Created by TheStudyFix

Endocrine — Disease Index & Clinical Criteria

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

Disease Index · 67 entries across 10 systems · deck-derived, finals-triage

Criteria & Scores · 39 criteria, scoring systems, classifications & protocols

C/P — Clinical Presentation

Inves — Investigations

Mng — Management

Special — Pathognomonic / disease-unique

Diabetes & Complications

13 entries

Type 1 Diabetes Mellitus (T1DM)

C/P

Polyuria, polydipsia, polyphagia, lassitude, nausea, blurred vision
Young lean patient; not obese; strikes children/young adults (any age)
Weight loss despite normal/increased appetite (catabolic state)
Severe nocturnal enuresis in children (2° polyuria)
May present initially with DKA; onset sudden or stress-precipitated

Inves

Islet autoantibodies — usually present (vs absent in T2DM)
C-peptide — undetectable/low (absent endogenous insulin)
FPG ≥7.0 mmol/L or random ≥11.1 mmol/L with symptoms
HbA1c ≥6.5% — but NOT valid for suspected T1DM
Venous pH/bicarbonate + ketones if DKA suspected

Mng

Lifelong insulin — basal-bolus (MDI) or continuous SC infusion (CSII pump)
Rapid-acting analogs (lispro/aspart/glulisine) — reduce hypoglycaemia risk
Starting dose 0.2–1 U/kg/day (½ basal at bedtime + ½ bolus in 3 divided doses)
CGM + sensor-augmented pump with low-glucose suspend — nocturnal hypoglycaemia

Special

Explosive onset in a young lean patient with ketoacidosis — diagnostic of T1DM
Autoimmune β-cell destruction → absolute insulin deficiency
Highest susceptibility: HLA-DR3-DQB1*0201 + HLA-DR4-DQB1*0302 heterozygote; monozygotic twin concordance >50%

physiology · background · low-yield

Mechanism

Environmental triggers for β-cell autoimmunity — viruses (enterovirus, mumps, rubella, coxsackievirus B4), toxic chemicals, cow's milk in infancy, cytotoxins
Acute presentation — acute fatty liver distends the hepatic capsule → RUQ pain (flood of FFAs); persistent pain → suspect pancreatitis

Background

Insulin injection-site absorption — abdomen fastest/preferred > upper arm intermediate > thigh slowest
Split-mixed regimen — 2/3 intermediate-acting + 1/3 short-acting

Epidemiology/Risk

Twin concordance — dizygotic 5–6% vs monozygotic >50%

Type 2 Diabetes Mellitus (T2DM)

C/P

Often asymptomatic for years; may present after microvascular complications
Polyuria, polydipsia, polyphagia, weight loss; blurred vision, lower-limb paraesthesia, genital candida/balanitis
Signs: acanthosis nigricans, central obesity, hypertension, absent ankle reflexes, foot ulcers
Associated: older age, obesity, family history, GDM history, physical inactivity, ethnicity

Inves

FPG ≥7.0 / HbA1c ≥6.5% / 2h-OGTT ≥11.1 / random ≥11.1 mmol/L (repeat if asymptomatic)
Islet autoantibodies absent; C-peptide normal/high
Screen from age 45 (or BMI ≥25 + ≥1 risk factor); repeat at min 3-year intervals if normal

Mng

Lifestyle + Metformin first-line
ASCVD → add SGLT2i or GLP-1 RA with proven CV benefit
Heart failure → SGLT2i preferred
Needs injectable → GLP-1 RA preferred over insulin
Start insulin if A1C >10%, BG ≥300 mg/dL, or ongoing catabolism; dual therapy if A1C ≥1.5% over target
Stop metformin before IV-contrast procedures — ideally 48 h (contrast-induced nephropathy → lactic acidosis)
Metformin stopped ~6 months post-MI; start inpatient basal-bolus or premixed insulin during hospital stay
Pre-operative target HbA1c <8.5% (unless emergency); switch hospitalised patients from oral agents to basal-bolus insulin
Do not combine DPP-4 inhibitor with GLP-1 RA (contraindicated combination — both incretin-based)

Special

Progressive β-cell failure on background insulin resistance + hyperglucagonaemia
Macrovascular disease often already present at diagnosis

physiology · background · low-yield

Background

Medical nutrition therapy — low-glycaemic complex carbs (brown rice, quinoa, oats, legumes), avoid simple/processed carbs; GI High ≥70 / Med 56–69 / Low ≤55
Exercise — ≥150 min/wk moderate-vigorous over ≥3 days + resistance 3×/wk; exercise ECG stress test before vigorous exercise if high CVD risk
Individualise A1C target upward (~7.5%) with associated comorbidities
Fasting/Ramadan — insulin & sulfonylureas carry the highest hypoglycaemia risk (reduce/adjust); low-GI Sohour, hydration 2–3 L/day

Exam technique

Pre-operative diabetes workup — FBG, HbA1c, CBC, urea/creatinine, CXR, ECG, history of diabetic complications

Monogenic Diabetes (MODY / Neonatal)

C/P

Usually onset <25 yr; weight similar to general population
Multigenerational autosomal inheritance pattern
Examples: neonatal diabetes, MODY (maturity-onset diabetes of the young)

Inves

Islet autoantibodies absent; C-peptide normal; insulin production usually present

Mng

First-line treatment depends on subtype

Special

DKA rare except neonatal; distinguished from T1DM by absent antibodies + strong AD family history

Gestational Diabetes Mellitus (GDM)

C/P

Glucose intolerance first recognised in 2nd/3rd trimester; 90% of DM in pregnancy
Persistent metabolic dysfunction at ~3 yr post-delivery

Inves

Screen at 24–28 weeks — one-step 75g OGTT (fasting ≥92, 1h ≥180, 2h ≥153 mg/dL) OR two-step (50g GLT nonfasting → if 1h ≥130–140, 100g OGTT)
1st-trimester labs — HbA1c, BUN, creatinine, TSH, free T4, spot urine protein:creatinine
Dating USS 1st trimester; anatomic USS + fetal echo at 18–20 wks; growth USS every 4–6 wks from 26–36 wks

Mng

Diet first-line — avoid large meals + simple carbs; complex carbs (whole grains, legumes)
Early insulin when diet fails — target non-diabetic glucose profiles

Special

Pre-existing DM carries higher fetal risk than GDM — double birth injury, triple caesarean, quadruple NICU admission

Diabetic Ketoacidosis (DKA)

C/P

1–2 days polyuria, polydipsia, nausea/vomiting, fatigue → stupor/coma
Abdominal pain + tenderness (present without abdominal disease)
Acetone (fruity) breath; Kussmaul respiration (blows off CO₂)
Hypotension + compensatory tachycardia (dehydration); mostly T1DM

Inves

Definitive: glucose >250 mg/dL, bicarbonate <15 mEq/L, pH <7.3, ketonaemia + moderate ketonuria
Pseudohyponatraemia (dilutional); K normal/high despite total-body K depletion

Mng

IV fluid + electrolyte replacement — restore perfusion, clear ketones renally (critical first step)
Insulin — stops ketogenesis + drives K⁺ intracellular, so replace K⁺ to prevent arrhythmia
Correct acidosis/electrolytes + treat the underlying cause (infection, insulin omission)
Insulin/fluid protocol: regular insulin IV bolus 0.1 U/kg then infusion 0.1 U/kg/hr; start normal saline 500–1000 mL/hr; when glucose falls to 250 mg/dL switch fluid to dextrose and halve insulin to 0.05 U/kg/hr

Special

Lack of insulin → unsuppressed adipose lipase → FFA to liver → excess hepatic ketones
Persistent abdominal pain → look for another cause (e.g. pancreatitis)
Correct glucose gradually — rapid glucose correction risks cerebral (brain) oedema

Hyperosmolar Hyperglycaemic State (HHS / HHNK)

C/P

Insidious onset over weeks; profound dehydration + depressed sensorium
Neurologic — seizures, stroke-like events, fasciculations, hyperthermia, nystagmus, hallucinations
Excessive thirst; mostly type 2 diabetes

Inves

Glucose >600 mg/dL; osmolarity >310 mOsm/L; NO significant ketoacidosis

Mng

Judicious rehydration + correct extensive K⁺ losses
Careful monitoring — rapid osmolar correction risks cerebral oedema (water re-enters adapted brain cells)

Special

Enough endogenous insulin to suppress ketogenesis but not hyperglycaemia
Precipitants — severe infection, acute pancreatitis, MI, TPN, excess carbohydrate
Raised serum osmolarity dehydrates the brain → risk of thromboembolic events

Hypoglycaemia

C/P

Onset — parasympathetic hunger → sympathetic (anxiety, tachycardia, sweating, cool clammy skin)
Neuroglycopenic — headache, poor problem-solving, disturbed behaviour, coma, seizures
Blood glucose <70 mg/dL

Inves

Capillary/venous glucose <70 mg/dL

Mng

Conscious — fast-acting carbohydrate (juice, honey, candy, sugar) — most effective
Cannot swallow — glucagon IM/SC
Severe/life-threatening — IV glucose (dextrose)

Special

Predominantly iatrogenic (insulin / long-acting secretagogues)
Risk ↑ in renal failure (reduced insulin clearance) + adrenal insufficiency
Whipple's triad — hypoglycaemic symptoms + documented low glucose + relief on raising glucose (LGW)

Diabetic Neuropathy

C/P

Peripheral sensory polyneuropathy — commonest; stocking-glove, bilateral symmetrical; paraesthesia, ↓ ankle/knee reflexes
Mononeuropathy — focal, one nerve territory (sensory loss + pain + motor weakness)
Amyotrophy — proximal pelvic-girdle/thigh wasting, painful, often asymmetric
Autonomic — postural hypotension, gastric atony/gastroparesis, nocturnal diarrhoea, paralytic bladder, impotence, retrograde ejaculation

Inves

Clinical — impaired pain/temp/light-touch/vibration; decreased deep tendon reflexes

Mng

Glycaemic control — hyperglycaemia is the key microvascular risk factor
Painful neuropathy — gabapentin or pregabalin (LGW)

Special

Loss of protective sensation → substrate for diabetic foot ulceration

physiology · background · low-yield

Other

Autonomic cranial-nerve involvement — impaired pupillary responses + impaired special senses

