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Lipoprotein Structure and Apolipoprotein Function

Total questions: 139

Worksheet time: 1hrs 10mins

Name
Class
Date
1.

Which apolipoprotein directly activates lipoprotein lipase (LPL) on VLDL and chylomicrons?

a)

ApoB-100 on LDL particles

b)

ApoE on remnant lipoproteins

c)

ApoC-II on triglyceride-rich lipoproteins

d)

ApoA-I on HDL particles

2.

Which apolipoprotein is essential for activating LCAT to enable HDL-mediated reverse cholesterol transport?

a)

ApoC-II activating LPL

b)

ApoB-48 guiding remnants

c)

ApoA-I stimulating LCAT activity

d)

ApoE binding hepatic receptors

3.

Which apolipoprotein serves as the ligand allowing LDL to be taken up by the LDL receptor (LDLR) in the liver?

a)

ApoA-I as HDL structural core

b)

ApoE as remnant clearance tag

c)

ApoB-100 as the LDL ID tag

d)

ApoC-II as enzyme activator

4.

Which apolipoprotein mediates hepatic clearance of chylomicron remnants and IDL via LRP/LDLR?

a)

ApoC-II LPL activator

b)

ApoE hepatic receptor ligand

c)

ApoA-I LCAT activator

d)

ApoB-48 structural protein

5.

Which structural apolipoprotein is unique to chylomicrons and their remnants?

a)

ApoB-100 on LDL and VLDL

b)

ApoA-I on HDL

c)

ApoB-48 on chylomicrons

d)

ApoC-II on VLDL

6.

Which lipoprotein class is richest in triglycerides and initially transports dietary fat?

a)

IDL with intermediate density

b)

LDL delivering cholesterol

c)

HDL carrying cholesterol esters

d)

Chylomicrons transporting dietary triglycerides

7.

Which apolipoprotein combination characterizes Lp(a) particles?

a)

ApoA-I plus ApoC-II

b)

ApoB-100 plus Apo(a)

c)

ApoE plus ApoB-48

d)

ApoB-100 plus ApoE

8.

What proportion of Lp(a) levels is largely determined by genetics rather than environment?

a)

About ten to twenty percent

b)

Nearly one hundred percent always

c)

Approximately seventy to ninety percent

d)

Roughly forty to fifty percent

9.

Which statement best explains why lifestyle changes often fail to lower elevated Lp(a)?

a)

Lp(a) is mainly diet dependent

b)

Lp(a) is primarily exercise regulated

c)

Lp(a) level is genetically fixed

d)

Lp(a) fluctuates with medications

10.

Which apolipoprotein acts as the primary structural protein of LDL particles?

a)

ApoC-II on VLDL surface

b)

ApoB-100 on LDL surface

c)

ApoA-I forming HDL core

d)

ApoE on remnant particles

11.

Which enzyme catalyzes cholesterol esterification on HDL to enable maturation?

a)

Lipoprotein lipase in capillaries

b)

HMG-CoA reductase in liver

c)

Hormone-sensitive lipase in adipose

d)

LCAT on HDL surface

12.

Which tag identifiers commonly mark lipoproteins for receptor recognition according to the diagram?

a)

ApoD and ApoF proteins

b)

ApoB-48, ApoB-100, ApoE, Apo(a)

c)

ApoA-IV and ApoC-I

d)

ApoA-II and ApoC-III

13.

Which lipoprotein primarily mediates reverse cholesterol transport to the liver?

a)

VLDL exporting hepatic TGs

b)

Chylomicrons carrying dietary fat

c)

LDL delivering cholesterol

d)

HDL performing reverse transport

14.

Which apolipoprotein is required for efficient lipolysis of triglyceride-rich lipoproteins in capillaries?

a)

ApoA-I activating HSL

b)

ApoB-48 structural tag

c)

ApoC-II activating LPL

d)

ApoE binding LDLR

15.

Which lipoprotein class is most enriched in cholesteryl esters and delivers cholesterol to tissues?

a)

HDL transporting excess cholesterol

b)

LDL delivering cholesteryl esters

c)

VLDL carrying triglycerides

d)

Chylomicrons moving dietary TG

16.

Which particle is depicted with an LDL-like core and additional apolipoprotein called Apo(a)?

a)

HDL mature sphere

b)

IDL transition particle

c)

Lp(a) composite lipoprotein

d)

Chylomicron large particle

17.

Which mechanism explains the atherogenicity of high Lp(a) levels?

a)

Improved hepatic clearance via ApoE

b)

Accelerated triglyceride hydrolysis

c)

Proinflammatory and prothrombotic effects

d)

Enhanced reverse transport efficiency

18.

