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KMTC/QP-08/EPS - Full Exam Explanation

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SECTION 1: MULTIPLE CHOICE QUESTIONS

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Q1. Which one of the following is true about natural killer (NK) cells?

• How they kill: NK cells release perforin (punches holes in the target cell membrane) and granzymes (enzymes that trigger apoptosis/programmed cell death inside the target). This process is called lysis.
• They target virus-infected cells and tumor (cancer) cells - not just bacteria, so option D is wrong.
• They do not engulf pathogens (that is phagocytosis, done by neutrophils and macrophages) - so option A is wrong.
• They definitely DO attack microbes/infected cells - so option C is wrong.

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Q2. The disease that causes large lips, nose, and tongue is called:

• GH causes soft tissue overgrowth - hence enlarged lips, tongue (macroglossia), nose, hands, and feet.
• Other features: protruding jaw (prognathism), large hands/feet, coarse facial features, joint pain, headaches.
• It differs from gigantism (same cause but happens before growth plates close, so the person grows very tall).
• Parkinson's and Alzheimer's are neurological diseases - they don't cause physical enlargement of features.
• Cancer can cause mass effects locally but not this characteristic pattern.

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Q3. The following are side effects of opioids EXCEPT:

• Constipation ✔ - opioids slow gut motility (very common, doesn't go away with tolerance)
• Sedation ✔ - CNS depression
• Respiratory depression ✔ - the most dangerous/life-threatening effect; opioids suppress the brainstem respiratory centers
• Miosis (pin-point pupils), nausea, vomiting, urinary retention, euphoria

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Q4. The following is NOT a route of exposure to organophosphate poisoning:

• Inhalation ✔ - breathing in sprayed pesticides
• Ingestion ✔ - swallowing (common in intentional poisoning/suicide attempts)
• Skin/mucous membrane contact ✔ - absorbed through the skin (especially in farm workers)

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Q5. The emerging infectious disease is:

• HIV/AIDS - emerged in the 1980s; now well-established, classified as an established disease
• TB - ancient disease, re-emerging in some contexts but not "newly emerging"
• Cancer - not an infectious disease
• COVID-19 - caused by SARS-CoV-2, first identified in Wuhan, China in December 2019, declared a global pandemic by WHO in March 2020. This is the classic example of an emerging infectious disease.

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Q6. The following is NOT a clinical feature of Diabetic Ketoacidosis (DKA):

• Polyuria ✔ - excess urination due to osmotic diuresis from high blood glucose
• Polydipsia ✔ - excessive thirst
• Polyphagia ✔ - excessive hunger (cells starving despite high blood glucose)
• Also: Kussmaul breathing (deep rapid breaths), fruity/acetone breath, nausea, vomiting, abdominal pain, altered consciousness

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Q7. Which one of the following is the link between innate and adaptive immunity?

• Innate immunity - fast, non-specific (NK cells, neutrophils, macrophages)
• Adaptive immunity - slow, specific (T cells, B cells, antibodies)

• They act immediately like innate cells (no prior sensitization needed)
• But they can be activated and regulated by adaptive immune cytokines (like IL-2, IL-12, IFN-γ from T-cells)
• NK cells also interact with antibodies via ADCC (Antibody-Dependent Cell-Mediated Cytotoxicity) - using antibodies from the adaptive system to target cells
• They communicate with dendritic cells, which present antigens to T-cells (adaptive system)

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Q8. The following infections are caused by Staphylococcus aureus EXCEPT:

• A. Furuncles (boils)
• B. Sinusitis
• C. Endocarditis
• D. Headache

• Furuncles (boils) ✔ - classic staph skin infection
• Sinusitis ✔ - S. aureus can cause sinusitis
• Endocarditis ✔ - S. aureus is the most common cause of acute bacterial endocarditis (infects heart valves, especially in IV drug users)

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Q9. Which among the following is NOT a congenital heart disease?

• Septal defect ✔ - ASD (Atrial Septal Defect) or VSD (Ventricular Septal Defect) - holes in the heart walls - classic CHD
• Obstruction defect ✔ - e.g., pulmonary stenosis, aortic stenosis, coarctation of aorta - CHD
• Cyanotic heart disease ✔ - e.g., Tetralogy of Fallot, Transposition of Great Arteries - CHD causing blue discoloration

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Q10. The following is NOT an example of an NSAID:

• Ibuprofen ✔ - classic NSAID
• Aspirin ✔ - also an NSAID (though unique in its irreversible COX inhibition)
• Diclofenac ✔ - NSAID
• Others: naproxen, indomethacin, celecoxib

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Q11. Type of antibody that assumes a major role in bloodborne and tissue infections:

• It is the only antibody that crosses the placenta (providing passive immunity to newborns)
• It plays the major role in secondary immune responses (long-term memory)
• It opsonizes pathogens (coats them for phagocytosis)
• Effective against bloodborne and tissue infections (bacteria, viruses, toxins)

• IgA - found in secretions (saliva, tears, breast milk, gut) - mucosal immunity
• IgM - first antibody produced in a new infection (primary response); also activates complement
• IgE - allergic reactions and combating parasites
• IgD - B-cell receptor; function not fully understood

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Q12. The following is supportive management of DKA before referral:

• ABC = Airway, Breathing, Circulation - the foundation of emergency management
• Fluid resuscitation - DKA patients are severely dehydrated due to osmotic diuresis. IV normal saline (0.9% NaCl) is started immediately.

• Inject antibiotics - only if there's a known infection precipitating DKA, not routine
• Send to lab - labs are important but NOT before stabilizing the patient
• Administer painkillers - not a priority in DKA management

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Q13. Which type of antibody is responsible for combating parasitic infections?