Diabetic Nephropathy

C/P

Leading cause of ESRD (40% of new cases); silent early
Risk factors — genetic/familial, elevated BP, poor glycaemic control, smoking, hyperlipidaemia

Inves

Microalbuminuria — 1st investigation (albumin rises in urine BEFORE creatinine rises in blood)
Histology — capillary basement-membrane thickening, diffuse + nodular glomerulosclerosis

Mng

Tight glycaemic + BP control; smoking cessation; treat hyperlipidaemia
ACEI/ARB for renoprotection; screen microalbuminuria (30–300 mg/dL) yearly (LGW)

Special

Nodular glomerulosclerosis — hallmark lesion affecting the glomeruli

Diabetic Retinopathy (Eye Disease)

C/P

Commonest diabetic eye disease — abnormal vascular permeability, microaneurysms, neovascularization, haemorrhage, scarring, retinal detachment
Macular oedema — leaked fluid/lipid onto macula → blurred central vision

Inves

Regular fundus examination
R0–R3 grading — R0 = maculopathy/oedema only (no infarcts or haemorrhage); R1 = non-proliferative (mild: microaneurysms; moderate: microaneurysms + haemorrhages <20); R2 = severe non-proliferative (haemorrhages >20); R3 = proliferative (neovascularisation)

Mng

Glycaemic + BP + lipid control

Special

Also causes cataract + glaucoma → blindness

Diabetic Foot

C/P

Sensory neuropathy — unaware of trauma from shoes/weight-bearing/infection
Motor neuropathy — intrinsic muscle weakness → deformity (claw toes) → focal high-pressure areas
Common trauma sites — back of heel, plantar metatarsal area, great toe

Inves

Assess distal symmetric neuropathy (major RF) + vascular disease

Mng

Foot surveillance — patient self-exam nightly; clinician foot exam every 3–6 months (LGW)

Special

60–70% neuropathy alone · 15–20% vascular alone · 15–20% both

Diabetic Macrovascular Disease

C/P

CAD → coronary syndrome/MI/CHF; cerebrovascular → stroke; PVD → ulceration, gangrene, amputation
Heart failure attributed to diabetic cardiomyopathy

Inves

Risk-factor assessment — obesity, HTN, hyperglycaemia, hyperlipidaemia, altered platelet function, ↑ fibrinogen

Mng

Manage macrovascular risk factors — HTN, dyslipidaemia, smoking
SGLT2i / GLP-1 RA for demonstrated cardiovascular benefit

Special

In T2DM may be present at diagnosis; in T1DM correlates with age + disease duration

12b

Diabetic Infections

C/P

Soft-tissue infections of the extremities; osteomyelitis
UTI / pyelonephritis; candidal skin & mucous-membrane infections
Dental caries + infections; TB & pneumonia

Inves

Clinical + site-directed cultures/imaging

Mng

Glycaemic control — hyperglycaemia + glycosuria fuel microorganism growth and worsen severity

Special

Suboptimal immune response — depressed neutrophil adherence, chemotaxis + phagocytosis (worse with poor control), plus vascular disease + neuropathy

Adrenal Cortex

7 entries

Primary Hyperaldosteronism (Conn's)

C/P

Hypertension (often resistant) — major finding
Hypokalaemia in ~30% — muscle weakness, paraesthesia, peripheral neuropathy, arrhythmia
Metabolic alkalosis; greater CV risk than other hypertension

Inves

Aldosterone/Renin ratio (ARR) — first-line; elevated (high aldo, low renin); take morning, upright, ≥2h after waking
High-resolution CT abdomen first for localisation, then AVS if inconclusive
Adrenal vein sampling (AVS) — unilateral ~4-fold aldosterone rise = adenoma; bilateral little difference = hyperplasia
Urine K⁺ >30 mmol/L — inappropriate renal potassium wasting in the face of hypokalaemia supports the diagnosis

Mng

Adenoma → laparoscopic adrenalectomy
Bilateral hyperplasia → MRA first-line — spironolactone (or eplerenone if intolerant)
2nd-line → K-sparing diuretic (amiloride) if MRA-intolerant

Special

Commonest cause = bilateral idiopathic adrenal hyperplasia (60–70%) > adrenal adenoma (20–30%)
Low renin / high aldosterone (inverse relation)

physiology · background · low-yield

Epidemiology/Risk

Accounts for ~10–20% of resistant hypertension and ~20% of secondary hypertension

Exam technique

~25% have a normal absolute aldosterone — rely on the ARR, not the aldosterone level alone

Physiology

Aldosterone acts on the distal tubule + collecting duct (retains Na⁺, excretes K⁺); genomic but relatively fast onset (~20 min)

Mechanism

Pseudohyperaldosteronism (low renin / low aldosterone) — licorice or Cushing's (11β-HSD2 inhibition), Liddle's syndrome (ENaC gain-of-function), SAME (11β-HSD2 loss-of-function)
MRA choice — spironolactone (non-selective: gynaecomastia, menstrual irregularity, impotence); eplerenone selective but less potent; finerenone non-steroidal

Background

Rare causes — unilateral hyperplasia, familial hyperaldosteronism, adrenal carcinoma

Secondary Hyperaldosteronism

C/P

Hypertensive (vascular causes) or normotensive (salt-wasting tubulopathies)

Inves

High renin + high aldosterone (direct relation)

Mng

MRAs (e.g. finerenone) — block the receptor

Special

Excessive RAAS activation — renal artery stenosis, renal ischaemia, renin-secreting tumour, diuretics, CHF/nephrotic/cirrhosis/pregnancy
Normotensive causes → Gitelman's / Bartter's syndromes

physiology · background · low-yield

Background

Aortic coarctation is a high-renin (hypertensive) cause of secondary hyperaldosteronism

Cushing's Syndrome

C/P

Fat — moon face (plethoric), buffalo hump, supraclavicular pads, truncal/pendulous obesity, thin arms + legs
Skin — thin, easy bruising, purple striae, poor wound healing, acne, hirsutism
Osteoporosis + codfish vertebrae; glucose intolerance/diabetes, HTN, proximal myopathy, psychosis
Hyperpigmentation only if ACTH high (pituitary/ectopic)

Inves

Loss of cortisol circadian rhythm (high am + pm); 24h urinary free cortisol
Overnight/low-dose DST — not suppressible (<1.8 mcg/dL / <50 nmol/L excludes Cushing's)
K low + metabolic alkalosis; plasma ACTH to split dependent vs independent
High-dose DST (pituitary suppresses, ectopic does not) + MRI pituitary / CT chest / CT abdomen; BIPSS if MRI negative

Mng

Surgery main modality — trans-sphenoidal (pituitary), adrenalectomy (adrenal)
Medical — ketoconazole, metyrapone, mitotane, mifepristone, osilodrostat, etomidate; pasireotide (if pituitary + no surgery)
2nd-line — bilateral adrenalectomy + radiotherapy

Special

Iatrogenic glucocorticoids = commonest cause overall
Pseudo-Cushing (obesity, depression, alcoholism) — excluded by overnight DST
Causes — ACTH-dependent: Cushing's disease = pituitary adenoma (80%), ectopic ACTH (small-cell lung cancer commonest, bronchial/pancreatic carcinoid); ACTH-independent: adrenal adenoma/carcinoma, micronodular adrenal dysplasia

physiology · background · low-yield

Other

Complications — visual loss (optic chiasm compression), increased infection susceptibility, menstrual abnormalities

Congenital Adrenal Hyperplasia (CAH)

C/P

21-OH deficiency (90%) — salt-wasting (hypovolaemic shock, low Na, high K, low BP) OR simple virilizing (ambiguous genitalia in 46,XX; precocious puberty/short stature in 46,XY)
Non-classic (late-onset) — premature pubarche, acne, hirsutism, oligomenorrhoea (mimics PCOS)
11β-OH — hypertension + virilization (DOC excess)
17α-OH — hypertension, low androgens, undervirilized 46,XY males

Inves

High serum 17-hydroxyprogesterone (21-OH deficiency marker)
Autosomal recessive

Mng

Glucocorticoids — replace cortisol + suppress ACTH-driven androgens
Mineralocorticoids (fludrocortisone) — for classic salt-wasting form
Anti-androgens (females, 2nd line); GnRH analogues — suppress puberty + preserve height

Special

Enzyme block ↓ cortisol → ↑ ACTH → adrenal hyperplasia + androgen hypersecretion
21-OH = low BP (salt-wasting); 11β-OH & 17α-OH = hypertension

physiology · background · low-yield

Other

11β-OH deficiency marker — raised 11-deoxycortisol (and DOC); distinguishes it from 21-OH (17-OHP)

Addison's Disease (Primary Adrenal Insufficiency)

C/P

Insidious onset; bronze hyperpigmentation; weakness, weight loss, profound fatigue, GI disturbance
Postural hypotension / vascular collapse
Hyponatraemia, hyperkalaemia, hypoglycaemia

Inves

Low cortisol + high ACTH; aldosterone low, renin high
Short synacthen (250 µg ACTH) — peak cortisol >18–20 mcg/dL (>550 nmol/L) excludes primary failure
Hyponatraemia, hyperkalaemia, eosinophilia, lymphocytosis

Mng

Hydrocortisone 15–20 mg/day (or prednisolone) glucocorticoid replacement
Fludrocortisone mineralocorticoid — needed in primary (RAAS lost)
Stress-dose (surgery/infection) — normal stress output ~250–300 mg cortisol/24h

Special

Autoimmune (>80%, anti-21-hydroxylase, spares medulla); TB 2nd cause
Schmidt syndrome (Addison + Hashimoto); PAS-1 (APECED, AIRE gene) = Addison + hypoPTH + mucocutaneous candidiasis; PAS-2 = Addison + T1DM + thyroid
Other causes — adrenal metastases (lung, breast, colon, renal), infiltration (sarcoidosis, amyloidosis, haemochromatosis), fungal (histoplasmosis, blastomycosis, cryptococcosis), lymphoma/leukaemia, adrenal haemorrhage
Other autoimmune associations — vitiligo, pernicious anaemia, coeliac disease, T1DM, Graves', myasthenia gravis

physiology · background · low-yield

Other

Also — change/loss of body-hair distribution; >2-fold long-term mortality (CV, malignancy, infection)

