Comprehensive Systems & Pathophysiology Review Notes

Exam Scope & Strategy

• Cumulative final; GI + Reproductive content ≈ 20 % of grade
• PowerPoint lists ONLY what you must know; if it is not on the slides or said in review, do not study it
• Focus on high-yield contrasts (e.g., Crohn vs UC) and pathophysiologic links instead of memorising every detail

Gastro-Intestinal (GI) System

Inflammatory Bowel Disease (IBD)

• Crohn’s Disease
  • Trans-mural (full-thickness) inflammation that can strike anywhere mouth→anus
  • “Skip/patchy” lesions → multiple separated ulcerations
  • Higher risk of fistula, perforation, malabsorption
• Ulcerative Colitis (UC)
  • Continuous, shallow ulceration starting in rectum and moving proximally through colon only
  • Limited to innermost mucosal layer
  • Hallmark: bloody diarrhoea
• Compare/contrast matrix
  • Crohn’s: entire GI → full thickness → skip → perforation
  • UC: colon only → mucosa → continuous → bleeding

Liver Disorders & Portal System

• Cirrhosis
  • Hepatocytes replaced by irreversible fibrotic tissue → loss of function
  • Early S/Sx: malaise, flatulence, RUQ heaviness/discomfort
  • Late S/Sx (mnemonic "JAACP‐BP")
  • Jaundice (↑ bilirubin from failed clearance)
  • Ascites (↓ albumin → ↓ oncotic pull + portal HTN → fluid shifts)
  • Anasarca / peripheral oedema
  • Confusion (↑ ammonia → hepatic encephalopathy)
  • Portal Hypertension (↑ splenic & portal pressures)
  • Bleeding risk (↓ clotting factors, varices)
• Esophageal Varices
  • Dilated veins secondary to portal HTN → fragile, life-threatening upper GI bleed
• GERD
  • Reflux of gastric acid → night epigastric pain, chronic cough, sore throat, morning sour taste

Gallbladder Pathology

• Gallstone spectrum terminology
  • Cholelithiasis = stone(s) in gallbladder (may be asymptomatic)
  • Biliary colic = transient cystic-duct obstruction → intermittent RUQ pain after fatty meal
  • Cholecystitis = persistent cystic-duct obstruction → inflammation, fever, leukocytosis
  • Choledocholithiasis = stone in common bile duct → ↑ risk pancreatitis & cholangitis
• Stone chemistry → know “cholesterol vs pigment vs mixed”, but exam stresses location & clinical picture

Bowel Obstruction

• Small bowel
  • Structural role = absorption; diameter cannot expand → early severe N/V, minimal distension
  • Common causes: adhesions, incarcerated/strangulated hernia
• Large bowel
  • Role = storage; highly distensible → massive distension, crampy LLQ pain, late/absent vomiting
  • Common causes: colorectal cancer, volvulus, diverticular disease

Viral Hepatitis (A B C) – know transmission

• A = fecal–oral (contaminated water/shellfish)
• B = blood/body fluids & sexual; vertical
• C = blood-borne (IVDU, transfusion) – chronicity common

Malabsorption & Structural Disorders

• Celiac Disease
  • Autoimmune destruction of intestinal villi when gluten present → villous atrophy → malabsorption, steatorrhoea, weight loss
• Diverticulosis vs Diverticulitis
  • LLQ pseudodiverticula (sigmoid) formed by high pressure
  • “-itis” = inflammation → LLQ pain, fever, leukocytosis; avoid seeds/nuts controversial
• Peritonitis (surgical emergency)
  • Sterile peritoneum contaminated (perforation, appendicitis, blood-borne)
  • Classic findings: sudden severe, rigid "board-like" abdomen, tachycardia, rebound tenderness
• H. pylori
  • #1 cause of peptic ulcer disease; urease + → mucosal damage
• Abdominal hernias
  • Protrusion of bowel through weak fascia; painful bulge, worse w/ valsalva; strangulation = N/V + severe pain
• Pancreatitis
  • Premature enzymatic activation → autodigestion; gallstones & ETOH main triggers

Pathogens & Immune Disorders

Hypersensitivity & Allergy

• Anaphylaxis = IgE-mediated systemic reaction → airway oedema, wheeze, hives, hypotension; treat epinephrine

HIV / AIDS

• Retrovirus targets CD4 T-helper cells
• Diagnostic AIDS criteria (either)
  • \text{CD4} < 200 \text{ cells/mm}^3 OR
  • Presence of AIDS-defining illness (e.g., PCP, Kaposi’s sarcoma)

Immunity Types

Inflammation & Sepsis Continuum

• 5 cardinal signs: redness, heat, swelling, pain, loss of function
• SIRS = vitals ± WBC abnormalities (no infection proven)
• Sepsis = SIRS + suspected/confirmed infection
• Severe sepsis / Septic shock = sepsis + organ dysfunction, hypotension &/or \text{Lactate} > 2\,\text{mmol·L}^{-1}