• When IgE binds to a parasite, it activates mast cells and eosinophils (via Fc-epsilon receptors)
• Eosinophils release toxic granules that kill parasites
• Elevated IgE levels are a clue for parasitic infections or atopic conditions (asthma, eczema, allergic rhinitis)

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Q14. Which one of the following cells is responsible for humoral immunity?

• Humoral immunity - mediated by antibodies (immunoglobulins)
• Cell-mediated immunity - mediated by T-cells

• Helper T-cells - assist B-cells and cytotoxic T-cells; they don't directly produce antibodies
• Killer T-cells (Cytotoxic T-cells) - destroy infected or cancerous cells directly (cell-mediated)
• T-lymphocytes - cell-mediated immunity, NOT humoral

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Q15. Which type of condition is best known as an endocrine disorder?

• Cystic fibrosis - genetic disease affecting chloride channels (CFTR gene); primarily a respiratory and GI disease
• Heterochromia - different colored irises; a genetic pigmentation variation, not endocrine
• Chimerism - having two genetically distinct cell populations in one body; genetic, not endocrine

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Q16. Which one of the following innate cells is responsible for pus formation?

• Dead and dying neutrophils
• Dead bacteria
• Cellular debris
• Tissue fluid

• Mast cells - involved in allergic reactions and releasing histamine
• Monocytes - circulate in blood, mature into macrophages in tissue
• Macrophages - long-term cleanup cells, but neutrophils make the acute pus

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Q17. The following is NOT a risk factor for COPD:

• Cigarette smoking ✔ - #1 cause of COPD worldwide
• Mosquito coil ✔ - burning mosquito coils indoors produces particulate matter and chemicals that damage airways (biomass smoke is a major COPD risk factor in developing countries)
• Biogas fuel ✔ - indoor burning of biomass/solid fuels (wood, dung, crop waste) for cooking is a major COPD risk in low-income countries

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Q18. The following is NOT a factor affecting drug absorption:

• Drug solubility ✔ - lipid-soluble drugs cross membranes better; poorly soluble drugs are poorly absorbed
• pH ✔ - affects drug ionization; weak acids are better absorbed in acidic environments (stomach), weak bases in alkaline (intestine)
• Presence of food ✔ - food can increase or decrease absorption depending on the drug (some drugs must be taken on an empty stomach)
• Also: blood flow to absorption site, surface area, gastrointestinal motility, drug formulation

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Q19. The following are fungal infections EXCEPT:

• Valley fever (Coccidioidomycosis) ✔ - caused by the fungus Coccidioides immitis; affects the lungs
• Athlete's foot (Tinea pedis) ✔ - caused by dermatophyte fungi (Trichophyton spp.); affects feet
• Ringworm (Tinea corporis) ✔ - caused by dermatophyte fungi; despite the name, no worm involved - it's fungal

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Q20. The following is a WORRYING complication of NSAIDs:

• The stomach lining loses its protection
• This leads to peptic ulcers and gastrointestinal (GI) bleeding - the most serious/worrying complication
• GI bleeding can be life-threatening (hematemesis, melena)

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SECTION 2: SHORT ANSWER QUESTIONS

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Q21. List the bacterial infections of the skin (5 Marks)

1. Impetigo - Staphylococcus aureus or Streptococcus pyogenes; honey-colored crusting lesions
2. Furuncles (Boils) - S. aureus; painful hair follicle infections
3. Carbuncles - Multiple interconnected furuncles
4. Cellulitis - S. aureus or S. pyogenes; deep skin/subcutaneous tissue infection
5. Erysipelas - S. pyogenes; superficial skin infection with sharp borders
6. Folliculitis - S. aureus; hair follicle inflammation
7. Leprosy - Mycobacterium leprae; chronic skin/nerve disease

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Q22. Supportive management of organophosphate poisoning (5 Marks)

1. Remove from exposure - Remove contaminated clothing, wash skin with soap and water
2. Airway management - Ensure open airway; suction secretions; consider intubation if needed
3. Oxygen administration - High-flow O2 (organophosphates cause bronchoconstriction and respiratory failure)
4. IV fluid administration - Maintain circulation
5. Atropine - Antidote; blocks muscarinic effects (SLUDGE); give until secretions dry up
6. Pralidoxime (2-PAM) - Reactivates acetylcholinesterase if given early
7. Refer to higher facility immediately after stabilization

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Q23. Clinical signs and symptoms of coronavirus (COVID-19) infection (5 Marks)

• Fever (most common)
• Dry cough
• Fatigue/malaise
• Shortness of breath / difficulty breathing
• Loss of taste (ageusia) and loss of smell (anosmia) - hallmark features
• Headache
• Sore throat
• Muscle aches (myalgia)
• Diarrhea (in some patients)
• Severe: pneumonia, ARDS (Acute Respiratory Distress Syndrome), multi-organ failure

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Q24. Risk factors for hypertension (5 Marks)

1. Age - risk increases with age
2. Obesity/overweight - excess weight increases cardiac workload
3. Physical inactivity - sedentary lifestyle
4. High salt (sodium) diet - increases fluid retention and blood pressure
5. Smoking and alcohol - damage blood vessels
6. Diabetes mellitus - damages blood vessels
7. Family history/genetics
8. Stress
9. Kidney disease - secondary hypertension

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Q25. List 5 examples of opioids (5 Marks)

