MLT GlobeChemistry: Lipids – page 5
107 Chemistry MCQs on Lipids with answers and explanations.
A cholesterol sample was drawn after the tourniquet had been in place for 5 minutes. The result will most likely be:
Prolonged stasis forces water out of the vein while large particles such as lipoproteins stay, so cholesterol can rise by 5–10% or more. Tourniquet time should be kept under 1 minute.
A child with fat malabsorption, ataxia, acanthocytes on the blood film, very low cholesterol and absent apolipoprotein B most likely has a defect in:
Abetalipoproteinemia results from MTP deficiency, so apo B lipoproteins (chylomicrons, VLDL, LDL) cannot be assembled. Fat-soluble vitamin E deficiency causes the neurological signs.
PCSK9 inhibitor drugs lower LDL cholesterol because PCSK9 normally:
PCSK9 binds the LDL receptor and directs it to lysosomes for destruction. Blocking PCSK9 leaves more receptors on liver cells to clear LDL. Gain-of-function PCSK9 mutations cause familial hypercholesterolemia.
Serum triglycerides are 177 mg/dL. Using 1 mmol/L = 88.5 mg/dL, what is the result in SI units?
177 ÷ 88.5 = 2.0 mmol/L. Dividing by 38.67 (the cholesterol factor) gives the wrong answer of 4.6 mmol/L.
Total cholesterol is 5.8 mmol/L, HDL cholesterol 1.1 mmol/L and measured LDL cholesterol 3.6 mmol/L. What is the remnant cholesterol (TC − HDL − LDL)?
5.8 − 1.1 − 3.6 = 1.1 mmol/L, the cholesterol carried in triglyceride-rich lipoproteins (VLDL, IDL, remnants). 4.7 mmol/L is the non-HDL cholesterol.
A child with edema, urine protein 5 g/day and serum albumin 1.8 g/dL (18 g/L) has cholesterol 380 mg/dL (9.8 mmol/L). The main mechanism of the high cholesterol is:
In nephrotic syndrome the liver increases synthesis of albumin and apo B lipoproteins in response to low oncotic pressure; reduced clearance also contributes. It is a secondary, not a primary, hyperlipidemia.
In the enzymatic cholesterol method, cholesterol oxidase converts free cholesterol to cholest-4-en-3-one and:
Cholesterol oxidase uses oxygen and produces hydrogen peroxide, which peroxidase then uses to form a colored dye. Free fatty acids are released earlier by cholesterol esterase.
Serum triglycerides are 3000 mg/dL (34 mmol/L). Sodium is 124 mmol/L by indirect ISE and 139 mmol/L by direct ISE on a blood gas analyzer. The best explanation is:
Indirect ISE dilutes the sample and assumes normal plasma water; large lipid volumes reduce the water fraction, causing pseudohyponatremia. Direct ISE measures activity in plasma water and is not affected.
Cholesteryl ester transfer protein (CETP) moves cholesteryl esters from HDL to:
CETP exchanges cholesteryl ester from HDL for triglyceride from VLDL and LDL. Low CETP activity is associated with high HDL cholesterol.
An adult man has an HDL cholesterol of 30 mg/dL (0.78 mmol/L). How is this result interpreted?
An HDL cholesterol below 40 mg/dL (1.0 mmol/L) is classified as low and is a recognised risk factor for coronary heart disease.
An adult's LDL cholesterol is 195 mg/dL (5.0 mmol/L). By NCEP ATP III categories this is:
NCEP ATP III classifies LDL of 190 mg/dL (4.9 mmol/L) or more as very high. Optimal is below 100 mg/dL and borderline high is 130–159 mg/dL.
A patient forgot to fast before a lipid profile. Which result is least affected by the recent meal?
Total cholesterol changes very little after a meal, whereas triglycerides and chylomicrons rise, and Friedewald LDL is calculated from triglycerides so it is also affected.
Series-1 prostaglandins (e.g., PGE1) come from dihomo-γ-linolenic acid. Which dietary essential fatty acid is its ultimate source?
Linoleate (ω-6) is desaturated and elongated to dihomo-γ-linolenate, giving series-1 eicosanoids, then arachidonate (series 2). ω-3 EPA gives series 3.
Eicosapentaenoic acid (EPA, 20:5 ω-3) from fish oil is also known as:
Timnodonic acid is EPA. Arachidonic acid is 20:4, clupanodonic 22:5 and nervonic 24:1.
Long-chain fatty acids enter muscle and adipose cells largely through:
Fatty acids released from albumin are taken up mainly by membrane proteins such as CD36 and FATPs, with some passive flip-flop. No ATPase pumps them, and albumin itself is not internalised.
Every biologically active prostaglandin contains a trans double bond between carbons:
The Δ13 trans double bond is common to all active prostaglandins. The 5,6 double bond is found only in series-2, and the 17,18 bond only in series-3 prostaglandins.
Which membrane lipids, abundant in plant chloroplasts, have a sugar joined by a glycosidic bond directly to glycerol?
Galactolipids carry galactose linked directly to C-3 of diacylglycerol. Sphingolipids use a sphingosine backbone, and phosphoglycerides link head groups through phosphate.
α-Oxidation removes one carbon from the carboxyl end of branched fatty acids. Its defect causes accumulation of phytanic acid in:
Phytanic acid's β-methyl group blocks β-oxidation, so α-oxidation (in peroxisomes, notably in nervous tissue) must act first. Tay–Sachs and Gaucher are lysosomal storage diseases; MCAD affects β-oxidation.
A child has large orange tonsils, hepatosplenomegaly and almost no plasma HDL. Mutation of which gene is most likely?
Tangier disease is autosomal recessive ABCA1 deficiency. Cholesterol cannot be exported to apoA-I, so HDL is barely detectable and cholesteryl esters build up in tissues.
Using current P/O ratios (2.5 per NADH, 1.5 per FADH2), what is the net ATP yield from complete oxidation of one stearic acid (C18:0)?
Eight beta-oxidation cycles give 8 FADH2, 8 NADH and 9 acetyl-CoA: 12 + 20 + 90 = 122 ATP. Subtracting 2 for activation gives 120.