Comprehensive Medical-Surgical Nursing
Table of contents
Use the chapter links below to move through the textbook.
Cardiovascular Disorders
Disorders of the heart and circulation commonly alter perfusion, oxygen delivery, preload, afterload and cardiac output. Nursing priorities centre on rapid assessment, haemodynamic stability, symptom control, medication safety, patient education and early recognition of deterioration.
Anatomy overview
The cardiovascular system consists of the heart, blood vessels and circulating blood. The heart is a four-chambered muscular pump. The right side receives systemic venous blood and delivers it to the lungs, while the left side receives oxygenated pulmonary venous blood and pumps it into the systemic circulation. Cardiac valves preserve one-way flow. Coronary arteries supply the myocardium, and the electrical conduction system coordinates atrial and ventricular contraction.
Physiology and clinical significance
Cardiac output is determined mainly by heart rate and stroke volume. Stroke volume is influenced by preload, contractility and afterload. Blood pressure reflects cardiac output and systemic vascular resistance. When these relationships are disturbed, patients may develop impaired perfusion, congestion, myocardial ischaemia, dysrhythmia or shock. Nursing assessment therefore connects symptoms such as chest pain, dyspnoea, oedema and syncope with perfusion and haemodynamic status.
Conditions in this chapter
Clinical condition
Hypertension
Pathophysiology
Sustained elevation of systemic vascular resistance and/or circulating volume increases arterial pressure and progressively stresses vascular endothelium and target organs. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include ageing and family history; high dietary sodium intake; obesity and physical inactivity; diabetes, kidney disease and sleep apnoea; and tobacco and harmful alcohol use. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Frequently asymptomatic; severe elevations may cause headache, visual symptoms or neurological complaints; Assess cardiovascular risk factors, medication adherence and evidence of target-organ injury.
Assessment and diagnostic evaluation
Repeated accurate blood-pressure measurements, preferably with confirmation outside the clinic when appropriate; Basic evaluation commonly includes urinalysis, renal function, electrolytes, glucose/lipids and ECG based on clinical context.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Lifestyle and risk-factor management plus clinician-prescribed antihypertensive therapy selected for comorbidities and overall cardiovascular risk; Urgent treatment is required when marked hypertension is accompanied by acute target-organ injury.
Nursing management: applying the nursing process
Frequently asymptomatic; severe elevations may cause headache, visual symptoms or neurological complaints; Assess cardiovascular risk factors, medication adherence and evidence of target-organ injury; and Repeated accurate blood-pressure measurements, preferably with confirmation outside the clinic when appropriate.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Use correct cuff size and technique; trend readings rather than relying on a single value.
- Monitor for dizziness, orthostatic symptoms, electrolyte or renal changes when relevant to treatment.
- Teach adherence, reduced dietary sodium, activity appropriate to health status, smoking avoidance and follow-up.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially ageing and family history, high dietary sodium intake, obesity and physical inactivity.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Coronary Artery Disease and Stable Angina
Pathophysiology
Atherosclerotic plaque narrows coronary arteries so myocardial oxygen demand can exceed supply, particularly during exertion or emotional stress. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include hypertension; dyslipidaemia; diabetes mellitus; tobacco exposure; and age, family history and chronic kidney disease. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Pressure, heaviness or tightness in the chest may be triggered by exertion and relieved by rest or prescribed anti-anginal therapy; Associated dyspnoea, fatigue or reduced exercise tolerance may occur.
Assessment and diagnostic evaluation
Clinical history and ECG; functional or anatomical cardiac testing may be used according to risk and local protocols; Assess lipid profile, diabetes risk and other modifiable cardiovascular factors.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Risk-factor modification and guideline-directed anti-ischaemic and antiplatelet/lipid-lowering therapy when prescribed; Revascularisation may be considered when symptoms remain limiting or anatomy confers higher risk.
Nursing management: applying the nursing process
Pressure, heaviness or tightness in the chest may be triggered by exertion and relieved by rest or prescribed anti-anginal therapy; Associated dyspnoea, fatigue or reduced exercise tolerance may occur; and Clinical history and ECG; functional or anatomical cardiac testing may be used according to risk and local protocols.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Characterise pain using onset, provocation, quality, radiation, severity and timing.
- Monitor vital signs and response to prescribed therapy; reinforce recognition of pain that is new, prolonged or occurs at rest.
- Support graded activity, medication adherence and risk-factor control.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially hypertension, dyslipidaemia, diabetes mellitus.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Acute Coronary Syndrome / Myocardial Infarction
Pathophysiology
Plaque disruption with acute thrombosis can abruptly reduce coronary blood flow; persistent ischaemia causes irreversible myocardial cell injury. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include established atherosclerotic disease; smoking; hypertension and dyslipidaemia; diabetes; and advanced age and chronic kidney disease. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
New, severe or prolonged chest discomfort, dyspnoea, sweating, nausea, weakness or atypical symptoms in some patients; Haemodynamic instability, pulmonary congestion or arrhythmias indicate greater severity.
Assessment and diagnostic evaluation
Immediate 12-lead ECG and serial cardiac biomarkers are central; additional imaging and coronary evaluation depend on presentation; Continuous rhythm and vital-sign monitoring are usually required in the acute phase.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Time-sensitive antithrombotic, anti-ischaemic and reperfusion strategies are selected by the clinical team according to ACS type and contraindications; Treat complications such as arrhythmia, heart failure or shock promptly.
Nursing management: applying the nursing process
New, severe or prolonged chest discomfort, dyspnoea, sweating, nausea, weakness or atypical symptoms in some patients; Haemodynamic instability, pulmonary congestion or arrhythmias indicate greater severity; and Immediate 12-lead ECG and serial cardiac biomarkers are central; additional imaging and coronary evaluation depend on presentation.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Prioritise ABC assessment, rest, continuous monitoring, IV access and rapid escalation of recurrent pain or instability.
- Administer prescribed medicines safely and observe for bleeding, hypotension, bradycardia or allergic reactions.
- Begin secondary-prevention education once stable, including cardiac rehabilitation and symptom recognition.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially established atherosclerotic disease, smoking, hypertension and dyslipidaemia.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Heart Failure
Pathophysiology
Impaired ventricular filling or ejection activates neurohormonal responses that initially support circulation but ultimately promote sodium retention, vasoconstriction and congestion. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include coronary artery disease or previous infarction; long-standing hypertension; valvular disease; cardiomyopathy; and arrhythmia and cardiotoxic exposure. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Dyspnoea, orthopnoea, fatigue, peripheral oedema, weight gain, raised jugular venous pressure and pulmonary crackles may occur; Acute decompensation can present with severe breathlessness, hypoxaemia or poor perfusion.
Assessment and diagnostic evaluation
Clinical examination, natriuretic peptides where available, ECG, chest imaging and echocardiography to define structure and ejection fraction; Renal function and electrolytes guide treatment safety.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Guideline-directed heart-failure therapy, diuresis for congestion and treatment of precipitating factors such as ischaemia, arrhythmia or infection; Selected patients may need devices or advanced therapies.
Nursing management: applying the nursing process
Dyspnoea, orthopnoea, fatigue, peripheral oedema, weight gain, raised jugular venous pressure and pulmonary crackles may occur; Acute decompensation can present with severe breathlessness, hypoxaemia or poor perfusion; and Clinical examination, natriuretic peptides where available, ECG, chest imaging and echocardiography to define structure and ejection fraction.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Record daily weight, intake/output, oedema, lung sounds, oxygenation and exercise tolerance.
- Monitor renal function, potassium, blood pressure and symptoms during diuresis and chronic therapy.
- Teach fluid/sodium guidance if prescribed, medication adherence, daily weight tracking and early reporting of worsening symptoms.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially coronary artery disease or previous infarction, long-standing hypertension, valvular disease.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Atrial Fibrillation
Pathophysiology
Chaotic atrial electrical activity prevents organised atrial contraction, produces an irregular ventricular rhythm and permits blood stasis that can promote atrial thrombus formation. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include increasing age; hypertension; heart failure or valve disease; thyroid disease; and obesity, sleep apnoea and alcohol excess. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Palpitations, fatigue, dyspnoea, dizziness or no symptoms; pulse is typically irregularly irregular; New neurological deficits may indicate embolic stroke.
Assessment and diagnostic evaluation
ECG confirms the rhythm; evaluate reversible triggers, thyroid status, electrolytes and structural heart disease as appropriate; Stroke and bleeding risk are assessed when considering anticoagulation.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Management may include ventricular rate control, rhythm-control strategies and anticoagulation based on individual risk; Urgent electrical cardioversion may be used for haemodynamic instability under expert care.
Nursing management: applying the nursing process
Palpitations, fatigue, dyspnoea, dizziness or no symptoms; pulse is typically irregularly irregular; New neurological deficits may indicate embolic stroke; and ECG confirms the rhythm; evaluate reversible triggers, thyroid status, electrolytes and structural heart disease as appropriate.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Monitor rhythm, pulse, blood pressure and symptoms; assess for heart failure or poor perfusion.
- If anticoagulated, reinforce bleeding precautions and adherence without altering therapy independently.
- Teach pulse awareness and urgent recognition of stroke symptoms.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially increasing age, hypertension, heart failure or valve disease.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Valvular Heart Disease
Pathophysiology
Valve stenosis creates pressure overload while regurgitation produces volume overload; chronic chamber remodelling can eventually impair cardiac output. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include degenerative calcification; rheumatic heart disease; congenital abnormalities; infective endocarditis; and connective-tissue or aortic disease. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Murmur, exertional dyspnoea, fatigue, syncope, chest pain, palpitations or signs of heart failure depending on valve and severity; Symptoms may develop gradually despite significant structural disease.
Assessment and diagnostic evaluation
Echocardiography is the main test for valve anatomy and haemodynamic severity; ECG, chest imaging and exercise testing may support evaluation.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Treat congestion, arrhythmias and associated cardiovascular conditions; definitive therapy may require valve repair or replacement; Anticoagulation is necessary in selected patients, especially with certain prosthetic valves or atrial fibrillation.
Nursing management: applying the nursing process
Murmur, exertional dyspnoea, fatigue, syncope, chest pain, palpitations or signs of heart failure depending on valve and severity; Symptoms may develop gradually despite significant structural disease; and Echocardiography is the main test for valve anatomy and haemodynamic severity.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Monitor for reduced exercise tolerance, fluid overload, arrhythmia and syncope.
- After valve procedures, monitor wound/vascular sites, rhythm, perfusion and infection signs according to protocol.
- Educate about follow-up, prescribed anticoagulation and when to seek urgent care.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially degenerative calcification, rheumatic heart disease, congenital abnormalities.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Infective Endocarditis
Pathophysiology
Microorganisms adhere to damaged endocardial surfaces or prosthetic material, forming infected vegetations that can damage valves and embolise. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include prosthetic valves or previous endocarditis; certain congenital heart lesions; intravascular devices; poor dentition or invasive infection sources; and injection drug use in adults. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Persistent fever, malaise, new or changing murmur and signs of systemic infection; embolic manifestations may occur; Risk is increased with some prosthetic valves, prior endocarditis and certain cardiac lesions or intravascular infections.
Assessment and diagnostic evaluation
Multiple blood cultures before antibiotics when feasible and echocardiography are central to diagnosis; Inflammatory markers, full blood count and organ-function tests help assess severity.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Prolonged targeted antimicrobial therapy is guided by cultures and specialist advice; Surgery may be required for heart failure, uncontrolled infection or selected high-risk complications.
Nursing management: applying the nursing process
Persistent fever, malaise, new or changing murmur and signs of systemic infection; embolic manifestations may occur; Risk is increased with some prosthetic valves, prior endocarditis and certain cardiac lesions or intravascular infections; and Multiple blood cultures before antibiotics when feasible and echocardiography are central to diagnosis.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Obtain cultures using strict aseptic technique when ordered; monitor temperature, haemodynamics and neurological status.
- Observe vascular access sites and administer antimicrobial therapy on schedule as prescribed.
- Reinforce oral hygiene, follow-up and individual preventive guidance.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially prosthetic valves or previous endocarditis, certain congenital heart lesions, intravascular devices.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Chapter summary
This chapter links system physiology with assessment and nursing priorities. The major conditions discussed include Hypertension, Coronary Artery Disease and Stable Angina, Acute Coronary Syndrome / Myocardial Infarction, Heart Failure, Atrial Fibrillation, Valvular Heart Disease, Infective Endocarditis. Across these disorders, safe care depends on recognising physiological instability, obtaining focused assessment data, administering prescribed treatment safely, preventing avoidable complications, supporting function and teaching the patient how to monitor for deterioration.
- Hypertension: Persistent elevation of arterial blood pressure that increases cardiac, cerebral, renal and vascular risk, often without symptoms.
- Coronary Artery Disease and Stable Angina: Atherosclerotic narrowing of coronary arteries can produce predictable myocardial ischaemia during exertion or stress.
- Acute Coronary Syndrome / Myocardial Infarction: Acute reduction of coronary blood flow causes myocardial ischaemia; prolonged occlusion can result in myocardial necrosis.
- Heart Failure: A syndrome in which the heart cannot meet the body's metabolic demands without elevated filling pressures, causing congestion and/or low output.
- Atrial Fibrillation: A supraventricular tachyarrhythmia with disorganised atrial electrical activity, irregular ventricular response and increased thromboembolic risk.
Self-review questions
Open each item after attempting an answer yourself.
1. Why can heart failure cause peripheral oedema?
Answer: Raised venous pressures and sodium/water retention increase hydrostatic pressure and promote fluid movement into interstitial tissues.
2. What two tests are central early in suspected acute coronary syndrome?
Answer: A 12-lead ECG and serial cardiac biomarkers, interpreted in the clinical context.
3. Why is atrial fibrillation associated with stroke?
Answer: Loss of organised atrial contraction encourages blood stasis and thrombus formation, which may embolise to the brain.
4. Name three observations important during diuresis in heart failure.
Answer: Weight, fluid balance/urine output, blood pressure, renal function, electrolytes and symptoms are all important.
5. What makes hypertensive emergency different from severe asymptomatic hypertension?
Answer: Acute target-organ injury is present in hypertensive emergency.
Respiratory Disorders
Respiratory illness can impair ventilation, diffusion, perfusion or airway patency. Nursing care focuses on airway assessment, work of breathing, oxygenation, positioning, secretion management, infection control and rapid escalation when gas exchange deteriorates.
Anatomy overview
The respiratory tract extends from the nose and upper airway to the tracheobronchial tree and alveoli. The lungs are enclosed by visceral and parietal pleura. Air reaches the gas-exchanging alveoli through progressively smaller conducting airways, while pulmonary capillaries bring deoxygenated blood into close contact with the alveolar membrane.
Physiology and clinical significance
Effective respiration requires ventilation, diffusion and perfusion. Ventilation moves air, diffusion transfers oxygen and carbon dioxide across the alveolar-capillary membrane, and perfusion carries blood through the pulmonary circulation. Airway narrowing, alveolar filling, loss of elastic recoil, pleural air or fluid, and vascular obstruction can each produce distinct patterns of hypoxaemia and respiratory distress.
Conditions in this chapter
Clinical condition
Asthma
Pathophysiology
Airway inflammation and hyper-responsiveness cause variable bronchoconstriction, mucosal oedema and mucus production, producing reversible airflow limitation. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include personal or family atopy; allergen exposure; viral respiratory infections; occupational sensitising agents; and smoke and air pollution. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Episodic wheeze, cough, chest tightness and breathlessness, often varying over time and with triggers; Severe attacks may produce difficulty speaking, exhaustion, reduced air entry or altered consciousness.
Assessment and diagnostic evaluation
History plus variable expiratory airflow limitation demonstrated by spirometry/peak flow when feasible; Assess trigger pattern, inhaler technique, symptom frequency and previous severe exacerbations.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Controller therapy is based on inhaled anti-inflammatory treatment, with reliever therapy and escalation according to control and risk; Acute severe exacerbations require prompt bronchodilation, systemic anti-inflammatory therapy and oxygen/advanced support as indicated.
Nursing management: applying the nursing process
Episodic wheeze, cough, chest tightness and breathlessness, often varying over time and with triggers; Severe attacks may produce difficulty speaking, exhaustion, reduced air entry or altered consciousness; and History plus variable expiratory airflow limitation demonstrated by spirometry/peak flow when feasible.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Assess respiratory rate, accessory-muscle use, speech, peak flow if appropriate and oxygen saturation.
- Position upright, administer prescribed inhaled therapies correctly and reassess response.
