Microbiology & antimicrobials flashcards
27 high-yield MRCP Part 1 cards from the Intellect Medicos Infectious Diseases course. Try to answer each question before you open it — then study them properly with spaced repetition, which brings each card back just before you would forget it.
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What is the mechanism of action of beta-lactam antibiotics (penicillins, cephalosporins, carbapenems)?
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They bind penicillin-binding proteins and block peptidoglycan cross-linking, so the bacterial cell wall cannot be built.
Why? Without an intact cell wall the bacterium lyses, so beta-lactams are bactericidal.
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How does vancomycin kill bacteria?
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It binds the D-Ala-D-Ala terminus of peptidoglycan precursors and blocks cell wall synthesis.
Why? Because it acts at a different site from beta-lactams, it still works against MRSA.
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Aminoglycosides (e.g. gentamicin) bind the ______ ribosomal subunit and cause misreading of mRNA; their two classic toxicities are nephrotoxicity and ototoxicity.
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30S
Why? They are bactericidal protein-synthesis inhibitors; toxicity is dose- and level-related, so levels are monitored.
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Aminoglycosides (e.g. gentamicin) bind the 30S ribosomal subunit and cause misreading of mRNA; their two classic toxicities are ______.
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nephrotoxicity and ototoxicity
Why? They are bactericidal protein-synthesis inhibitors; toxicity is dose- and level-related, so levels are monitored.
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How do tetracyclines (e.g. doxycycline) inhibit bacterial growth?
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They bind the 30S ribosomal subunit and block attachment of aminoacyl-tRNA.
Why? This stops protein chain elongation; tetracyclines are bacteriostatic.
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Name two important side effects of doxycycline that patients should be warned about.
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Photosensitivity and oesophagitis/oesophageal ulceration (take upright with plenty of water).
Why? Both are common and preventable — sun protection and swallowing the tablet standing with a full glass of water.
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Which serious haematological adverse effect is classically linked to chloramphenicol?
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Aplastic anaemia (bone marrow suppression).
Why? Chloramphenicol binds the 50S subunit and inhibits peptidyl transferase; idiosyncratic aplastic anaemia limits systemic use.
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What is the mechanism of action of macrolides (e.g. clarithromycin)?
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They bind the 50S ribosomal subunit and block translocation.
Why? Bacteriostatic protein-synthesis inhibition; useful against atypical organisms and in penicillin allergy.
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A 68-year-old on simvastatin 40 mg is started on clarithromycin for pneumonia. Five days later he has diffuse muscle pain and dark urine. What is the mechanism of this interaction?
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Clarithromycin inhibits CYP3A4, raising simvastatin levels and causing myopathy/rhabdomyolysis.
Why? Clarithromycin and erythromycin are potent P450 inhibitors; simvastatin should be withheld during a course.
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Which antibiotic is classically most associated with Clostridioides difficile diarrhoea?
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Clindamycin.
Why? Broad anaerobic cover disrupts normal colonic flora, letting C. difficile overgrow. Cephalosporins, co-amoxiclav and quinolones are also high risk.
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What is the first-line treatment for a first episode of non-severe C. difficile infection (NICE)?
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Oral vancomycin for 10 days.
Why? Oral vancomycin stays in the gut lumen and acts where the infection is; stop the causative antibiotic if possible.
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What is the target of fluoroquinolones such as ciprofloxacin?
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Bacterial DNA gyrase (topoisomerase II) and topoisomerase IV.
Why? Blocking these enzymes stops DNA supercoiling and replication — bactericidal.
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Which musculoskeletal adverse effect led the MHRA to restrict fluoroquinolone use?
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Tendinitis and tendon rupture (especially Achilles), plus other disabling, long-lasting effects.
Why? Risk is higher in people over 60, in renal impairment, after solid-organ transplant and with corticosteroids. Since January 2024 the MHRA says systemic fluoroquinolones must only be prescribed when other commonly recommended antibiotics are inappropriate.
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Which enzyme does rifampicin inhibit?
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Bacterial DNA-dependent RNA polymerase.