Which apolipoprotein tag guides chylomicron remnants to hepatic receptors for clearance?

a)

Apo(a) attached to ApoB-100

b)

ApoC-II enzymatic activator

c)

ApoB-48 structural identifier

d)

ApoA-I HDL core protein

19.

Which lipoprotein primarily carries dietary triglycerides from the intestine to peripheral tissues in the exogenous pathway?

a)

LDL particles

b)

HDL particles

c)

IDL particles

d)

VLDL particles

e)

Chylomicrons

20.

In the endogenous pathway, which lipoprotein is secreted by the liver to deliver triglycerides to tissues?

a)

VLDL secreted by hepatocytes

b)

IDL released by enterocytes

c)

LDL formed in intestine

d)

Chylomicrons from bile

e)

HDL synthesized in adipose

21.

Which apolipoprotein is characteristic of LDL and mediates binding to LDL receptors?

a)

ApoC-II on LDL

b)

ApoE on LDL

c)

ApoA-I on LDL

d)

ApoB-48 on LDL

e)

ApoB-100 on LDL

22.

Reverse cholesterol transport is best described as which process?

a)

HDL removes excess cholesterol

b)

IDL converts to LDL in plasma

c)

LDL delivers cholesterol to cells

d)

Chylomicrons carry dietary cholesterol

e)

VLDL exports triglycerides to adipose

23.

Which enzyme hydrolyzes triglycerides in chylomicrons and VLDL within capillaries?

a)

HMG‑CoA reductase

b)

Hormone‑sensitive lipase

c)

Acyl‑CoA synthetase

d)

Phospholipase A2

e)

Lipoprotein lipase enzyme

24.

What happens to chylomicrons after delivering fatty acids to tissues?

a)

They become remnants cleared by liver

b)

They fuse with HDL permanently

c)

They convert directly to LDL

d)

They recycle to intestines intact

e)

They enter bile without processing

25.

Which sequence correctly orders particles in the endogenous pathway as triglycerides are delivered?

a)

IDL to VLDL to LDL

b)

LDL to IDL to VLDL

c)

Chylomicron to LDL to HDL

d)

HDL to IDL to chylomicron

e)

VLDL to IDL to LDL

26.

LDL and Lp(a) share which receptor for cellular uptake?

a)

NPC1L1 transporter

b)

ABCA1 transporter

c)

ApoA-I receptor

d)

SR-B1 receptor

e)

LDL receptor on cells

27.

In the normal state with PCSK9 present, what is the fate of LDLR after binding LDL and PCSK9?

a)

Export to Golgi apparatus

b)

Immediate recycling to surface

c)

Release into bloodstream

d)

Conversion into SR-B1 receptor

e)

Lysosomal degradation occurs

28.

PCSK9 inhibitors promote which outcome at the LDL receptor?

a)

Chylomicron formation increase

b)

Increased PCSK9 production

c)

LDLR permanent degradation

d)

ABCA1 efflux inhibition

e)

LDLR recycling to surface

29.

Which pathway primarily handles de novo synthesized cholesterol from the liver?

a)

Endogenous hepatic pathway

b)

Exogenous intestinal pathway

c)

Reverse transport pathway

d)

Biliary excretion pathway

e)

Enterohepatic circulation

30.

During reverse cholesterol transport, where is collected cholesterol ultimately processed?

a)

In intestinal mucosa reabsorption

b)

In the liver for use or excretion

c)

In pancreatic acinar secretion

d)

In adipose tissue storage

e)

In skeletal muscle oxidation

31.

Which apolipoprotein is unique to chylomicrons compared with LDL?

a)

ApoB-48 on chylomicrons

b)

ApoB-100 on chylomicrons

c)

ApoA-I on chylomicrons

d)

ApoE absent on chylomicrons

e)

ApoC-II absent on chylomicrons

32.

Which event increases cellular clearance of circulating LDL when PCSK9 is inhibited?

a)

Enhanced chylomicron remnant flow

b)

Greater IDL formation from LDL

c)

Reduced HDL-mediated efflux

d)

Less LDL binding to receptors

e)

More LDLR available at membrane

33.

Which hormone primarily activates acetyl-CoA carboxylase (ACC) to promote fatty acid synthesis?

a)

Insulin after feeding

b)

Glucagon in fasting state

c)

Epinephrine during stress

d)

Cortisol in catabolism

34.

During adipose fatty acid breakdown, which regulatory pattern is correct?

a)

Citrate activates lipase

b)

Glucagon inhibits lipase

c)

Glucagon activates lipase

d)

Insulin activates lipase

35.

Which molecule inhibits hepatic beta-oxidation by blocking carnitine shuttle CPT-1?

a)

Malonyl-CoA from synthesis

b)

Acetyl-CoA from TCA

c)

NADH from glycolysis

d)

AMP from low energy

36.

