L57, 58 Absorptive and post-absorptive states, vomiting reflex

Question 1

L57

What are the two main metabolic states of the body?

Answer 1

Absorptive state (after eating) and postabsorptive state (between meals or fasting).

Question 2

L57

What is the primary goal of the absorptive state?

Answer 2

To store nutrients and supply energy from food intake.

Question 3

L57

Which hormone dominates the absorptive state?

Answer 3

Insulin

Question 4

L57

What are insulin’s effects on adipose tissue?

Answer 4

Inhibits hormone-sensitive lipase (HSL) → reduces lipolysis.

Increases lipoprotein lipase (LPL) → enhances fat storage.

Question 5

L57

What are insulin’s effects on muscle tissue?

Answer 5

Promotes glucose uptake via GLUT4.

Increases glycogen synthesis.

Stimulates fatty acid uptake and storage.

Question 6

L57

What are insulin’s effects on the liver?

Answer 6

Enhances glucose uptake and glycogen storage.

Stimulates glycolysis and lipogenesis (fat synthesis).

Promotes oxidative phosphorylation.

Question 7

L57

What are the key glucose transporters and their features?

Answer 7

GLUT1: Found in brain, placenta – basal uptake.

GLUT2: Liver, kidney – high Km, allows glucose to equilibrate.

GLUT3: Neuronal – low Km, steady uptake.

GLUT4: Muscle, fat – insulin-regulated.

SGLT-1/2: Active transport in gut/kidneys.

Question 8

L57

What is the postabsorptive state?

Answer 8

The fasting state where the body maintains blood glucose via internal energy stores.

Question 9

L57

Which hormone dominates the postabsorptive state?

Answer 9

Glucagon (with reduced insulin)

Question 10

L57

What are the key processes in the postabsorptive state?

Answer 10

Glycogenolysis (glycogen breakdown)

Gluconeogenesis (new glucose synthesis)

Lipolysis (fat breakdown)

Question 11

L57

What fuels gluconeogenesis and where does it occur?

Answer 11

Occurs in the liver, using:

Lactate

Alanine

Glycerol

Question 12

L57

What are the main enzymes in gluconeogenesis?

Answer 12

Pyruvate carboxylase (PC)

PEP carboxykinase (PEPCK)

Fructose-1,6-bisphosphatase

Glucose-6-phosphatase

Question 13

L57

What is lipolysis and what drives it?

Answer 13

Breakdown of fat (triacylglycerols) into free fatty acids (NEFA) and glycerol.

Driven by adrenaline/noradrenaline

Inhibited by insulin

Question 14

L57

Which enzymes are involved in lipolysis?

Answer 14

ATGL: Adipose triglyceride lipase

HSL: Hormone-sensitive lipase

MGL: Monoacylglycerol lipase

Question 15

L57

What is obesity in metabolic terms?

Answer 15

A chronic condition due to energy imbalance: excessive storage of lipids and inadequate utilisation.

Question 16

L57

Name two key pharmacological treatments for obesity.

Answer 16

Orlistat: Inhibits fat absorption in the gut.

GLP-1 analogues (e.g., liraglutide): Suppress appetite, improve glucose metabolism.

Question 17

L57

What is the mechanism of action of Orlistat?

Answer 17

Blocks pancreatic lipase, preventing triglyceride breakdown and absorption.

Question 18

L57

What are examples of GLP-1 analogues?

Answer 18

Exenatide

Liraglutide

Branded: Saxenda, Wegovy

Question 19

L57

What new drug class supports weight loss by glucose excretion?

Answer 19

SGLT2 inhibitors (e.g., Canagliflozin)

Question 20

L57

What surgical options are used for obesity treatment?

Answer 20

Gastric bypass

Sleeve gastrectomy

Adjustable gastric banding

Question 21

L57

What vitamins are required post-bariatric surgery?

Answer 21

Iron, Vitamin B12, Calcium, Vitamin D

Zinc, Copper, Selenium, Folic acid, Thiamine

Question 22

L57

What happens to dietary protein during the absorptive state?

Answer 22

Amino acids are used for:

• Protein synthesis
• Transamination into keto acids for energy or fatty acid synthesis

Question 23

L57

What happens to dietary fat during the absorptive state?

Answer 23

Packaged into chylomicrons in enterocytes.

Transported via lymphatic system.

Delivered to adipose tissue, broken by lipoprotein lipase, stored as triacylglycerols.

Question 24

L57

What metabolic pathway is stimulated by insulin in the liver during the absorptive state?

Answer 24

Glycolysis: breakdown of glucose to pyruvate

Pyruvate can feed into:

• TCA cycle for energy
• De novo lipogenesis for fat synthesis

Question 25

# L57 What is the role of the brain in energy metabolism?

Answer 25

Depends almost entirely on glucose in the fed state. In prolonged fasting, uses ketone bodies (e.g., β-hydroxybutyrate).

Question 26

# L57 What happens to muscle protein in the postabsorptive state?

Answer 26

Broken down to release amino acids like alanine, which is transported to the liver for gluconeogenesis.

Question 27

# L57 How does the liver support glucose levels in the postabsorptive state?

Answer 27

Releases glucose via: - Glycogenolysis - Gluconeogenesis Converts fatty acids to ketone bodies during prolonged fasting.

Question 28

# L57 What is the Cori cycle?

Answer 28

Lactate produced by anaerobic glycolysis in muscles is transported to the liver. Converted back to glucose via gluconeogenesis.

Question 29

# L57 What is the Alanine cycle?

Answer 29

Muscle breaks down protein → releases alanine. Alanine goes to liver, converted into glucose.

Question 30

# L57 How are ketone bodies produced and used?

Answer 30

Produced in liver mitochondria from acetyl-CoA (from fatty acid oxidation). Used by brain and muscles during fasting/starvation.

Question 31

# L57 How does liraglutide work for weight loss?

Answer 31

Mimics GLP-1: delays gastric emptying, reduces appetite, enhances insulin secretion, reduces glucagon.

Question 32

# L57 What are common side effects of Orlistat?

Answer 32

Steatorrhoea (fatty stools) Flatulence Faecal urgency/incontinence Risk of fat-soluble vitamin deficiency (A, D, E, K)

Question 33

# L57 What are the mechanisms of SGLT2 inhibitors?

Answer 33

Inhibit sodium-glucose transport protein 2 in kidneys. Promote urinary glucose excretion → calorie loss and weight reduction.

Question 34

# L57 How does bariatric surgery affect drug absorption?

Answer 34

Alters gastrointestinal anatomy and pH, reducing bioavailability. May require liquid or crushed formulations post-op.

