Medical MCQ Practice

• Definition: Homeostasis is the body’s ability to maintain a stable internal environment despite external changes.
• Example: Regulation of body temperature via sweating and shivering.
• Core components:
  • Receptors detect deviation from set points.
  • Control centres (e.g. hypothalamus) process the signal.
  • Effectors restore balance (e.g. sweat glands, muscles).
• Mechanism: Mostly governed by negative feedback loops.
• Failure of homeostasis: Underlies diseases like diabetes, fever, and hypertension.

• Function: Maintains core body temperature (36.3–37.3°C).
• Skin blood flow regulation:
  • Glabrous skin: passive control via vasoconstriction.
  • Non-glabrous skin: active vasodilation via sympathetic cholinergic nerves.
• Raynaud’s Phenomenon:
  • Primary: exaggerated vasoconstriction to cold.
  • Secondary: linked with autoimmune diseases.
• Clinical tool: Sympathetic release test to assess thermoregulatory function.

• Acute inflammation: Neutrophil infiltration, vascular leakiness, cytokine surge.
• Chronic inflammation: Lymphocytes and plasma cells; common in autoimmune disease (e.g. RA).
• Granulomas: Collections of macrophages, often in TB or sarcoidosis.
• Key pathology terms:
  • Abscess: pus-filled cavity.
  • Empyema: pus in body cavity.
  • Ulcer: full-thickness epithelial loss with necrosis.
  • Sinus tract: blind-ended inflammatory tunnel.

• Structural types:
  • Fibrous: e.g. sutures, gomphosis.
  • Cartilaginous: synchondroses, symphyses.
  • Synovial: have cavity, membrane, capsule, e.g. knee joint.
• Synovial Joint Types: Hinge (elbow), Pivot (radioulnar), Ball & socket (hip), Saddle (thumb).
• Functional types:
  • Synarthrosis: no movement.
  • Amphiarthrosis: limited.
  • Diarthrosis: free movement.

• Definition: Chronic inflammation with granulomas—organized macrophage clusters.
• Classic causes: Tuberculosis (caseating), Sarcoidosis (non-caseating).
• Histology: Giant cells, central necrosis (caseous in TB), Ziehl-Neelsen stain + in TB.
• Clinical case relevance: Granulomas in sarcoidosis are non-caseating and ZN stain negative.

• Key Concept: Skin blood flow is critical for temperature control.
• Cutaneous vessels:
  • Controlled by sympathetic vasoconstrictors (tonic).
  • Glabrous (palms, soles) vs. non-glabrous (arms, back).
• Test: Sympathetic release test checks vasodilation via temperature plateau.
• Disorders: Raynaud’s, peripheral artery disease (gangrene risk).

• Definition: When regulatory systems can’t maintain stability.
• Examples:
  • Cardiovascular: chronic hypertension, heart failure.
  • Endocrine: diabetes mellitus (insulin deficiency).
• Mechanism: Positive feedback loops take over, e.g. fever.
• Clinical implication: Maintaining homeostasis is vital in all physiological systems.

• Coagulative: Seen in MI. Preserved architecture, pink eosinophilic cytoplasm.
• Liquefactive: Brain injury. Complete tissue digestion.
• Caseous: TB. Cheese-like appearance, seen in granulomas.
• Fat: Enzymatic destruction of adipose tissue, seen in pancreatitis.
• Fibrinoid: Vessel wall necrosis, seen in vasculitis.

• Key components:
  • Articular cartilage: hyaline, cushions joint ends.
  • Synovial membrane: secretes fluid.
  • Joint cavity: contains synovial fluid.
  • Capsule & ligaments: provide support.
• Function: Freely moveable (diarthrotic); supported by tendons, muscles, bursae.

• 3 parts:
  1. Sensor: detects change (e.g. thermal receptors).
  2. Control Centre: brain/hypothalamus.
  3. Effector: restores equilibrium (e.g. sweat glands, muscles).
• Feedback types:
  • Negative: stabilizing (e.g. BP regulation).
  • Positive: amplifying (e.g. clotting, fever).
• Quiz: What returns elevated body temp to normal? Answer: Sweating.