Secondary Adrenal Insufficiency

C/P

Not pigmented, no salt wasting, hypoglycaemia
Pituitary failure effects — GH (short stature), TSH (hypothyroid), FSH/LH (hypogonadism), ADH (DI)

Inves

Low cortisol + low/inappropriately-normal ACTH; aldosterone preserved (RAAS intact)
Long synacthen (depot ACTH ×3 days) — adrenals respond (rules out primary)

Mng

Glucocorticoid replacement only — NO fludrocortisone (RAAS/aldosterone intact)

Special

Commonest cause = sudden withdrawal of exogenous glucocorticoids (>30 mg HC/day for >3 weeks suppresses HPA axis)

Addisonian (Adrenal) Crisis

C/P

Hypovolaemic shock, vomiting, fever, confusion — medical emergency

Inves

Hyponatraemia, hyperkalaemia, hypoglycaemia, eosinophilia, lymphocytosis

Mng

Hydrocortisone 100 mg IV stat then 50 mg QDS — give before ACTH/cortisol result
Aggressive IV fluids (normal saline) + treat precipitant

Special

Precipitants — rapid steroid withdrawal, sepsis/stress on chronic insufficiency
Waterhouse-Friderichsen (meningococcal adrenal haemorrhage); Sheehan's (postpartum pituitary necrosis)

Adrenal Medulla & Familial Syndromes

7 entries

Phaeochromocytoma / Paraganglioma

C/P

"Spells"/paroxysms (50%) — 5 Ps: Headache (80%), Perspiration (71%), Palpitations (64%), Pallor (42%), Paroxysms; anxiety/fear of impending death
HTN — sustained 50% / paroxysmal 40% / normal 10%; orthostatic hypotension
Weight loss, hyperglycaemia, dilated/hypertrophic cardiomyopathy, arrhythmia

Inves

Fractionated metanephrines — plasma or 24h urine (acid preservative); most sensitive, best to rule out
Anatomical CT/MRI (MRI 98% for extra-adrenal); MIBG scan (80%) — stop TCAs/CCBs 48h prior; PET (¹⁸F-FDG)
Genetic testing — RET, VHL, NF1, SDH-A/B/C/D; urine VMA obsolete
Somatostatin / Octreotide scan — third functional-imaging modality (somatostatin receptors present in ~70% of cases), alongside MIBG and PET

Mng

Adrenalectomy (laparoscopic/open) — definitive
Alpha-blockade FIRST — phenoxybenzamine 7–10 days pre-op (target BP <120/80), doxazosin selective
Then beta-blockade — propranolol/bisoprolol 2–3 days, only after adequate alpha-blockade
Metyrosine if inoperable; crisis → IV phentolamine / nitroprusside / nicardipine
Post-op follow-up — immediate hypotension + hypoglycaemia; HTN may persist up to 2 months; monitor urine catecholamines annually

Special

Rule of 10s — 10% extra-adrenal / bilateral / malignant / familial / normotensive
"Alpha before beta" — beta-first → unopposed alpha vasoconstriction + BP crisis
Crisis triggers — anaesthesia, surgery, ↑ intra-abdominal pressure, tyramine-rich food, metoclopramide; extra-adrenal organ of Zuckerkandl
Pheo crisis (may be the INITIAL presentation) — hypertensive crisis, cardiomyopathy/heart failure, circulatory collapse (shock), pulmonary oedema, respiratory failure, acute kidney injury, seizures
Paraganglioma = chromaffin-cell tumour of sympathetic ganglia (extra-adrenal); phaeochromocytoma = intra-adrenal paraganglioma (85–90% intra-adrenal)

physiology · background · low-yield

Physiology

Chromaffin cells = modified postganglionic sympathetic neurons in the inner 10% of the adrenal, stain brown with chromium salts; catecholamine effects: bronchodilation, mydriasis, ↑glucose/fatty-acid release

Mechanism

Catecholamine metabolism — COMT → metanephrines, MAO → VMA (final product); plasma half-life 10–100 s, ~50% loosely albumin-bound (levels fluctuate widely)

Epidemiology/Risk

~10–30% are hereditary (higher than the classic '10% familial'); many drugs raise metanephrines falsely (TCAs, levodopa, decongestants, amphetamines, clonidine withdrawal); dopamine measurement not useful

Other

Imaging morphology — classically a vascular solid mass; can be cystic when large with enhancing septa; may compress liver / right kidney
Imaging — vascular adrenal mass; large tumours become cystic with enhancing septa and can mimic a necrotic renal-cell-carcinoma metastasis

Adrenocortical Carcinoma

C/P

Functioning adrenal mass — hypercortisolism (Cushing's) ± virilization — or mass effect

Inves

Adrenal CT/MRI; if cortisol-secreting → ACTH-independent (low ACTH, high cortisol)
CT — typically a large mass (e.g. 13.5 cm) with internal calcifications, no focal fat; displaces adjacent organs (pancreas/kidney) without frank invasion
Imaging — large mass (often >10 cm, e.g. 13.5 cm) with internal calcifications and no intracellular fat; displaces adjacent organs (pancreas/kidney) rather than invading

Mng

Surgical resection; mitotane (adrenolytic agent)

Special

Rare ACTH-independent Cushing's cause; adrenal malignancy rarely causes hypofunction

physiology · background · low-yield

Other

Benign vs malignant adrenal mass on imaging — lipid-rich adenoma = CT attenuation <10 HU (fat is negative HU, e.g. −12 HU) and signal drop on out-of-phase MRI (chemical shift phenomenon); carcinoma lacks fat

MEN 1

C/P

3 Ps — Pituitary adenoma + Primary hyperParathyroidism + Pancreatic tumour (insulin/gastrin-secreting)
Associated — thyroid adenoma, adrenal adenoma, thymic carcinoid, subcutaneous lipoma, collagenomas/angiofibromas

Inves

Screen the component organs — calcium/PTH, pituitary hormones, gut hormones

Mng

Manage each component tumour

Special

Menin tumour-suppressor gene (loss of function); autosomal dominant

MEN 2A

C/P

Medullary thyroid carcinoma + primary hyperparathyroidism + phaeochromocytoma (often bilateral); lichen planus

Inves

RET proto-oncogene; calcitonin (MTC), metanephrines (phaeo), calcium (PHPT)

Mng

Remove phaeochromocytoma first, then total thyroidectomy
Phaeo: cortical-sparing adrenalectomy preferred (bilateral disease in up to 50%); PHPT: subtotal parathyroidectomy with cryopreservation / implantation in neck or forearm

Special

RET mutation (chr 10, constitutive activation); AD, ~100% penetrance; more indolent than 2B

MEN 2B

C/P

Medullary thyroid carcinoma + phaeochromocytoma + mucosal neuromas (lips/tongue) + marfanoid habitus
Ganglioneuromatosis of bowel (Hirschsprung-like); NO hyperparathyroidism

Inves

RET proto-oncogene mutation

Mng

Aggressive — early prophylactic thyroidectomy in gene carriers

Special

Most aggressive variant — affects the very young, diagnosed at advanced stage; lacks parathyroid involvement (vs 2A)
Skeletal (marfanoid) associations — congenital hip dislocation, pes cavus, pectus excavatum, kyphosis

Von Hippel-Lindau (VHL)

C/P

Haemangioblastoma (CNS/retinal), renal cell carcinoma/cysts, phaeochromocytoma, pancreatic cysts/NETs, endolymphatic sac tumours

Inves

VHL tumour-suppressor gene; VHL-phaeo secretes norepinephrine / normetanephrine

Mng

Surveillance + treat individual tumours

Special

AD; offer genetic testing if bilateral phaeos, +FH, young age, or co-phenotype disorder (MTC, retinal haemangioma)

Neurofibromatosis Type 1 (NF1)

C/P

Neurofibromas, café-au-lait spots, Lisch nodules; 2% develop phaeochromocytoma (usually solitary)

Inves

NF1 gene (encodes neurofibromin)

Mng

— (manage phaeo per protocol if present)

Special

AD tumour-suppressor; phaeos usually solitary adenoma (not bilateral)

Secondary Hypertension

4 entries

Coarctation of the Aorta

C/P

2nd commonest secondary-HTN cause in children; 2–5× more common in boys
Neonate → heart failure; typically diagnosed age 5 (HTN or murmur)
Diminished femoral pulses; arm-leg BP discrepancy

Inves

Discrepancy between bilateral brachial or brachial/femoral BPs
CXR — classic "three" sign + rib notching
Echocardiography (children); MRI (adults)

Mng

— (surgical/interventional repair; not detailed in deck)

Special

Rib notching = collateral-vessel erosion; "three sign" = aortic indentation

Renal Artery Stenosis (RAS)

C/P

Older adults — atherosclerotic; young women — fibromuscular dysplasia
Renal bruit; late-onset / resistant hypertension

Inves

Creatinine rise >30% after ACEI/ARB — hallmark (GFR is angiotensin-dependent)
Colour doppler US (operator/habitus-dependent); MRA or CT renal angiography (equally accurate)
MRA preferred if avoiding radiation/contrast (safe in poor renal function)

Mng

Revascularization — curative in 20–85%, improves BP in nearly all

Special

FMD is the key cause in young women; atherosclerosis in the elderly

Obstructive Sleep Apnea (OSA)

C/P

Obese, large neck circumference; snoring / apnoeic episodes; nocturnal BP surges
Daytime BP can remain elevated even when breathing normal

Inves

Epworth Sleepiness Scale, Sleep Apnea Clinical Score + night pulse oximetry
Sleep study (polysomnography) — gold standard

Mng

CPAP — reduces blood pressure

Special

Sympathetic overactivity from repeated nocturnal hypoxic stress

physiology · background · low-yield

Mechanism

Pathophysiology — sympathetic overactivity plus oxidant stress and inflammation

Resistant Hypertension

C/P

BP uncontrolled despite therapy; ~12% of hypertensive patients
Definition — BP uncontrolled despite ≥3 antihypertensives (including a diuretic)

Inves

Exclude measurement error + white-coat effect first

Mng

Screen + treat the underlying secondary cause

Special

Reconsider the "big three" — aldosteronism, OSA, renal artery stenosis

Water & Sodium

4 entries

Central (Cranial) Diabetes Insipidus

C/P

Polyuria (>3 L/day), frequency/nocturia, polydipsia, craving cold liquids
Orthostatic hypotension, dehydration; severe → weakness, altered mental status, coma, seizures (hypernatraemia)

