RACP Divisional Written Exam · FRACP

Renal for the written exam

Everything Physify has for Renal: short lessons written to Australian guidance, exam-style questions with a worked explanation for each, and Bedside, our AI tutor, under every one. Try a question below, no sign-up.

courses: 30courses
lessons: 163lessons
exam-style questions: 801exam-style questions
figures in the lessons: 21figures in the lessons

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Renal

A 44-year-old woman has had 3 episodes of immune TTP in 2 years, each needing plasma exchange, despite azathioprine maintenance. She is well, with platelets 240 x 10^9/L and normal LDH, and ADAMTS13 activity was 15 per cent at her last two visits. Which long-term strategy has the strongest evidence for preventing further relapse?

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What's covered

30 courses, each a set of lessons with a quiz after them. The bar shows how many questions each has. Open a course to see its lesson outline.

From the lessons

21 figures sit in the Renal lessons: ECGs, diagrams, films and clinical images, each with what to look for. Here are 4. Tap one to enlarge it.

Schematic glomerular capillary loop: the lumen lined by fenestrated endothelium, the glomerular basement membrane (GBM) around it, podocyte foot processes on the outer surface facing the urinary space, and the mesangium in the stalk beneath the loop. Marked sites: subepithelial deposits under the foot processes (membranous) and a large subepithelial hump; subendothelial deposits between the endothelium and the GBM; mesangial deposits in the stalk; foot process effacement over one segment; and linear staining along the GBM. The table below lists each site. Podocyte: minimal change disease (immunofluorescence negative) and FSGS, both nephrotic. Subepithelial: membranous nephropathy (granular IgG; also lupus class V), nephrotic; post-infectious glomerulonephritis with humps (granular IgG and C3), nephritic. Subendothelial: lupus nephritis class IV (wire loops), nephritic; MPGN (double contours), both nephrotic and nephritic. Mesangial: IgA nephropathy (dominant IgA), nephritic. Linear GBM: anti-GBM disease (linear IgG, no deposits), nephritic. A note explains that membranous deposits form outside the GBM with no inflammatory infiltrate and so present nephrotic, whereas post-infectious humps come with endocapillary proliferation and present nephritic; in IgA nephropathy nephrotic-range proteinuria is uncommon (about 5 to 20 per cent); lupus class IV plus V and MPGN give both. A key gives the colours (endothelium dashed red, GBM grey, podocyte foot processes blue, mesangium lilac), and a footnote says the drawing is schematic and not to scale. — Physify teaching diagram (schematic). Tap the image to zoom.

From the lesson “Approach, Classification and Biopsy” in Nephrotic vs. Nephritic Syndromes

Flowchart of the stepwise approach to a blood gas, numbered as the nine steps in the text. 1: read the clinical context first; the history predicts the disorder. 2: check the gas is internally consistent, hydrogen ion in nmol/L = 24 x PaCO2 / bicarbonate. 3: acidaemia or alkalaemia from the pH, then the primary process; normal pH 7.35 to 7.45, with reference PaCO2 40 mmHg and bicarbonate 24 mmol/L; below 7.35 is acidaemia (high PaCO2 respiratory acidosis, low bicarbonate metabolic acidosis), above 7.45 alkalaemia (low PaCO2 respiratory alkalosis, high bicarbonate metabolic alkalosis). 4: PaCO2 and bicarbonate moving the same way allow compensation; opposite directions mean a mixed disorder. 5: expected compensation, outside which there is a second primary disorder: metabolic acidosis, Winters formula PaCO2 = 1.5 x bicarbonate + 8, plus or minus 2; metabolic alkalosis PaCO2 = 0.7 x bicarbonate + 20, plus or minus 5; respiratory acidosis bicarbonate up 1 (acute) or 3.5 to 4 (chronic) and respiratory alkalosis bicarbonate down 2 (acute) or 4 to 5 (chronic) for each 10 mmHg change in PaCO2. 6: anion gap on every gas = sodium minus (chloride + bicarbonate), normal about 12 mmol/L without potassium, corrected for albumin by adding 0.25 x (40 minus albumin in g/L). 7: if the gap is high, delta ratio = (anion gap minus 12) / (24 minus bicarbonate): below 0.4 normal anion gap acidosis, 0.4 to 1 high plus normal anion gap acidosis, 1 to 2 high anion gap acidosis alone, above 2 an added metabolic alkalosis or a high baseline bicarbonate from chronic respiratory acidosis; also consider the osmolar gap, lactate, ketones and drug levels. 8: classify the cause with targeted urine tests: urine anion gap or urine osmolar gap for a normal anion gap acidosis, urine chloride and blood pressure for a metabolic alkalosis. 9: synthesise: list every process present and the clinical cause of each. — Physify teaching diagram. Tap the image to zoom.

