Hematology Quiz | Practice MCQ #mcq.ImBooz

• (A) Iron deficiency
• (B) Pregnancy
• (C) Hypoxia
• (D) Alkaline pH of stomach

Check AnswerSolution[D]:-Alkaline pH of stomach

• (A) Oxalates
• (B) Ascorbate
• (C) Phytates
• (D) Phosphates

Check AnswerSolution[B]:-These reducing substances in diet will lead to increased iron absorption. Hydroquinone, lactate, ascorbate, pyruvate, succinate, fructose, cysteine and sorbitol.

• (A) Increased TIBC
• (B) Decreased S. iron
• (C) Decreased S. ferritin
• (D) Decreased % saturation

Check AnswerSolution[C]:-Decreased S. ferritin

• (A) If 300 mg elemental iron given only 100 mg gets absorbed
• (B) Reticulocytosis appears in 1-2 weeks and then peaks in 3-4 weeks
• (C) Hemoglobin levels are usually corrected in 6 weeks after starting therapy
• (D) Decrease in absorption of iron with improvement of Hb

Check AnswerSolution[D]:-Decrease in absorption of iron with improvement of Hb

• (A) Anemia of chronic disease
• (B) Sideroblastic anemia
• (C) Iron deficiency anemia
• (D) Thalassemia major

Check AnswerSolution[B]:-Sideroblastic anemia

• (A) Esophageal web in post-cricoid region
• (B) Iron deficiency
• (C) Koilonychia
• (D) Gum Hypertrophy

Check AnswerSolution[D]:-Gum Hypertrophy

• (A) Liver disease
• (B) Copper deficiency
• (C) Thiamine deficiency
• (D) Orotic aciduria

Check AnswerSolution[B]:-Microcytic hypochromic anemia is caused due to copper deficiency. Rest other conditions are associated with macrocytic anemia. Copper deficiency is unresponsive to iron therapy and is associated with hypoferrimia, neutropenia and usually the presence of vacuolated erythroid precursors in the bone marrow.

• (A) Low EPO level
• (B) Decreased RBC renewal
• (C) Decreased RBC supply
• (D) Decreased plasma volume

Check AnswerSolution[D]:-Decreased plasma volume

• (A) Polycythemia vera
• (B) Renal failure
• (C) AIHA
• (D) Anemia of chronic disease

Check AnswerSolution[C]:-AIHA

• (A) Negative iron balance
• (B) Decreased iron stores
• (C) Decrease MCV
• (D) Decrease in Hemoglobin

Check AnswerSolution[A]:-Negative iron balance

• (A) Treatment should be given with alongwith vitamin C
• (B) Enteric coated and prolonged release preparations should be given
• (C) Best given after meals
• (D) Maximum dose is 200 mg of elemental iron/day

Check AnswerSolution[D]:-Maximum dose is 200 mg of elemental iron/day

• (A) Pregnancy
• (B) Chronic inflammation
• (C) Iron overload
• (D) Phosphates

Check AnswerSolution[A]:-Pregnancy

• (A) It is low in anemia of chronic disease
• (B) Raised in hemochromatosis
• (C) Transported by ferritin
• (D) Shows a diurnal variation

Check AnswerSolution[C]:-Physiologically, the serum iron concentration has a diurnal rhythm; it decreases in late afternoon and evening, reaching a nadir near 9:00 pm and increases to its maximum between 7:00 am and 10:00 pm. Iron is transported by Transferrin in Fe3+ form and not by Ferritin (Storage protein for iron).

• (A) Cyanosis due to abnormal Hb is inherited as autosomal recessive trait
• (B) Cyanosis due to NADH diaphorase deficiency is inherited as autosomal recessive trait
• (C) Most accurate method of diagnosing methemoglobinemia is by spectrophotometric analysis
• (D) Hereditary methemoglobinemia due to NADH-diaphorase deficiency is readily treated by ascorbic acid

Check AnswerSolution[A]:-Methemoglobinemia is due to abnormal Hb and NADH-diaphorase deficiency which is autosomal dominant and autosomal recessive, respectively. Can be misinterpreted when automated instruments designed to estimate levels of reduced Hb, oxygenated Hb, Met Hb and Carboxy Hb are used. Direct spectrophotometric analysis is required to diagnose methemoglobinemia or sulphemoglobinemia. For hereditary methemoglobinemia due to NADH diaphorase deficiency, treatment is ascorbic acid, 300-600 mg/day. Acute toxic methemoglobinemia is treated with methylene blue. NADPH rapidly reduces Methylene blue to Leukomethylene blue which nonenzymatically reduce Met Hb to Hb.Dose is 1-2 mg/kg over 5 min for rapid action. Cimetidine is a selective inhibitor of M-hydroxylation, so it is used in methemoglobinemia produced by dapsone. Unlike methemoglobinemia sulph hemoglobin cannot be converted to Hb

• (A) Methemoglobinuria
• (B) Methemoglobinemia
• (C) CDA
• (D) Carboxyhemoglobinemia

Check AnswerSolution[B]:-Methemoglobinemia can occur due to abnormal Hb (called Hb-M) or due to deficiency of NADH – diaphorase. In most Hb-M tyrosine is substituted for either proximal or distal histidine and this tyrosine can form iron – phenolate complex that resist reduction to divalent iron state by the. NADH-diaphorase engyme.

