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General Surgery - Physiotherapy Exam Answers

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Q1. What is Shock? Classify Types of Shock. Describe Clinical Features and Management of Haemorrhagic Shock. (15 marks)

Definition of Shock

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Classification of Shock

                          SHOCK
                            |
    ┌───────────┬───────────┼───────────┬───────────┐
    ▼           ▼           ▼           ▼           ▼
Haemorrhagic/ Cardiogenic  Obstructive Distributive Endocrine
Hypovolaemic              Shock       Shock        Shock
Shock
    |               |           |           |
- Haemorrhage   - MI        - PE        - Septic
- Burns         - Arrhythmia - Cardiac   - Anaphylactic
- Vomiting      - Valvular     tamponade - Neurogenic
- Diarrhoea       disease   - Tension
- Third-spacing              pneumothorax

Source: Bailey and Love's Short Practice of Surgery, 28th Ed

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Haemorrhagic Shock - Pathophysiology

Blood Loss
    ↓
↓ Circulating Volume
    ↓
↓ Cardiac Output & ↓ BP
    ↓
Baroreceptor activation
    ↓
Sympathoadrenal response
    ↓
↑ Heart rate, Vasoconstriction, ↑ ADH, ↑ Renin-Angiotensin
    ↓
Compensated Shock (maintained BP)
    ↓ (if loss continues)
Decompensated Shock (↓ BP, ↓ urine output)
    ↓
Organ hypoperfusion → Anaerobic metabolism → Lactic acidosis
    ↓
Multiple Organ Failure → Death

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Clinical Features of Haemorrhagic Shock

Blood pressure is usually well maintained until 30-40% of circulating volume is lost. A 15% loss is within normal compensatory limits.

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Classes of Haemorrhagic Shock (ATLS Classification)

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Management of Haemorrhagic Shock

MANAGEMENT FLOWCHART
        ↓
    1. STOP THE BLEEDING
       - Direct pressure / tourniquet
       - Surgical haemostasis
        ↓
    2. AIRWAY & BREATHING
       - High-flow O₂ (15 L/min via non-rebreather mask)
       - Intubate if GCS < 8
        ↓
    3. IV ACCESS & FLUID RESUSCITATION
       - 2 large-bore peripheral IV lines (16G or larger)
       - Warm IV crystalloid (Hartmann's / Normal saline)
       - Permissive hypotension in penetrating trauma (SBP ~80-90 mmHg)
        ↓
    4. BLOOD PRODUCTS (if Class III/IV)
       - Packed Red Blood Cells
       - Fresh Frozen Plasma (FFP)
       - Platelets (1:1:1 ratio)
        ↓
    5. MONITORING
       - Urine output (target ≥0.5 mL/kg/hr)
       - BP, HR, SpO₂, ABG, Lactate
        ↓
    6. DEFINITIVE CARE
       - Surgical / interventional radiology to stop bleeding
       - ICU admission
        ↓
    7. PREVENT COMPLICATIONS
       - Hypothermia prevention (warm fluids, blankets)
       - Correct coagulopathy (avoid "lethal triad":
         hypothermia + acidosis + coagulopathy)

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Q2. What is Gangrene? Classify Types. Clinical Features and Management of Gas Gangrene. (15 marks)

Definition of Gangrene

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Classification of Gangrene

                        GANGRENE
                           |
           ┌───────────────┼───────────────┐
           ▼               ▼               ▼
         DRY             WET             GAS
       Gangrene         Gangrene        Gangrene
           |               |               |
    (Ischaemia,      (Infection +     (Clostridium
    no infection)    Ischaemia)       perfringens)
                           |
                    ┌──────┴──────┐
                    ▼             ▼
              Moist/Wet     Gas Gangrene
              Gangrene    (Clostridial)
                                  |
                           ┌──────┴──────┐
                           ▼             ▼
                    Necrotising     Fournier's
                    Fasciitis       Gangrene

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Gas Gangrene

Causative Organism

• Clostridium perfringens - Gram-positive, anaerobic, spore-bearing bacillus
• Found widely in soil and faeces
• Produces: collagenase, hyaluronidase, alpha toxin (lecithinase)

Predisposing Factors

• Immunocompromised state
• Diabetes mellitus
• Malignant disease
• Wounds with necrotic tissue, foreign material, or devascularised tissue
• Military wounds (high-velocity missile injuries cause extensive tissue damage)
• Amputation for peripheral vascular disease with open necrotic ulceration

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Clinical Features of Gas Gangrene

