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GROUP-A — Respiratory Physiology

Q.1 — Respiratory Unit & Gas Diffusion Factors

1. Thickness of the membrane — increased thickness (e.g., pulmonary edema, fibrosis) decreases diffusion
2. Surface area — decreased surface area (e.g., emphysema) decreases diffusion
3. Diffusion coefficient of the gas — CO₂ diffuses ~20× faster than O₂
4. Partial pressure difference — greater gradient = faster diffusion
5. Molecular weight & solubility of the gas

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Q.2 — O₂-Hb Dissociation Curve, P50, & Sigmoid Shape

• Hemoglobin has 4 subunits with cooperative binding (allosteric effect)
• Binding of the first O₂ molecule increases the affinity of subsequent subunits (T-state → R-state conformational change)
• This cooperative binding creates the characteristic S-shape (sigmoid)
• The flat upper portion ensures near-complete saturation at pulmonary capillaries; the steep lower portion facilitates O₂ unloading in tissues

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Q.3 — Lung Capacities, Vital Capacity & Affecting Factors

1. Age — decreases with age
2. Sex — higher in males than females
3. Height/Body size — taller individuals have greater VC
4. Posture — lower in supine position
5. Physical fitness — athletes have higher VC
6. Lung disease — restrictive diseases (fibrosis) decrease VC; obstructive diseases may also reduce it
7. Respiratory muscle strength

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Q.4 — Hypoxia: Definition, Classification, Causes & Cyanosis

• Cyanosis (bluish discoloration) occurs when reduced Hb > 5 g/dL in capillary blood
• Hypoxic hypoxia → can cause central cyanosis
• Anemic hypoxia → usually NO cyanosis (not enough Hb to reach 5 g/dL threshold)
• CO poisoning → NO cyanosis (cherry-red appearance)
• Histotoxic hypoxia → NO cyanosis (blood is well-oxygenated)
• So hypoxia is not always associated with cyanosis

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Q.5 — GIT Movements & Mass Movement

• Mouth: Mastication, deglutition
• Esophagus: Peristalsis (primary & secondary), lower esophageal sphincter relaxation
• Stomach: Receptive relaxation, tonic contraction, peristaltic waves (mixing/propulsion), pyloric pump
• Small intestine: Segmentation (mixing), peristalsis (propulsion), migrating motor complex (MMC) in fasting
• Large intestine: Haustral churning, peristalsis, mass movement

• Mechanism: A large segment of colon contracts simultaneously and the contents are pushed toward the rectum
• Initiated by gastrocolic reflex (after a meal) and duodenocolic reflex
• Mediated by: distension of the stomach → long (vagal) and short (myenteric) reflexes → colon contracts
• Occurs 1–3 times/day; propels fecal content toward rectum → urge to defecate

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Q.6 — Spirometry Calculations

• Tidal Volume (TV) = 500 mL
• IRV = 3000 mL
• ERV = 1200 mL
• RV = 1200 mL

• Prevents lung collapse between breaths (maintains alveolar patency)
• Dilutes incoming fresh air to prevent sudden changes in alveolar gas concentrations (ensures continuous, smooth gas exchange)
• Maintains FRC (~2300 mL), which keeps alveoli open and acts as an O₂ reservoir
• RV cannot be expelled even with maximal effort — lungs never fully empty

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Q.7 (SEQ) — Respiratory Centers, Chemical Regulation & Exercise

• Central chemoreceptors (medullary): Respond to ↑PCO₂ → ↑H⁺ in CSF → stimulate ventilation (most powerful)
• Peripheral chemoreceptors (carotid & aortic bodies): Respond to ↓PO₂ (<60 mmHg), ↑PCO₂, ↑H⁺

• Ventilation increases proportionally with CO₂ production and O₂ consumption
• Mechanisms: Proprioceptors in joints/muscles → immediate increase; rising CO₂ & H⁺ sustain it; body temperature stimulus
• PaO₂ and PaCO₂ remain nearly normal during moderate exercise