Astrocytes: Maintain BBB integrity, regulate ionic environment, support neurons.

Microglia: CNS macrophages, key in immune surveillance and phagocytosis.

Oligodendrocytes: Myelinate multiple CNS axons.

Ependymal Cells: Line ventricles, produce & circulate CSF.

Clinical Relevance: BBB breakdown occurs in MS, infections, trauma.

Schwann cells: Myelinate single PNS axons; promote regeneration.

Oligodendrocytes: CNS equivalent; no regeneration.

Saltatory Conduction: APs jump between nodes of Ranvier — increases speed.

Diseases: Demyelination in MS (CNS) and Guillain-Barré (PNS).

Slide Tip: Myelinated axons = fast, white matter; unmyelinated = slow, grey matter.

Sympathetic: "Fight or flight" — ↑ HR, bronchodilation, pupil dilation.

Parasympathetic: "Rest and digest" — ↓ HR, ↑ GI motility.

Neurotransmitters:
Sympathetic: ACh (pre), Noradrenaline (post).
Parasympathetic: ACh both pre- and post-ganglionic.

Clinical Cases: Beta-blockers inhibit sympathetic HR response.

Layers (deep to superficial): Basale, Spinosum, Granulosum, Lucidum (palms/soles), Corneum.

Keratinocytes: Major cell; produce keratin for waterproofing.

Melanocytes: Pigment production, located in basal layer.

Clinical Example: Psoriasis = hyperproliferation of keratinocytes, ↑ stratum corneum.

Na⁺/K⁺ ATPase: 3 Na⁺ out, 2 K⁺ in — maintains resting potential.

Calcium Channels: Involved in muscle contraction, NT release.

Passive vs Active Transport:
Passive: Diffusion, facilitated (e.g. GLUT).
Active: Uses ATP (e.g. Na⁺/K⁺ pump).

Osmosis: Water moves toward hypertonic solution.

Definition: Insertion/deletion not divisible by 3 → shifts reading frame.

Consequence: Alters entire downstream amino acid sequence.

Example: In CFTR gene → cystic fibrosis.

Compare:
Missense: 1 base → different aa.
Nonsense: Premature stop codon.
Silent: No aa change.

Slide Detail: tRNA reads mRNA in 3-base codons.

Autonomy: Respect patient choice — even refusal of treatment.

Beneficence: Act in patient’s best interest.

Non-maleficence: “Do no harm.”

Justice: Fair access to healthcare.

Clinical Dilemma: Jehovah's Witness refusing transfusion — autonomy respected.

Carbohydrates: Energy — glucose, glycogen (liver & muscle).

Proteins: Structure (collagen), transport (Hb), enzymes.

Lipids: Long-term energy (triglycerides), membranes (phospholipids).

Nucleic Acids: DNA (genetic storage), RNA (expression).

Lecture Highlight: ATP is not a storage molecule, but an energy currency.

Apoptosis:
Programmed, energy-dependent.
Cell shrinkage, chromatin condensation, apoptotic bodies.
No inflammation.

Necrosis:
Unregulated cell death (e.g. hypoxia).
Cell swelling, rupture, inflammation.

Clinical Insight: Chemotherapy often induces apoptosis in cancer cells.

Cerebrum: Sensory processing, voluntary movement, higher cognition.

Cerebellum: Balance, coordination.

Brainstem: Autonomic control (breathing, HR); midbrain, pons, medulla.

Spinal Cord: Reflex arcs, ascending (sensory) & descending (motor) tracts.

Case Link: Stroke in cerebellum → ataxia; brainstem stroke → life-threatening.

Components: Sensory receptor → Afferent neuron → Integration center → Efferent neuron → Effector.

Example: Patellar reflex (monosynaptic).

Clinical note: Hyperreflexia = UMN lesion; Hyporeflexia = LMN or peripheral neuropathy.

