Oxazolidinones and streptogramins US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Oxazolidinones and streptogramins. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Oxazolidinones and streptogramins US Medical PG Question 1: Part of the success of the Streptococcus pyogenes bacterium lies in its ability to evade phagocytosis. Which of the following helps in this evasion?
- A. Streptolysin S
- B. Streptolysin O
- C. Streptokinase
- D. M protein (Correct Answer)
- E. Pyrogenic toxin
Oxazolidinones and streptogramins Explanation: ***M protein***
- The **M protein** is a major virulence factor of *Streptococcus pyogenes* that **inhibits phagocytosis** by binding to factor H, a host complement regulatory protein, preventing C3b deposition.
- It also helps the bacterium adhere to host cells and resist killing by neutrophils.
*Streptolysin S*
- **Streptolysin S** is a **hemolysin** that causes beta-hemolysis on blood agar and contributes to tissue damage by lysing cells.
- While contributing to virulence, its primary role is not direct inhibition of phagocytosis but rather cell lysis.
*Streptolysin O*
- **Streptolysin O (SLO)** is another **hemolysin** that produces pore-forming toxins, leading to cell lysis and tissue destruction.
- It is highly antigenic and often used as a diagnostic marker (ASO titer) for past *S. pyogenes* infections, but it does not directly prevent phagocytosis.
*Streptokinase*
- **Streptokinase** is an enzyme that activates plasminogen, leading to the breakdown of fibrin clots, which helps in the **spread of infection** within tissues.
- Its main function is not to evade phagocytosis but rather to facilitate invasion by dissolving blood clots that would typically wall off the infection.
*Pyrogenic toxin*
- **Pyrogenic toxins** (also known as erythrogenic toxins) are superantigens that cause symptoms like fever and rash (e.g., in scarlet fever) by stimulating a massive, non-specific T-cell activation.
- These toxins contribute to the systemic manifestations of infection but do not directly interfere with the process of phagocytosis.
Oxazolidinones and streptogramins US Medical PG Question 2: An 18-year old college freshman presents to his university clinic because he has not been feeling well for the past two weeks. He has had a persistent headache, occasional cough, and chills without rigors. The patient’s vital signs are normal and physical exam is unremarkable. His radiograph shows patchy interstitial lung infiltrates and he is diagnosed with atypical pneumonia. The patient is prescribed azithromycin and takes his medication as instructed. Despite adherence to his drug regimen, he returns to the clinic one week later because his symptoms have not improved. The organism responsible for this infection is likely resistant to azithromycin through which mechanism?
- A. Mutation in topoisomerase II
- B. Methylation of ribosomal binding site
- C. Presence of a beta-lactamase
- D. Decreased binding to RNA polymerase
- E. Insertion of drug efflux pumps (Correct Answer)
Oxazolidinones and streptogramins Explanation: ***Insertion of drug efflux pumps***
- **Azithromycin** is a macrolide antibiotic that inhibits bacterial protein synthesis by binding to the **50S ribosomal subunit**.
- In **Mycoplasma pneumoniae** (the most common cause of atypical pneumonia in young adults), the **most common** mechanism of macrolide resistance is through **efflux pumps**, particularly the **mef genes**.
- These efflux pumps actively transport macrolides out of the bacterial cell, reducing intracellular drug concentration and conferring resistance.
- This mechanism is responsible for the majority of macrolide-resistant *M. pneumoniae* isolates worldwide.
*Methylation of ribosomal binding site*
- **Methylation** of the ribosomal binding site (specifically the **23S rRNA** via erm genes) does prevent azithromycin from binding effectively.
- While this is a valid macrolide resistance mechanism seen in organisms like *Streptococcus pneumoniae* and *Streptococcus pyogenes*, it is **less common** in *Mycoplasma pneumoniae*.
- Efflux pumps (mef) are the predominant mechanism in *M. pneumoniae* resistant strains.
*Mutation in topoisomerase II*
- **Topoisomerase II** (DNA gyrase) is the target of **fluoroquinolone antibiotics**, not macrolides.
- Mutations in this enzyme lead to resistance against fluoroquinolones, such as **ciprofloxacin**.