• (A) Sulfonamide
• (B) Chloroquine
• (C) Dapsone
• (D) All of the above

Check AnswerSolution[D]:-Acquired methemoglobinemia can be caused due to multiple drugs and toxins including aniline dyes, benzene, chloroquine, dapsone, local anesthetic agents, reglan, primaquine, phenazopyridine, sulphonamides, acetanilid, alloxan, benzocaine, bivalent copper, bismuth subnitrate, bupivacaine hydrochloride, chlorates, chloroquine, chromates, clofazimine, dimethyl sulfoxide, dinitrophenol, exhaust fumes, ferricyanide, flutamide, hydroxylamine, lidocaine hydrochloride, metoclopramide, methylene blue, naphthalene, nitrates, nitric oxide, nitrites, nitrofuran, nitroglycerin, sodium nitroprusside, phenacetin, phenazopyridine hydrochloride, phenytoin, prilocaine, rifampin, silver nitrate, sodium valproate, smoke inhalation and sulfasalazine trinitrotoluene. Hemoglobin M is used to designate several variants of abnormal hemoglobin associated with genetic methemoglobinemia. In most of the hemoglobin M, tyrosine has been substituted for either the proximal or the distal histidine. This results in reduced capacity of the enzymatic machinery of the erythrocyte to efficiently reduce the iron to the divalent form and thus predisposes to methemoglobinemia. These hemoglobin variants are associated with cyanosis, which is present from early life.

• (A) Cyanosis
• (B) Hemolysis
• (C) Normal PaO2 in arterial blood gas analysis
• (D) All of the above

Check AnswerSolution[D]:-Methemoglobinemia may be acute or chronic. The physiologic level of methemoglobin in the blood is 0% to 2%. Methemoglobin concentrations of 10% to 20% are tolerated well, but levels above this are often associated with symptoms. Levels above 70% may cause death. Symptoms also depend on the rapidity of its formation. Many patients with lifelong methemoglobinemia are asymptomatic, but patients exposed to drugs and toxins who abruptly develop the same levels of methemoglobinemia may be severely symptomatic. Dyspnea, nausea, and tachycardia occur at methemoglobin levels of 30% or more. Lethargy, stupor, and deteriorating consciousness occur as methemoglobin levels approach 55%. Higher levels may cause cardiac arrhythmias and circulatory failure. Druginduced methemoglobinemia may be followed by Hemolytic anemia especially with exposure to dapsone, sulfasalazine, or phenacetin. Heinz bodies (precipitated hemoglobin or globin subunits due to denaturation of hemoglobin in erythrocytes) and fragmented red blood cells characterize this type of anemia. Acute intravascular hemolysis may occasionally lead to renal failure. Blood containing high concentrations of methemoglobin appears chocolate brown. Subjects with methemoglobinemia may have normal partial pressures of oxygen, despite life-threatening methemoglobinemia. The oxygen saturation values, measured by a pulse oximeter, are falsely elevated.

• (A) Exchange transfusion
• (B) Hyperbaric oxygen
• (C) Methylene blue
• (D) Dialysis

Check AnswerSolution[C]:-The possible diagnosis of methemoglobinemia should be suspected because the patient is cyanosed, the cyanosis is unresponsive to ventilation, there is no prior history of respiratory problems, and the patient had been exposed to a topical anesthetic that is known to cause methemoglobinemia. Cyanosis, low hemoglobin oxygen saturation on pulse oximetry (typically 85-89% representing the absorbance spectrum of methemoglobin), normal PaO2 on ABG, “chocolate blood”. (Methemoglobinemia does not change color with the addition of oxygen whereas dark blood due to deoxyhemoglobin will turn red with oxygen).Co-oximetry of ABG will quantify the percent of methemoglobinemia in a fresh arterial sample. For methemoglobinemia due to drug exposure, traditional first-line therapy consists of an infusion of methylene blue (1%; 1-2 mg/kg IV over 5 minutes), whose action depends on the availability of reduced nicotinamide adenine nucleotide phosphate (NADPH) within the red blood cells. After an acute exposure to an oxidizing agent, treatment should be considered when the methemoglobin is 30% in an asymptomatic patient and 20% in a symptomatic patient. Patients with anemia or cardiorespiratory problems should be treated at lower levels of methemoglobin. Dextrose should be given because the major source of NADH in the red blood cells is the catabolism of sugar through glycolysis. Dextrose is also necessary to form NADPH through the hexose monophosphate shunt, which is necessary for methylene blue to be effective. Exchange transfusion is reserved for patients in whom methylene blue therapy is ineffective.

• (A) Primaquine
• (B) Chloroquine
• (C) Pyrimethamine
• (D) Quinine

Check AnswerSolution[C]:-Pyrimethamine

• (A) G6PD deficiency
• (B) P K deficiency
• (C) Triosephosphate isomerase deficiency
• (D) None of the above

Check AnswerSolution[B]:-P K deficiency