TIMELINE OF GAS GANGRENE PROGRESSION

Hour 0-6:         Contaminated wound (trauma, surgery)
                           ↓
Hour 6-24:        Severe, disproportionate LOCAL PAIN
                  Wound oedema, pallor, tense skin
                           ↓
Hour 24-48:       CREPITUS (gas in tissues - palpable crackle)
                  Thin, brown, sweet-smelling discharge
                  Gas visible on plain X-ray
                  Skin becomes bronze/purple → black
                           ↓
Hour 48-72:       SYSTEMIC FEATURES:
                  - High fever, tachycardia
                  - Circulatory collapse
                  - Jaundice (haemolysis)
                  - Renal failure
                  - Multi-organ failure → DEATH if untreated

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Management of Gas Gangrene

MANAGEMENT ALGORITHM
         ↓
  1. IMMEDIATE RESUSCITATION
     - IV access, fluids, O₂
     - Blood cultures, FBC, coagulation, renal function
         ↓
  2. HIGH-DOSE ANTIBIOTICS (IMMEDIATELY)
     - IV Penicillin G (large doses) - FIRST LINE
     - + Clindamycin (stops toxin production)
     - + Metronidazole (for anaerobes)
         ↓
  3. URGENT SURGICAL DEBRIDEMENT
     - Radical excision of ALL necrotic tissue
     - Fasciotomy if compartment syndrome
     - Amputation may be necessary (limb sacrifice to save life)
         ↓
  4. HYPERBARIC OXYGEN THERAPY (if available)
     - Creates unfavourable anaerobic environment
     - Reduces toxin production
     - Adjunct - NOT a substitute for surgery
         ↓
  5. SUPPORTIVE ICU CARE
     - Mechanical ventilation if needed
     - Vasopressors for haemodynamic support
     - Renal replacement therapy
     - Nutritional support
         ↓
  6. PREVENTION
     - Antibiotic prophylaxis before amputations
     - Adequate wound debridement after trauma
     - Tetanus prophylaxis

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Q3. Causes of Cancer + Warburg Effect + Benign vs Malignant Tumour (15 marks)

Causes of Cancer

CAUSES OF CANCER

┌─────────────────────────────────────────────────────┐
│                                                     │
│   GENETIC          ENVIRONMENTAL      BIOLOGICAL    │
│   FACTORS          FACTORS            FACTORS       │
│                                                     │
│ - Inherited gene   - Radiation        - Viruses     │
│   mutations        - Chemical         - Bacteria    │
│ - Proto-oncogene     carcinogens      - Parasites   │
│   activation       - Tobacco smoke    - Chronic     │
│ - Tumour           - Alcohol            inflammation│
│   suppressor gene  - UV radiation                   │
│   loss (p53, Rb)   - Asbestos                       │
│ - DNA repair gene  - Aflatoxin                      │
│   mutations        - Diet (processed                │
│ - Chromosomal        foods, red meat)               │
│   instability      - Obesity                        │
└─────────────────────────────────────────────────────┘

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The Warburg Effect

NORMAL CELL METABOLISM vs WARBURG EFFECT (Cancer Cells)

NORMAL CELLS (Aerobic):
Glucose → Pyruvate → Krebs Cycle → Oxidative Phosphorylation → 36-38 ATP
                                          (requires O₂)

CANCER CELLS (Warburg Effect):
Glucose → Pyruvate → LACTATE
(Even in presence of O₂ - "aerobic glycolysis")
→ Only 2 ATP per glucose
→ BUT rapid glucose uptake compensates

WHY do cancer cells do this?
↓
1. Rapid ATP production (speed > efficiency)
2. Lactate creates acidic tumour microenvironment (promotes invasion)
3. Glycolytic intermediates used for biosynthesis of:
   - Nucleotides (DNA/RNA for cell division)
   - Lipids (cell membranes)
   - Amino acids (proteins)
4. Supports rapid, uncontrolled proliferation

• PET scan (FDG-PET) exploits it - cancer cells take up more radiolabelled glucose (¹⁸F-FDG) than normal cells, lighting up on scan
• Target for cancer therapy (glycolysis inhibitors under research)
• Associated with poor prognosis (high metabolic activity = aggressive tumour)

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Differences Between Benign and Malignant Tumours

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Q4. Stages of Pregnancy, Management of Full-Term Pregnancy, Complications (15 marks)

Stages of Pregnancy

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Stages of Labour (Full-Term Pregnancy Management)

