Sulfonamides and trimethoprim US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Sulfonamides and trimethoprim. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Sulfonamides and trimethoprim US Medical PG Question 1: A 68-year-old man comes to the physician because of headache, fatigue, and nonproductive cough for 1 week. He appears pale. Pulmonary examination shows no abnormalities. Laboratory studies show a hemoglobin concentration of 9.5 g/dL and an elevated serum lactate dehydrogenase concentration. A peripheral blood smear shows normal red blood cells that are clumped together. Results of cold agglutinin titer testing show a 4-fold elevation above normal. An x-ray of the chest shows diffuse, patchy infiltrates bilaterally. Treatment is begun with an antibiotic that is also used to promote gut motility. Which of the following is the primary mechanism of action of this drug?
- A. Inhibition of bacterial RNA polymerase
- B. Inhibition of folic acid synthesis
- C. Free radical creation within bacterial cells
- D. Inhibition of transpeptidase cross-linking at the cell wall
- E. Inhibition of peptide translocation at the 50S ribosomal subunit (Correct Answer)
Sulfonamides and trimethoprim Explanation: ***Inhibition of peptide translocation at the 50S ribosomal subunit***
- This drug described is likely **erythromycin** or another **macrolide antibiotic**, which inhibits bacterial protein synthesis by binding to the **50S ribosomal subunit** and preventing translocation.
- Macrolides are used to treat **atypical pneumonia** caused by *Mycoplasma pneumoniae*, which is indicated by the patient's symptoms (headache, fatigue, nonproductive cough, bilateral patchy infiltrates) and **cold agglutinin disease**.
*Inhibition of bacterial RNA polymerase*
- This is the mechanism of action of **rifampin**, which is primarily used for **tuberculosis** and **meningitis prophylaxis**, not for atypical pneumonia.
- Rifampin's side effects and spectrum of activity do not align with the implied clinical scenario, especially the gut motility promotion.
*Inhibition of folic acid synthesis*
- This is the mechanism for **sulfonamides** and **trimethoprim**, which are bacteriostatic and target different pathogens than those causing cold agglutinin positive pneumonia.
- These drugs are not known for promoting gut motility.
*Free radical creation within bacterial cells*
- This mechanism is characteristic of **metronidazole**, an antibiotic used for anaerobic bacterial and parasitic infections.
- Metronidazole does not fit the clinical context of atypical pneumonia with cold agglutinins, nor is it a macrolide that promotes gut motility.
*Inhibition of transpeptidase cross-linking at the cell wall*
- This describes the mechanism of **beta-lactam antibiotics** (e.g., penicillins, cephalosporins), which are ineffective against **atypical pneumonia** because *Mycoplasma* lacks a cell wall.
- Beta-lactams do not typically promote gut motility.
Sulfonamides and trimethoprim US Medical PG Question 2: A 49-year-old woman comes to the physician because of a 4-month history of fatigue and recurrent pain in both of her wrists and her fingers. During this time, she has also had stiffness of her joints for about 80 minutes after waking up in the morning. Examination shows swelling and tenderness of the wrists and metacarpophalangeal joints bilaterally. Her serum erythrocyte sedimentation rate is 42 mm/h and rheumatoid factor is positive. Treatment is begun with a drug that results in decreased synthesis of deoxythymidine monophosphate. This mechanism is most similar to the mechanism of action of which of the following drugs?