1. Morphine - gold standard for severe pain
2. Codeine - mild-moderate pain; also antitussive
3. Fentanyl - very potent; used in anesthesia and chronic pain patches
4. Tramadol - synthetic opioid; moderate pain
5. Pethidine (Meperidine) - used in labor pain
6. Methadone - used in opioid dependence treatment
7. Oxycodone - moderate-severe pain

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Q26. Classification of antimicrobial agents (5 Marks)

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Q27. List 5 indications of muscle relaxants (5 Marks)

1. Surgical anesthesia - to facilitate intubation and surgery
2. Muscle spasms - back pain, neck pain, spasms from injury
3. Spasticity - in multiple sclerosis, cerebral palsy, stroke
4. Tetanus - to manage severe muscle rigidity
5. Electroconvulsive therapy (ECT) - to prevent fractures during seizures
6. Facilitation of mechanical ventilation

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Q28. Risk factors for hypoglycemia (5 Marks)

1. Excessive insulin dose - in diabetic patients
2. Skipping meals / inadequate food intake
3. Strenuous exercise - increases glucose consumption
4. Alcohol use - inhibits hepatic gluconeogenesis
5. Oral hypoglycemic drugs (e.g., sulfonylureas like glibenclamide)
6. Liver disease - impaired glycogen stores
7. Kidney disease - reduced insulin clearance
8. Insulinoma - insulin-secreting tumor

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SECTION 3: LONG ESSAY QUESTIONS

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Q29. Diabetic Ketoacidosis (DKA) - 20 Marks

• Missed insulin dose - most common
• Infection (pneumonia, UTI)
• New-onset Type 1 Diabetes (first presentation)
• Trauma, surgery, myocardial infarction, stroke

• The "3 Polys": Polyuria, Polydipsia, Polyphagia
• Nausea, vomiting, abdominal pain
• Kussmaul breathing (deep, rapid)
• Fruity/acetone breath
• Dehydration (dry mucous membranes, sunken eyes)
• Altered consciousness, coma in severe cases

• Blood glucose (elevated >11 mmol/L)
• Blood gases (low pH, low bicarbonate)
• Urine dipstick (ketones +++)
• Serum electrolytes (low K+ initially; total body K+ depleted)
• Full Blood Count (look for infection)
• ECG (K+ changes affect the heart)

1. IV fluids (0.9% NaCl)
2. Insulin infusion
3. Potassium replacement (critically important - serum K+ drops as insulin drives K+ into cells)
4. Monitor and treat precipitating cause
5. Antibiotics if infection confirmed

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Q30. Life Cycle of Plasmodium falciparum (Malaria) - 20 Marks

1. Infected female Anopheles mosquito bites → injects sporozoites into bloodstream
2. Sporozoites travel to liver → infect hepatocytes → multiply → form merozoites (hepatic/pre-erythrocytic stage, ~5-7 days)
3. Merozoites released into blood → infect red blood cells (RBCs)
4. Inside RBCs: ring stage → trophozoite → schizont → rupture releases more merozoites (every 48 hours for P. falciparum - causing tertian fever pattern)
5. Some merozoites develop into gametocytes (male/female forms)

1. Mosquito bites infected human → ingests gametocytes
2. In the mosquito gut: gametocytes mature → fertilization → zygote → ookinete → oocyst
3. Oocyst ruptures → releases sporozoites → migrate to salivary glands
4. Mosquito bites next human → cycle repeats

• Infects all ages of RBCs (others prefer young or old RBCs only)
• Causes cytoadherence - infected RBCs stick to blood vessel walls → blockage → cerebral malaria, organ failure
• No dormant liver stage (unlike P. vivax and P. ovale)

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KMTC/QP-08/EPS - General Medicine

Complete Exam Explanation (All 30 Questions)

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SECTION 1: MULTIPLE CHOICE QUESTIONS

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Q1. Which one of the following is true about natural killer (NK) cells?

✅ Answer: B - They kill the invading microorganism by lysis

1. Perforin-granzyme pathway: NK cells release perforin, a protein that punches circular pores (holes) into the membrane of the target cell. Through these pores, granzymes (proteolytic enzymes) enter the target cell and activate caspases, triggering apoptosis (programmed cell death from inside the cell).
2. Death receptor pathway: NK cells express FasL on their surface, which binds to Fas on the target cell surface and directly triggers apoptosis.

• Virus-infected cells - NK cells detect cells that have LOST MHC class I molecules (viruses often downregulate MHC-I to hide from cytotoxic T-cells; NK cells exploit this "missing self" recognition)
• Tumor/cancer cells - which also often lose MHC-I expression
• They are NOT limited to bacteria only (option D is wrong)
• They do NOT engulf pathogens - phagocytosis is done by neutrophils and macrophages (option A is wrong)

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Q2. The disease that causes large lips, nose, and tongue is called:

✅ Answer: C - Acromegaly

• Enlarged, coarsened facial features
• Macroglossia (large tongue)
• Enlarged lips and nose
• Protruding jaw (prognathism)
• Prominent forehead (frontal bossing)
• Enlarged hands and feet (patients notice rings no longer fit, shoe size increases)
• Enlarged internal organs (heart, liver - organomegaly)

• Gigantism = excess GH occurs BEFORE puberty (growth plates still open) → person grows extremely tall
• Acromegaly = excess GH occurs AFTER puberty (growth plates closed) → features enlarge but height does not increase much

• Diabetes mellitus (GH is anti-insulin / diabetogenic)
• Hypertension and cardiomegaly
• Sleep apnea (enlarged tongue/soft tissues obstruct airway)
• Arthritis (joint changes)
• Hyperprolactinemia in 20-40% of cases (co-secretion with prolactin)