- Teach spacer/inhaler technique, adherence, trigger reduction and use of an individual action plan.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially personal or family atopy, allergen exposure, viral respiratory infections.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Chronic Obstructive Pulmonary Disease (COPD)
Pathophysiology
Chronic airway inflammation and/or alveolar destruction causes persistent expiratory airflow limitation, air trapping and impaired gas exchange. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include tobacco smoke; biomass or occupational exposure; air pollution; recurrent respiratory injury; and alpha-1 antitrypsin deficiency. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Progressive exertional dyspnoea, chronic cough, sputum production, wheeze and reduced exercise tolerance; Exacerbations present with increased breathlessness, cough or sputum change.
Assessment and diagnostic evaluation
Post-bronchodilator spirometry confirms persistent airflow obstruction; Assess smoking/biomass exposure, exacerbation history, nutrition, oxygenation and functional limitation.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Smoking cessation and inhaled bronchodilator-based therapy form the foundation; selected patients benefit from inhaled anti-inflammatory therapy, vaccination, pulmonary rehabilitation or long-term oxygen; Exacerbations may require short-acting bronchodilators, systemic anti-inflammatory treatment, antimicrobials when indicated and ventilatory support.
Nursing management: applying the nursing process
Progressive exertional dyspnoea, chronic cough, sputum production, wheeze and reduced exercise tolerance; Exacerbations present with increased breathlessness, cough or sputum change; and Post-bronchodilator spirometry confirms persistent airflow obstruction.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Monitor breathing pattern, sputum, oxygenation, fatigue and nutrition/hydration.
- Teach pursed-lip breathing, energy conservation and correct inhaler use.
- For patients at risk of carbon-dioxide retention, oxygen is titrated to the prescribed target rather than given without monitoring.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially tobacco smoke, biomass or occupational exposure, air pollution.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Pneumonia
Pathophysiology
Infection triggers inflammation and fluid/cellular exudate within alveoli, reducing effective ventilation of affected lung regions. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include older age or frailty; chronic lung or cardiac disease; aspiration risk; immunosuppression; and recent viral infection or healthcare exposure. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Fever, cough, sputum, pleuritic chest pain, tachypnoea and dyspnoea; older or frail patients may present atypically; Severe disease may cause hypoxaemia, hypotension or confusion.
Assessment and diagnostic evaluation
Clinical assessment with chest imaging; microbiological tests are selected according to severity and setting; Assess oxygenation, hydration, renal function and sepsis indicators.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Appropriate antimicrobial therapy for suspected bacterial infection, supportive care and treatment of hypoxaemia or sepsis; Hospitalisation level is guided by severity and comorbidities.
Nursing management: applying the nursing process
Fever, cough, sputum, pleuritic chest pain, tachypnoea and dyspnoea; older or frail patients may present atypically; Severe disease may cause hypoxaemia, hypotension or confusion; and Clinical assessment with chest imaging; microbiological tests are selected according to severity and setting.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Monitor vital signs, respiratory effort, mental status and oxygen saturation.
- Promote upright positioning, hydration if appropriate, coughing/deep breathing and mobilisation as tolerated.
- Administer antimicrobials on time and watch for clinical deterioration or treatment adverse effects.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially older age or frailty, chronic lung or cardiac disease, aspiration risk.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Pulmonary Tuberculosis
Pathophysiology
Mycobacterium tuberculosis induces a cell-mediated immune response with granuloma formation; active disease can destroy lung tissue and spread by airborne droplets. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include close exposure to infectious TB; HIV or other immunosuppression; undernutrition; crowded living conditions; and diabetes and tobacco exposure. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Persistent cough, fever, night sweats, weight loss, fatigue and sometimes haemoptysis; Symptoms can be subtle, so exposure history and local epidemiology matter.
Assessment and diagnostic evaluation
Sputum molecular testing and/or microscopy/culture with chest imaging according to national TB protocols; Evaluate HIV status and other risk factors using appropriate consent and local guidance.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Combination anti-tuberculosis therapy is given for a defined course under national programme guidance; drug susceptibility influences regimen choice; Public-health contact evaluation and infection-control measures are important.
Nursing management: applying the nursing process
Persistent cough, fever, night sweats, weight loss, fatigue and sometimes haemoptysis; Symptoms can be subtle, so exposure history and local epidemiology matter; and Sputum molecular testing and/or microscopy/culture with chest imaging according to national TB protocols.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Implement airborne precautions in healthcare settings when infectious pulmonary TB is suspected.
- Support adherence, monitor for medication toxicity as directed and reinforce scheduled follow-up.
- Provide respectful education on cough hygiene, ventilation and reducing transmission without stigma.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially close exposure to infectious TB, HIV or other immunosuppression, undernutrition.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Pleural Effusion
Pathophysiology
Excess fluid accumulates between visceral and parietal pleura, compressing adjacent lung and restricting expansion. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include heart failure; infection; malignancy; liver or kidney disease; and pulmonary embolism. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Dyspnoea, pleuritic discomfort, reduced chest expansion, dullness to percussion and diminished breath sounds on the affected side; Large effusions can significantly impair ventilation.
Assessment and diagnostic evaluation
Chest radiograph and ultrasound identify fluid; diagnostic thoracentesis is often used when the cause is uncertain; Pleural fluid analysis helps distinguish transudative from exudative processes.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Treat the underlying cause; therapeutic drainage may be needed for large symptomatic effusions; Infected collections may require antibiotics and tube drainage.
Nursing management: applying the nursing process
Dyspnoea, pleuritic discomfort, reduced chest expansion, dullness to percussion and diminished breath sounds on the affected side; Large effusions can significantly impair ventilation; and Chest radiograph and ultrasound identify fluid; diagnostic thoracentesis is often used when the cause is uncertain.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Monitor respiratory status before and after drainage procedures and observe puncture/drain sites.
- Maintain prescribed chest-drain system position and document output when present.
- Escalate sudden dyspnoea, chest pain, hypotension or reduced breath sounds after a procedure.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially heart failure, infection, malignancy.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Pneumothorax
Pathophysiology
Air in the pleural space abolishes the normal negative pressure that keeps the lung expanded, allowing partial or complete lung collapse. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include underlying lung disease; smoking; chest trauma or procedures; tall thin body habitus in primary spontaneous cases; and positive-pressure ventilation. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Sudden unilateral pleuritic pain, dyspnoea and reduced breath sounds; severe cases may cause hypoxaemia and haemodynamic instability; Tension physiology can produce profound distress and shock.
Assessment and diagnostic evaluation
Clinical assessment plus chest imaging when the patient is stable; unstable tension pneumothorax is treated as a clinical emergency without delaying for imaging; Ultrasound may assist rapid bedside assessment where available.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Management ranges from observation in selected small stable cases to pleural drainage; tension pneumothorax requires emergency decompression by trained clinicians; Treat the precipitating cause and prevent recurrence when indicated.
Nursing management: applying the nursing process
Sudden unilateral pleuritic pain, dyspnoea and reduced breath sounds; severe cases may cause hypoxaemia and haemodynamic instability; Tension physiology can produce profound distress and shock; and Clinical assessment plus chest imaging when the patient is stable; unstable tension pneumothorax is treated as a clinical emergency without delaying for imaging.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Provide rapid ABC assessment, prescribed oxygen and continuous observation for worsening distress.
- With a chest drain, keep the system below chest level, check connections and document bubbling/swinging and drainage according to local policy.
- Do not clamp a chest tube routinely unless specifically directed by a competent clinician/protocol.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially underlying lung disease, smoking, chest trauma or procedures.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Pulmonary Embolism
Pathophysiology
A thrombus—most often originating in deep veins—lodges in the pulmonary arterial circulation, creating abrupt vascular obstruction and V/Q mismatch. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include recent surgery or immobility; active cancer; previous venous thromboembolism; pregnancy/postpartum or oestrogen exposure; and inherited/acquired thrombophilia. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Sudden dyspnoea, pleuritic chest pain, tachycardia, hypoxaemia, syncope or haemoptysis; massive PE can present with shock; Symptoms may be nonspecific, so risk-factor assessment is important.
Assessment and diagnostic evaluation
Clinical probability tools and D-dimer testing guide imaging in appropriate patients; CT pulmonary angiography is commonly used when imaging is required; ECG, biomarkers and echocardiography help risk-stratify more severe cases.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Anticoagulation is the main treatment when not contraindicated; unstable high-risk PE may require reperfusion therapy by specialist teams; Treat hypoxaemia and circulatory compromise supportively.
Nursing management: applying the nursing process
Sudden dyspnoea, pleuritic chest pain, tachycardia, hypoxaemia, syncope or haemoptysis; massive PE can present with shock; Symptoms may be nonspecific, so risk-factor assessment is important; and Clinical probability tools and D-dimer testing guide imaging in appropriate patients; CT pulmonary angiography is commonly used when imaging is required.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Monitor oxygenation, respiratory rate, pain, heart rate and blood pressure closely.
- Administer anticoagulants safely as prescribed and observe for bleeding.
- Educate about adherence, warning signs of bleeding/recurrent thrombosis and mobility measures after stabilisation.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially recent surgery or immobility, active cancer, previous venous thromboembolism.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Chapter summary
This chapter links system physiology with assessment and nursing priorities. The major conditions discussed include Asthma, Chronic Obstructive Pulmonary Disease (COPD), Pneumonia, Pulmonary Tuberculosis, Pleural Effusion, Pneumothorax, Pulmonary Embolism. Across these disorders, safe care depends on recognising physiological instability, obtaining focused assessment data, administering prescribed treatment safely, preventing avoidable complications, supporting function and teaching the patient how to monitor for deterioration.
- Asthma: A chronic inflammatory airway disorder characterised by variable airflow obstruction and bronchial hyper-responsiveness.
- Chronic Obstructive Pulmonary Disease (COPD): Persistent airflow limitation, usually due to emphysema and/or chronic bronchitis, associated with chronic airway inflammation and structural lung damage.
- Pneumonia: Infection and inflammation of lung parenchyma cause alveolar filling, impaired gas exchange and systemic inflammatory response.
- Pulmonary Tuberculosis: Tuberculosis is an airborne infection caused by Mycobacterium tuberculosis, most often affecting the lungs but capable of involving many organs.
- Pleural Effusion: Excess fluid accumulates in the pleural space because of heart failure, infection, malignancy, inflammation or other causes.
Self-review questions
Open each item after attempting an answer yourself.
1. What are the three linked processes required for effective gas exchange?
Answer: Ventilation, diffusion and perfusion.
2. Why can pneumothorax impair ventilation?
Answer: Air in the pleural space reduces the negative pressure that normally keeps the lung expanded.
3. What clinical change may make severe asthma especially concerning?
Answer: A very quiet chest or reduced air entry in a distressed patient can indicate critically low airflow.
4. Why is pulmonary embolism a V/Q problem?
Answer: Ventilated lung may lose blood flow because an embolus obstructs pulmonary perfusion.
5. What should respiratory nursing assessment trend over time?
Answer: Work of breathing, respiratory rate, oxygenation, breath sounds, sputum, mental state and response to therapy.
Neurological Disorders
Neurological disorders can change consciousness, motor function, sensation, speech, swallowing and autonomic control. Nursing assessment depends on careful neurological observation, airway protection, aspiration prevention, pressure-injury prevention, mobility support and recognition of sudden change.
Anatomy overview
The nervous system comprises the brain, spinal cord, peripheral nerves and autonomic pathways. The cerebral hemispheres support higher function, sensation and voluntary movement; the brainstem controls vital functions and cranial nerve activity; the cerebellum coordinates balance and movement. The meninges and cerebrospinal fluid protect the central nervous system within the rigid skull and vertebral canal.
Physiology and clinical significance
Neurones communicate by electrical impulses and chemical neurotransmitters. Cerebral function depends on uninterrupted oxygen and glucose delivery. Because the skull cannot expand significantly, oedema or bleeding can raise intracranial pressure and reduce cerebral perfusion. Neurological nursing therefore relies on repeated observations for changes in consciousness, pupils, motor function, speech, swallowing, sensation and respiratory pattern.
Conditions in this chapter
Clinical condition
Acute Ischaemic Stroke
Pathophysiology
Arterial occlusion deprives a region of brain tissue of oxygen and glucose, creating an infarct core surrounded by potentially salvageable ischaemic tissue. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include hypertension; atrial fibrillation; diabetes and dyslipidaemia; tobacco use; and carotid or other vascular disease. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Sudden facial weakness, arm weakness, speech difficulty, visual loss, imbalance or other focal deficits; Time last known well is essential because reperfusion treatments are time-dependent.
Assessment and diagnostic evaluation
Immediate brain imaging distinguishes haemorrhage from ischaemia; vascular imaging and laboratory tests guide treatment; Use a structured stroke scale and assess glucose because hypoglycaemia can mimic stroke.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Eligible patients may receive reperfusion therapy, including thrombolysis and/or mechanical thrombectomy, according to specialist criteria; Secondary prevention targets antithrombotic therapy, risk factors and the identified cause.
Nursing management: applying the nursing process
Sudden facial weakness, arm weakness, speech difficulty, visual loss, imbalance or other focal deficits; Time last known well is essential because reperfusion treatments are time-dependent; and Immediate brain imaging distinguishes haemorrhage from ischaemia; vascular imaging and laboratory tests guide treatment.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Activate the stroke pathway immediately; maintain airway, oxygenation and frequent neurological observations.
- Keep the patient nil by mouth until a swallow screen is completed; use aspiration precautions.
- Support early mobilisation and rehabilitation once medically stable, with communication and pressure-area care.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially hypertension, atrial fibrillation, diabetes and dyslipidaemia.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Epilepsy and Seizures
Pathophysiology
Abnormal synchronous neuronal electrical activity produces transient neurological events that vary according to the brain region involved. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include genetic predisposition; previous brain injury or stroke; central nervous system infection; brain tumour or structural lesion; and metabolic disturbance. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Episodes may involve altered awareness, focal motor/sensory symptoms or generalised convulsions; Postictal confusion, fatigue or transient neurological deficits can follow.
Assessment and diagnostic evaluation
Detailed witness history, neurological assessment and EEG; MRI or other imaging is used in selected patients; Check metabolic or toxic triggers when an acute symptomatic seizure is suspected.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Antiseizure medicine is selected according to seizure type, comorbidities and patient factors; Prolonged or repeated seizures without recovery require emergency treatment by trained clinicians.
Nursing management: applying the nursing process
Episodes may involve altered awareness, focal motor/sensory symptoms or generalised convulsions; Postictal confusion, fatigue or transient neurological deficits can follow; and Detailed witness history, neurological assessment and EEG; MRI or other imaging is used in selected patients.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- During a convulsive seizure, protect from injury, clear nearby hazards, support the airway and time the event; do not forcibly restrain or place objects in the mouth.
- Afterwards place the patient in a safe recovery position when appropriate and reassess breathing and consciousness.
- Teach adherence, sleep regularity, seizure first aid and individual safety advice.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially genetic predisposition, previous brain injury or stroke, central nervous system infection.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Meningitis
Pathophysiology
Inflammation of the meninges and cerebrospinal fluid can cause cerebral oedema, raised intracranial pressure and systemic inflammatory complications. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include close-contact exposure to transmissible pathogens; immunosuppression; CSF leak or neurosurgery; extremes of age; and incomplete vaccination depending on organism. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Fever, severe headache, neck stiffness, photophobia, vomiting or altered mental state; rash may occur in meningococcal disease; Infants, older adults and immunocompromised patients may present atypically.
Assessment and diagnostic evaluation
Blood cultures and lumbar puncture when safe, with cerebrospinal-fluid analysis; neuroimaging is used before LP in selected patients; Do not delay urgent treatment when bacterial meningitis is strongly suspected.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Prompt empiric antimicrobial therapy tailored to age/risk and local guidance, then targeted to results; Adjunctive therapy and intensive support may be required for severe disease.
Nursing management: applying the nursing process
Fever, severe headache, neck stiffness, photophobia, vomiting or altered mental state; rash may occur in meningococcal disease; Infants, older adults and immunocompromised patients may present atypically; and Blood cultures and lumbar puncture when safe, with cerebrospinal-fluid analysis; neuroimaging is used before LP in selected patients.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Apply appropriate infection precautions based on suspected organism and local policy.
- Perform frequent neurological observations and monitor temperature, perfusion, urine output and seizures.
- Reduce environmental stimuli when photophobia/headache is severe and support family communication.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially close-contact exposure to transmissible pathogens, immunosuppression, CSF leak or neurosurgery.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Parkinson Disease
Pathophysiology
Progressive loss of dopaminergic neurones in the substantia nigra disrupts basal ganglia circuits responsible for smooth initiation and control of movement. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include increasing age; family/genetic susceptibility; male sex; certain environmental exposures; and history of specific parkinsonian syndromes. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Slowness of movement, resting tremor, rigidity, shuffling gait, reduced facial expression and non-motor symptoms such as constipation or sleep disturbance; Swallowing and communication may become impaired later.
