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KATHMANDU UNIVERSITY - JULY 2025

Bachelor of Physiotherapy - Year I

Paper I: Basic Concepts, Genetics, Integumentary and Autonomic Nervous System

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SECTION "B"

A. Short Answer Questions

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Q1. Explain in brief about types of cartilaginous joint with example. [2]

• Bones are united by hyaline cartilage
• These are temporary joints - the cartilage is eventually replaced by bone (ossification)
• Movement: None (immovable / synarthrosis)
• Examples:
  • Epiphyseal growth plates (between epiphysis and diaphysis of long bones)
  • First sternocostal joint (1st rib with manubrium)
  • Spheno-occipital synchondrosis (base of skull)

• Bones are united by fibrocartilage disc
• Supported by periarticular ligaments
• Movement: Slight (amphiarthrosis)
• Examples:
  • Pubic symphysis (between two pubic bones)
  • Intervertebral discs (between vertebral bodies)
  • Manubriosternal joint

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Q2. Define carbohydrates. Classify it with examples. [2]

• Trioses (3C): Glyceraldehyde, Dihydroxyacetone
• Pentoses (5C): Ribose, Deoxyribose, Xylulose
• Hexoses (6C): Glucose, Fructose, Galactose, Mannose

• Raffinose, Stachyose (found in legumes)

• Homopolysaccharides: Starch, Glycogen, Cellulose (all made of glucose)
• Heteropolysaccharides: Heparin, Hyaluronic acid, Chondroitin sulfate

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Q3. What are the sources, functions, and deficiency manifestations of Vitamin C? [2]

• Water-soluble vitamin
• Not synthesized endogenously in humans (unlike most mammals)
• RDA: 60-90 mg/day

• Citrus fruits (lemon, orange, lime)
• Amla (Indian gooseberry) - richest source
• Guava, tomatoes, green peppers, broccoli
• Fresh leafy vegetables

1. Collagen synthesis - hydroxylation of proline and lysine residues in procollagen
2. Antioxidant - scavenges free radicals
3. Iron absorption - reduces Fe³⁺ to Fe²⁺ in the gut
4. Hormone synthesis - dopamine to noradrenaline conversion
5. Wound healing
6. Immune function

• Perifollicular hemorrhages (earliest sign)
• Bleeding gums (gingivitis), loose teeth
• Corkscrew hair
• Subperiosteal hemorrhages (painful swollen joints in children)
• Poor wound healing
• Anemia (due to impaired iron absorption)
• Scorbutic rosary (beading of ribs at costochondral junction) in children
• Woody leg (Barlow's disease in children)

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Q4. Define and classify neurotransmitters. [2]

• Excitatory: Glutamate, Aspartate
• Inhibitory: GABA (gamma-aminobutyric acid), Glycine

• Catecholamines: Dopamine, Norepinephrine (Noradrenaline), Epinephrine (Adrenaline)
• Indoleamines: Serotonin (5-HT), Melatonin
• Others: Histamine

• Acetylcholine (ACh) - at neuromuscular junction, all autonomic ganglia, parasympathetic postganglionic

• Substance P (pain), Enkephalins, Endorphins, Somatostatin, VIP (Vasoactive Intestinal Peptide)

• Nitric oxide (NO), Carbon monoxide (CO)

• ATP, Adenosine

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Q5. Differentiate between RNA and DNA viruses. [2]

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Q6. Explain bacteria growth curve. [2]

• No increase in cell number
• Bacteria adapt to new environment
• Active metabolic activity - synthesis of enzymes, proteins
• Duration varies with species and conditions

• Rapid doubling of bacteria at a constant rate
• Most metabolically active phase
• Most susceptible to antibiotics
• Generation time is shortest here
• Straight line when plotted on semi-log scale

• Growth rate = Death rate (net growth = zero)
• Nutrients depleted, toxic products accumulate
• Spore formation occurs in some bacteria

