Topic: Renal Physiology
Subtopic: Carbonic Anhydrase Enzyme
Keyword Definitions
• Carbonic Anhydrase – enzyme catalyzing conversion of CO₂ and H₂O to H₂CO₃.
• RBC – Red Blood Cells, transport oxygen and carbon dioxide.
• Plasma – liquid part of blood without cells.
• Kidney – organ filtering blood and maintaining acid-base balance.
• Brain – organ controlling body functions and maintaining pH balance.
Lead Question (2013)
Carbonic anhydrase activity found in all except?
a) Brain
b) Kidney
c) RBC
d) Plasma
Explanation: Carbonic anhydrase is present in kidney tubular cells, RBCs, and brain tissues where it helps in acid-base regulation. Plasma lacks carbonic anhydrase activity. Therefore, the correct answer is Plasma. This absence helps maintain compartmental differences in CO₂ buffering and bicarbonate regulation within the body fluids.
1) Guessed Question
Which type of carbonic anhydrase is abundant in RBCs?
a) CA I
b) CA II
c) CA III
d) CA IV
Explanation: RBCs predominantly contain Carbonic Anhydrase II, a cytoplasmic isoenzyme that rapidly catalyzes the hydration of carbon dioxide. This process is essential for CO₂ transport and bicarbonate buffer system. Hence, the correct answer is CA II, which is the most active isoenzyme in red blood cells.
2) Guessed Question
A patient with renal tubular acidosis has a defect in which enzyme?
a) Na⁺/K⁺ ATPase
b) Carbonic Anhydrase
c) Renin
d) Aldolase
Explanation: Renal tubular acidosis type II is due to defective carbonic anhydrase in the proximal tubules. This enzyme normally facilitates bicarbonate reabsorption. Without it, bicarbonate is wasted in urine, leading to acidosis. Thus, the correct answer is Carbonic Anhydrase, showing its crucial role in kidney function.
3) Guessed Question
Which drug is a carbonic anhydrase inhibitor?
a) Furosemide
b) Acetazolamide
c) Spironolactone
d) Hydrochlorothiazide
Explanation: Acetazolamide is a diuretic that inhibits carbonic anhydrase, reducing bicarbonate reabsorption in proximal tubules, causing alkaline urine and metabolic acidosis. It is used in glaucoma, altitude sickness, and some seizure disorders. Hence, the correct answer is Acetazolamide, the prototype carbonic anhydrase inhibitor drug.
4) Guessed Question
Which of the following conditions benefits from carbonic anhydrase inhibitors?
a) Glaucoma
b) Hypothyroidism
c) Hypertension only
d) Parkinson’s disease
Explanation: Carbonic anhydrase inhibitors decrease aqueous humor secretion in the eye, lowering intraocular pressure. Therefore, they are widely used in the treatment of glaucoma. While they may have other clinical uses, the main therapeutic indication remains glaucoma. Thus, the correct answer is Glaucoma, showing their ophthalmic importance.
5) Guessed Question
A mountaineer develops acute mountain sickness. Which drug helps?
a) Mannitol
b) Acetazolamide
c) Furosemide
d) Amiloride
Explanation: At high altitude, hypoxia leads to respiratory alkalosis. Acetazolamide, a carbonic anhydrase inhibitor, induces metabolic acidosis by bicarbonate excretion, which stimulates ventilation and relieves symptoms. Therefore, the correct answer is Acetazolamide. This drug is commonly used prophylactically for altitude sickness prevention in climbers.
6) Guessed Question
Carbonic anhydrase in gastric parietal cells helps in secretion of:
a) HCl
b) HCO₃⁻
c) Pepsin
d) Mucus
Explanation: In gastric parietal cells, carbonic anhydrase generates H⁺ and HCO₃⁻ from CO₂ and H₂O. The H⁺ is secreted into the stomach lumen to form hydrochloric acid (HCl). Thus, the correct answer is HCl. This mechanism is central to acid secretion in the stomach’s digestive process.
7) Guessed Question
Patient with seizures and glaucoma is prescribed a drug inhibiting carbonic anhydrase. Likely drug is:
a) Phenytoin
b) Valproate
c) Acetazolamide
d) Carbamazepine
Explanation: Acetazolamide, by inhibiting carbonic anhydrase, reduces intraocular pressure in glaucoma and also has anticonvulsant activity in absence seizures. Hence, in a patient with both glaucoma and seizures, acetazolamide is the drug of choice. Therefore, the correct answer is Acetazolamide, highlighting its dual clinical usefulness.
8) Guessed Question
Which statement about carbonic anhydrase is true?
a) Found only in plasma
b) Inhibitors cause metabolic alkalosis
c) Essential for acid-base balance
d) Not present in kidneys
Explanation: Carbonic anhydrase catalyzes CO₂ hydration, playing a vital role in maintaining acid-base homeostasis. It is widely present in RBCs, kidneys, and other tissues. Plasma lacks it. Inhibitors cause metabolic acidosis, not alkalosis. Therefore, the correct answer is “Essential for acid-base balance,” showing its systemic importance.
9) Guessed Question
In the proximal tubule, carbonic anhydrase inhibition leads to:
a) Increased HCO₃⁻ excretion
b) Increased Na⁺ reabsorption
c) Increased H⁺ secretion
d) Increased water reabsorption
Explanation: Inhibition of carbonic anhydrase reduces bicarbonate reabsorption in proximal tubule, leading to increased urinary excretion of bicarbonate. This results in alkaline urine and mild metabolic acidosis. Thus, the correct answer is Increased HCO₃⁻ excretion. This mechanism underlies the diuretic action of carbonic anhydrase inhibitors.
10) Guessed Question
Which isoform of carbonic anhydrase is membrane-bound and found in kidneys?
a) CA I
b) CA II
c) CA IV
d) CA IX
Explanation: Carbonic Anhydrase IV is a membrane-bound isoform located in the proximal tubular brush border of kidneys. It facilitates extracellular conversion of bicarbonate, essential for reabsorption processes. Therefore, the correct answer is CA IV. This demonstrates the tissue-specific isoform distribution of the enzyme in human physiology.
Topic: Liver and Plasma Proteins
Subtopic: Albumin Metabolism
Keyword Definitions
• Albumin – major plasma protein synthesized by the liver, maintaining oncotic pressure.
