• Examples: penicillins, cephalosporins, carbapenems, monobactams
• Mechanism: inhibit transpeptidase enzyme → block cell wall (peptidoglycan) synthesis
• Spectrum:
o Penicillin G: streptococci, syphilis
o Amoxicillin: broader (e.g., E. coli, H. influenzae), often combined with clavulanate
o Piperacillin-tazobactam: pseudomonas coverage
• Resistance: β-lactamases, altered penicillin-binding proteins (e.g., MRSA)
• Examples: erythromycin, clarithromycin, azithromycin
• Mechanism: bind 50S ribosomal subunit → inhibit protein synthesis
• Uses: atypical pneumonia (Mycoplasma, Chlamydia), pertussis, alternative for penicillin allergy
• Side effects:
o QT prolongation
o Cholestatic hepatitis
• Examples: ciprofloxacin, levofloxacin, moxifloxacin
• Mechanism: inhibit DNA gyrase (topoisomerase II) and topoisomerase IV
• Uses: Gram-negative UTIs, severe GI infections, pseudomonas (cipro)
• Side effects:
o QT prolongation
o Tendonitis, tendon rupture
o Contraindicated in pregnancy & children (cartilage damage)
• Examples: gentamicin, amikacin, tobramycin
• Mechanism: bind 30S ribosomal subunit → misreading of mRNA → defective protein synthesis
• Uses: severe Gram-negative infections, synergy in endocarditis
• Side effects:
o Nephrotoxicity (proximal tubular necrosis)
o Ototoxicity (vestibular & cochlear damage)
o Neuromuscular blockade
• Example: doxycycline
• Mechanism: bind 30S ribosomal subunit → inhibit protein synthesis
• Uses: Lyme disease, chlamydia, acne, malaria prophylaxis
• Precautions:
o Avoid in children <8 years and pregnancy (teeth staining, bone effects)
o Photosensitivity
• C. difficile colitis: clindamycin, cephalosporins, fluoroquinolones
• QT prolongation: macrolides, fluoroquinolones
• β-lactam allergy: consider aztreonam (monobactam) or macrolide
• Rifampicin:
o Orange secretions
o Potent CYP450 enzyme inducer → interacts with warfarin, OCP
o Peripheral neuropathy (due to B6 deficiency; give pyridoxine)
o Hepatotoxicity
• Pyrazinamide:
o Hyperuricaemia → gout flares
o Hepatotoxicity
• Ethambutol:
o Optic neuritis → red-green colour blindness
o Visual acuity monitoring
Herpesviruses
• Aciclovir: HSV, VZV; nephrotoxicity if not adequately hydrated
• Ganciclovir: CMV; myelosuppression, neutropenia
Influenza
• Oseltamivir (neuraminidase inhibitor): effective if started within 48 hours
HIV therapy
• Drug classes:
o NRTIs (e.g., tenofovir, abacavir)
o NNRTIs (e.g., efavirenz)
o Protease inhibitors (e.g., lopinavir, darunavir)
o Integrase inhibitors (e.g., raltegravir)
• Key side effects:
o Lactic acidosis (esp. NRTIs)
o Lipodystrophy (PIs)
o Hyperlipidaemia, insulin resistance
o Hepatotoxicity
o Inhibit ergosterol synthesis (via CYP inhibition)
o Side effects: hepatotoxicity, QT prolongation, drug interactions
o Binds ergosterol → pore formation → cell death
o "Amphoterrible": nephrotoxicity, electrolyte loss (hypokalaemia, hypomagnesaemia), infusion reactions
o Inhibit β-glucan synthesis in fungal cell wall
o Useful for Candida (esp. fluconazole-resistant), Aspergillus
Malaria
• Artemether-lumefantrine: first-line in uncomplicated falciparum malaria
• Quinine: severe malaria; side effects include cinchonism (tinnitus, headache), hypoglycaemia
• Mefloquine: neuropsychiatric side effects
Schistosomiasis
• Praziquantel: increases calcium permeability → spastic paralysis of worms
Helminths
• Albendazole: inhibits microtubule formation
• Ivermectin: increases chloride permeability → paralysis (useful in strongyloidiasis, onchocerciasis)
• Select right drug, dose, and duration
• Empirical therapy guided by local resistance patterns and severity
• De-escalation once culture results are available
• Avoid unnecessary broad-spectrum use to reduce Clostridioides difficile risk and resistance
• Educate patients about adherence and adverse effects
• Penicillin anaphylaxis: cross-reactivity ~1% with first-generation cephalosporins
• Vancomycin: "red man syndrome" if infused too quickly (histamine-mediated)
• Linezolid: risk of serotonin syndrome if combined with SSRIs, also causes thrombocytopenia
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Author & Educational Disclaimer
Author:
Dr Phillip Cockrell BM FRCP DipClinEd
Dr Phillip Cockrell is a UK Consultant Physician in Internal Medicine, currently working at Queen Alexandra Hospital, Portsmouth University Hospitals NHS Trust. He has previously worked as a registrar across Intensive Care Medicine, Gastroenterology, Cardiology, Stroke Medicine, Acute Medicine, and Respiratory Medicine.
He has held senior leadership roles including Associate Clinical Director of the Acute Medical Unit, Clinical Director of Internal Medicine, and Chief of Medicine. Dr Cockrell has over 15 years’ experience in postgraduate medical education, having lectured extensively across the MRCP syllabus and contributed to MRCP revision teaching and course development.
Dr Cockrell holds a Bachelor of Medicine (BM), Fellowship of the Royal College of Physicians (FRCP), and a Diploma in Clinical Education (DipClinEd). His teaching approach is based on structured consolidation of complex medical topics to support efficient and effective revision for postgraduate examinations.
Purpose of this content:
The material on this page is intended solely for educational purposes to support revision for the MRCP (UK) Part 1 examination. It reflects examination-relevant principles of internal medicine and is designed to aid learning and pattern recognition.
Medical disclaimer:
This content is designed for postgraduate medical examination revision and does not constitute medical advice, diagnosis, or treatment guidance and must not be used as a substitute for professional clinical judgement, local guidelines, or specialist consultation. Clinical decisions should always be made in the context of individual patient circumstances and current national guidance.