Inves

High serum osmolality (>300), inappropriately low urine osmolality (50–200), specific gravity <1.005, Na normal/high
Water deprivation test — fails to concentrate; then desmopressin → urine osmolality rises ≥50% (responds)
Partial cranial DI — urine partially concentrates on deprivation, then rises further to normal with desmopressin (vs complete DI: no change on deprivation, marked rise with desmopressin)

Mng

Desmopressin (vasopressin analogue) — nasal spray or tablet
Chlorpropamide for partial deficiency (prolongs vasopressin action/release)

Special

Deficiency of ADH secretion (like T1DM); causes — idiopathic, head trauma, postsurgical, tumours, TB/meningitis, sarcoidosis/Wegener's

physiology · background · low-yield

Background

Polyuria thresholds — adults >30–50 mL/kg/24h, children >100 mL/kg/24h; up to 10–15 L/day in severe disease
Further causes — cerebrovascular disease, encephalitis; postsurgical DI develops 1–6 days after surgery (may recur/become chronic); head-trauma DI may remit after 6 months
Gestational DI — a further recognised subtype (analogous to gestational DM)

Mechanism

ADH synthesised in hypothalamus, stored/released by posterior pituitary; V1 = vasoconstriction, V2 = water reabsorption via aquaporin-2 channels

Nephrogenic Diabetes Insipidus

C/P

Polyuria, polydipsia, craving cold liquids (same DI picture)

Inves

High serum osmolality, low urine osmolality
Water deprivation — no change; desmopressin → NO change (kidney unresponsive)

Mng

Stop offending drug + correct electrolytes; low-solute diet
Thiazide diuretic — mild volume depletion → ↑ proximal reabsorption (diminishes polyuria)
Amiloride for lithium-induced; indomethacin (NSAID) to reduce output

Special

End-organ ADH unresponsiveness (like T2DM); acquired — lithium, hypercalcaemia, hypokalaemia, amphotericin B

physiology · background · low-yield

Epidemiology/Risk

Fuller cause list — congenital (rare inherited); drugs aminoglycosides, vincristine; renal (polycystic kidney disease, obstructive uropathy, papillary necrosis); systemic (sickle cell, multiple myeloma, amyloidosis)

Psychogenic Polydipsia

C/P

Excessive water intake with normal ADH

Inves

Low plasma osmolality (dilute) at baseline
Water deprivation — urine markedly concentrates; desmopressin — no further improvement

Mng

Restrict water intake

Special

Both plasma and urine diluted — the exception to the plasma-urine inverse rule

SIADH

C/P

Euvolaemic; acute — nausea/malaise (Na <125–130) → headache, lethargy, seizures, coma (Na <115–120, cerebral oedema)
Chronic — fatigue, dizziness, gait disturbance, falls in elderly (cerebral adaptation)

Inves

Hyponatraemia + hypo-osmolality + urine osmolality >100; euvolaemic
Low BUN + low uric acid; exclude cardiac/renal/adrenal/hepatic/thyroid dysfunction
Increased urinary sodium excretion (inappropriate natriuresis); serum K unchanged

Mng

Fluid restriction (500–1500 mL/day) — mainstay
Acute/symptomatic — 3% hypertonic saline; loop diuretics (increase free-water excretion)
Vaptans (tolvaptan, conivaptan) — V2 receptor antagonists
Correct slowly 0.5–1 mEq/h, max 10–12 mEq/24h

Special

ADH release not suppressed by low osmolality; osmotic demyelination (central pontine myelinolysis) if corrected too fast
Small cell lung carcinoma = classic ectopic ADH producer
Causes beyond small cell — drugs (carbamazepine, SSRIs, cyclophosphamide, chlorpropamide, NSAIDs, vincristine), CNS (stroke, haemorrhage, trauma, infection, psychosis), pulmonary (pneumonia, asthma, pneumothorax), post trans-sphenoidal pituitary surgery (Na nadir postop day 6–7), hypothyroidism/hypopituitarism

physiology · background · low-yield

Mechanism

Pathophysiology — ADH not suppressed by low osmolality → water retention → transient volume expansion → natriuretic peptides → natriuresis → returns to euvolaemia (worsens hyponatraemia)

Calcium & Bone

13 entries

Hypocalcaemia

C/P

Circumoral paraesthesia, muscle cramps, tetany, convulsions, laryngeal spasm
Chvostek + Trousseau signs; chronic — lenticular cataracts; behavioural disturbance

Inves

ECG — prolonged QT + T-wave peaking
Low/undetectable PTH → hypoparathyroidism; elevated PTH → non-parathyroid cause (except pseudohypoPTH)
Always measure serum magnesium (low Mg blocks PTH release/action)

Mng

Acute tetany — IV calcium gluconate 20–30 mL of 10% over 15–20 min (less vein-irritant than CaCl₂); never in a bicarbonate line
Long-term — calcium carbonate 2 g/day + calcitriol 0.5–1.0 mcg/day (calcifediol for liver disease)
Replace magnesium (IV magnesium chloride) if low — hypocalcaemia stays refractory to calcium until coexisting hypomagnesaemia is corrected; phenytoin (diphenylhydantoin) for tetanic convulsions

Special

Chvostek + Trousseau signs pathognomonic of neuromuscular excitability
Post-thyroidectomy hypoparathyroidism — Ca nadir 48–72h; "hungry bone" syndrome after parathyroidectomy
Causes — vitamin D deficiency, hypoparathyroidism, pseudohypoparathyroidism (PTH resistance), renal failure, acute pancreatitis, magnesium depletion, massive transfusion (citrate binds Ca), artefactual (EDTA/citrate sample)

physiology · background · low-yield

Other

CV — arrhythmia, tachycardia, hypotension (in addition to prolonged QT / T-wave peaking)
Post-thyroid/parathyroid surgery monitoring — plasma calcium the morning after operation and again 24h later (nadir 48–72h)

Mechanism

Hypoalbuminaemia lowers total plasma calcium while ionised calcium stays normal → patient asymptomatic (pseudohypocalcaemia); other causes — osteoblastic (prostate) metastases, acute hyperphosphataemia (phosphate load / tumour-lysis chemotherapy)

Hypercalcaemia

C/P

"Stones, bones, groans, moans"; often asymptomatic/incidental
Renal — polyuria/dehydration, renal calculi, nephrocalcinosis
GI — anorexia, N&V, abdominal pain, constipation, peptic ulcer, acute pancreatitis
Neuro — mental changes, lassitude, weakness

Inves

Suppressed PTH → non-parathyroid cause; raised/detectable PTH → PTH-mediated cause
PTHrP if malignancy suspected (solid tumours)

Mng

Acute — IV saline rehydration, bisphosphonates, calcitonin (see Hypercalcaemic Crisis criteria)

Special

Primary hyperPTH (outpatient) + malignancy (inpatient) = 90% of cases
Solid tumours → PTHrP (↑Ca, ↓PO4, ↑urinary cAMP); haematologic → cytokines (↑Ca, ↑PO4)
Other causes — granulomatous disease (sarcoidosis, TB → convert inactive vit D to active), thiazide diuretics, vitamin D/A intoxication, milk-alkali syndrome, lithium, immobilization, hyperthyroidism, Addison's disease, FHH, tertiary hyperPTH

physiology · background · low-yield

Other

Common humoral (solid) tumours — lung (25%), breast (20%), squamous cell (head/neck/oesophagus), renal cell (8%); haematologic — myeloma, lymphoma, leukaemia

Familial Hypocalciuric Hypercalcaemia (FHH)

C/P

Mild, benign asymptomatic hypercalcaemia

Inves

24h urine calcium <100 mg/24h (usually <50); calcium:creatinine clearance ratio <0.01
Autosomal dominant; exclude thiazides + vit D deficiency before genetic testing

Mng

No treatment — benign

Special

Calcium-sensing receptor mutation (higher Ca set-point); must exclude before parathyroidectomy for PHPT

Primary Hyperparathyroidism

C/P

Often asymptomatic/incidental; "bones, stones, groans, psychic moans"
Kidney stones (15–20%), severe bone disease (5%, osteitis fibrosa cystica), muscle weakness, polyuria, psychiatric
Parathyroid crisis (1–2%) — Ca >15 mg/dL, coma/confusion

Inves

High Ca + high (or inappropriately-normal) PTH simultaneously = diagnostic; low phosphate; Cl:PO4 ratio >33
Albumin-corrected Ca = serum Ca + 0.8 × (4.0 − albumin)
Exclude FHH with 24h urine calcium; localise pre-op with neck US → sestamibi / 4D-CT
Hands/skull X-ray — cystic formations from calcium resorption

Mng

Focused/unilateral parathyroidectomy with IOPM (Miami: PTH drop ≥50% at 10 min) or bilateral neck exploration
Surgery for asymptomatic if any: age <50, Ca >1 mg/dL over normal, CrCl <60, T-score <−2.5, urine Ca >400, fracture/stones — else surveillance
Post-op oral calcium ~2 weeks; cinacalcet not for surgical candidates

Special

Single adenoma 80–85%; MEN1/2A association; hyperplasia is the rule in familial/MEN/ESRD

physiology · background · low-yield

Epidemiology/Risk

~1% of adults; women outnumber men 2:1 (1 in 500 women vs 1 in 2000 men >40); ~100,000 new US cases/yr

Other

Localisation imaging — adenoma is homogeneously hypoechoic vs the echogenic thyroid on high-frequency US; Tc-99m sestamibi is retained in the mitochondria-rich adenoma while washing out of thyroid (Tc-99m pertechnetate marks thyroid only)

Secondary Hyperparathyroidism

C/P

Chronic renal failure setting; renal osteodystrophy — bone/joint/muscle pain
Calciphylaxis, pruritus

Inves

High PTH + low/normal Ca + high phosphate

Mng

Surgery (3½/4-gland resection) if calciphylaxis, PTH >800 pg/mL, or failed maximal medical management

Special

Physiological compensation for chronic hypocalcaemia (CKD: low vit D + high PO4)
Calciphylaxis — painful purpuric cutaneous lesions → tissue calcification + ischaemic necrosis → dry gangrene