• Half-life – time required for half of a substance to be eliminated from plasma.
• Plasma Proteins – proteins present in plasma, mainly albumin, globulins, fibrinogen.
• Liver – organ responsible for synthesis of albumin and other plasma proteins.
• Oncotic Pressure – osmotic pressure exerted by plasma proteins, preventing edema.
Lead Question (2013)
Half-life of albumin is:
a) 5 days
b) 10 days
c) 20 days
d) 40 days
Explanation: Albumin is synthesized in the liver and has an average plasma half-life of 20 days. Its relatively long half-life reflects stability and slow catabolism. Conditions like malnutrition, chronic liver disease, or nephrotic syndrome affect albumin turnover. Hence, the correct answer is 20 days, indicating albumin’s metabolic persistence.
1) Guessed Question
Which organ is primarily responsible for albumin synthesis?
a) Kidney
b) Spleen
c) Liver
d) Bone marrow
Explanation: Albumin is exclusively synthesized in the liver hepatocytes. It represents the most abundant plasma protein, maintaining osmotic balance and transporting hormones, fatty acids, and drugs. Any impairment of liver function directly decreases albumin production. Therefore, the correct answer is Liver, which plays a central role in protein synthesis.
2) Guessed Question
A patient with cirrhosis presents with low albumin and edema. Cause of edema is?
a) Increased hydrostatic pressure
b) Decreased oncotic pressure
c) Increased lymphatic drainage
d) Increased protein intake
Explanation: Hypoalbuminemia due to liver failure reduces plasma oncotic pressure, leading to movement of fluid into interstitial spaces causing edema and ascites. This clinical manifestation is typical of cirrhosis and chronic liver disease. Hence, the correct answer is Decreased oncotic pressure, directly linked to reduced plasma albumin levels.
3) Guessed Question
Normal serum albumin level in adults is:
a) 1–2 g/dL
b) 2–3 g/dL
c) 3.5–5.5 g/dL
d) 6–8 g/dL
Explanation: The normal serum albumin concentration in adults is 3.5–5.5 g/dL. Levels below 3.5 g/dL indicate hypoalbuminemia, often associated with malnutrition, nephrotic syndrome, or liver disease. Maintaining this concentration is essential for fluid balance and nutrient transport. Thus, the correct answer is 3.5–5.5 g/dL.
4) Guessed Question
Which vitamin deficiency decreases albumin synthesis?
a) Vitamin A
b) Vitamin B12
c) Vitamin C
d) Vitamin K
Explanation: Protein synthesis, including albumin, is impaired in Vitamin B12 deficiency due to defective DNA synthesis and ineffective erythropoiesis. Although other vitamins influence metabolism, Vitamin B12 deficiency is strongly linked with reduced albumin production in chronic deficiency states. Therefore, the correct answer is Vitamin B12, highlighting its metabolic importance.
5) Guessed Question
A nephrotic syndrome patient has albuminuria. What happens to oncotic pressure?
a) Increases
b) Decreases
c) Remains unchanged
d) Doubles
Explanation: In nephrotic syndrome, albumin is lost in urine, resulting in hypoalbuminemia. The decline in plasma albumin reduces oncotic pressure, causing edema and fluid accumulation. This is a hallmark of nephrotic syndrome pathophysiology. Hence, the correct answer is Decreases, demonstrating the direct relationship between albumin and oncotic balance.
6) Guessed Question
Albumin binds and transports all except:
a) Bilirubin
b) Calcium
c) Thyroxine
d) Hemoglobin
Explanation: Albumin transports bilirubin, calcium, fatty acids, and hormones like thyroxine. However, hemoglobin is not carried by albumin; it is bound by haptoglobin when free in plasma. Therefore, the correct answer is Hemoglobin, as albumin is not responsible for its transport. This highlights albumin’s selective transport functions.
7) Guessed Question
Patient with protein-energy malnutrition (kwashiorkor) presents with edema. Cause is?
a) Hypoalbuminemia
b) Hypernatremia
c) Increased vascular resistance
d) Hyperkalemia
Explanation: In kwashiorkor, inadequate dietary protein reduces hepatic albumin synthesis, causing hypoalbuminemia. This decreases plasma oncotic pressure, leading to edema despite adequate caloric intake. Therefore, the correct answer is Hypoalbuminemia, a classic mechanism explaining edema in malnourished children. This condition exemplifies the vital role of albumin in nutrition.
8) Guessed Question
Which test is most specific for assessing hepatic synthetic function?
a) Serum bilirubin
b) Serum albumin
c) Prothrombin time
d) ALT/AST
Explanation: Serum albumin reflects chronic hepatic synthetic capacity, but prothrombin time is more sensitive for acute changes. Since albumin has a long half-life, its fall indicates prolonged liver dysfunction. Therefore, the correct answer is Serum albumin, which is a reliable marker of chronic liver synthetic function over time.
9) Guessed Question
Which of the following increases albumin catabolism?
a) Burns
b) Hypothyroidism
c) Renal artery stenosis
d) Addison’s disease
Explanation: Severe burns increase vascular permeability, leading to albumin leakage and accelerated catabolism. This results in hypoalbuminemia and edema, complicating patient recovery. Hence, the correct answer is Burns, which significantly increase albumin breakdown and loss from circulation. This emphasizes albumin’s vulnerability in catabolic stress states.
10) Guessed Question
Which plasma protein has the longest half-life?
a) Albumin
b) Fibrinogen
c) Transferrin
d) Immunoglobulin G
Explanation: Immunoglobulin G (IgG) has the longest half-life among plasma proteins, around 23 days. Albumin has a shorter half-life of about 20 days. This long half-life makes IgG suitable for passive immunity through maternal transfer and therapeutic use. Thus, the correct answer is Immunoglobulin G, not albumin.
Topic: Plasma Proteins
Subtopic: Half-life of Plasma Proteins
Keyword Definitions:
• Prealbumin: Plasma protein also called transthyretin, transports thyroxine and retinol-binding protein.
• Albumin: Most abundant plasma protein, maintains oncotic pressure and transports molecules.
• Half-life: Time taken for half of the protein amount to degrade or be eliminated.
• Plasma Proteins: Proteins circulating in blood, important in transport, immunity, and clotting.
