Upper Gastrointestinal Bleeding: MCCQE Notes
Resuscitate, risk-stratify, scope within 24 hours — and know which patients get antibiotics and a vasoactive drug before the endoscope.
Structured the way you revise — mechanism, discriminators, first-line management, and the details that separate the right answer from the plausible one.
58 notes
Resuscitate, risk-stratify, scope within 24 hours — and know which patients get antibiotics and a vasoactive drug before the endoscope.
Acute onset with fluctuating attention is delirium until proven otherwise — and it is a medical emergency, not a behavioural problem.
A first unprovoked seizure does not automatically mean antiepileptic drugs; status is a timed protocol you should know by heart.
Pre-renal, renal, post-renal — and an ultrasound plus a urinalysis will usually tell you which.
The CTFPHC recommendations differ from the American ones in ways the exam deliberately targets — breast, cervical and prostate especially.
Post-bronchodilator spirometry makes the diagnosis, and only three interventions change mortality.
Pretest probability comes first. Order a D-dimer without it and you have made the problem worse.
Non-contrast CT first, then the two time windows — thrombolysis and thrombectomy — and the secondary prevention that starts the same admission.
Four diagnostic tests, an individualised A1C target, and drug choice driven by cardiovascular and renal disease rather than by glucose alone.
Fluid first, then insulin, and never start insulin before you know the potassium.
TSH plus free T4 resolves nearly every stem — once you know the four patterns and the two traps.
Confidentiality is the rule; the exceptions are a short, memorisable list. Knowing which are mandatory and which are discretionary is the whole question.
Capacity is decision-specific, not a label on a patient — and in Canada a capable minor can consent for themselves. The two ideas the exam tests hardest.
Ascites, SBP, encephalopathy, varices and hepatorenal syndrome — each with a treatment the exam expects verbatim.
Sensitivity and specificity, predictive values that move with prevalence, and the difference between relative and absolute risk.
Volume status plus urine sodium and osmolality gets you to the cause, and the rate of correction is what keeps the patient safe.
The MCV splits the differential three ways, and the reticulocyte count tells you whether the marrow is trying.
Diagnostic thresholds depend on how the pressure was measured, and the treatment target depends on the patient. Both are commonly examined.
The first decision is STEMI or not, because it changes the clock. Everything else follows from that fork.
The nomogram, the eight-hour window, and the King's College criteria — and why a normal patient at four hours proves nothing.
Under 28 days, fever means a full septic work-up and admission — no exceptions, however well the baby looks.
Efficacy in typical use, the absolute contraindications to oestrogen, and emergency contraception — the three things reliably examined.
Four drug classes change mortality and everything else treats symptoms. Knowing which is which answers most questions.
Diagnosis needs demonstrated variable airflow obstruction, and escalation decisions are driven by a short list of control questions.
Preeclampsia no longer requires proteinuria, magnesium is for seizures rather than blood pressure, and delivery is the only cure.
Diagnosis by criteria, treatment by evidence, and a risk assessment that asks directly rather than inferring.
Fever, jaundice and acute kidney injury after freshwater or occupational exposure — the classic Weil's disease vignette.
Atypical pneumonia with hyponatraemia, deranged LFTs and confusion after foreign travel or air-conditioning exposure — diagnosed on a urinary antigen.
The serology table is the exam. Learn to read HBsAg, anti-HBc and anti-HBs and every hepatitis B question becomes a pattern match.
Large urine volumes with a short differential — sort them into osmotic, water diuresis and drug causes.
Removing pathogenic antibodies and immune complexes from plasma — key in anti-GBM disease, TTP and severe vasculitis.
Home dialysis using the peritoneum as a membrane — with peritonitis as its defining complication.
Ischaemic death of the renal papillae — think analgesic nephropathy, diabetes and sickle cell disease.
An acute kidney injury a few days after iodinated contrast — largely preventable with hydration and risk-factor control.
Heavy urinary protein loss brings predictable complications — thrombosis, infection and hyperlipidaemia chief among them.
A mixed nephritic-nephrotic glomerulonephritis with 'tram-track' basement membranes and low complement — think hepatitis C and complement dysregulation.
The physiology of clearance — inulin for GFR, PAH for renal plasma flow, and why creatinine clearance overestimates GFR.
The world's commonest glomerulonephritis — visible haematuria a day or two after an upper respiratory infection.
Low potassium sorted by whether it comes with alkalosis or acidosis — plus the classic U-wave ECG and safe replacement.
Dilatation of the renal pelvis and calyces from obstruction — with useful mnemonics for the unilateral and bilateral causes.
A collapsing FSGS of advanced HIV — heavy proteinuria, large echogenic kidneys and rapid progression, best treated with antiretrovirals.
A thrombotic microangiopathy with a classic triad — usually following Shiga-toxin E. coli, occasionally from complement dysregulation.
A framework for the glomerular diseases — splitting them along the nephritic-to-nephrotic spectrum.
The NICE framework for prescribing IV fluids — resuscitation, routine maintenance, replacement, redistribution and reassessment.
Generalised proximal tubular failure — leaking glucose, amino acids, phosphate and bicarbonate into the urine.
Often the first warning sign of cardiovascular disease — with a useful organic-versus-psychogenic split guiding assessment.
Polyuria from ADH deficiency (cranial) or ADH resistance (nephrogenic) — distinguished by the water deprivation test.
An inherited defect in dibasic amino-acid reabsorption causing recurrent, poorly soluble cystine stones from a young age.
Persistent pelvic pain and urinary symptoms — most cases are non-bacterial chronic pelvic pain syndrome rather than infection.
A normochromic normocytic anaemia driven by erythropoietin deficiency — correct iron first, then use ESAs to a modest haemoglobin target.
The childhood form of polycystic kidney disease — presenting antenatally or in infancy, with congenital hepatic fibrosis.
A pulmonary-renal syndrome from antibodies against type IV collagen — rapidly progressive glomerulonephritis with lung haemorrhage.
A simple calculation that splits metabolic acidosis into raised-gap and normal-gap causes — and points you to the diagnosis.
Extracellular deposition of misfolded protein causing nephrotic syndrome, cardiac and multi-system disease — diagnosed by Congo red staining.
A rare syndrome combining acute interstitial nephritis with anterior uveitis, classically in young women.
An immune-mediated cause of acute kidney injury — usually drug-induced — with eosinophilia, sterile pyuria and white cell casts.
A flagellate protozoan causing non-bloody, fatty diarrhoea and malabsorption — diagnosed by stool antigen assay and treated with metronidazole.
The commonest cause of nephrotic syndrome in older Caucasian adults — with a signature anti-PLA2R antibody and subepithelial deposits.