• Surgical removal of pituitary adenoma (transsphenoidal surgery)
• Somatostatin analogues (octreotide, lanreotide) - suppress GH secretion
• GH receptor antagonist (pegvisomant) for resistant cases

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Q3. The following are side effects of opioids EXCEPT:

✅ Answer: B - Cough

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Q4. The following is NOT a route of exposure to organophosphate poisoning:

✅ Answer: D - Injection

• Inhalation - Agricultural workers breathing in pesticide spray; industrial accidents; nerve agent exposure (e.g., sarin gas)
• Ingestion - Deliberate self-poisoning (common in developing countries); accidental ingestion of contaminated food
• Skin and mucous membrane contact - OPs are highly lipid-soluble and penetrate intact skin readily; farm workers who handle pesticides without gloves

• Salivation, Lacrimation, Urination, Defecation, GI cramps, Emesis (muscarinic effects)
• Defecation, Urination, Miosis, Bradycardia, Bronchospasm/Bronchorrhea, Emesis, Lacrimation, Salivation
• Nicotinic effects: muscle weakness, fasciculations, paralysis
• CNS: anxiety, seizures, coma

1. Remove from exposure - remove clothes, wash skin
2. Atropine - blocks muscarinic receptors (stops SLUDGE); given until secretions dry
3. Pralidoxime (2-PAM) - reactivates AChE if given within hours (before "aging" occurs)
4. Diazepam - for seizures
5. Airway support / mechanical ventilation

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Q5. The emerging infectious disease is:

✅ Answer: D - COVID-19

• Has recently appeared in a population for the first time, OR
• Has existed previously but is rapidly increasing in incidence, geographic range, or severity

• Caused by SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus 2)
• First identified in Wuhan, Hubei Province, China in December 2019
• Spread globally within weeks; WHO declared a pandemic on March 11, 2020
• A brand-new pathogen, previously unknown to science - the textbook definition of "emerging"

• HIV/AIDS - emerged in the 1970s-1980s; now well characterized, with established treatments (ART)
• TB (Tuberculosis) - one of the oldest diseases known to humanity; Mycobacterium tuberculosis has infected humans for thousands of years; it is "re-emerging" in some contexts but not truly "emerging"
• Cancer - not an infectious disease; cannot be spread person to person (except for virus-associated cancers like cervical cancer with HPV, but cancer itself is not infectious)

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Q6. The following is NOT a clinical feature of Diabetic Ketoacidosis (DKA):

✅ Answer: D - Hematuria

1. Hyperglycemia (blood glucose >11 mmol/L or >200 mg/dL)
2. Ketonemia/Ketonuria (ketones in blood and urine)
3. Metabolic acidosis (pH <7.3, bicarbonate <18 mmol/L)

• Polyuria - glucose spills into urine, pulls water by osmosis → large urine output
• Polydipsia - dehydration triggers thirst
• Polyphagia - cells starving despite high blood sugar (insulin absent, so cells cannot uptake glucose)
• Weakness, lethargy, nausea, anorexia
• Kussmaul breathing - deep, rapid, labored breathing; the body tries to blow off CO2 to compensate for acidosis
• Fruity/acetone smell on breath - from exhaled acetone (a volatile ketone)
• Dehydration signs - dry skin, dry mucous membranes, sunken eyes, tachycardia
• Abdominal pain (can mimic acute abdomen)
• Altered consciousness/coma in severe cases

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Q7. Which one of the following is the LINK between innate and adaptive immunity?

✅ Answer: C - Natural Killer cells

• NK cells are classified as innate lymphoid cells - they act immediately without prior sensitization
• However, they communicate extensively with the adaptive system:
  • They interact with dendritic cells (which present antigens to T-cells)
  • They are upregulated by adaptive cytokines like IL-2 (from T-helper cells), IL-12, and IFN-γ
  • They perform ADCC (Antibody-Dependent Cell-mediated Cytotoxicity) - they use IgG antibodies (adaptive system product) bound to targets as signals to kill (via Fc receptors on NK cell surface)
• They produce IFN-γ, which activates macrophages (innate) and promotes Th1 differentiation (adaptive)

• Neutrophils - purely innate; short-lived; don't interact with adaptive system in a bridging capacity
• Mast cells - innate; mainly allergic reactions; interact with IgE but don't bridge the systems
• Basophils - innate; allergic responses; not considered the bridge

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Q8. Infections caused by Staphylococcus aureus EXCEPT:

✅ Answer: D - Headache

• Furuncles (boils) - painful, pus-filled skin infections around hair follicles. Classic S. aureus infection.
• Sinusitis - S. aureus is one of the causes of bacterial sinusitis (along with S. pneumoniae and H. influenzae)
• Endocarditis - S. aureus is the MOST COMMON cause of acute bacterial endocarditis; it aggressively destroys heart valves; very common in IV drug users (skin bacteria introduced via injection)
• Cellulitis, impetigo, wound infections, osteomyelitis, septic arthritis, pneumonia, septicemia, toxic shock syndrome, food poisoning (via enterotoxins)

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Q9. Which is NOT a congenital heart disease?