Assessment and diagnostic evaluation
Primarily clinical neurological diagnosis; imaging may exclude alternative causes; Response to dopaminergic therapy can support diagnosis but is not the only criterion.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Treatment is individualised and may include dopaminergic medicines, rehabilitation and selected advanced device/surgical approaches; Non-motor symptoms are treated specifically.
Nursing management: applying the nursing process
Slowness of movement, resting tremor, rigidity, shuffling gait, reduced facial expression and non-motor symptoms such as constipation or sleep disturbance; Swallowing and communication may become impaired later; and Primarily clinical neurological diagnosis; imaging may exclude alternative causes.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Give time-critical Parkinson medicines exactly as scheduled in hospital unless changed by the prescriber.
- Assess falls risk, swallowing, constipation, communication and activities of daily living.
- Encourage physiotherapy, cueing strategies, safe mobility and medication education.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially increasing age, family/genetic susceptibility, male sex.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Multiple Sclerosis
Pathophysiology
Immune-mediated inflammation damages central nervous system myelin and axons, causing lesions disseminated in time and anatomical location. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include young adult age; female sex; genetic susceptibility; low vitamin D / limited sunlight association; and smoking and previous EBV infection association. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Visual symptoms, limb weakness, sensory change, ataxia, bladder dysfunction, fatigue or cognitive symptoms may occur in episodes or progression; Heat and fatigue can transiently worsen symptoms.
Assessment and diagnostic evaluation
MRI is central; cerebrospinal-fluid analysis and evoked potentials may support diagnosis; Exclude alternative inflammatory, infectious and metabolic conditions.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Acute relapses may be treated with clinician-directed anti-inflammatory therapy; disease-modifying therapies reduce relapse/activity in appropriate patients; Symptom-specific treatment and rehabilitation are important.
Nursing management: applying the nursing process
Visual symptoms, limb weakness, sensory change, ataxia, bladder dysfunction, fatigue or cognitive symptoms may occur in episodes or progression; Heat and fatigue can transiently worsen symptoms; and MRI is central; cerebrospinal-fluid analysis and evoked potentials may support diagnosis.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Assess mobility, fatigue, bladder/bowel function, vision, pain and mood.
- Plan care to conserve energy while preserving independence and activity.
- Teach infection awareness and monitoring relevant to prescribed disease-modifying therapy.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially young adult age, female sex, genetic susceptibility.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Guillain–Barré Syndrome
Pathophysiology
An acute immune-mediated peripheral neuropathy damages myelin or axons, producing rapidly progressive weakness and possible autonomic or respiratory dysfunction. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include recent gastrointestinal or respiratory infection; Campylobacter infection; some viral illnesses; rare post-surgical or immune triggers; and history of prior GBS warrants individual vaccine discussion. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Symmetric progressive weakness, tingling, reduced reflexes, facial/bulbar weakness and autonomic instability; Respiratory muscles may weaken rapidly.
Assessment and diagnostic evaluation
Clinical pattern supported by nerve-conduction studies and cerebrospinal-fluid findings; Serial respiratory measurements and cardiac monitoring are crucial in moderate-to-severe disease.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Intravenous immunoglobulin or plasma exchange are standard disease-modifying treatments in appropriate patients; Ventilatory and autonomic support may be needed.
Nursing management: applying the nursing process
Symmetric progressive weakness, tingling, reduced reflexes, facial/bulbar weakness and autonomic instability; Respiratory muscles may weaken rapidly; and Clinical pattern supported by nerve-conduction studies and cerebrospinal-fluid findings.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Closely monitor respiratory effort, cough strength, swallowing, vital capacity where ordered and autonomic changes.
- Use DVT prevention, pressure-area care, pain management and passive/active rehabilitation as tolerated.
- Provide communication support for patients with severe weakness while preserving autonomy.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially recent gastrointestinal or respiratory infection, Campylobacter infection, some viral illnesses.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Traumatic Brain Injury and Raised Intracranial Pressure
Pathophysiology
Primary mechanical injury may be followed by oedema, bleeding and impaired cerebral perfusion; rising intracranial pressure can further compromise brain tissue. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include falls; road traffic injury; sports or occupational trauma; anticoagulation increasing bleeding risk; and intracranial haemorrhage or cerebral oedema. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Headache, vomiting, confusion, reduced consciousness, focal deficits, seizures or unequal pupils can occur; Deteriorating consciousness is an emergency sign.
Assessment and diagnostic evaluation
Serial Glasgow Coma Scale/neurological assessment and urgent CT imaging according to clinical criteria; Assess for other trauma and maintain cervical-spine precautions until cleared when indicated.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Management focuses on preventing secondary brain injury, treating intracranial bleeding/oedema and neurosurgical intervention when required; Ventilation, haemodynamic support and seizure management are individualised in severe TBI.
Nursing management: applying the nursing process
Headache, vomiting, confusion, reduced consciousness, focal deficits, seizures or unequal pupils can occur; Deteriorating consciousness is an emergency sign; and Serial Glasgow Coma Scale/neurological assessment and urgent CT imaging according to clinical criteria.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Prioritise airway and oxygenation; perform frequent neurological observations and report any decline immediately.
- Keep head and neck aligned; elevate the head of bed when prescribed and not contraindicated.
- Avoid unnecessary stimulation, prevent fever and monitor fluid balance, glucose and seizure activity according to protocol.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially falls, road traffic injury, sports or occupational trauma.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Chapter summary
This chapter links system physiology with assessment and nursing priorities. The major conditions discussed include Acute Ischaemic Stroke, Epilepsy and Seizures, Meningitis, Parkinson Disease, Multiple Sclerosis, Guillain–Barré Syndrome, Traumatic Brain Injury and Raised Intracranial Pressure. Across these disorders, safe care depends on recognising physiological instability, obtaining focused assessment data, administering prescribed treatment safely, preventing avoidable complications, supporting function and teaching the patient how to monitor for deterioration.
- Acute Ischaemic Stroke: Abrupt interruption of cerebral blood flow causes focal neurological dysfunction and brain infarction unless perfusion is restored quickly.
- Epilepsy and Seizures: Epilepsy is a tendency to recurrent unprovoked seizures caused by abnormal synchronous neuronal activity; seizures vary by onset and manifestations.
- Meningitis: Inflammation of the meninges is commonly infectious and can progress rapidly to neurological injury, sepsis and death.
- Parkinson Disease: A progressive neurodegenerative disorder involving dopaminergic pathways, producing bradykinesia plus tremor, rigidity and postural instability.
- Multiple Sclerosis: An immune-mediated demyelinating disorder of the central nervous system characterised by neurological lesions separated in time and space.
Self-review questions
Open each item after attempting an answer yourself.
1. Why are repeated neurological observations important?
Answer: Trends can reveal evolving cerebral injury or raised intracranial pressure earlier than a single examination.
2. What time detail is crucial in acute stroke?
Answer: The time the patient was last known well.
3. Why is swallowing assessment important after stroke?
Answer: Dysphagia raises the risk of aspiration, pneumonia and inadequate nutrition.
4. What major function must be watched closely in Guillain–Barré syndrome?
Answer: Respiratory muscle function, together with autonomic status.
5. Why can intracranial pressure rise after head injury?
Answer: Bleeding and oedema increase intracranial volume within the fixed skull.
Gastrointestinal & Hepatobiliary Disorders
Gastrointestinal and hepatobiliary disorders may affect digestion, absorption, elimination, fluid balance and metabolic function. Nursing care emphasises pain assessment, hydration, nutrition, bleeding surveillance, bowel function, infection prevention and peri-operative support where indicated.
Anatomy overview
The gastrointestinal tract extends from the mouth through the oesophagus, stomach, small intestine, colon, rectum and anus. Accessory organs—the liver, gallbladder and pancreas—support digestion through bile production, nutrient processing and digestive enzymes. The mucosa provides a large absorptive surface and also forms an important immune and barrier interface.
Physiology and clinical significance
Digestion depends on motility, secretion, enzymatic breakdown, absorption and coordinated elimination. The liver regulates metabolism, detoxification, protein synthesis and bile formation. Disruption may present as pain, reflux, vomiting, bleeding, obstruction, malabsorption, jaundice or altered bowel habit. Fluid balance can deteriorate rapidly when vomiting, diarrhoea, haemorrhage or third-spacing occurs.
Conditions in this chapter
Clinical condition
Gastro-oesophageal Reflux Disease (GORD/GERD)
Pathophysiology
Incompetence or inappropriate relaxation of the lower oesophageal sphincter permits gastric contents to reflux and irritate oesophageal mucosa. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include obesity; pregnancy; hiatal hernia; large/fatty meals or late eating; and medicines that reduce lower oesophageal sphincter tone. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Heartburn, acid regurgitation, chest discomfort and sometimes chronic cough or hoarseness; Alarm features include dysphagia, gastrointestinal bleeding, unexplained anaemia or persistent vomiting.
Assessment and diagnostic evaluation
Often clinical; endoscopy or reflux testing is used for alarm features, refractory symptoms or diagnostic uncertainty; Review medicine and lifestyle contributors.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Lifestyle measures and acid-suppressive treatment are commonly used; selected refractory cases may require anti-reflux procedures; Treat complications such as strictures or Barrett oesophagus according to specialist care.
Nursing management: applying the nursing process
Heartburn, acid regurgitation, chest discomfort and sometimes chronic cough or hoarseness; Alarm features include dysphagia, gastrointestinal bleeding, unexplained anaemia or persistent vomiting; and Often clinical; endoscopy or reflux testing is used for alarm features, refractory symptoms or diagnostic uncertainty.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Teach smaller meals if helpful, avoidance of lying down soon after eating and trigger identification.
- Support adherence to prescribed acid-suppressive therapy and monitor response.
- Escalate alarm symptoms for medical evaluation.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially obesity, pregnancy, hiatal hernia.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Peptic Ulcer Disease
Pathophysiology
Breakdown of gastric or duodenal mucosal defence allows acid-peptic injury, commonly associated with Helicobacter pylori or ulcerogenic medicines. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include Helicobacter pylori infection; NSAID use; previous ulcer; tobacco use; and critical illness and selected other medicines. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Epigastric burning or pain, dyspepsia, nausea; bleeding may present with haematemesis or melaena; Sudden severe abdominal pain may indicate perforation.
Assessment and diagnostic evaluation
H. pylori testing and upper endoscopy when indicated, especially with alarm symptoms or bleeding; Check haemoglobin and haemodynamic status if bleeding is suspected.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Acid suppression plus H. pylori eradication when present; review and minimise ulcerogenic medications when clinically possible; Bleeding or perforation may require endoscopic, radiological or surgical intervention.
Nursing management: applying the nursing process
Epigastric burning or pain, dyspepsia, nausea; bleeding may present with haematemesis or melaena; Sudden severe abdominal pain may indicate perforation; and H. pylori testing and upper endoscopy when indicated, especially with alarm symptoms or bleeding.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Monitor pain, stool/emesis for blood, vital signs and haemoglobin in complicated disease.
- Administer prescribed therapy accurately and reinforce completion of eradication treatment.
- Teach avoidance of unsupervised ulcerogenic medicines and smoking.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially Helicobacter pylori infection, NSAID use, previous ulcer.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Upper Gastrointestinal Bleeding
Pathophysiology
Bleeding proximal to the ligament of Treitz may arise from ulcers, varices or mucosal lesions and can rapidly reduce circulating blood volume. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include peptic ulcer disease; portal hypertension and varices; NSAID/anticoagulant use; severe vomiting causing mucosal tears; and upper GI malignancy. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Haematemesis, coffee-ground emesis, melaena, dizziness, syncope or signs of shock; Tachycardia and postural or persistent hypotension suggest significant volume loss.
Assessment and diagnostic evaluation
Full blood count, coagulation profile, renal/liver tests, blood grouping/crossmatch and urgent endoscopy according to severity; Risk stratification helps determine level of care.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Resuscitation, blood products when indicated, acid-suppressive therapy for non-variceal bleeding and specific vasoactive/antimicrobial therapy for suspected variceal bleeding under specialist care; Endoscopic haemostasis is central for many causes.
Nursing management: applying the nursing process
Haematemesis, coffee-ground emesis, melaena, dizziness, syncope or signs of shock; Tachycardia and postural or persistent hypotension suggest significant volume loss; and Full blood count, coagulation profile, renal/liver tests, blood grouping/crossmatch and urgent endoscopy according to severity.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Perform frequent haemodynamic observations, establish/maintain IV access and document emesis/stool characteristics.
- Keep the patient nil by mouth when appropriate for urgent endoscopy and administer prescribed therapies.
- Monitor for rebleeding, reduced urine output, worsening shock or altered consciousness.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially peptic ulcer disease, portal hypertension and varices, NSAID/anticoagulant use.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Acute Appendicitis
Pathophysiology
Luminal obstruction and bacterial proliferation cause progressive inflammation of the appendix with risk of ischaemia, perforation and peritonitis. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include luminal obstruction; lymphoid hyperplasia; faecolith; younger age groups though any age is possible; and rare tumour or foreign-body obstruction. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Pain often begins centrally then localises to the right lower abdomen, with anorexia, nausea and fever; Presentation varies in pregnancy, older adults and children.
Assessment and diagnostic evaluation
Clinical examination, inflammatory markers and ultrasound or CT depending on patient group and local practice; Pregnancy testing is relevant when appropriate because it changes differential diagnosis and imaging choices.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Appendicectomy is common definitive management; selected uncomplicated cases may be managed non-operatively by specialist teams; Antimicrobial therapy is used when perforation, abscess or operative protocols indicate.
Nursing management: applying the nursing process
Pain often begins centrally then localises to the right lower abdomen, with anorexia, nausea and fever; Presentation varies in pregnancy, older adults and children; and Clinical examination, inflammatory markers and ultrasound or CT depending on patient group and local practice.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Monitor pain, temperature, abdominal signs and hydration; maintain fasting when surgery is planned.
- Provide pre-operative preparation and post-operative wound, pain, mobility and bowel-function care.
- Report sudden worsening pain with rigidity, fever or haemodynamic change.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially luminal obstruction, lymphoid hyperplasia, faecolith.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Intestinal Obstruction
Pathophysiology
Mechanical blockage or failure of motility prevents normal passage of intestinal contents, causing distension, fluid sequestration and possible bowel ischaemia. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include previous abdominal surgery and adhesions; hernia; tumour; volvulus; and inflammatory or stricturing bowel disease. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Colicky pain, abdominal distension, vomiting and reduced passage of stool/flatus; high obstruction may cause early vomiting; Constant severe pain, fever or peritonism raises concern for ischaemia/strangulation.
Assessment and diagnostic evaluation
Abdominal imaging, often CT, defines level, cause and complications; Assess electrolytes, renal function, lactate and hydration.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Initial treatment generally includes fasting, IV fluid/electrolyte correction and selective nasogastric decompression; Surgery is required for strangulation, perforation, certain mechanical causes or failure of conservative care.
Nursing management: applying the nursing process
Colicky pain, abdominal distension, vomiting and reduced passage of stool/flatus; high obstruction may cause early vomiting; Constant severe pain, fever or peritonism raises concern for ischaemia/strangulation; and Abdominal imaging, often CT, defines level, cause and complications.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Measure abdominal girth when useful, bowel sounds, pain, vomiting, intake/output and nasogastric drainage if present.
- Maintain fluid balance and oral care while fasting.
- Escalate increasing continuous pain, fever, tachycardia, guarding or falling urine output.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially previous abdominal surgery and adhesions, hernia, tumour.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Acute Pancreatitis
Pathophysiology
Premature activation of pancreatic digestive enzymes triggers autodigestive inflammation, which can extend systemically in severe disease. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include gallstones; alcohol misuse in adults; marked hypertriglyceridaemia; certain medicines; and post-ERCP or abdominal trauma. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Severe persistent epigastric pain often radiating to the back, nausea and vomiting; Severe cases may develop hypoxaemia, hypotension or oliguria.
Assessment and diagnostic evaluation
Characteristic pain plus raised pancreatic enzymes and/or imaging findings establish diagnosis; Ultrasound evaluates gallstones; CT is used selectively for complications or diagnostic uncertainty.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Early supportive care includes IV fluids adjusted to clinical response, analgesia, antiemetics and early enteral nutrition when tolerated; Treat causes such as gallstones and complications; prophylactic antibiotics are not routine in uncomplicated sterile pancreatitis.
