Disorders of lipid metabolism – Obesity MCQs With Answer

Introduction: Disorders of lipid metabolism and obesity are central topics in pharmacology and therapeutics for B. Pharm students. Understanding dyslipidemia, altered lipoprotein metabolism, and obesity-related biochemical changes helps in selecting appropriate pharmacotherapy and counseling on lifestyle interventions. Key concepts include cholesterol and triglyceride transport, lipoprotein classes (LDL, HDL, VLDL), enzymatic regulators (HMG-CoA reductase, lipoprotein lipase), genetic disorders (familial hypercholesterolemia), and modern drugs (statins, fibrates, PCSK9 inhibitors, GLP‑1 agonists). This concise guide emphasizes mechanisms, clinical implications, lab interpretation, and drug actions to prepare you for exams and practice. Now let’s test your knowledge with 50 MCQs on this topic.

Q1. Which statement best defines disorders of lipid metabolism?

• Conditions causing abnormal synthesis, transport, or degradation of lipids leading to altered plasma lipoprotein levels
• Any disease of the liver unrelated to lipid levels
• Only genetic diseases that affect cholesterol synthesis
• Exclusive increase of body fat without biochemical abnormalities

Correct Answer: Conditions causing abnormal synthesis, transport, or degradation of lipids leading to altered plasma lipoprotein levels

Q2. Which lipoprotein is the main carrier of cholesterol to peripheral tissues and most strongly associated with atherosclerotic risk?

• High-density lipoprotein (HDL)
• Very low-density lipoprotein (VLDL)
• Low-density lipoprotein (LDL)
• Chylomicrons

Correct Answer: Low-density lipoprotein (LDL)

Q3. The Friedewald formula estimates LDL cholesterol using which measured parameters?

• Total cholesterol minus HDL minus (triglycerides/5)
• Total cholesterol divided by HDL
• Direct LDL measurement and HDL subtraction
• Triglycerides minus VLDL

Correct Answer: Total cholesterol minus HDL minus (triglycerides/5)

Q4. Which enzyme is the rate-limiting step in cholesterol biosynthesis and target of statins?

• Lipoprotein lipase (LPL)
• HMG-CoA reductase
• Acyl-CoA:cholesterol acyltransferase (ACAT)
• Cholesteryl ester transfer protein (CETP)

Correct Answer: HMG-CoA reductase

Q5. Familial hypercholesterolemia is most commonly due to a defect in which protein?

• Low-density lipoprotein (LDL) receptor
• Apolipoprotein A-I
• Lipoprotein lipase (LPL)
• HMG-CoA synthase

Correct Answer: Low-density lipoprotein (LDL) receptor

Q6. Which lipid pattern is classically seen with insulin resistance and obesity?

• Increased HDL, low triglycerides
• Increased triglycerides, low HDL, small dense LDL
• Isolated high LDL with normal TG and HDL
• Decreased VLDL and high HDL

Correct Answer: Increased triglycerides, low HDL, small dense LDL

Q7. Which apolipoprotein is the major structural protein of HDL and important for reverse cholesterol transport?

• Apolipoprotein B-100 (ApoB-100)
• Apolipoprotein C-II (ApoC-II)
• Apolipoprotein A-I (ApoA-I)
• Apolipoprotein E (ApoE)

Correct Answer: Apolipoprotein A-I (ApoA-I)

Q8. Which drug class primarily lowers triglycerides by activating peroxisome proliferator-activated receptor-alpha (PPAR-α)?

• Statins
• Fibrates
• Bile acid sequestrants
• PCSK9 inhibitors

Correct Answer: Fibrates

Q9. Mechanism of action of ezetimibe involves:

• Inhibition of intestinal cholesterol absorption via NPC1L1 transporter
• Inhibition of HMG-CoA reductase in the liver
• Enhancement of bile acid reabsorption
• Activation of lipoprotein lipase

Correct Answer: Inhibition of intestinal cholesterol absorption via NPC1L1 transporter

Q10. Which adverse effect is classically associated with statin therapy and requires monitoring?

• Hypoglycemia
• Hepatotoxicity and myopathy (elevated transaminases and creatine kinase)
• Hypertriglyceridemia
• Pancreatitis

Correct Answer: Hepatotoxicity and myopathy (elevated transaminases and creatine kinase)

Q11. Which Friedewald formula limitation must be noted when triglycerides are very high (>400 mg/dL)?