• Loss of inhibition of inspiration → apneusis (prolonged gasping inspiration with brief expiration)
• Breathing rate decreases; depth increases markedly

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GROUP-B — Renal Physiology

Q.8 — Nephron Diagram & Cortical vs. Juxtamedullary Nephrons

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Q.9 — GFR: Definition, Factors, Net Filtration Pressure

1. Net filtration pressure
2. Glomerular capillary permeability (Kf)
3. Surface area of glomerular capillaries
4. Renal plasma flow
5. Afferent/efferent arteriolar tone
6. Hormones: angiotensin II (↓GFR), prostaglandins (↑), ANP (↑)

• Glomerular capillary hydrostatic pressure (GCHP) = 60 mmHg (favors filtration)
• Bowman's capsule hydrostatic pressure (BCHP) = 18 mmHg (opposes)
• Glomerular oncotic pressure (GOP) = 32 mmHg (opposes)
• Bowman's capsule oncotic pressure = ~0 mmHg (negligible)

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Q.10 — Water Reabsorption Sites & Urine Concentration in Collecting Duct

1. ADH (vasopressin) released from posterior pituitary in response to ↑plasma osmolarity
2. ADH binds V2 receptors on collecting duct cells → activates adenylyl cyclase → ↑cAMP
3. Aquaporin-2 (AQP-2) channels inserted into luminal membrane
4. Water moves from tubular lumen into hyperosmotic medullary interstitium
5. The countercurrent multiplier (loop of Henle) and countercurrent exchanger (vasa recta) create and maintain the medullary osmotic gradient (up to 1200 mOsm/kg)
6. Urea also contributes to medullary hyperosmolarity via UT-A1/UT-A3 transporters in inner medullary collecting duct

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Q.11 — Na⁺ Reabsorption Mechanism & TmG

• PCT: Na⁺-K⁺-ATPase on basolateral side creates low intracellular Na⁺; Na⁺ enters from lumen via co-transporters (Na-glucose, Na-amino acid) and Na-H exchanger
• Loop of Henle (thick ascending): Na-K-2Cl cotransporter (NKCC2) on luminal side; impermeably to water → dilutes tubular fluid
• DCT: Na-Cl cotransporter (thiazide-sensitive); aldosterone acts here
• Collecting duct: ENaC (epithelial Na channel); aldosterone ↑ Na⁺ reabsorption via ↑ENaC expression

• Maximum rate at which glucose can be reabsorbed by tubular carriers
• Normal TmG = 375 mg/min (males) / 300 mg/min (females)
• Renal threshold for glucose = ~180 mg/dL plasma glucose (carriers saturated)
• Above this, glucose spills into urine (glycosuria) — as in uncontrolled diabetes mellitus

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Q.12 — Diuresis: Classification & Osmotic Diuresis in Diabetes

1. Blood glucose >> renal threshold (180 mg/dL) → glucose not fully reabsorbed
2. Unabsorbed glucose in tubular lumen retains water osmotically
3. This overwhelms the Na⁺ reabsorption mechanism → polyuria (3–15 L/day)
4. Loss of water → dehydration → polydipsia
5. Glycosuria is the hallmark

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Q.13 — Involuntary Urination in 6-Month-Old Infant

• In infants, micturition is purely a spinal reflex (sacral micturition reflex center, S2–S4)
• When bladder fills to ~150 mL → stretch receptors in detrusor muscle are activated → afferent signals via pelvic nerves → sacral cord → efferent signals → detrusor contraction + internal urethral sphincter relaxation → involuntary voiding
• The pontine micturition center (Barrington's nucleus) and higher cortical centers (prefrontal cortex) normally inhibit this reflex and allow voluntary postponement
• These descending pathways are not functional in infants → reflex micturition is uninhibited
• Voluntary control typically develops by 2–3 years of age with maturation of these pathways

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Q.14 (SEQ) — Functions of Kidney, BP Regulation, Kidney Function Tests & Micturition