*Presence of a beta-lactamase*
- **Beta-lactamase enzymes** inactivate **beta-lactam antibiotics** (e.g., penicillin, cephalosporins) by hydrolyzing their beta-lactam ring.
- Additionally, *Mycoplasma pneumoniae* **lacks a cell wall**, making it inherently resistant to all beta-lactam antibiotics regardless of beta-lactamase production.
*Decreased binding to RNA polymerase*
- **RNA polymerase** is the target for antibiotics like **rifampin**, which inhibits bacterial transcription.
- Decreased binding to RNA polymerase would lead to rifampin resistance, not azithromycin resistance.
Oxazolidinones and streptogramins US Medical PG Question 3: A 51-year-old man with alcohol use disorder comes to the physician because of a fever and productive cough. An x-ray of the chest shows a right lower lobe consolidation and a diagnosis of aspiration pneumonia is made. The physician prescribes a drug that blocks peptide transfer by binding to the 50S ribosomal subunit. Which of the following drugs was most likely prescribed?
- A. Ceftriaxone
- B. Doxycycline
- C. Metronidazole
- D. Clindamycin (Correct Answer)
- E. Azithromycin
Oxazolidinones and streptogramins Explanation: ***Clindamycin***
- **Clindamycin** is a lincosamide antibiotic that **blocks peptide transfer** by binding to the **50S ribosomal subunit**, inhibiting bacterial protein synthesis.
- It is a highly effective treatment for **aspiration pneumonia** due to its excellent activity against the **anaerobic bacteria** commonly found in oral flora, which are the primary pathogens in this condition.
*Ceftriaxone*
- **Ceftriaxone** is a third-generation cephalosporin that inhibits bacterial cell wall synthesis by binding to **penicillin-binding proteins**, not the 50S ribosomal subunit.
- While it has broad-spectrum activity, it is typically used for community-acquired pneumonia and is less effective against the **anaerobic organisms** predominant in aspiration pneumonia.
*Doxycycline*
- **Doxycycline** is a tetracycline antibiotic that binds to the **30S ribosomal subunit**, preventing the attachment of aminoacyl-tRNA.
- While effective against some respiratory pathogens, it is not the first-line choice for **aspiration pneumonia** as its anaerobic coverage is insufficient.
*Metronidazole*
- **Metronidazole** acts by forming **cytotoxic compounds** that damage bacterial DNA after reduction by anaerobic enzymes, rather than binding to ribosomal subunits.
- While effective against many **anaerobes**, it is often used in combination with other antibiotics for aspiration pneumonia, and its mechanism of action is distinct from that described.
*Azithromycin*
- **Azithromycin** is a macrolide antibiotic that also binds to the **50S ribosomal subunit**, but it **inhibits translocation** of the growing peptide chain, not primarily peptide transfer.
- While used for community-acquired pneumonia, its coverage for **oropharyngeal anaerobes** can be inconsistent, making clindamycin a more reliable choice for aspiration pneumonia.
Oxazolidinones and streptogramins US Medical PG Question 4: A 65-year-old man with chronic obstructive lung disease, depression, and type 2 diabetes mellitus comes to the physician with fever, chills, dyspnea, and a productive cough for 5 days. His temperature is 38.8°C (101.8°F) and respirations are 30/min. An x-ray of the chest shows a right lower lobe infiltrate, and sputum culture grows bacteria that are sensitive to fluoroquinolone antibiotics. Pharmacotherapy with oral moxifloxacin is initiated. Three days later, the patient continues to have symptoms despite being compliant with the antibiotic. Serum moxifloxacin levels are undetectable. The lack of response to antibiotic therapy in this patient is most likely due to the concurrent ingestion of which of the following medications?
- A. Theophylline
- B. Multivitamin (Correct Answer)
- C. Glimepiride
- D. Prednisone
- E. Amitriptyline
Oxazolidinones and streptogramins Explanation: ***Multivitamin***
- **Moxifloxacin is a fluoroquinolone** that undergoes chelation with **divalent and trivalent cations** (e.g., magnesium, calcium, iron, zinc), which are commonly found in multivitamins.
- This chelation forms **insoluble complexes** that significantly reduce the gastrointestinal absorption of moxifloxacin, leading to undetectable serum levels and treatment failure.
*Theophylline*
- Theophylline is a **bronchodilator** used for COPD, but it does not interact with fluoroquinolones to reduce their absorption.