Tertiary Hyperparathyroidism

C/P

Renal transplant patients; osteoporosis, symptomatic hyperparathyroidism

Inves

High PTH + high Ca + high phosphate (autonomous)

Mng

3½- or 4-gland resection with autotransplantation (brachioradialis muscle)
Surgery if Ca >12.5 mg/dL, or persistent Ca >10.2 >3 months post-transplant

Special

Hyperplastic glands become autonomous after prolonged secondary state

Parathyroid Carcinoma

C/P

~1% of primary HPT; very high Ca (>3.5 mmol/L, 70%); palpable neck mass (50%); severe bone disease (60%)

Inves

Firm, adherent grey-white gland / local invasion intra-op; biopsy contraindicated

Mng

En bloc resection — parathyroid gland + thyroid lobe + isthmus + involved tissue

Special

Thick fibrous capsule with trabeculated bands; recurrence within 3 years; 50% favourable prognosis

Osteomalacia & Rickets

C/P

Spontaneous fractures (femur + other sites); rickets in children, osteomalacia in adults

Inves

Low Ca + low phosphate, high ALP, low 25-OH vit D, elevated PTH (secondary hyperparathyroidism)

Mng

Cholecalciferol 20,000 IU weekly × 6 weeks, then 800–1000 IU daily

Special

Defect of bone mineralization 2° vit D deficiency; causes — diet/sunlight, malabsorption, renal disease, anticonvulsants, 1α-hydroxylase deficiency (VDDR)

Osteoporosis

C/P

Silent until fracture — neck of femur, vertebral, Colles' (wrist); fragility fractures

Inves

DEXA T-score <−2.5 = osteoporosis (osteopenia −1 to −2.5)
FRAX — 10-year major osteoporotic fracture probability

Mng

Base — calcium 1000–1500 mg/day + vitamin D 400–800 IU/day
Bisphosphonates first-line — alendronate (weekly), ibandronate (monthly), zoledronate (yearly IV); avoid oral if upper-GI problem
Denosumab (RANKL inhibitor, SC 6-monthly); teriparatide (PTH analogue, SC — severe cases)
Strontium ranelate / raloxifene — no longer used (DVT/CV risk)

Special

Secondary causes — corticosteroids, hyperPTH, alcohol, immobilization, RA, PPIs
Bisphosphonate SEs — osteonecrosis of jaw, atypical femoral fracture, oesophagitis
Denosumab — potent resorption blockade can precipitate hypocalcaemia (also muscle pain, constipation, rash)

physiology · background · low-yield

Epidemiology/Risk

Further secondary causes — adrenal disease, osteogenesis imperfecta, Turner syndrome, malignancy, systemic mastocytosis
Higher-risk racial groups — Caucasians and Asians (lower peak bone mass)

Other

Teriparatide — increases bone turnover & serum Ca²⁺; osteosarcoma risk (reserved for severe cases)

Mechanism

Vitamin D deficiency drives bone loss via secondary ↑PTH → ↑bone resorption

Paget's Disease of Bone

C/P

Often asymptomatic; pain, deformity, fracture, nerve compression
High-output cardiac failure; commonly misdiagnosed as bone malignancy

Inves

Raised ALP with otherwise normal LFTs / Ca / vit D
Abnormal appearance of pelvis, long bones & skull on X-ray

Mng

Bisphosphonates, calcitonin, surgery

Special

Localized chaotic remodelling (osteoblastic + osteosclerotic); <1% osteosarcoma
High-output failure from hypervascular new bone (acts as an AV shunt)

Metastatic Bone Disease

C/P

Pathological fracture; commonly spine + hip

Inves

Bone scan; Ca may be normal in osteosclerotic mets (prostate, breast)

Mng

— (not detailed in deck)

Special

Primaries — Breast, Lung, Prostate, Kidney, Thyroid

Primary Bone Cancer

C/P

Night pain, unremitting pain (red flags); pathological fracture
Osteosarcoma (children); osteoid osteoma + myeloma (adults)

Inves

— (imaging/biopsy; not detailed in deck)

Mng

— (not detailed in deck)

Special

Tissues of origin — bone, cartilage, vascular structures, marrow

Osteonecrosis (Avascular Necrosis)

C/P

Pain on weight-bearing (some rest/night pain); sites — femoral head, distal femur, proximal humerus, scaphoid, talus

Inves

X-ray may be normal early → bone scan or MRI if suspected

Mng

Conservative — bed rest, non-weight-bearing, analgesia
Surgical — core decompression, osteotomy, replacement

Special

RFs — fracture, steroids, alcohol, sickle cell, radiation, decompression sickness (Caisson)

Pituitary

4 entries

Hypopituitarism

C/P

Sequential hormone loss → hypogonadism, growth failure, hypothyroidism, adrenal insufficiency

Inves

Static + dynamic pituitary function tests per axis

Mng

Replace deficient target-organ hormones

Special

Order of loss — LH/FSH → GH → prolactin → TSH → ACTH (ACTH preserved until late)
Causes — hypophysectomy, radiotherapy, tumour, congenital
Sheehan's syndrome — postpartum pituitary necrosis; a cause of hypopituitarism / secondary hypothyroidism
Pituitary apoplexy — sudden haemorrhage/infarction of the gland; rare catastrophic acute presentation (emergency)

physiology · background · low-yield

Epidemiology/Risk

Functioning pituitary tumours most commonly secrete prolactin & GH; less commonly ACTH; rarely TSH/FSH

Other

Pituitary adenoma (PitNET) — micro <10 mm vs macro >10 mm; ~65% secretory (prolactin ~50% > GH 10% > ACTH 6% > TSH 1%), ~35% non-secretory (usually macroadenomas presenting with mass effect)
Dynamic MRI is needed to see a microadenoma — the normal gland (arterial supply) enhances immediately whereas the adenoma (portal supply) is a focal defect early with delayed enhancement; sudden haemorrhage/infarction = pituitary apoplexy

Acromegaly / Gigantism

C/P

Enlarged hands/feet, coarse facies, prognathism, enlarged nose/tongue/lips, deep voice, skin tags, sweating
Carpal tunnel syndrome, spinal cord compression, osteoarthritis
Organomegaly (cardiomegaly, hepatomegaly, nephromegaly), colonic polyps/cancer; HTN, diabetes, sleep apnea
Gigantism if excess GH before epiphyseal closure (children)
Visual impairment / visual field defect from suprasellar (optic chiasm) mass effect of the adenoma
Reproductive hypogonadism — erectile dysfunction & ↓ libido (men); menstrual irregularity & ↓ libido (women)
Thyroid hypertrophy (goitre)

Inves

OGTT — GH fails to suppress (GH >10 ng/mL after oral glucose) — diagnostic
Elevated IGF-1 (stable screening marker); MRI pituitary adenoma; colonoscopy

Mng

Trans-sphenoidal surgery — 1st line
Somatostatin analogues (octreotide) when surgery not possible; radiotherapy adjunct for huge adenomas

Special

Mortality — cardiomyopathy/HF, stroke, sleep apnea, colon cancer
Ectopic GH/GHRH (lung, pancreas) is a rare non-pituitary cause

Hyperprolactinaemia / Prolactinoma

C/P

Women — galactorrhoea, menstrual irregularity, infertility
Men — impotence, ↓ libido, infertility
Compressive — visual field defects, headache; micro <10 mm, macro >10 mm
Compressive — extraocular muscle weakness (alongside visual field defects & headache)

Inves

Prolactin (morning, fasting); MRI; exclude drugs (antipsychotics, metoclopramide, methyldopa) + hypothyroidism (high TRH)
Also exclude pregnancy (physiological) and further drug causes — verapamil, opiates, TCAs, reserpine, cocaine (add to antipsychotics/metoclopramide/methyldopa)

Mng

Medical first-line — dopamine agonists: bromocriptine (DOC), cabergoline (long-acting) — shrink tumour + lower prolactin
Trans-sphenoidal surgery only if not responding to medical therapy

Special

Medical therapy is first-line (unlike other pituitary tumours)
Primary hypothyroidism raises TRH → stimulates prolactin

physiology · background · low-yield

Epidemiology/Risk

Pituitary adenoma frequency — ~65% secretory (prolactin ~50%, GH 10%, ACTH 6%, TSH 1%) vs ~35% non-secretory (usually macroadenomas)

Background

Pituitary adenomas now termed PitNET (pituitary neuroendocrine tumours); micro <10 mm vs macro >10 mm

Other

Microadenomas may be invisible on standard MRI — dynamic (contrast) MRI is modality of choice (portal supply → late-delayed-phase enhancement / arterial-phase focal defect)

GH Deficiency

C/P

Children — growth retardation; adults — GH deficiency features

Inves

Random GH limited value (pulsatile); IGF-1 gives integrated summary
Stimulation tests — ITT (gold standard), glucagon; deficient if adult GH <2.7 / child <4.5 µg/L
Stimulation-test agents — pharmacological: insulin (ITT), arginine, L-dopa, clonidine, glucagon, GHRH; physiological: sleep, exercise, stress, protein
ITT validity — valid only if glucose falls <2.5 mmol/L (usually by 20 min); insulin IV, sample glucose + GH every 30 min for 2 h; reverse hypo once validated

Mng

GH replacement

Special

Diagnosed by failure to rise on stimulation; ITT is gold standard but hazardous (needs 2 staff)

physiology · background · low-yield

Physiology

GH is secreted in a pulsatile pattern; stimulated by GHRH, inhibited by somatostatin; drives hepatic IGF-1 which exerts negative feedback; somatic effects = femur & muscle growth

Other

Glucagon stimulation test — safer but less sensitive alternative to ITT; glucose rises then falls (60–90 min) to provoke GH release

Thyroid — Hyperfunction

6 entries

Graves' Disease

C/P

Thyrotoxic — weight loss + ↑ appetite, heat intolerance, palpitations/AF, tremor, sweating, diarrhoea, irritability
Diffuse goitre + bruit; 5:1 female, peak 20–40 yr
Ophthalmopathy — exophthalmos, proptosis, diplopia, grittiness
Eponymous eye signs — von Graefe's (upper lid lags behind the globe on downgaze), Stellwag's (widened palpebral fissure / lid retraction, infrequent blinking), Joffroy's (absent forehead wrinkling when looking up with head bent down), Möbius' (impaired convergence on near objects)
Pretibial myxedema (pathognomonic, rare 2–3%); thyroid acropachy
Neuromuscular — proximal myopathy, periodic hypokalaemic (thyrotoxic) paralysis, hyper-reflexia/clonus, myasthenia gravis association
Systemic — osteoporosis; reproductive: amenorrhoea/oligomenorrhoea, infertility, gynaecomastia
Thyrotoxic heart — high-output cardiac failure (CHF/dyspnoea) and angina, in addition to AF/palpitations