Lead Question – 2013
Half life of Prealbumin is?
a) 2 days
b) 10 days
c) 20 days
d) 40 days
Explanation: The half-life of prealbumin (transthyretin) is approximately 2 days. This short half-life makes it a sensitive marker for acute changes in nutritional status, unlike albumin, which has a longer half-life of around 20 days. Hence, the correct answer is 2 days.
1) Half-life of Albumin is:
a) 5 days
b) 10 days
c) 20 days
d) 40 days
Explanation: Albumin has a half-life of approximately 20 days. It is a major plasma protein synthesized in the liver, responsible for oncotic pressure maintenance and substance transport. Its long half-life makes it unsuitable for acute nutritional assessment. Correct answer is 20 days.
2) Half-life of Fibrinogen is:
a) 1 day
b) 3 days
c) 7 days
d) 14 days
Explanation: Fibrinogen, a coagulation factor, has a half-life of about 3 to 5 days. It plays a key role in blood clotting by being converted to fibrin during hemostasis. The correct answer is 3 days, making it an important acute phase reactant.
3) Half-life of Transferrin is:
a) 2 days
b) 8 days
c) 20 days
d) 40 days
Explanation: Transferrin is an iron-binding plasma protein with a half-life of about 8 days. It transports iron in circulation and is used as an indicator in nutritional and iron metabolism assessment. The correct answer is 8 days.
4) Clinical: A malnourished patient is monitored for improvement. Which plasma protein with the shortest half-life is the best marker?
a) Albumin
b) Prealbumin
c) Transferrin
d) Fibrinogen
Explanation: Prealbumin, with a half-life of 2 days, is the best marker for short-term changes in nutritional status. Albumin has a longer half-life, thus not suitable for acute monitoring. Hence, the correct answer is Prealbumin.
5) Clinical: In liver failure, which plasma protein level decreases first due to its short half-life?
a) Albumin
b) Prealbumin
c) Transferrin
d) Ceruloplasmin
Explanation: Prealbumin is synthesized in the liver and has a short half-life. In liver failure, its level drops quickly, making it an early marker. The correct answer is Prealbumin.
6) Which protein has the longest half-life among plasma proteins?
a) Albumin
b) Transferrin
c) Immunoglobulin G
d) Prealbumin
Explanation: Immunoglobulin G (IgG) has the longest half-life, approximately 23 days, which helps in maintaining long-term immunity. This property also makes IgG suitable for passive immunization. The correct answer is IgG.
7) Clinical: A child with protein-energy malnutrition is treated. Which plasma protein will reflect improvement within 48 hours?
a) Albumin
b) Prealbumin
c) IgG
d) Transferrin
Explanation: Prealbumin responds rapidly due to its 2-day half-life, showing improvement within 48 hours. Albumin, with a longer half-life, changes slowly. Thus, the correct answer is Prealbumin.
8) Which protein has a half-life of around 5 days?
a) Retinol-binding protein
b) Fibrinogen
c) Albumin
d) Transferrin
Explanation: Retinol-binding protein (RBP) has a very short half-life of around 12 hours, not 5 days. Fibrinogen half-life is 3–5 days, so the closest is Fibrinogen with 5 days. Correct answer: Fibrinogen.
9) Clinical: Which plasma protein is used as a sensitive marker for protein-calorie malnutrition because of its short half-life?
a) Albumin
b) Prealbumin
c) Transferrin
d) Ceruloplasmin
Explanation: Prealbumin, due to its very short half-life, is a sensitive marker for protein-calorie malnutrition. Its levels reflect recent nutritional status better than albumin or transferrin. The correct answer is Prealbumin.
10) Which plasma protein has the shortest half-life?
a) Prealbumin
b) Albumin
c) Fibrinogen
d) Transferrin
Explanation: Among plasma proteins, prealbumin has the shortest half-life (2 days), making it useful in clinical monitoring. Albumin and transferrin have longer half-lives, hence are less sensitive for acute nutritional changes. The correct answer is Prealbumin.
Topic: Calcium Signaling
Subtopic: Calmodulin and Enzyme Activation K
Keyword Definitions:
• Calmodulin: A calcium-binding messenger protein regulating many enzymes and cellular processes.
• Protein Kinase: Enzyme that phosphorylates proteins, altering activity.
• Phosphorylase: Enzyme breaking glycogen into glucose-1-phosphate.
• 2,3-DPG: Regulator of hemoglobin’s oxygen affinity.
• Glucokinase: Enzyme phosphorylating glucose in hepatocytes and pancreatic β-cells.
Lead Question – 2013
Calmodulin activates?
a) Muscle phosphorylase
b) Protein kinase
c) 2, 3 DPG
d) Glucokinase
Explanation: Calmodulin is a calcium-binding protein that activates several enzymes, most notably protein kinases. It does not directly activate phosphorylase, glucokinase, or 2,3-DPG. Calmodulin works by binding Ca²⁺ and changing shape to activate target proteins. The correct answer is Protein kinase.
1) Which of the following is a direct target of calmodulin?
a) Myosin light chain kinase
b) Hexokinase
c) Pyruvate dehydrogenase
d) Glycogen synthase
Explanation: Calmodulin directly activates myosin light chain kinase (MLCK) in smooth muscle. This leads to phosphorylation of myosin light chains and contraction. Other listed enzymes are not directly activated by calmodulin. The correct answer is Myosin light chain kinase.
2) Clinical: A patient has defective smooth muscle contraction. Which calmodulin-dependent enzyme is most likely impaired?
a) Myosin light chain kinase
b) Pyruvate carboxylase
c) Lactate dehydrogenase
d) Adenylate cyclase
Explanation: Smooth muscle contraction requires MLCK activation by Ca²⁺-calmodulin. A defect here impairs contraction. Other enzymes are not directly involved in this process. The correct answer is Myosin light chain kinase.
3) Calmodulin regulates which of the following?
a) Adenylate cyclase
b) Glycogen phosphorylase
c) Pyruvate kinase
d) Fructose bisphosphatase
Explanation: Calmodulin can regulate adenylate cyclase in some tissues by binding Ca²⁺ and altering cyclic AMP production. Other enzymes listed are not directly regulated by calmodulin. The correct answer is Adenylate cyclase.