- While fluoroquinolones can inhibit the metabolism of theophylline (**CYP1A2 inhibition**), leading to increased theophylline levels, this interaction would not explain undetectable moxifloxacin levels.
*Glimepiride*
- Glimepiride is a **sulfonylurea for type 2 diabetes** and does not interact with fluoroquinolones in a way that would decrease moxifloxacin absorption.
- Fluoroquinolones can increase the risk of **hypoglycemia** when co-administered with sulfonylureas, but they do not affect each other's absorption.
*Prednisone*
- Prednisone is a **corticosteroid** often used for COPD exacerbations; it does not interfere with the absorption of moxifloxacin.
- There are no known significant pharmacokinetic interactions between corticosteroids and fluoroquinolones that would lead to undetectable moxifloxacin levels.
*Amitriptyline*
- Amitriptyline is a **tricyclic antidepressant** used for depression; it does not interact with fluoroquinolones to reduce their absorption.
- While fluoroquinolones can prolong the **QT interval** which could add to the **arrhythmogenic risk** of amitriptyline, this interaction does not affect moxifloxacin absorption.
Oxazolidinones and streptogramins US Medical PG Question 5: A 33-year-old woman presents to her local clinic in rural eastern India complaining of neck pain and fever. She reports a 4 day history of severe neck pain, neck stiffness, mild diarrhea, and fever. She has not taken her temperature. She works as a laborer and frequently carries heavy weights on her back. She is prescribed a medication and told to come back if her symptoms do not improve. Her symptoms resolve after a couple days. Six months later, she gives birth to a newborn male at 34 weeks gestation. His temperature is 97.8°F (36.6°C), blood pressure is 90/55 mmHg, pulse is 110/min, and respirations are 24/min. On examination, the baby is irritable with a weak cry. Ashen gray cyanosis is noted diffusely. What is the mechanism of action of the drug responsible for this child's presentation?
- A. DNA-dependent RNA polymerase inhibitor
- B. Dihydropteroate synthase inhibitor
- C. DNA gyrase inhibitor
- D. 30S ribosomal subunit inhibitor
- E. 50S ribosomal subunit inhibitor (Correct Answer)
Oxazolidinones and streptogramins Explanation: ***50S ribosomal subunit inhibitor***
- The mother's symptoms (neck pain, stiffness, fever, mild diarrhea) and rapid improvement suggest a bacterial infection treated with an antibiotic. Given the newborn's presentation of **gray baby syndrome** (ashen gray cyanosis, irritability, weak cry, hypothermia, hypotension), the likely causative drug is **chloramphenicol**.
- **Chloramphenicol** inhibits bacterial protein synthesis by binding to the **50S ribosomal subunit**, which can cause idiosyncratic toxicity in neonates due to underdeveloped glucuronidation enzymes needed for its metabolism.
*DNA-dependent RNA polymerase inhibitor*
- This mechanism describes drugs like **rifampin**, which is primarily used for **tuberculosis** and does not cause gray baby syndrome.
- Rifampin's side effects include **red-orange discoloration** of bodily fluids and **hepatotoxicity**, which are distinct from the described neonatal symptoms.
*Dihydropteroate synthase inhibitor*
- This mechanism is characteristic of **sulfonamides** (e.g., sulfamethoxazole), which inhibit folic acid synthesis in bacteria.
- Sulfonamides are associated with **kernicterus** in neonates (due to displacement of bilirubin from albumin), not gray baby syndrome.
*DNA gyrase inhibitor*
- This describes **fluoroquinolones** (e.g., ciprofloxacin), which block bacterial DNA replication and transcription.
- Fluoroquinolones are generally **contraindicated in pregnancy and children** due to concerns about cartilage damage, but they do not cause gray baby syndrome.
*30S ribosomal subunit inhibitor*
- This mechanism is used by **tetracyclines** and **aminoglycosides**.
- **Tetracyclines** can cause **tooth discoloration** and **bone growth inhibition** in children, while **aminoglycosides** are associated with **ototoxicity** and **nephrotoxicity**; neither causes gray baby syndrome.