• It underestimates HDL cholesterol
• It accurately estimates LDL regardless of TG level
• It becomes invalid and LDL should be measured directly
• It provides overestimation of total cholesterol

Correct Answer: It becomes invalid and LDL should be measured directly

Q12. ApoB-100 is primarily found in which lipoprotein and is an indicator of atherogenic particle number?

• HDL
• LDL and VLDL
• Chylomicrons only
• Intestinal bile salts

Correct Answer: LDL and VLDL

Q13. Which enzyme hydrolyzes triglycerides in circulating chylomicrons and VLDL to release free fatty acids?

• HMG-CoA reductase
• Lipoprotein lipase (LPL)
• Acyl-CoA synthetase
• LCAT (lecithin–cholesterol acyltransferase)

Correct Answer: Lipoprotein lipase (LPL)

Q14. Which dyslipidemia is characterized by elevated chylomicrons and very high triglycerides, often presenting in childhood?

• Type I hyperlipoproteinemia (familial LPL deficiency)
• Type IIa familial hypercholesterolemia
• Type III dysbetalipoproteinemia
• Type V hyperlipidemia due to isolated LDL elevation

Correct Answer: Type I hyperlipoproteinemia (familial LPL deficiency)

Q15. Which drug lowers LDL by increasing hepatic LDL receptor expression via inhibition of cholesterol synthesis?

• Niacin
• Statins
• Fibrates
• Omega-3 fatty acids

Correct Answer: Statins

Q16. Which biochemical change is commonly observed with niacin therapy?

• Increased HDL and decreased triglycerides but causes flushing due to prostaglandin release
• Marked decrease in HDL and increase in LDL
• Renal failure as a common side effect
• Direct inhibition of HMG-CoA reductase

Correct Answer: Increased HDL and decreased triglycerides but causes flushing due to prostaglandin release

Q17. PCSK9 inhibitors reduce LDL mainly by which mechanism?

• Increasing intestinal cholesterol excretion
• Promoting hepatic LDL receptor recycling and preventing their degradation
• Directly inhibiting cholesterol biosynthesis enzyme
• Enhancing cholesteryl ester transfer protein activity

Correct Answer: Promoting hepatic LDL receptor recycling and preventing their degradation

Q18. The role of HDL in lipid metabolism is primarily:

• Delivering triglycerides to adipose tissue
• Reverse cholesterol transport from peripheral tissues to the liver
• Acting as the main carrier of dietary triglycerides
• Activating HMG-CoA reductase

Correct Answer: Reverse cholesterol transport from peripheral tissues to the liver

Q19. Which laboratory finding best correlates with increased atherosclerotic cardiovascular disease risk?

• Low LDL and high HDL
• High LDL cholesterol and elevated ApoB levels
• Normal lipid profile but elevated albumin
• Isolated low triglycerides

Correct Answer: High LDL cholesterol and elevated ApoB levels

Q20. Cholestyramine and other bile acid sequestrants lower LDL cholesterol by:

• Binding bile acids in the intestine, increasing hepatic conversion of cholesterol to bile acids
• Inhibiting HMG-CoA reductase directly
• Activating LPL in adipose tissue
• Stimulating intestinal absorption of cholesterol

Correct Answer: Binding bile acids in the intestine, increasing hepatic conversion of cholesterol to bile acids

Q21. Which genetic mutation causes familial dysbetalipoproteinemia (Type III) leading to accumulation of remnant particles?

• Mutations in apolipoprotein E (ApoE2 homozygosity)
• LDL receptor null mutation
• HMG-CoA reductase overexpression
• LPL gene duplication

Correct Answer: Mutations in apolipoprotein E (ApoE2 homozygosity)

Q22. Which therapeutic approach is recommended first-line for obesity-related dyslipidemia in B. Pharm counseling?

• Immediate initiation of PCSK9 inhibitors
• Lifestyle modification including diet, exercise, and weight loss
• High-dose niacin without lifestyle changes
• Use of bile acid sequestrants as primary therapy for obesity

Correct Answer: Lifestyle modification including diet, exercise, and weight loss

Q23. Which marker is most appropriate to monitor statin efficacy in a patient?

• Serum creatinine
• Fasting LDL cholesterol
• Blood urea nitrogen (BUN)
• Serum amylase

Correct Answer: Fasting LDL cholesterol

Q24. Which drug indicated for severe hypertriglyceridemia reduces hepatic VLDL synthesis and may cause gallstones?

• Fibrates (e.g., gemfibrozil)
• Statins
• Bile acid sequestrants
• PCSK9 inhibitors

Correct Answer: Fibrates (e.g., gemfibrozil)

Q25. In the management of dyslipidemia, combination therapy of statins with fibrates increases risk of which adverse event?

