Drug-Induced Blood Dyscrasias — MCQs

10 questions

Which of the following statements best describes the underlying mechanism of heparin-induced thrombocytopenia?

A patient of schizophrenia is being treated with clozapine. For which rare but serious side effects should he be monitored?

Which of the following types of leukemia is administered prophylactic methotrexate for CNS prophylaxis –

Which of the following statements is true regarding drug-induced lupus erythematosus (DILE)?

Which of the following hematological problems may be precipitated by parvovirus?

A patient with a history of penicillin allergy is admitted with bacterial meningitis. After receiving intravenous antibiotics, she develops a severe reaction. Which of the following drugs is most likely responsible for her condition?

The most classic dietary trigger for acute hemolytic anemia in G6PD deficiency is which of the following?

Drug Induced Lupus is caused by all except

Ulipristal acetate (progesterone receptor modulator) should not be prescribed as emergency contraceptive in women with

Q10

Which of the following drugs can lead to pemphigus?

Drug-Induced Blood Dyscrasias Indian Medical PG Practice Questions and MCQs

Question 1: Which of the following statements best describes the underlying mechanism of heparin-induced thrombocytopenia?

A. Low molecular weight heparin can also cause heparin-induced thrombocytopenia.
B. Vitamin K is not an antidote for heparin-induced thrombocytopenia.
C. Heparin-induced thrombocytopenia can occur after several days of heparin therapy.
D. Antibodies are formed against heparin-platelet factor 4 complexes. (Correct Answer)

Explanation: **_Antibodies are formed against platelet factor 4._** - The underlying mechanism of **heparin-induced thrombocytopenia (HIT)** involves the formation of antibodies against complexes of **heparin and platelet factor 4 (PF4)** [2]. - These antibodies bind to the **heparin-PF4 complexes** on the surface of platelets, leading to platelet activation, aggregation, and consumption, which results in thrombocytopenia and a prothrombotic state [2]. *Low molecular weight heparin can also cause heparin-induced thrombocytopenia.* - While **low molecular weight heparin (LMWH)** has a lower incidence of causing HIT compared to unfractionated heparin, it can still trigger the condition [1], [2]. - This is because LMWH, like unfractionated heparin, can form complexes with PF4, leading to the same immune response in susceptible individuals [2]. *Vitamin K is not an antidote for heparin-induced thrombocytopenia.* - **Vitamin K** is the antidote for warfarin overdose, which works by reversing its anticoagulant effects [3]. - It has no role as an antidote for HIT because HIT is an **immune-mediated reaction** involving platelet activation, not a direct anticoagulant effect that can be reversed by Vitamin K [2]. *Heparin-induced thrombocytopenia can occur after several days of heparin therapy.* - HIT typically manifests after **5 to 10 days of heparin exposure**, as it takes time for the immune system to produce antibodies against the heparin-PF4 complexes [2]. - However, in patients with prior exposure to heparin, HIT can occur much sooner, even within **24 hours**, due to pre-existing antibodies.

Question 2: A patient of schizophrenia is being treated with clozapine. For which rare but serious side effects should he be monitored?

A. Seizures
B. Agranulocytosis (Correct Answer)
C. Hepatomegaly
D. Renal bleed

Explanation: ***Agranulocytosis*** - **Agranulocytosis** is a severe and potentially fatal reduction in white blood cells (specifically neutrophils) that can occur with clozapine use [2, 3]. - This is the **rare but serious side effect** that requires mandatory monitoring, occurring in **0.8-2%** of patients. - Patients on clozapine require routine **complete blood count (CBC)** monitoring: **weekly for the first 6 months**, then biweekly for months 6-12, then monthly thereafter . - This is the primary reason clozapine has restricted use despite being the most effective antipsychotic for treatment-resistant schizophrenia. *Seizures* - While clozapine can lower the **seizure threshold** (especially at higher doses), seizures occur in **1-2%** of patients and are **dose-dependent** . - Seizures are a known side effect that warrants dosage adjustment, but they are **not as rare** as agranulocytosis and do not require the same intensive blood monitoring protocol. - Management involves dose reduction or adding anticonvulsants. *Hepatomegaly* - **Hepatic dysfunction** can occur with clozapine, but **hepatomegaly** (enlarged liver) itself is not one of its rare, life-threatening side effects requiring specific monitoring above other, more severe issues. - Liver enzyme elevation may be monitored, but this is not the primary "rare but serious" concern. *Renal bleed* - **Renal complications** or **renal bleeding** are not recognized as significant or specifically monitored rare side effects of clozapine. - Clozapine's major concerns primarily involve hematologic (agranulocytosis), cardiovascular (myocarditis), and metabolic systems.