1. Excretion of metabolic waste (urea, creatinine, uric acid)
2. Fluid balance regulation (water excretion)
3. Electrolyte regulation (Na⁺, K⁺, Ca²⁺, phosphate)
4. Acid-base balance (H⁺ secretion, HCO₃⁻ reabsorption/generation)
5. Blood pressure regulation (renin-angiotensin system, pressure natriuresis)
6. Erythropoietin production (stimulates RBC formation)
7. Vitamin D activation (1α-hydroxylase: 25-OH D₃ → 1,25-(OH)₂D₃)
8. Gluconeogenesis (especially during prolonged fasting)
9. Clearance of hormones and drugs

1. Pressure natriuresis/diuresis — ↑BP → ↑Na⁺ & water excretion → ↓blood volume → ↓BP
2. Renin-Angiotensin-Aldosterone System (RAAS) — ↓BP/volume → renin → angiotensin II → vasoconstriction + aldosterone → Na⁺ retention → ↑BP
3. ADH/Vasopressin — ↑plasma osmolarity → ADH → water retention → ↑blood volume → ↑BP
4. Prostaglandins (PGE₂, PGI₂) — vasodilatory, natriuretic (counterregulatory)
5. Kallikrein-kinin system — kinins → vasodilation, natriuresis

1. Serum creatinine (normal: 0.6–1.2 mg/dL) — most commonly used
2. Blood urea nitrogen (BUN) (normal: 7–20 mg/dL)
3. GFR estimation (eGFR via CKD-EPI or MDRD equations)
4. Creatinine clearance (approximates GFR, ~125 mL/min)
5. Urine analysis — proteinuria, hematuria, casts
6. Inulin clearance (gold standard for GFR)
7. PAH clearance (renal plasma flow)
8. 24-hour urine protein
9. Serum electrolytes
10. Urine osmolality/specific gravity

• Bladder fills → stretch receptors fire → pelvic nerve afferents → sacral cord (S2–S4) + pontine micturition center → detrusor contraction (parasympathetic) + internal sphincter relaxation → voiding
• Voluntary control: cortex can inhibit pontine center until appropriate time
• External sphincter under voluntary somatic control (pudendal nerve)

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MCQ Answers (True/False & Single Best Answer)

Q.1 — Hormones/Autacoids that DECREASE GFR (T/F)

Q.2 — FEV₁ (T/F)

Q.3 — Medullary Collecting Duct (T/F)

Q.4 — Plasma Clearance (T/F)

Q.5 — O₂ Carrying Capacity Depends On (T/F)

Q.6 — Regarding Diuretics (T/F)

Q.7 — Stomach Emptying is Inhibited By (T/F)

Q.8 — Gastric HCl Secretion (T/F)

Q.9 — Respiratory Dead Space (T/F)

Q.10 — GIT Hormones (T/F)

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Single Best Answer (Q.11–Q.20)

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Q.1 — Nephron: Parts & Cortical vs. Juxtamedullary Differences

a) Nephron — Parts (Diagram)

                    AFFERENT ARTERIOLE
                          ↓
                    GLOMERULUS ←→ BOWMAN'S CAPSULE
                          ↓
              PROXIMAL CONVOLUTED TUBULE (PCT)
                          ↓
                 LOOP OF HENLE
              ┌───────────────────┐
              ↓                   ↑
      Descending Limb      Ascending Limb
      (thin, permeable     (thick, impermeable
       to water)            to water)
              └───────────────────┘
                          ↓
              DISTAL CONVOLUTED TUBULE (DCT)
                          ↓
                  COLLECTING DUCT
                          ↓
                  RENAL PELVIS → URETER

1. Renal corpuscle — Glomerulus + Bowman's capsule (site of filtration)
2. Proximal Convoluted Tubule (PCT) — in cortex; major reabsorption site
3. Loop of Henle — descending thin limb + ascending thin limb + ascending thick limb; dips into medulla
4. Distal Convoluted Tubule (DCT) — in cortex; hormone-regulated reabsorption
5. Collecting Duct — cortex → medulla; urine concentration under ADH