• Death rate exceeds growth rate
• Number of viable bacteria decreases
• Autolysis of cells occurs

         Stationary
         /‾‾‾‾‾‾‾‾‾\
Log      |           |  Decline
phase   /             \
       /               \
Lag--/                   \

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Q7. Enumerate Koch's postulates. Define sterilization. [1+1]

1. The organism must be found in all cases of the disease and absent from healthy individuals.
2. The organism must be isolated from the diseased host and grown in pure culture.
3. The pure culture must produce the same disease when inoculated into a healthy susceptible host.
4. The organism must be re-isolated from the experimentally diseased host and shown to be identical to the original organism.

Limitation: Does not apply to organisms that cannot be cultured (e.g., Mycobacterium leprae) or obligate intracellular parasites.

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Q8. Enumerate four differences between benign and malignant tumors. [2]

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Q9. Define Necrosis. Enumerate different types of necrosis with examples. [1+1]

1. Coagulative Necrosis
   • Most common type
   • Architecture of tissue preserved but cells are dead (ghostly outlines)
   • Caused by ischemia in most organs
   • Example: Myocardial infarction, renal infarct
2. Liquefactive Necrosis
   • Tissue is digested and converted to liquid
   • Seen in brain infarction and bacterial abscesses
   • Example: Cerebral infarction (brain softening), lung abscess
3. Caseous Necrosis
   • Soft, cheese-like, friable material
   • Characteristic of tuberculosis
   • Example: TB lymph nodes (caseum)
4. Fat Necrosis
   • Enzymatic fat necrosis: release of lipases (acute pancreatitis)
   • Traumatic fat necrosis: blunt trauma to fat (e.g., breast)
   • Example: Acute pancreatitis (chalky white saponification deposits)
5. Fibrinoid Necrosis
   • Deposition of fibrin-like eosinophilic material in vessel walls
   • Seen in immune complex-mediated vasculitis, malignant hypertension
   • Example: Rheumatoid arthritis, Polyarteritis nodosa
6. Gangrenous Necrosis
   • Coagulative necrosis + putrefactive bacterial infection
   • Dry gangrene (ischemia without infection) vs. Wet gangrene (with infection)
   • Example: Diabetic foot

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Q10. Describe in brief about the pathophysiology of edema. [2]

• Capillary hydrostatic pressure pushes fluid OUT
• Plasma oncotic pressure pulls fluid IN

• Venous obstruction → back-pressure → fluid forced out
• Example: Cardiac failure (right-sided), deep vein thrombosis (DVT), portal hypertension

• Less protein to retain fluid intravascularly → fluid leaks out
• Example: Nephrotic syndrome, liver cirrhosis, malnutrition (kwashiorkor)

• Inflammation mediators (histamine, bradykinin) increase vessel permeability
• Example: Burns, anaphylaxis, acute inflammation

• Lymph cannot drain → fluid accumulates
• Example: Filariasis (elephantiasis), post-mastectomy lymphedema

• Hormonal (RAAS activation in heart failure) → sodium retention → water follows
• Example: Hyperaldosteronism, renal failure

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Q11. Explain the factors that influence drug absorption. [2]

1. Lipid solubility - Lipophilic drugs cross membranes more easily
2. Ionization (pKa) - Non-ionized form is absorbed better; Henderson-Hasselbalch equation applies
3. Molecular size - Smaller molecules absorbed faster
4. Formulation - Tablet < Capsule < Suspension < Solution

• IV (100% bioavailability) > Inhalation > Sublingual > IM > SC > Oral > Rectal > Topical

1. Gastric pH - Acid drugs absorbed in stomach; basic drugs in intestine
2. Gastric emptying time - Faster emptying = faster absorption
3. Gut motility - Increased motility = decreased absorption time
4. Presence of food - Can delay absorption (e.g., tetracycline chelated by food)
5. Surface area - Small intestine has large surface (villi, microvilli)
6. First-pass metabolism - Oral drugs metabolized in gut wall + liver before reaching circulation (e.g., lignocaine, propranolol - high first pass)

