MLT GlobeChemistry: TDM, toxicology & vitamins – page 4
109 Chemistry MCQs on TDM, toxicology & vitamins with answers and explanations.
Pantothenic acid forms part of coenzyme A and of the acyl carrier protein used in:
Its 4′-phosphopantetheine arm is the acyl carrier of fatty acid synthase. Pyruvate carboxylase uses biotin, and glycolysis needs no CoA.
The yellow colour of egg yolk is due mainly to:
Yolk colour comes from dietary xanthophylls (lutein, zeaxanthin) deposited by the hen. Riboflavin gives only a faint greenish-yellow tint, mostly to the egg white.
Erythrocyte transketolase activity, with and without added TPP, is used to assess nutritional status of:
Transketolase needs thiamine pyrophosphate; a large rise in activity when TPP is added indicates thiamine deficiency. Riboflavin status is tested with erythrocyte glutathione reductase.
The Schilling test has been withdrawn. Which test is now used to show pernicious anaemia as the cause of B12 deficiency?
Intrinsic factor antibodies are highly specific for pernicious anaemia; parietal cell antibodies are more sensitive but less specific. Ferritin, electrophoresis and osmotic fragility investigate other anaemias.
A patient has paraesthesia, loss of vibration sense, macrocytic anaemia and raised methylmalonic acid. The likely deficiency is:
Subacute combined degeneration with raised MMA indicates B12 deficiency. Folate deficiency causes similar anaemia but normal MMA and no dorsal column disease.
Which one-carbon unit is NOT carried by tetrahydrofolate?
Tetrahydrofolate carries formyl, methenyl, methylene and methyl groups. CO2 is carried by biotin in carboxylation reactions.
A patient has a microcytic anaemia, and ring sideroblasts are seen on the iron-stained marrow. Lack of which vitamin can impair haem synthesis in this way?
Pyridoxal phosphate is the cofactor for ALA synthase, the first step of haem synthesis. B12 deficiency causes megaloblastic, not sideroblastic, anaemia.
In collagen synthesis, vitamin C is the cofactor for hydroxylating which amino acid residue?
Prolyl and lysyl hydroxylases need ascorbate to keep their iron reduced. Without it, collagen is unstable and scurvy develops. Glycine is abundant in collagen but is not hydroxylated.
A patient on long-term broad-spectrum antibiotics has a prolonged PT. Loss of which vitamin-dependent step best explains this?
Vitamin K is the cofactor for gamma-carboxylating factors II, VII, IX and X. Gut bacteria supply some vitamin K, so antibiotics can cause deficiency.
Which fat-soluble vitamin acts as a membrane antioxidant alongside the selenium-containing enzyme glutathione peroxidase?
Vitamin E breaks lipid-peroxidation chains in membranes. Selenium-dependent glutathione peroxidase removes peroxides, so the two nutrients spare each other.
'Burning feet' paraesthesia in prisoners of war was linked to deficiency of which B vitamin?
Experimental and wartime pantothenate deficiency caused burning feet together with fatigue and GI upset. Isolated deficiency is rare because the vitamin is found in most foods.
Which functional group is attached to the pyridine ring of nicotinic acid (niacin)?
Nicotinic acid is pyridine-3-carboxylic acid. Its amide, nicotinamide, is the form built into NAD+ and NADP+.
A young adult with liver disease and neuropsychiatric symptoms is suspected of Wilson disease. Which serum finding supports this?
Wilson disease (ATP7B defect) impairs copper incorporation into ceruloplasmin and biliary excretion, so ceruloplasmin is low while urinary copper rises.
Which of the following is NOT a recognized treatment for Wilson disease?
Penicillamine and trientine chelate copper, and zinc blocks intestinal copper absorption by inducing metallothionein. Potassium iodide is used for thyroid conditions, not copper overload.
Digoxin toxicity is more likely at a given serum digoxin level when the patient has:
Digoxin and potassium compete for the same site on the Na-K ATPase. Low potassium increases digoxin binding and its toxic effects, so potassium is checked with digoxin levels.
For an aminoglycoside given as a 30-minute IV infusion, the peak level is usually drawn:
Waiting about 30 minutes after the end of the infusion allows distribution to finish. A sample just before the dose is a trough, not a peak.
A drug level is 40 mg/L at 08:00 and 10 mg/L at 16:00, with no dose in between. The half-life is:
40 to 20 is one half-life and 20 to 10 is a second, so two half-lives took 8 hours. Each half-life is therefore 4 hours.
A patient on lithium has a very high result with no signs of toxicity. The sample was collected in a green-top tube. The most likely cause is:
Lithium heparin tubes add lithium to the sample and falsely raise the result. Lithium should be measured in serum or a lithium-free tube, about 12 hours after the last dose.
A patient with low albumin has toxic signs while the total phenytoin level is within range. The best next test is:
Phenytoin is about 90% protein-bound; with low albumin or uremia the free, active fraction rises. Free phenytoin reflects the true effect better than total.
Methotrexate levels are monitored after high-dose therapy mainly to decide:
Delayed methotrexate clearance leads to severe toxicity; timed levels guide how much and how long leucovorin (folinic acid) is given.