HMG-CoA reductase activity increases under which physiological condition?

a)

AMPK activation high

b)

Insulin signaling rise

c)

Glucagon signaling rise

d)

High cholesterol feedback

37.

Which statement best describes insulin’s overall effect on lipid metabolism?

a)

Raises CETP-mediated transfer

b)

Promotes synthesis and storage

c)

Stimulates breakdown in adipose

d)

Blocks esterification by LCAT

38.

Which reference value aligns with normal fasting LDL cholesterol?

a)

LDL-C below 100 mg/dL

b)

LDL-C between 120–160 mg/dL

c)

LDL-C above 150 mg/dL

d)

LDL-C around 200 mg/dL

39.

Which HDL threshold is considered normal for men?

a)

HDL-C over 70 mg/dL

b)

HDL-C over 30 mg/dL

c)

HDL-C over 40 mg/dL

d)

HDL-C over 50 mg/dL

40.

Which lipid panel value indicates normal total cholesterol?

a)

Over 220 mg/dL

b)

Around 250 mg/dL

c)

Between 210–240 mg/dL

d)

Under 200 mg/dL

41.

Which triglyceride level is within the normal reference range?

a)

Under 150 mg/dL

b)

Around 180 mg/dL

c)

Between 160–190 mg/dL

d)

Above 200 mg/dL

42.

A patient has fasting LDL-C 160 mg/dL and HDL-C 35 mg/dL. Which risk interpretation fits best?

a)

LDL low, HDL high

b)

LDL high, HDL low

c)

LDL normal, HDL optimal

d)

Both LDL and HDL normal

43.

In reverse cholesterol transport, which enzyme esterifies cholesterol on nascent HDL?

a)

LCAT on HDL surface

b)

CETP between lipoproteins

c)

HMG-CoA reductase hepatic

d)

ACC in cytosol

44.

Which pathway step moves cholesteryl esters from HDL to VLDL/LDL?

a)

LCAT-mediated synthesis

b)

LDLR-mediated uptake

c)

CETP-mediated transfer

d)

SR-BI efflux to liver

45.

A 60-year-old man with obesity (BMI 34) has total cholesterol 240 mg/dL, LDL-C 155 mg/dL, HDL-C 35 mg/dL, and triglycerides 320 mg/dL. Which abnormal process best explains this pattern?

a)

Reverse cholesterol transport is defective

b)

Conversion of HDL to LDL is blocked

c)

Intestinal fat absorption is markedly reduced

d)

Reduced hepatic VLDL secretion

e)

Impaired hepatic LDL receptor uptake

46.

In obesity, which lipoprotein is most directly elevated due to increased hepatic triglyceride export?

a)

VLDL particles carrying ApoB-100

b)

IDL remnants rich in cholesterol

c)

LDL particles depleted of triglyceride

d)

Chylomicrons formed postprandially

e)

HDL particles synthesized in liver

47.

A 60-year-old man with ASCVD shows very high VLDL, normal LDL, and normal ApoB-100 production. Which mechanism best accounts for high VLDL with normal LDL?

a)

Lipoprotein lipase deficiency reduces VLDL clearance

b)

LCAT deficiency increases VLDL formation from HDL

c)

Inability to convert VLDL to LDL at LDL receptor

d)

Malabsorption lowers chylomicron formation markedly

e)

Elevated CETP directly raises LDL synthesis

48.

Which enzyme primarily hydrolyzes triglycerides in circulating VLDL to permit their clearance?

a)

LCAT catalyzing cholesterol ester formation

b)

Hormone-sensitive lipase active in adipocytes

c)

HMG-CoA reductase synthesizing cholesterol

d)

CETP exchanging cholesterol esters

e)

Lipoprotein lipase anchored to endothelium

49.

Which finding is most consistent with defective reverse cholesterol transport?

a)

Isolated increase of IDL particles

b)

Elevated ApoB-100 with low VLDL

c)

Normal HDL with high chylomicrons

d)

High LDL with normal triglycerides

e)

Low HDL with elevated triglycerides

50.

Calculate BMI for a patient weighing 90 kg and 1.70 m tall. Use BMI=weight(height2)BMI = \frac{weight}{(height^2)} .

a)

27.5 kg/m² indicating overweight

b)

29.0 kg/m² indicating overweight

c)

31.1 kg/m² indicating obesity

d)

24.1 kg/m² indicating optimal

e)

33.8 kg/m² indicating severe obesity

51.

According to the shown thresholds, which BMI range is labeled optimal for adults?

a)

16.0–18.0 kg/m² as optimal

b)

25.0–29.9 kg/m² as optimal

c)

30.0–34.9 kg/m² as optimal

d)

23.0–24.9 kg/m² as optimal

e)

18.5–22.9 kg/m² as optimal

52.