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b) 4 Important Differences: Cortical vs. Juxtamedullary Nephrons

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Q.2 — GFR: Definition, NFP Calculation & Autoregulation

a) Define GFR & Calculate Net Filtration Pressure

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b) GFR Autoregulation

1. Myogenic Mechanism

• ↑BP → stretch of afferent arteriole wall → automatic vasoconstriction → ↓blood flow into glomerulus → GFR maintained
• Conversely, ↓BP → vasodilation → maintained GFR
• Rapid response (seconds)

2. Tubuloglomerular Feedback (TGF)

• ↑GFR → ↑NaCl delivery to macula densa (in DCT wall)
• Macula densa detects ↑NaCl via NKCC2 co-transporter
• Releases adenosine and TXA₂ → afferent arteriolar constriction → ↓GFR back to normal
• ↓GFR → opposite occurs → ↑renin release → angiotensin II → efferent arteriolar constriction → maintains GFR

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Q.3 — Completely Reabsorbed Substances & Glucose Reabsorption from PCT

a) Substances Completely Reabsorbed

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b) Mechanism of Glucose Reabsorption from PCT

1. Na⁺/K⁺-ATPase on the basolateral membrane pumps 3 Na⁺ out and 2 K⁺ in → creates low intracellular Na⁺ concentration (electrochemical gradient)
2. On the luminal membrane, the SGLT2 (Sodium-Glucose Linked Transporter 2) co-transports 1 Na⁺ and 1 glucose from tubular lumen into the cell (secondary active — driven by Na⁺ gradient)
   • SGLT1 (in S3 segment) transports 2 Na⁺ : 1 glucose
3. Glucose accumulates inside the cell, then exits across the basolateral membrane via GLUT2 (facilitated diffusion) into the peritubular capillary
4. Transport maximum (TmG): ~375 mg/min in males, ~300 mg/min in females
   • Below renal threshold (~180 mg/dL plasma): all glucose reabsorbed
   • Above threshold: carriers saturated → glycosuria (as in uncontrolled DM)

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Q.4 — Hormones Acting on Renal Tubule & ADH Mechanism

a) Hormones Acting on Renal Tubule

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b) How ADH Helps in Water Reabsorption from Kidney

1. ADH binds V2 receptors on basolateral membrane of principal cells
2. → Activates Gs protein → adenylyl cyclase → ↑cAMP
3. ↑cAMP → activates protein kinase A (PKA)
4. PKA phosphorylates aquaporin-2 (AQP-2) vesicles in cytoplasm
5. AQP-2 vesicles fuse with the luminal membrane → water channels inserted
6. Water moves osmotically from tubular lumen into the hyperosmotic interstitium
7. Water exits cell via AQP-3 and AQP-4 on the basolateral side → into peritubular capillary

In the absence of ADH (e.g., diabetes insipidus): collecting duct is impermeable to water → large volumes of dilute urine

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Q.5 — Stomach Emptying & Peristalsis in Small Intestine

a) Stomach Emptying — Definition & Duration

• Carbohydrates: 1–2 hours
• Proteins: 3–4 hours
• Fats: 4–5 hours (slowest — due to CCK-mediated inhibition)
• Mixed meal: ~3–4 hours typically

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b) How Peristalsis Occurs in the Small Intestine

1. Stimulus: Distension of the intestinal wall by a bolus of chyme
2. Stretch activates the myenteric (Auerbach's) plexus via mechanoreceptors
3. Oral (proximal) side: Release of ACh and Substance-P → contraction of circular muscle (ascending excitation)
4. Aboral (distal) side: Release of VIP and NO → relaxation of circular muscle (descending inhibition)
5. The bolus is squeezed forward
6. Longitudinal muscle assists by shortening the segment ahead

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Q.6 (PBQ — Compulsory) — 60-year-old Woman with Urinary Urgency/Incontinence

• Frequent urination
• Inability to hold urine even when bladder is partially filled
• Involuntary detrusor contractions on cystometry even with small urine volumes

a) Abnormal Bladder Condition Suggested:

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b) Physiological Mechanism Responsible

1. Lesion occurs above the sacral cord but below the cortex (e.g., stroke, Parkinson's, MS, cervical spondylosis, or age-related loss of cortical inhibition)
2. The descending inhibitory pathways from cortex/PMC are damaged or weakened
3. The sacral micturition reflex (S2–S4) is released from cortical inhibition → becomes hyperactive
4. Even small volumes of urine cause bladder stretch receptors to fire → afferent signals reach sacral cord → uninhibited detrusor contractions
5. Patient experiences urgency (cannot suppress the reflex), frequency, and urge incontinence
6. In a 60-year-old woman: age-related cortical neuronal loss + possible subcortical white matter changes reduce inhibitory control over the bladder

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Q.7 (SEQ — Compulsory)

a) Functions of the Kidney

1. Excretion of metabolic waste — urea (from protein metabolism), creatinine, uric acid, bilirubin metabolites
2. Regulation of water balance — adjusts urine volume (0.5 to 20 L/day)
3. Regulation of electrolytes — Na⁺, K⁺, Ca²⁺, Mg²⁺, PO₄³⁻, Cl⁻
4. Acid-base balance — secretes H⁺, reabsorbs HCO₃⁻, produces ammonium
5. Blood pressure regulation — renin-angiotensin-aldosterone, pressure natriuresis, prostaglandins
6. Erythropoietin production — stimulates RBC formation in bone marrow (responds to hypoxia)
7. Vitamin D activation — converts 25-OH cholecalciferol → 1,25-(OH)₂D₃ (calcitriol) via 1α-hydroxylase
8. Gluconeogenesis — contributes ~20% of total gluconeogenesis during prolonged fasting
9. Clearance of hormones & drugs — insulin, PTH, many medications

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b) Renal Function Tests

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c) Plasma Clearance

• Cₓ = clearance of substance X (mL/min)
• Uₓ = urine concentration of X (mg/mL)
• V̇ = urine flow rate (mL/min)
• Pₓ = plasma concentration of X (mg/mL)

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d) Measuring GFR by Inulin Clearance

• Is freely filtered at glomerulus
• Is not reabsorbed, not secreted, not metabolized by the tubule
• Is not toxic, not protein-bound

1. Patient is given a continuous IV infusion of inulin to achieve a stable plasma concentration
2. Urine is collected over a timed period (e.g., 1 hour) via catheter
3. Measure:
   • P_in = plasma inulin concentration (e.g., 1 mg/mL)
   • U_in = urine inulin concentration (e.g., 125 mg/mL)
   • V̇ = urine flow rate (e.g., 1 mL/min)

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Q.7 (Or) — GIT Movements

a) Movements of Different Parts of GIT

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b) Mass Movement — Definition, Mechanism & Physiological Importance

1. Triggered by the gastrocolic reflex (food entering the stomach distends it → long vagal reflex → colon contracts) and the duodenocolic reflex
2. A distended segment of colon causes the entire segment proximal to it to contract simultaneously (similar to "clearing" the colon)
3. The longitudinal and circular muscles of a long segment (20–30 cm) contract en masse
4. Fecal material is propelled rapidly toward the rectum
5. Mediated by: myenteric plexus (intrinsic) + parasympathetic stimulation (extrinsic)

• Propels fecal matter from transverse/descending colon to sigmoid/rectum
• Triggers the urge to defecate when rectum fills
• Occurs 1–3 times/day, typically after meals (gastrocolic reflex)
• Impaired mass movement → constipation; exaggerated → diarrhea

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c) Law of the Gut (Bayliss & Starling, 1899)

• Oral (proximal) side: Circular muscle contracts (ascending excitation) — via ACh, Substance-P
• Aboral (distal) side: Circular muscle relaxes (descending inhibition) — via VIP, NO, ATP
• This ensures one-way (aboral) propulsion of gut contents
• Mediated entirely by the myenteric plexus — works even after complete extrinsic denervation