4) Clinical: A hypertensive patient is treated with calcium channel blockers. Which calmodulin-mediated process is most affected?
a) Smooth muscle contraction
b) Glycolysis
c) Urea cycle
d) Beta-oxidation
Explanation: Calcium entry is needed to activate calmodulin and MLCK, leading to smooth muscle contraction. Blocking calcium channels decreases contraction, lowering blood pressure. Correct answer is Smooth muscle contraction.
5) Which secondary messenger works in conjunction with calmodulin?
a) Cyclic AMP
b) Cyclic GMP
c) Calcium ions
d) Inositol triphosphate
Explanation: Calmodulin is activated by calcium ions (Ca²⁺). IP₃ can release calcium from stores, indirectly aiding calmodulin. But the direct activator is calcium. The correct answer is Calcium ions.
6) Clinical: A mutation in calmodulin would primarily affect which system?
a) Calcium-mediated signaling
b) Glycogen synthesis
c) DNA replication
d) Fatty acid synthesis
Explanation: Calmodulin mediates calcium signaling and regulates kinases and enzymes. A mutation would disrupt many calcium-dependent pathways, including muscle contraction and secretion. The correct answer is Calcium-mediated signaling.
7) Calmodulin-dependent protein kinase II is important in:
a) Memory and learning
b) Lipid metabolism
c) Urea synthesis
d) Cholesterol transport
Explanation: CaMKII is a calmodulin-dependent protein kinase important in neuronal plasticity, memory, and learning. This highlights calmodulin’s role in the nervous system. Correct answer is Memory and learning.
8) Clinical: A patient has defective neurotransmitter release. Which calmodulin-related mechanism may be impaired?
a) Synaptic vesicle exocytosis
b) Glycogen storage
c) Fatty acid oxidation
d) DNA repair
Explanation: Calmodulin regulates exocytosis of neurotransmitters by activating calcium-dependent proteins. A defect impairs synaptic transmission. Correct answer is Synaptic vesicle exocytosis.
9) Which enzyme is calmodulin-dependent?
a) Phosphodiesterase
b) Succinyl-CoA synthetase
c) Enolase
d) Aldolase
Explanation: Calmodulin activates certain phosphodiesterases that degrade cyclic nucleotides, regulating signaling. Other enzymes listed are not dependent on calmodulin. The correct answer is Phosphodiesterase.
10) Clinical: A patient with asthma benefits from a drug reducing calmodulin activity. Which effect helps relieve symptoms?
a) Decreased smooth muscle contraction
b) Increased glycolysis
c) Enhanced fatty acid metabolism
d) Increased urea cycle activity
Explanation: Calmodulin is crucial for smooth muscle contraction via MLCK. Inhibiting calmodulin decreases airway smooth muscle contraction, relieving bronchospasm in asthma. The correct answer is Decreased smooth muscle contraction.
Topic: Endocrinology
Subtopic: Hormonal Regulation during Starvation
Keyword Definitions:
• Leptin: Hormone from adipose tissue that suppresses appetite and regulates energy balance.
• MSH (Melanocyte Stimulating Hormone): Hormone affecting skin pigmentation and appetite control.
• Ghrelin: Stomach hormone that increases hunger and stimulates growth hormone release.
• Insulin: Pancreatic hormone promoting glucose uptake and storage.
• Starvation: Condition of prolonged fasting leading to metabolic and hormonal adaptations.
Lead Question – 2013
During starvation, which level increases?
a) Leptin
b) MSH
c) Ghrelin
d) Insulin
Explanation: Starvation reduces leptin and insulin levels due to fat and glucose depletion. Ghrelin, secreted by the stomach, rises to stimulate appetite and increase growth hormone release. This adaptive mechanism drives hunger and promotes energy mobilization. The correct answer is Ghrelin.
1) Which hormone decreases during starvation?
a) Leptin
b) Ghrelin
c) Cortisol
d) Glucagon
Explanation: Leptin, secreted by adipose tissue, decreases during starvation because fat stores decline. Ghrelin and cortisol increase, while glucagon also rises to maintain glucose. Thus, leptin falls significantly. The correct answer is Leptin.
2) Clinical: A fasting patient experiences extreme hunger. Which hormone is responsible?
a) Insulin
b) Ghrelin
c) Leptin
d) Thyroxine
Explanation: Ghrelin, released from the stomach during fasting, stimulates appetite and signals hunger to the hypothalamus. Its levels rise significantly in starvation. Hence, the correct answer is Ghrelin.
3) Which hormone increases lipolysis during starvation?
a) Insulin
b) Glucagon
c) Leptin
d) Ghrelin
Explanation: Glucagon promotes lipolysis and ketogenesis during starvation. Insulin normally inhibits lipolysis, but it decreases during fasting. Ghrelin and leptin are not directly responsible for lipolysis. Correct answer is Glucagon.
4) Clinical: A malnourished child with very low fat stores will have low levels of?
a) Leptin
b) Ghrelin
c) Cortisol
d) Glucagon
Explanation: With low adipose tissue, leptin secretion falls drastically. Ghrelin may rise, while cortisol and glucagon increase to provide alternative fuels. The correct answer is Leptin.
5) Which hormone helps maintain blood glucose during prolonged fasting?
a) Insulin
b) Glucagon
c) Ghrelin
d) Leptin
Explanation: Glucagon stimulates gluconeogenesis and glycogenolysis in the liver, maintaining blood glucose during fasting. Insulin falls, while ghrelin and leptin play appetite-related roles. The correct answer is Glucagon.
6) Clinical: A starving patient develops ketone breath odor. Which hormone promoted this adaptation?
a) Glucagon
b) Insulin
c) Leptin
d) Ghrelin
Explanation: Glucagon stimulates fatty acid oxidation and ketogenesis in the liver during prolonged fasting, leading to ketone body production. Insulin normally inhibits ketogenesis, but it is suppressed during starvation. Correct answer is Glucagon.
7) Which hormone rises immediately after a meal and falls during starvation?
a) Insulin
b) Ghrelin
c) Glucagon
d) Cortisol
Explanation: Insulin rises after a meal to promote glucose storage. During fasting or starvation, insulin levels fall, while glucagon and ghrelin increase. Correct answer is Insulin.
8) Clinical: A patient with chronic starvation has hyperpigmentation due to increased?
a) ACTH
b) MSH
c) Leptin
d) Insulin
Explanation: MSH levels may rise as a derivative of ACTH in prolonged starvation and stress, causing hyperpigmentation. Leptin and insulin decrease, while ghrelin increases. Correct answer is MSH.