- A. Trimethoprim (Correct Answer)
- B. Gentamicin
- C. Sulfamethoxazole
- D. Doxycycline
- E. Azithromycin
Sulfonamides and trimethoprim Explanation: ***Trimethoprim***
- The patient has **rheumatoid arthritis** being treated with **methotrexate**, which inhibits **dihydrofolate reductase** leading to decreased **deoxythymidine monophosphate (dTMP)** synthesis
- **Trimethoprim** also inhibits **dihydrofolate reductase** in bacteria, targeting the same enzyme in the folate metabolism pathway as methotrexate
- This makes their mechanisms of action most similar among the options provided
*Gentamicin*
- Aminoglycoside antibiotic that inhibits bacterial protein synthesis by irreversibly binding to the **30S ribosomal subunit**
- Mechanism is entirely different from inhibition of dTMP synthesis
*Sulfamethoxazole*
- Sulfonamide antibiotic that inhibits bacterial **dihydropteroate synthase** by competing with para-aminobenzoic acid (PABA)
- While it targets the folate pathway, it acts **earlier** in the pathway than trimethoprim or methotrexate (before dihydrofolate reductase)
*Doxycycline*
- Tetracycline antibiotic that inhibits bacterial protein synthesis by reversibly binding to the **30S ribosomal subunit**
- Does not involve the folate pathway or dTMP synthesis
*Azithromycin*
- Macrolide antibiotic that inhibits bacterial protein synthesis by binding to the **50S ribosomal subunit**
- Unrelated to dTMP synthesis or folate metabolism
Sulfonamides and trimethoprim US Medical PG Question 3: A 67-year-old man is seen on the surgical floor after a transplant procedure. The previous day, the patient had a renal transplant from a matched donor. He is currently recovering and doing well. The patient has a past medical history of IV drug use, diabetes mellitus, oral cold sores, hypertension, renal failure, and dyslipidemia. The patient's current medications include lisinopril, atorvastatin, insulin, and aspirin. Prior to the procedure, he was also on dialysis. The patient is started on cyclosporine. The patient successfully recovers over the next few days. Which of the following medications should be started in this patient?
- A. Azithromycin
- B. TMP-SMX (Correct Answer)
- C. Acyclovir
- D. Low dose acyclovir
- E. Penicillin
Sulfonamides and trimethoprim Explanation: ***TMP-SMX***
- **TMP-SMX (trimethoprim-sulfamethoxazole)** is the **most critical** prophylactic medication for all solid organ transplant recipients on immunosuppression.
- It provides essential prophylaxis against **Pneumocystis jirovecii pneumonia (PJP)**, a life-threatening opportunistic infection with high mortality if not prevented.
- PJP prophylaxis is a **universal recommendation** for all transplant patients and is typically continued for 6-12 months post-transplant.
- Additionally offers protection against **Toxoplasma gondii**, **Nocardia**, and common urinary tract infections, making it particularly valuable in renal transplant recipients.
*Azithromycin*
- Azithromycin is a macrolide antibiotic used for specific bacterial infections and sometimes for **Mycobacterium avium complex (MAC)** prophylaxis in severely immunocompromised patients.
- It is not standard prophylaxis in routine post-transplant care and does not protect against PJP, the most critical opportunistic infection in this setting.
*Acyclovir*
- High-dose acyclovir is used to **treat active HSV or VZV infections**, not for routine prophylaxis.
- This patient has no active viral infection requiring treatment doses at this time.
*Low dose acyclovir*
- Low-dose acyclovir (or valacyclovir) is indeed used for **HSV/VZV prophylaxis** in transplant patients, especially those with a history of cold sores.
- Many transplant centers do initiate this medication alongside TMP-SMX in the post-transplant period.
- However, in a **single-best-answer** context, **TMP-SMX takes priority** as it prevents PJP, which is universally life-threatening and has higher incidence without prophylaxis compared to severe HSV reactivation.
- TMP-SMX is considered the **essential first-line** prophylaxis that all transplant patients must receive.
*Penicillin*
- Penicillin is a narrow-spectrum antibiotic effective against certain gram-positive bacteria.
- It has no role in post-transplant opportunistic infection prophylaxis and does not protect against PJP, HSV, or other transplant-related infections.
Sulfonamides and trimethoprim US Medical PG Question 4: A 15-year-old boy presents with his father to the urgent care department with a 5-day history of frequent diarrhea, occasionally mixed with streaks of blood. Stool cultures are pending, but preliminary stool samples demonstrate fecal leukocytes and erythrocytes. The patient's vital signs are within normal limits, and he is started on outpatient therapy for presumed Shigella infection. Which of the following was the young man most likely started on?