Sympathetic (Adrenergic):

• α₁: Vasoconstriction (↑BP)
• β₁: ↑HR, ↑contractility
• β₂: Bronchodilation, vasodilation in muscle

Parasympathetic (Cholinergic):

• M₂: ↓HR
• M₃: Gland secretion, smooth muscle contraction (e.g. bladder)

Pharmacology tie-in: β-blockers block β₁; antimuscarinics block M₃.

Thoracolumbar origin: T1–L2.

Preganglionic fibres: Short, release ACh.

Postganglionic fibres: Long, release NE (except sweat glands: ACh).

Chain ganglia: Allow signal to travel above/below initial spinal segment.

"Brain of the gut": Can function independently but modulated by ANS.

Plexuses:

• Myenteric (Auerbach’s): Motility
• Submucosal (Meissner’s): Secretion, blood flow

Clinical relevance: Hirschsprung's = absence of ENS ganglia → megacolon.

Brain:

• Internal carotids → Anterior circulation
• Vertebral arteries → Posterior circulation
• Circle of Willis = anastomotic loop

Spinal cord:

• Anterior spinal artery (motor)
• Posterior spinal arteries (sensory)

Clinical: Anterior spinal artery syndrome = bilateral motor loss.

Produced by: Choroid plexus (ependymal cells).

Flow: Lateral → 3rd → 4th ventricle → subarachnoid space.

Reabsorbed by: Arachnoid granulations into venous sinuses.

Clinical: Hydrocephalus = CSF accumulation due to obstruction or impaired drainage.

Dura mater: Tough outer layer.

Arachnoid mater: CSF flows beneath.

Pia mater: Directly covers brain/spinal cord.

Subarachnoid space: Site of lumbar puncture (L3–L4 in adults).

Clinical: Subarachnoid haemorrhage → "thunderclap" headache.

Glutamate: Major excitatory neurotransmitter.

Excess → Overactivation of NMDA/AMPA receptors → Ca²⁺ influx → Cell death.

Pathology: Seen in stroke, ALS, Alzheimer's.

Therapeutics: Riluzole reduces glutamate transmission (ALS).

Increased by: Myelination, larger axon diameter.

Decreased by: Demyelination (e.g. MS), compression injuries.

Clinical: Nerve conduction studies assess peripheral neuropathies.

Anterior spinal artery: Supplies 2/3 of spinal cord (motor tracts).

Posterior spinal arteries: Supply dorsal columns (sensory).

Great radicular artery (of Adamkiewicz): Vital for thoracolumbar supply.

Infarct presentation: Paraparesis, loss of pain/temp, preserved proprioception.

• Diabetes Mellitus:
  • Type 1: autoimmune destruction of beta cells, absolute insulin deficiency.
  • Type 2: insulin resistance ± relative deficiency. Linked to obesity, lifestyle.
• Hormone axes: HPA (cortisol), HPT (thyroxine), HPG (sex hormones).
• Adrenal disorders: Addison’s disease = primary adrenal insufficiency. Symptoms include fatigue, hyperpigmentation, low BP.
• Endocrine feedback: Negative feedback predominant, e.g. cortisol suppressing ACTH.

• Innate Immunity: First-line defense; includes neutrophils, macrophages, dendritic cells.
• Adaptive Immunity: Specific; B-cells (humoral), T-cells (cell-mediated).
• Antigen presentation: Via MHC I (all nucleated cells) to CD8+ T-cells, MHC II (APCs) to CD4+ T-cells.
• Cytokines: Signaling molecules like IL-1, TNF-alpha, IFN-gamma.

• Anaemia types:
  • Microcytic: iron deficiency, thalassemia.
  • Normocytic: blood loss, chronic disease.
  • Macrocytic: B12/folate deficiency.
• Clotting Cascade: Intrinsic (aPTT), Extrinsic (PT), Common pathway leads to fibrin clot.
• Platelet function: Adhesion (vWF), activation, aggregation (fibrinogen bridging via GPIIb/IIIa).

• Pharmacokinetics: ADME – Absorption, Distribution, Metabolism, Excretion.
• Pharmacodynamics: Drug-receptor interactions, dose-response curves.
• Tyrosine Kinase Inhibitors: e.g. Imatinib for CML, blocks BCR-ABL fusion protein.
• Drug metabolism: Liver CYP450 enzymes – important for interactions.