Question 3: Which of the following types of leukemia is administered prophylactic methotrexate for CNS prophylaxis –

A. AML
B. CLL
C. CML
D. ALL (Correct Answer)

Explanation: ***ALL*** - **Acute Lymphoblastic Leukemia (ALL)** has a high propensity for **central nervous system (CNS) involvement**, necessitating prophylactic intrathecal methotrexate to prevent CNS relapse [1]. - Prophylactic treatment of the CNS is a standard component of ALL treatment protocols due to the risk of leukemic cell infiltration into the brain and spinal cord [1]. *AML* - **Acute Myeloid Leukemia (AML)** has a lower incidence of CNS involvement compared to ALL, so prophylactic CNS treatment is generally not routine unless specific risk factors are present. - While CNS involvement can occur in AML, it is more commonly treated with systemic chemotherapy that has CNS penetration or intrathecal treatment only when CNS disease is confirmed. *CLL* - **Chronic Lymphocytic Leukemia (CLL)** rarely involves the CNS, and prophylactic CNS treatment is not part of standard management. - When CNS involvement does occur in CLL, it is an aggressive, late-stage complication and typically requires specific, targeted therapy rather than prophylaxis. *CML* - **Chronic Myeloid Leukemia (CML)** has an extremely low risk of CNS involvement, especially in the chronic phase, and therefore, prophylactic CNS treatment is not administered. - CNS involvement in CML is usually seen during a blast crisis and is rare, making prophylaxis unnecessary.

Question 4: Which of the following statements is true regarding drug-induced lupus erythematosus (DILE)?

A. CNS manifestations are common in DILE.
B. Renal involvement is common in DILE.
C. Antihistone antibodies are commonly found in DILE. (Correct Answer)
D. All patients with antibodies progress to systemic lupus erythematosus.

Explanation: ***Antihistone antibodies are commonly found in DILE.*** - The presence of **antihistone antibodies** is a hallmark of drug-induced lupus erythematosus, detected in a majority of cases. - This antibody profile helps differentiate DILE from idiopathic systemic lupus erythematosus (SLE), where other autoantibodies like anti-dsDNA are more prominent. *CNS manifestations are common in DILE.* - **Central nervous system (CNS) involvement** is rare in DILE, distinguishing it from idiopathic SLE where neuropsychiatric symptoms are more prevalent. - While headaches and mild cognitive changes can occur, severe manifestations like seizures or psychosis are not typical of DILE. *Renal involvement is common in DILE.* - **Renal involvement**, such as glomerulonephritis, is highly uncommon in DILE, unlike idiopathic SLE where it is a significant cause of morbidity. - If significant renal disease is present in a patient suspected of DILE, it warrants a re-evaluation for idiopathic SLE or another diagnosis. *All patients with antibodies progress to systemic lupus erythematosus.* - Not all patients who develop antibodies, such as **antihistone antibodies**, will progress to full-blown DILE or systemic lupus erythematosus. - The condition typically resolves upon discontinuation of the offending drug, and the presence of antibodies alone is not sufficient for diagnosis, requiring clinical symptoms.

Question 5: Which of the following hematological problems may be precipitated by parvovirus?