Nursing management: applying the nursing process
Severe persistent epigastric pain often radiating to the back, nausea and vomiting; Severe cases may develop hypoxaemia, hypotension or oliguria; and Characteristic pain plus raised pancreatic enzymes and/or imaging findings establish diagnosis.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Monitor pain, respiratory status, haemodynamics, urine output, glucose and electrolytes.
- Support early oral/enteral nutrition as prescribed rather than prolonged unnecessary fasting.
- Observe for worsening abdominal signs, fever or organ dysfunction.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially gallstones, alcohol misuse in adults, marked hypertriglyceridaemia.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Cirrhosis and Portal Hypertension
Pathophysiology
Chronic liver injury causes fibrosis and regenerative nodules that distort hepatic architecture, impair function and increase resistance to portal blood flow. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include chronic viral hepatitis; harmful alcohol use; metabolic dysfunction-associated steatotic liver disease; autoimmune/cholestatic liver disease; and hereditary metabolic disorders. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Fatigue, jaundice, ascites, peripheral oedema, bruising, varices, splenomegaly and hepatic encephalopathy may develop; Decompensation is marked by ascites, variceal bleeding, encephalopathy or jaundice.
Assessment and diagnostic evaluation
Liver tests, coagulation profile, blood count, ultrasound/elastography and evaluation of cause; endoscopy screens for varices when indicated; Assess renal function and infection because decompensated patients can deteriorate quickly.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Treat the underlying cause and complications such as ascites, varices and encephalopathy; transplantation assessment is appropriate in advanced disease; Avoid hepatotoxic exposures and adjust medicines to liver function.
Nursing management: applying the nursing process
Fatigue, jaundice, ascites, peripheral oedema, bruising, varices, splenomegaly and hepatic encephalopathy may develop; Decompensation is marked by ascites, variceal bleeding, encephalopathy or jaundice; and Liver tests, coagulation profile, blood count, ultrasound/elastography and evaluation of cause; endoscopy screens for varices when indicated.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Monitor mental status, bleeding, abdominal girth, weight, oedema, stool, fluid balance and infection signs.
- Use prescribed sodium/fluid guidance and administer therapies for encephalopathy/ascites exactly as ordered.
- Educate on medication safety, alcohol avoidance and urgent reporting of bleeding or confusion.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially chronic viral hepatitis, harmful alcohol use, metabolic dysfunction-associated steatotic liver disease.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Chapter summary
This chapter links system physiology with assessment and nursing priorities. The major conditions discussed include Gastro-oesophageal Reflux Disease (GORD/GERD), Peptic Ulcer Disease, Upper Gastrointestinal Bleeding, Acute Appendicitis, Intestinal Obstruction, Acute Pancreatitis, Cirrhosis and Portal Hypertension. Across these disorders, safe care depends on recognising physiological instability, obtaining focused assessment data, administering prescribed treatment safely, preventing avoidable complications, supporting function and teaching the patient how to monitor for deterioration.
- Gastro-oesophageal Reflux Disease (GORD/GERD): Reflux of gastric contents into the oesophagus causes troublesome symptoms and/or mucosal injury.
- Peptic Ulcer Disease: A mucosal defect in the stomach or duodenum is commonly associated with Helicobacter pylori infection or ulcerogenic medicines.
- Upper Gastrointestinal Bleeding: Bleeding proximal to the ligament of Treitz commonly results from peptic ulcer disease, varices or mucosal lesions and may cause major blood loss.
- Acute Appendicitis: Obstruction and inflammation of the appendix can progress to ischaemia, perforation and peritonitis.
- Intestinal Obstruction: Mechanical blockage or functional ileus prevents normal movement of bowel contents and can impair perfusion if strangulation occurs.
Self-review questions
Open each item after attempting an answer yourself.
1. What are haematemesis and melaena?
Answer: Haematemesis is vomiting blood; melaena is black tarry stool caused by digested blood, usually from an upper GI source.
2. Why can intestinal obstruction cause dehydration?
Answer: Vomiting, reduced intake and sequestration of fluid into the bowel/third space reduce effective circulating volume.
3. Why is pancreatitis sometimes a systemic disease?
Answer: Pancreatic inflammation can trigger a widespread inflammatory response and organ dysfunction.
4. What causes ascites in cirrhosis?
Answer: Portal hypertension, sodium/water retention and low effective circulating volume are major contributors.
5. What is a key nursing priority in major GI bleeding?
Answer: Rapid haemodynamic assessment and escalation while supporting circulation and preparing for definitive evaluation.
Renal & Urinary Disorders
Renal and urinary disease can alter fluid volume, electrolytes, acid–base balance, blood pressure, erythropoiesis and excretion of metabolic waste. Precise fluid balance, renal-function trends, medication safety and early recognition of obstruction or infection are core nursing priorities.
Anatomy overview
The kidneys lie retroperitoneally and contain millions of nephrons, each with a glomerulus and tubular system. Blood is filtered at the glomerulus; tubular segments then reabsorb needed water and solutes, secrete selected substances and determine the final composition of urine. Urine passes through the ureters to the bladder and leaves through the urethra.
Physiology and clinical significance
Kidneys regulate extracellular volume, electrolytes, acid-base balance and excretion of metabolic waste. They also contribute to blood pressure control, erythropoiesis and vitamin D activation. Renal disorders can therefore produce fluid overload, dehydration, electrolyte disturbance, acidosis, anaemia and uraemic manifestations in addition to urinary symptoms.
Conditions in this chapter
Clinical condition
Acute Kidney Injury (AKI)
Pathophysiology
An abrupt fall in renal filtration results from reduced perfusion, intrinsic renal injury and/or urinary outflow obstruction, causing waste and fluid/electrolyte accumulation. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include sepsis and shock; dehydration or haemorrhage; nephrotoxic medicines/contrast exposure; major surgery; and urinary obstruction. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Reduced urine output may occur but is not universal; oedema, dyspnoea, nausea or confusion can develop; Common causes are reduced renal perfusion, intrinsic renal injury and urinary obstruction.
Assessment and diagnostic evaluation
Trend serum creatinine and urine output; assess urinalysis, electrolytes and renal imaging when obstruction is possible; Review volume status, sepsis, nephrotoxins and recent procedures.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Correct the underlying cause, optimise haemodynamics and discontinue/adjust nephrotoxic or renally cleared medicines where appropriate; Dialysis is used for selected severe complications such as refractory electrolyte, acid–base, fluid or uraemic problems.
Nursing management: applying the nursing process
Reduced urine output may occur but is not universal; oedema, dyspnoea, nausea or confusion can develop; Common causes are reduced renal perfusion, intrinsic renal injury and urinary obstruction; and Trend serum creatinine and urine output; assess urinalysis, electrolytes and renal imaging when obstruction is possible.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Strict intake/output, daily weight, oedema, lung sounds and blood-pressure monitoring.
- Observe potassium, acid–base status and ECG when hyperkalaemia risk is present.
- Avoid unprescribed nephrotoxic medicines and ensure dose adjustments are followed.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially sepsis and shock, dehydration or haemorrhage, nephrotoxic medicines/contrast exposure.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Chronic Kidney Disease (CKD)
Pathophysiology
Progressive irreversible nephron loss reduces filtration and endocrine function, leading to uraemia, fluid/electrolyte imbalance and systemic complications. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include diabetes mellitus; hypertension; glomerular disease; recurrent kidney injury; and hereditary or structural kidney disease. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Early CKD may be asymptomatic; advanced disease causes fatigue, pruritus, oedema, nausea, anaemia, bone-mineral problems and uraemic symptoms; Hypertension and diabetes are common associated conditions.
Assessment and diagnostic evaluation
Estimated GFR and urine albumin assessment stage disease; repeat testing confirms chronicity; Investigate cause and complications including electrolytes, haemoglobin and bone-mineral parameters.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Slow progression through blood-pressure/diabetes control, kidney-protective therapies where indicated, and avoidance of nephrotoxins; Advanced disease may require dialysis or kidney transplantation planning.
Nursing management: applying the nursing process
Early CKD may be asymptomatic; advanced disease causes fatigue, pruritus, oedema, nausea, anaemia, bone-mineral problems and uraemic symptoms; Hypertension and diabetes are common associated conditions; and Estimated GFR and urine albumin assessment stage disease; repeat testing confirms chronicity.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Track weight, blood pressure, fluid status, renal labs, anaemia symptoms and medication adherence.
- Provide individual dietary education with renal specialists rather than overly restrictive unsupervised diets.
- For dialysis patients, assess access sites and reinforce infection prevention and treatment attendance.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially diabetes mellitus, hypertension, glomerular disease.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Acute Glomerulonephritis
Pathophysiology
Immune-mediated glomerular inflammation reduces filtration and permits blood and protein to enter urine. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include recent streptococcal infection; autoimmune disease; vasculitis; infective endocarditis; and other immune-complex disorders. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Haematuria, oedema, hypertension and reduced urine output are typical nephritic features; Some forms follow infection; others reflect autoimmune or systemic disease.
Assessment and diagnostic evaluation
Urinalysis, renal function, complement/serology and infection studies; renal biopsy is used in selected cases; Assess blood pressure and pulmonary oedema because fluid overload may be rapid.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Treat the cause and complications, control blood pressure and fluid overload, and use immunosuppression only for appropriate immune-mediated forms under specialist care; Dialysis may be needed for severe kidney failure complications.
Nursing management: applying the nursing process
Haematuria, oedema, hypertension and reduced urine output are typical nephritic features; Some forms follow infection; others reflect autoimmune or systemic disease; and Urinalysis, renal function, complement/serology and infection studies; renal biopsy is used in selected cases.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Strict fluid balance, daily weight, blood-pressure checks and assessment for oedema or breathlessness.
- Monitor urine colour/output and laboratory trends.
- Reinforce prescribed sodium/fluid guidance and follow-up.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially recent streptococcal infection, autoimmune disease, vasculitis.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Nephrotic Syndrome
Pathophysiology
Marked glomerular protein loss causes hypoalbuminaemia, reduced plasma oncotic pressure, oedema and compensatory lipid abnormalities. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include primary glomerular diseases; diabetes mellitus; systemic lupus erythematosus; amyloidosis; and selected infections or medicines. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Generalised oedema, frothy urine and weight gain; severe cases can develop ascites or pleural fluid; Underlying causes vary with age and systemic disease.
Assessment and diagnostic evaluation
Quantify urinary protein, serum albumin, renal function and lipid profile; investigate secondary causes; Renal biopsy may be needed depending on age and suspected pathology.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Treat the underlying glomerular disease, manage oedema and blood pressure, and consider thrombosis prevention/treatment based on individual risk; Kidney-protective therapies are used where appropriate.
Nursing management: applying the nursing process
Generalised oedema, frothy urine and weight gain; severe cases can develop ascites or pleural fluid; Underlying causes vary with age and systemic disease; and Quantify urinary protein, serum albumin, renal function and lipid profile; investigate secondary causes.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Daily weight, abdominal girth when relevant, skin care for oedema and monitoring of urine output.
- Observe for infection and venous-thromboembolism symptoms.
- Support prescribed dietary and medication plan without encouraging high-protein self-treatment.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially primary glomerular diseases, diabetes mellitus, systemic lupus erythematosus.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Urinary Tract Infection and Pyelonephritis
Pathophysiology
Ascending bacterial infection inflames the lower urinary tract and may extend to the renal pelvis and parenchyma. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include female urinary anatomy; sexual activity; pregnancy; urinary obstruction or stones; and catheterisation or impaired bladder emptying. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Dysuria, frequency and urgency suggest cystitis; fever, flank pain, nausea or systemic features suggest pyelonephritis; Older adults may have atypical symptoms, but asymptomatic bacteriuria should not be assumed to explain confusion without assessment.
Assessment and diagnostic evaluation
Urinalysis and urine culture when indicated, particularly in pyelonephritis, pregnancy, recurrent or complicated infection; Imaging is considered when obstruction, stones or abscess are suspected.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Appropriate antimicrobial therapy based on syndrome, local resistance and culture when available; Severe infection may require IV therapy and sepsis management.
Nursing management: applying the nursing process
Dysuria, frequency and urgency suggest cystitis; fever, flank pain, nausea or systemic features suggest pyelonephritis; Older adults may have atypical symptoms, but asymptomatic bacteriuria should not be assumed to explain confusion without assessment; and Urinalysis and urine culture when indicated, particularly in pyelonephritis, pregnancy, recurrent or complicated infection.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Monitor temperature, pain, hydration, urine characteristics and response to treatment.
- Encourage appropriate fluid intake if not contraindicated and timely voiding.
- Teach completion of prescribed therapy and urgent review for worsening fever, vomiting, flank pain or sepsis signs.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially female urinary anatomy, sexual activity, pregnancy.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Renal / Ureteric Calculi
Pathophysiology
Crystals precipitate and aggregate within the urinary tract, producing obstruction, ureteric spasm and intense colicky pain. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include low urine volume; high urinary calcium/oxalate/uric acid; dietary and metabolic factors; family history; and recurrent urinary infection for some stone types. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Severe flank pain radiating toward the groin, haematuria, nausea and restlessness; Fever or rigors with obstruction suggests infected hydronephrosis.
Assessment and diagnostic evaluation
Urinalysis and non-contrast CT are common diagnostic tools; ultrasound is preferred in some groups such as pregnancy; Check renal function and signs of infection.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Analgesia, antiemetics and selected medical expulsive strategies may be used for suitable stones; Urgent decompression is required for infected obstruction or threatened renal function; definitive procedures depend on stone size/location.
Nursing management: applying the nursing process
Severe flank pain radiating toward the groin, haematuria, nausea and restlessness; Fever or rigors with obstruction suggests infected hydronephrosis; and Urinalysis and non-contrast CT are common diagnostic tools; ultrasound is preferred in some groups such as pregnancy.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Monitor pain, urine output, fever and hydration; strain urine if requested for stone analysis.
- Administer prescribed analgesia and antiemetics and reassess effect.
- Escalate fever, reduced urine output, uncontrolled pain or haemodynamic change promptly.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially low urine volume, high urinary calcium/oxalate/uric acid, dietary and metabolic factors.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Chapter summary
This chapter links system physiology with assessment and nursing priorities. The major conditions discussed include Acute Kidney Injury (AKI), Chronic Kidney Disease (CKD), Acute Glomerulonephritis, Nephrotic Syndrome, Urinary Tract Infection and Pyelonephritis, Renal / Ureteric Calculi. Across these disorders, safe care depends on recognising physiological instability, obtaining focused assessment data, administering prescribed treatment safely, preventing avoidable complications, supporting function and teaching the patient how to monitor for deterioration.
- Acute Kidney Injury (AKI): A sudden decline in kidney function causes retention of nitrogenous wastes and disturbances of fluid, electrolyte and acid–base balance.
- Chronic Kidney Disease (CKD): Persistent kidney structural or functional abnormality for at least three months can progress to kidney failure and increases cardiovascular risk.
- Acute Glomerulonephritis: Immune-mediated inflammation of glomeruli reduces filtration and permits blood/protein to enter urine.
- Nephrotic Syndrome: Heavy glomerular protein loss causes hypoalbuminaemia, oedema and hyperlipidaemia, with increased risk of thrombosis and infection.
- Urinary Tract Infection and Pyelonephritis: Bacterial infection may involve the lower urinary tract or ascend to the kidneys, where systemic illness is more likely.
Self-review questions
Open each item after attempting an answer yourself.
1. What three broad mechanisms cause AKI?
Answer: Reduced renal perfusion, intrinsic renal injury and urinary outflow obstruction.
2. Why does CKD commonly cause anaemia?
Answer: Diseased kidneys produce less erythropoietin, and other factors can also impair red-cell production.
3. What urinary pattern is typical of nephrotic syndrome?
Answer: Heavy proteinuria with hypoalbuminaemia and oedema.
4. Why is urine output useful clinically?
Answer: It is a practical indicator of renal perfusion and function when interpreted with the overall clinical picture.
5. What symptom pattern suggests ureteric colic?
Answer: Severe fluctuating flank pain that may radiate toward the groin, often with nausea and haematuria.
Endocrine & Metabolic Disorders
Endocrine disorders alter hormonal regulation of glucose, metabolism, water, electrolytes and stress responses. Nursing care requires vigilant observation for acute metabolic decompensation, safe medication administration and clear self-management education tailored by the clinical team.
Anatomy overview
The endocrine system includes the hypothalamus, pituitary, thyroid, parathyroids, adrenals, pancreatic islets, gonads and other hormone-producing tissues. Hormones travel through the circulation and act on specific receptors to coordinate metabolism, growth, stress responses, fluid balance and reproduction.