Question 35

# L57 What is the difference between short-acting and long-acting GLP-1 analogues?

Answer 35

Short-acting: Exenatide (BID), mainly affects gastric emptying. Long-acting: Liraglutide, Semaglutide (weekly), affect appetite regulation in CNS more prominently.

Question 36

# L57 Which other hormones influence the absorptive/postabsorptive states?

Answer 36

Cortisol: Stimulates gluconeogenesis and protein catabolism. Growth hormone: Antagonises insulin, promotes lipolysis. Adrenaline: Stimulates glycogenolysis and lipolysis during stress. Somatostatin: Inhibits insulin and glucagon secretion.

Question 37

# L57 What are the main forms of energy storage in the body?

Answer 37

1. Glycogen (liver & muscle) – short-term, fast access. 2. Triglycerides (adipose) – long-term, high energy yield. 3. Proteins (muscles) – functional mass, used in prolonged starvation.

Question 38

# L57 What are the metabolic phases of starvation?

Answer 38

1. Postabsorptive (0–6 hrs): Glycogenolysis. 2. Early fasting (6–24 hrs): Gluconeogenesis begins. 3. Prolonged fasting (1–5 days): Ketone production rises. 4.Long-term starvation (>5 days): Brain uses ketones, protein sparing begins.

Question 39

# L57 What are the primary ketone bodies and their origins?

Answer 39

Acetoacetate, β-hydroxybutyrate, and acetone Formed in liver mitochondria from acetyl-CoA via β-oxidation of fats

Question 40

# L57 What is the role of lipoprotein lipase (LPL) in adipose tissue?

Answer 40

Stimulated by insulin Hydrolyses triglycerides in chylomicrons/VLDL → stores fat

Question 41

# L57 How is gluconeogenesis regulated in the liver?

Answer 41

Stimulated by: Glucagon, cortisol Inhibited by: Insulin Key enzymes regulated: PEPCK, Fructose-1,6-bisphosphatase, Glucose-6-phosphatase

Question 42

# L57 What is the Randle Cycle (glucose-fatty acid cycle)?

Answer 42

A metabolic process where increased fatty acid oxidation in muscle inhibits glucose utilisation — relevant in insulin resistance and diabetes.

Question 43

# L57 What happens to chylomicrons after delivering triglycerides?

Answer 43

They become chylomicron remnants, which are taken up by the liver via apoE recognition.

Question 44

# L57 What is the role of the liver in lipid metabolism during the absorptive state?

Answer 44

Converts excess glucose to fatty acids (de novo lipogenesis). Packages them as VLDL for export to adipose tissue.

Question 45

# L57 What triggers ketogenesis?

Answer 45

Low insulin, high glucagon Occurs when acetyl-CoA accumulates from β-oxidation and TCA cycle is saturated or suppressed

Question 46

# L57 Why can the liver not use ketone bodies?

Answer 46

Liver lacks the enzyme thiophorase (succinyl-CoA:acetoacetate CoA transferase), so it cannot metabolise ketones it produces.

Question 47

# L57 What stimulates GLUT4 translocation to the cell membrane?

Answer 47

Insulin binding to its receptor activates PI3K-Akt signalling, promoting GLUT4 translocation to increase glucose uptake in muscle and adipose tissue.

Question 48

# L57 How does muscle use glucose and fat differently during fed and fasted states?

Answer 48

Fed: Prefers glucose via insulin-stimulated uptake. Fasted: Uses fatty acids and ketones; glucose is spared for the brain.

Question 49

# L57 What inhibits hormone-sensitive lipase (HSL)?

Answer 49

Insulin is the key inhibitor, preventing lipolysis during the fed state.

Question 50

# L57 What are the clinical consequences of uncontrolled lipolysis?

Answer 50

Excess NEFA in blood → taken up by liver → increases VLDL, fatty liver, and insulin resistance

Question 51

# L57 What is insulin resistance and how does it affect metabolism?

Answer 51

Cells become less responsive to insulin → reduced glucose uptake → increased gluconeogenesis, lipolysis, and hyperglycaemia.

Question 52

# L57 What happens to protein metabolism during prolonged starvation?

Answer 52

Initially broken down for gluconeogenesis. Later conserved when brain switches to ketone bodies → protein sparing.

Question 53

# L57 What is metabolic flexibility?

Answer 53

The body's ability to switch between carbohydrate and fat oxidation depending on availability and energy needs — reduced in obesity and type 2 diabetes.

Question 54

# L57 What does GLP-1 stand for and what are its effects?

Answer 54

Glucagon-Like Peptide-1: Enhances glucose-dependent insulin secretion Suppresses glucagon Slows gastric emptying Promotes satiety

Question 55

# L57 Which of the following hormones primarily promotes glycogen synthesis in the absorptive state? A) Glucagon B) Cortisol C) Insulin D) Adrenaline E) Growth hormone

Answer 55

✅ Correct: C) Insulin Insulin promotes glycogenesis, lipogenesis, and protein synthesis in the absorptive state.

Question 56

# L57 During the postabsorptive state, which of the following is the major source of blood glucose? A) Glycolysis B) Gluconeogenesis C) Glycogenolysis D) Lipolysis E) Ketogenesis

Answer 56

✅ Correct: C) Glycogenolysis Initially, glycogenolysis is the major source before gluconeogenesis takes over during prolonged fasting.

Question 57

# L57 Which of the following is most likely to increase during prolonged starvation? A) Insulin secretion B) Liver glycogen stores C) Ketone body production D) Muscle glycogen synthesis E) Lipoprotein lipase activity

Answer 57

✅ Correct: C) Ketone body production Prolonged starvation triggers ketogenesis from fatty acid-derived acetyl-CoA.

Question 58

# L57 Which transporter is responsible for insulin-mediated glucose uptake in adipose tissue? A) GLUT1 B) GLUT2 C) GLUT3 D) GLUT4 E) SGLT1

Answer 58

✅ Correct: D) GLUT4 GLUT4 is translocated to the membrane in response to insulin in muscle and adipose tissue.

Question 59

# L57 Which enzyme is directly activated by glucagon to increase hepatic glucose output? A) Hexokinase B) Glycogen synthase C) Glucose-6-phosphatase D) Acetyl-CoA carboxylase E) Hormone-sensitive lipase

Answer 59

✅ Correct: C) Glucose-6-phosphatase It’s a key enzyme in gluconeogenesis and glycogenolysis, allowing glucose release from liver.