1. Age (neonates and elderly have altered absorption)
2. Disease states (Crohn's disease, heart failure with gut congestion)
3. Drug interactions (antacids reduce absorption of tetracyclines, fluoroquinolones)

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Q12. Define agonist and antagonist with suitable examples. [2]

• Full agonist: Produces maximal response - e.g., Morphine (μ-opioid receptor), Adrenaline (adrenergic receptor)
• Partial agonist: Produces submaximal response even when all receptors are occupied - e.g., Buprenorphine (partial μ-opioid agonist), Buspirone (partial 5-HT1A agonist)

• Competitive antagonist: Competes with agonist for the same receptor site; reversible - e.g., Atropine (blocks ACh at muscarinic receptors), Propranolol (blocks adrenaline at β receptors)
• Non-competitive antagonist: Binds irreversibly or at allosteric site; cannot be overcome by increasing agonist dose - e.g., Phenoxybenzamine (irreversible α-blocker)

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Q13. Classify beta blockers with examples. [2]

• With ISA (Intrinsic Sympathomimetic Activity): Pindolol, Acebutolol (cause less bradycardia)
• With membrane-stabilizing activity: Propranolol, Acebutolol
• Cardioselective: Atenolol, Metoprolol, Bisoprolol

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Q14. Explain briefly regarding the pharmacological management of organophosphorous poisoning. [2]

• Remove from exposure, decontaminate skin
• ABC (Airway, Breathing, Circulation)
• Suction secretions

• Competitive muscarinic receptor antagonist
• Reverses muscarinic effects (bradycardia, bronchospasm, hypersecretions)
• Dose: 2-4 mg IV every 5-10 min until atropinization (dry secretions, tachycardia, dry skin)
• Does NOT reverse nicotinic effects (muscle paralysis)

• Reactivates inhibited AChE (if given early, before "aging")
• Reverses BOTH muscarinic AND nicotinic effects
• Dose: 1-2 g IV over 15-30 min
• Must be given within 24-48 hours (before irreversible aging of AChE)

• To control seizures

• Mechanical ventilation if respiratory failure

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Q15. Explain active transport across membrane. [2]

• Requires energy (ATP hydrolysis)
• Moves substances AGAINST concentration/electrochemical gradient
• Requires specific carrier proteins
• Saturable (Tm - transport maximum)
• Can be inhibited

• Energy comes DIRECTLY from ATP hydrolysis
• Example: Na⁺/K⁺-ATPase pump (Sodium-Potassium pump)
  • Pumps 3 Na⁺ out and 2 K⁺ in per cycle
  • Maintains resting membrane potential
  • Inhibited by digoxin (cardiac glycoside)
• Example: Ca²⁺-ATPase pump, H⁺/K⁺-ATPase (proton pump in stomach parietal cells - blocked by omeprazole)

• Energy comes INDIRECTLY from the electrochemical gradient created by primary transport
• Cotransport (Symport): Both substances move in the same direction
  • Example: Na⁺-glucose cotransporter (SGLT) in intestinal cells; Na⁺-amino acid cotransport
• Countertransport (Antiport): Substances move in opposite directions
  • Example: Na⁺/Ca²⁺ exchanger, Na⁺/H⁺ exchanger

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B. Clinical Based Questions [4Q × 5 = 20 marks]

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Q16. Clinical Case - Anatomy [10 marks]