9) Ghrelin is primarily secreted from?
a) Adipose tissue
b) Pancreas
c) Stomach
d) Hypothalamus
Explanation: Ghrelin is secreted mainly from the stomach, especially the fundus, and acts on the hypothalamus to increase hunger. Adipose tissue secretes leptin, and pancreas secretes insulin. Correct answer is Stomach.
10) Clinical: In starvation, why does blood insulin level fall?
a) Low glucose availability
b) High ghrelin secretion
c) Increased leptin action
d) Excess fat breakdown
Explanation: Insulin secretion depends on glucose. During starvation, blood glucose decreases, leading to reduced insulin secretion. Ghrelin increases hunger, while leptin falls, but insulin is directly linked to glucose availability. Correct answer is Low glucose availability.
Subtopic: Hepatic Blood Flow
Keyword Definitions:
• Liver: Largest internal organ, vital for metabolism and detoxification.
• Blood supply: Dual supply via hepatic artery and portal vein.
• Portal vein: Carries nutrient-rich blood from intestines.
• Hepatic artery: Supplies oxygen-rich blood.
• Perfusion rate: Blood flow through tissue per unit weight.
Lead Question - 2013
Blood supply of liver [ml/100g/min]
a) 1500-2000
b) 1000-1500
c) 50-60
d) 250-300
Explanation:
The liver receives dual blood supply, about 25% from the hepatic artery and 75% from the portal vein. Normal perfusion of liver tissue is approximately 1000–1500 ml/100g/min. This ensures metabolic, detoxification, and synthetic functions. Answer: b) 1000–1500.
1) Which vessel supplies 75% of blood flow to the liver?
a) Hepatic artery
b) Portal vein
c) Hepatic vein
d) Inferior vena cava
Explanation:
The portal vein carries nutrient-rich blood from intestines and supplies nearly 75% of hepatic blood flow. The hepatic artery contributes the remaining 25%. This dual system supports liver’s metabolic activity. Answer: b) Portal vein.
2) During portal vein thrombosis, which vessel compensates blood flow?
a) Inferior vena cava
b) Hepatic artery
c) Renal vein
d) Splenic vein
Explanation:
When the portal vein is obstructed, the hepatic artery increases blood flow to maintain perfusion. This autoregulatory mechanism protects hepatocytes temporarily but cannot fully replace portal supply. Answer: b) Hepatic artery.
3) In cirrhosis, portal hypertension occurs due to:
a) Increased hepatic artery flow
b) Increased resistance in liver sinusoids
c) Decreased portal vein inflow
d) Increased hepatic vein drainage
Explanation:
Cirrhosis increases resistance within liver sinusoids and portal tracts, leading to portal hypertension. This causes ascites, varices, and splenomegaly. Answer: b) Increased resistance in liver sinusoids.
4) A 50-year-old man with cirrhosis presents with hematemesis. Most likely cause?
a) Gastric ulcer
b) Variceal bleed
c) Mallory-Weiss tear
d) Duodenal ulcer
Explanation:
In cirrhosis with portal hypertension, esophageal varices rupture commonly causing hematemesis. Portal-systemic shunts lead to dilated veins that rupture easily. Answer: b) Variceal bleed.
5) Oxygen content of hepatic arterial blood is:
a) High
b) Low
c) Moderate
d) Absent
Explanation:
Hepatic arterial blood is oxygen-rich, supplying hepatocytes with required oxygen. Portal vein blood is nutrient-rich but relatively low in oxygen. Answer: a) High.
6) A patient with Budd-Chiari syndrome presents with hepatomegaly. Blockage site is:
a) Hepatic veins
b) Portal vein
c) Hepatic artery
d) Inferior vena cava below diaphragm
Explanation:
Budd-Chiari syndrome results from obstruction of hepatic veins draining the liver, leading to hepatomegaly, ascites, and abdominal pain. Answer: a) Hepatic veins.
7) Functional unit of liver is:
a) Lobule
b) Acinus
c) Sinusoid
d) Portal triad
Explanation:
The hepatic acinus is the functional unit based on blood supply, oxygenation, and metabolism, divided into zones 1–3. Answer: b) Acinus.
8) A 45-year-old alcoholic develops ascites. Primary mechanism?
a) Decreased albumin
b) Increased portal pressure
c) Increased aldosterone
d) Lymphatic obstruction
Explanation:
Portal hypertension due to cirrhosis increases hydrostatic pressure, pushing fluid into peritoneal cavity. Hypoalbuminemia and aldosterone excess worsen ascites. Answer: b) Increased portal pressure.
9) Liver receives what percent of cardiac output?
a) 10%
b) 15%
c) 25%
d) 40%
Explanation:
Liver receives approximately 25% of cardiac output via portal vein and hepatic artery, essential for metabolism and detoxification. Answer: c) 25%.
10) In hepatic encephalopathy, toxin accumulation is mainly:
a) Ammonia
b) Urea
c) Bilirubin
d) Lactate
Explanation:
Ammonia accumulates due to impaired detoxification in liver failure, crossing blood-brain barrier and altering neurotransmission. This causes hepatic encephalopathy. Answer: a) Ammonia.
Chapter: Physiology
Topic: Gastrointestinal Physiology
Subtopic: Exocrine Pancreatic Secretion
Keyword Definitions:
• Centroacinar cells: Specialized duct cells in the pancreas that secrete bicarbonate.
• Pancreas: Gland with both exocrine (enzymes, bicarbonate) and endocrine (hormones) functions.
• Parotid gland: Major salivary gland secreting saliva.
• Prostate: Male gland contributing fluid to semen.
• Bicarbonate: Neutralizes gastric acid in the duodenum.
Lead Question - 2013
Centroacinar cells are present in?
a) Pancreas
b) Parotid gland
c) Prostate
d) None
Explanation:
Centroacinar cells are located in the exocrine pancreas, forming part of the ductal system. They secrete bicarbonate and water under stimulation by secretin. These cells are absent in parotid or prostate glands. Their role is crucial in neutralizing acidic chyme. Answer: a) Pancreas.