Question 60

# L57 What is the primary fate of dietary triglycerides during the absorptive state? A) Oxidised for immediate energy B) Stored in the liver C) Converted to glucose D) Packaged into chylomicrons for storage E) Excreted via bile

Answer 60

✅ Correct: D) Packaged into chylomicrons for storage Triglycerides are transported via chylomicrons to adipose for storage.

Question 61

# L57 Which drug acts by inhibiting pancreatic and gastric lipases? A) Liraglutide B) Semaglutide C) Orlistat D) Metformin E) Dapagliflozin

Answer 61

✅ Correct: C) Orlistat Orlistat blocks fat absorption by inhibiting lipases.

Question 62

# L57 . In the fasting state, which tissue continues to require glucose as a primary fuel source? A) Skeletal muscle B) Brain C) Adipose tissue D) Liver E) Kidney medulla

Answer 62

✅ Correct: B) Brain The brain is highly dependent on glucose, although it can adapt to ketones during prolonged fasting.

Question 63

# L57 Which metabolic pathway is upregulated in adipose tissue by insulin in the fed state? A) Gluconeogenesis B) Glycogenolysis C) Lipolysis D) Lipogenesis E) Ketogenesis

Answer 63

✅ Correct: D) Lipogenesis Insulin promotes fat synthesis and storage in adipose tissue.

Question 64

# L57 Why can't the liver utilise ketone bodies? A) Lacks mitochondria B) Cannot oxidise fatty acids C) Does not express GLUT4 D) Lacks thiophorase enzyme E) Converts ketones to glucose

Answer 64

✅ Correct: D) Lacks thiophorase enzyme The liver produces but does not use ketone bodies due to lack of thiophorase.

Question 65

# L57 Which of the following best explains the increase in hepatic gluconeogenesis during the postabsorptive state? A) Increased insulin sensitivity B) Activation of lipoprotein lipase C) Suppression of glucagon secretion D) Stimulation by cortisol and glucagon E) Decreased β-oxidation of fatty acids

Answer 65

✅ Correct: D) Stimulation by cortisol and glucagon Both hormones upregulate gluconeogenic enzymes to maintain blood glucose.

Question 66

# L57 Which tissue relies heavily on anaerobic glycolysis during hypoglycaemia? A) Brain B) Liver C) Renal medulla D) Skeletal muscle (resting) E) Adipose tissue

Answer 66

✅ Correct: C) Renal medulla The renal medulla lacks mitochondria and depends on glycolysis even in normal states.

Question 67

# L57 Which of the following changes occurs in the transition from the fed to the fasted state? A) Increased glycogen synthesis in the liver B) Increased GLUT4 expression on muscle cells C) Increased release of fatty acids from adipose tissue D) Increased insulin release E) Increased amino acid uptake into muscle

Answer 67

✅ Correct: C) Increased release of fatty acids from adipose tissue Insulin falls, hormone-sensitive lipase is activated, and lipolysis increases.

Question 68

# L57 Which of the following correctly matches a transporter with its tissue and role? A) GLUT2 – skeletal muscle – insulin-mediated glucose uptake B) GLUT1 – erythrocytes – basal glucose uptake C) GLUT4 – liver – glucose export D) SGLT1 – brain – glucose sensing E) GLUT3 – adipose – insulin-dependent uptake

Answer 68

✅ Correct: B) GLUT1 – erythrocytes – basal glucose uptake GLUT1 ensures constant glucose supply to red blood cells and the blood–brain barrier.

Question 69

# L57 A drug that mimics GLP-1 would be expected to: A) Increase glucagon secretion B) Promote weight gain C) Slow gastric emptying D) Increase appetite E) Stimulate hepatic ketone production

Answer 69

✅ Correct: C) Slow gastric emptying GLP-1 agonists (e.g. liraglutide) slow gastric emptying and promote satiety, aiding weight loss.

Question 70

# L57 In the absence of insulin, which process is likely to be impaired? A) Gluconeogenesis in the liver B) Lipolysis in adipose tissue C) Glucose uptake into skeletal muscle D) Ketogenesis E) Glycogen breakdown

Answer 70

✅ Correct: C) Glucose uptake into skeletal muscle GLUT4-mediated uptake is insulin-dependent; without insulin, muscle cannot efficiently take up glucose.

Question 71

# L57 A patient has been fasting for 48 hours. Which metabolic change is expected? A) Decreased plasma glucagon B) Increased muscle protein synthesis C) Increased liver glycogen content D) Increased ketone body concentration E) Increased insulin secretion

Answer 71

✅ Correct: D) Increased ketone body concentration By 48 hours, ketogenesis is active as fat stores are used for energy.

Question 72

# L57 Which of the following enzymes is rate-limiting for lipolysis in adipose tissue? A) Lipoprotein lipase B) Glucose-6-phosphatase C) Hormone-sensitive lipase D) Acetyl-CoA carboxylase E) Phosphofructokinase-1

Answer 72

✅ Correct: C) Hormone-sensitive lipase Activated during fasting to mobilise stored triglycerides.

Question 73

# L57 What effect does insulin have on hormone-sensitive lipase (HSL)? A) Activates HSL to break down triglycerides B) Inhibits HSL to suppress lipolysis C) Has no effect on HSL D) Stimulates expression of HSL E) Enhances ketogenesis via HSL

Answer 73

✅ Correct: B) Inhibits HSL to suppress lipolysis Insulin promotes fat storage by inhibiting HSL activity.

Question 74

# L57 Which of the following best explains why the liver produces but does not utilise ketone bodies? A) Lacks enzymes to convert fatty acids to acetyl-CoA B) Cannot perform gluconeogenesis C) Cannot activate acetoacetate D) Cannot perform β-oxidation E) Uses ketone bodies for rapid energy

Answer 74

✅ Correct: C) Cannot activate acetoacetate The liver lacks thiophorase (SCOT enzyme) needed for ketone body oxidation.

Question 75

# L57 A diabetic patient presents with weight loss, ketone breath, and hyperglycaemia. Which metabolic process is most upregulated? A) Glycogenesis B) Glycolysis C) Ketogenesis D) Lipogenesis E) Insulin secretion

Answer 75

✅ Correct: C) Ketogenesis Low insulin and high glucagon promote fatty acid oxidation and ketone production.

Question 76

# L57 uring prolonged fasting, how is muscle protein conserved? A) Increased insulin sensitivity B) Brain switches to glucose usage C) Increased glycogenolysis D) Brain switches to ketone usage E) Enhanced gluconeogenesis from amino acids

Answer 76

✅ Correct: D) Brain switches to ketone usage This shift spares protein breakdown for gluconeogenesis.