SURFACE
────────────────────────────────
  STRATUM CORNEUM
  (dead, flattened, anucleate 
   keratinocytes / corneocytes)
────────────────────────────────
  STRATUM GRANULOSUM
  (granular cells with 
   keratohyalin granules)
────────────────────────────────
  STRATUM SPINOSUM
  (prickle cells with desmosomes
   Langerhans cells present here)
────────────────────────────────
  STRATUM BASALE
  (single layer of 
   columnar/cuboidal cells, 
   mitotic figures present,
   melanocytes present)
────────────────────────────────
  BASEMENT MEMBRANE
  (DEJ - Dermo-epidermal junction)
────────────────────────────────
         DERMIS
  (Papillary dermis - loose CT
   with blood vessels)
  (Reticular dermis - dense CT
   with collagen bundles)
  Hair follicles, sebaceous glands,
  arrector pili muscle present
────────────────────────────────
     HYPODERMIS (SUBCUTIS)
  (Adipose tissue, sweat glands)

• Thin skin: 4 epidermal layers (NO stratum lucidum)
• Hair follicles and sebaceous glands PRESENT in thin skin
• Fewer sweat glands than thick skin
• Thinner stratum corneum

• Found in all skin except palms, soles, glans penis, labia minora
• Parts: Shaft (above skin), root (below skin), follicle (surrounding sheath)
• Hair bulb at base contains matrix cells (actively dividing) and melanocytes
• Arrector pili muscle attached - causes goosebumps (piloerection) on sympathetic stimulation

• Holocrine glands (entire cell disintegrates to form secretion)
• Produce sebum (oily secretion - lubricates skin and hair)
• Open into hair follicle
• Absent on palms and soles
• Stimulated by androgens

• Eccrine glands: Found all over body; open directly on skin surface; produce watery sweat; important in thermoregulation; cholinergic innervation
• Apocrine glands: Found in axilla, groin, areola; open into hair follicle; produce viscous secretion; become active at puberty

• Keratinized plates on dorsal surface of terminal phalanges
• Parts: Nail plate, nail bed, nail root (matrix), lunula, eponychium (cuticle)
• Nail matrix produces nail cells

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Q17. Clinical Case - Anatomy [5 marks]

• Length > width
• Have a diaphysis (shaft), two epiphyses, medullary cavity, periosteum
• Example: Femur, tibia, fibula, humerus, radius, ulna, metacarpals, metatarsals, phalanges
• This child has a fracture of a long bone (humerus/radius/ulna)

• Roughly cuboidal in shape, length ≈ width ≈ breadth
• Cancellous bone covered by thin compact bone, no medullary cavity
• Example: Carpal bones (scaphoid, lunate, triquetrum, pisiform, trapezium, trapezoid, capitate, hamate), Tarsal bones (calcaneus, talus, navicular, cuboid, cuneiforms)

• Flat, plate-like shape
• Two layers of compact bone (tables) with diploë (cancellous bone) in between
• Function: Protection and provide large surface area for muscle attachment
• Example: Skull bones (parietal, frontal, occipital), scapula, ilium, sternum, ribs

• Do not fit into above categories
• Example: Vertebrae, sphenoid bone, ethmoid bone, hip bone (os coxae), maxilla, mandible

• Develop within tendons
• Function: Protect tendons, alter angle of muscle pull
• Example: Patella (largest sesamoid), pisiform bone, sesamoids under 1st metatarsal head

• Contain air-filled cavities (sinuses)
• Example: Frontal bone, maxilla, ethmoid, sphenoid (paranasal sinuses)

• Enters the diaphysis through the nutrient foramen (obliquely)
• Divides into ascending and descending branches inside medullary cavity
• Supplies: Inner 2/3 of cortex of diaphysis and medullary bone marrow
• Derived from: Systemic arteries (e.g., in humerus: from brachial artery)

• Numerous small arteries from surrounding muscles/periosteum
• Supplies: Outer 1/3 of cortex of diaphysis

• Enter through the epiphyseal surface
• Supply: Epiphyseal bone and articular surface
• Important in children: These are separate from metaphyseal vessels at the growth plate

• Branches from periosteal vessels entering the metaphysis
• Supply: Metaphyseal spongy bone

Epiphyseal artery ──→ [EPIPHYSIS]
                         |
               - - - GROWTH PLATE - - -  (Epiphyseal plate)
                         |
Metaphyseal artery──→ [METAPHYSIS]
                         |
                      [DIAPHYSIS]  ←── Nutrient artery (enters via nutrient foramen)
                         |               ↑ Periosteal arteries
               - - - GROWTH PLATE - - -
                         |
Epiphyseal artery ──→ [EPIPHYSIS]

Clinical note: In children, the epiphyseal plate acts as a barrier separating epiphyseal and metaphyseal circulations. Infections (osteomyelitis) tend to begin in the metaphysis due to sluggish blood flow there.