Inves

Low TSH, high FT4/FT3; TSH-R Ab (stim) — specific for Graves'
If eye signs present → diagnose clinically; if absent → radioiodine uptake (diffuse increased uptake); anti-TPO

Mng

Symptomatic — propranolol 10–40 mg q8h (also blocks peripheral T4→T3 conversion)
Antithyroid — carbimazole/methimazole (30–40 mg → 5–20 mg) or PTU, 12–18 months, ~50% relapse; watch agranulocytosis (fever + sore throat)
Surgery preferred for very large glands, compressive symptoms, or pregnancy — SSKI 5 drops BID 2 wks pre-op to reduce vascularity
RAI preferred in most — >80% become hypothyroid, may worsen eye disease, no pregnancy 6–12 months
Thyroidectomy complications (~1%) — hypoparathyroidism; recurrent laryngeal nerve injury (hoarseness of voice); external laryngeal nerve injury (poor vocal volume)
Ophthalmopathy — prednisone 100 mg/day immediately post-RAI (7–14 days, then taper over 6–12 wk), external retrobulbar radiotherapy if steroids fail, orbital decompression for threatened vision

Special

Pretibial myxedema — pathognomonic; TSH-R stimulating antibody
NO SPECS ophthalmopathy classification; PTU preferred in pregnancy (esp 1st trimester)

physiology · background · low-yield

Epidemiology/Risk

Precipitating factors — pregnancy, iodide excess, viral/bacterial infections, lithium therapy, glucocorticoid withdrawal
15% have a close relative with the same disorder

Mechanism

Tachycardia and tremor due to hyperreactivity to catecholamines (not raised catecholamine levels)
Autoimmune pathogenesis — T lymphocytes sensitize to thyroid antigens → stimulate B lymphocytes to make TSH-R (stim) antibody

Other

Thionamide side effects beyond agranulocytosis — cholestatic jaundice, hepatocellular toxicity, angioneurotic oedema/acute arthralgia
Immediate RAI contraindicated (achieve euthyroid first) — elderly, IHD/comorbidity, severe thyrotoxicosis, large glands >100 g
Skin — pruritus, onycholysis, vitiligo/hair thinning, palmar erythema, spider naevi
Breastfeeding allowed on PTU (not concentrated in milk)

Exam technique

True exophthalmos on exam — white rim of sclera visible between the upper cornea and upper eyelid (vs lid lag)

Toxic Adenoma (Plummer's)

C/P

Older person (>40) with recent growth of a long-standing nodule
Thyrotoxic symptoms but NO infiltrative ophthalmopathy; nodule on one side

Inves

Low TSH, high T3, slightly high T4
Scan — hot nodule with suppressed contralateral uptake

Mng

Surgery preferred

Special

Autonomous follicular adenoma — almost never malignant; lacks Graves' autoimmune features

Toxic Multinodular Goitre

C/P

Older patients with long-standing MNG; goitre may be small or large, may extend substernally
Pressure symptoms if compressive — tracheal shift/compression, retrosternal extension

Inves

RAI scan — multiple functioning nodules / patchy distribution
CXR if compressive — scabbard trachea (narrowing + lateral deviation of the tracheal air column); retrosternal mass below the clavicles

Mng

Surgery (see Compressive Thyroid Mass — Surgical Approach framework for the pressure-symptom algorithm)

Special

Jod-Basedow phenomenon — iodide-precipitated hyperthyroidism (iodide load / amiodarone)
Scabbard trachea — severe lateral tracheal compression; causes also include Riedel's thyroiditis, poorly differentiated carcinoma, tracheomalacia

Subacute Thyroiditis (de Quervain's)

C/P

Post-viral; triphasic — hyper → hypo → normal; fever, malaise, palpitations
Exquisitely tender thyroid, soreness in neck (no redness/heat)

Inves

Initially T4/T3 high + TSH low → later T4/T3 drop + TSH rises
RAI uptake initially LOW (rises as recovers); ESR up to 100; antibodies usually not detectable

Mng

Symptomatic — paracetamol 0.5 g QDS; severe — NSAID or prednisone 20 mg TDS × 7–10 days
L-thyroxine during hypothyroid phase; 10% need long-term therapy

Special

Destructive viral inflammation → preformed hormone leak → thyrotoxicosis with LOW RAI uptake; self-limiting

Thyroid Storm

C/P

Severely hyperthyroid + precipitant (infection, surgical stress, stopping antithyroids)
Anorexia, tachycardia, tachyarrhythmias, confusion; fever/hyperthermia, hypotension → shock
Agitation → coma; pulmonary oedema / cardiac failure

Inves

Clinical diagnosis — draw TFTs but start therapy without waiting for confirmation

Mng

Supportive — fluids/electrolytes, vasopressors, cooling blanket + acetaminophen
Propranolol — 1 mg/min IV or 60–80 mg q4h (blocks adrenergic tone + T4→T3)
PTU — 1000 mg loading then 250 mg q6h; iodide 1h AFTER PTU (Lugol's / SSKI) — blocks hormone release
Dexamethasone 2 mg IV q6h — blocks peripheral T4→T3; treat precipitant

Special

Iodide given AFTER PTU — giving it first would provide fuel for hormone synthesis

Other Thyrotoxicosis

C/P

Thyrotoxicosis factitia (exogenous thyroxine); struma ovarii; hydatidiform mole; TSH-secreting pituitary adenoma

Inves

Factitia — RAI uptake nil + low thyroglobulin; struma ovarii — nil neck uptake but pelvic uptake
Mole — HCG (TSH-like activity); TSH-oma — high FT4/FT3 with normal/high TSH

Mng

Cause-specific

Special

Factitia has low thyroglobulin (suppressed gland); TSH-oma = inappropriately normal/high TSH + temporal field defect

physiology · background · low-yield

Other

Neonatal thyrotoxicosis — listed among the causes of thyrotoxicosis

Thyroid — Hypofunction

3 entries

Hypothyroidism

C/P

Weakness (99%), fatigue, weight gain, cold intolerance, lethargy, constipation
Bradycardia, pericardial effusion, low-voltage/flat-T ECG
Dry cool skin, non-pitting myxedema, loss of outer ⅓ of eyebrows (Queen Anne's sign), puffy face, thick tongue, hoarse voice
Menorrhagia, hyperlipidaemia, anaemia; slow-relaxing tendon reflexes
Causes — most common Hashimoto's/autoimmune (95% primary); iatrogenic post-RAI or post-thyroidectomy; drugs (amiodarone, lithium, interferon); iodine excess or deficiency; secondary = Sheehan's/hypopituitarism
Cognitive/psychiatric — depression, slow thinking, poor concentration, slow speech; carpal tunnel syndrome, paraesthesias, ataxia

Inves

Primary — low FT4 + high TSH; subclinical — high TSH + normal FT4
Central — low FT4 + inappropriately normal/low TSH (→ brain MRI)
TPO antibodies (Hashimoto)

Mng

L-thyroxine 50–100 mcg PO OD (start 25 mcg if elderly/IHD — avoid precipitating angina)
Recheck TSH after 4–6 weeks to titrate; monitor FT4 (not TSH) in secondary; in pregnancy check TFTs monthly + ↑ dose ~30%
Subclinical (high TSH, normal FT4) — treat with L-thyroxine if TPOAb+ or symptomatic; annual follow-up if TPOAb− and asymptomatic

Special

Non-pitting myxedema — glycosaminoglycan deposition (not fluid); loss of lateral eyebrow; delayed reflex relaxation

physiology · background · low-yield

Background

Hair — thinning/loss, coarse sparse dry hair, loss of body hair; goitre may be present
Treat concomitant hyperprolactinaemia/hypercholesterolaemia if not normalised after adequate thyroid replacement

Mechanism

Anaemia subtypes — iron deficiency (menorrhagia/malabsorption), folate deficiency, or autoimmune pernicious anaemia; impaired Hb synthesis

Background

Further primary causes — infiltrative disease (sarcoidosis, amyloidosis, haemochromatosis, scleroderma), late-stage invasive fibrous (Riedel's) thyroiditis, and peripheral resistance to thyroid hormone

Hashimoto's Thyroiditis

C/P

Painless goitre, euthyroid or mild hypothyroid; young females (4:1)
Hashitoxicosis — transient thyrotoxicosis; older patients → severe hypothyroid with small firm atrophic gland

Inves

High anti-TPO Ab and/or anti-thyroglobulin; TSH high if hypothyroid
FNA — lymphocytic infiltration + Hürthle cells

Mng

L-thyroxine replacement

Special

Autoimmune lymphocytic destruction; Hürthle cells on FNA; rare complication → thyroid lymphoma; Schmidt-syndrome association
Autoimmune clustering — associated with pernicious anaemia, adrenal insufficiency, idiopathic hypoparathyroidism, vitiligo

physiology · background · low-yield

Background

Schmidt's syndrome components — Hashimoto's, adrenal insufficiency, hypoparathyroidism, DM, ovarian failure, candidal infection; permanent hypothyroidism in 10–15% of young patients

Myxedema Coma

C/P

Obese elderly woman in winter — yellowish skin, hoarse voice, large tongue, altered mental status, hypothermia
Lethargy → stupor/coma; hypoventilation, hypotension, bradycardia; signs of infection masked

Inves

Low FT4 + TSH high/normal/low; hyponatraemia + hypoglycaemia; low WBC/platelets
EKG — bradycardia, low voltage, prolonged QTc; elevated CK

Mng

Treat on clinical suspicion — draw TSH/FT3/FT4/cortisol/ACTH first
IV L-thyroxine 0.2–0.5 mg bolus then 0.1 mg IV OD
Hydrocortisone 100 mg IV q8h — before/with T4 to prevent precipitating adrenal crisis
Passive warming only; support ventilation (main cause of death); IV glucose