STAGES OF LABOUR

STAGE 1: LATENT PHASE
  - Onset of regular contractions → Cervix fully dilated (10 cm)
  - Primigravida: up to 12-14 hrs | Multigravida: up to 6-8 hrs
  - Early: 0-6 cm dilation (slow)
  - Active: 6-10 cm dilation (faster, ~1 cm/hr)

        ↓

STAGE 2: EXPULSION
  - Full dilation → Delivery of baby
  - Pushing (maternal effort)
  - Primigravida: up to 2 hrs (3 hrs with epidural)
  - Crowning → Delivery of head → Body

        ↓

STAGE 3: PLACENTAL
  - Delivery of baby → Delivery of placenta + membranes
  - Active management: oxytocin 10 IU IM + cord traction
  - Normally within 30 minutes

        ↓

STAGE 4: RECOVERY
  - First 1-2 hours post-delivery
  - Monitor for PPH, vital signs stabilisation

Antenatal Management Visits

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Complications During Management of Full-Term Pregnancy

COMPLICATIONS

MATERNAL                           FETAL/NEONATAL
    |                                    |
┌───────────────────┐         ┌──────────────────────┐
│ Antepartum:       │         │ - Fetal distress      │
│ - Placenta praevia│         │ - Cord prolapse       │
│ - Abruption       │         │ - IUGR                │
│ - Pre-eclampsia   │         │ - Macrosomia          │
│ - GDM             │         │ - Premature delivery  │
│ - PROM            │         │ - Shoulder dystocia   │
│                   │         │ - Birth asphyxia      │
│ Intrapartum:      │         └──────────────────────┘
│ - PPH             │
│ - Obstructed      │
│   labour          │
│ - Uterine rupture │
│ - Eclampsia       │
│                   │
│ Postpartum:       │
│ - PPH (>500 mL)   │
│ - Infection       │
│ - DVT/PE          │
│ - Retained        │
│   placenta        │
└───────────────────┘

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Q5. Short Notes (3 × 5 marks)

(a) Common Causes of Blindness and Prevention

PRIMARY:    - Vitamin A supplementation (children)
            - Eye protection (workplace, UV protection)
            - Vaccination (measles, which can cause corneal scarring)
            - Vector control (trachoma, onchocerciasis)

SECONDARY:  - Screening (diabetics, elderly for glaucoma/ARMD)
            - Early treatment of infections
            - Refractive error correction

TERTIARY:   - Surgical rehabilitation (cataract, corneal transplant)
            - Low vision aids
            - Rehabilitation services

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(b) Keloid

COMPARISON: NORMAL SCAR vs HYPERTROPHIC SCAR vs KELOID

                    Normal      Hypertrophic    Keloid
                    Scar        Scar
                      |              |             |
Boundaries:       Within       Within           BEYOND
                  wound        wound            wound
Regression:       Yes          Yes (often)      NO
Time to appear:   Months       Early            Late (months-years)
Symptoms:         None         Itch/pain        Itch, pain, tenderness
Recurrence:       No           Low              HIGH after excision
Histology:        Organised    Nodular          Thick, hyalinised
                  collagen     collagen         collagen bundles
Sites affected:   Any          Any              Ear lobes, sternum,
                                               shoulder, upper back

• Overactive fibroblasts → Excess collagen (Type I > Type III) production
• Defective apoptosis of fibroblasts
• ↑ TGF-β signalling
• More common in dark-skinned individuals

1. PREVENTION:    - Avoid unnecessary surgery in prone individuals
                  - Tension-free wound closure
                  - Silicone gel sheets (prophylactic)

2. TREATMENT (least to most invasive):
   - Silicone gel/sheets (1st line)
   - Intralesional corticosteroids (triamcinolone) - most common
   - Compression therapy (pressure garments)
   - Cryotherapy
   - Laser therapy
   - Surgical excision (ONLY combined with adjuvant - radiation or steroids; high recurrence if excision alone)
   - Radiotherapy (post-excision)

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(c) Types of Anaesthesia

                    ANAESTHESIA
                        |
          ┌─────────────┼─────────────┐
          ▼             ▼             ▼
      GENERAL        REGIONAL       LOCAL
    ANAESTHESIA     ANAESTHESIA   ANAESTHESIA
          |               |             |
   Unconscious,    Block of           Small
   complete loss   nerve pathway      area
   of sensation              |
                    ┌────────┴────────┐
                    ▼                 ▼
                CENTRAL           PERIPHERAL
                NEURAXIAL         NERVE BLOCKS
                    |                 |
              ┌─────┴─────┐     - Brachial plexus
              ▼           ▼     - Femoral nerve
           Spinal      Epidural  - Sciatic nerve
          (subarachnoid)          - Intercostal