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Q18. Clinical Case - Physiology [10 marks]

1. Chronotropic effect (Positive): Increases heart rate (SA node - increases automaticity and depolarization rate)
2. Inotropic effect (Positive): Increases force of myocardial contraction (increases stroke volume)
3. Dromotropic effect (Positive): Increases velocity of conduction through AV node (shortens AV nodal delay/PR interval)
4. Bathmotropic effect (Positive): Increases excitability of all cardiac tissue
5. Lusitropic effect (Positive): Enhances relaxation during diastole (improves ventricular filling)

• Noradrenaline + β1 receptor → adenylyl cyclase activated → ↑ cAMP → Protein kinase A activation → Phosphorylation of L-type Ca²⁺ channels → ↑ Ca²⁺ influx → Stronger contraction and faster rate

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Q19. Clinical Case - Physiology [5 marks]

• Skin radiates heat in the form of infrared rays to surrounding environment
• In warm environment: vasodilation of cutaneous vessels increases blood flow to skin → more heat radiated

• Direct transfer of heat from skin surface to surrounding air/objects
• Convection occurs as warm air near skin rises and cool air replaces it

• Most important mechanism when environmental temperature > body temperature
• Eccrine sweat glands (cholinergic) are stimulated by hypothalamus
• Evaporation of 1L of sweat dissipates ~580 kcal of heat
• Effective even in hot environments as long as humidity is low

• Vasoconstriction in cold: Reduces blood flow to skin → conserves heat (arteriovenous anastomoses close)
• Vasodilation in heat: Increases blood flow to skin up to 30% of cardiac output → facilitates heat loss
• Countercurrent heat exchange: Arteries and veins run alongside, warm arterial blood transfers heat to cool venous blood returning from periphery

• Arrector pili muscles contract (goosebumps) → traps insulating air layer in furry animals (limited use in humans)

• Despite the pathologically elevated set-point, skin still participates in heat loss when the set-point is being reset during defervescence: sweating and vasodilation occur → fever breaks with diaphoresis

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• Anterior hypothalamus (preoptic area): Heat-sensitive neurons - activated when temperature rises; triggers heat-LOSS mechanisms
• Posterior hypothalamus: Activated by cold; triggers heat-CONSERVATION and heat-PRODUCTION mechanisms

• Anterior hypothalamus activates:
  1. Cutaneous vasodilation → increased heat loss via radiation
  2. Sweating (eccrine glands) → heat loss by evaporation
  3. Decreased metabolic rate
  4. Behavioral responses: seeks cool environment, removes clothing

• Posterior hypothalamus activates:
  1. Cutaneous vasoconstriction → reduces heat loss
  2. Shivering (rhythmic skeletal muscle contractions) → generates heat
  3. Non-shivering thermogenesis: adrenaline release → brown adipose tissue metabolism (important in neonates)
  4. Piloerection
  5. Behavioral responses: seeks warmth, adds clothing

• Pyrogens (bacterial LPS, IL-1, IL-6, TNF) → stimulate COX-2 in hypothalamus → PGE2 production → RAISES the thermostat set-point
• Body responds as if it is cold → shivering (chills/rigors) and vasoconstriction until new higher set-point is reached → fever of 40°C
• Antipyretics (paracetamol, ibuprofen) work by inhibiting COX-2 → reduce PGE2 → reset thermostat to normal

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