- A. Oral vancomycin
- B. Oral erythromycin
- C. Oral metronidazole
- D. An oral quinolone
- E. Oral trimethoprim-sulfamethoxazole (TMP-SMX) (Correct Answer)
Sulfonamides and trimethoprim Explanation: **Oral trimethoprim-sulfamethoxazole (TMP-SMX)**
- **TMP-SMX** is a traditional first-line treatment for **Shigella infection** in settings where susceptibility is expected or confirmed.
- The patient's presentation with **bloody diarrhea**, **fecal leukocytes**, and **erythrocytes** is classic for **Shigella dysentery**.
- While **resistance rates vary by region**, TMP-SMX remains an appropriate choice when local susceptibility patterns support its use.
- It is cost-effective, well-tolerated, and appropriate for outpatient management of uncomplicated cases.
*Oral vancomycin*
- Vancomycin is specifically used for **Clostridioides difficile infection** and does not treat Shigella.
- It has **poor oral absorption** and no activity against Gram-negative enteric pathogens like Shigella.
*Oral erythromycin*
- Erythromycin is primarily effective against **Campylobacter jejuni** and respiratory pathogens.
- It has **limited activity against Shigella** and resistance rates are high, making it an inappropriate choice.
*Oral metronidazole*
- Metronidazole treats **anaerobic bacteria** and protozoal infections (*Giardia*, *Entamoeba histolytica*).
- It has **no significant activity against Shigella**, a facultative anaerobic Gram-negative bacillus.
*An oral quinolone*
- **Fluoroquinolones** (e.g., ciprofloxacin) are highly effective against Shigella and often used as first-line therapy, particularly in areas with high TMP-SMX resistance.
- They are increasingly preferred in current guidelines due to rising resistance to TMP-SMX.
- However, in the context of empiric outpatient treatment where susceptibility is presumed, **TMP-SMX** may still be chosen initially as a narrower-spectrum, cost-effective option, with fluoroquinolones reserved based on culture results or treatment failure.
Sulfonamides and trimethoprim US Medical PG Question 5: A 6-year-old boy is brought to the physician because of headache, cough, runny nose, and a low-grade fever since waking up that morning. He has been healthy except for a urinary tract infection one week ago that has resolved with trimethoprim-sulfamethoxazole therapy. Both parents have a history of allergic rhinitis. His temperature is 37.8°C (100°F). Physical exam shows rhinorrhea and tenderness over the frontal and maxillary sinuses. There is cervical lymphadenopathy. Laboratory studies show:
Hemoglobin 14.2 g/dL
Leukocyte count 2,700/mm3
Segmented neutrophils 30%
Bands 1%
Eosinophils 4%
Basophils 0%
Lymphocytes 56%
Monocytes 9%
Platelet count 155,000/mm3
Which of the following is the most likely underlying cause of this patient's symptoms?
- A. CMV infection
- B. EBV infection
- C. Acute lymphocytic leukemia
- D. Medication side effect (Correct Answer)
- E. Acute myelogenous leukemia
Sulfonamides and trimethoprim Explanation: ***Medication side effect***
- The patient's recent **trimethoprim-sulfamethoxazole (TMP-SMX)** treatment and current **leukopenia** (WBC 2,700/mm³, normal 5,000-10,000/mm³) with **neutropenia** (absolute neutrophil count ~840/mm³) strongly suggest **drug-induced bone marrow suppression**.
- TMP-SMX is a folate antagonist known to cause dose-dependent bone marrow suppression, particularly affecting neutrophils and occasionally platelets. The platelet count (155,000/mm³) is at the lower limit of normal, which may represent early marrow effect.
- While the patient's current symptoms (rhinorrhea, cough, sinus tenderness, low-grade fever) suggest an **acute viral upper respiratory infection**, the question asks for the "most likely underlying cause." The **leukopenia with neutropenia** is the most significant abnormal finding and represents the drug effect that predisposes to or complicates infections.
- The combination of recent antibiotic exposure and cytopenias makes medication side effect the primary diagnosis.
*CMV infection*
- CMV can cause **leukopenia**, but typically presents with more prominent constitutional symptoms including prolonged fever, malaise, hepatosplenomegaly, and atypical lymphocytosis.
- The acute onset of URI symptoms and temporal relationship to antibiotic use makes drug-induced marrow suppression more likely.