Which lab pattern most strongly suggests insulin-resistant dyslipidemia commonly seen with high BMI?

a)

Isolated high LDL with normal HDL

b)

Low LDL with high triglycerides

c)

Low triglycerides with high HDL

d)

High triglycerides with low HDL

e)

Normal triglycerides with high HDL

53.

For a patient with triglycerides 320 mg/dL and low HDL, which first-line therapeutic target best reduces VLDL burden?

a)

Stimulate CETP-mediated lipid exchange

b)

Improve insulin sensitivity and weight loss

c)

Increase dietary cholesterol intake

d)

Block intestinal bile acid reabsorption

e)

Inhibit LCAT activity in plasma

54.

A patient has normal ApoB-100 production but elevated VLDL. Which lab change after fibrate therapy would indicate improved clearance?

a)

Increased LDL with constant triglycerides

b)

Unchanged VLDL with higher ApoB-100

c)

Lower HDL with increased CETP activity

d)

Decreased triglycerides with reduced VLDL

e)

Higher total cholesterol with lower LDL

55.

Which statement best distinguishes primary from secondary dyslipidemia?

a)

Primary is more common in the population; secondary is rare and neonatal

b)

Primary causes triglyceride elevations only; secondary affects HDL exclusively

c)

Primary results from diet-induced lipid excess; secondary is always genetic

d)

Primary involves inherited metabolic mutation; secondary involves external disruption

56.

Which classification system organizes dyslipidemias by the predominant raised lipoprotein?

a)

WHO/Fredrickson types I–V classification

b)

ATP III metabolic syndrome score

c)

Framingham risk percentage tiers

d)

NYHA functional cardiac classes

57.

Which scenario most likely represents secondary dyslipidemia?

a)

Functional lipid pathways disrupted by diabetes or drugs

b)

Congenital LDL receptor deletion at birth

c)

Autosomal dominant inheritance of PCSK9 variant

d)

ApoB-100 defect causing LDL binding failure

58.

Which complication is a recognized consequence of secondary dyslipidemia?

a)

Peptic ulcer disease and celiac sprue

b)

Asthma exacerbations and chronic bronchitis

c)

Osteoporosis with fractures and anemia

d)

Atherosclerotic cardiovascular disease and pancreatitis

59.

A patient with familial hypercholesterolemia typically shows which laboratory feature?

a)

HDL-C below 20 mg/dL

b)

Triglycerides above 600 mg/dL

c)

LDL-C greater than 190 mg/dL

d)

Lipoprotein(a) exceeding 300 mg/dL

60.

Which visible sign is classically associated with familial hypercholesterolemia?

a)

Tendon xanthomas on extensor surfaces

b)

Palmar erythema over metacarpals

c)

Digital clubbing of distal phalanges

d)

Petechial rash on lower extremities

61.

Which ocular finding supports a diagnosis of familial hypercholesterolemia in a young adult?

a)

Bilateral conjunctival pallor from anemia

b)

Kayser–Fleischer rings from copper deposition

c)

Papilledema during acute hypertension

d)

Corneal arcus present before age forty-five

62.

What is the most common molecular defect in familial hypercholesterolemia?

a)

LDL receptor loss-of-function mutation

b)

Apolipoprotein A-I structural alteration

c)

LPL overexpression in adipose tissue

d)

CETP gain-of-function increasing HDL

63.

Which mechanism explains high LDL in LDL receptor deficiency?

a)

Reduced hepatic clearance prolongs LDL half-life

b)

Enhanced intestinal cholesterol absorption

c)

Increased HDL cholesteryl ester transfer

d)

Accelerated VLDL synthesis in the liver

64.

Which rarer cause of familial hypercholesterolemia involves impaired LDL binding?

a)

ABCA1 loss increasing macrophage cholesterol

b)

ApoB-100 mutation causing defective LDLR interaction

c)

ApoA-II deletion reducing HDL formation

d)

LPL truncation reducing chylomicron hydrolysis

65.

A gain-of-function mutation in PCSK9 leads to which outcome?

a)

Increased LDL receptor degradation and high LDL

b)

Improved ApoB editing reducing LDL production

c)

Suppressed VLDL secretion and low LDL

d)

Enhanced LDL receptor recycling lowering LDL

66.

Which inheritance pattern fits familial hypercholesterolemia in most families?

a)

Mitochondrial maternal inheritance only

b)

X-linked recessive affecting males predominantly

c)

Autosomal recessive requiring two mutant alleles

d)

Autosomal dominant with 50% transmission risk

67.