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d) Peristaltic Rush

• Intense irritation of the intestinal mucosa (e.g., severe gastroenteritis, toxins, chemical irritants)
• Extreme bowel distension

• Rapid expulsion of irritants/toxins from the small intestine
• Results in profuse watery diarrhea (contents propelled to colon before water can be absorbed)
• Protective mechanism — clears harmful substances quickly
• Mediated by exaggerated myenteric reflex activity + possibly serotonin (5-HT) release from enterochromaffin cells

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GIT & Renal Physiology — MCQ & SBA Answers

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Part 1: True (T) / False (F) — Q.1 to Q.5

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Q.1 — Following is/are Cholagogue(s)

Cholagogues = substances that stimulate gallbladder contraction and bile ejection into duodenum

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Q.2 — Factors That Delay Gastric Emptying

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Q.3 — Examples of Freely Filterable Substances

Freely filterable = small, unbound molecules that pass freely through the glomerular filtration barrier

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Q.4 — GFR is Reduced Due To

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Q.5 — Completely Reabsorbed Substances

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Part 2: Single Best Answer (SBA) — Q.11 to Q.15

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Q.11 — Macula Densa is Present In:

The macula densa is a specialized cluster of cells in the wall of the DCT at the point where it contacts the afferent arteriole of its own glomerulus (part of the juxtaglomerular apparatus). It senses NaCl concentration in tubular fluid and regulates GFR via tubuloglomerular feedback.

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Q.12 — Which Movement Has a Housekeeping Role in GIT?

The MMC occurs during fasting (interdigestive period). It sweeps the intestine clean of residual food, bacteria, and debris every ~90 minutes, preventing bacterial overgrowth. It is called the "intestinal housekeeper." It is initiated by motilin (released from duodenum during fasting).

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Q.13 — Function of Myenteric Plexus (Auerbach's Plexus):

The myenteric (Auerbach's) plexus lies between the longitudinal and circular muscle layers and primarily controls GIT motility (peristalsis, segmentation, mass movement). The submucosal (Meissner's) plexus controls secretion and absorption.

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Q.14 — Which Part of the Nephron is Completely Impermeable to Water?

The thick ascending limb is completely impermeable to water (lacks aquaporins) but actively transports Na⁺, K⁺, and Cl⁻ via NKCC2 co-transporter. This makes the tubular fluid hypotonic (diluting segment) and builds up the medullary osmotic gradient. This is why it is also called the "diluting segment."

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Q.15 — Urea Reabsorption Occurs In:

Urea is passively reabsorbed (~40–50% of filtered urea) in the inner medullary collecting duct via UT-A1 and UT-A3 urea transporters (stimulated by ADH). This urea reabsorption is critical for maintaining the medullary hyperosmotic gradient needed for urine concentration. The PCT reabsorbs some urea passively, but the primary site for regulated urea recycling is the inner medullary collecting duct.

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Summary Answer Key

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Complete MCQ Answers — GIT, Renal & Respiratory Physiology

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IMAGE 1: Single Best Answers (Q.11–Q.20)

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Q.11 — Juxtaglomerular Cells are Located In:

JG cells (granular cells) are modified smooth muscle cells of the afferent arteriole wall. They contain renin granules and are part of the juxtaglomerular apparatus (JGA). They sense stretch/pressure and release renin.

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Q.12 — Maximum H⁺ Secretion Occurs In:

The PCT secretes the largest absolute amount of H⁺ (~65% of total H⁺ secretion) via the Na⁺/H⁺ exchanger (NHE3) on the luminal membrane. The collecting duct secretes H⁺ maximally in terms of concentration (can acidify urine to pH 4.5), but the PCT handles the greatest volume.