Why? This blocks transcription. For active infection (e.g. TB, staphylococcal infection) rifampicin is not used alone because resistance develops quickly.
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Sulfonamides inhibit ______ and trimethoprim inhibits dihydrofolate reductase, blocking bacterial folate synthesis.
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dihydropteroate synthase
Why? Acting at two steps of the same pathway makes co-trimoxazole synergistic.
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Sulfonamides inhibit dihydropteroate synthase and trimethoprim inhibits ______, blocking bacterial folate synthesis.
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dihydrofolate reductase
Why? Acting at two steps of the same pathway makes co-trimoxazole synergistic.
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Linezolid plus an SSRI can cause which dangerous reaction?
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Serotonin syndrome — linezolid is a weak, reversible MAO inhibitor.
Why? Linezolid inhibits monoamine oxidase, so serotonergic drugs accumulate.
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What reaction occurs if a patient taking metronidazole drinks alcohol?
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A disulfiram-like reaction: flushing, nausea, vomiting, headache and palpitations.
Why? Classically explained by impaired acetaldehyde breakdown (acetaldehyde accumulates), although the exact mechanism is debated. The BNF advises avoiding alcohol during treatment and for 48 hours after.
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Name two situations in which nitrofurantoin should be avoided.
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eGFR below 45 mL/min/1.73 m², and at term in pregnancy (risk of neonatal haemolysis).
Why? In poor renal function it is ineffective in urine and accumulates; near term it can haemolyse fetal red cells.
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How do azole antifungals (e.g. fluconazole) work?
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They inhibit fungal 14α-demethylase (a cytochrome P450 enzyme), blocking ergosterol synthesis.
Why? Ergosterol is the main sterol in the fungal cell membrane.
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What are the two classic adverse effects of amphotericin B?
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Nephrotoxicity and electrolyte loss (hypokalaemia and hypomagnesaemia); also infusion reactions.
Why? Amphotericin binds ergosterol and forms membrane pores, but also binds human cholesterol, damaging renal tubules.
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How does aciclovir selectively act on herpes-infected cells?
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It is phosphorylated by viral thymidine kinase, then inhibits viral DNA polymerase.
Why? Only infected cells activate the drug, so toxicity to normal cells is low.
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Which electrolyte problems does foscarnet classically cause?
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Hypocalcaemia and hypomagnesaemia (also nephrotoxicity).
Why? Foscarnet is a pyrophosphate analogue that chelates divalent cations; it does not need viral thymidine kinase.
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What is the main dose-limiting toxicity of ganciclovir/valganciclovir?
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Myelosuppression, especially neutropenia.
Why? Ganciclovir is more toxic to marrow than aciclovir, so FBC must be monitored.
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Which simple lab test separates Staphylococcus from Streptococcus?
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Catalase test: staphylococci are catalase positive, streptococci catalase negative.
Why? Then coagulase separates S. aureus (positive) from coagulase-negative staphylococci such as S. epidermidis.
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What is the first-choice antibiotic for lower UTI in a non-pregnant woman with eGFR ≥45 (NICE NG109)?
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Nitrofurantoin modified-release 100 mg twice daily for 3 days.
Why? Resistance to nitrofurantoin is low and it concentrates in urine. Trimethoprim for 3 days is the other first choice, but only if the risk of resistance is low.
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What is a first-choice oral antibiotic for acute pyelonephritis in a non-pregnant adult (NICE NG111)?
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Cefalexin for 7–10 days. Ciprofloxacin is now listed only if the other first choices are unsuitable (MHRA 2024).
Why? Upper UTI needs a drug with good tissue levels. Co-amoxiclav or trimethoprim are first choices only when culture shows the organism is susceptible. Cefalexin is also the oral first choice in pregnancy.
More Infectious Diseases topics
- Skin, soft tissue & Gram-positive infections
- Pneumonia & tuberculosis
- Meningitis & encephalitis
- Gastrointestinal infections
- Viral infections & hepatitis
- HIV & opportunistic infections
- Zoonoses & rickettsial infections
- Malaria & tropical infections
- Worms & helminths
- Sexually transmitted infections
- Vaccines, PEP & asplenia