A 32-year-old runner presents with chest pain during exertion, tendon xanthomas, corneal arcus, and LDL-C of 388 mg/dL. What is the most likely diagnosis?

a)

Heterozygous familial hypercholesterolemia causing premature CAD

b)

Secondary dyslipidemia due to vegetarian diet alone

c)

Familial hypertriglyceridemia with pancreatitis risk

d)

Hypoalphalipoproteinemia with isolated low HDL

68.

In the runner case, why is lifestyle modification alone insufficient?

a)

Dietary saturated fat intake is the sole driver

b)

Exercise acutely raises LDL during training

c)

Genetic clearance defect drives extreme LDL levels

d)

Obesity is the underlying cause of dyslipidemia

69.

With a zero-cholesterol diet, where does the patient’s high LDL primarily originate in familial hypercholesterolemia?

a)

Adipose tissue lipolysis during fasting

b)

Endogenous hepatic production with impaired clearance

c)

Increased chylomicron remnants after meals

d)

Excess intestinal absorption from plant sterols

70.

What immediate therapy strategy best addresses the runner’s condition?

a)

Aggressive pharmacotherapy with high-intensity statin

b)

Intermittent fasting as sole intervention

c)

Low-dose aspirin alone without lipid therapy

d)

Omega-3 supplements as monotherapy

71.

In the patient diagram, which combination most directly contributes to increased free fatty acid flux to the liver?

a)

Low-carbohydrate diet with fasting

b)

Normal BMI with insulin sensitivity

c)

High-protein diet with exercise

d)

Poorly controlled diabetes with obesity

72.

According to the pathophysiology diagram, insulin resistance most immediately causes which hepatic lipoprotein change?

a)

LDL receptor upregulation in muscle

b)

HDL hypersecretion from intestine

c)

VLDL overproduction by the liver

d)

Chylomicron clearance acceleration

73.

Which lipoprotein phenotype in the diagram is associated with higher atherogenic risk?

a)

Large, buoyant HDL particles

b)

Small, dense LDL particles

c)

Chylomicrons after meals

d)

IDL with high apoE content

74.

Which enzymatic activity is shown as reduced due to insulin resistance, impairing triglyceride-rich lipoprotein clearance?

a)

Lipoprotein lipase activity

b)

Hormone-sensitive lipase activity

c)

CETP transfer activity

d)

HMG-CoA reductase activity

75.

From the lipid panel, which parameter is flagged as very high at baseline?

a)

Triglycerides at 350 mg/dL

b)

LDL-C at 135 mg/dL

c)

Total cholesterol at 240 mg/dL

d)

HDL-C at 35 mg/dL

76.

After 6 months, which change best reflects improved cardiometabolic risk in the follow-up table?

a)

Triglycerides decreased to 145 mg/dL

b)

LDL-C increased to 160 mg/dL

c)

Total cholesterol unchanged at 240 mg/dL

d)

HDL-C decreased to 25 mg/dL

77.

Which management focus in the diagram is described as the cornerstone for treating secondary dyslipidemia?

a)

Add high-dose omega-3 therapy

b)

Increase refined carbohydrate intake

c)

Replace saturated fat with trans fat

d)

Improve diabetes control and exercise

78.

In the atherosclerosis diagram, what modification turns LDL-C into a form readily taken up by macrophages?

a)

Glycosylation of apoB-100

b)

Acetylation of HDL proteins

c)

Oxidative modification of LDL

d)

Phosphorylation of cholesterol

79.

What cell type forms foam cells after ingesting oxidized LDL in the depicted pathway?

a)

Macrophages in the intima

b)

Adipocytes in visceral fat

c)

Hepatocytes in the liver

d)

Enterocytes in the ileum

80.

What is the immediate vascular consequence shown after foam cell accumulation?

a)

Venous thrombosis development

b)

Capillary angiogenesis

c)

Arteriolar vasodilation

d)

Atherosclerotic plaque formation

81.

In the ASCVD progression diagram, which clinical event is linked to a vulnerable plaque rupture?

a)

Acute coronary syndrome

b)

Benign heart murmur

c)

Stable angina without thrombus

d)

Mitral valve prolapse

82.

Which feature along the plaque progression pathway indicates increased inflammatory activity?

a)

Myeloperoxidase elevation within plaque

b)

Reduced monocyte recruitment

c)

Decreased endothelial nitric oxide

d)

Lower plasma fibrinogen levels

83.

Which statement best explains why small, dense LDL elevates ASCVD risk compared with larger LDL?

a)

It has lower affinity for arterial proteoglycans

b)

It is cleared faster by hepatic LDL receptors

c)

It carries fewer apoB molecules overall

d)

It penetrates the intima and oxidizes readily

84.

Considering the baseline panel, which single intervention aligns with the diagrammed management to improve both TG and HDL?

a)

Weight loss with regular aerobic exercise

b)

Supplement-only approach without lifestyle

c)

High-fructose diet to boost energy

d)

Eliminating all dietary fat intake

85.