• Cell cycle checkpoints: G1/S (DNA damage), G2/M (replication), M (spindle).
• Oncogenes: Gain of function → uncontrolled growth. e.g. RAS, HER2.
• Tumour suppressors: Loss of function. e.g. p53, RB.
• Apoptosis: Programmed cell death; p53 activates intrinsic mitochondrial pathway via Bax/Bak.

• Type I: Immediate, IgE-mediated. e.g. Anaphylaxis, hay fever.
• Type II: Antibody-mediated cytotoxicity. e.g. Autoimmune haemolytic anaemia.
• Type III: Immune complex deposition. e.g. SLE, post-strep glomerulonephritis.
• Type IV: Delayed-type, T-cell mediated. e.g. TB skin test, contact dermatitis.

• G protein-coupled receptors (GPCRs): 7-transmembrane receptors coupled to G proteins (alpha, beta, gamma subunits).
• Gs (stimulatory): Activates adenylate cyclase → ↑ cAMP → activates PKA. Example: β-adrenergic receptors.
• Gi (inhibitory): Inhibits adenylate cyclase → ↓ cAMP. Example: α2-adrenergic receptors, M2 receptors.
• Gq: Activates phospholipase C → ↑ IP3/DAG → ↑ intracellular Ca²⁺ → activates PKC. Example: α1-adrenergic receptors, M1/M3 receptors.
• Clinical: Cholera toxin locks Gs ON; Pertussis toxin locks Gi OFF.

• Type I: Bone, skin, tendon – strongest. Defective in osteogenesis imperfecta.
• Type II: Cartilage (hyaline), vitreous body, nucleus pulposus.
• Type III: Reticulin – found in skin, vessels, uterus. Defective in vascular Ehlers-Danlos syndrome.
• Type IV: Basement membranes. Affected in Alport syndrome & Goodpasture’s disease.
• Type V: Found in cornea, placenta, and skin. Also involved in some types of EDS.

• Essential AA: Cannot be synthesized – must be obtained from diet. e.g. Leucine, Lysine, Tryptophan.
• Non-essential AA: Can be synthesized. e.g. Alanine, Glutamate.
• Polar AA: Serine, Threonine, Asparagine, Glutamine.
• Non-polar AA: Glycine, Alanine, Valine, Leucine, Isoleucine.
• Aromatic: Phenylalanine (Phe, F), Tyrosine (Tyr, Y), Tryptophan (Trp, W).
• Acidic: Aspartic acid (Asp, D), Glutamic acid (Glu, E).
• Basic: Arginine (Arg, R), Lysine (Lys, K), Histidine (His, H).
• Shorthand Tip: Know both 1-letter (e.g. F for Phe) and 3-letter codes (e.g. Phe).

• Lecture: Case+1+Overview+2024.pdf
• Type: Autosomal recessive metabolic disorder.
• Defect: Cystathionine beta-synthase (CBS) deficiency.
• Features: Marfanoid habitus, lens dislocation, thromboembolic events, intellectual disability.
• Treatment: Vitamin B6 (pyridoxine), low-methionine diet, betaine, folic acid, B12.

• Lecture: Case+1+Overview+2024.pdf
• Type: Autosomal recessive disorder.
• Defect: Phenylalanine hydroxylase deficiency → phenylalanine accumulation.
• Symptoms: Intellectual disability, microcephaly, fair complexion, musty odor.
• Management: Low phenylalanine diet, newborn screening critical.

• Lecture: Neoplastic+%26+Non+Neoplastic+Growth+Disorders+23s.pdf
• Definition: Metaplasia of lower oesophageal squamous epithelium to columnar epithelium.
• Cause: Gastro-oesophageal reflux disease (GORD).
• Risk: Progression to oesophageal adenocarcinoma.

• Lecture: Neoplastic+%26+Non+Neoplastic+Growth+Disorders+23s.pdf
• Change: Cerebral atrophy.
• Histology: Narrowed gyri, widened sulci.
• Mechanism: Atrophy from neuronal loss and apoptosis.

