RACP Divisional Written Exam · FRACP

Endocrinology for the written exam

Everything Physify has for Endocrinology: 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.

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Endocrinology

A 55-year-old woman has LDL 2.9 mmol/L, HDL 1.6 mmol/L, triglycerides 1.1 mmol/L and lipoprotein(a) 180 nmol/L, measured after her mother's myocardial infarction at 61. BP is 126/78 mmHg, she has never smoked and her 5-year risk is 6 per cent. After discussion she has started atorvastatin 20 mg. How should the lipoprotein(a) be managed?

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What's covered

27 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

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

Schematic of calcium and phosphate regulation. The parathyroid, sensing ionised calcium through the calcium-sensing receptor (low ionised calcium raises PTH, and phosphate raises it too), releases PTH, which acts on bone through osteoblasts and osteocytes (RANKL up) to release calcium and phosphate, and on the kidney to increase distal calcium reabsorption, cause proximal phosphaturia and increase 1-alpha-hydroxylase. Vitamin D3 from skin and diet becomes 25-hydroxyvitamin D in the liver, and renal 1-alpha-hydroxylase converts it into calcitriol, which raises gut absorption of calcium and phosphate, suppresses PTH and, by an arrow from kidney to bone, raises FGF23. Osteocytes and osteoblasts make FGF23, also raised by phosphate, PTH and iron deficiency; FGF23 causes phosphaturia, lowers 1-alpha-hydroxylase, raises 24-hydroxylase and suppresses PTH in health. PTH has no direct action on the gut. Calcitonin from thyroid C cells makes osteoclasts retract, is mildly calciuretic and matters least. A table of net effects: PTH raises calcium and calcitriol and lowers phosphate; calcitriol raises calcium and phosphate; FGF23 lowers phosphate and calcitriol; calcitonin causes a minor fall in calcium. Notes: in CKD the parathyroid loses Klotho, so FGF23 still lowers calcitriol but PTH rises; calcitriol also induces 24-hydroxylase (CYP24A1), its own off switch.
Physify teaching diagram (schematic). Tap the image to zoom.

From the lesson “Calcium and Phosphate: Gut, Kidney and Bone with PTH, Vitamin D and FGF23” in Bone Remodelling and Mineral Homeostasis

Schematic of adrenal steroid synthesis in three columns. StAR carries cholesterol into the mitochondrion and CYP11A1 makes pregnenolone. The mineralocorticoid column runs pregnenolone, progesterone, deoxycorticosterone, corticosterone and aldosterone; the glucocorticoid column runs 17-OH pregnenolone, 17-OH progesterone, 11-deoxycortisol and cortisol; the androgen column runs DHEA, androstenedione and testosterone, then oestradiol and dihydrotestosterone. 21-hydroxylase converts 17-OH progesterone to 11-deoxycortisol and progesterone to deoxycorticosterone; 11-beta-hydroxylase makes cortisol, and 11-beta-hydroxylation makes corticosterone (by CYP11B1 in the fasciculata, CYP11B2 in the glomerulosa); 17-alpha-hydroxylase and the 17,20-lyase (CYP17A1) lead into the glucocorticoid and androgen columns; 3-beta-HSD acts in all three. Drugs marked: abiraterone at CYP17A1, metyrapone and osilodrostat at 11-beta-hydroxylase, anastrozole and letrozole at aromatase, finasteride and dutasteride at 5-alpha-reductase. A table gives the congenital adrenal hyperplasia patterns, in each of which ACTH rises and drives the columns still open: 21-hydroxylase (about 95 per cent) with low cortisol, salt wasting, androgen excess and a very high 17-hydroxyprogesterone; 11-beta-hydroxylase with low cortisol, hypertension and hypokalaemia, androgen excess and high 11-deoxycortisol and deoxycorticosterone; 17-alpha-hydroxylase with low cortisol, hypertension and hypokalaemia, low androgens and high deoxycorticosterone and corticosterone; and 3-beta-HSD with salt wasting and a high DHEA. Notes say deoxycorticosterone is a mineralocorticoid, so blocks that let it accumulate (11-beta- and 17-alpha-hydroxylase) cause hypertension, hypokalaemia and suppressed renin, and a virilised 46,XX infant points to 21- or 11-beta-hydroxylase deficiency while an undervirilised 46,XY infant points to 17-alpha-hydroxylase, 3-beta-HSD or an earlier block.
Physify teaching diagram (schematic). Tap the image to zoom.

From the lesson “Congenital Adrenal Hyperplasia: 21-Hydroxylase Deficiency, Genetics and Diagnosis” in Adrenal Disorders

Schematic map of TSH on a log scale (0.01 to 100 mIU/L) against free T4 in three categories (low, normal, high), with the reference ranges shaded (TSH about 0.4 to 4.0 mIU/L and free T4 about 10 to 20 pmol/L in the course; ranges vary by laboratory). Raised TSH with low free T4: primary hypothyroidism. Raised TSH with normal free T4: subclinical hypothyroidism, mild below 10 and marked at 10 or above; a mildly raised TSH is repeated in 2 to 3 months before labelling. Low free T4 with a low, normal or mildly raised TSH: central hypothyroidism; non-thyroidal illness overlaps it with a normal or low TSH. Normal TSH and free T4: euthyroid. Low TSH with normal free T4: subclinical hyperthyroidism, grade 1 0.1 to 0.4 and grade 2 below 0.1, also seen with non-thyroidal illness, high-dose glucocorticoids, dopamine and the first trimester. Low TSH, below 0.1 and usually below 0.01, with high free T4: primary hyperthyroidism. High free T4 with a TSH that is not suppressed: a TSH-secreting adenoma or resistance to thyroid hormone, once assay interference and familial dysalbuminaemic hyperthyroxinaemia are excluded. Dashed arrows show assay interference: biotin moves a euthyroid result towards apparent hyperthyroidism (falsely low TSH, falsely high free T4 and T3), and macro-TSH or heterophile antibodies move it towards apparent subclinical hypothyroidism (falsely raised TSH with a normal free T4). A caution box adds that heparin raises measured free T4 in vitro, and that results that do not fit a clinically stable patient should be repeated on a different platform before acting.
Physify teaching diagram (schematic). Tap the image to zoom.

From the lesson “Central Hypothyroidism and Test Interference” in Hypothyroidism

Schematic of the hypothalamic-pituitary-adrenal axis: hypothalamic CRH drives pituitary ACTH, which drives adrenal cortisol, and cortisol feeds back negatively on both the pituitary and the hypothalamus, as does exogenous glucocorticoid. Five disorders are marked with their expected results: primary adrenal insufficiency at the adrenal (ACTH high, cortisol low); secondary adrenal insufficiency from pituitary disease or exogenous steroid (ACTH low or inappropriately normal, cortisol low); Cushing disease from a pituitary corticotroph adenoma (ACTH normal or high, cortisol high); ectopic ACTH from a tumour such as a bronchial carcinoid or small cell lung cancer (ACTH and cortisol high, often very high); and a cortisol-secreting adrenal adenoma (ACTH suppressed, cortisol high). A note says mineralocorticoid is lost only in primary insufficiency (renin high, hyperkalaemia), and pigmentation comes from the high ACTH, so it too is primary only.
Physify teaching diagram (schematic). Tap the image to zoom.

From the lesson “Feedback, Localising the Lesion, and the Growth Hormone and Prolactin Axes” in Hormone Axes: Synthesis, Feedback and Receptor Action

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Endocrinology in the clinical exam

14 interactive short cases and 3 long cases for the RACP Divisional Clinical Exam: you examine, present and are marked on the five RACP domains.

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Endocrinology on the blog

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