Physiology and clinical significance
Most endocrine systems operate through feedback loops. Small alterations in hormone production or tissue response can have widespread consequences because endocrine signals affect many organs simultaneously. Nursing assessment therefore pays attention to weight change, temperature tolerance, pulse, blood pressure, glucose, mental state, hydration and electrolyte patterns.
Conditions in this chapter
Clinical condition
Diabetes Mellitus
Pathophysiology
Insufficient insulin action—because of autoimmune beta-cell loss, insulin resistance or both—causes chronic hyperglycaemia and metabolic/vascular injury. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include family history and genetics; overweight/central adiposity for type 2; physical inactivity; history of gestational diabetes; and autoimmune susceptibility for type 1. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Polyuria, polydipsia, fatigue, weight change, recurrent infections or no symptoms early in type 2 diabetes; Hypoglycaemia can occur as a treatment complication.
Assessment and diagnostic evaluation
Diagnosis uses standard glucose or HbA1c criteria with repeat confirmation when appropriate; Assess cardiovascular risk, renal status, feet, eyes and medication safety regularly.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Individualised nutrition/activity support plus glucose-lowering medication; insulin is essential in type 1 diabetes and used in many other situations; Cardiovascular and kidney risk reduction is part of modern diabetes care.
Nursing management: applying the nursing process
Polyuria, polydipsia, fatigue, weight change, recurrent infections or no symptoms early in type 2 diabetes; Hypoglycaemia can occur as a treatment complication; and Diagnosis uses standard glucose or HbA1c criteria with repeat confirmation when appropriate.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Monitor capillary glucose as ordered and recognise hypo/hyperglycaemia.
- Teach medicine/insulin technique only within the patient's prescribed plan, along with foot care and sick-day contact guidance.
- Promote regular follow-up for eyes, kidneys, cardiovascular risk and feet.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially family history and genetics, overweight/central adiposity for type 2, physical inactivity.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Diabetic Ketoacidosis (DKA) / Hyperosmolar Hyperglycaemic State (HHS)
Pathophysiology
Severe insulin deficiency or ineffective insulin action produces marked hyperglycaemia and osmotic diuresis; DKA additionally features ketone production and metabolic acidosis. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include new or poorly controlled diabetes; infection; missed or insufficient insulin; myocardial infarction or stroke; and medicines or major physiological stress. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Polyuria, dehydration, nausea/vomiting, abdominal symptoms and altered consciousness; DKA may include deep respirations and ketotic breath; Precipitants include infection, missed insulin and acute illness.
Assessment and diagnostic evaluation
Urgent glucose, ketones, electrolytes, renal function, venous/arterial acid–base assessment and osmolality as appropriate; Search for the trigger while monitoring potassium closely.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Protocol-based IV fluid replacement, insulin therapy and careful electrolyte correction under continuous clinical monitoring; Treat the precipitating cause and avoid overly rapid osmotic shifts.
Nursing management: applying the nursing process
Polyuria, dehydration, nausea/vomiting, abdominal symptoms and altered consciousness; DKA may include deep respirations and ketotic breath; Precipitants include infection, missed insulin and acute illness; and Urgent glucose, ketones, electrolytes, renal function, venous/arterial acid–base assessment and osmolality as appropriate.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Frequent vital signs, neurological observations, glucose, fluid balance and laboratory monitoring.
- Use infusion pumps and independent safety checks where required for high-alert insulin/electrolyte therapy.
- When stable, review the precipitating factor and reinforce the patient's individual sick-day plan.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially new or poorly controlled diabetes, infection, missed or insufficient insulin.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Hypothyroidism
Pathophysiology
Insufficient thyroid hormone slows metabolic processes across multiple organ systems. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include autoimmune thyroiditis; thyroid surgery or radioiodine; iodine imbalance; certain medicines; and pituitary/hypothalamic disease. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Fatigue, cold intolerance, constipation, dry skin, slow pulse, weight gain and cognitive slowing may occur; Severe decompensation can cause hypothermia, bradycardia and reduced consciousness.
Assessment and diagnostic evaluation
TSH and free thyroid hormone levels establish most primary cases; evaluate cause and associated autoimmune disease when appropriate; Review medicines that can affect thyroid function.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Thyroid hormone replacement is titrated to clinical and biochemical response; Severe decompensated hypothyroidism requires urgent inpatient care.
Nursing management: applying the nursing process
Fatigue, cold intolerance, constipation, dry skin, slow pulse, weight gain and cognitive slowing may occur; Severe decompensation can cause hypothermia, bradycardia and reduced consciousness; and TSH and free thyroid hormone levels establish most primary cases; evaluate cause and associated autoimmune disease when appropriate.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Monitor energy, bowel pattern, heart rate, temperature and treatment adherence.
- Teach consistent timing of prescribed thyroid replacement and separation from interfering medicines/foods as advised by the clinician/pharmacist.
- Escalate marked drowsiness, hypothermia or cardiovascular instability.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially autoimmune thyroiditis, thyroid surgery or radioiodine, iodine imbalance.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Hyperthyroidism / Thyrotoxicosis
Pathophysiology
Excess circulating thyroid hormone increases metabolic activity and sympathetic responsiveness. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include Graves disease; toxic multinodular goitre; toxic adenoma; thyroiditis; and excess thyroid hormone exposure. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Heat intolerance, sweating, tremor, weight loss despite appetite, palpitations, anxiety and frequent stools; Graves disease may include eye manifestations.
Assessment and diagnostic evaluation
Suppressed TSH with elevated thyroid hormones; antibodies and imaging help determine cause; ECG is useful when palpitations or arrhythmia are present.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Therapy may include antithyroid medicines, symptom control, radioactive iodine or surgery depending on cause and patient factors; Thyroid storm requires urgent intensive treatment.
Nursing management: applying the nursing process
Heat intolerance, sweating, tremor, weight loss despite appetite, palpitations, anxiety and frequent stools; Graves disease may include eye manifestations; and Suppressed TSH with elevated thyroid hormones; antibodies and imaging help determine cause.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Monitor pulse, temperature, weight and symptoms of arrhythmia or heart failure.
- Teach adherence and urgent reporting of severe sore throat/fever if taking certain antithyroid medicines because of rare blood dyscrasias.
- Support eye comfort measures in Graves orbitopathy as directed.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially Graves disease, toxic multinodular goitre, toxic adenoma.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Adrenal Insufficiency (Addison Disease)
Pathophysiology
Deficient adrenal glucocorticoid production, with mineralocorticoid deficiency in primary disease, impairs stress response and fluid/electrolyte regulation. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include autoimmune adrenal destruction; tuberculosis or other adrenal infection; adrenal haemorrhage/infiltration; pituitary disease; and abrupt withdrawal after prolonged glucocorticoid therapy for secondary insufficiency. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Fatigue, weight loss, postural dizziness, nausea, abdominal symptoms and hyperpigmentation in primary disease; Adrenal crisis may cause severe hypotension, vomiting, hypoglycaemia and electrolyte disturbance.
Assessment and diagnostic evaluation
Morning cortisol and dynamic endocrine testing with ACTH/electrolytes help establish the diagnosis and cause; Consider adrenal insufficiency in unexplained shock, especially with relevant history.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Long-term hormone replacement is individualised; acute adrenal crisis requires urgent glucocorticoid and fluid therapy by clinicians; Patients need a personalised stress-dose plan for illness/procedures.
Nursing management: applying the nursing process
Fatigue, weight loss, postural dizziness, nausea, abdominal symptoms and hyperpigmentation in primary disease; Adrenal crisis may cause severe hypotension, vomiting, hypoglycaemia and electrolyte disturbance; and Morning cortisol and dynamic endocrine testing with ACTH/electrolytes help establish the diagnosis and cause.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Monitor blood pressure, glucose, sodium/potassium, hydration and symptoms during acute illness.
- Do not omit prescribed steroid replacement in hospital without medical review.
- Teach emergency identification, illness planning and when to seek urgent care.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially autoimmune adrenal destruction, tuberculosis or other adrenal infection, adrenal haemorrhage/infiltration.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Cushing Syndrome
Pathophysiology
Chronic excessive glucocorticoid exposure alters glucose, protein and fat metabolism and suppresses immune, bone and connective-tissue function. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include exogenous glucocorticoid therapy; pituitary ACTH-secreting adenoma; adrenal cortisol-producing tumour; ectopic ACTH production; and rare familial endocrine syndromes. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Proximal muscle weakness, easy bruising, hypertension, glucose intolerance, skin changes and increased infection risk; Long-term exogenous steroid exposure is a common cause.
Assessment and diagnostic evaluation
Endocrine testing confirms hypercortisolism and identifies the source when endogenous disease is suspected; Medication history is essential.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Treat the cause, which may involve carefully supervised reduction of exogenous steroids, surgery or medicines that reduce cortisol production/action; Manage hypertension, diabetes, osteoporosis and infection risk.
Nursing management: applying the nursing process
Proximal muscle weakness, easy bruising, hypertension, glucose intolerance, skin changes and increased infection risk; Long-term exogenous steroid exposure is a common cause; and Endocrine testing confirms hypercortisolism and identifies the source when endogenous disease is suspected.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Monitor blood pressure, glucose, skin integrity, infection signs and muscle weakness.
- Never advise abrupt discontinuation of long-term prescribed corticosteroids; tapering is clinician-directed.
- Provide falls and bone-health education based on individual risk.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially exogenous glucocorticoid therapy, pituitary ACTH-secreting adenoma, adrenal cortisol-producing tumour.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Chapter summary
This chapter links system physiology with assessment and nursing priorities. The major conditions discussed include Diabetes Mellitus, Diabetic Ketoacidosis (DKA) / Hyperosmolar Hyperglycaemic State (HHS), Hypothyroidism, Hyperthyroidism / Thyrotoxicosis, Adrenal Insufficiency (Addison Disease), Cushing Syndrome. Across these disorders, safe care depends on recognising physiological instability, obtaining focused assessment data, administering prescribed treatment safely, preventing avoidable complications, supporting function and teaching the patient how to monitor for deterioration.
- Diabetes Mellitus: Chronic hyperglycaemia results from impaired insulin secretion, insulin action or both and can damage blood vessels, nerves, kidneys, eyes and other organs.
- Diabetic Ketoacidosis (DKA) / Hyperosmolar Hyperglycaemic State (HHS): Severe insulin deficiency or relative deficiency causes dangerous hyperglycaemia, dehydration and metabolic disturbance; DKA includes ketoacidosis, while HHS has extreme hyperosmolality with little ketosis.
- Hypothyroidism: Insufficient thyroid hormone slows metabolic processes and can affect cardiovascular, neurological, gastrointestinal and reproductive function.
- Hyperthyroidism / Thyrotoxicosis: Excess thyroid hormone increases metabolic activity and sympathetic effects; Graves disease is a common cause.
- Adrenal Insufficiency (Addison Disease): Deficient adrenal glucocorticoid production, with or without mineralocorticoid deficiency, impairs stress response and fluid/electrolyte regulation.
Self-review questions
Open each item after attempting an answer yourself.
1. What distinguishes DKA from HHS physiologically?
Answer: DKA has significant ketone production and metabolic acidosis; HHS usually has more extreme hyperosmolality with minimal ketonaemia.
2. Why must potassium be monitored closely during DKA treatment?
Answer: Insulin and correction of acidosis shift potassium into cells, so serum potassium can fall quickly.
3. What does thyroid hormone excess do to metabolism?
Answer: It increases metabolic activity and sympathetic responsiveness.
4. Why is adrenal crisis dangerous?
Answer: Severe cortisol deficiency can cause hypotension, electrolyte disturbance, hypoglycaemia and shock.
5. What is the basic principle of endocrine feedback?
Answer: Hormone levels or their effects feed back to regulate upstream hormone release and maintain homeostasis.
Haematology & Oncology
Haematological disorders affect oxygen transport, immunity and haemostasis, while malignancy may involve marrow, lymphatic tissue or solid organs. Nursing priorities include infection prevention, bleeding precautions, transfusion safety, symptom control and psychosocial support.
Anatomy overview
Blood contains red cells, white cells, platelets and plasma. Bone marrow produces the cellular components through haematopoiesis. Red cells carry oxygen with haemoglobin, leukocytes defend against infection, and platelets cooperate with plasma clotting factors to achieve haemostasis.
Physiology and clinical significance
Haematological disease may arise from underproduction, excessive destruction, abnormal cell proliferation or disordered coagulation. Symptoms often reflect impaired oxygen delivery, infection susceptibility or bleeding. Because blood disorders affect every organ, nursing care requires careful monitoring of fatigue, fever, bleeding, pain, transfusion reactions and treatment-related complications.
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Conditions in this chapter
Clinical condition
Iron-Deficiency Anaemia
Pathophysiology
Insufficient available iron limits haemoglobin synthesis, producing smaller, paler red cells and reduced oxygen-carrying capacity. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include chronic blood loss; inadequate dietary iron; increased demand such as pregnancy; malabsorption; and gastrointestinal blood loss. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Fatigue, pallor, exertional dyspnoea, dizziness and sometimes pica or restless legs; Severe anaemia can cause tachycardia or cardiac strain.
Assessment and diagnostic evaluation
Full blood count typically shows microcytosis; ferritin and iron studies support diagnosis; The underlying cause, especially occult gastrointestinal or menstrual blood loss, must be assessed.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Iron replacement and treatment of the source of iron loss; route depends on severity, tolerance and absorption; Transfusion is reserved for selected severe/symptomatic cases according to clinical context.
Nursing management: applying the nursing process
Fatigue, pallor, exertional dyspnoea, dizziness and sometimes pica or restless legs; Severe anaemia can cause tachycardia or cardiac strain; and Full blood count typically shows microcytosis; ferritin and iron studies support diagnosis.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Monitor fatigue, exercise tolerance and haemoglobin response.
- Teach correct use and expected effects of prescribed iron, including possible gastrointestinal side effects.
- Encourage iron-containing foods as part of a balanced diet without replacing investigation of the cause.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially chronic blood loss, inadequate dietary iron, increased demand such as pregnancy.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Sickle Cell Disease
Pathophysiology
Polymerisation of abnormal haemoglobin S during deoxygenation distorts red cells, causing haemolysis and episodic microvascular obstruction. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include inheritance of sickle haemoglobin genes; dehydration can precipitate crises; infection can precipitate crises; hypoxia can precipitate sickling; and extreme temperature or physiological stress. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Pain crises, chronic anaemia, jaundice and increased infection risk; acute chest syndrome can cause fever, chest pain and hypoxaemia; Stroke, splenic dysfunction and organ damage may develop.
Assessment and diagnostic evaluation
Haemoglobin analysis confirms the diagnosis; routine monitoring assesses organ complications; During acute illness evaluate infection, oxygenation, hydration and haemoglobin change.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Acute crises require prompt analgesia, hydration tailored to status and treatment of triggers; transfusion is used for specific indications; Disease-modifying therapy and vaccination/infection prevention reduce long-term complications.
Nursing management: applying the nursing process
Pain crises, chronic anaemia, jaundice and increased infection risk; acute chest syndrome can cause fever, chest pain and hypoxaemia; Stroke, splenic dysfunction and organ damage may develop; and Haemoglobin analysis confirms the diagnosis; routine monitoring assesses organ complications.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Assess pain promptly and use the prescribed analgesia plan without stigmatising the patient.
- Monitor oxygenation, temperature, hydration and signs of acute chest syndrome or neurological change.
- Teach trigger awareness, hydration, adherence and when to seek urgent care.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially inheritance of sickle haemoglobin genes, dehydration can precipitate crises, infection can precipitate crises.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Leukaemia
Pathophysiology
Clonal malignant proliferation of haematopoietic precursor cells crowds marrow and may infiltrate organs, impairing normal blood-cell production. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include increasing age for many subtypes; specific genetic syndromes; previous chemotherapy/radiation; benzene exposure; and certain marrow disorders. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Fatigue, infection, fever, bruising/bleeding, bone pain, lymphadenopathy or organ enlargement; Cytopenias may be severe at presentation.
Assessment and diagnostic evaluation
Full blood count and peripheral smear followed by bone-marrow and immunophenotypic/molecular studies; Tumour-lysis risk and infection status are assessed before treatment.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Therapy depends on subtype and may include chemotherapy, targeted/immunologic therapy and stem-cell transplantation; Supportive treatment includes antimicrobials, transfusion and tumour-lysis prevention when indicated.