• Lecture: Cell+Death+24sh.pdf
• Necrosis Type: Caseous necrosis.
• Histology: Amorphous pink material, granulomatous inflammation.

• Lecture: Cell+Death+24sh.pdf
• Mechanism: Fat necrosis due to enzymatic digestion of fat.
• Cause: Alcohol or gallstones.

• Lecture: Cell+Death+24sh.pdf
• Feature: Fibrinoid necrosis in vessel walls.
• Example: Seen in autoimmune vasculitis and immune complex deposition.

• Lecture: Cell+Death+24sh.pdf
• Necrosis Type: Coagulative necrosis.
• Microscopy: Loss of nuclei, eosinophilic cytoplasm, acute inflammation.

• Lecture: Cell+Death+24sh.pdf
• Necrosis Type: Liquefactive necrosis.
• Unique: Brain lacks structural support → liquefaction into cysts.

• Lecture: Cell+Death+24sh.pdf
• Feature: Overexpression of Bcl-2 → inhibition of apoptosis.
• Pathology: Enhanced survival of abnormal lymphocytes.

• Lecture: Cell+Death+24sh.pdf
• Mechanism: Defective apoptosis clearance → nuclear antigens → autoimmunity.
• Result: Production of autoantibodies.

• Lecture: Cell+Death+24sh.pdf
• Mechanism: Autoimmune-mediated apoptosis of pancreatic β-cells.
• Result: Insulin deficiency.

• Lecture: Cell+Death+24sh.pdf
• Mechanism: Induces apoptosis in both infected and uninfected CD4+ T-cells.
• Result: Progressive immune suppression.

• Lecture: MED1028-Microbiome.pdf
• Link: Dysbiosis in GF mice → altered sociability and repetitive behavior.
• Relevance: Studied via gut-brain axis.

• Lecture: MED1028-Microbiome.pdf
• Link: Result of antibiotic-induced dysbiosis.
• Symptoms: Diarrhoea, inflammation, and pseudomembranous colitis.

• Genetics: Autosomal recessive; mutation in the ACADM gene.
• Mechanism: Impaired fatty acid oxidation during fasting or stress → energy failure.
• Presentation: Often in infancy (1–24 months); hypoglycaemia, seizures, lethargy, coma, sudden death.
• Diagnosis: Newborn screening (blood spot).
• Treatment: Avoid fasting, emergency glucose during illness, carnitine supplementation (sometimes).

• Cause: Severe hypersensitivity reaction to certain medications (e.g. allopurinol, anticonvulsants).
• Presentation: Rash, fever, lymphadenopathy, eosinophilia, liver/kidney involvement.
• Histopathology: Eosinophil-rich inflammation and necrotic keratinocytes.
• Treatment: Stop offending drug, corticosteroids, supportive care.

• Cause: Infection of dermis and subcutaneous tissue, often due to Streptococcus pyogenes or Staphylococcus aureus.
• Histology: Neutrophilic infiltration through epidermis, dermis, and subcutaneous fat.
• Clinical: Rapid onset redness, warmth, swelling, pain. May follow skin trauma (e.g. cat scratch).
• Treatment: Empirical antibiotics (e.g. flucloxacillin).

• Cause: Superficial skin infection, typically caused by Staphylococcus aureus or Streptococcus pyogenes.
• Clinical: Golden, crusted lesions, usually around nose and mouth in children.
• Histology: Intraepidermal vesicles with neutrophils and bacteria.
• Treatment: Topical or oral antibiotics (e.g. fusidic acid or flucloxacillin).

• Cause: Foreign body reaction to tattoo pigment.
• Histology: Non-caseating granulomas in skin containing pigment.
• Clinical: Papular or nodular overgrowths developing over tattooed skin weeks after procedure.
• Differential: Must exclude sarcoidosis or cutaneous TB.

• Cause: Peripheral neuropathy and vascular insufficiency in diabetes.
• Clinical: Chronic foot ulcers, usually painless, often infected.
• Histology: Ulceration with granulation tissue and possible secondary infection.
• Treatment: Glycaemic control, offloading pressure, wound care, antibiotics.