*EBV infection*
- EBV (infectious mononucleosis) characteristically causes **lymphocytosis with atypical lymphocytes**, not leukopenia.
- Classic features include **pharyngitis**, **posterior cervical lymphadenopathy**, **splenomegaly**, and fatigue, which are not present here.
- The lymphocyte percentage (56%) is within normal range for age, not elevated.
*Acute lymphocytic leukemia*
- **ALL** would present with more severe constitutional symptoms (high fever, bone pain, significant fatigue) and typically shows **circulating blasts** on peripheral smear.
- The cytopenias in ALL are usually more profound (severe anemia, marked thrombocytopenia <50,000/mm³).
- The absence of blasts in the differential and relatively preserved hemoglobin (14.2 g/dL) argue against leukemia.
*Acute myelogenous leukemia*
- **AML** presents with severe symptoms including fatigue, bleeding diathesis, and recurrent infections.
- Peripheral smear typically shows **myeloblasts** with Auer rods in some cases.
- The patient's mild symptoms, absence of blasts, and normal hemoglobin make AML highly unlikely.
Sulfonamides and trimethoprim US Medical PG Question 6: A 55-year-old man with a history of hypertension and benign prostate hyperplasia presents for follow-up 4 days into the treatment of a urinary tract infection with trimethoprim-sulfamethoxazole. His symptoms have resolved, and he reports no problems with urination, with the exception of a weak urine stream and hesitancy, which he has had for the past 2 years. At the time of this visit, the patient is afebrile; the blood pressure is 130/88 mm Hg and the heart rate is 80/min. There is no flank tenderness. A urinalysis reveals no leukocytes and is negative for esterase. The urinalysis reveals 2 red blood cells (RBCs)/ high power field (HPF), and there are no casts on urinary sediment analysis. The physician, however, notices the following abnormality:
Prior treatment
BUN 12 mg/dL
Creatinine 1.2 mg/dL
Today’s visit
BUN 13 mg/dL
Creatinine 2.1 mg/dL
- A. Admit the patient for further management of acute interstitial nephritis
- B. Admit the patient for further management of acute tubular necrosis
- C. Schedule a cystoscopy for urethral obstruction
- D. Schedule an intravenous pyelography for urinary obstruction
- E. Reassure the patient, stop trimethoprim-sulfamethoxazole and repeat the measurement in 1–2 weeks (Correct Answer)
Sulfonamides and trimethoprim Explanation: ***Reassure the patient, stop trimethoprim-sulfamethoxazole and repeat the measurement in 1–2 weeks***
- The patient's **creatinine elevation** from 1.2 to 2.1 mg/dL after starting **trimethoprim-sulfamethoxazole** is likely due to the drug's known effect of inhibiting **creatinine secretion** in the renal tubules, leading to a rise in serum creatinine without actual kidney injury, and this effect is often reversible upon discontinuation.
- Given that the patient's symptoms of UTI have resolved, and there are no signs of active kidney injury (afebrile, no flank tenderness, normal urinalysis for leukocytes/casts, mild RBCs), the most appropriate step is to stop the medication and monitor kidney function.
*Admit the patient for further management of acute interstitial nephritis*
- **Acute interstitial nephritis** typically presents with systemic symptoms like **fever**, **rash**, and **eosinophilia**, none of which are present in this case.
- The urinalysis would typically show **white blood cells** and possibly **eosinophils**, which are absent here.
*Admit the patient for further management of acute tubular necrosis*
- **Acute tubular necrosis** (ATN) usually causes a more significant and rapid rise in creatinine, often accompanied by **oliguria** or **anuria**, and a urinalysis showing muddy brown casts, which are not seen here.
- The patient's symptoms have improved, suggesting no severe acute kidney injury requiring admission for ATN.
*Schedule a cystoscopy for urethral obstruction*
- While the patient has a history of benign prostatic hyperplasia (BPH) and symptoms of weak stream and hesitancy, these are chronic issues and do not explain the acute rise in creatinine.
- A **cystoscopy** is an invasive procedure and is not indicated as an immediate response to this reversible creatinine elevation.