Which liver enzyme initiates primary bile acid synthesis from cholesterol?

a)

HMG‑CoA reductase

b)

CYP3A4

c)

CYP7A1

d)

Pancreatic lipase

86.

What is the main functional advantage of conjugating bile acids with glycine or taurine?

a)

Increases detergent activity

b)

Enhances bilirubin excretion

c)

Raises blood glucose

d)

Stimulates insulin secretion

87.

Which component forms micelles to emulsify dietary fat in the intestine?

a)

Phosphatases

b)

Bile salts

c)

Pepsin enzymes

d)

Lipoprotein lipase

88.

Where is bile primarily stored and concentrated before meals?

a)

Portal vein

b)

Gallbladder

c)

Pancreatic duct

d)

Ileal mucosa

89.

Which hormone chiefly triggers gallbladder contraction postprandially?

a)

Glucagon

b)

Secretin

c)

Cholecystokinin (CCK)

d)

Gastrin

90.

Approximately what percentage of bile salts is recycled during enterohepatic circulation?

a)

About 20%

b)

About 75%

c)

About 50%

d)

About 95%

91.

Which statement best describes enterohepatic circulation of bile salts?

a)

Pulmonary uptake then systemic release

b)

Direct secretion into lymphatic vessels

c)

Renal filtration then urinary loss

d)

Intestinal reabsorption with portal return

92.

Which major component makes up most of bile by volume?

a)

Cholesterol at forty percent

b)

Phospholipids at sixty percent

c)

Bile pigments at fifty percent

d)

Water at roughly ninety‑seven percent

93.

What is the amphipathic but less soluble product directly formed from cholesterol in the liver?

a)

Primary bile acids

b)

Triglycerides

c)

Very low‑density lipoproteins

d)

Ketone bodies

94.

Which pair correctly matches term roots with the affected site: cholangitis and cholecystitis?

a)

Bile duct inflammation; gallbladder inflammation

b)

Pancreas stones; liver inflammation

c)

Ileum obstruction; portal vein thrombosis

d)

Gallbladder stones; bile duct stones

95.

Cholelithiasis most accurately refers to which condition?

a)

Autoimmune destruction of hepatocytes

b)

Inflammation of the pancreatic duct

c)

Gallstone formation within biliary tract

d)

Infection of the ileal mucosa

96.

Which imbalance most predisposes to cholesterol gallstone formation?

a)

Low cholesterol with abundant bile acids

b)

Excess water with reduced electrolytes

c)

High bilirubin with excess phospholipids

d)

Too much cholesterol with fewer bile salts

97.

During fat digestion, how do bile salts enhance absorption?

a)

By hydrolyzing triglycerides directly

b)

By forming micelles around lipids

c)

By inhibiting pancreatic enzymes

d)

By raising gastric acid secretion

98.

Secretin primarily promotes which process in the biliary system?

a)

Gallstone dissolution by acids

b)

Bile secretion from hepatocytes

c)

Pancreatic zymogen activation

d)

Ileal peristalsis of bile salts

99.

Which route correctly traces bile flow from storage to intestinal lumen during digestion?

a)

Pancreas to Wirsung duct to jejunum

b)

Ileum to lymphatics to hepatic artery

c)

Liver to portal vein to pancreatic duct

d)

Gallbladder to cystic duct to common bile duct

100.

Which lipid parameter is the primary therapeutic target due to its atherogenic role?

a)

LDL cholesterol promoting plaque formation

b)

Total cholesterol concentration in plasma

c)

Triglycerides reflecting metabolic syndrome

d)

HDL cholesterol providing reverse transport

101.

Which LDL-C level is categorized as very high on a standard lipid panel?

a)

< 100 mg/dL indicating optimal

b)

130–159 mg/dL indicating borderline high

c)

160–189 mg/dL indicating high risk

d)

>= 190 mg/dL indicating severe risk

102.

An HDL-C value is considered a poor level in men when it is below which threshold?

a)

< 50 mg/dL increasing risk

b)

< 40 mg/dL increasing risk

c)

< 35 mg/dL increasing risk

d)

< 60 mg/dL increasing risk

103.

Which triglyceride range is classified as high and linked to acute pancreatitis risk when extreme?

a)

< 150 mg/dL protective level

b)

>= 500 mg/dL optimal level

c)

200–499 mg/dL high range

d)

150–199 mg/dL borderline high

104.

Total cholesterol on the lipid panel represents which sum?

a)

Triglycerides converted to cholesterol

b)

LDL, HDL, and VLDL combined

c)

LDL plus HDL only measured

d)

HDL and chylomicrons combined

105.