1) Which hormone stimulates pancreatic bicarbonate secretion?
a) Secretin
b) Gastrin
c) CCK
d) Somatostatin
Explanation:
Secretin, released from duodenum in response to acidic chyme, stimulates centroacinar and ductal cells of pancreas to secrete bicarbonate-rich fluid. This neutralizes gastric acid and prepares the duodenum for digestion. Answer: a) Secretin.
2) Which enzyme is secreted in inactive form from pancreas?
a) Trypsinogen
b) Amylase
c) Lipase
d) Nuclease
Explanation:
Trypsinogen is secreted as inactive zymogen by pancreatic acinar cells. It is activated in the small intestine by enterokinase to form trypsin, which activates other zymogens. This prevents autodigestion. Answer: a) Trypsinogen.
3) A 45-year-old man presents with severe epigastric pain radiating to back after alcohol binge. Serum amylase is elevated. Most probable diagnosis?
a) Acute pancreatitis
b) Peptic ulcer
c) Cholecystitis
d) Myocardial infarction
Explanation:
Alcohol binge and severe epigastric pain with raised serum amylase suggest acute pancreatitis. The pancreas is inflamed due to autodigestion by its own enzymes. Answer: a) Acute pancreatitis.
4) In cystic fibrosis, pancreatic insufficiency occurs due to:
a) Blocked pancreatic ducts
b) Increased enzyme secretion
c) Autoimmune destruction
d) Lack of blood supply
Explanation:
In cystic fibrosis, defective CFTR channel leads to thick secretions blocking pancreatic ducts. This prevents digestive enzymes from reaching intestine, causing malabsorption. Answer: a) Blocked pancreatic ducts.
5) Which enzyme activates trypsinogen in intestine?
a) Pepsin
b) Enterokinase
c) Lipase
d) Elastase
Explanation:
Enterokinase (enteropeptidase) from intestinal brush border activates trypsinogen to trypsin. Trypsin then activates other pancreatic proenzymes. Answer: b) Enterokinase.
6) A patient develops steatorrhea. Which pancreatic enzyme deficiency most likely?
a) Amylase
b) Lipase
c) Trypsin
d) Chymotrypsin
Explanation:
Steatorrhea (fatty stools) is due to pancreatic lipase deficiency, impairing fat digestion and absorption. Lipase is essential for triglyceride hydrolysis. Answer: b) Lipase.
7) Which of the following is not secreted by pancreas?
a) Insulin
b) Glucagon
c) Somatostatin
d) Gastrin
Explanation:
The pancreas secretes insulin, glucagon, and somatostatin from islets of Langerhans. Gastrin is secreted mainly by G cells of stomach. Answer: d) Gastrin.
8) A 30-year-old woman presents with recurrent hypoglycemia. MRI shows pancreatic tumor. Most likely tumor?
a) Insulinoma
b) Glucagonoma
c) Somatostatinoma
d) Gastrinoma
Explanation:
Insulinoma is a pancreatic β-cell tumor producing excess insulin, causing recurrent hypoglycemia. It is the most common functioning pancreatic neuroendocrine tumor. Answer: a) Insulinoma.
9) Which ion exchange occurs in pancreatic ductal cells?
a) Cl⁻ in, HCO₃⁻ out
b) HCO₃⁻ in, Cl⁻ out
c) Na⁺ in, K⁺ out
d) K⁺ in, Na⁺ out
Explanation:
In pancreatic ductal cells, Cl⁻/HCO₃⁻ exchanger secretes bicarbonate into lumen in exchange for chloride, aiding in neutralization of gastric acid. Answer: a) Cl⁻ in, HCO₃⁻ out.
10) A 60-year-old smoker presents with painless jaundice and weight loss. Which part of pancreas is commonly involved?
a) Head
b) Body
c) Tail
d) Uncinate process
Explanation:
Carcinoma of pancreatic head obstructs common bile duct, causing painless progressive jaundice with weight loss. This is the most common site of pancreatic cancer. Answer: a) Head.
Chapter: Physiology
Topic: Cell Signaling
Subtopic: G Protein Coupled Receptors (GPCRs)
Keyword Definitions:
• G Protein: Guanine nucleotide-binding protein involved in signal transduction.
• GPCR: Membrane receptor coupled with G proteins to transmit extracellular signals.
• Alpha subunit: Determines stimulatory or inhibitory action by binding GTP or GDP.
• Second messenger: Intracellular mediator like cAMP or IP3.
• Signal transduction: Process of converting extracellular signals into cellular responses.
Lead Question - 2013
True about G protein coupled receptors is:
a) G proteins bind to hormones on the cell surface
b) All the three subunits alpha, beta and gamma should bind to each other for G protein to act
c) G proteins act as inhibitory and excitatory because of difference in alpha subunit
d) G protein is bound to GTP in resting state
Explanation:
G proteins are inactive in the GDP-bound state. On activation, GDP is exchanged for GTP on alpha subunit. Depending on alpha subunit type (Gs, Gi), they stimulate or inhibit target enzymes. They do not bind hormones directly. Answer: c) G proteins act as inhibitory and excitatory because of difference in alpha subunit.
1) Which second messenger is increased by Gs protein activation?
a) IP3
b) DAG
c) cAMP
d) cGMP
Explanation:
Gs protein stimulates adenylate cyclase, which converts ATP to cAMP. Increased cAMP activates protein kinase A, leading to multiple cellular responses. Answer: c) cAMP.
2) Which of the following hormones acts via Gq protein?
a) ADH (V2 receptor)
b) TSH
c) Angiotensin II
d) ACTH
Explanation:
Angiotensin II acts through Gq protein, stimulating phospholipase C, generating IP3 and DAG, leading to Ca²⁺ release and smooth muscle contraction. Answer: c) Angiotensin II.
3) A 40-year-old woman develops flushing and watery diarrhea. Lab shows elevated VIP levels. Which receptor pathway is involved?
a) Tyrosine kinase
b) GPCR with Gs
c) GPCR with Gi
d) Nuclear receptor
Explanation:
VIP acts via Gs protein-coupled receptors, increasing cAMP and stimulating secretion. VIPoma causes watery diarrhea, hypokalemia, and achlorhydria (WDHA syndrome). Answer: b) GPCR with Gs.
4) Which of the following uses Gi protein mechanism?
a) Glucagon
b) Dopamine D2 receptor
c) ACTH
d) Vasopressin (V2)
Explanation:
Dopamine D2 receptors act via Gi proteins, which inhibit adenylate cyclase, reducing cAMP levels. This leads to inhibitory signaling. Answer: b) Dopamine D2 receptor.