Question 77

# L57 Which of the following is most likely during the early absorptive state (first 2 hours post-meal)? A) Increased ketone body synthesis B) Increased gluconeogenesis C) Increased plasma glucagon D) Increased activity of lipoprotein lipase E) Increased proteolysis

Answer 77

✅ Correct: D) Increased activity of lipoprotein lipase LPL hydrolyses chylomicron triglycerides for storage in adipose.

Question 78

# L57 A drug that enhances insulin sensitivity in muscle and liver would most likely: A) Decrease glucose uptake B) Increase ketogenesis C) Reduce hepatic gluconeogenesis D) Inhibit GLUT2 expression E) Promote protein breakdown

Answer 78

✅ Correct: C) Reduce hepatic gluconeogenesis Improved insulin signalling suppresses glucose production.

Question 79

# L57 Which of the following best describes the metabolic fate of dietary amino acids in the absorptive state? A) Used exclusively for energy production B) Converted to glycogen directly C) Used for protein synthesis and excess converted to fat D) Stored as amino acids in the liver E) Excreted unchanged in urine

Answer 79

✅ Correct: C) Used for protein synthesis and excess converted to fat Amino acids are not stored; surplus is deaminated and used for fat synthesis.

Question 80

# L57 What is the main function of glucagon during the postabsorptive state? A) Stimulate glucose uptake into cells B) Inhibit gluconeogenesis C) Activate glycogen synthase D) Mobilise energy stores E) Promote lipogenesis

Answer 80

✅ Correct: D) Mobilise energy stores Glucagon activates glycogenolysis, gluconeogenesis, and lipolysis.

Question 81

# L57 Which of the following metabolic hormones is primarily secreted by intestinal L-cells? A) Insulin B) Amylin C) GLP-1 D) Glucagon E) Somatostatin

Answer 81

✅ Correct: C) GLP-1 Secreted in response to food; enhances insulin secretion, satiety, and delays gastric emptying.

Question 82

# L57 What effect does cortisol have on metabolism during prolonged stress or fasting? A) Decreases gluconeogenesis B) Inhibits proteolysis C) Promotes glycogen synthesis D) Enhances gluconeogenesis and proteolysis E) Inhibits fatty acid oxidation

Answer 82

✅ Correct: D) Enhances gluconeogenesis and proteolysis Cortisol increases glucose availability by breaking down muscle protein for gluconeogenesis.

Question 83

# L57 Which of the following most accurately explains the brain's adaptation to starvation? A) Switches fully to fatty acid oxidation B) Reduces metabolic rate to zero C) Converts lactate to glucose D) Utilises ketone bodies to spare glucose E) Uses triglycerides directly

Answer 83

✅ Correct: D) Utilises ketone bodies to spare glucose After ~3 days, ketones become the main energy source for the brain, reducing protein breakdown.

Question 84

# L57 A patient taking orlistat is at risk of deficiency in which of the following? A) Vitamin B12 B) Vitamin C C) Vitamin D D) Vitamin B1 E) Folate

Answer 84

✅ Correct: C) Vitamin D Orlistat inhibits fat absorption, which reduces absorption of fat-soluble vitamins (A, D, E, K).

Question 85

# L58 What is emesis, and what is its physiological purpose?

Answer 85

Emesis (vomiting) is a defence reflex designed to expel harmful substances from the stomach. It can be triggered by unpleasant sights, smells, tastes, toxins, or inner ear disturbances.

Question 86

# L58 Name 3 non-pathological triggers of emesis.

Answer 86

1. Sight & smell (e.g., spoiled food) 2. Taste (e.g., bitterness → spit it out) 3. Anticipatory/emotional stimuli (e.g., before chemotherapy)

Question 87

# L58 Name 4 pathological causes of vomiting.

Answer 87

Uraemia (kidney failure) Gastroduodenal disorders (e.g., ulcers) Hepatic disease (e.g., cirrhosis) Infections (e.g., gastroenteritis)

Question 88

# L58 Which drugs commonly induce vomiting?

Answer 88

Chemotherapy agents (e.g., cisplatin) Dopamine agonists (e.g., L-dopa, bromocriptine) Opiates Alcohol Ipecacuanha (historically used to induce vomiting)

Question 89

# L58 What is PONV?

Answer 89

Post-operative nausea and vomiting — common after anaesthesia or surgery.

Question 90

# L58 What brain areas control vomiting?

Answer 90

Higher centres (e.g., cortex — emotions, anticipation) Vomiting centre in lateral reticular formation (brainstem) Chemoreceptor trigger zone (CTZ) — detects blood-borne emetics

Question 91

# L58 What is the CTZ and where is it located?

Answer 91

The chemoreceptor trigger zone (CTZ) is located in the area postrema (medulla) and lacks a blood-brain barrier, allowing it to detect toxins and drugs.

Question 92

# L58 Name 4 classes of anti-emetic drugs.

Answer 92

Dopamine antagonists (neuroleptics) 5-HT3 receptor antagonists NK1 (neurokinin) receptor antagonists Antihistamines / Antimuscarinics (for motion sickness)

Question 93

# L58 Name 3 dopamine (D2) antagonists used as anti-emetics.

Answer 93

Chlorpromazine Haloperidol Metoclopramide (also weak 5-HT3 antagonist) 📝 Domperidone = fewer CNS side effects (doesn’t cross BBB well)

Question 94

# L58 Side effects of neuroleptics?

Answer 94

Extrapyramidal symptoms (e.g., dystonia, tremor), especially at high doses Domperidone = fewer side effects

Question 95

# L57 How does metoclopramide work?

Answer 95

D2 receptor antagonist Weak 5-HT3 antagonist Enhances gastric emptying High doses = more effective but ↑ side effects

Question 96

# L57 What are 5-HT3 receptor antagonists used for?

Answer 96

Treat chemotherapy-induced nausea, e.g. cisplatin Examples: Ondansetron, Granisetron, Tropisetron

Question 97

# L58 What makes palonosetron special?

Answer 97

Second-generation 5-HT3 antagonist Very long half-life Causes 5-HT3 receptor internalisation (stronger effect)

Question 98

# L58 What is aprepitant, and what is its mechanism?

Answer 98

NK1 receptor antagonist (blocks substance P) Works at CTZ and vagus Effective for delayed emesis from chemo Often combined with 5-HT3 antagonists

Question 99

# L58 What is dexamethasone used for in emesis?

Answer 99

Glucocorticoid with anti-inflammatory action Used as adjunct therapy with ondansetron/aprepitant Improves anti-emetic effect (synergy)

Question 100

# L58 Which benzodiazepine is used for nausea?

Answer 100

Diazepam – suppresses neuronal excitability Used in combo: ondansetron + dexamethasone + diazepam

