MRCP Part 1
MRCP Part 1 revision notes
Free, full-length MRCP Part 1 revision notes from Examrix — acid–base, acute kidney injury, diabetic emergencies, thyroid disease, ECG interpretation and more, each written to Best of Five depth.
Nephrology
- Acid-Base DisordersMetabolic acid-base disorders represent complex alterations in systemic bicarbonate concentrations and extracellular fluid volume. Evaluation must begin with arterial or venous blood gas analysis to establish the primary process, followed by calculation of the anion gap (corrected for albumin) and assessment of respiratory compensation using Winter's formula. Metabolic acidosis is divided into high anion gap (accumulation of unmeasured organic acids) and normal anion gap (bicarbonate loss or renal tubular dysfunction) variants, while metabolic alkalosis is subclassified by its responsiveness to saline resuscitation, guided by urinary chloride levels. Comprehensive metabolic and urinary electrolyte profiles remain the cornerstone of differential diagnosis. Free to read 30 min read
- Acute Kidney InjuryAcute Kidney Injury (AKI) is a rapid decline in renal excretory function characterized by accumulation of nitrogenous waste products and inability to maintain fluid and electrolyte homeostasis. Diagnosed and staged using the KDIGO criteria (based on serum creatinine rises and urine output decline), its etiology is categorized into prerenal (hypoperfusion), intrinsic (ATN, AIN, glomerulonephritis), and postrenal (obstructive) pathways. Systematic investigation requires clinical volume status assessment, urinary biochemistry (FE Na , FE Urea ), urine sediment microscopy, and renal tract imaging. Management is centered around treating the underlying cause, hemodynamic optimization via balanced crystalloids, strict avoidance of nephrotoxins, and timely correction of life-threatening complications like hyperkalemia, metabolic acidosis, and fluid overload, with RRT reserved for refractory cases. Free to read 30 min read
- CKD Complications and TreatmentManagement of advanced CKD complications requires balancing haematological, metabolic, and immunological systems. Anaemia of CKD is managed with targeted iron replacement followed by ESA therapy to a strict target Hb of 100–120 g/L. CKD-MBD is managed by controlling hyperphosphataemia and secondary hyperparathyroidism using dietary restriction, calcium-free binders (e.g., Sevelamer), and calcimimetics, with the goal of avoiding adynamic bone disease and vascular calcification. When GFR falls below 15 mL/min/1.73m², preparation for renal replacement therapy is mandatory. Renal transplantation offers the best survival advantage; success relies on HLA-DR matching and triple immunosuppressive therapy, while vigilantly monitoring for CNI nephrotoxicity, BK virus nephropathy, and acute rejection. Free to read 30 min read
Endocrinology
- Adrenal DiseaseAdrenal disorders present high-yield diagnostic dilemmas in post-graduate examinations. Addison's disease demands urgent recognition of mineralocorticoid and glucocorticoid deficiency, confirmed via Synacthen testing and treated with physiological hormone replacement. Cushing's syndrome requires a meticulous two-step approach: first establishing hypercortisolism using screening tests (such as the 1mg ONDST), followed by ACTH-driven localization (distinguishing adrenal, pituitary, and ectopic sources). Primary Hyperaldosteronism represents the most common secondary cause of hypertension, requiring careful medication washouts prior to ARR screening, confirmation via saline suppression, and localization via adrenal vein sampling before surgical intervention. Free to read 30 min read
- Calcium DisordersCalcium homeostasis is tightly regulated by the feedback loop between ionized calcium, the calcium-sensing receptor (CaSR), PTH, and active vitamin D. Hypercalcaemia is most commonly driven by primary hyperparathyroidism in the outpatient setting and malignancy (via PTHrP or osteolytic lesions) in hospitalised patients. Acute severe hypercalcaemia requires immediate volume expansion with isotonic saline followed by intravenous bisphosphonates or denosumab. Hypocalcaemia requires step-wise assessment of magnesium, renal function, and PTH levels to differentiate between hypoparathyroidism, vitamin D deficiency, and pseudohypoparathyroidism. Free to read 30 min read
- Diabetic EmergenciesDiabetic emergencies demand a highly structured, biomarker-driven therapeutic approach. DKA is characterized by absolute insulin deficiency leading to uncontrolled ketogenesis and metabolic acidosis; its resolution requires fixed-rate insulin to clear ketones, co-administered with dextrose to prevent hypoglycemia, and meticulous potassium replacement. HHS represents a state of relative insulin sufficiency that prevents ketogenesis but permits extreme hyperglycemia, causing profound osmotic diuresis and dehydration; its management focuses primarily on gradual fluid resuscitation and cautious osmolality reduction. Hypoglycemia represents an immediate neurological threat requiring rapid, graded glucose replacement, with special strategies like octreotide reserved for sulfonylurea-induced refractory cases. Free to read 30 min read