Oxazolidinones and streptogramins US Medical PG Question 6: A 61-year-old woman who recently emigrated from India comes to the physician because of a 2-month history of fever, fatigue, night sweats, and a productive cough. She has had a 5-kg (11-lb) weight loss during this period. She has a history of type 2 diabetes mellitus and poorly controlled asthma. She has had multiple asthma exacerbations in the past year that were treated with glucocorticoids. An x-ray of the chest shows a cavitary lesion of the posterior apical segment of the left upper lobe with consolidation of the surrounding parenchyma. The pathogen identified on sputum culture is found to be resistant to multiple drugs, including streptomycin. Which of the following mechanisms is most likely involved in bacterial resistance to this drug?
- A. Alteration in the sequence of gyrA genes
- B. Upregulation of arabinosyl transferase production
- C. Upregulation of mycolic acid synthesis
- D. Alteration in 30S ribosomal subunit (Correct Answer)
- E. Inhibition of bacterial synthesis of RNA
Oxazolidinones and streptogramins Explanation: ***Alteration in 30S ribosomal subunit***
- Streptomycin is an **aminoglycoside antibiotic** that acts by binding to the **16S rRNA of the 30S ribosomal subunit**, which interferes with bacterial protein synthesis.
- **Resistance to streptomycin** most commonly arises from mutations in the genes encoding ribosomal proteins (e.g., *rpsL*) or the 16S rRNA that alter the drug's binding site on the 30S ribosomal subunit, preventing its inhibitory effect.
*Alteration in the sequence of gyrA genes*
- Mutations in the *gyrA* gene typically confer resistance to **fluoroquinolone antibiotics**, such as ciprofloxacin and levofloxacin.
- Fluoroquinolones target **DNA gyrase (topoisomerase II)**, which is encoded by *gyrA*, not the ribosomes.
*Upregulation of arabinosyl transferase production*
- **Arabinogalactan**, a major component of the mycobacterial cell wall, is synthesized by **arabinosyl transferases** (e.g., EmbB).
- Resistance to **ethambutol** is often associated with mutations or upregulation of these enzymes, leading to increased synthesis of the arabinogalactan layer.
*Upregulation of mycolic acid synthesis*
- **Mycolic acid** is a crucial component of the mycobacterial cell wall, and its synthesis is inhibited by drugs like **isoniazid**.
- Upregulation of mycolic acid synthesis or mutations in genes related to its production (e.g., *kasA*) can lead to **isoniazid resistance**, but not directly to streptomycin resistance.
*Inhibition of bacterial synthesis of RNA*
- **Rifampin** is an antibiotic that inhibits bacterial RNA synthesis by binding to the **DNA-dependent RNA polymerase**.
- While resistance to rifampin often involves mutations in the *rpoB* gene, this mechanism is specific to rifampin and not streptomycin.
Oxazolidinones and streptogramins US Medical PG Question 7: A 22-year-old woman presents to the emergency department because of agitation and sweating. History shows she is currently being treated for depression with citalopram. She also takes tramadol for back pain. Her temperature is 38.6°C (101.5°F), the pulse is 108/min, the respirations are 18/min, and the blood pressure is 165/110 mm Hg. Physical examination shows hyperreflexia and mild tremors in all 4 extremities. Which of the following should be used in the next step of management for this patient?
- A. Diazepam
- B. Chlorpromazine
- C. Cyproheptadine
- D. Selegiline
- E. Discontinue tramadol and citalopram (Correct Answer)
Oxazolidinones and streptogramins Explanation: ***Discontinue tramadol and citalopram***
- This patient presents with symptoms highly suggestive of **serotonin syndrome**, characterized by **agitation, sweating, hyperthermia, tachycardia, hypertension, hyperreflexia, and tremors**, stemming from the concomitant use of **citalopram (SSRI)** and **tramadol (serotonergic properties)**.
- The immediate priority in managing serotonin syndrome is to **discontinue all serotonergic agents** definitively, as continued exposure can worsen symptoms and lead to severe complications.
*Diazepam*
- While **benzodiazepines** like diazepam are often used to manage agitation and hyperreflexia in serotonin syndrome, they are **symptomatic treatments** and do not address the underlying cause.
- Their use would be **adjunctive to discontinuing the causative agents**, not the primary next step.