Question 101

# L58 Cannabinoids in emesis treatment?

Answer 101

Nabilone (synthetic cannabinoid) Used for chemotherapy-related nausea Effects: anti-emetic, euphoria, sedation

Question 102

# L58 Which drugs are used for motion sickness?

Answer 102

Anti-muscarinics: Scopolamine, hyoscine Anti-histamines: Dimenhydrinate, cyclizine, cinnarizine, promethazine

Question 103

# L58 How do anti-muscarinics work in emesis?

Answer 103

Block muscarinic receptors in vestibular system Inhibit cholinergic signals from inner ear → vomiting centre Used in motion sickness, vertigo

Question 104

# L58 Mechanism of anti-histamines in vomiting?

Answer 104

Block H1 receptors in vestibular nuclei and vomiting centre Effective for motion sickness, vestibular disorders

Question 105

# L58 What are the primary reasons we vomit?

Answer 105

As a defence reflex due to sight/smell, taste, or toxins (ingested or endogenous).

Question 106

# L58 What diseases are commonly associated with vomiting?

Answer 106

Uraemia, gastroduodenal disorders, hepatic disease, infections.

Question 107

# L58 Name common causes of drug-induced emesis.

Answer 107

Cancer chemo, dopamine agonists (e.g. L-dopa), opiates, ipecacuanha, alcohol.

Question 108

# L58 What is anticipatory emesis?

Answer 108

Vomiting triggered by expectation, often seen in patients undergoing repeated chemotherapy.

Question 109

# L58 What brain region controls the vomiting reflex?

Answer 109

The vomiting centre in the lateral reticular formation of the brainstem.

Question 110

# L58 Name four neuroleptics used as anti-emetics.

Answer 110

Chlorpromazine, haloperidol, domperidone, metoclopramide.

Question 111

# L58 What side-effects are associated with neuroleptics?

Answer 111

Extra-pyramidal side-effects (not with domperidone); sometimes lack efficacy.

Question 112

# L58 How does metoclopramide work?

Answer 112

High-affinity D2 receptor antagonist; weak 5-HT3 receptor antagonist.

Question 113

# L58 Q10: Name three potent 5-HT3 receptor antagonists.

Answer 113

Ondansetron, granisetron, tropisetron.

Question 114

# L58 What are the advantages of 5-HT3 receptor antagonists?

Answer 114

Block cisplatin-induced emesis, complete blockade with less emetogenic drugs, no extrapyramidal side effects.

Question 115

# L58 What’s unique about palonosetron?

Answer 115

Long half-life and causes 5-HT3 receptor internalisation (2nd gen).

Question 116

# L58 What does aprepitant block?

Answer 116

NK1 (neurokinin 1) receptors; effective against acute & delayed cisplatin-induced emesis and PONV.

Question 117

# L58 What is aprepitant often combined with?

Answer 117

5-HT3 receptor antagonists.

Question 118

# L58 What is the role of dexamethasone in anti-emesis?

Answer 118

Reduces inflammation; synergistic with 5-HT3 and NK1 antagonists.

Question 119

# L58 How do benzodiazepines like diazepam help in emesis?

Answer 119

They cause neuronal suppression; often combined with ondansetron and dexamethasone.

Question 120

# L58 What are two cannabinoid agents used for emesis?

Answer 120

Cannabis sativa and nabilone.

Question 121

# L58 Name one anti-muscarinic used for motion sickness.

Answer 121

Scopolamine (± hyoscine).

Question 122

# L58 What pathway is targeted by anti-muscarinics in motion sickness?

Answer 122

Labyrinthine-vestibular-cerebellar pathway (cholinergic).

Question 123

# L58 Name some anti-histamines used in motion sickness.

Answer 123

Dimenhydrinate, cinnarizine, cyclizine, promethazine.

Question 124

# L58 What receptors do anti-histamines block in the vomiting pathway?

Answer 124

H1 receptors (especially in the LVC pathway and CTZ).

Question 125

# L58 What is the role of the Chemoreceptor Trigger Zone (CTZ)?

Answer 125

Detects emetogenic substances in blood/CSF; rich in dopamine (D2), serotonin (5-HT3), acetylcholine (muscarinic), and NK1 receptors.

Question 126

# L58 Which neurotransmitter receptors are mainly involved in the vomiting reflex?

Answer 126

Dopamine (D2), serotonin (5-HT3), acetylcholine (muscarinic), histamine (H1), and substance P (NK1).

Question 127

# L58 Where are 5-HT3 receptors located?

Answer 127

On vagal afferents in the gut, in the CTZ, and the nucleus tractus solitarius (NTS).

Question 128

# L58 What causes 5-HT3 receptor activation in chemotherapy-induced vomiting?

Answer 128

Release of serotonin from enterochromaffin cells in the GI tract after chemotherapy.

Question 129

# L58 What makes domperidone safer than other neuroleptics?

Answer 129

Does not cross the blood-brain barrier significantly → fewer CNS side effects like extrapyramidal symptoms.

Question 130

# L58 How do 5-HT3 antagonists compare to neuroleptics in efficacy and side effects?

Answer 130

5-HT3 antagonists are more effective in chemo-induced emesis and have fewer neurological side effects.

Question 131

# L58 Why might metoclopramide be used in higher doses?

Answer 131

Higher doses offer increased efficacy, especially for chemotherapy-induced vomiting, though side effects may increase.

Question 132

# L58 Why are 5-HT3 antagonists often combined with other drugs?

Answer 132

For synergistic effect, especially in delayed-phase emesis or resistant cases (e.g. add dexamethasone or NK1 antagonist).

Question 133

# L58 What makes palonosetron superior for some patients?

Answer 133

Longer duration of action (long t½), better for delayed emesis; induces internalisation of 5-HT3 receptors for prolonged blockade.

Question 134

# L58 What is the mechanism behind cannabinoid anti-emetics like nabilone?

Answer 134

Activate CB1 receptors in the CNS; provide euphoria and sedation, which helps in refractory cases like chemotherapy.

Question 135

# L58 What benefit do benzodiazepines bring to anti-emetic regimens?

Answer 135

Reduce anxiety and anticipatory nausea; work via GABAergic neuronal suppression.

Question 136

# L58 In what context are steroids like dexamethasone particularly useful?

Answer 136

Enhance efficacy of 5-HT3 or NK1 antagonists in chemotherapy and post-operative nausea; also reduce inflammation.

Question 137

# L58 What combination of drugs is typically used for chemotherapy-induced nausea and vomiting (CINV)?

Answer 137

: 5-HT3 receptor antagonist (e.g. ondansetron) + NK1 receptor antagonist (e.g. aprepitant) ± dexamethasone ± benzodiazepine.