Nursing management: applying the nursing process
Fatigue, infection, fever, bruising/bleeding, bone pain, lymphadenopathy or organ enlargement; Cytopenias may be severe at presentation; and Full blood count and peripheral smear followed by bone-marrow and immunophenotypic/molecular studies.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Use infection-prevention and bleeding precautions according to neutrophil/platelet status.
- Monitor temperature, mucositis, nutrition, transfusion reactions and chemotherapy adverse effects.
- Escalate fever in a neutropenic patient urgently according to protocol.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially increasing age for many subtypes, specific genetic syndromes, previous chemotherapy/radiation.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Lymphoma
Pathophysiology
Malignant transformation of lymphocytes produces clonal growth in lymph nodes or extranodal tissue and may involve bone marrow. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include immune dysregulation; selected viral infections; family susceptibility; immunosuppressive therapy; and age patterns varying by subtype. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Persistent painless lymphadenopathy, fever, drenching night sweats, weight loss, pruritus or fatigue; Mass effect may cause respiratory or abdominal symptoms.
Assessment and diagnostic evaluation
Excisional or core lymph-node biopsy establishes subtype; imaging and marrow studies are used for staging when indicated; Baseline organ-function tests guide therapy.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Treatment may include combination systemic therapy, immunotherapy, targeted therapy and/or radiotherapy based on subtype/stage; Some indolent lymphomas can be observed initially under specialist care.
Nursing management: applying the nursing process
Persistent painless lymphadenopathy, fever, drenching night sweats, weight loss, pruritus or fatigue; Mass effect may cause respiratory or abdominal symptoms; and Excisional or core lymph-node biopsy establishes subtype; imaging and marrow studies are used for staging when indicated.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Monitor infection, bleeding, fatigue, nutrition and treatment toxicity.
- Provide education about chemotherapy/radiotherapy schedules and fertility or survivorship concerns where relevant.
- Assess psychosocial needs and support continuity of care.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially immune dysregulation, selected viral infections, family susceptibility.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Immune Thrombocytopenia (ITP)
Pathophysiology
Immune-mediated platelet destruction and impaired platelet production reduce circulating platelet numbers and increase mucocutaneous bleeding risk. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include autoimmune tendency; recent viral illness; pregnancy in some adults; other autoimmune disorders; and certain medicines. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Petechiae, easy bruising, mucosal bleeding or heavy menstrual bleeding; many patients have no symptoms; Major internal bleeding is uncommon but risk rises with very low platelets and other factors.
Assessment and diagnostic evaluation
Diagnosis is clinical after excluding alternative causes; full blood count typically shows isolated thrombocytopenia; Review medicines, infection history and peripheral smear.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Observation is appropriate for some patients; others require therapies that reduce immune platelet destruction or increase production; Urgent treatment is required for clinically significant bleeding.
Nursing management: applying the nursing process
Petechiae, easy bruising, mucosal bleeding or heavy menstrual bleeding; many patients have no symptoms; Major internal bleeding is uncommon but risk rises with very low platelets and other factors; and Diagnosis is clinical after excluding alternative causes; full blood count typically shows isolated thrombocytopenia.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Use bleeding precautions: minimise trauma, avoid unnecessary invasive procedures and monitor urine/stool/mucosa.
- Administer treatment and blood products only as prescribed and monitor response.
- Teach patients to seek help for significant bleeding or head injury.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially autoimmune tendency, recent viral illness, pregnancy in some adults.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Disseminated Intravascular Coagulation (DIC)
Pathophysiology
Widespread pathological activation of coagulation consumes platelets and clotting factors while generating microvascular thrombosis and bleeding. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include sepsis; major trauma; obstetric emergencies; malignancy; and severe tissue injury or shock. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Oozing from puncture sites, bruising, bleeding, organ dysfunction and shock in a critically ill patient; Common triggers include severe sepsis, trauma, obstetric catastrophe and malignancy.
Assessment and diagnostic evaluation
Falling platelets, prolonged coagulation tests, low fibrinogen in many cases and elevated fibrin-degradation markers support diagnosis; Serial trends are more useful than a single result.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Treat the underlying trigger urgently and provide blood-component support when clinically indicated; Critical-care support is required when organ failure or shock is present.
Nursing management: applying the nursing process
Oozing from puncture sites, bruising, bleeding, organ dysfunction and shock in a critically ill patient; Common triggers include severe sepsis, trauma, obstetric catastrophe and malignancy; and Falling platelets, prolonged coagulation tests, low fibrinogen in many cases and elevated fibrin-degradation markers support diagnosis.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Monitor all bleeding sites, perfusion, urine output and neurological status; minimise venepuncture and invasive procedures.
- Use careful pressure after necessary punctures and follow transfusion-safety protocols.
- Escalate new bleeding or worsening organ dysfunction immediately.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially sepsis, major trauma, obstetric emergencies.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Chapter summary
This chapter links system physiology with assessment and nursing priorities. The major conditions discussed include Iron-Deficiency Anaemia, Sickle Cell Disease, Leukaemia, Lymphoma, Immune Thrombocytopenia (ITP), Disseminated Intravascular Coagulation (DIC). Across these disorders, safe care depends on recognising physiological instability, obtaining focused assessment data, administering prescribed treatment safely, preventing avoidable complications, supporting function and teaching the patient how to monitor for deterioration.
- Iron-Deficiency Anaemia: Insufficient iron limits haemoglobin synthesis and reduces oxygen-carrying capacity; chronic blood loss and inadequate intake/absorption are common causes.
- Sickle Cell Disease: An inherited haemoglobin disorder causes red-cell sickling, haemolysis and episodic vaso-occlusion with multi-organ complications.
- Leukaemia: Malignant proliferation of haematopoietic cells disrupts normal marrow function and may infiltrate tissues.
- Lymphoma: Malignancies of lymphoid tissue include Hodgkin and non-Hodgkin lymphomas with varied biological behaviour.
- Immune Thrombocytopenia (ITP): Immune-mediated platelet destruction and impaired production cause isolated thrombocytopenia with variable bleeding risk.
Self-review questions
Open each item after attempting an answer yourself.
1. Why does anaemia cause fatigue and dyspnoea?
Answer: Reduced haemoglobin lowers oxygen-carrying capacity, so tissues receive less oxygen during activity.
2. What drives vaso-occlusive pain in sickle cell disease?
Answer: Sickled cells obstruct small vessels and provoke ischaemia and inflammation.
3. Why are patients with leukaemia at risk of infection and bleeding?
Answer: Malignant marrow cells can suppress normal leukocyte and platelet production.
4. What is DIC?
Answer: Systemic uncontrolled coagulation activation that consumes platelets/factors while causing microthrombi and bleeding.
5. What precautions are important in severe thrombocytopenia?
Answer: Reduce trauma and invasive procedures where possible, observe closely for bleeding and follow local bleeding-precaution protocols.
Musculoskeletal Disorders
Musculoskeletal conditions can cause pain, deformity, loss of mobility and neurovascular compromise. Nursing care combines pain control, safe mobilisation, pressure prevention, neurovascular assessment, rehabilitation and education that protects independence.
Anatomy overview
The musculoskeletal system includes bones, joints, cartilage, ligaments, tendons and skeletal muscle. Bones provide structural support and mineral storage; joints permit movement; muscles generate force and maintain posture. Healthy movement depends on intact neurovascular supply and coordinated mechanical alignment.
Physiology and clinical significance
Bone is continuously remodelled, while articular cartilage reduces friction across joints. Trauma, inflammation, degeneration, infection and loss of bone density can impair mobility and independence. Nursing priorities include pain control, neurovascular assessment, safe mobilisation, prevention of pressure injury and thromboembolism, and rehabilitation.
Conditions in this chapter
Clinical condition
Fractures
Pathophysiology
Mechanical force exceeds bone strength, disrupting bone continuity and surrounding soft tissue with potential bleeding and neurovascular compromise. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include trauma; osteoporosis; falls; sports injury; and pathological bone lesions. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Pain, swelling, deformity, bruising and loss of function; open fractures communicate with the external environment; Neurovascular compromise or compartment syndrome are limb-threatening emergencies.
Assessment and diagnostic evaluation
X-ray is first-line for most fractures; CT/MRI may define complex or occult injuries; Document distal pulses, capillary refill, movement and sensation before and after immobilisation.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Reduction and immobilisation are chosen according to fracture type; some fractures require internal or external fixation; Open fractures require urgent wound/antimicrobial/tetanus management under trauma protocols.
Nursing management: applying the nursing process
Pain, swelling, deformity, bruising and loss of function; open fractures communicate with the external environment; Neurovascular compromise or compartment syndrome are limb-threatening emergencies; and X-ray is first-line for most fractures; CT/MRI may define complex or occult injuries.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Perform frequent neurovascular observations and assess pain beyond the expected pattern.
- Elevate/ice when appropriate and prescribed; maintain cast, splint or traction safety.
- Support early safe mobility, DVT prevention and nutrition for healing.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially trauma, osteoporosis, falls.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Osteoarthritis
Pathophysiology
Loss and remodelling of articular cartilage and subchondral bone produce mechanical joint pain, stiffness and reduced mobility. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include ageing; obesity; previous joint injury; repetitive mechanical loading; and joint malalignment or genetic susceptibility. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Activity-related joint pain, brief morning stiffness, reduced range of motion and crepitus; Symptoms can fluctuate and do not always correlate with imaging severity.
Assessment and diagnostic evaluation
Usually clinical; imaging is used when diagnosis is uncertain or surgery is considered; Assess functional limitation, falls risk and comorbidities.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Education, exercise/physiotherapy and weight-neutral functional strategies form the foundation; analgesic options are individualised; Joint replacement is considered for severe persistent pain and disability.
Nursing management: applying the nursing process
Activity-related joint pain, brief morning stiffness, reduced range of motion and crepitus; Symptoms can fluctuate and do not always correlate with imaging severity; and Usually clinical; imaging is used when diagnosis is uncertain or surgery is considered.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Support pacing, low-impact strengthening and use of mobility aids when needed.
- Monitor pain and function rather than focusing only on radiographic changes.
- After arthroplasty, follow wound, DVT prevention and mobilisation protocols.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially ageing, obesity, previous joint injury.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Rheumatoid Arthritis
Pathophysiology
Systemic autoimmunity drives chronic synovial inflammation that can erode cartilage and bone and affect extra-articular organs. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include female sex; genetic susceptibility; smoking; middle adulthood though any age can occur; and other autoimmune risk. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Symmetrical small-joint pain/swelling, prolonged morning stiffness, fatigue and reduced function; Extra-articular eye, lung, vascular or neurological involvement can occur.
Assessment and diagnostic evaluation
Clinical synovitis plus inflammatory markers, rheumatoid factor/anti-CCP and imaging as appropriate; Early specialist assessment improves outcomes.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Disease-modifying antirheumatic therapy is started early and escalated to control inflammation; short-term symptom therapy may be used; Screening for infection and treatment-related risks is required for immunomodulatory medicines.
Nursing management: applying the nursing process
Symmetrical small-joint pain/swelling, prolonged morning stiffness, fatigue and reduced function; Extra-articular eye, lung, vascular or neurological involvement can occur; and Clinical synovitis plus inflammatory markers, rheumatoid factor/anti-CCP and imaging as appropriate.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Assess pain, joint swelling, fatigue and ability to perform daily activities.
- Balance rest during flares with regular range-of-motion and strengthening under rehabilitation guidance.
- Educate about monitoring required for prescribed disease-modifying therapy and infection warning signs.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially female sex, genetic susceptibility, smoking.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Osteoporosis
Pathophysiology
Bone resorption exceeds formation, reducing bone mass and microarchitectural strength so fragility fractures occur more easily. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include increasing age; post-menopausal oestrogen loss; low body weight; long-term glucocorticoid exposure; and low calcium/vitamin D, smoking and inactivity. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Often silent until fracture; vertebral fractures may cause back pain or height loss; Risk rises with age, certain endocrine conditions and prolonged corticosteroid exposure.
Assessment and diagnostic evaluation
Bone-mineral-density testing and clinical fracture-risk assessment are used in at-risk patients; Evaluate secondary causes and vitamin/mineral status as appropriate.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Fall prevention, adequate calcium/vitamin D intake when appropriate and anti-osteoporosis medicines for people at sufficient fracture risk; Treat secondary causes and review medicines that increase falls risk.
Nursing management: applying the nursing process
Often silent until fracture; vertebral fractures may cause back pain or height loss; Risk rises with age, certain endocrine conditions and prolonged corticosteroid exposure; and Bone-mineral-density testing and clinical fracture-risk assessment are used in at-risk patients.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Perform falls assessment and promote safe strength/balance activity.
- Teach adherence and administration precautions for prescribed bone medicines.
- After fragility fracture, support rehabilitation and secondary-fracture prevention.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially increasing age, post-menopausal oestrogen loss, low body weight.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Osteomyelitis
Pathophysiology
Microorganisms infect bone through bloodstream spread, contiguous tissue or direct inoculation, producing inflammation and possible bone necrosis. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include open fracture or surgery; diabetes/foot ulcers; poor peripheral circulation; bacteraemia; and implanted orthopaedic hardware. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Localised bone pain, tenderness, swelling and fever; chronic disease may form draining sinuses; Diabetes, vascular disease and orthopaedic implants increase risk in some patients.
Assessment and diagnostic evaluation
Inflammatory markers and imaging, often MRI; cultures from bone/deep tissue provide the best microbiological diagnosis when obtainable; Blood cultures are useful when systemic infection is present.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Prolonged targeted antimicrobial therapy and source control/debridement when necessary; Optimise perfusion, glycaemic control and wound care in relevant patients.
Nursing management: applying the nursing process
Localised bone pain, tenderness, swelling and fever; chronic disease may form draining sinuses; Diabetes, vascular disease and orthopaedic implants increase risk in some patients; and Inflammatory markers and imaging, often MRI; cultures from bone/deep tissue provide the best microbiological diagnosis when obtainable.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Monitor pain, fever, wound/drainage and inflammatory markers.
- Administer antimicrobials on schedule and care for long-term IV access using infection-prevention standards.
- Support off-loading or mobility restrictions prescribed by orthopaedic teams.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially open fracture or surgery, diabetes/foot ulcers, poor peripheral circulation.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Chapter summary
This chapter links system physiology with assessment and nursing priorities. The major conditions discussed include Fractures, Osteoarthritis, Rheumatoid Arthritis, Osteoporosis, Osteomyelitis. Across these disorders, safe care depends on recognising physiological instability, obtaining focused assessment data, administering prescribed treatment safely, preventing avoidable complications, supporting function and teaching the patient how to monitor for deterioration.
- Fractures: A fracture is loss of bone continuity caused by trauma, stress or pathological weakening and may be closed or open.
- Osteoarthritis: Degenerative joint disease involves cartilage loss, subchondral bone change and variable synovial inflammation, commonly affecting knees, hips, hands and spine.
- Rheumatoid Arthritis: A systemic autoimmune inflammatory arthritis primarily affects synovial joints and can cause progressive erosion and extra-articular disease.
- Osteoporosis: Reduced bone strength increases fragility-fracture risk, especially at the hip, spine and wrist.
- Osteomyelitis: Bone infection can be acute or chronic and may arise from bloodstream spread, contiguous infection or direct inoculation after trauma/surgery.
Self-review questions
Open each item after attempting an answer yourself.
1. What must be checked distal to a limb fracture?
Answer: Perfusion, pulse if palpable, capillary refill, sensation, movement, temperature and pain should be assessed and trended.
2. Why is compartment syndrome urgent?
Answer: Rising pressure in a closed muscle compartment can stop tissue perfusion and cause irreversible nerve and muscle injury.
3. How does rheumatoid arthritis differ from osteoarthritis?
Answer: Rheumatoid arthritis is systemic autoimmune synovitis; osteoarthritis is primarily degenerative mechanical joint disease.
4. Why does osteoporosis increase fracture risk?
Answer: Bone mass and microarchitectural strength are reduced.
5. What makes osteomyelitis difficult to treat?
Answer: Infected or necrotic bone has impaired perfusion and may require prolonged antimicrobial therapy and sometimes surgery.
Common Surgical & Oncological Conditions
Many surgical disorders require coordinated assessment, imaging, peri-operative optimisation and postoperative recovery. Nursing care spans pre-operative preparation, infection prevention, pain control, mobilisation, nutrition, drain/wound observation and patient education.
Anatomy overview
Surgical nursing integrates disease-specific anatomy with perioperative assessment. Abdominal, breast, thoracic, urinary and hepatobiliary procedures can alter organ function, fluid balance, pain, mobility and infection risk. Understanding surgical anatomy allows nurses to interpret drains, wounds, stomas and expected postoperative recovery.