Special

Precipitant — sepsis #1, cold exposure; steroids before/with thyroxine; active warming → vasodilatory shock
Medical emergency — 20–30% mortality
Precipitants also include medication non-adherence, drugs (amiodarone, lithium, narcotics), trauma/burns, MI, CHF, PE, stroke, DKA

physiology · background · low-yield

Background

Pituitary myxedema clue — scanty pubic/axillary hair; clinically hard to distinguish from sepsis and adrenal crisis

Thyroid — Nodules & Cancer

6 entries

Thyroid Nodule

C/P

Usually asymptomatic/incidental; compressive in large (dysphagia, dyspnoea, dysphonia, hoarseness)
Sudden pain → haemorrhage into cyst; rapid enlargement → anaplastic / lymphoma
Malignancy features — firm/hard, fixed, ill-defined margins, cervical adenopathy
Malignancy risk ↑ at age <20 or >60 and male sex; vocal cord paralysis, fixation to neck structures and enlarged regional nodes are the most specific signs

Inves

TSH/FT4/FT3 (mostly euthyroid); US suspicious features — microcalcifications, taller-than-wide, irregular margins, very hypoechoic
TI-RADS → FNAC by category/size; radionuclide scan if TSH low (hot = almost never malignant; cold = 5–8% malignant)
FNAC size thresholds by TI-RADS — TR3 ≥2.5 cm, TR4 ≥1.5 cm, TR5 ≥1.0 cm
Focal thyroid uptake on FDG-PET (incidentaloma) → ~33% prove malignant

Mng

Levothyroxine if hypothyroid (shrinks goitre as TSH normalises)
Surgery — malignant, toxic, compressive, or retrosternal extension
Thyroidectomy complications — recurrent laryngeal nerve (hoarseness), external laryngeal nerve (loss of vocal volume), hypoparathyroidism → hypocalcaemia, bleeding

Special

Pemberton's sign — retrosternal goitre; arms overhead → facial plethora + JVD
5–15% of nodules malignant; radiation (Chernobyl <14 yr) is a key risk factor

physiology · background · low-yield

Epidemiology/Risk

Prevalence — 3–7% by palpation, up to 50–67% by US/autopsy; ↑ with age, female sex and iodine deficiency; ~50% of clinically "solitary" nodules are multinodular on US
Differentiated thyroid cancer (DTC) = ~90% of thyroid cancers; thyroid cancer ~1% of all cancers; DTC 10-yr survival ~90% (local recurrence 5–20%, distant mets 10–15%)

Background

Benign DDx — multinodular goitre, Hashimoto's, simple/haemorrhagic cyst, parathyroid cyst, follicular adenoma, subacute (de Quervain's) thyroiditis
Metastases to the thyroid (blood-borne) — renal, breast, lung, colon, melanoma
Molecular testing (ThyroSeq — BRAF, RAS, RET, PAX8/PPARγ, TERT) for indeterminate Bethesda III/IV nodules can avoid surgery in ~60%

Papillary Thyroid Carcinoma

C/P

Young adults; slow-growing; commonest thyroid cancer (85% of WDTC); nodal involvement common

Inves

FNA — Orphan Annie-eyed nuclei; often multifocal; US microcalcifications
Thyroglobulin should be undetectable after total thyroidectomy ± RAI; a rising level signals recurrence — unreliable if anti-Tg antibodies present

Mng

<1 cm → lobectomy + isthmusectomy; 1–4 cm → total thyroidectomy OR lobectomy; >4 cm / extension / nodes → total thyroidectomy + central node dissection
RAI ablation by ATA risk; TSH suppression (levothyroxine); thyroglobulin surveillance
TSH-suppression targets (2015 ATA) — low-risk 0.5–2.0, intermediate 0.1–0.5, high-risk <0.1 mU/L; RAI dose — none (low-risk), 30 mCi (intermediate), 100–150 mCi (high-risk)

Special

Orphan Annie-eyed nuclei; lymphatic spread; excellent prognosis (96% overall survival) even with mets

Follicular & Hürthle Cell Carcinoma

C/P

Unifocal; older patients; haematogenous (blood-borne) spread common, nodes uncommon

Inves

FNA cannot distinguish adenoma from carcinoma — microfollicular = "suspicious" → diagnostic lobectomy
Diagnosis needs histology — capsular or vascular invasion; Hürthle = oncocytes rich in mitochondria (FTC subtype)

Mng

Diagnostic hemithyroidectomy → total thyroidectomy if malignant; RAI; thyroglobulin surveillance

Special

Capsular/vascular invasion diagnostic; blood-borne mets common; worse prognosis than papillary (follicular 91%, Hürthle 85% overall survival)
Skull / bone metastasis is classic — reflects blood-borne (haematogenous) spread

Medullary Thyroid Carcinoma (MTC)

C/P

~5% of thyroid malignancies, 20% inherited; upper/middle thirds (C-cell zone)
Secretes calcitonin (also somatostatin, serotonin, VIP → carcinoid syndrome, Cushing's, diarrhoea)

Inves

Calcitonin >100 pg/L (100% PPV); >400 pg/L suggests distant mets; CEA; RET testing
Amyloid stroma; screen every new MTC for phaeo (metanephrines) + PHPT (calcium) before surgery

Mng

Total thyroidectomy + bilateral central neck dissection; MEN2A prophylactic — central dissection not needed
Lateral dissection only if FNA-proven spread; remove phaeo FIRST if synchronous
Advanced/systemic disease — tyrosine kinase inhibitors (TKI); EBRT to neck for residual MTC, extensive nodal disease or extra-thyroidal extension

Special

Parafollicular C-cell / neural-crest origin; amyloid stroma (from calcitonin); familial = bilateral/multicentric + more aggressive; NOT radioiodine-avid

physiology · background · low-yield

Epidemiology/Risk

Sporadic MTC — unilateral, 5th–6th decade; familial (RET) — bilateral/multicentric, 2nd–3rd decade, screening-detected disease may be microscopic only

Anaplastic Thyroid Carcinoma

C/P

Appears late in life; rapid, invasive, non-encapsulated growth; airway compromise

Inves

FNA/histology — small or large anaplastic cells

Mng

Multimodal — surgery + radiation + chemotherapy (poor outcomes)

Special

Succumb within 6 months; death from local recurrence + pulmonary metastasis; overall 5-yr survival ~7%

Thyroid Lymphoma

C/P

Rapid enlargement of the thyroid; arises on a background of Hashimoto's thyroiditis

Inves

FNA / biopsy

Mng

— (not detailed in deck)

Special

Rare complication of Hashimoto's thyroiditis
Arises in the hypothyroid stage of Hashimoto's, driven by ongoing cell destruction; a non-epithelial thyroid malignancy

Additions — Approach & OSCE

2 entries

Secondary Hypertension — Approach & Evaluation

C/P

History clues: paroxysmal flushing → phaeochromocytoma; cold/heat intolerance → thyroid dysfunction; snoring/apnoeic episodes → obstructive sleep apnoea
Exam signs: arm–leg BP discrepancy / diminished femoral pulses → coarctation; renal bruit → renal artery stenosis; buffalo hump + moon facies → Cushing's

Inves

Lab clues: unprovoked hypokalaemia → aldosteronism; ↑ haematocrit → polycythaemia; azotaemia/proteinuria → renal disease; creatinine rise >30% after ACEI/ARB → renal artery stenosis
Test-by-cause: coarctation → echocardiography; Cushing's → 24h urinary free cortisol + dexamethasone suppression; phaeo → plasma/urinary metanephrines; RAS → CT/MRA renal arteries + colour Doppler; renal parenchymal → renal US, creatinine/eGFR, urine albumin ± biopsy
Age-stratified algorithm when no clinical clues: child → renal US; young adult → renal-artery MRI/CTA; middle-aged → renin–aldosterone levels

Mng

New-patient evaluation goals — identify comorbidities/risk factors, assess target-organ damage, exclude secondary causes (most have no identifiable secondary cause)

Special

ABCDE of secondary HTN: A — Accuracy/Apnoea/Aldosteronism; B — Bad kidneys/Bruits; C — Coarctation/Catecholamines/Cortisol (Cushing's); D — Drugs/Diet; E — Endocrine/Erythropoietin
Epidemiology: 1 in 3 adults hypertensive, mostly essential; secondary cause in ~5–10% of adults but up to 85% of young children
Age-based secondary prevalence: children 70–85% (renal parenchymal, coarctation); young adults ~5% (FMD in women, thyroid); middle-aged 8–12% (aldosteronism, OSA, Cushing's, phaeo); ≥65y ~17% (atherosclerotic RAS, renal failure, hypothyroidism)

physiology · background · low-yield

Mechanism

Drugs/substances raising BP: oestrogen (OCP), NSAIDs, corticosteroids, decongestants, antidepressants, diet pills; illicit/herbal — ephedra, ginseng, amphetamines, cocaine
Pathophysiologic drivers — ↑ cardiac output, renal Na⁺/water retention, arteriolar smooth-muscle constriction (endothelin vs nitric oxide), sympathetic activation, endocrine (insulin, aldosterone), genetic (angiotensinogen genes; GRA, AME, Liddle syndrome)

Thyroid Examination (OSCE)

Special

Moves up on swallowing = thyroid mass or lymph node; moves up on tongue protrusion = thyroglossal cyst
Thyroid bruit over the upper pole (superior thyroid artery entry) = Graves' hypervascularity; sternal dullness on percussion = retrosternal goitre
Fixity to skin (pinch test) or to strap muscle (hold sternomastoid while patient swallows) suggests malignant infiltration

physiology · background · low-yield

Exam technique

Equipment — glass of water (swallowing), paper (fine tremor), stethoscope (bruit), tendon hammer (reflex relaxation phase)
Palpate from behind, ask about pain first; isthmus overlies the 1st–2nd tracheal rings just below the cricoid, then move laterally to the lobes; comment on site/size/shape/symmetry, surface/consistency/borders/tenderness, tracheal deviation, thrill and cervical nodes

Diagnostic Criteria & Targets

9 entries

Diabetes Diagnosis Criteria

Test	Diagnostic level
FPG	≥7.0 mmol/L (126 mg/dL) — ≥8 h no caloric intake
A1C	≥6.5% — not valid for suspected T1DM
2h-PG in 75g OGTT	≥11.1 mmol/L (200 mg/dL)
Random PG	≥11.1 mmol/L (200 mg/dL) with symptoms

Confirmation: single test result in diabetes range sufficient if symptomatic; asymptomatic requires a repeat confirmatory test on another day.

