• Beta-blockers
o ↓ HR and BP via β1 blockade
o Indications: angina, HF, AF, post-MI
o Cautions: avoid in asthma/COPD (bronchospasm), bradycardia, fatigue
o Examples: bisoprolol, atenolol
• ACE inhibitors (ACEi)
o ↓ BP, proteinuria, post-MI and HF mortality
o Adverse effects: cough, angioedema, hyperkalaemia, ↑ creatinine
o Monitor U&Es 1–2 weeks after initiation
o Example: ramipril
• Angiotensin receptor blockers (ARBs)
o Similar to ACEi but no cough
o Monitor for hyperkalaemia, renal function
o Example: losartan
• Calcium channel blockers (CCBs)
o Dihydropyridines (e.g. amlodipine): vasodilation → ankle oedema, flushing
o Non-dihydropyridines (e.g. verapamil, diltiazem): rate control, avoid with beta-blockers
• Diuretics
o Loop diuretics (furosemide): potent; risk of hypokalaemia, hypovolaemia, ototoxicity
o Thiazides (bendroflumethiazide, indapamide): cause hypercalcaemia,
hyponatraemia, gout, impaired glucose tolerance
• Anticoagulants
o Warfarin: inhibits vitamin K-dependent factors (II, VII, IX, X); INR monitoring required
o Many interactions (e.g. antibiotics, amiodarone)
o DOACs (rivaroxaban, apixaban): fixed doses, renal dose adjustment, no monitoring
• Antiplatelets
o Aspirin: irreversible COX-1 inhibitor; risk of GI irritation, bleeding
o Clopidogrel: P2Y12 inhibitor; metabolised by CYP2C19 → variable response
• Insulin
o Types: rapid (aspart), long-acting (glargine), premixed
o Basal–bolus regimen preferred in Type 1
o Risk: hypoglycaemia (tremor, confusion, seizures)
• Oral hypoglycaemics
o Metformin: 1st line in T2DM; GI upset; risk of lactic acidosis if eGFR <30
o Sulfonylureas (gliclazide): risk of hypoglycaemia, weight gain
o SGLT2 inhibitors (dapagliflozin): CV benefit, ↓ HbA1c, weight loss; UTI, DKA risk even with normal glucose
• Thyroid drugs
o Levothyroxine: monitor TSH every 6–8 weeks when starting or adjusting
o Carbimazole/PTU: risk of agranulocytosis (check FBC with sore throat/fever)
• Steroids
o Routes: oral, IV, inhaled, topical
o Adverse effects: weight gain, osteoporosis, diabetes, psychosis, infections
o Long-term use → consider bisphosphonates and PPI cover
• PPIs (omeprazole, lansoprazole)
o Indications: GORD, PUD, Barrett’s
o Risks with long-term use: ↓ Mg²⁺, ↓ B12, C. difficile, fractures
• Laxatives
o Stimulant (senna): risk of cramping, dependence
o Osmotic (lactulose): draws fluid in; also used in hepatic encephalopathy to ↓ ammonia
• Anti-emetics
o Metoclopramide: risk of extrapyramidal side effects, avoid long-term
o Ondansetron: QT prolongation, constipation
• Antiepileptics
o Phenytoin: narrow therapeutic index, zero-order kinetics, enzyme inducer
o Valproate: hepatotoxic, teratogenic (NTDs); avoid in women of childbearing age if possible
• Antipsychotics
o Typical (haloperidol): EPS, QT prolongation
o Atypical (risperidone): less EPS, ↑ prolactin
o Clozapine: reserved for resistant schizophrenia; agranulocytosis, myocarditis → requires regular FBC
• Antidepressants
o SSRIs (sertraline, citalopram): 1st line; hyponatraemia, GI bleeding (esp. with NSAIDs), serotonin syndrome
o TCAs (amitriptyline): anticholinergic, cardiotoxic in overdose, QT prolongation
• Mood stabilisers
o Lithium: narrow therapeutic index, nephrotoxic, thyroid dysfunction
o Monitor levels, U&Es, TFTs every 3–6 months
• NSAIDs
o Risks: renal impairment, peptic ulcers, cardiovascular events
o Use gastroprotection (e.g. PPI) in high-risk patients
• Methotrexate
o Weekly dosing; co-prescribe folic acid
o Monitor FBC, LFTs, renal function
o Contraindicated in pregnancy
• Biologics (e.g. infliximab, etanercept)
o Screen for latent TB and hepatitis B/C before initiation
o Risk of reactivation and infections
• Steroids
o Taper if >3 weeks to avoid adrenal suppression
o Bone protection (vitamin D + calcium ± bisphosphonate) if long-term
• Antibiotics
o Penicillins: common cause of rash, anaphylaxis
o Aminoglycosides (gentamicin): nephrotoxic, ototoxic; monitor levels
o Macrolides (erythromycin): enzyme inhibitors, QT prolongation
o Quinolones (ciprofloxacin): tendon rupture, QT risk
• Antivirals
o Aciclovir: risk of crystalluria, AKI if IV without adequate hydration
• Anti-TB therapy
o Rifampicin: enzyme inducer, orange secretions
o Isoniazid: peripheral neuropathy (prevent with pyridoxine)
o Pyrazinamide: hepatotoxic, hyperuricaemia
o Ethambutol: optic neuritis (check visual acuity)
Principles of drug metabolism and interactions
Clinical pharmacology and prescribing in special situations
System-based theraputics and core drug classes
————————————————————————————————————————————————————————————————————————————————————————————————————————-
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.