Physiology and clinical significance
Surgery triggers neuroendocrine stress responses and inflammation. Recovery requires adequate oxygenation, circulation, analgesia, nutrition, mobility and wound healing. Cancer surgery may be combined with systemic therapy or radiotherapy, and care often extends from diagnosis through treatment, rehabilitation and survivorship.
Conditions in this chapter
Clinical condition
Cholelithiasis and Acute Cholecystitis
Pathophysiology
Gallstones may obstruct the cystic duct, causing gallbladder distension and inflammation; persistent obstruction can lead to infection or other biliary complications. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include female sex; increasing age; obesity or rapid weight loss; pregnancy; and haemolytic disorders for pigment stones. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Right-upper-quadrant or epigastric pain, often after meals, with nausea; fever and persistent tenderness suggest acute cholecystitis; Jaundice raises concern for common bile duct obstruction.
Assessment and diagnostic evaluation
Ultrasound is first-line; liver tests help identify biliary obstruction; Further biliary imaging is used when duct stones are suspected.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Analgesia, fluids and antibiotics when acute infection is suspected; laparoscopic cholecystectomy is definitive for many symptomatic patients; Endoscopic bile-duct therapy may be required for choledocholithiasis.
Nursing management: applying the nursing process
Right-upper-quadrant or epigastric pain, often after meals, with nausea; fever and persistent tenderness suggest acute cholecystitis; Jaundice raises concern for common bile duct obstruction; and Ultrasound is first-line; liver tests help identify biliary obstruction.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Monitor pain, fever, jaundice, nausea and oral tolerance.
- Provide pre/post-operative care including early mobilisation and wound assessment.
- Escalate hypotension, confusion, worsening jaundice or sepsis signs.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially female sex, increasing age, obesity or rapid weight loss.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Colorectal Cancer
Pathophysiology
Accumulated genetic and epigenetic changes transform colonic epithelial cells, often through an adenoma-to-carcinoma sequence. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include increasing age; family history or hereditary syndromes; inflammatory bowel disease; processed/red meat and obesity associations; and smoking and alcohol. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Rectal bleeding, change in stool pattern, iron-deficiency anaemia, abdominal pain or weight loss; Right-sided tumours may present predominantly with anaemia; distal tumours can obstruct.
Assessment and diagnostic evaluation
Colonoscopy with biopsy, followed by imaging and pathology-based staging; Tumour markers may support surveillance but do not replace diagnostic evaluation.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Surgical resection is central for many localised cancers; chemotherapy, radiotherapy and targeted/immunologic treatments depend on stage and tumour biology; Stoma creation may be temporary or permanent in selected cases.
Nursing management: applying the nursing process
Rectal bleeding, change in stool pattern, iron-deficiency anaemia, abdominal pain or weight loss; Right-sided tumours may present predominantly with anaemia; distal tumours can obstruct; and Colonoscopy with biopsy, followed by imaging and pathology-based staging.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Prepare patients for bowel surgery according to protocol and provide postoperative pain, mobility and bowel-function care.
- If a stoma is formed, teach pouch care, skin protection and supply planning with a stoma specialist.
- Monitor for anastomotic leak, ileus, infection and nutritional problems.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially increasing age, family history or hereditary syndromes, inflammatory bowel disease.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Breast Cancer
Pathophysiology
Malignant breast epithelial cells acquire invasive potential and may spread through lymphatic and haematogenous routes. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include increasing age; family/genetic susceptibility; prolonged lifetime oestrogen exposure; alcohol and obesity after menopause; and previous chest irradiation. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
New breast lump, skin/nipple change, nipple discharge or axillary lymphadenopathy; many cancers are screen-detected before symptoms; Not every lump is malignant, but persistent changes require assessment.
Assessment and diagnostic evaluation
Triple assessment typically combines clinical examination, imaging and tissue biopsy; Pathology establishes receptor status and grade; staging is performed when indicated.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Treatment may include breast-conserving surgery or mastectomy, radiotherapy and systemic endocrine, chemotherapy, targeted or immunologic therapy; Genetic assessment is offered when family/personal history suggests inherited risk.
Nursing management: applying the nursing process
New breast lump, skin/nipple change, nipple discharge or axillary lymphadenopathy; many cancers are screen-detected before symptoms; Not every lump is malignant, but persistent changes require assessment; and Triple assessment typically combines clinical examination, imaging and tissue biopsy.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Provide peri-operative wound/drain care and monitor for seroma or infection.
- Teach gradual arm/shoulder rehabilitation and lymphoedema risk-reduction guidance provided by the treating team.
- Support body-image concerns, treatment adherence and symptom reporting.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially increasing age, family/genetic susceptibility, prolonged lifetime oestrogen exposure.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Lung Cancer
Pathophysiology
Malignant transformation of bronchial or pulmonary epithelial cells produces locally invasive tumours that can metastasise early depending on subtype. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include tobacco exposure; second-hand smoke; radon; occupational carcinogens; and air pollution and prior lung disease associations. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Persistent cough, haemoptysis, chest pain, dyspnoea, recurrent pneumonia, hoarseness or unexplained weight loss; Some tumours are detected incidentally on imaging.
Assessment and diagnostic evaluation
Chest CT and tissue diagnosis by bronchoscopy, needle biopsy or other route; staging includes nodal and metastatic assessment; Molecular testing guides targeted treatment in many non-small-cell cancers.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Depending on stage and biology: surgery, radiotherapy, chemotherapy, targeted therapy and immunotherapy may be used alone or combined; Palliative care can be integrated early for symptom burden.
Nursing management: applying the nursing process
Persistent cough, haemoptysis, chest pain, dyspnoea, recurrent pneumonia, hoarseness or unexplained weight loss; Some tumours are detected incidentally on imaging; and Chest CT and tissue diagnosis by bronchoscopy, needle biopsy or other route; staging includes nodal and metastatic assessment.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Monitor respiratory symptoms, nutrition, fatigue and treatment adverse effects.
- Support smoking cessation without blame and teach early reporting of fever or worsening breathlessness.
- After thoracic surgery, support pulmonary hygiene, pain control and early mobilisation.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially tobacco exposure, second-hand smoke, radon.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Benign Prostatic Hyperplasia (BPH)
Pathophysiology
Non-malignant hyperplasia within the periurethral prostate narrows the prostatic urethra and increases resistance to urinary flow. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include increasing age; androgen-related prostatic growth; family history; metabolic syndrome associations; and obesity associations. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Hesitancy, weak stream, incomplete emptying, frequency and nocturia; Acute urinary retention causes painful inability to void.
Assessment and diagnostic evaluation
History, examination, urinalysis and assessment of post-void residual/renal function when indicated; PSA and further testing are used selectively to evaluate cancer risk or complications.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Watchful waiting, medicines that improve urinary flow or reduce prostate size, and minimally invasive/surgical therapy for refractory or complicated disease; Acute retention requires clinician-managed bladder drainage.
Nursing management: applying the nursing process
Hesitancy, weak stream, incomplete emptying, frequency and nocturia; Acute urinary retention causes painful inability to void; and History, examination, urinalysis and assessment of post-void residual/renal function when indicated.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Monitor voiding pattern, bladder distension, urine output and signs of infection.
- After catheterisation or prostate procedures, observe urine colour, clots and catheter patency according to protocol.
- Teach patients to review over-the-counter medicines that may worsen retention with a clinician/pharmacist.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially increasing age, androgen-related prostatic growth, family history.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Prostate Cancer
Pathophysiology
Malignant prostate gland cells grow locally and may spread to lymph nodes and bone, particularly in advanced disease. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include increasing age; family history/genetic susceptibility; Black ancestry; selected hereditary cancer syndromes; and diet/lifestyle factors under continuing study. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Often asymptomatic when localised; advanced disease may cause urinary obstruction, bone pain or systemic symptoms; PSA elevation is not specific for cancer.
Assessment and diagnostic evaluation
PSA-based assessment, prostate imaging and biopsy when indicated; histology and staging guide management; Bone or advanced imaging is used according to risk.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Options include active surveillance, surgery, radiotherapy, androgen-deprivation and additional systemic therapies depending on risk/stage; Treatment decisions consider life expectancy, comorbidity and patient preferences.
Nursing management: applying the nursing process
Often asymptomatic when localised; advanced disease may cause urinary obstruction, bone pain or systemic symptoms; PSA elevation is not specific for cancer; and PSA-based assessment, prostate imaging and biopsy when indicated; histology and staging guide management.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Provide education on urinary, bowel and sexual side effects without assumptions.
- After prostate surgery, monitor catheter function, bleeding, infection and pelvic-floor recovery per protocol.
- Support adherence and monitoring during hormonal therapy, including bone and metabolic health.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially increasing age, family history/genetic susceptibility, Black ancestry.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Bladder Cancer
Pathophysiology
Urothelial malignancy commonly arises from cumulative carcinogenic exposure and may remain superficial or invade bladder muscle. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include tobacco smoking; occupational aromatic amine exposure; chronic bladder irritation in selected settings; prior pelvic radiation; and certain chemotherapy exposures. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Visible or microscopic haematuria, urinary frequency/urgency or irritative symptoms; Persistent unexplained haematuria requires evaluation.
Assessment and diagnostic evaluation
Cystoscopy with biopsy/resection, urinary tract imaging and pathology staging; Urine cytology can help in selected high-grade disease.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Non-muscle-invasive tumours are treated with transurethral resection plus risk-adapted intravesical therapy/surveillance; Muscle-invasive disease may require radical surgery and systemic therapy and/or radiotherapy strategies.
Nursing management: applying the nursing process
Visible or microscopic haematuria, urinary frequency/urgency or irritative symptoms; Persistent unexplained haematuria requires evaluation; and Cystoscopy with biopsy/resection, urinary tract imaging and pathology staging.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Monitor haematuria, urinary retention and infection after cystoscopic procedures.
- For urinary diversion, teach stoma/appliance care and hydration guidance with specialist nurses.
- Support smoking cessation because tobacco exposure is a major modifiable risk factor.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially tobacco smoking, occupational aromatic amine exposure, chronic bladder irritation in selected settings.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Chapter summary
This chapter links system physiology with assessment and nursing priorities. The major conditions discussed include Cholelithiasis and Acute Cholecystitis, Colorectal Cancer, Breast Cancer, Lung Cancer, Benign Prostatic Hyperplasia (BPH), Prostate Cancer, Bladder Cancer. Across these disorders, safe care depends on recognising physiological instability, obtaining focused assessment data, administering prescribed treatment safely, preventing avoidable complications, supporting function and teaching the patient how to monitor for deterioration.
- Cholelithiasis and Acute Cholecystitis: Gallstones may obstruct the cystic duct, causing gallbladder inflammation; migration can also cause jaundice or pancreatitis.
- Colorectal Cancer: Malignancy of the colon or rectum may present through bleeding, altered bowel habit, anaemia or obstruction and is often curable when localised.
- Breast Cancer: Malignant breast tumours vary in receptor status and biological behaviour; treatment is tailored to stage and tumour biology.
- Lung Cancer: Primary lung malignancy is commonly classified as non-small-cell or small-cell cancer and may present locally or with metastatic/systemic effects.
- Benign Prostatic Hyperplasia (BPH): Non-malignant prostate enlargement can obstruct bladder outflow and cause lower urinary tract symptoms.
Self-review questions
Open each item after attempting an answer yourself.
1. What are core postoperative nursing priorities?
Answer: Airway/breathing, circulation, pain, wound/drains, fluid balance, nausea, mobility, thrombosis prevention and detection of complications.
2. Why is early mobilisation encouraged after many operations?
Answer: It supports lung expansion, circulation, bowel function and reduces risks such as venous thromboembolism and deconditioning.
3. What is cancer staging used for?
Answer: To describe disease extent and guide treatment planning and prognosis discussions.
4. Why can BPH cause urinary retention?
Answer: Enlarged periurethral prostate tissue increases resistance to bladder outflow.
5. What should patients with a new stoma receive before discharge?
Answer: Practical stoma-care teaching, supplies planning, warning signs and follow-up support tailored to the procedure.
Skin, Wounds & Systemic Infection
Skin integrity protects against fluid loss, infection and temperature disturbance. Wound and infection care requires systematic assessment of depth, perfusion, pressure, exudate, pain, systemic response and the patient's mobility and nutritional context.
Anatomy overview
Skin consists of epidermis, dermis and subcutaneous tissue. It protects against infection and fluid loss, contributes to temperature regulation and sensation, and participates in vitamin D metabolism. Its integrity depends on perfusion, nutrition, mobility and freedom from prolonged pressure or excessive moisture.
Physiology and clinical significance
Skin injury initiates haemostasis, inflammation, proliferation and remodelling. Burns, pressure, infection and chronic inflammatory disease disturb these processes in different ways. Extensive skin loss can also alter fluid balance and temperature control, while infection can progress from local tissue to systemic sepsis.
Conditions in this chapter
Clinical condition
Burns
Pathophysiology
Thermal, chemical, electrical or radiation injury damages skin and deeper tissues; extensive burns disrupt barrier function, fluid balance and temperature regulation. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include open flame or hot liquids; electrical sources; chemicals; radiation; and unsafe cooking/heating environments. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Pain, blistering or tissue destruction; major burns can cause fluid shifts, hypothermia and systemic inflammatory response; Airway injury is suspected after enclosed-space fire exposure, facial burns, soot, hoarseness or respiratory distress.
Assessment and diagnostic evaluation
Assess burn depth, percentage body-surface area and special areas; evaluate airway and associated trauma first; Laboratory and imaging evaluation depend on severity and mechanism.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Major burns require protocol-based resuscitation, temperature control, analgesia, wound care and specialist burn-centre input; Surgical debridement/grafting may be needed; infection is treated when clinically present rather than with routine systemic prophylaxis.
Nursing management: applying the nursing process
Pain, blistering or tissue destruction; major burns can cause fluid shifts, hypothermia and systemic inflammatory response; Airway injury is suspected after enclosed-space fire exposure, facial burns, soot, hoarseness or respiratory distress; and Assess burn depth, percentage body-surface area and special areas; evaluate airway and associated trauma first.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Prioritise ABCs, keep the patient warm and monitor circulation to burned limbs.
- Use prescribed wound dressings, aseptic technique, pain control and nutritional support.
- Monitor urine output and fluid balance closely in major burns according to resuscitation protocol.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially open flame or hot liquids, electrical sources, chemicals.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Pressure Injury
Pathophysiology
Sustained pressure, often combined with shear, compromises tissue perfusion over vulnerable areas and leads to local tissue damage. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include immobility; reduced sensation; poor perfusion; malnutrition; and moisture, friction and shear. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Non-blanching erythema, skin loss or deeper tissue exposure depending on stage; Darkly pigmented skin may show colour, temperature or consistency changes before obvious redness.
Assessment and diagnostic evaluation
Systematic skin assessment and pressure-injury staging where appropriate; Assess mobility, nutrition, moisture, perfusion and device-related pressure.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Pressure redistribution, treatment of infection when present, debridement in selected wounds and advanced wound/surgical care when indicated; Nutrition and management of underlying illness support healing.
Nursing management: applying the nursing process
Non-blanching erythema, skin loss or deeper tissue exposure depending on stage; Darkly pigmented skin may show colour, temperature or consistency changes before obvious redness; and Systematic skin assessment and pressure-injury staging where appropriate.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Reposition according to individual risk and tolerance, use pressure-redistributing surfaces and protect from moisture/shear.
- Document wound size, tissue, exudate, surrounding skin and pain using consistent methods.
- Do not massage reddened bony prominences; escalate rapidly worsening wounds or systemic infection.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially immobility, reduced sensation, poor perfusion.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Cellulitis
Pathophysiology
Bacterial infection spreads through dermis and subcutaneous tissue, triggering local inflammation that can extend systemically. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include breaks in the skin; oedema/lymphoedema; diabetes; venous insufficiency; and previous cellulitis. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Tender expanding redness with local warmth; fever or systemic symptoms may accompany more severe infection; Purulent lesions suggest abscess or different microbiology and require assessment.
Assessment and diagnostic evaluation
Usually clinical; cultures are reserved for selected cases with drainage, unusual exposure or severe systemic illness; Assess for deeper infection, necrosis and sepsis if pain/systemic toxicity is disproportionate.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Appropriate antimicrobial therapy targeting likely organisms; drainage is required when a true abscess is present; Treat portals of entry such as ulcers or fungal foot disease.