✅ Answer: D - Cerebrovascular disease

1. Septal defects (holes between heart chambers):
   • ASD (Atrial Septal Defect) - hole between right and left atria
   • VSD (Ventricular Septal Defect) - hole between right and left ventricles; most common CHD overall
   • Blood shunts left → right (oxygenated → deoxygenated side) initially
2. Obstructive defects (narrowing that obstructs blood flow):
   • Pulmonary stenosis - narrowed pulmonary valve
   • Aortic stenosis - narrowed aortic valve
   • Coarctation of the aorta - narrowing of the aorta itself
3. Cyanotic heart disease (right-to-left shunts causing blue baby):
   • Tetralogy of Fallot (TOF) - VSD + pulmonary stenosis + overriding aorta + right ventricular hypertrophy; most common cyanotic CHD
   • Transposition of the Great Arteries (TGA)
   • Truncus arteriosus

• Acquired (develop during life, often due to hypertension, atherosclerosis, diabetes)
• Not structural heart defects
• Not present at birth as congenital abnormalities
• Located in the brain, not the heart

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Q10. The following is NOT an example of an NSAID:

✅ Answer: D - Amoxicillin

• Analgesia (pain relief) - by reducing prostaglandin sensitization of pain receptors
• Anti-inflammatory - by reducing prostaglandin-mediated inflammation
• Antipyretic (fever reduction) - by reducing PGE2 in the hypothalamus

• Ibuprofen - most widely used OTC NSAID
• Aspirin (acetylsalicylic acid) - unique: irreversibly inhibits COX-1 and COX-2; low-dose used for antiplatelet effect
• Diclofenac - commonly prescribed; injectable and oral forms
• Naproxen, Indomethacin, Ketorolac, Celecoxib (COX-2 selective)

• No COX inhibition
• No anti-inflammatory effect
• No antipyretic action
• A completely different target and mechanism

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Q11. Type of antibody that plays a major role in bloodborne and tissue infections:

✅ Answer: A - IgG

• IgG is the dominant antibody in blood and interstitial fluid - precisely where bloodborne pathogens circulate
• It opsonizes bacteria (coats them) - marks them for phagocytosis by neutrophils and macrophages
• It activates complement (via classical pathway) → destroys bacteria
• It neutralizes bacterial toxins and viruses
• The ONLY antibody that crosses the placenta - provides passive immunity to the neonate for the first 3-6 months of life
• Mediates ADCC with NK cells

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Q12. Supportive management of DKA before referral:

✅ Answer: C - Do ABC and fluid administration

• Ensure the airway is open and clear
• DKA patients may have reduced consciousness and risk aspiration
• Position patient appropriately; suction if needed

• Assess respiratory rate and effort
• Kussmaul breathing is expected but monitor for respiratory fatigue
• Provide supplemental oxygen

• DKA patients lose massive amounts of fluid through osmotic diuresis
• Fluid deficit is typically 3-6 liters in an adult
• Start IV Normal Saline (0.9% NaCl) immediately: replaces volume, corrects hypotension, dilutes glucose
• Fluids are the single most important pre-hospital/pre-referral intervention

• Inject antibiotics - only if there is a confirmed/strongly suspected infection triggering DKA; not routine pre-referral management
• Send to lab - critical labs are needed, but NOT before ABC and stabilization; labs do not treat the patient
• Painkillers - abdominal pain in DKA is expected and usually resolves with DKA treatment; opioids may mask abdominal signs and are not indicated

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Q13. Which antibody is responsible for combating parasitic infections?

✅ Answer: B - IgE

1. IgE antibodies bind to parasite antigens
2. The Fc portion of IgE binds to Fc-epsilon receptors on eosinophils and mast cells
3. Eosinophils degranulate and release major basic protein (MBP), eosinophil cationic protein (ECP), and peroxidase - these are directly toxic to parasites
4. This is called Antibody-Dependent Cell-mediated Cytotoxicity (ADCC) by eosinophils

• Elevated serum IgE + eosinophilia = strongly suggests parasitic infection (or atopic disease)
• Parasitic infections: Ascaris, Strongyloides, Toxocara, Schistosoma, hookworm

• Type I hypersensitivity (immediate allergic reactions) - asthma, anaphylaxis, urticaria, hay fever
• Binds to mast cells → cross-linking by allergen → mast cell degranulation → histamine release → allergic symptoms

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Q14. Which cell is responsible for humoral immunity?

✅ Answer: B - B-lymphocytes

• Carried out by B-lymphocytes
• "Humoral" refers to body fluids (humors) - antibodies circulate in blood and lymph
• When activated (requires antigen + T-helper cell signals), B-cells differentiate into:
  • Plasma cells - antibody-secreting factories (produce thousands of antibody molecules per second)
  • Memory B-cells - long-lived; respond rapidly if the same antigen is encountered again
• Effective against: extracellular bacteria, toxins, free viruses (before they enter cells)

• Carried out by T-lymphocytes
• Cytotoxic T-cells (CD8+) - kill virus-infected cells and tumor cells directly
• Helper T-cells (CD4+) - coordinate the immune response; activate B-cells and cytotoxic T-cells; produce cytokines
• Effective against: intracellular pathogens (viruses, mycobacteria), cancer cells

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Q15. Which type of condition is best known as an endocrine disorder?

✅ Answer: B - Hyperthyroidism

• The thyroid gland overproduces T3 (triiodothyronine) and T4 (thyroxine)
• Most common cause: Graves' disease (autoimmune - TSH receptor antibodies stimulate the thyroid)
• Other causes: toxic multinodular goiter, toxic adenoma, thyroiditis

• Weight loss despite increased appetite (hypermetabolism)
• Heat intolerance, excessive sweating
• Palpitations/tachycardia (heart racing)
• Tremor (fine tremor of hands)
• Anxiety, irritability, restlessness
• Diarrhea (increased gut motility)
• Exophthalmos (bulging eyes) - specific to Graves' disease
• Goiter (enlarged thyroid gland)
• Menstrual irregularities

• Cystic fibrosis - single gene disorder (CFTR mutation) affecting chloride transport; primarily causes thick mucus in lungs, pancreas, GI tract - NOT hormonal
• Heterochromia - different colored irises; caused by differential melanin distribution in the iris; genetic, developmental, or due to trauma - no hormone involvement
• Chimerism - a person who has two genetically distinct cell populations in their body (e.g., from twin embryo fusion); genetic condition, not endocrine

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Q16. Which innate cell is responsible for pus formation?