*Schedule an intravenous pyelography for urinary obstruction*
- An **intravenous pyelography** (IVP) is used to visualize the urinary tract and might detect a urinary obstruction, but the history of BPH and chronic symptoms don't point towards a new, acute obstructive process causing the creatinine increase.
- Furthermore, an IVP involves contrast dye, which could be nephrotoxic, especially in a patient with elevated creatinine, making it an inappropriate initial step.
Sulfonamides and trimethoprim US Medical PG Question 7: A 29-year-old female presents to her gynecologist complaining of a painful rash around her genitals. She has multiple sexual partners and uses condoms intermittently. Her last STD screen one year ago was negative. On examination, she has bilateral erosive vesicles on her labia majora and painful inguinal lymphadenopathy. She is started on an oral medication that requires a specific thymidine kinase for activation. Which of the following adverse effects is associated with this drug?
- A. Photosensitivity
- B. Deafness
- C. Renal failure (Correct Answer)
- D. Gingival hyperplasia
- E. Pulmonary fibrosis
Sulfonamides and trimethoprim Explanation: ***Renal failure***
- The patient's symptoms (painful genital rash, erosive vesicles, inguinal lymphadenopathy) are highly suggestive of **herpes simplex virus (HSV) infection**, likely genital herpes.
- The drug described is an antiviral agent like **acyclovir, valacyclovir, or famciclovir**, which require **viral thymidine kinase** for activation and are known to cause **renal impairment** (nephrotoxicity) as an adverse effect, especially with high doses or in dehydrated patients due to crystal nephropathy.
*Photosensitivity*
- **Photosensitivity** is a common side effect of some antibiotics (e.g., tetracyclines, sulfonamides), diuretics (e.g., thiazides), and antifungals, but it is **not a prominent adverse effect of acyclovir or its derivatives**.
- While theoretical, it is not a clinically significant or frequently observed adverse effect associated with the class of antiviral drugs used for HSV.
*Deafness*
- **Ototoxicity**, leading to deafness or hearing loss, is a well-known adverse effect of certain classes of drugs, such as **aminoglycoside antibiotics** (e.g., gentamicin) and **loop diuretics** (e.g., furosemide).
- It is **not an adverse effect** associated with antiviral medications like acyclovir.
*Gingival hyperplasia*
- **Gingival hyperplasia** (overgrowth of gum tissue) is a recognized side effect of specific medications including **phenytoin** (an anticonvulsant), **cyclosporine** (an immunosuppressant), and **calcium channel blockers** (e.g., nifedipine, amlodipine).
- This adverse effect is **not associated with antiviral drugs** used to treat herpes simplex.
*Pulmonary fibrosis*
- **Pulmonary fibrosis** is a serious adverse effect linked to various drugs like **amiodarone** (an antiarrhythmic), **bleomycin** (a chemotherapeutic agent), **methotrexate** (an immunosuppressant/chemotherapeutic), and **nitrofurantoin** (an antibiotic).
- **Antiviral medications for HSV** do not typically cause pulmonary fibrosis.
Sulfonamides and trimethoprim US Medical PG Question 8: A 30-year-old man comes to the emergency department because of the sudden onset of back pain beginning 2 hours ago. Beginning yesterday, he noticed that his eyes started appearing yellowish and his urine was darker than normal. Two months ago, he returned from a trip to Greece, where he lived before immigrating to the US 10 years ago. Three days ago, he was diagnosed with latent tuberculosis and started on isoniazid. He has worked as a plumber the last 5 years. His temperature is 37.4°C (99.3°F), pulse is 80/min, and blood pressure is 110/70 mm Hg. Examination shows back tenderness and scleral icterus. Laboratory studies show:
Hematocrit 29%
Leukocyte count 8000/mm3
Platelet count 280,000/mm3
Serum
Bilirubin
Total 4 mg/dL
Direct 0.7 mg/dL
Haptoglobin 15 mg/dL (N=41–165 mg/dL)
Lactate dehydrogenase 180 U/L
Urine
Blood 3+
Protein 1+
RBC 2–3/hpf
WBC 2–3/hpf
Which of the following is the most likely underlying cause of this patient's anemia?