Nursing management: applying the nursing process
Tender expanding redness with local warmth; fever or systemic symptoms may accompany more severe infection; Purulent lesions suggest abscess or different microbiology and require assessment; and Usually clinical; cultures are reserved for selected cases with drainage, unusual exposure or severe systemic illness.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Mark/measure margins when useful, monitor pain, temperature and spread, and elevate affected limb when appropriate.
- Administer antimicrobials as prescribed and monitor response.
- Escalate rapidly progressive pain, blistering, hypotension or systemic toxicity.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially breaks in the skin, oedema/lymphoedema, diabetes.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Psoriasis
Pathophysiology
Immune dysregulation accelerates keratinocyte turnover and creates chronic inflammatory plaques with potential joint involvement. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include genetic susceptibility; immune dysregulation; infection or skin injury triggers; stress; and certain medicines. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Scaly erythematous plaques commonly affect extensor surfaces and scalp; nail changes and pruritus can occur; Joint pain/swelling may indicate psoriatic arthritis.
Assessment and diagnostic evaluation
Usually clinical; biopsy is rarely needed; Assess cardiovascular/metabolic comorbidity and impact on quality of life in moderate-to-severe disease.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Topical therapy for limited disease; phototherapy and systemic/biologic treatments are used for more extensive or resistant disease under specialist care; Psoriatic arthritis needs rheumatology management.
Nursing management: applying the nursing process
Scaly erythematous plaques commonly affect extensor surfaces and scalp; nail changes and pruritus can occur; Joint pain/swelling may indicate psoriatic arthritis; and Usually clinical; biopsy is rarely needed.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Promote gentle skin care, moisturising and adherence to prescribed topical application technique.
- Assess itching, sleep and psychosocial impact without stigmatising visible lesions.
- For systemic therapy, reinforce required monitoring and infection precautions.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially genetic susceptibility, immune dysregulation, infection or skin injury triggers.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Sepsis and Septic Shock
Pathophysiology
A dysregulated host response to infection causes organ dysfunction; profound circulatory and cellular abnormalities define septic shock. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include serious infection; older age or frailty; immunosuppression; invasive devices or recent surgery; and major chronic disease. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Fever or hypothermia, tachycardia, tachypnoea, altered mental state, hypotension, reduced urine output or mottled skin; Any infection with new organ dysfunction should raise concern.
Assessment and diagnostic evaluation
Clinical recognition plus blood tests, cultures and source-directed imaging; lactate and organ-function markers help assess severity; Do not wait for all results before treating a strongly suspected severe infection.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Rapid antimicrobial therapy, source control, fluid resuscitation when indicated and vasopressors for persistent shock under critical-care guidance; Oxygen/ventilatory and organ support are provided as required.
Nursing management: applying the nursing process
Fever or hypothermia, tachycardia, tachypnoea, altered mental state, hypotension, reduced urine output or mottled skin; Any infection with new organ dysfunction should raise concern; and Clinical recognition plus blood tests, cultures and source-directed imaging; lactate and organ-function markers help assess severity.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Escalate immediately using the local sepsis pathway; monitor airway, breathing, circulation, mental status and urine output.
- Obtain cultures promptly when ordered without causing harmful treatment delay.
- Track response to fluids/vasopressors and watch for pulmonary oedema, arrhythmia or worsening perfusion.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially serious infection, older age or frailty, immunosuppression.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Chapter summary
This chapter links system physiology with assessment and nursing priorities. The major conditions discussed include Burns, Pressure Injury, Cellulitis, Psoriasis, Sepsis and Septic Shock. Across these disorders, safe care depends on recognising physiological instability, obtaining focused assessment data, administering prescribed treatment safely, preventing avoidable complications, supporting function and teaching the patient how to monitor for deterioration.
- Burns: Thermal, chemical, electrical or other injury damages skin and sometimes deeper tissues; severity depends on depth, extent, location and associated injury.
- Pressure Injury: Localised damage to skin and/or underlying tissue develops from pressure or pressure combined with shear, often over bony prominences or beneath devices.
- Cellulitis: An acute bacterial infection of dermis and subcutaneous tissue causes spreading erythema, warmth, swelling and pain.
- Psoriasis: A chronic immune-mediated inflammatory disorder accelerates keratinocyte turnover, producing well-demarcated plaques and sometimes systemic joint disease.
- Sepsis and Septic Shock: Sepsis is life-threatening organ dysfunction caused by a dysregulated response to infection; septic shock involves severe circulatory/metabolic abnormalities with higher mortality.
Self-review questions
Open each item after attempting an answer yourself.
1. What are the main layers of skin?
Answer: Epidermis, dermis and subcutaneous tissue.
2. Why does immobility increase pressure-injury risk?
Answer: Prolonged pressure compresses small vessels, reducing tissue perfusion, especially over bony prominences.
3. Why are large burns associated with fluid problems?
Answer: Loss of capillary and skin barrier integrity causes substantial fluid shifts and evaporative loss.
4. What finding suggests cellulitis may be becoming systemic?
Answer: Fever, hypotension, tachycardia, confusion or other organ dysfunction should prompt urgent escalation.
5. What defines sepsis conceptually?
Answer: Organ dysfunction caused by a dysregulated host response to infection.
Eye & Ear Disorders
Eye and ear disorders can threaten vision, hearing, balance and independence. Nursing care includes symptom recognition, medication safety, fall prevention, infection control and urgent escalation of sudden vision loss, severe eye pain or acute neurological symptoms.
Anatomy overview
The eye focuses light through the cornea and lens onto the retina, where photoreceptors convert light into neural signals that pass through the optic nerve. The ear contains external, middle and inner components; the cochlea supports hearing while the vestibular apparatus contributes to balance.
Physiology and clinical significance
Vision depends on clear optical media, controlled intraocular pressure, intact retina and optic pathways. Hearing and balance depend on transmission of sound energy and normal inner-ear function. Sudden visual loss, severe painful red eye, acute neurological symptoms with vertigo, or postauricular swelling can signal emergencies requiring rapid specialist review.
Conditions in this chapter
Clinical condition
Cataract
Pathophysiology
Progressive opacification of the crystalline lens scatters light and reduces visual acuity. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include ageing; diabetes; long-term corticosteroid exposure; eye trauma; and smoking and ultraviolet exposure. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Painless gradual blurred vision, glare, reduced contrast and difficulty with night vision; Symptoms may significantly impair reading, driving or daily activities.
Assessment and diagnostic evaluation
Visual-acuity testing and slit-lamp examination; Assess functional impact and other ocular disease before surgery.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Definitive treatment is cataract extraction with intraocular lens implantation when visual impairment justifies surgery; Temporary optical correction may help earlier stages.
Nursing management: applying the nursing process
Painless gradual blurred vision, glare, reduced contrast and difficulty with night vision; Symptoms may significantly impair reading, driving or daily activities; and Visual-acuity testing and slit-lamp examination.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Pre-operatively reinforce eye-drop and fasting instructions according to the surgical team.
- Post-operatively teach eye protection, prescribed drops and avoidance of eye rubbing.
- Urgently report severe pain, sudden vision reduction, increasing redness or discharge after surgery.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially ageing, diabetes, long-term corticosteroid exposure.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Glaucoma
Pathophysiology
Progressive optic nerve injury, often related to susceptibility to intraocular pressure, leads to irreversible loss of retinal ganglion cells and visual field. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include increasing age; family history; African ancestry for open-angle glaucoma; high intraocular pressure; and steroid exposure or ocular anatomy risk. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Open-angle glaucoma is usually silent until peripheral vision is lost; Acute angle-closure glaucoma can cause severe eye pain, headache, blurred vision, halos, nausea and a red eye.
Assessment and diagnostic evaluation
Tonometry, optic-nerve assessment and visual-field testing; gonioscopy helps assess angle anatomy; Regular follow-up is needed because damage is irreversible.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Pressure-lowering eye drops, laser or surgery are selected according to glaucoma type and progression; Acute angle closure is an ophthalmic emergency requiring immediate specialist treatment.
Nursing management: applying the nursing process
Open-angle glaucoma is usually silent until peripheral vision is lost; Acute angle-closure glaucoma can cause severe eye pain, headache, blurred vision, halos, nausea and a red eye; and Tonometry, optic-nerve assessment and visual-field testing; gonioscopy helps assess angle anatomy.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Teach correct eye-drop administration and punctal occlusion when instructed to reduce systemic absorption.
- Emphasise adherence even when vision feels normal.
- Escalate acute severe eye pain with visual disturbance urgently.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially increasing age, family history, African ancestry for open-angle glaucoma.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Retinal Detachment
Pathophysiology
The neurosensory retina separates from the retinal pigment epithelium, interrupting photoreceptor support and threatening permanent vision. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include posterior vitreous changes with ageing; high myopia; eye trauma; previous eye surgery; and personal/family history of retinal tear/detachment. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Sudden flashes, new floaters or a curtain/shadow across the visual field, usually without pain; Central vision falls if the macula becomes detached.
Assessment and diagnostic evaluation
Urgent dilated retinal examination, often with ocular ultrasound if the fundus cannot be visualised; Identify tears, trauma and high-risk ocular history.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Laser/cryotherapy can treat selected tears; established detachments often require urgent surgical repair; Positioning instructions vary by procedure and must come from the ophthalmic team.
Nursing management: applying the nursing process
Sudden flashes, new floaters or a curtain/shadow across the visual field, usually without pain; Central vision falls if the macula becomes detached; and Urgent dilated retinal examination, often with ocular ultrasound if the fundus cannot be visualised.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Treat new flashes/floaters with a field defect as urgent and minimise delays in ophthalmic review.
- After repair, follow prescribed positioning and eye-protection instructions exactly.
- Teach warning symptoms of recurrence or infection.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially posterior vitreous changes with ageing, high myopia, eye trauma.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Otitis Media
Pathophysiology
Inflammation and fluid accumulation in the middle ear commonly follow Eustachian tube dysfunction and upper respiratory infection. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include recent upper respiratory infection; Eustachian tube dysfunction; young age; smoke exposure; and craniofacial abnormalities. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Ear pain, fever, reduced hearing and a bulging/inflamed tympanic membrane; rupture may cause discharge and pain relief; Recurrent disease may affect hearing.
Assessment and diagnostic evaluation
Otoscopy is central; pneumatic otoscopy/tympanometry can confirm middle-ear effusion; Assess mastoid tenderness or neurological signs in severe disease.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Pain control is important; antibiotics are used selectively based on age, severity and local guidelines; Persistent effusion or recurrent infection may require ENT review.
Nursing management: applying the nursing process
Ear pain, fever, reduced hearing and a bulging/inflamed tympanic membrane; rupture may cause discharge and pain relief; Recurrent disease may affect hearing; and Otoscopy is central; pneumatic otoscopy/tympanometry can confirm middle-ear effusion.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- Assess pain, fever and hearing changes; administer prescribed medicines safely.
- Keep the ear canal free from non-prescribed objects or drops when perforation status is uncertain.
- Escalate post-auricular swelling, severe headache, neck stiffness or systemic illness.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially recent upper respiratory infection, Eustachian tube dysfunction, young age.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Clinical condition
Ménière Disease
Pathophysiology
Disordered inner-ear fluid homeostasis is associated with episodic vestibular and cochlear dysfunction, producing vertigo, tinnitus and fluctuating hearing loss. The clinical picture develops from these physiological changes and from the degree to which compensatory mechanisms can maintain organ function. In practice, severity is judged by symptoms, vital signs, organ function, examination findings and response to initial management rather than by the diagnosis label alone.
Causes and risk factors
Important associations include exact cause often uncertain; inner-ear fluid dysregulation; autoimmune or viral associations proposed; migraine association in some patients; and family susceptibility in a minority. Risk factors do not confirm the diagnosis; they help establish pre-test probability, guide prevention and identify modifiable contributors.
Clinical manifestations
Recurrent spontaneous vertigo episodes with nausea, tinnitus and variable hearing loss; Balance impairment increases fall risk during attacks.
Assessment and diagnostic evaluation
Clinical pattern plus audiometry; alternative vestibular and neurological causes must be excluded; ENT assessment guides diagnosis and treatment.
A focused nursing assessment should establish onset and progression, current physiological stability, relevant past history, medicines/allergies, functional impact and safety concerns. Investigations are interpreted alongside the clinical picture; abnormal results require correlation rather than isolated treatment.
Medical and surgical management
Acute symptom control and longer-term lifestyle/medical strategies are individualised; refractory disease may require procedural treatment; Hearing rehabilitation may be needed.
Nursing management: applying the nursing process
Recurrent spontaneous vertigo episodes with nausea, tinnitus and variable hearing loss; Balance impairment increases fall risk during attacks; and Clinical pattern plus audiometry; alternative vestibular and neurological causes must be excluded.
- Identify the priority nursing problem from the patient’s actual presentation (for example pain, impaired gas exchange, reduced perfusion, fluid imbalance, activity intolerance, infection risk or knowledge deficit).
- Set measurable goals based on physiological stability, symptom relief, function, safety and the patient’s individual plan of care.
- During severe vertigo, reduce falls risk, assist mobility and provide a quiet safe environment.
- Monitor hydration if vomiting is persistent and administer prescribed antiemetic/vestibular medicines.
- Teach patients to sit/lie down when attacks begin and follow specialist hearing/balance plans.
Reassess the patient after interventions. Compare symptoms, vital signs, functional status, fluid balance, relevant laboratory trends and treatment tolerance with the goals of care. Escalate deterioration promptly.
Patient education and discharge planning
- Discuss modifiable risk factors relevant to this patient, especially exact cause often uncertain, inner-ear fluid dysregulation, autoimmune or viral associations proposed.
- Explain the purpose of prescribed treatment, expected monitoring and the importance of follow-up; do not stop or change prescribed medicines without clinician guidance.
- Teach the patient and family which worsening symptoms require urgent review, using the complication/red-flag section below as a guide.
Chapter summary
This chapter links system physiology with assessment and nursing priorities. The major conditions discussed include Cataract, Glaucoma, Retinal Detachment, Otitis Media, Ménière Disease. Across these disorders, safe care depends on recognising physiological instability, obtaining focused assessment data, administering prescribed treatment safely, preventing avoidable complications, supporting function and teaching the patient how to monitor for deterioration.
- Cataract: Progressive opacification of the crystalline lens reduces transmission and focus of light onto the retina.
- Glaucoma: A group of optic neuropathies characterised by progressive retinal ganglion-cell loss, often associated with elevated intraocular pressure.
- Retinal Detachment: Separation of the neurosensory retina from the underlying retinal pigment epithelium threatens permanent vision loss if untreated.
- Otitis Media: Inflammation/infection of the middle ear commonly follows upper respiratory infection, especially in children, but can affect adults.
- Ménière Disease: An inner-ear disorder causes episodic vertigo with fluctuating sensorineural hearing loss, tinnitus and aural fullness.
Self-review questions
Open each item after attempting an answer yourself.
1. Why is glaucoma dangerous even when symptoms are absent?
Answer: Optic nerve damage can progress silently, and lost visual field is irreversible.
2. What symptoms suggest retinal detachment?
Answer: New flashes, a sudden increase in floaters, or a curtain/shadow over the visual field.
3. What is a cataract?
Answer: Opacification of the crystalline lens that reduces the clarity of light reaching the retina.
4. Why are falls precautions relevant in Ménière disease?
Answer: Sudden vertigo and imbalance can cause falls.
5. What postoperative eye symptoms require urgent review?
Answer: Severe pain, sudden reduction in vision, marked increasing redness or discharge, depending on the procedure and instructions.
Core references and guideline sources
The explanatory text in this edition is original educational synthesis. Clinical recommendations should always be checked against current local protocols and full source guidance.
- World Health Organization. Guideline for the pharmacological treatment of hypertension in adults. Geneva: WHO; 2021. Source
- Global Initiative for Asthma (GINA). Global Strategy for Asthma Management and Prevention, 2026 update. Source
- Global Initiative for Chronic Obstructive Lung Disease (GOLD). Global strategy reports and current COPD resources. Source
- KDIGO. Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease, 2024. Source
- American Diabetes Association. Standards of Care in Diabetes—2026. Source
- American Heart Association/American Stroke Association. 2026 Guideline for the Early Management of Patients With Acute Ischemic Stroke. Source
- NICE. Clinical knowledge summaries and guidelines for adult medical and surgical conditions. Source
- World Health Organization. Global tuberculosis programme: consolidated guidance and operational handbooks. Source
- Surviving Sepsis Campaign. International guidelines for management of sepsis and septic shock. Source
- National Institutes of Health and relevant institutes (NHLBI, NIDDK, NCI, NEI): patient and professional disease resources. Source
- Wikimedia Commons file pages listed beneath each image provide the image creator, source and reuse licence. Source