Pathophysiology of Common Diseases

Understanding pathophysiology — the disordered physiological processes that underlie disease — is essential for nursing practice in the UAE. It allows you to anticipate complications, interpret clinical findings, and make sound nursing judgments. For the DOH (UAE) examination, pathophysiology questions are integrated into clinical scenarios rather than tested as pure science. This topic covers the key disease processes encountered in UAE clinical practice, with particular emphasis on the conditions that are most prevalent in the Gulf region.

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🟢 Lite — Quick Review (1h–1d)

Rapid summary for last-minute revision before your exam.

Cellular Adaptation — Key Concepts:

• Hypertrophy: Cell enlargement (muscle with exercise, cardiac muscle in hypertension)
• Hyperplasia: Cell number increase (thyroid goitre in iodine deficiency)
• Atrophy: Cell size decrease (muscle wasting from disuse)
• Metaplasia: One mature cell type replaced by another (smoker’s bronchial epithelium)
• Dysplasia: Abnormal cell appearance (pre-malignant; CIN cervical intraepithelial neoplasia)
• Neoplasia: Uncontrolled cell proliferation (benign vs malignant)

Cell Death:

• Necrosis: Cell death from injury (coagulative, liquefactive, caseous, fat, gangrenous)
• Apoptosis: Programmed cell death (normal; excessive = degenerative diseases; deficient = cancer)

Inflammation — The Classic Signs (Celsus):

• Rubor (redness)
• Tumor (swelling)
• Calor (heat)
• Dolor (pain)
• Functio laesa (loss of function) — added by Galen

⚡ Exam Tip: Acute inflammation is a protective response — it is only harmful when excessive, prolonged, or misdirected (autoimmune disease). Knowing when inflammation is helpful vs. harmful is a key examination concept.

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🟡 Standard — Regular Study (2d–2mo)

Standard content for students with a few days to months.

1. Atherosclerosis — The Root of Cardiovascular Disease

Pathophysiology:

1. Endothelial injury — Hypertension, hyperlipidaemia, smoking, diabetes damage the endothelium
2. Lipid accumulation — LDL cholesterol enters arterial wall; oxidised LDL is taken up by macrophages → foam cells
3. Fatty streak formation — Earliest visible lesion; occurs in childhood
4. Fibrous plaque — Smooth muscle cells proliferate; collagen deposited; plaque forms
5. Complicated plaque — Calcification, rupture, thrombosis, haemorrhage

Key Clinical Sequelae:

• Coronary artery disease → Angina → MI
• Cerebral vessels → Stroke (ischaemic or haemorrhagic)
• Peripheral arteries → Peripheral vascular disease → claudication, gangrene
• Renal arteries → Renovascular hypertension → chronic kidney disease

Risk Factors — UAE Context:

• Modifiable: Smoking (including shisha), hypertension, hyperlipidaemia, diabetes mellitus, obesity, sedentary lifestyle, diet high in saturated fats
• Non-modifiable: Age, male gender, family history, genetic predisposition
• South Asian and Arab populations have higher cardiovascular risk at lower BMIs

2. Diabetes Mellitus — Complications

Acute Complications:

Diabetic Ketoacidosis (DKA):

• Occurs in Type 1 DM (can occur in Type 2 under stress)
• Absolute insulin deficiency → hyperglycaemia → osmotic diuresis → dehydration and electrolyte loss
• Ketosis → metabolic acidosis
• Signs: Polyuria, polydipsia, nausea/vomiting, abdominal pain, Kussmaul breathing, confusion, Fruity breath (acetone), Hypotension
• DKA criteria: Blood glucose > 250 mg/dL; pH < 7.3; HCO₃⁻ < 18; serum ketones positive; anion gap elevated

Hyperosmolar Hyperglycaemic State (HHS):

• Occurs in Type 2 DM; more insidious onset
• Severe hyperglycaemia (>600 mg/dL) without significant ketosis
• Severe dehydration (osmotic diuresis)
• Altered consciousness, seizures, coma
• More fatal than DKA due to extreme dehydration

Hypoglycaemia:

• Blood glucose < 70 mg/dL
• Adrenergic symptoms: Sweating, tremor, tachycardia, anxiety, hunger
• Neuroglycopenic symptoms: Confusion, slurred speech, seizures, coma
• Treatment: 15 g fast-acting carbohydrate (4 glucose tablets, 150 mL juice); repeat in 15 min; if unconscious, IV dextrose or IM glucagon

Chronic Complications:

• Microvascular: Retinopathy (→ blindness), nephropathy (→ renal failure), neuropathy (→ foot ulcers, Charcot joint)
• Macrovascular: MI, stroke, peripheral vascular disease
• Other: Increased infection risk, cataracts, gastroparesis