• Gastrointestinal bleeding
• Myopathy and rhabdomyolysis
• Hypertension
• Hypoglycemia

Correct Answer: Myopathy and rhabdomyolysis

Q26. Which adipokine is typically decreased in obesity and is associated with insulin sensitivity?

• Leptin
• TNF-α
• Adiponectin
• Resistin

Correct Answer: Adiponectin

Q27. The primary action of lipoprotein lipase is stimulated by which apolipoprotein cofactor?

• Apolipoprotein C-II (ApoC-II)
• Apolipoprotein A-I (ApoA-I)
• Apolipoprotein B-100 (ApoB-100)
• Apolipoprotein E (ApoE)

Correct Answer: Apolipoprotein C-II (ApoC-II)

Q28. Which statement about HDL-raising therapies and cardiovascular outcomes is most accurate?

• All HDL-raising drugs unequivocally reduce cardiovascular events
• Raising HDL pharmacologically does not always translate to reduced cardiovascular events
• HDL level is irrelevant to cardiovascular risk
• Increasing HDL via CETP inhibitors consistently reduces mortality

Correct Answer: Raising HDL pharmacologically does not always translate to reduced cardiovascular events

Q29. Which outcome is expected from orlistat therapy used for obesity management?

• Inhibition of pancreatic and gastric lipases leading to reduced fat absorption
• Central appetite suppression via serotonin receptors
• Direct stimulation of lipoprotein lipase activity
• Inhibition of HMG-CoA reductase

Correct Answer: Inhibition of pancreatic and gastric lipases leading to reduced fat absorption

Q30. Which lipid abnormality increases the risk of pancreatitis if very elevated?

• Isolated low HDL
• Markedly elevated triglycerides (>1000 mg/dL)
• Moderately elevated LDL only
• Low total cholesterol

Correct Answer: Markedly elevated triglycerides (>1000 mg/dL)

Q31. Lecithin–cholesterol acyltransferase (LCAT) enzyme is crucial for which process?

• Converting free cholesterol into cholesteryl esters on HDL during reverse cholesterol transport
• Synthesizing triglycerides in adipose tissue
• Hydrolyzing triglycerides in chylomicrons
• Catalyzing bile acid synthesis directly

Correct Answer: Converting free cholesterol into cholesteryl esters on HDL during reverse cholesterol transport

Q32. Which class of drugs can increase the risk of cholesterol gallstone formation by reducing biliary cholesterol solubility?

• Fibrates
• Statins
• PCSK9 inhibitors
• Ezetimibe

Correct Answer: Fibrates

Q33. Which of the following best describes the mechanism of action of bile acid sequestrants on LDL lowering?

• They block intestinal cholesterol absorption by inhibiting NPC1L1 transporter
• They bind bile acids preventing their reabsorption, increasing hepatic conversion of cholesterol to bile acids and upregulating LDL receptors
• They directly degrade LDL particles in plasma
• They activate PPAR-α to reduce VLDL secretion

Correct Answer: They bind bile acids preventing their reabsorption, increasing hepatic conversion of cholesterol to bile acids and upregulating LDL receptors

Q34. In metabolic syndrome diagnostic criteria, which lipid abnormality is included?

• High HDL and low triglycerides
• Elevated triglycerides (≥150 mg/dL) and/or reduced HDL
• Isolated low LDL cholesterol
• Low total cholesterol only

Correct Answer: Elevated triglycerides (≥150 mg/dL) and/or reduced HDL

Q35. Which oral antihyperlipidemic drug should be avoided with concurrent gemfibrozil due to drug interaction increasing myopathy risk?

• Atorvastatin
• Niacin
• Bile acid sequestrant
• PCSK9 inhibitor

Correct Answer: Atorvastatin

Q36. Which physiological effect of obesity contributes to dyslipidemia?

• Decreased free fatty acid release from adipose tissue
• Increased adipose tissue lipolysis leading to elevated circulating free fatty acids and hepatic VLDL synthesis
• Decreased hepatic VLDL production
• Enhanced insulin sensitivity in adipose tissue

Correct Answer: Increased adipose tissue lipolysis leading to elevated circulating free fatty acids and hepatic VLDL synthesis

Q37. Which medication primarily reduces LDL by inhibiting the intestinal bile acid reabsorption transporter (ASBT)?

• Ezetimibe
• Bile acid sequestrants like colesevelam
• Statins
• Fibrates

Correct Answer: Bile acid sequestrants like colesevelam

Q38. A patient with very high LDL despite maximally tolerated statin therapy may be considered for which additional therapy to further reduce LDL?