From the lesson “Physiology and a Stepwise Approach to the Blood Gas” in Acid-Base Disorders

Flowchart for sodium below 135 mmol/L. First, severe symptoms (vomiting, seizures, GCS 8 or less, arrest) need 3 per cent saline 100 to 150 mL over 10 to 20 minutes whatever the duration (taught in the next lesson). Step 1, serum osmolality: high means hypertonic hyponatraemia from hyperglycaemia or mannitol; normal means pseudohyponatraemia from lipid or paraprotein, or glycine or sorbitol irrigation; below 275 mOsm/kg means hypotonic, the only form that causes cerebral oedema. Step 2, urine osmolality: below 100 mOsm/kg means ADH is suppressed (primary polydipsia, water intoxication, low solute intake such as beer potomania or tea and toast); above 100 mOsm/kg means ADH is acting. Step 3, urine sodium with volume status: below 30 mmol/L means low effective arterial volume, either volume depleted (diarrhoea, burns, remote diuretic use) or oedematous (heart failure, cirrhosis, nephrotic syndrome); above 30 mmol/L means the kidney is losing sodium, either volume depleted (current diuretic, salt-wasting nephropathy, mineralocorticoid deficiency, cerebral salt wasting, vomiting with bicarbonaturia) or euvolaemic (SIADH, hypothyroidism, glucocorticoid deficiency: check morning cortisol before calling it SIADH). An oedematous patient with kidney failure, or one on a diuretic, can have urine sodium above 30, so it cannot sort that patient into these groups. Notes give the SIADH criteria (effective osmolality below 275 mOsm/kg, urine osmolality above 100, urine sodium above 30 mmol/L, clinical euvolaemia, normal thyroid and adrenal function, no recent diuretic), that thiazides are the commonest drug cause and loop diuretics rarely cause it, and the chronic correction limits (eTG, October 2026): no more than 1 mmol/L every 2 hours and 8 mmol/L in 24 hours, or 6 in 24 hours with risk factors for osmotic demyelination (sodium 105 or below, alcohol use disorder, malnutrition, hypokalaemia, advanced liver disease). — Physify teaching diagram (schematic). Tap the image to zoom.

From the lesson “Hyponatraemia: Classification and Diagnosis” in Electrolyte Abnormalities

Schematic nephron showing where diuretics act. Proximal tubule, about 65 per cent of filtered sodium: SGLT2 inhibitors block SGLT2, and acetazolamide inhibits carbonic anhydrase. Thick ascending limb of the loop of Henle, about 25 per cent: loop diuretics block NKCC2. Distal convoluted tubule, 5 to 10 per cent: thiazides block NCC. Collecting duct principal cell: amiloride blocks ENaC, and spironolactone and eplerenone block the mineralocorticoid receptor. In the medullary collecting duct ADH (vasopressin) acts on the V2 receptor to insert aquaporin-2 so water is reabsorbed. The thin descending limb is water permeable, and the cortex and medulla are marked. — Physify teaching diagram (schematic). Tap the image to zoom.

From the lesson “Tubular Transport by Segment” in Renal Physiology

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Renal in the clinical exam

7 interactive short cases and 4 long cases for the RACP Divisional Clinical Exam: you examine, present and are marked on the five RACP domains.

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Renal on the blog

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