Question 138

# L58 Which drugs are best for motion sickness and why?

Answer 138

Anti-muscarinics (scopolamine) and anti-histamines (cyclizine, cinnarizine) — effective on vestibular system and LVC pathway.

Question 139

# L58 What type of vomiting is best treated by dopamine antagonists?

Answer 139

Drug-induced vomiting (e.g. from opioids or L-dopa), as these target D2 receptors in the CTZ.

Question 140

How is pregnancy-induced vomiting (hyperemesis gravidarum) commonly treated?

Answer 140

Often with antihistamines or metoclopramide; choice depends on severity and safety in pregnancy.

Question 141

# L58 What is the functional role of the vomiting centre?

Answer 141

It integrates signals from the CTZ, vagal afferents, vestibular system, and higher centres to coordinate the act of vomiting.

Question 142

# L58 Which cranial nerves are involved in the vomiting reflex?

Answer 142

Vagus (X), glossopharyngeal (IX), facial (VII), and spinal nerves for motor output (e.g. abdominal muscle contraction).

Question 143

# L58 What are the efferent outputs from the vomiting centre?

Answer 143

Signals to salivary, respiratory, GI, and abdominal muscles to produce coordinated vomiting.

Question 144

# L58 What are the phases of vomiting?

Answer 144

1. Nausea – conscious awareness and discomfort. 2. Retching – unproductive rhythmic contractions. 3. Vomiting – expulsion of stomach contents.

Question 145

# L58 What distinguishes nausea from vomiting physiologically?

Answer 145

Nausea involves cortical processing and autonomic symptoms (sweating, pallor); vomiting is a brainstem-controlled motor act.

Question 146

# L58 What makes NK1 receptor antagonists unique in emesis management?

Answer 146

They block substance P centrally in the NTS and vomiting centre, covering both acute and delayed phases of chemotherapy-induced vomiting.

Question 147

# L58 What is receptor internalisation and how does it apply to palonosetron?

Answer 147

It refers to the removal of receptors from the cell surface, reducing responsiveness. Palonosetron causes 5-HT3 receptor internalisation for prolonged action.

Question 148

# L58 Why don’t 5-HT3 antagonists work for motion sickness?

Answer 148

Because motion sickness is primarily mediated by cholinergic and histaminergic pathways from the vestibular system, not serotonin.

Question 149

# L58 Why are elderly patients more susceptible to extrapyramidal side effects?

Answer 149

They may have increased sensitivity to dopamine antagonism, especially from drugs like metoclopramide or haloperidol.

Question 150

# L58 Why is domperidone preferred over metoclopramide in some cases?

Answer 150

Due to its lower risk of CNS side effects and better safety profile in long-term use.

Question 151

# L58 Why is anticipatory vomiting difficult to treat pharmacologically?

Answer 151

It is conditioned and driven by higher centres; best managed with behavioural therapy ± benzodiazepines.

Question 152

# L58 What role does the area postrema play in emesis?

Answer 152

It is the anatomical site of the CTZ; located in the medulla outside the blood-brain barrier, ideal for detecting toxins in blood.

Question 153

# L58 Why is the half-life of anti-emetics important in clinical use?

Answer 153

It determines dosing frequency and duration of action; e.g. palonosetron (long t½) is preferred for delayed-phase CINV.

Question 154

# L58 Why is intravenous administration used for some anti-emetics?

Answer 154

Ensures rapid onset and bypasses GI tract, which may be non-functional during vomiting.

Question 155

# L58 Why do some anti-emetics have sedative side effects?

Answer 155

Drugs like H1 antagonists and antimuscarinics cross the BBB and act centrally, causing drowsiness.

Question 156

# L58 Which pathway do H1 and muscarinic antagonists primarily block?

Answer 156

The vestibular system (inner ear) to vomiting centre pathway — important in motion sickness.

Question 157

# L58 Why are D2 antagonists not first-line for motion sickness?

Answer 157

The vestibular system is not dopamine-driven; D2 antagonists are more effective in CTZ-mediated nausea (e.g. opioids, uraemia).

Question 158

# L58 What are key side effects of metoclopramide?

Answer 158

Extrapyramidal symptoms (e.g. dystonia, Parkinsonism), especially in younger patients and high doses.

Question 159

# L58 Why should metoclopramide be avoided in Parkinson’s disease?

Answer 159

It blocks D2 receptors and can worsen motor symptoms due to reduced dopamine activity.

Question 160

# L58 What are the potential cardiac effects of 5-HT3 antagonists?

Answer 160

May prolong QT interval — monitor in patients with existing cardiac issues or those on other QT-prolonging drugs.

Question 161

# L58 What should be done if first-line anti-emetics fail?

Answer 161

Consider combination therapy, assess for underlying cause, or add corticosteroids/NK1 antagonists in chemo-induced cases.

Question 162

# L58 Why are corticosteroids useful despite unclear mechanisms?

Answer 162

Likely reduce inflammation and prostaglandin-mediated nausea; potentiate effect of other anti-emetics.

Question 163

# L58 What is anticipatory nausea and how is it triggered?

Answer 163

A conditioned response seen in chemotherapy patients due to past unpleasant experiences; triggered before treatment.

Question 164

# L58 What non-pharmacological techniques can help with anticipatory nausea?

Answer 164

Behavioural therapy, relaxation training, hypnosis, or distraction techniques; benzodiazepines may help short-term.

Question 165

# L58 Which area is considered the chemoreceptor trigger zone (CTZ)? A) Nucleus tractus solitarius B) Cerebellum C) Area postrema D) Hypothalamus

Answer 165

C) Area postrema ✅ ✅ Explanation: The CTZ is located in the area postrema of the medulla oblongata, just outside the blood-brain barrier. It detects emetogenic substances in the blood and CSF.

Question 166

# L58 Which receptor is primarily targeted by ondansetron? A) D2 B) NK1 C) H1 D) 5-HT3

Answer 166

D) 5-HT3 ✅ ✅ Explanation: Ondansetron is a selective serotonin 5-HT3 receptor antagonist, primarily used to treat nausea and vomiting, especially post-operative and chemotherapy-induced.

Question 167

# L58 Which anti-emetic is most associated with extrapyramidal side effects? A) Promethazine B) Metoclopramide C) Ondansetron D) Scopolamine

Answer 167

B) Metoclopramide ✅ ✅ Explanation: Metoclopramide is a D2 receptor antagonist that can cross the BBB and affect the basal ganglia, leading to EPS such as dystonia and parkinsonism.

