Which of the following statements about prostaglandins is most accurate?
AThey are derived from cholesterol
BThey are derived from 20-carbon polyunsaturated fatty acids (arachidonic acid)
CThey are amino acid derivatives
DThey are carbohydrate-based molecules
Correct Answer:
B. They are derived from 20-carbon polyunsaturated fatty acids (arachidonic acid)
EXPLANATION
Prostaglandins are eicosanoids derived from arachidonic acid (20-carbon polyunsaturated fatty acid). They act as paracrine and autocrine signaling molecules.
A patient with severely elevated serum triglycerides (>1000 mg/dL) is at immediate risk of:
AOnly hypercholesterolemia
BAcute pancreatitis
CPeripheral neuropathy
DMyocardial infarction only
Correct Answer:
B. Acute pancreatitis
EXPLANATION
Severe hypertriglyceridemia (>1000 mg/dL) significantly increases the risk of acute pancreatitis due to pancreatic inflammation caused by triglyceride-rich lipoproteins.
Which of the following correctly describes the role of carnitine in fatty acid metabolism?
AIt synthesizes fatty acids
BIt transports long-chain fatty acids across the mitochondrial membrane
CIt activates fatty acids to acyl-CoA
DIt directly oxidizes fatty acids
Correct Answer:
B. It transports long-chain fatty acids across the mitochondrial membrane
EXPLANATION
Carnitine, via carnitine palmitoyltransferase (CPT), transfers long-chain fatty acyl groups across the inner mitochondrial membrane, enabling their oxidation in the matrix.
What is the primary product of the initial step of ketogenesis?
AAcetoacetate
BAcetyl-CoA
CBeta-hydroxybutyrate
DAcetone
Correct Answer:
A. Acetoacetate
EXPLANATION
Acetoacetate is the first ketone body formed from two molecules of Acetyl-CoA via HMG-CoA synthase. It can be reduced to beta-hydroxybutyrate or decarboxylated to acetone.
In the condition of hypertriglyceridemia with normal LDL levels, which genetic defect is most likely?
ALDL receptor deficiency
BLipoprotein lipase or apoC-II deficiency
CCETP deficiency
DApoB gene mutation
Correct Answer:
B. Lipoprotein lipase or apoC-II deficiency
EXPLANATION
Deficiency of lipoprotein lipase or its cofactor apoC-II results in severe hypertriglyceridemia with elevated chylomicrons and VLDL but relatively normal LDL levels.
Myelin contains approximately 80% lipid by weight, with cholesterol being the most abundant lipid (27% of total myelin mass), followed by galactocerebroside.
Which of the following best explains the inverse relationship between LDL and HDL cholesterol in atherogenesis?
ALDL deposits cholesterol while HDL removes it from arterial walls
BThey compete for the same enzyme
CHDL synthesis inhibits LDL synthesis
DBoth have the same apolipoprotein composition
Correct Answer:
A. LDL deposits cholesterol while HDL removes it from arterial walls
EXPLANATION
LDL carries cholesterol into arterial walls and can be oxidized, promoting atherosclerosis. HDL mediates reverse cholesterol transport, removing cholesterol from tissues and delivering it to the liver.
Tangier disease is associated with deficiency of which protein?
AApoA-I
BABCA1 transporter
CLipoprotein lipase
DApoB-100
Correct Answer:
B. ABCA1 transporter
EXPLANATION
Tangier disease results from mutations in the ABCA1 gene, which encodes a cholesterol transporter. This leads to severe HDL deficiency and accumulation of cholesterol esters in tissues.
Which of the following statements about saturated fatty acids is correct?
AThey have lower melting points than unsaturated fatty acids
BThey are liquid at room temperature
CThey lack double bonds and are more prone to oxidation
DThey enhance HDL cholesterol levels
Correct Answer:
A. They have lower melting points than unsaturated fatty acids
EXPLANATION
Saturated fatty acids have higher melting points and are typically solid at room temperature due to tight packing. They are more stable and less prone to oxidation than unsaturated fatty acids.