Which finding is a red flag suggesting a primary lipid disorder?

a)

Family history of late-life stroke

b)

Transient low HDL after illness

c)

LDL-C ≥190 mg/dL in screening

d)

Mildly elevated triglycerides after a meal

106.

A 12-year-old with tendon xanthomas and very high LDL cholesterol most likely has which diagnosis?

a)

Secondary dyslipidemia from hypothyroidism

b)

Niemann–Pick disease type C causing neurodegeneration

c)

Familial combined hyperlipidemia with high TGs

d)

Familial hypercholesterolemia due to LDLR mutation

107.

In untreated hypothyroidism, levothyroxine lowers LDL-C primarily by which mechanism?

a)

Increasing hepatic LDL receptor expression

b)

Enhancing lipoprotein lipase in adipose

c)

Inhibiting intestinal cholesterol absorption

d)

Upregulating HMG‑CoA reductase activity

108.

Which HDL-C level is considered optimal or better for cardiovascular protection?

a)

> 40–50 mg/dL favorable level

b)

< 35 mg/dL favorable level

c)

35–45 mg/dL favorable level

d)

>= 190 mg/dL favorable level

109.

Triglycerides ≥500 mg/dL raise immediate concern for which complication?

a)

Atherosclerotic plaque rupture events

b)

Acute pancreatitis due to hypertriglyceridemia

c)

Gallstone formation from cholesterol supersaturation

d)

Fatty liver cirrhosis in childhood

110.

In fatty acid oxidation defects like MCAD deficiency, which fasting presentation is typical?

a)

Severe hypertriglyceridemia without symptoms

b)

Hypoketotic hypoglycemia during illness

c)

Hyperketotic hyperglycemia after short fast

d)

Elevated HDL-C with normal triglycerides

111.

Which standard lipid panel threshold defines optimal LDL-C?

a)

130–159 mg/dL optimal category

b)

160–189 mg/dL optimal category

c)

< 100 mg/dL optimal category

d)

>= 190 mg/dL optimal category

112.

Which protein is defective in Tangier disease, leading to impaired cholesterol efflux from cells?

a)

ABCA1 transporter protein

b)

SR-BI receptor protein

c)

ApoB structural protein

d)

LCAT catalytic enzyme

113.

In Tangier disease, what lipid profile finding best supports the diagnosis?

a)

Elevated triglyceride levels

b)

Markedly high LDL levels

c)

Normal HDL with high apoA-I

d)

Markedly low HDL levels

114.

What is the immediate consequence when ABCA1 function is lost in peripheral cells?

a)

VLDL cannot be secreted by the liver

b)

LDL cannot deliver cholesterol to cells

c)

Nascent HDL cannot acquire cholesterol

d)

Triglycerides cannot be stored in adipocytes

115.

Which clinical feature is classically associated with Tangier disease?

a)

Orange enlarged tonsils

b)

Xanthomas over elbows

c)

Corneal arcus in youth

d)

Kayser–Fleischer rings

116.

Reverse cholesterol transport primarily depends on which process that is disrupted in Tangier disease?

a)

Cholesterol loading onto nascent HDL

b)

Cholesterol ester hydrolysis by CEH

c)

LDL receptor–mediated endocytosis

d)

Bile acid–dependent micelle formation

117.

Lysosomal storage diseases share what core pathophysiologic mechanism?

a)

Excess beta-oxidation in mitochondria

b)

Increased lipoprotein lipase activity

c)

Overproduction of simple fatty acids

d)

Failure to degrade complex lipids

118.

Which enzyme deficiency causes Tay-Sachs disease?

a)

Beta-glucocerebrosidase deficiency

b)

Alpha-galactosidase A deficiency

c)

Hexosaminidase A deficiency

d)

Sphingomyelinase deficiency

119.

Gaucher disease results from a deficiency of which enzyme?

a)

Beta-glucocerebrosidase

b)

Alpha-galactosidase A

c)

Hexosaminidase A

d)

Sphingomyelinase

120.

Niemann–Pick disease is most directly linked to a deficiency in which enzyme?

a)

Apolipoprotein E

b)

Beta-glucocerebrosidase

c)

Hexosaminidase A

d)

Sphingomyelinase

121.

Fabry disease involves accumulation of globotriaosylceramide due to deficiency of which enzyme?

a)

Alpha-galactosidase A

b)

Hexosaminidase A

c)

Sphingomyelinase

d)

Beta-glucocerebrosidase

122.

What accumulated substrate characterizes Tay-Sachs disease?

a)

Triglyceride in lysosomes

b)

GM2 ganglioside in neurons

c)

Cholesteryl esters in macrophages

d)

Ceramide in hepatocytes

123.

A patient with hepatosplenomegaly and bone pain is suspected of having Gaucher disease. Which substrate accumulates?

a)

Glucocerebroside in macrophages

b)

GM2 ganglioside in neurons

c)

Sphingomyelin in hepatocytes

d)

Globotriaosylceramide in endothelium

124.