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(d) Causes of Sudden Hearing Loss (Sudden Sensorineural Hearing Loss - SSNHL)

CAUSES OF SUDDEN HEARING LOSS

CONDUCTIVE                    SENSORINEURAL
     |                              |
- Foreign body              Vascular:
- Cerumen impaction          - Cochlear infarction
- Otitis media (acute)       - Microvascular disease
- Otitis media with          - Vertebrobasilar insufficiency
  effusion ("glue ear")      
- Perforated TM             Infectious:
- Otosclerosis               - Viral (mumps, measles,
- Trauma                       herpes zoster = Ramsay Hunt)
                             - Bacterial (meningitis)
                             
                            Autoimmune:
                             - Autoimmune inner ear disease
                             - SLE, Wegener's
                             
                            Neoplastic:
                             - Acoustic neuroma (CN VIII)
                             - Cerebellopontine angle tumour
                             
                            Trauma:
                             - Temporal bone fracture
                             - Barotrauma (perilymph fistula)
                             - Noise-induced
                             
                            Drugs/Ototoxicity:
                             - Aminoglycosides (gentamicin)
                             - Loop diuretics (furosemide)
                             - Cisplatin, quinine
                             
                            Idiopathic (majority, ~85%):
                             - Presumed viral or vascular

• Oral corticosteroids (prednisolone) within 2 weeks - mainstay
• Intratympanic steroids if systemic not possible
• MRI brain/internal auditory meatus - exclude acoustic neuroma
• Audiogram

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Q6. Blood Groups, Transfusion Indications, Haemolytic Disease of the Newborn (15 marks)

Blood Group Systems

• Based on presence/absence of D antigen
• Rh positive (Rh+): has D antigen (~85% of population)
• Rh negative (Rh-): lacks D antigen

BLOOD GROUP COMPATIBILITY

                O-
                ↓ (can donate to all)
        O+   A-   B-   AB-
         ↓    ↓    ↓    ↓
        A+   B+        AB+
                        ↓ (can only receive from all)
                       AB+

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Indications for Blood Transfusion

• General guideline: Hb <7 g/dL - restrictive strategy (transfuse 1 unit, re-check)
• Cardiac/older patients: Hb <8 g/dL
• Symptomatic patients: Regardless of absolute Hb number - treat symptoms
• "One unit at a time, then reassess" - current best practice

TRANSFUSION DECISION FLOWCHART

         Patient has anaemia/blood loss
                    ↓
         Is patient SYMPTOMATIC?
         (breathlessness, chest pain,
          syncope, tachycardia, hypotension)
                    ↓
          YES                    NO
           ↓                      ↓
     Transfuse                  Check Hb
     regardless                    ↓
     of Hb           Hb <7 g/dL?  (8 g/dL in cardiac)
                        ↓
              YES               NO
               ↓                 ↓
           Transfuse         Conservative management
           1 unit             Iron supplementation
           reassess           Treat underlying cause

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Haemolytic Disease of the Newborn (HDN)

PATHOPHYSIOLOGY OF HDN

1st PREGNANCY (Rh- mother + Rh+ father):
    Fetal RBCs (Rh+) enter maternal circulation
    (especially at delivery - "fetomaternal haemorrhage")
                    ↓
    Maternal immune system SENSITISED → produces Anti-D IgG antibodies
    (usually NO disease in 1st pregnancy as antibodies form after delivery)

2nd PREGNANCY (with Rh+ fetus):
    Maternal Anti-D IgG crosses placenta (IgG crosses; IgM does not)
                    ↓
    Binds to fetal Rh+ RBCs → opsonisation
                    ↓
    Fetal RBC destruction (extravascular haemolysis in spleen)
                    ↓
         ┌─────────────────────────────┐
         ▼                             ▼
   FETAL ANAEMIA                 Excess BILIRUBIN
         ↓                             ↓
  Extramedullary                Kernicterus (if
  haemopoiesis                  bilirubin crosses
  (liver, spleen,               blood-brain barrier)
  "erythroblastosis")
         ↓
  Hydrops fetalis
  (severe: oedema,
   ascites, death)

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Sources: Bailey and Love's Short Practice of Surgery (28th Ed); Pye's Surgical Handicraft (22nd Ed) | Bailey and Love's Short Practice of Surgery, pp. 33-36, 79