- A. Absence of reduced glutathione (Correct Answer)
- B. Absence of uridine 5'-monophosphate
- C. Crescent-shaped erythrocytes
- D. Defective ankyrin in the RBC membrane
- E. Inhibition of aminolevulinate dehydratase
Sulfonamides and trimethoprim Explanation: ***Absence of reduced glutathione***
- This patient's presentation with anemia, jaundice, dark urine, and particularly the low **haptoglobin** and elevated **LDH**, points to **hemolysis**. The recent initiation of **isoniazid** (an oxidative stressor) and his Greek ancestry strongly suggest **G6PD deficiency**, where a lack of reduced glutathione leads to oxidative damage and hemolysis.
- **Glucose-6-phosphate dehydrogenase (G6PD) deficiency** is an X-linked recessive disorder common in populations of Mediterranean and African descent. It impairs the **hexose monophosphate shunt**, reducing the cell's ability to produce **NADPH**, which is crucial for reducing **oxidative stress** via **reduced glutathione**.
*Absence of uridine 5'-monophosphate*
- Absence of **uridine 5'-monophosphate (UMP)** is associated with **hereditary orotic aciduria**, a rare metabolic disorder.
- This condition typically presents with **megaloblastic anemia** (not hemolytic anemia), growth retardation, and orotic acid crystals in the urine, none of which are consistent with this patient's findings.
*Crescent-shaped erythrocytes*
- **Crescent-shaped erythrocytes** (sickle cells) are characteristic of **sickle cell anemia**, a genetic disorder causing chronic hemolytic anemia, vaso-occlusive crises, and pain.
- While it can cause hemolytic anemia, the triggers and specific laboratory findings (e.g., absence of a specific oxidative stressor like isoniazid causing acute hemolysis, the sudden onset in an adult not previously diagnosed) make it less likely than G6PD deficiency in this context.
*Defective ankyrin in the RBC membrane*
- Defective **ankyrin** in the red blood cell membrane is characteristic of **hereditary spherocytosis**, an inherited disorder causing hemolytic anemia.
- This condition typically presents with **spherocytes** on the blood smear, increased **MCHC**, and a positive **osmotic fragility test**, which are not indicated by the provided lab results.
*Inhibition of aminolevulinate dehydratase*
- Inhibition of **aminolevulinate dehydratase** is associated with **lead poisoning**, which impairs **heme synthesis**.
- This would typically cause a **microcytic or normocytic anemia** with **basophilic stippling** and elevated **protoporphyrin levels**, not an acute hemolytic crisis with jaundice, low haptoglobin, and elevated LDH.
Sulfonamides and trimethoprim US Medical PG Question 9: An 8-year-old boy is brought to the emergency department by his parents because of sudden onset of abdominal pain beginning an hour ago. The parents report that their son has also had an episode of dark urine earlier that morning. Three days ago, he was diagnosed with a urinary tract infection and was treated with trimethoprim-sulfamethoxazole. He emigrated from Liberia to the US with his family 3 years ago. There is no personal history of serious illness. His immunizations are up-to-date. Vital signs are within normal limits. Examination shows diffuse abdominal tenderness and scleral icterus. The spleen is palpated 1–2 cm below the left costal margin. Laboratory studies show:
Hemoglobin 10 g/dL
Mean corpuscular volume 90 μm3
Reticulocyte count 3%
Serum
Bilirubin
Total 3 mg/dL
Direct 0.5 mg/dL
Haptoglobin 20 mg/dL (N=41–165 mg/dL)
Lactate dehydrogenase 160 U/L
Urine
Blood 3+
Protein 1+
RBC 2–3/hpf
WBC 2–3/hpf
Which of the following is the most likely underlying cause of this patient's symptoms?
- A. Production of hemoglobin S
- B. Deficient glucose-6-phosphate dehydrogenase (Correct Answer)
- C. Lead poisoning
- D. Cold agglutinins
- E. Defective RBC membrane proteins
Sulfonamides and trimethoprim Explanation: ***Deficient glucose-6-phosphate dehydrogenase***
- The patient's presentation with **hemolytic anemia** (low hemoglobin, elevated reticulocytes, low haptoglobin, elevated LDH, elevated indirect bilirubin) following **trimethoprim-sulfamethoxazole** administration, along with dark urine (hemoglobinuria), is highly suggestive of G6PD deficiency.