✅ Answer: D - Neutrophils

• Dead and dying neutrophils (the main component)
• Dead bacteria
• Destroyed tissue debris
• Plasma proteins
• Enzymes from neutrophil granules

1. Margination - neutrophils roll along blood vessel walls near infection
2. Diapedesis - they squeeze through blood vessel walls into tissue
3. Chemotaxis - they follow chemical signals (IL-8, C5a, LTB4) toward the bacteria
4. Phagocytosis - engulf bacteria into phagosomes
5. Killing - respiratory burst produces reactive oxygen species (superoxide, H2O2, hypochlorous acid); also release proteases and defensins
6. Death - neutrophils die in large numbers after killing bacteria

• Abscess = localized collection of pus
• Neutrophil count in blood (WBC) rises during bacterial infection = leukocytosis (diagnostic indicator)

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Q17. The following is NOT a risk factor for COPD:

✅ Answer: B - Drinking dirty water

1. Cigarette smoking - accounts for ~80% of COPD cases worldwide. Smoke causes chronic airway inflammation, mucus hypersecretion, and destroys alveolar walls (emphysema). Dose-response: measured in pack-years (packs/day × years smoked)
2. Indoor biomass fuel combustion - burning wood, coal, dung, crop waste for cooking/heating. Major risk factor in developing countries. Produces fine particulate matter and toxic gases that damage airways. Mosquito coils and biogas fuel both produce fine particles and chemicals when burned indoors.
3. Occupational dust/fumes - coal dust, grain dust, silica, welding fumes
4. Outdoor air pollution
5. Genetic factors - Alpha-1 antitrypsin deficiency causes early, severe emphysema in non-smokers (rare)
6. Recurrent childhood respiratory infections

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Q18. The following is NOT a factor affecting drug absorption:

✅ Answer: B - Dosages

• Dosage (the quantity of drug) determines how much drug is available to be absorbed, but it does NOT change the rate, mechanism, or efficiency of absorption
• A larger dose doesn't make the drug absorb faster or better per unit - the same proportion of the dose will still be absorbed
• Dosage is a factor affecting drug concentration/exposure, not the absorption process itself

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Q19. The following are fungal infections EXCEPT:

✅ Answer: C - Bordetella pertussis

• It is a gram-negative coccobacillus
• Causes Whooping cough (pertussis) - a severe respiratory illness
• Transmitted by respiratory droplets
• Classic: paroxysmal cough ending in an inspiratory "whoop", followed by vomiting
• Vaccine-preventable (DTP/DTaP vaccine)

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Q20. The following is a WORRYING complication of NSAIDs:

✅ Answer: B - Gastrointestinal bleeding

• COX-1 produces prostaglandins PGE2 and PGI2 in the stomach
• These prostaglandins normally:
  • Stimulate mucus and bicarbonate secretion (mucosal barrier)
  • Maintain blood flow to the stomach mucosa
  • Inhibit acid secretion
• When COX-1 is inhibited → less protective prostaglandins → stomach lining becomes vulnerable to acid damage → peptic ulcers → GI bleeding

• 3× in patients under 65 years
• 8× in patients over 75 years (Source: Mulholland & Greenfield's Surgery)
• Risk increases further with: higher doses, longer duration, concomitant steroids, anticoagulants, H. pylori infection

• GI bleeding can present as hematemesis (vomiting blood) or melena (black tarry stools)
• Can be life-threatening requiring blood transfusion, endoscopy, surgery
• Can be silent (no pain) in elderly patients
• Unlike cough, vomiting, or headache (minor nuisances), GI bleeding can kill

• Co-prescribe Proton Pump Inhibitors (PPIs) e.g., omeprazole with NSAIDs in at-risk patients
• Use COX-2 selective inhibitors (celecoxib) which spare COX-1 → less GI toxicity

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SECTION 2: SHORT ANSWER QUESTIONS

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Q21. List the bacterial infections of the skin (5 Marks)

1. Impetigo - Staphylococcus aureus or Streptococcus pyogenes; most common in children; superficial honey-colored crusts; non-bullous and bullous forms
2. Folliculitis - S. aureus; infection of hair follicles; red papules/pustules at follicle bases
3. Furuncle (Boil) - S. aureus; deep painful hair follicle infection with central pus; common on neck, axilla, buttocks
4. Carbuncle - S. aureus; multiple interconnected furuncles; may cause systemic features (fever, malaise)
5. Cellulitis - S. aureus or S. pyogenes; spreading infection of dermis and subcutaneous tissue; red, hot, swollen, painful skin; no clear demarcation
6. Erysipelas - S. pyogenes; superficial cellulitis with SHARP raised borders; bright red; affects face and legs; high fever
7. Leprosy - Mycobacterium leprae; chronic infection causing skin patches with loss of sensation, nerve thickening

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Q22. Supportive management of organophosphate poisoning (5 Marks)