5) Which intracellular change occurs after β-adrenergic receptor stimulation?
a) Increase in cAMP
b) Decrease in IP3
c) Increase in cGMP
d) Increase in DAG
Explanation:
β-adrenergic receptors act via Gs protein, stimulating adenylate cyclase, increasing cAMP levels, which activate PKA and enhance heart rate and contractility. Answer: a) Increase in cAMP.
6) A 32-year-old male ingests cholera toxin. Which step is affected?
a) Inhibition of adenylate cyclase
b) Activation of Gs by ADP ribosylation
c) Stimulation of Gi
d) Inhibition of cAMP
Explanation:
Cholera toxin ADP ribosylates Gs protein, locking it in active form, causing persistent activation of adenylate cyclase and massive cAMP increase, leading to fluid secretion. Answer: b) Activation of Gs by ADP ribosylation.
7) Which receptor is NOT mediated by GPCR?
a) Muscarinic receptor
b) β-adrenergic receptor
c) Insulin receptor
d) Dopamine receptor
Explanation:
Insulin receptor is a receptor tyrosine kinase, not a GPCR. GPCRs mediate muscarinic, β-adrenergic, and dopamine receptors. Answer: c) Insulin receptor.
8) A patient presents with whooping cough. Pertussis toxin inhibits which function?
a) Gi protein function
b) Gs protein activation
c) Tyrosine kinase activity
d) Nuclear receptor action
Explanation:
Pertussis toxin ADP ribosylates Gi protein, preventing inhibition of adenylate cyclase, resulting in persistently high cAMP. Answer: a) Gi protein function.
9) Which G protein subunit binds GTP during activation?
a) Alpha
b) Beta
c) Gamma
d) Delta
Explanation:
The alpha subunit binds GDP in inactive state and GTP in active state, leading to dissociation from beta and gamma subunits and activation of downstream signaling. Answer: a) Alpha.
10) A 55-year-old man with pheochromocytoma shows hypertension and tachycardia due to catecholamine excess. Which receptor is involved in heart stimulation?
a) α1 receptor
b) β1 receptor
c) β2 receptor
d) α2 receptor
Explanation:
β1 adrenergic receptors in the heart mediate increased heart rate and contractility via Gs protein and cAMP pathway, contributing to symptoms of pheochromocytoma. Answer: b) β1 receptor.
Chapter: Physiology
Topic: Cell Signaling
Subtopic: G Protein Coupled Receptors (GPCRs) and Neurotransmission
Keyword Definitions:
• GPCR (G Protein Coupled Receptor): Membrane receptor activating intracellular G proteins upon ligand binding.
• Muscarinic receptors: Cholinergic receptors acting via GPCRs, affecting heart, smooth muscle, and glands.
• Nicotinic receptors: Ligand-gated ion channels, not GPCRs, mediating fast synaptic transmission.
• Insulin receptor: Tyrosine kinase receptor, not GPCR, regulating glucose uptake.
• GABA-A receptor: Ligand-gated chloride channel, mediating inhibitory neurotransmission.
Lead Question - 2013
Which of the following act through G protein coupled receptors?
a) Ach Muscarinic receptors
b) Insulin receptors
c) Ach Nicotinic receptors
d) GABA-A receptors
Explanation:
Muscarinic acetylcholine receptors are classic GPCRs, mediating parasympathetic effects via G proteins. Insulin receptors are tyrosine kinases, nicotinic receptors and GABA-A are ligand-gated ion channels. Therefore, only muscarinic receptors act through GPCRs. Answer: a) Ach Muscarinic receptors.
1) Which second messenger is increased by M2 muscarinic receptor activation in heart?
a) cAMP decrease
b) cAMP increase
c) IP3 increase
d) DAG increase
Explanation:
M2 muscarinic receptors are Gi-coupled in the heart. Activation inhibits adenylate cyclase, decreasing cAMP, slowing heart rate and contractility. Answer: a) cAMP decrease.
2) Which receptor type is involved in fast skeletal muscle contraction?
a) Nicotinic Ach receptor
b) Muscarinic Ach receptor
c) β1 adrenergic receptor
d) GABA-B receptor
Explanation:
Nicotinic acetylcholine receptors are ligand-gated ion channels at the neuromuscular junction, allowing rapid sodium influx, depolarization, and muscle contraction. Answer: a) Nicotinic Ach receptor.
3) A patient with bradycardia is given atropine. Which receptor is blocked?
a) M2 muscarinic receptor
b) β1 receptor
c) Nicotinic receptor
d) α1 receptor
Explanation:
Atropine is a muscarinic antagonist that blocks M2 receptors in the heart, preventing parasympathetic-mediated slowing of heart rate. Answer: a) M2 muscarinic receptor.
4) Which receptor mediates parasympathetic glandular secretion via GPCR?
a) M3 muscarinic receptor
b) Nicotinic receptor
c) β2 adrenergic receptor
d) GABA-A receptor
Explanation:
M3 muscarinic receptors are Gq-coupled GPCRs, stimulating phospholipase C, IP3 production, and intracellular Ca²⁺ increase, leading to glandular secretion. Answer: a) M3 muscarinic receptor.
5) Which GPCR mediates bronchodilation by sympathetic stimulation?
a) β2 adrenergic receptor
b) M3 receptor
c) Nicotinic receptor
d) GABA-A receptor
Explanation:
β2 adrenergic receptors are Gs-coupled GPCRs in bronchial smooth muscle. Activation increases cAMP, causing relaxation and bronchodilation. Answer: a) β2 adrenergic receptor.
6) Clinical: A patient has hypotension due to septic shock. Which GPCR pathway is targeted by norepinephrine infusion?
a) α1 receptor
b) M2 receptor
c) Nicotinic receptor
d) GABA-B receptor
Explanation:
Norepinephrine acts on α1 adrenergic receptors (Gs/PLC-coupled) causing vasoconstriction, raising blood pressure. These are GPCR-mediated effects. Answer: a) α1 receptor.
7) GABA-B receptor is coupled to:
a) Gi protein
b) Gs protein
c) Gq protein
d) Ion channel
Explanation:
GABA-B receptors are GPCRs coupled to Gi/o proteins, inhibiting adenylate cyclase, opening K⁺ channels, and producing slow inhibitory postsynaptic potentials. Answer: a) Gi protein.