- G6PD deficiency is common in individuals of African descent (patient emigrated from Liberia) and certain medications like sulfa drugs can trigger **oxidative stress** leading to hemolysis in affected individuals.
*Production of hemoglobin S*
- While **sickle cell anemia** (due to hemoglobin S) can cause hemolytic anemia and abdominal pain (**vaso-occlusive crisis**), the sudden onset linked to a specific medication and the absence of a prior history of serious illness make G6PD deficiency more likely.
- Sickle cell disease typically presents with recurrent painful crises, dactylitis in infancy, and chronic hemolytic anemia, which are not described here.
*Lead poisoning*
- **Lead poisoning** can cause abdominal pain and anemia, but it typically presents with a **microcytic hypochromic anemia** and **basophilic stippling** on peripheral smear.
- It does not directly cause an acute hemolytic crisis triggered by trimethoprim-sulfamethoxazole.
*Cold agglutinins*
- **Cold agglutinin disease** involves hemolytic anemia triggered by cold exposure, and the antibodies react optimally at cold temperatures.
- The patient's symptoms are acute and triggered by a medication known to induce oxidative stress, which is not characteristic of cold agglutinin disease.
*Defective RBC membrane proteins*
- **Hereditary spherocytosis** (a defect in RBC membrane proteins like spectrin or ankyrin) causes chronic hemolytic anemia and splenomegaly.
- While it can manifest with jaundice, it typically does not cause an acute, drug-induced hemolytic crisis with hemoglobinuria as seen here.
Sulfonamides and trimethoprim US Medical PG Question 10: A 45-year-old woman presents to the emergency department with fever, cough, tonsillar enlargement, and bleeding lips. She has a diffuse blistering rash that encompasses the palms and soles of her feet, in total covering 55% of her total body surface area (TBSA). The upper epidermal layer easily slips away with slight rubbing. Within 24 hours the rash progresses to 88% TBSA involvement and the patient requires mechanical ventilation for respiratory distress. Which of the following is the most likely etiology of this patient’s condition?
- A. Cytomegalovirus
- B. Deficiency of C-1 esterase inhibitor
- C. Exposure to carbamazepine (Correct Answer)
- D. Herpes simplex virus
- E. Molluscum contagiosum
Sulfonamides and trimethoprim Explanation: ***Exposure to carbamazepine***
- The rapid progression of a widespread blistering rash, **positive Nikolsky's sign** (skin slipping away), significant TBSA involvement (55% rapidly increasing to 88%), and systemic symptoms (fever, respiratory distress) are highly characteristic of **Stevens-Johnson Syndrome/Toxic Epidermal Necrolysis (SJS/TEN)**.
- **Carbamazepine** is a well-known medication trigger for SJS/TEN, a severe cutaneous adverse drug reaction.
*Cytomegalovirus*
- While CMV can cause a rash and systemic symptoms, it typically manifests as a **maculopapular rash** or purpura, not extensive blistering with a positive Nikolsky's sign.
- CMV infection usually presents with features like mononucleosis-like syndrome, hepatitis, or retinitis, which are not described here as the primary concern.
*Deficiency of C-1 esterase inhibitor*
- This deficiency causes **hereditary angioedema**, characterized by recurrent episodes of localized swelling, typically affecting the face, airways, and gastrointestinal tract.
- It does not cause a blistering rash or the extensive epidermal detachment seen in this patient.
*Herpes simplex virus*
- HSV can cause blistering lesions, but these are typically **localized vesicles** that progress to ulcers, such as cold sores or genital herpes.
- While widespread HSV infection can occur in immunocompromised patients, it does not typically present as a diffuse blistering rash with such extensive epidermal detachment and high TBSA involvement as described.
*Molluscum contagiosum*
- This is a viral skin infection that causes characteristic **dome-shaped, umbilicated papules**.
- It does not cause a widespread blistering rash, fever, or the severe systemic symptoms and epidermal detachment seen in this patient.
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