1. Remove from exposure: Remove all contaminated clothing; wash skin/hair thoroughly with soap and water (healthcare workers should wear gloves to avoid secondary contamination)
2. Airway management: Position patient (recovery position if unconscious); suction secretions; prepare for intubation if respiratory failure imminent
3. High-flow Oxygen: OPs cause bronchoconstriction and respiratory muscle paralysis; 100% O2 via face mask
4. IV access and fluids: Establish IV line; administer normal saline for hypotension/shock
5. Antidote - Atropine: IV atropine 2-4 mg every 5-10 minutes until secretions dry (salivation, lacrimation, bronchorrhea controlled). Atropine competes with ACh at muscarinic receptors. LARGE doses may be needed.
6. Pralidoxime (2-PAM): IV; reactivates acetylcholinesterase by cleaving the OP-AChE bond; must be given EARLY (before "aging" - irreversible binding - occurs within hours)
7. Diazepam (benzodiazepine): For seizure control and to reduce anxiety/fasciculations
8. Refer immediately to a higher-level facility with ICU capabilities

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Q23. Clinical signs and symptoms of COVID-19 (5 Marks)

• Fever (>38°C) - most common presenting feature
• Dry cough - persistent, non-productive
• Fatigue and malaise
• Loss of taste (ageusia) - hallmark, very specific for COVID-19
• Loss of smell (anosmia) - hallmark
• Headache
• Sore throat
• Myalgia (muscle aches)
• Nasal congestion / runny nose
• Diarrhea, nausea (GI manifestations in ~20% of patients)

• Shortness of breath / dyspnea - indicates pneumonia
• Chest tightness/pain
• Hypoxia (SpO2 <94%) - requires oxygen
• Pneumonia visible on chest X-ray (bilateral ground-glass opacities)
• ARDS (Acute Respiratory Distress Syndrome)
• Multi-organ failure in critical cases

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Q24. Risk factors for hypertension (5 Marks)

1. Age - vessels stiffen progressively; prevalence rises sharply after age 55
2. Family history/genetics - polygenic inheritance; 50% heritability
3. Race - higher prevalence and severity in people of African descent

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Q25. List 5 examples of opioids (5 Marks)

1. Morphine - gold standard opioid analgesic; severe pain; post-op, cancer, MI
2. Codeine - mild-moderate pain; cough suppression; prodrug (converted to morphine by CYP2D6)
3. Fentanyl - 100× more potent than morphine; used in surgery, ICU sedation, cancer pain patches (transdermal)
4. Tramadol - weak opioid + serotonin/norepinephrine reuptake inhibitor; moderate pain; lower risk of dependence
5. Pethidine (Meperidine) - used in labor analgesia; short-acting; toxic metabolite (norpethidine) can cause seizures
6. Methadone - long-acting; used for chronic pain and opioid dependence treatment (maintenance therapy)
7. Oxycodone - moderate-severe pain; found in combination with acetaminophen (Percocet)
8. Buprenorphine - partial agonist; used for pain and opioid dependence (with naloxone as Suboxone)

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Q26. Classify antimicrobial agents (5 Marks)

• Beta-lactams: Penicillins (Amoxicillin, Ampicillin), Cephalosporins (Ceftriaxone), Carbapenems (Meropenem) - inhibit cell wall synthesis
• Macrolides: Erythromycin, Azithromycin, Clarithromycin - inhibit 50S ribosome (protein synthesis)
• Fluoroquinolones: Ciprofloxacin, Levofloxacin - inhibit DNA gyrase and topoisomerase IV
• Aminoglycosides: Gentamicin, Streptomycin, Amikacin - inhibit 30S ribosome
• Tetracyclines: Doxycycline, Tetracycline - inhibit 30S ribosome; broad spectrum
• Sulfonamides: Cotrimoxazole (Sulfamethoxazole + Trimethoprim) - inhibit folate synthesis

• Azoles: Fluconazole, Ketoconazole, Itraconazole - inhibit ergosterol synthesis
• Polyenes: Amphotericin B - binds ergosterol; disrupts fungal membrane

• Antiretrovirals: Zidovudine (AZT), Tenofovir - for HIV
• Acyclovir - for Herpes viruses (HSV, VZV)
• Oseltamivir (Tamiflu) - for Influenza

• Antiprotozoals: Metronidazole (amoebiasis, giardiasis), Chloroquine/Artemisinin (malaria)
• Antihelminthics: Albendazole, Mebendazole (worms/helminths)

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Q27. List 5 indications of muscle relaxants (5 Marks)

1. Surgical anesthesia - neuromuscular blockers (succinylcholine, rocuronium, vecuronium) facilitate tracheal intubation and provide skeletal muscle relaxation during surgery
2. Mechanical ventilation - relax respiratory muscles to allow the ventilator to breathe for the patient in ICU
3. Acute muscle spasms - back pain, neck injury, torticollis; centrally acting drugs (diazepam, baclofen, methocarbamol, tizanidine)
4. Spasticity - chronic muscle rigidity in multiple sclerosis, cerebral palsy, spinal cord injury; baclofen (GABA-B agonist), tizanidine (alpha-2 agonist)
5. Tetanus - generalized muscle rigidity and spasms; IV diazepam + neuromuscular blockade in severe cases
6. Electroconvulsive Therapy (ECT) - succinylcholine given before ECT to prevent fractures from convulsions
7. Endotracheal intubation - to allow insertion of the breathing tube without resistance

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Q28. Risk factors for hypoglycemia (5 Marks)