Question 168

# L58 Which neurotransmitter is involved in motion sickness? A) Dopamine B) Serotonin C) Acetylcholine D) Substance P

Answer 168

C) Acetylcholine ✅ ✅ Explanation: The vestibular system transmits signals via histamine (H1) and acetylcholine (muscarinic M1) receptors—important in motion sickness.

Question 169

# L58 Palonosetron has a long duration of action because: A) It is lipophilic B) It causes receptor internalisation C) It blocks multiple receptor types D) It is not metabolised by the liver

Answer 169

B) It causes receptor internalisation ✅ ✅ Explanation: Palonosetron causes 5-HT3 receptor internalisation, which prolongs its anti-emetic effect, making it effective for delayed CINV.

Question 170

# L58 Domperidone has fewer CNS side effects than metoclopramide because: A) It blocks muscarinic receptors B) It doesn’t bind dopamine receptors C) It cannot cross the blood-brain barrier D) It is given intravenously

Answer 170

C) It cannot cross the blood-brain barrier ✅ ✅ Explanation: Domperidone acts on peripheral D2 receptors but does not significantly cross the BBB, reducing the risk of central dopamine-related side effects.

Question 171

# L58 Which cranial nerve is involved in afferent signalling to the vomiting centre? A) CN V B) CN IX C) CN X D) CN VII

Answer 171

Answer: C) CN X ✅ ✅ Explanation: The vagus nerve (cranial nerve X) carries visceral afferent signals from the GI tract to the nucleus tractus solitarius and the vomiting centre.

Question 172

# L58 Which phase of vomiting involves rhythmic abdominal contractions without expulsion? A) Nausea B) Vomiting C) Retching D) Post-ictal

Answer 172

Answer: C) Retching ✅ ✅ Explanation: Retching is a preparatory phase involving dry heaves—muscle contractions without vomit expulsion—commonly preceding full emesis.

Question 173

# L58 NK1 antagonists prevent vomiting by blocking: A) Dopamine B) Histamine C) Acetylcholine D) Substance P

Answer 173

Answer: D) Substance P ✅ ✅ Explanation: NK1 receptors bind substance P, a key neurotransmitter in the vomiting reflex. NK1 antagonists like aprepitant block this pathway effectively.

Question 174

# L58 What is the most appropriate anti-emetic for post-operative nausea and vomiting (PONV)? A) Metoclopramide B) Ondansetron C) Cyclizine D) Lorazepam

Answer 174

Answer: B) Ondansetron ✅ ✅ Explanation: 5-HT3 antagonists such as ondansetron are first-line treatment for PONV due to their high efficacy and favourable safety profile.

Question 175

# L58 A 70-year-old man develops parkinsonian symptoms after taking an anti-emetic. Which is the likely cause? A) Cyclizine B) Domperidone C) Metoclopramide D) Ondansetron

Answer 175

Answer: C) Metoclopramide ✅ ✅ Explanation: Metoclopramide crosses the blood-brain barrier and blocks central D2 receptors, increasing the risk of extrapyramidal symptoms, especially in older adults.

Question 176

# L58 A patient is receiving chemotherapy and has persistent vomiting 3 days later. Which is most appropriate? A) Lorazepam B) Metoclopramide C) Palonosetron D) Cyclizine

Answer 176

Answer: C) Palonosetron ✅ ✅ Explanation: Palonosetron is ideal for delayed-phase chemotherapy-induced nausea and vomiting (CINV) due to its long half-life and receptor internalisation effect.

Question 177

# L58 A patient with a history of cardiac arrhythmia should avoid: A) Dexamethasone B) Palonosetron C) Ondansetron D) Domperidone

Answer 177

Answer: C) Ondansetron ✅ ✅ Explanation: Ondansetron can prolong the QT interval, increasing the risk of arrhythmias like torsades de pointes, especially in those with existing cardiac conditions.

Question 178

# L58 A child with motion sickness is prescribed an anti-emetic. Which is most appropriate? A) Ondansetron B) Scopolamine C) Promethazine D) Metoclopramide Answer: C) Promethazine ✅

Answer 178

✅ Explanation: Promethazine, an H1 receptor antagonist, is suitable for motion sickness and is commonly used in paediatrics, though caution is needed due to sedation.

Question 179

# L58 A patient experiencing anticipatory nausea before chemotherapy may benefit from: A) Ondansetron B) Cyclizine C) Lorazepam D) Domperidone

Answer 179

Answer: C) Lorazepam ✅ ✅ Explanation: Anticipatory nausea is often psychological; benzodiazepines like lorazepam provide anxiolytic and amnesic effects to help manage it.

Question 180

# L58 Why is combination therapy often used for CINV? A) To improve compliance B) To reduce cost C) To cover multiple emetogenic pathways D) To reduce drug resistance

Answer 180

Answer: C) To cover multiple emetogenic pathways ✅ ✅ Explanation: Combining anti-emetics with different mechanisms (e.g. 5-HT3 + NK1 + corticosteroid) targets multiple neurotransmitter systems involved in emesis.

Question 181

# L58 A young woman on high-dose metoclopramide develops acute dystonia. What is the most likely cause? A) Dopamine receptor upregulation B) Dopamine antagonism in the basal ganglia C) Serotonin excess D) Histamine depletion

Answer 181

Answer: B) Dopamine antagonism in the basal ganglia ✅ ✅ Explanation: Blocking D2 receptors in the basal ganglia can lead to extrapyramidal symptoms such as acute dystonia—a known adverse effect of metoclopramide.

Question 182

# L58 Which anti-emetic is LEAST likely to cause sedation? A) Cyclizine B) Promethazine C) Ondansetron D) Scopolamine

Answer 182

Answer: C) Ondansetron ✅ ✅ Explanation: Unlike antihistamines and antimuscarinics, ondansetron does not block histamine or acetylcholine receptors, making sedation unlikely.

Question 183

# L58 In which situation is dexamethasone typically used as an anti-emetic? A) Gastroenteritis B) Migraine-associated nausea C) Chemotherapy-induced vomiting D) Motion sickness

Answer 183

Answer: C) Chemotherapy-induced vomiting ✅ ✅ Explanation: Dexamethasone enhances the effect of other anti-emetics (like 5-HT3 antagonists) and is commonly used in CINV protocols.

Question 184

# L58 A patient on opioids is experiencing nausea. Which anti-emetic is most effective for this cause? A) Ondansetron B) Metoclopramide C) Aprepitant D) Promethazine

Answer 184

Answer: B) Metoclopramide ✅ ✅ Explanation: Opioids trigger CTZ-mediated nausea through dopamine receptors, and metoclopramide’s D2 antagonism counteracts this effect effectively.