A. Aplastic crisis (Correct Answer)
B. Hemolytic crisis
C. Thrombocytopenia
D. Pancytopenia

Explanation: ***Aplastic crisis*** - Parvovirus B19 preferentially infects and destroys **erythroid progenitor cells** in the bone marrow, leading to a temporary halt in red blood cell production [1]. - This can precipitate an **aplastic crisis**, especially in individuals with underlying chronic hemolytic anemias (e.g., **sickle cell disease** or **hereditary spherocytosis**), where red blood cell lifespan is already shortened [2]. *Hemolytic crisis* - A hemolytic crisis involves an **accelerated destruction of red blood cells**, leading to a sudden drop in hemoglobin. - While parvovirus can indirectly worsen anemia, it primarily affects red cell production rather than directly increasing their destruction, acting more as a trigger for a production problem than a hemolytic one [1]. *Thrombocytopenia* - **Thrombocytopenia** is characterized by a low platelet count, which can lead to bleeding disorders. - While viral infections can sometimes cause mild myelosuppression affecting platelets, parvovirus B19 is not typically associated with severe or primary thrombocytopenia. *Pancytopenia* - **Pancytopenia** is a reduction in all three blood cell lines (red blood cells, white blood cells, and platelets). - While parvovirus can cause a transient aplastic crisis (affecting red cells), it rarely causes a severe, sustained suppression of all cell lines to be classified as true pancytopenia, though some transient leukopenia may occur [1].

Question 6: A patient with a history of penicillin allergy is admitted with bacterial meningitis. After receiving intravenous antibiotics, she develops a severe reaction. Which of the following drugs is most likely responsible for her condition?

A. Chloramphenicol
B. Gentamicin
C. Doxycycline
D. Vancomycin (Correct Answer)

Explanation: ***Vancomycin*** - **Vancomycin infusion reaction** (formerly "red man syndrome") is a common adverse effect, especially with rapid intravenous administration, characterized by **flushing, rash, pruritus**, and sometimes **hypotension** or **angioedema**. - This reaction results from **non-IgE-mediated mast cell degranulation**, leading to histamine release, and is not directly related to penicillin allergy but can be mistaken for an allergic reaction. *Gentamicin* - Gentamicin is an **aminoglycoside** and is not typically associated with severe immediate hypersensitivity reactions like the one described. - Its main toxicities include **nephrotoxicity** and **ototoxicity**, often occurring with prolonged use or high concentrations. *Chloramphenicol* - Chloramphenicol is associated with serious but less common adverse effects such as **bone marrow suppression** (aplastic anemia) or **grey baby syndrome** in neonates. - It does not commonly cause acute, severe hypersensitivity reactions presenting as a rash and flushing. *Doxycycline* - Doxycycline is a **tetracycline antibiotic** and is generally well-tolerated, though it can cause photosensitivity, gastrointestinal upset, and esophageal irritation. - Like the other incorrect options, it does not typically induce acute, severe infusion reactions mimicking an allergic response in the way vancomycin does, especially in a penicillin-allergic patient.

Question 7: The most classic dietary trigger for acute hemolytic anemia in G6PD deficiency is which of the following?

A. Viral upper respiratory infections only
B. Vitamin C supplements
C. Fava beans (Correct Answer)
D. Folic acid deficiency

Explanation: **Fava beans** - **Fava beans** contain high concentrations of **vicine and convicine**, which are converted into **divicine and isouramil**. These compounds produce **reactive oxygen species** that overwhelm the erythrocyte's antioxidant defense mechanisms, especially in individuals with **G6PD deficiency** [2]. - In individuals with **G6PD deficiency**, the inability to produce sufficient **NADPH** results in inadequate levels of **reduced glutathione**, making red blood cells vulnerable to **oxidative stress** induced by these fava bean metabolites, leading to **hemolysis** [1, 3]. *Viral upper respiratory infections only* - While **infections (bacterial or viral)** can trigger **hemolytic crises** in G6PD deficient individuals by causing **oxidative stress** and inflammation, they are not a dietary trigger [3, 4]. - The question specifically asks for a **dietary trigger**, which excludes infections as the primary cause. *Vitamin C supplements* - While **large doses of vitamin C (ascorbic acid)** can act as a **pro-oxidant** and potentially induce some oxidative stress, it is generally not considered a classic or strong trigger for acute hemolytic anemia in G6PD deficiency at typical supplement doses. - **Fava beans** are far more potent and well-documented as a dietary trigger for this condition [2]. *Folic acid deficiency* - **Folic acid deficiency** does not directly cause acute hemolytic anemia in G6PD deficiency; it typically leads to **megaloblastic anemia** due to impaired DNA synthesis [4]. - While folic acid supplementation is often given to G6PD deficient patients with chronic hemolysis to support increased red blood cell production, its deficiency does not induce oxidative hemolysis.