3. COPD and Asthma — Obstructive Lung Disease

COPD — Chronic Obstructive Pulmonary Disease:

• Progressive, partially reversible airflow obstruction
• Emphysema: Alveolar wall destruction → loss of elastic recoil → air trapping → barrel chest, pink puffer, hyperinflation
• Chronic bronchitis: Airway inflammation and mucus hypersecretion → blue bloater, cyanosis, oedema
• Both often coexist

Asthma:

• Reversible airway inflammation and bronchoconstriction
• Triggers: Allergens, cold air, exercise, infection, stress
• Inflammation → smooth muscle spasm → mucosal oedema → mucus plugging → airway narrowing
• Eosinophils are the predominant inflammatory cells in asthma

Acute Severe Asthma (Status Asthmaticus):

• Silent chest (no air movement — ominous sign of severe obstruction)
• Cyanosis, bradycardia, hypotension (impending respiratory arrest)
• SpO₂ < 92% despite oxygen
• Unable to speak in full sentences

4. Acute Kidney Injury (AKI)

Pre-renal AKI (60–70% of cases):

• Caused by decreased renal perfusion (hypovolaemia, shock, sepsis)
• BUN:Creatinine ratio > 20:1 (urea disproportionately elevated because decreased GFR + increased passive reabsorption)
• Reversible if perfusion restored promptly

Intrinsic Renal AKI:

• Acute tubular necrosis (ATN) — most common (ischaemia or nephrotoxins); aminoglycosides, contrast media, myoglobin
• Acute interstitial nephritis — drug reaction (NSAIDs, penicillins, PPIs)
• Glomerulonephritis — haematuria, proteinuria, oedema

Post-renal AKI:

• Obstruction of urine outflow (stones, BPH, bilateral ureteric obstruction)
• Relieved by removing obstruction

AKI vs CKD:

• AKI: Acute onset; potentially reversible; normal/small kidneys on ultrasound
• CKD: Chronic; irreversible; small, scarred kidneys

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🔴 Extended — Deep Study (3m+)

Comprehensive coverage for students on a longer study timeline.

5. Cancer Biology — Key Concepts

Characteristics of Malignant Cells (Hallmarks of Cancer):

1. Self-sufficiency in growth signals
2. Insensitivity to growth inhibitory signals
3. Evasion of apoptosis
4. Unlimited replicative potential (telomerase activation)
5. Sustained angiogenesis
6. Invasion and metastasis
7. Reprogramming energy metabolism
8. Immune evasion

TNM Staging System:

• Tumour size and local extent
• N regional lymph node involvement
• M distant metastasis
• Higher T, N, M = more advanced disease

Metastasis Pathways:

• Direct extension (local spread)
• Lymphatic spread (most common for carcinomas)
• Haematogenous spread (most common for sarcomas)
• Transcoelomic (across body cavities — e.g., ovarian cancer spreading to peritoneum)

Tumour Markers (used in monitoring, not primary diagnosis):

• CEA: Colorectal cancer (and others)
• CA-125: Ovarian cancer
• CA 19-9: Pancreatic cancer
• AFP: Hepatocellular carcinoma, testicular cancer
• PSA: Prostate cancer (but elevated in BPH and prostatitis too)

6. Shock — Types and Progression

Hypovolaemic Shock:

• Causes: Haemorrhage, dehydration, burns, vomiting, diarrhoea
• Early: Cool extremities, tachycardia, narrow pulse pressure, increased diastolic
• Late: Hypotension, metabolic acidosis, multi-organ failure

Cardiogenic Shock:

• Pump failure (MI, arrhythmias, cardiomyopathy)
• Signs: Pulmonary oedema, elevated JVP, cold extremities

Distributive Shock (Vasodilatory):

• Septic shock: Vasodilation from inflammatory mediators; warm extremities initially (warm shock); fever, elevated WBC, source of infection; cold shock in late/refractory stages
• Anaphylactic shock: Type I hypersensitivity; histamine release → vasodilation, bronchospasm, urticaria; requires IM adrenaline immediately
• Neurogenic shock: Loss of sympathetic tone after spinal cord injury; bradycardia, hypotension, warm/dry skin; treated with vasopressors

Obstructive Shock:

• Cardiac tamponade, tension pneumothorax, massive PE
• All cause impaired cardiac output due to mechanical obstruction

Shock Progression: Compensated → Decompensated → Irreversible (multi-organ failure → death)

Exam Watch: In septic shock, the hallmark is vasodilation causing warm extremities and a bounding pulse early on, combined with hypotension that doesn’t respond well to fluids alone — vasopressors are required early. This distinguishes it from hypovolaemic shock where fluids are the primary treatment.

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