Which statement best differentiates lysosomal storage diseases from fatty acid beta-oxidation defects?

a)

LSDs increase LDL uptake; FAO defects increase HDL synthesis

b)

LSDs cause hyperketotic hypoglycemia; FAO defects cause anemia

c)

LSDs impair lipid recycling; FAO defects impair energy generation

d)

LSDs raise ketones; FAO defects lower ketones

125.

Medium-chain acyl-CoA dehydrogenase (MCAD) deficiency typically presents with which metabolic pattern during fasting?

a)

Hypoketotic hypoglycemia

b)

Normoketotic euglycemia

c)

Hyperketotic hypoglycemia

d)

Hyperketotic hyperglycemia

126.

Which transport step is necessary for reverse cholesterol transport and is defective in Tangier disease?

a)

SR-BI–mediated HDL uptake by liver

b)

ABCA1-mediated efflux to nascent HDL

c)

LDL receptor internalization in hepatocytes

d)

LCAT-mediated cholesterol ester formation

127.

In lysosomal storage diseases, what cellular outcome results from persistent undegraded lipid accumulation?

a)

Cell dysfunction and eventual death

b)

Enhanced beta-oxidation capacity

c)

Rapid cholesterol export to HDL

d)

Increased mitochondrial biogenesis

128.

Which lysosomal storage disease most classically presents with a cherry-red spot in the macula and lacks hepatomegaly?

a)

Fabry with angiokeratomas

b)

Niemann–Pick with hepatosplenomegaly

c)

Tay–Sachs with neurodegeneration

d)

Gaucher disease with bone crises

129.

In Tay–Sachs disease, deficiency of which enzyme leads to GM2 ganglioside accumulation in neurons?

a)

Alpha-galactosidase A deficiency

b)

Beta-hexosaminidase A deficiency

c)

Glucocerebrosidase deficiency

d)

Sphingomyelinase deficiency

130.

Which accumulated lipid is characteristic of Gaucher disease?

a)

Globotriaosylceramide in vessels

b)

GM2 ganglioside in neurons

c)

Glucocerebroside in macrophages

d)

Sphingomyelin in lysosomes

131.

A patient has hepatosplenomegaly and poor muscle control due to lysosomal storage. Which enzyme is most likely deficient?

a)

Hexosaminidase A in neurons

b)

Alpha-galactosidase A in endothelium

c)

Sphingomyelinase in macrophages

d)

Glucocerebrosidase in bone

132.

Which clinical feature pair best matches Gaucher disease?

a)

Hepatosplenomegaly and bone crises

b)

Neurodegeneration and poor muscle control

c)

Peripheral neuropathy and renal failure

d)

Cherry-red macula and no hepatomegaly

133.

Which disease involves alpha-galactosidase A deficiency leading to GL-3 accumulation?

a)

Gaucher with glucocerebroside

b)

Tay–Sachs with GM2 storage

c)

Niemann–Pick with sphingomyelin

d)

Fabry with globotriaosylceramide

134.

Which lysosomal storage disease typically features 'crumpled tissue paper' macrophages?

a)

Fabry angiokeratoma lesions

b)

Tay–Sachs neurodegenerative inclusions

c)

Gaucher with Gaucher cells

d)

Niemann–Pick foamy cells

135.

Which therapeutic approach directly replaces the missing lysosomal enzyme?

a)

Dietary restriction of sphingolipids

b)

Gene therapy correcting mutations

c)

Bone marrow transplantation alone

d)

Enzyme replacement therapy (ERT)

136.

What pathologic change in neurons is depicted in Tay–Sachs disease images?

a)

Swollen neurons with lamellar inclusions

b)

Ischemic necrosis with edema

c)

Axonal demyelination with plaques

d)

Neuronal apoptosis with microglia

137.

Which disease listed commonly causes angiokeratomas and progressive renal failure?

a)

Fabry due to GL-3 accumulation

b)

Gaucher due to bone crises

c)

Niemann–Pick with poor muscle control

d)

Tay–Sachs with cherry-red spot

138.

A child with neurodegeneration and a cherry-red macula but normal liver size most likely has accumulation of which substrate?

a)

GL-3 in endothelium

b)

GM2 ganglioside in neurons

c)

Sphingomyelin in hepatocytes

d)

Glucocerebroside in macrophages

139.

Which pair correctly matches the deficient enzyme with the disease causing hepatosplenomegaly and neurodegeneration?

a)

Hexosaminidase A in Tay–Sachs

b)

Glucocerebrosidase in Gaucher

c)

Alpha-galactosidase A in Fabry

d)

Sphingomyelinase in Niemann–Pick

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