- Thyrotoxicosis and HypothyroidismThyroid disorders present along a spectrum of metabolic activity defined by synthesis and destruction. Hyperthyroidism is categorized into high-uptake states (Graves' disease, toxic multinodular goiter, toxic adenoma) and low-uptake states (destructive thyroiditis, exogenous levothyroxine excess). Hypothyroidism primarily arises from autoimmune destruction (Hashimoto's thyroiditis), post-ablative therapy, or drug-induced states (amiodarone, lithium, checkpoint inhibitors). Accurate clinical assessment requires integrating serological profiles (TSH, free T4/T3, TRAb, anti-TPO) with functional imaging, ensuring that treatment is tailored specifically to the underlying pathophysiology rather than biochemically abnormal numbers alone. Free to read 30 min read
Cell Biology
Gastroenterology
- Chronic Liver DiseaseChronic liver disease progresses through a spectrum of metabolic (NAFLD/MASLD) or toxic (alcohol-related) insults toward liver cirrhosis and portal hypertension. Management requires strict adherence to evidence-based scoring systems for risk stratification (FIB-4, ELF) and clinical decision-making. Decompensated cirrhosis represents a medical emergency where the physiological consequences of splanchnic vasodilation—namely ascites, spontaneous bacterial peritonitis, variceal hemorrhage, and hepatorenal syndrome—must be addressed using targeted vasoactive drugs (terlipressin), volume expansion (20% human albumin), and prompt antimicrobial therapy. Free to read 30 min read
- Decompensated CirrhosisDecompensated cirrhosis is characterized by portal hypertension and a hyperdynamic circulatory state, leading to a spectrum of critical complications. Ascites is managed with sodium restriction and dual-diuretic therapy, with large-volume paracentesis (>5L) requiring albumin replacement to prevent circulatory collapse. Spontaneous bacterial peritonitis requires urgent diagnostic tap (PMNs ≥ 250 cells/mm³), prompt empiric 3rd-generation cephalosporins, and renal protection with albumin. Acute variceal hemorrhage is a medical emergency managed with early vasoactive agents, prophylactic antibiotics, and urgent endoscopic ligation. Hepatic encephalopathy is a clinical diagnosis triggered by identifiable factors, managed with lactulose and rifaximin. Hepatorenal syndrome represents functional renal failure due to extreme splanchnic vasodilation, requiring volume expansion with albumin and splanchnic vasoconstrictor therapy with terlipressin. Free to read 30 min read
Anatomy
Cardiology
- Congenital Heart Disease: Shunts and Structural LesionsAdult Congenital Heart Disease (ACHD) represents a rapidly growing cohort in clinical cardiology due to highly successful pediatric surgical interventions. Internists must recognize the long-term sequelae of repaired lesions (e.g., pulmonary regurgitation and ventricular arrhythmias decades after Tetralogy of Fallot repair) as well as newly presenting, unrepaired lesions such as ostium secundum ASDs, bicuspid aortic valves, or coarctation of the aorta. Diagnostic evaluation relies heavily on transthoracic and transesophageal echocardiography, supplemented by Cardiac MRI for gold-standard quantification of ventricular volumes and shunt fractions (Qp:Qs). Managing these complex patients requires a multidisciplinary approach, balancing intervention criteria against the irreversible pulmonary vascular changes of Eisenmenger syndrome. Free to read 30 min read
- ECG, Exercise Testing and Cardiac BiomarkersThis tutorial reviews the advanced clinical and electrophysiological aspects of electrocardiogram interpretation, exercise tolerance testing, and cardiac biomarkers required for postgraduate medical examinations. Accurate diagnosis of myocardial ischemia requires recognizing specific infarct equivalents like Wellens' and de Winter T-wave patterns, and applying the Sgarbossa criteria in patients with baseline LBBB. When performing exercise tolerance tests, strict adherence to absolute contraindications and ensuring the patient achieves 85% of their age-predicted maximal heart rate is mandatory. Finally, interpreting cardiac biomarkers requires a nuanced understanding of high-sensitivity troponin kinetics, the multi-factorial etiologies of myocardial injury, and the physiological clearers of natriuretic peptides, such as obesity and renal impairment. Free to read 30 min read
- Inherited Arrhythmia and Sudden Cardiac Death SyndromesInherited arrhythmia syndromes encompass channelopathies (such as LQTS, Brugada syndrome, and CPVT) and desmosomal cardiomyopathies (such as ARVC). LQTS subtypes (LQT1, LQT2, LQT3) are distinguished by their specific mutated potassium or sodium ion channels and distinct clinical triggers. Brugada syndrome involves a loss-of-function sodium channel mutation (SCN5A) presenting with characteristic right precordial coved ST elevation and is managed with trigger avoidance, quinidine, or ICDs. CPVT results from leaky intracellular calcium release channels (RyR2) triggered by catecholamines, requiring high-dose beta-blockers (nadolol) and flecainide. ARVC is a progressive desmosomal disease causing fibrofatty replacement of the RV, presenting with localized ECG abnormalities (Epsilon waves, V1-V3 T-wave inversions) and carrying a high risk of exercise-induced ventricular arrhythmias. Free to read 30 min read