Question 8: Drug Induced Lupus is caused by all except

A. Hydralazine
B. Sulphonamides
C. Isoniazid
D. Procaine (Correct Answer)

Explanation: ***Procaine*** - While **procainamide**, a derivative of procaine, is a known cause of **drug-induced lupus (DIL)**, **procaine** itself is not typically implicated. - Procaine is a **local anesthetic** and its mechanism of action does not commonly lead to the immunological reactions seen in DIL. *Hydralazine* - **Hydralazine** is a well-established cause of **drug-induced lupus (DIL)**, particularly with higher doses and prolonged use. - It frequently results in the development of **anti-histone antibodies**, a hallmark of DIL. *Sulphonamides* - Various **sulphonamide antibiotics** (e.g., sulfasalazine, sulfamethoxazole) are known to induce **lupus-like syndromes**. - These drugs can trigger immune responses leading to symptoms characteristic of **systemic lupus erythematosus (SLE)**. *Isoniazid* - **Isoniazid**, an anti-tuberculosis medication, is a recognized cause of **drug-induced lupus (DIL)**. - It often leads to the formation of **anti-histone antibodies** and clinical manifestations resembling spontaneous lupus.

Question 9: Ulipristal acetate (progesterone receptor modulator) should not be prescribed as emergency contraceptive in women with

A. liver dysfunction (Correct Answer)
B. glaucoma
C. coagulopathy
D. kidney failure

Explanation: ***Correct: liver dysfunction*** - **Ulipristal acetate** is extensively metabolized in the **liver** by the CYP450 enzyme system, predominantly CYP3A4. - In individuals with **severe hepatic impairment**, the metabolism of ulipristal acetate can be impaired, leading to increased plasma concentrations and potential adverse effects. - **Severe liver dysfunction** is a documented contraindication in product labeling. *Incorrect: glaucoma* - There is **no known contraindication** for ulipristal acetate use in individuals with **glaucoma**. - Its mechanism of action primarily involves progesterone receptors and does not directly impact intraocular pressure. *Incorrect: coagulopathy* - Ulipristal acetate does **not significantly affect blood coagulation** parameters or platelet function. - It is not contraindicated in individuals with **coagulopathy**, unlike some estrogen-containing contraceptives. *Incorrect: kidney failure* - While urinary excretion of ulipristal acetate metabolites occurs, the **primary elimination pathway is fecal** (approximately 90%). - **Kidney failure** is not considered a contraindication, and dose adjustments are generally not required.

Question 10: Which of the following drugs can lead to pemphigus?

A. Carbamazepine
B. Penicillamine (Correct Answer)
C. Isoniazid
D. Furosemide

Explanation: ***Penicillamine*** - **Penicillamine** is a well-known drug that can induce **pemphigus**, often through mechanisms involving alterations in **desmosome structure** or function. - The drug's sulfhydryl groups are thought to interfere with the integrity of **desmoglein proteins**, leading to blister formation. *Isoniazid* - **Isoniazid** is a first-line antituberculosis drug primarily associated with **hepatotoxicity** and **peripheral neuropathy**. - It is not typically implicated in the development of **pemphigus**. *Carbamazepine* - **Carbamazepine** is an anticonvulsant that can cause various cutaneous reactions, most notably **Stevens-Johnson syndrome (SJS)** and **toxic epidermal necrolysis (TEN)**. - While it can cause severe skin reactions, **pemphigus** is not a common side effect of carbamazepine. *Furosemide* - **Furosemide** is a loop diuretic that can cause **photosensitivity**, rashes, and rarely, severe skin reactions like **erythema multiforme**. - It is not recognized as a drug that induces **pemphigus**.

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