Cram sheet

Endocrinology — 5-min cram sheet

Written by Betra Youhanna, a medical student and not a doctor — check every detail against your own teaching.

A quick revision sheet. Check current teaching and clinical guidance before using any detail in patient care.

Endocrinology — 5-min cram sheet

_Built from the endo disease index. Deck-faithful._

Buzzword → answer (the vignette reflex)

Dynamic test / hormone pattern → diagnosis

Test / patternResultDiagnosis
Overnight 1 mg DSTNot suppressible (cortisol >1.8 mcg/dL / >50 nmol/L)Cushing's syndrome
High-dose DST (2 mg q6h)Pituitary suppresses, ectopic does notCushing's disease vs ectopic ACTH
Short synacthen (250 µg)Peak cortisol >18–20 mcg/dL (>550 nmol/L)Excludes primary adrenal failure
Water deprivation → desmopressinFails to concentrate, then urine osmo rises ≥50%Central (cranial) DI
Water deprivation → desmopressinNo change on deprivation AND no change with desmopressinNephrogenic DI
Water deprivationUrine markedly concentratesPsychogenic polydipsia
OGTTGH fails to suppress (>10 ng/mL after oral glucose)Acromegaly
Aldosterone/Renin ratioElevated — high aldosterone, low reninPrimary hyperaldosteronism (Conn's)
Renin + aldosteroneHigh renin + high aldosteroneSecondary hyperaldosteronism
Adrenal vein sampling (aldo/cortisol)>4 = adenoma (surgical); <3 = bilateral hyperplasia (medical)Localises Conn's
ITT (GH/cortisol)Failure to rise (valid only if glucose <2.5 mmol/L)GH deficiency
Calcitonin>100 pg/L (100% PPV); >400 suggests distant metsMedullary thyroid carcinoma
Ca + PTHHigh Ca + high/inappropriately-normal PTHPrimary hyperparathyroidism
Ca + PTHHigh Ca + suppressed PTH (→ PTHrP)Malignancy / non-parathyroid hypercalcaemia
TSH + T4/T3↑TSH ↓T4 primary hypo · ↓TSH ↑T4 primary hyper · ↓TSH ↓T4 central · ↑TSH ↑T4 TSH-omaTFT interpretation
ACTH + cortisol↓cort/↑ACTH Addison's · ↓cort/↓ACTH steroid or hypopituitarism · ↑cort/↑ACTH Cushing's disease OR ectopic · ↑cort/↓ACTH adrenal adenomaACTH/cortisol patterns
Radioiodine scanDiffuse hot = Graves · multiple hot/patchy = toxic MNG · one super-hot = toxic adenoma · cold = 5–8% malignantThyrotoxicosis / nodule
RAI uptakeNil neck uptake + low thyroglobulinThyrotoxicosis factitia

Criteria / staging / scores at a glance

Discriminators that decide questions

  1. T1DM vs T2DM — T1: islet autoantibodies usually present, C-peptide undetectable/low, first-line insulin, DKA common; T2: antibodies absent, C-peptide normal/high, non-insulin agents, DKA rare.
  2. DKA vs HHS — DKA: glucose >250, bicarb <15, pH <7.3, ketones present (mostly T1DM); HHS: glucose >600, osmolarity >310, NO significant ketoacidosis (mostly T2DM, enough insulin to suppress ketogenesis but not hyperglycaemia).
  3. Primary vs secondary hyperaldosteronism — Primary (Conn's): low renin / high aldosterone (inverse); Secondary: high renin + high aldosterone (direct, e.g. renal artery stenosis; normotensive causes = Gitelman's/Bartter's).
  4. Primary vs secondary adrenal insufficiency — Primary (Addison's): pigmented + salt-wasting, high ACTH, aldosterone low/renin high, needs fludrocortisone; Secondary: not pigmented, no salt-wasting, low/inappropriately-normal ACTH, aldosterone preserved, NO fludrocortisone.
  5. Central vs nephrogenic DI — Central: desmopressin makes urine concentrate (ADH secretion deficit); Nephrogenic: desmopressin → no change (end-organ ADH unresponsiveness — lithium, hypercalcaemia, hypokalaemia).
  6. Papillary vs follicular carcinoma — Papillary: lymphatic spread, multifocal, Orphan Annie nuclei, good prognosis; Follicular: bloodstream (haematogenous) spread, unifocal, capsular/vascular invasion diagnostic, worse prognosis.