Rheumatology
Psychiatry
Biostatistics and Evidence-Based Medicine
Geriatric Medicine
Physiology and Biochemistry
Genetics
Immunology
Respiratory
Metabolic Disorders
Haematology
- Microcytic AnaemiaMicrocytic anaemia (MCV <80 fL) is a common diagnostic challenge in postgraduate examinations. The three primary differentials—Iron Deficiency Anaemia, Anaemia of Chronic Disease, and Sideroblastic Anaemia—can be systematically distinguished by evaluating iron kinetics, inflammatory markers, and peripheral blood or bone marrow morphology. Hepcidin is the master regulator, determining whether microcytosis is due to absolute iron depletion (IDA) or iron sequestration (ACD). Accurate differentiation is vital, as it guides appropriate intervention, from urgent gastrointestinal cancer screening in IDA to intravenous iron therapy in chronic cardiorenal syndromes, or cofactor replenishment in sideroblastic states. Free to read 30 min read
- Transfusion MedicinePostgraduate mastery of transfusion medicine requires distinguishing between specific blood components, recognizing precise physiologic transfusion thresholds (e.g., <70 g/L for RBCs, <10 x 10 9 /L for prophylactic platelets), and accurately identifying immunological versus non-immunological transfusion reactions. TACO and TRALI remain high-yield emergency differentials requiring diametrically opposed management strategies. Clinicians must ensure strict clerical accuracy to prevent fatal acute ABO hemolytic reactions and understand the niche indications for modified products (irradiated vs. CMV-negative) to protect highly vulnerable patient populations. Free to read 30 min read
Neurology
- Movement DisordersA precise approach to movement disorders on the MRCP exam relies on classifying the patient's phenomenology as hypokinetic (Parkinson's disease and parkinsonian mimics) or hyperkinetic (essential tremor, chorea, and dystonia). Parkinson's disease is diagnosed clinically through asymmetric bradykinesia, rigidity, and rest tremor, with first-line treatments selected based on age and cognitive profile. Atypical parkinsonian syndromes (PSP, MSA, CBD) must be ruled out using characteristic red flags like early falls, gaze palsies, or early autonomic failure. Essential tremor presents with action-induced bilateral arm tremors that respond to beta-blockers or primidone. Hyperkinetic disorders like Huntington's chorea and primary dystonias represent genetic and physiological abnormalities within the basal ganglia's direct and indirect pathways, managed symptomatically with VMAT-2 inhibitors, anticholinergics (such as trihexyphenidyl), or targeted botulinum toxin injections. Free to read 30 min read
- Stroke and TIAStroke and TIA demand urgent, protocol-driven investigation and management. The Oxford/Bamford schema provides rapid bedside localization into TACS, PACS, LACS, or POCS. Acute ischemic stroke management centers on immediate reperfusion via intravenous alteplase within 4.5 hours and mechanical thrombectomy within 6 to 24 hours for large vessel occlusions. Once hemorrhage is excluded, immediate antiplatelet therapy is initiated—utilizing short-term dual antiplatelets (Aspirin and Clopidogrel) for minor strokes and high-risk TIAs to optimize secondary prevention. Long-term risk reduction mandates strict blood pressure control, high-intensity statin therapy, timely carotid endarterectomy for significant symptomatic stenosis, and oral anticoagulation if atrial fibrillation is identified. Free to read 30 min read
Oncology
Palliative and end of life care
Clinical Pharmacology and Therapeutics
Medical Ophthalmology
Infectious Diseases
- SepsisMastering sepsis requires an advanced clinical synthesis of the Sepsis-3 diagnostic criteria, the pathophysiological transition from sepsis to septic shock, and the precision-driven interpretation of microbiological diagnostics. Management relies on the rapid deployment of the 1-hour bundle, early initiation of first-line vasopressors (Norepinephrine) when fluid resuscitation fails, timely and definitive physical source control, and a systematic approach to identifying true bacteremia versus contaminants in blood cultures. Free to read 30 min read
- Skin and Soft-Tissue InfectionThis tutorial covers the spectrum of skin and soft-tissue infections, highlighting key distinctions between cellulitis, erysipelas, and mimicking non-infectious inflammatory states. Particular emphasis is placed on the rapid recognition and surgical management of necrotising fasciitis, where the addition of clindamycin to standard beta-lactams is essential for toxin suppression. For diabetic foot infections, a multidisciplinary approach focusing on vascular assessment, targeted bone biopsy for osteomyelitis, and broad-spectrum polymicrobial coverage is the gold standard for clinical care and board examination success. Free to read 30 min read