• PCSK9 inhibitor therapy
• Increase dietary saturated fat intake
• Stop statin and use fibrate only
• Use oral glucocorticoids

Correct Answer: PCSK9 inhibitor therapy

Q39. In severe hypertriglyceridemia, which acute therapy may be used to rapidly lower triglycerides and reduce pancreatitis risk?

• Intravenous insulin infusion and plasmapheresis in certain cases
• Switching to bile acid sequestrants only
• Oral statin monotherapy
• Long-term niacin therapy as first acute measure

Correct Answer: Intravenous insulin infusion and plasmapheresis in certain cases

Q40. Which transporter is targeted by ezetimibe to reduce intestinal cholesterol uptake?

• NPC1L1 (Niemann-Pick C1-Like 1)
• ASBT (apical sodium–bile acid transporter)
• GLUT4
• OATP1B1

Correct Answer: NPC1L1 (Niemann-Pick C1-Like 1)

Q41. Which of the following describes the primary benefit of GLP-1 receptor agonists in obesity management beyond weight loss?

• They increase LDL cholesterol substantially
• They improve glycemic control and may improve lipid profile and cardiovascular risk markers
• They primarily cause gallstone formation as the main benefit
• They inhibit lipoprotein lipase directly

Correct Answer: They improve glycemic control and may improve lipid profile and cardiovascular risk markers

Q42. Which lipoprotein fraction is richest in triglycerides and is responsible for transporting dietary fat from intestine to tissues?

• LDL
• HDL
• Chylomicrons
• IDL (intermediate-density lipoprotein)

Correct Answer: Chylomicrons

Q43. Which laboratory test specifically quantifies the number of atherogenic particles better than LDL-C alone?

• AST/ALT
• ApoB measurement
• Urine protein
• Serum amylase

Correct Answer: ApoB measurement

Q44. Which enzyme esterifies cholesterol in HDL and is essential for maturation of HDL particles?

• LCAT (lecithin–cholesterol acyltransferase)
• ACAT
• HMG-CoA reductase
• Lipoprotein lipase

Correct Answer: LCAT (lecithin–cholesterol acyltransferase)

Q45. Which of the following is a common non-pharmacologic strategy to improve dyslipidemia in obese patients?

• High saturated fat diet
• Caloric restriction, increased physical activity, and dietary modification to reduce trans fats and simple sugars
• Complete bed rest to reduce metabolic demands
• Frequent high-glycemic meals

Correct Answer: Caloric restriction, increased physical activity, and dietary modification to reduce trans fats and simple sugars

Q46. Which lipid-lowering agent is contraindicated in pregnancy due to essential roles of cholesterol in fetal development?

• Bile acid sequestrants
• Statins
• Fish oil (omega-3 fatty acids)
• Colesevelam

Correct Answer: Statins

Q47. Which measure is most appropriate to assess visceral adiposity related cardiovascular risk in obesity?

• Weight alone
• BMI without waist measurement
• Waist circumference and waist-to-hip ratio
• Fasting insulin only

Correct Answer: Waist circumference and waist-to-hip ratio

Q48. A gain-of-function mutation in which gene can cause familial hypercholesterolemia by increasing LDL receptor degradation?

• PCSK9
• LCAT
• ApoA-I
• ACAT

Correct Answer: PCSK9

Q49. Which therapeutic agent lowers triglycerides by providing highly purified omega-3 fatty acids and is used for severe hypertriglyceridemia?

• Fenofibrate
• Lovastatin
• High-dose EPA/DHA (prescription omega-3 fatty acids)
• Colestipol

Correct Answer: High-dose EPA/DHA (prescription omega-3 fatty acids)

Q50. Which lipid-related target is the main goal for primary prevention in most guidelines when treating high cardiovascular risk patients?

• Reducing HDL to lower levels
• Lowering LDL cholesterol to guideline-specific targets
• Raising triglycerides above 500 mg/dL
• Increasing total cholesterol

Correct Answer: Lowering LDL cholesterol to guideline-specific targets

G S Sachin

I am a Registered Pharmacist under the Pharmacy Act, 1948, and the founder of PharmacyFreak.com. I hold a Bachelor of Pharmacy degree from Rungta College of Pharmaceutical Science and Research. With a strong academic foundation and practical knowledge, I am committed to providing accurate, easy-to-understand content to support pharmacy students and professionals. My aim is to make complex pharmaceutical concepts accessible and useful for real-world application.

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