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Q.13 — Widely Used Clinical Test for Estimation of GFR:

• Inulin clearance = gold standard but cumbersome (requires IV infusion; not routine)
• Creatinine clearance = most widely used clinically (~125 mL/min); slightly overestimates GFR due to tubular secretion but is practical
• Urea clearance is unreliable (urea is reabsorbed variably)
• PAH clearance measures renal plasma flow, not GFR

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Q.14 — Most Powerful Feedback System for Controlling Plasma Osmolarity:

The ADH-thirst mechanism is the primary and most powerful regulator of plasma osmolarity:

• ↑Osmolarity → hypothalamic osmoreceptors → ↑ADH (water retention) + ↑thirst (water intake) → osmolarity normalized
• The renin-angiotensin system primarily regulates volume/BP, not osmolarity
• Countercurrent system creates the gradient but doesn't "control" osmolarity

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Q.15 — In Children Below 3 Years, Micturition Is:

In infants/children <2–3 years, the descending corticospinal inhibitory pathways to the sacral micturition center (S2–S4) are not yet myelinated. Micturition is purely a spinal reflex — bladder fills → stretch receptors → sacral cord → detrusor contraction → voiding. Voluntary cortical control develops around age 2–3 years.

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Q.16 — Cyanide Poisoning Causes Death Due To:

Cyanide (CN⁻) binds irreversibly to the Fe³⁺ of cytochrome c oxidase (Complex IV) of the mitochondrial electron transport chain → blocks oxidative phosphorylation → cells cannot use O₂ → histotoxic hypoxia → lactic acidosis → cell death. Blood remains well-oxygenated (cherry-red), so no cyanosis.

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Q.17 — Surfactant Causes:

Pulmonary surfactant (dipalmitoylphosphatidylcholine, DPPC) is produced by type II pneumocytes:

• Reduces alveolar surface tension → prevents alveolar collapse → ↑lung compliance
• Present at birth (after ~26 weeks gestation); absent/deficient in premature infants → Respiratory Distress Syndrome (RDS)
• Secreted by alveolar type II cells (not bronchus)

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Q.18 — Which Causes a LEFT Shift of the Oxy-Hemoglobin Dissociation Curve?

Left shift = ↑Hb affinity for O₂ (harder to unload O₂ to tissues). Causes — mnemonic "CADET, face Left":

• ↓CO₂, ↓H⁺ (Alkalosis), ↓Temperature, ↓2,3-BPG, CO (carbon monoxide), Fetal Hb

Among the options:

• Increased lactate → acidosis → RIGHT shift
• Decreased 2,3-BPG → LEFT shift ✓ (also correct)
• Alkalosis → LEFT shift ✓
• Increased 2,3-BPG → RIGHT shift

Both b and c are correct, but alkalosis (c) is the more classically tested single answer.

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Q.19 — Cholagogues are Substances Which Cause:

Cholagogue = substance that causes gallbladder contraction + relaxation of sphincter of Oddi → bile ejected into duodenum (e.g., CCK, magnesium sulfate, fatty acids)

• Choleretics = substances that increase bile secretion by the liver (e.g., bile salts, secretin)
• Increasing bile concentration = choleretic effect
• Acidification = not a cholagogue effect

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Q.20 — The Usual Stimulus of Peristalsis:

Distension of the gut wall by luminal contents is the primary stimulus for peristalsis. It activates mechanoreceptors → myenteric plexus → Law of the Intestine: contraction above + relaxation below the bolus → propulsion. Sympathetic stimulation inhibits peristalsis; acid/alkaline chyme are not the primary stimuli.

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IMAGE 2: True (T) / False (F) — Q.1 to Q.10 (Renal & Respiratory)

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Q.1 — Hormones & Autacoids That DECREASE GFR

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Q.2 — FEV₁

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Q.3 — The Medullary Collecting Duct Is

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Q.4 — Plasma Clearance Rate Of

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Q.5 — O₂ Carrying Capacity of Blood Depends On

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Q.6 — Regarding Diuretics

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Q.7 — Stomach Emptying is Inhibited By

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Q.8 — Gastric HCl Secretion Is

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Q.9 — Respiratory Dead Space

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Q.10 — GIT Hormones Are

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Quick Reference Summary