Autoimmune & Toxin Disorders

• Rheumatoid Arthritis: B-cell auto-Ab vs synovial joints → symmetric pain, stiffness, deformation
• Botulism: Clostridium botulinum neurotoxin (canned foods) → descending flaccid paralysis
• Tetanus: C. tetani toxin via wound → trismus, risus sardonicus, severe muscle spasm “lock-jaw”

Renal & Urinary System

Acute Kidney Injury (AKI)

• Prerenal = perfusion/volume problem (dehydration, hemorrhage)
• Intrarenal = nephron damage (ATN, nephrotoxic drugs)
• Postrenal = obstruction (BPH, stones)
• Recovery Phases
  1. Oliguric: ↓ U/O <400 mL/d, ↑ BUN/Cr, hyperkalaemia
  2. Diuretic: ↑ U/O, hypovolaemia, still ↑ labs
  3. Recovery: GFR & labs normalise

Chronic Kidney Disease (CKD)

• Progressive ↓ GFR for ≥3 months; staged by GFR value

Glomerular Syndromes

• Nephrotic ("O" = protein): massive proteinuria (>3.5 g/d), hypoalbuminaemia → generalised oedema, compensatory hyperlipidaemia
• Nephritic: inflammation → haematuria, oliguria, cola-coloured urine, mild proteinuria

Infection & Tract Disorders

• Lower UTI (Acute cystitis) – dysuria, frequency, urgency; elderly = confusion
• Upper UTI (Pyelonephritis) – cystitis S/Sx + fever, flank pain, N/V, chills
• Incontinence Types
  • Stress: weak sphincter (laugh, cough)
  • Urge: detrusor overactivity (OAB)
  • Overflow: retention + dribble (obstruction, neurogenic)
  • Functional: cognitive/physical inability to reach toilet
• Nephrolithiasis (kidney stone)
  • Sudden colicky flank pain radiating groin; hematuria; NO dysuria usually
  • Calcium-oxalate stones: high Ca²⁺ + low fluid intake

Reproductive Disorders

Female

• Cervical Cancer: strong association with HPV strains 16/18; PAP & HPV vaccine for prevention
• Pelvic Inflammatory Disease (PID): ascending polymicrobial infection; risks: multiple partners, unprotected sex, prior PID

Male

• Testicular Torsion: adolescent rapid growth; acute severe scrotal pain, swelling, N/V; surgical emergency to preserve perfusion
• Benign Prostatic Hyperplasia (BPH): hyperplasia of prostatic cells → weak stream, hesitancy, frequency, nocturia → risk retention/UTI

Cellular Injury & Cancer Biology

• Most common cellular insult = hypoxia
  • Forces anaerobic glycolysis → ↓ ATP → pump failure → swelling, acidosis, death
• Cellular adaptations
  • Hypertrophy (↑ size), Atrophy (↓ size), Hyperplasia (↑ number), Metaplasia (one cell type replaced by another), Dysplasia (abnormal, precancerous)
• Neoplasia
  • Benign = slow, well-differentiated, non-invasive
  • Malignant = autonomous, poorly differentiated, invasive, metastatic, angiogenic, immune-evasive
• Warning signs (CAUTION mnemonic) – especially unintended weight loss & fatigue
• Grading (microscopic appearance, differentiation) vs Staging (extent/spread, TNM)

Genetic Concepts & Inheritance

• Nondisjunction (meiosis error) → aneuploidies: trisomy 21, monosomy X
• Inheritance Patterns
  • Autosomal Dominant: 1 mutant allele → dz (no carriers). e.g., Huntington, Marfan, AD-PKD
  • Autosomal Recessive: need 2 mutant alleles; heterozygotes = carriers. e.g., CF, Sickle Cell, Tay-Sachs, PKU
  • X-Linked Recessive: mutated X; males affected/not, females affected/carrier/unaffected. e.g., Haemophilia A/B, red-green colour blindness

Blood & Platelets

Anaemias (focus table)

• Shared general S/Sx: fatigue, pallor, dyspnoea, dizziness
  

• Sympathetic compensation: ↑ HR, ↑ contractility, peripheral vasoconstriction
• Hormonal: ADH & RAAS → Na⁺ + H₂O reabsorption, vasoconstriction to maintain BP

Acute Haemolytic Transfusion Reaction

• ABO mismatch → intravascular haemolysis, fever, flank pain, shock
• Major complication: DIC (Disseminated Intravascular Coagulation)
  • Systemic micro-clots and consumption of clotting factors → simultaneous bleeding
  • Labs: ↑ D-dimer, ↓ platelets & fibrinogen, prolonged PT/aPTT

Study tip: Pair each disorder with (1) key pathophysiology sentence, (2) defining clinical sign, (3) must-know lab/criterion. Re-create small comparison tables from memory until effortless recall.