*Chlorpromazine*
- **Chlorpromazine** is an antipsychotic with **dopamine-blocking effects** and anticholinergic properties; it is **not indicated** for the treatment of serotonin syndrome.
- In fact, its use could **exacerbate certain symptoms** or lead to adverse effects due to its other pharmacological actions.
*Cyproheptadine*
- **Cyproheptadine** is a **serotonin antagonist** that can be used in some cases of severe serotonin syndrome to counteract the excessive serotonin activity.
- However, the **initial and most critical step** is to discontinue the offending medications before considering pharmacologic interventions like cyproheptadine, which is typically reserved for moderate to severe cases after initial drug cessation.
*Selegiline*
- **Selegiline** is a **monoamine oxidase B (MAO-B) inhibitor** that increases dopamine levels and, at higher doses, can also inhibit MAO-A, leading to increased serotonin.
- Administering another serotonergic agent would be **contraindicated** and potentially fatal in a patient experiencing serotonin syndrome.
Oxazolidinones and streptogramins US Medical PG Question 8: A patient on SSRI sertraline was also prescribed amitriptyline and subsequently developed serotonin toxicity. What is the likely treatment for serotonin toxicity?
- A. Flumazenil
- B. Cyproheptadine (Correct Answer)
- C. L-Carnitine
- D. Leucovorin
- E. Naloxone
Oxazolidinones and streptogramins Explanation: ***Cyproheptadine***
- **Cyproheptadine** is a serotonin antagonist that can help reverse the effects of excessive serotonin in the central nervous system.
- It works by blocking **serotonin 5-HT2A receptors**, which are implicated in the pathophysiology of serotonin toxicity.
*Flumazenil*
- **Flumazenil** is a benzodiazepine receptor antagonist used to reverse the effects of benzodiazepine overdose.
- It has no role in the treatment of **serotonin toxicity**, as it does not affect serotonin pathways.
*L-Carnitine*
- **L-Carnitine** is a mitochondrial co-factor used in fatty acid metabolism, sometimes supplemented for certain metabolic disorders or muscle pain.
- It does not have any direct action on **serotonin receptors** or the serotonin system, making it ineffective for serotonin toxicity.
*Leucovorin*
- **Leucovorin** (folinic acid) is used to counteract the effects of methotrexate toxicity or to enhance the effects of fluorouracil in chemotherapy.
- It is not involved in modulating **neurotransmitter levels** or reversing the symptoms of serotonin toxicity.
*Naloxone*
- **Naloxone** is an opioid receptor antagonist used to reverse opioid overdose.
- It has no effect on **serotonin receptors** or serotonergic pathways, making it ineffective for treating serotonin toxicity.
Oxazolidinones and streptogramins US Medical PG Question 9: A 50-year-old woman presents with acute onset fever and chills for the past hour. She mentions earlier in the day she felt blue, so she took some St. John’s wort because she was told by a friend that it helps with depression. Past medical history is significant for hypertension, diabetes mellitus, and depression managed medically with captopril, metformin, and fluoxetine. She has no history of allergies. Her pulse is 130/min, the respiratory rate is 18/min, the blood pressure is 176/92 mm Hg, and the temperature is 38.5°C (101.3°F). On physical examination, the patient is profusely diaphoretic and extremely irritable when asked questions. Oriented x 3. The abdomen is soft and nontender with no hepatosplenomegaly. Increased bowel sounds are heard in the abdomen. Deep tendon reflexes are 3+ bilaterally and clonus is elicited. The sensation is decreased in the feet bilaterally. Mydriasis is present. Fingerstick glucose is 140 mg/dL. An ECG shows sinus tachycardia but is otherwise normal. Which of the following is the most likely cause of this patient’s condition?
- A. Sepsis
- B. Anaphylactic reaction
- C. Diabetic ketoacidosis
- D. Neuroleptic malignant syndrome
- E. Serotonin syndrome (Correct Answer)
Oxazolidinones and streptogramins Explanation: ***Serotonin syndrome***
- The patient's presentation with **fever, diaphoresis, hypertension, tachycardia, hyperreflexia, clonus, mydriasis**, and **agitation** after combining an **SSRI (fluoxetine)** with **St. John's wort** (a serotonin-enhancing herbal supplement) is highly characteristic of serotonin syndrome.