8) Which GPCR mediates vasopressin’s antidiuretic effect?
a) V2 receptor
b) V1 receptor
c) Nicotinic receptor
d) M3 receptor
Explanation:
V2 vasopressin receptors in renal collecting ducts are Gs-coupled GPCRs. Activation increases cAMP, promoting insertion of aquaporin-2 channels and water reabsorption. Answer: a) V2 receptor.
9) Which subunit of G protein activates adenylate cyclase?
a) Gαs
b) Gαi
c) Gβ
d) Gγ
Explanation:
Gαs subunit of stimulatory G protein activates adenylate cyclase, increasing cAMP levels. Gαi inhibits adenylate cyclase. Beta and gamma subunits regulate signaling but do not directly activate adenylate cyclase. Answer: a) Gαs.
10) Clinical: A patient with overactive parasympathetic activity shows bradycardia and hypotension. Which receptor blockade can correct this?
a) Muscarinic receptor antagonist
b) Nicotinic receptor antagonist
c) β1 receptor blocker
d) GABA-A antagonist
Explanation:
Muscarinic antagonists like atropine block M2 receptors in the heart, preventing excessive parasympathetic slowing, correcting bradycardia and hypotension. Nicotinic, β1, and GABA-A are not involved in parasympathetic heart rate regulation. Answer: a) Muscarinic receptor antagonist.
Chapter: Physiology
Topic: Gastrointestinal Physiology
Subtopic: Hormonal Regulation of Digestion
Keyword Definitions:
• Cholecystokinin (CCK): Gastrointestinal hormone secreted by I-cells of duodenum and jejunum.
• IP3-DAG system: Intracellular signaling pathway activated by Gq protein-coupled receptors.
• Adenylyl cyclase: Enzyme converting ATP to cAMP in Gs protein pathways.
• Gallbladder contraction: Stimulated by CCK to release bile into duodenum.
• Pancreatic enzyme secretion: Stimulated by CCK to aid digestion of fats and proteins.
Lead Question - 2013
Mechanism of action of cholecystokinin?
a) Activation of adenylyl cyclase
b) Opening of ion channels
c) Through IP3-DAG system
d) Transcription factors
Explanation:
CCK acts via Gq protein-coupled receptors on pancreatic acinar and gallbladder smooth muscle cells. Activation triggers phospholipase C, generating IP3 and DAG, raising intracellular Ca²⁺, and stimulating enzyme secretion and gallbladder contraction. Answer: c) Through IP3-DAG system.
1) CCK release is stimulated mainly by:
a) Fats and proteins in duodenum
b) Glucose in blood
c) Gastric distension
d) Acidic pH
Explanation:
CCK secretion is triggered by fat and protein digestion products entering duodenum, stimulating gallbladder contraction and pancreatic enzyme secretion for proper digestion. Answer: a) Fats and proteins in duodenum.
2) Which receptor mediates CCK effects on gallbladder?
a) CCK-A receptor
b) CCK-B receptor
c) M3 receptor
d) β2 adrenergic receptor
Explanation:
CCK-A receptors are expressed on gallbladder smooth muscle and pancreatic acinar cells, mediating contraction and enzyme secretion via IP3-DAG pathway. Answer: a) CCK-A receptor.
3) Clinical: A patient has gallstones and impaired CCK response. Which effect is expected?
a) Impaired bile release
b) Increased gastric acid
c) Hypoglycemia
d) Constipation
Explanation:
Failure of CCK signaling prevents gallbladder contraction, reducing bile flow into duodenum, impairing fat digestion, leading to steatorrhea. Answer: a) Impaired bile release.
4) Which enzyme system is activated by CCK in pancreatic acinar cells?
a) Phospholipase C
b) Adenylyl cyclase
c) Tyrosine kinase
d) Guanylyl cyclase
Explanation:
CCK binds Gq-coupled receptors, activating phospholipase C, which generates IP3 and DAG, increases intracellular Ca²⁺, and stimulates secretion of digestive enzymes. Answer: a) Phospholipase C.
5) CCK effect on sphincter of Oddi is:
a) Contraction
b) Relaxation
c) No effect
d) Inhibition of nerve
Explanation:
CCK causes relaxation of sphincter of Oddi via smooth muscle relaxation, allowing bile and pancreatic juice to enter duodenum. Answer: b) Relaxation.
6) A patient with pancreatitis has impaired enzyme secretion. Which hormone primarily stimulates enzyme release?
a) CCK
b) Secretin
c) Gastrin
d) Motilin
Explanation:
CCK is the main hormone stimulating pancreatic enzyme secretion. Secretin mainly increases bicarbonate secretion. Answer: a) CCK.
7) Which intracellular messenger causes smooth muscle contraction by CCK?
a) Calcium
b) cAMP
c) cGMP
d) Nitric oxide
Explanation:
CCK increases intracellular calcium via IP3 pathway, activating calmodulin and myosin light chain kinase, causing gallbladder and sphincter smooth muscle contraction. Answer: a) Calcium.
8) Which organ’s enzyme secretion is primarily controlled by CCK?
a) Pancreas
b) Liver
c) Stomach
d) Kidney
Explanation:
CCK acts on pancreatic acinar cells via IP3-DAG signaling to stimulate secretion of amylase, lipase, and proteases for digestion of nutrients. Answer: a) Pancreas.
9) CCK and secretin act together to:
a) Enhance pancreatic secretion
b) Inhibit gastric emptying
c) Stimulate bile synthesis
d) Increase motilin
Explanation:
CCK and secretin synergistically increase pancreatic fluid and enzyme secretion: CCK stimulates enzymes via IP3-DAG, secretin stimulates bicarbonate via cAMP, optimizing digestion. Answer: a) Enhance pancreatic secretion.
10) Clinical: A patient has fat malabsorption and low enzyme output. Which deficiency is likely?
a) CCK deficiency
b) Secretin deficiency
c) Gastrin deficiency
d) Motilin deficiency
Explanation:
Deficient CCK impairs pancreatic enzyme secretion and gallbladder contraction, leading to poor fat digestion, steatorrhea, and nutrient malabsorption. Answer: a) CCK deficiency.