Question 185

# L58 Which structure is outside the blood-brain barrier and directly detects emetogenic toxins? A) Vestibular nucleus B) Cerebellum C) Chemoreceptor trigger zone (CTZ) D) Nucleus tractus solitarius (NTS)

Answer 185

Answer: C) Chemoreceptor trigger zone (CTZ) ✅ ✅ Explanation: The CTZ, located in the area postrema, lies outside the BBB, making it sensitive to circulating toxins and drugs.

Question 186

# L58 Which neurotransmitter is primarily involved in the vestibular system’s role in motion sickness? A) Dopamine B) Serotonin C) Histamine D) Substance P

Answer 186

Answer: C) Histamine ✅ ✅ Explanation: The vestibular nuclei use histaminergic and muscarinic pathways to transmit signals contributing to motion sickness.

Question 187

# L58 Which of the following enhances gastrointestinal motility in addition to anti-emetic effects? A) Ondansetron B) Metoclopramide C) Promethazine D) Aprepitant

Answer 187

Answer: B) Metoclopramide ✅ ✅ Explanation: Metoclopramide is both a D2 antagonist and prokinetic agent that promotes gastric emptying, reducing nausea.

Question 188

# L58 What is the mechanism of scopolamine in preventing nausea? A) Dopamine antagonism B) Histamine antagonism C) NK1 receptor blockade D) Muscarinic receptor antagonism

Answer 188

Answer: D) Muscarinic receptor antagonism ✅ ✅ Explanation: Scopolamine blocks muscarinic (M1) receptors, particularly effective for motion sickness due to vestibular pathway involvement.

Question 189

# L58 Which anti-emetic is most appropriate for a patient with Parkinson’s disease? A) Metoclopramide B) Domperidone C) Prochlorperazine D) Promethazine

Answer 189

Answer: B) Domperidone ✅ ✅ Explanation: Domperidone does not cross the BBB, so it won’t worsen Parkinsonian symptoms by blocking central dopamine receptors.

Question 190

# L58 A patient with chemotherapy-induced nausea has failed ondansetron. What is the next best step? A) Increase ondansetron dose B) Add lorazepam C) Add aprepitant D) Switch to cyclizine

Answer 190

Answer: C) Add aprepitant ✅ ✅ Explanation: For moderate-to-high emetogenic chemotherapy, combining 5-HT3 antagonists with NK1 antagonists (like aprepitant) and dexamethasone provides superior control.

Question 191

# L58 Which of the following is a known side effect of 5-HT3 antagonists? A) Parkinsonism B) QT interval prolongation C) Sedation D) Hepatic necrosis

Answer 191

Answer: B) QT interval prolongation ✅ ✅ Explanation: 5-HT3 antagonists such as ondansetron are associated with QT prolongation, a potentially serious cardiac effect.

Question 192

# L58 What role does the nucleus tractus solitarius (NTS) play in vomiting? A) Primary site for visual processing of emetogenic stimuli B) Initiates retching movements C) Coordinates afferent signals to the vomiting centre D) Acts as the site of serotonin release

Answer 192

Answer: C) Coordinates afferent signals to the vomiting centre ✅ ✅ Explanation: The NTS integrates signals from various sources (GI tract, CTZ, vestibular system) and relays them to the vomiting centre in the medulla.

Question 193

# L58 A patient undergoing cisplatin chemotherapy experiences delayed nausea 3 days after treatment. Which anti-emetic is most suitable? A) Cyclizine B) Ondansetron C) Aprepitant D) Domperidone

Answer 193

Answer: C) Aprepitant ✅ ✅ Explanation: Aprepitant, an NK1 antagonist, is effective for delayed chemotherapy-induced nausea, which occurs >24 hours after treatment.

Question 194

# L58 A pregnant woman in her first trimester presents with severe nausea. Which anti-emetic is considered safe in early pregnancy? A) Metoclopramide B) Ondansetron C) Prochlorperazine D) Cyclizine

Answer 194

Answer: D) Cyclizine ✅ ✅ Explanation: Cyclizine is an antihistamine often used for nausea in pregnancy. Though others may be used cautiously, cyclizine has a longer track record of safe use in early gestation.

Question 195

# L58 An elderly patient with heart failure is prescribed ondansetron. What is the most important monitoring parameter? A) Liver enzymes B) Visual acuity C) QT interval D) Blood glucose

Answer 195

Answer: C) QT interval ✅ ✅ Explanation: Ondansetron can prolong the QT interval, increasing the risk of arrhythmias, especially in elderly or cardiac patients.

Question 196

# L58 A patient with Parkinson’s disease requires anti-emetic treatment. Which drug is most appropriate to avoid exacerbation of symptoms? A) Metoclopramide B) Prochlorperazine C) Domperidone D) Haloperidol

Answer 196

Answer: C) Domperidone ✅ ✅ Explanation: Domperidone does not cross the BBB, avoiding central D2 antagonism and worsening of Parkinsonian symptoms.

Question 197

# L58 A patient taking opioids is experiencing nausea due to reduced GI motility. Which anti-emetic also improves gastric emptying? A) Ondansetron B) Promethazine C) Metoclopramide D) Aprepitant

Answer 197

Answer: C) Metoclopramide ✅ ✅ Explanation: Metoclopramide acts centrally as a D2 antagonist and peripherally as a prokinetic agent, enhancing GI motility.

Question 198

# L58 Which drug is least likely to cause sedation as a side effect? A) Cyclizine B) Promethazine C) Domperidone D) Prochlorperazine

Answer 198

Answer: C) Domperidone ✅ ✅ Explanation: As domperidone acts peripherally and doesn’t cross the BBB significantly, it’s less associated with sedation than centrally acting agents.

Question 199

# L58 A patient develops extrapyramidal symptoms after anti-emetic use. Which drug is most likely responsible? A) Domperidone B) Metoclopramide C) Cyclizine D) Aprepitant

Answer 199

Answer: B) Metoclopramide ✅ ✅ Explanation: Metoclopramide blocks central D2 receptors and can cause extrapyramidal symptoms like dystonia or akathisia, especially in young adults.

Question 200

# L58 Which anti-emetic class is most effective for post-operative nausea and vomiting (PONV)? A) NK1 antagonists B) Antihistamines C) 5-HT3 antagonists D) Antimuscarinics

Answer 200

Answer: C) 5-HT3 antagonists ✅ ✅ Explanation: 5-HT3 antagonists like ondansetron are first-line for PONV due to their effectiveness and relatively clean side effect profile.