- This condition results from excessive serotonergic activity in the central and peripheral nervous system.
*Sepsis*
- While **fever, chills, and tachycardia** can be indicators of sepsis, the presence of specific neurological and neuromuscular signs like **hyperreflexia, clonus, and mydriasis** points away from it.
- The patient's **irritable state and normal mental orientation** is less typical for severe sepsis, which often involves altered mental status.
*Anaphylactic reaction*
- **Anaphylaxis** presents with rapid onset of symptoms such as **urticaria, angioedema, bronchospasm, and hypotension**, which are not observed in this patient.
- There is no history of allergen exposure, and the prominent neurological symptoms are not typical of anaphylaxis.
*Diabetic ketoacidosis*
- **DKA** is characterized by **hyperglycemia, metabolic acidosis, and ketonemia**, often presenting with Kussmaul respirations and fruity breath odor.
- The patient's **fingerstick glucose (140 mg/dL)** is not significantly elevated, and there is no mention of deep, rapid breathing or other DKA-specific symptoms.
*Neuroleptic malignant syndrome*
- **NMS** is typically associated with exposure to **dopamine antagonists (antipsychotics)** and is characterized by **severe muscle rigidity, hyperthermia, altered mental status, and autonomic instability.**
- While some symptoms overlap, this patient's history of St. John's wort and fluoxetine points to increased serotonin, and the specific neuromuscular findings like clonus are more indicative of serotonin syndrome.
Oxazolidinones and streptogramins US Medical PG Question 10: A 58-year-old female presents to her primary care physician with a 1-month history of facial and chest flushing, as well as intermittent diarrhea and occasional difficulty breathing. On physical exam, a new-onset systolic ejection murmur is auscultated and is loudest at the left second intercostal space. Subsequent echocardiography reveals leaflet thickening secondary to fibrous plaque deposition on both the pulmonic and tricuspid valves. Which of the following laboratory abnormalities would most likely be found in this patient?
- A. Elevated urinary 5-hydroxyindoleacetic acid (Correct Answer)
- B. Elevated serum bicarbonate
- C. Elevated serum potassium
- D. Decreased serum chromogranin A
- E. Elevated urinary vanillylmandelic acid
Oxazolidinones and streptogramins Explanation: **Elevated urinary 5-hydroxyindoleacetic acid**
* This patient's symptoms (flushing, diarrhea, dyspnea, and cardiac valve abnormalities, especially right-sided with fibrous plaque deposition) are classic for **carcinoid syndrome**. This syndrome is caused by neuroendocrine tumors, often in the gastrointestinal tract, that secrete large amounts of serotonin.
* **5-hydroxyindoleacetic acid (5-HIAA)** is the main metabolite of **serotonin**, and its elevated levels in urine are a key diagnostic marker for carcinoid syndrome.
*Elevated serum bicarbonate*
* **Elevated serum bicarbonate** is typically associated with **metabolic alkalosis**, which is not a direct or expected finding in carcinoid syndrome.
* Carcinoid syndrome can lead to electrolyte imbalances due to diarrhea, but metabolic alkalosis through elevated bicarbonate is not a primary or characteristic feature.
*Elevated serum potassium*
* **Elevated serum potassium** (hyperkalemia) is not a common or direct consequence of carcinoid syndrome.
* While severe diarrhea can sometimes lead to electrolyte disturbances, it more typically causes **hypokalemia** due to potassium loss, not hyperkalemia.
*Decreased serum chromogranin A*
* **Chromogranin A** is a general marker for neuroendocrine tumors; however, in actively secreting tumors like those causing carcinoid syndrome, **serum chromogranin A** levels would most likely be **elevated**, not decreased.
* It serves as a useful diagnostic and prognostic marker for neuroendocrine tumors, indicating tumor burden and activity.
*Elevated urinary vanillylmandelic acid*
* **Elevated urinary vanillylmandelic acid (VMA)** is a diagnostic marker for **pheochromocytoma** and **paraganglioma**, tumors that secrete catecholamines (epinephrine and norepinephrine).
* While some symptoms like flushing can overlap, the specific cardiac and gastrointestinal symptoms described, along with the right-sided valvular lesions, are characteristic of carcinoid syndrome, not pheochromocytoma.
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