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Review of Pharmacology - 9E (2015)

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<strong>Review</strong> <strong>of</strong> <strong>Pharmacology</strong><br />

8. Ans. (b) It results in decrease in reticulocyte count (Ref: Katzung 10/e p537-538;KDT 6/e p592)<br />

• Erythropoietin is a hematopoietic growth factor that is normally produced by the kidneys.<br />

• Normally, there is an inverse relationship between serum erythropoietin levels and hemoglobin levels. When<br />

Hb decreases and anemia becomes more severe, serum erythropoietin level increases exponentially. But,<br />

anemia due to chronic renal failure is an exception to this inverse relationship. In CRF, erythropoietin is not<br />

produced, that results in anemia. So, exogenous erythropoietin will markedely improve anemia in CRF patients<br />

whereas there is less likelihood <strong>of</strong> response in other anemias.<br />

• Erythropoietin consistently improves the hematocrit and Hb levels and usually eliminates the need <strong>of</strong> blood<br />

transfusions in CRF patients.<br />

• An increase in reticulocyte count is usually observed in 10 days and increase in hematocrit and Hb levels in<br />

about 2-6 weeks.<br />

Hematology<br />

9. Ans. (b) Folic acid alone causes improvement <strong>of</strong> anemic symptoms but neurological dysfunction continues (Ref: Katzung<br />

10/e p532; KDT 6/e p591)<br />

• Vitamin B 12<br />

is required for conversion <strong>of</strong> methionine to homocysteine and for formation <strong>of</strong> succinyl CoA from methylmalonyl<br />

CoA.<br />

• Deficiency <strong>of</strong> vitamin B 12<br />

results in megaloblastic anemia, GI manifestations and neurological abnormalities (due to<br />

demyelination).<br />

• Folic acid alone will correct the symptoms <strong>of</strong> megaloblastic anemia but it does not prevent neurological abnormalities,<br />

which continue to proceed.<br />

• Neurological abnormalities manifests intially in the form <strong>of</strong> loss <strong>of</strong> posterior column sensations (vibration, proprioception<br />

etc.), but later on can result in subacute combined degeneration <strong>of</strong> spinal cord.<br />

10. Ans. (a) Neutropenia (Ref: Katzung’s 11/e p580-581)<br />

• Filgrastim (G-CSF) and sargramostim (GM-CSF) are used to prevent or treat chemotherapy induced neutropenia.<br />

• Erythropoietin is used to treat anemia associated with chronic renal failure and cancer chemotherapy.<br />

• Oprelvekin (1L-11) is used to prevent and treat thrombocytopenia.<br />

11. Ans. (b) Oral Deferiprone (Ref: KDT 6/e p868)<br />

• Drug <strong>of</strong> choice for acute iron poisoning is desferrioxamine, however it has to be administered parenterally. It is not<br />

effective by oral route.<br />

• In beta thalassemia major, iron excess can result due to repeated blood transfusions and massive hemolysis. Chelating<br />

agent has to be administered for long time in this case. Therefore, oral Deferiprone is preferred in this case.<br />

12. Ans. (a) Duodenum and upper jejunum (Ref: KK Sharma 2007/675, Katzung 11/e p/571)<br />

• Maximum iron absorption occurs in duodenum and proximal jejunum.<br />

• Vitamin B 12<br />

is absorbed in distal ileum whereas folic acid is absorbed in proximal jejunum.<br />

13. Ans. (c) Erythropoietin (Ref: KDT 6/e p592)<br />

Chronic renal failure may result in anemia due to deficient production <strong>of</strong> erythropoietin.<br />

14. Ans. (a) Cannot be injected i.v. (Ref: KDT 6/e p586)<br />

Iron sorbitol citrate should not be used i.v. because it may rapidly saturate the transferrin receptors and can result in high<br />

concentrations <strong>of</strong> free iron.<br />

15. Ans. (a) Conversion <strong>of</strong> malonic acid to succinic acid (Ref: KDT 6/e p588)<br />

Conversion <strong>of</strong> malonic acid to succinic acid requires vitamin B 12<br />

but not folate. This reaction is required for myelin formation<br />

and deficiency <strong>of</strong> B 12<br />

is responsible for demyelination.<br />

16. Ans. (b) Counteracting toxicity <strong>of</strong> high dose methotrexate therapy (Ref: KDT 6/e p592)<br />

• Prophylaxis <strong>of</strong> neural tube defects require treatment with folic acid.<br />

• Methotrexate toxicity can be prevented by 5′-formyltetrahydr<strong>of</strong>olate (folinic acid).<br />

• Pernicious anemia requires the therapy with vitamin B 12<br />

.<br />

• Anemia associated with chronic renal failure is treated with erythropoietin.<br />

460<br />

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