1. Excess insulin dose - most common in Type 1 DM; miscalculated insulin dose or accidental overdose
2. Oral hypoglycemic drugs - sulfonylureas (glibenclamide, glipizide, glimepiride) stimulate insulin release regardless of blood glucose; high risk of hypoglycemia
3. Skipping meals / inadequate carbohydrate intake - insulin injected but insufficient glucose absorbed
4. Excessive physical exercise - muscles consume large amounts of glucose; if insulin dose not adjusted, hypoglycemia follows
5. Alcohol consumption - ethanol inhibits hepatic gluconeogenesis (liver's ability to make new glucose from amino acids/lactate); heavy drinkers who skip meals at highest risk
6. Liver disease - impaired gluconeogenesis and glycogen storage; liver cannot maintain blood glucose during fasting
7. Kidney disease - kidneys normally degrade insulin; in renal failure, insulin persists longer → prolonged hypoglycemic effect
8. Insulinoma - rare insulin-secreting pancreatic tumor; causes fasting hypoglycemia

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SECTION 3: LONG ESSAY QUESTIONS

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Q29. Diabetic Ketoacidosis (DKA) - Full Discussion

Definition

• Hyperglycemia (blood glucose >11 mmol/L / 200 mg/dL)
• Ketonemia and ketonuria (elevated ketone bodies in blood and urine)
• Metabolic acidosis (arterial pH <7.3, serum bicarbonate <18 mmol/L)

Causes / Precipitating Factors

1. Missed insulin dose - most common cause (non-compliance, deliberate omission to control weight)
2. Intercurrent illness/Infection - any infection (UTI, pneumonia, gastroenteritis) increases counter-regulatory hormones (glucagon, cortisol, catecholamines, GH) which worsen insulin resistance
3. New-onset Type 1 DM - DKA may be the first presentation; undiagnosed diabetes
4. Trauma or surgery - physiologic stress raises counter-regulatory hormones
5. Myocardial infarction (heart attack) or stroke
6. Certain drugs - corticosteroids, thiazide diuretics, atypical antipsychotics

Pathophysiology

Insulin deficiency
      ↓
Cells cannot take up glucose → HYPERGLYCEMIA
      ↓
Fatty acids released from adipose tissue (lipolysis)
      ↓
Liver converts fatty acids → KETONE BODIES
(acetoacetate, beta-hydroxybutyrate, acetone)
      ↓
Ketones are acids → METABOLIC ACIDOSIS
      ↓
High blood glucose → glucose spills into urine → osmotic diuresis
      ↓
DEHYDRATION + ELECTROLYTE LOSS (Na+, K+, Cl-, PO4, Mg)

Clinical Features (from Goldman-Cecil Medicine)

• Progressive polyuria (frequent, large volume urination)
• Polydipsia (intense thirst)
• Polyphagia (hunger - cells starving)
• Nausea, vomiting
• Abdominal pain (can mimic surgical emergency)
• Weakness, fatigue, lethargy

• Kussmaul breathing - deep, sighing, rapid respirations (compensatory respiratory alkalosis trying to blow off CO2 to raise pH)
• Fruity/acetone smell on breath (exhaled acetone)
• Dehydration - dry skin, dry mucous membranes, sunken eyes, reduced skin turgor, tachycardia, hypotension (orthostatic → frank shock)
• Depressed consciousness ranging from drowsiness to coma (severe cases)
• Fever (if precipitated by infection)

Investigations

Management

1. IV fluids - 0.9% NaCl 1 liter in first 30-60 minutes; then 500 ml/hour for 4 hours
2. Insulin infusion - Regular (soluble) insulin IV; DO NOT give insulin before checking K+ (insulin drives K+ into cells; if K+ already low, could cause fatal hypokalemia and cardiac arrest)
3. Potassium replacement - Add K+ to IV fluids once serum K+ <5.5 mmol/L; monitor closely
4. Treat precipitating cause - Antibiotics if infection identified; treat MI if present

• Hourly blood glucose
• 2-hourly electrolytes (especially K+)
• 4-hourly blood gases
• Fluid balance (urine output, IV input)

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Q30. Life Cycle of Plasmodium falciparum (Malaria)

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PHASE 1: HEPATIC (LIVER) STAGE - In the Human

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PHASE 2: ERYTHROCYTIC (RED BLOOD CELL) STAGE - In the Human

• Ring trophozoite (early ring form - this is what you see on a blood film)
• Trophozoite (feeding stage; digests hemoglobin → produces hemozoin/malaria pigment)
• Schizont (divides to produce 16-32 new merozoites)

• Cytoadherence - infected RBCs stick to blood vessel walls → capillary blockage
• Cerebral malaria - when cerebral vessels blocked → brain damage

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PHASE 3: MOSQUITO STAGE (Sexual Reproduction)

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Life Cycle Diagram (Robbins & Kumar Basic Pathology)

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Why P. falciparum is the Deadliest

1. Cytoadherence - PfEMP1 causes infected RBCs to stick to vessel walls → capillary occlusion → organ failure
2. Cerebral malaria - congestion of brain capillaries → seizures, coma, death (especially in children)
3. Infects ALL ages of RBCs - so the parasitemia can be very high (>5% of RBCs infected)
4. No dormant liver stage - no relapses, but the acute infection is overwhelming
5. Severe anemia - massive RBC destruction
6. Metabolic acidosis, hypoglycemia, ARDS, acute kidney injury - multi-organ failure in severe cases

Complications

• Cerebral malaria (most feared)
• Severe anemia
• Acute kidney injury (blackwater fever - hemoglobinuria from hemolysis)
• Acute Respiratory Distress Syndrome (ARDS)
• Hypoglycemia (parasite consumes glucose; quinine treatment also lowers glucose)
• Splenic rupture
• Death if untreated

Treatment

• Artemisinin-based Combination Therapy (ACT) - Artemether-Lumefantrine (Coartem) - first-line for uncomplicated falciparum malaria
• IV Artesunate - severe/cerebral malaria (hospital setting)
• Supportive care - IV fluids, anti-seizure drugs, blood transfusion

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