Prediabetes Categories

Category	Threshold
IFG (Impaired Fasting Glucose)	FPG 6.1–6.9 mmol/L
IGT (Impaired Glucose Tolerance)	2h-PG in 75g OGTT 7.8–11.0 mmol/L
Prediabetes (A1C)	A1C 6.0–6.4%

GDM Screening Strategies

Screen at 24–28 weeks gestation.

One-step

75g OGTT (fasting) — diagnose GDM if any value met/exceeded: fasting ≥92 · 1h ≥180 · 2h ≥153 mg/dL.

Two-step

Step 1 — 50g GLT (non-fasting); if 1h ≥130–140 mg/dL → Step 2 — 100g OGTT (fasting), diagnose if ≥2 values met/exceeded.

DKA Diagnostic Criteria

Glucose >250 mg/dL
Bicarbonate <15 mEq/L
pH <7.3
Ketonaemia + moderate ketonuria

Triad: hyperglycaemia + ketosis + metabolic acidosis.

HHS Diagnostic Criteria

Glucose >600 mg/dL
Osmolarity >310 mOsm/L
Dehydration + depressed sensorium
NO ketoacidosis

DM Management Targets

Parameter	Target
A1C	<7.0%
Preprandial PG	90–130 mg/dL
Postprandial PG	<180 mg/dL
Blood pressure	<130/80 mmHg
Lipids	LDL <100 · TG <150 · HDL >40 mg/dL

Glucose Monitoring Methods

Method	Reflects
SMBG	One point in time
CGM	5–10 min real-time (correlates with A1C)
HbA1C	~3-month average

Acromegaly OGTT Criterion

Oral glucose tolerance test — GH clearly elevated (>10 ng/mL) after oral glucose = diagnostic
Normal response — glucose suppresses GH
Elevated IGF-1 — stable integrated screening marker

Cushing's Screening Cutoffs

Overnight 1 mg DST (11 PM → cortisol 8 AM) — <1.8 mcg/dL (50 nmol/L) excludes Cushing's
24h urinary free cortisol — elevated
Loss of cortisol circadian rhythm (high am + pm; midnight cortisol not suppressed)

Dynamic Endocrine Tests

6 entries

Dexamethasone Suppression Tests

Variant	Dose	Use / interpretation
Overnight low-dose	1–2 mg at 11 PM, cortisol 8 AM	Screen; suppress to <50 nmol/L = normal; excludes pseudo-Cushing
48-h low-dose	0.5 mg q6h	Confirmatory for Cushing's syndrome (after failed overnight)
48-h high-dose	2 mg q6h	Localises — pituitary suppresses, ectopic does not

Significant failure to suppress = cortisol >1.7 mcg/dL (>50 nmol/L).

Synacthen (ACTH Stimulation) Test

Short test

250 µg Synacthen IV, cortisol at 0/30/60 min. Normal — increment >200 to peak >550 nmol/L (>18 mcg/dL) → excludes primary failure.

Long test

Depot ACTH × 3 days — differentiates: secondary (adrenal eventually responds, increment >200) vs primary/Addison's (little change, no response).

Water Deprivation Test

Restrict fluids (stop if weight ↓3%), then give desmopressin 0.03 mcg/kg SC.

Pattern	Urine osmo after deprivation	After desmopressin
Complete cranial DI	No change (stays low)	Marked improvement
Partial cranial DI	Partial rise	Additional rise to normal
Nephrogenic DI	No change	No change
Psychogenic polydipsia	Markedly increases	No further improvement

DI confirmed if plasma osmo >300 with urine osmo <600 (fails to concentrate).

Insulin Tolerance Test (ITT)

Gold standard for GH / cortisol reserve; hazardous — always 2 staff
Insulin IV; measure glucose + GH every 30 min for 2h
Valid only if glucose <2.5 mmol/L (usually by 20 min); reverse hypo after validation
Contraindicated in epilepsy / ischaemic heart disease

GH Deficiency Cutoffs

	Not deficient	Deficient
Adult	GH >6 µg/L	GH <2.7 µg/L
Child	GH >7.5 µg/L	GH <4.5 µg/L

Values between the cutoffs = grey zone requiring correlation.

Aldosterone-Renin Ratio (ARR) & AVS

ARR (first-line)

Elevated (high aldosterone, suppressed renin). Take morning, upright, ≥2h after waking. Stop first: spironolactone/eplerenone/amiloride, K-wasting diuretics, liquorice, ACEI/ARB, β-blockers. OK to use: verapamil, hydralazine, α-blockers.

Adrenal vein sampling (AVS)

Aldosterone/cortisol ratio	Interpretation
>4	Diagnostic of adenoma (surgical)
>3 to <4	Suggestive of adenoma
<3	Bilateral hyperplasia (medical)

Endocrine Classifications

7 entries

Diabetes Classification (ADA)

4 classes — Type 1 · Type 2 · Gestational · Specific types (monogenic [MODY, neonatal], exocrine pancreas [CF, pancreatitis], drug/chemical [glucocorticoids, HIV Rx, transplant]).

Feature	Monogenic	T1DM	T2DM
Age	<25	Most <25	Usually >24
Islet autoantibodies	Absent	Usually present	Absent
C-peptide	Normal	Undetectable/low	Normal/high
First-line Rx	Depends on subtype	Insulin	Non-insulin agents
Family history	Multigenerational/AD	Infrequent (5–10%)	Frequent (75–90%)
DKA	Rare (except neonatal)	Common	Rare

CAH Enzyme Deficiencies

	21-OH (90%)	11β-OH	17α-OH
Mineralocorticoid	Low	High (DOC)	High
Androgens	High	High	Low
Metabolite	17-OH-progesterone	11-deoxycortisol + DOC	—
Genitalia	Ambiguous ♀	Ambiguous ♀	Undervirilised ♂
Blood pressure	Low (salt-wasting)	High	High

Diagnostic marker for 21-OH = high serum 17-hydroxyprogesterone. Autosomal recessive.

Hyperaldosteronism Classification

Type	Renin	Aldosterone	Cause
Primary (Conn's)	Low	High	Adenoma / bilateral hyperplasia / CAH
Secondary	High	High	Renovascular disease, renin tumour, oedematous states
Pseudo (low renin/low aldo)	Low	Low	Cushing's, liquorice (11β-HSD2 block), SAME, Liddle's (ENaC gain)

All forms → hypertension (mineralocorticoid excess).

ACTH / Cortisol Patterns

Condition	Cortisol	ACTH
Primary adrenal failure (Addison's)	Low	High
Steroid Rx / hypopituitarism	Low	Low
Cushing's disease (pituitary)	High	High
Adrenal adenoma	High	Low
Ectopic ACTH	High	High

MEN Syndromes

Syndrome	Components	Gene
MEN 1	Pituitary + Parathyroid + Pancreatic tumours (3 Ps)	Menin (tumour suppressor)
MEN 2A	Medullary thyroid Ca + Phaeochromocytoma + Hyperparathyroidism	RET (chr 10)
MEN 2B	Medullary thyroid Ca + Phaeo + Mucosal neuromas + Marfanoid (no PHPT)	RET
FMTC	Medullary thyroid Ca only	RET

MEN 2 — autosomal dominant, ~100% penetrance; MEN 2B most aggressive, MEN 2A / FMTC more indolent.

Polyglandular Autoimmune Syndromes

Schmidt syndrome — Addison's + Hashimoto's thyroiditis
PAS type 1 (APECED, AIRE gene, AR) — Addison's + hypoparathyroidism + mucocutaneous candidiasis
PAS type 2 — Addison's + type 1 DM + Hashimoto's or Graves'

Rule of 10s (Phaeochromocytoma)

10% extra-adrenal
10% bilateral
10% malignant
10% familial
10% normotensive

Modern genetics — familial fraction actually up to ~30%.

Thyroid Frameworks

10 entries

TFT Interpretation Patterns

Condition	TSH	T4 / T3
Primary hypothyroidism	↑	↓
Primary hyperthyroidism	↓	↑
Hypopituitarism (central)	↓	↓
TSH-secreting tumour	↑	↑

TSH normal range 0.5–5 µU/ml; assess with free hormone, not bound.

Isotope Scan Patterns

Pattern	Diagnosis
Diffuse hot thyroid	Graves' disease
Multiple hot nodules / patchy	Toxic MNG
One super-hot nodule	Toxic adenoma
Cold nodule	Non-functioning — 5–8% malignant

Hot nodule almost never malignant; do scan if TSH low.

ACR TI-RADS Scoring

Category	Feature → points
Composition	Cystic/spongiform 0 · mixed 1 · solid 2
Echogenicity	Anechoic 0 · hyper/iso 1 · hypoechoic 2 · very hypoechoic 3
Shape	Wider-than-tall 0 · taller-than-wide 3
Margin	Smooth/ill-defined 0 · lobulated/irregular 2 · extra-thyroidal extension 3
Echogenic foci	None/comet-tail 0 · macrocalcification 1 · peripheral 2 · punctate 3

TI-RADS Categories & FNA Cutoffs

TR	Points	Malignancy	FNA if
TR1	0	0.3%	No
TR2	2	1.5%	No
TR3	3	4.8%	≥2.5 cm
TR4	4–6	9.1%	≥1.5 cm
TR5	≥7	35%	≥1.0 cm

Follow-up thresholds — TR3 ≥1.5 cm · TR4 ≥1.0 cm · TR5 ≥0.5 cm.

Bethesda FNA Cytology

Category	Malignancy risk	Action
I — Non-diagnostic	5–10%	Repeat US-guided FNA
II — Benign	0–3%	Clinical follow-up / US 12–24 mo
III — AUS/FLUS	6–18%	Molecular test, repeat FNA (3 mo), or lobectomy
IV — Follicular neoplasm	10–40%	Molecular test or lobectomy
V — Suspicious for malignancy	45–60%	Near-total thyroidectomy / lobectomy
VI — Malignant	94–96%	Near-total thyroidectomy / lobectomy

Molecular testing (ThyroSeq — BRAF, RAS, RET, PAX8/PPARγ, TERT) can avoid surgery in ~60% of Bethesda III/IV nodules.

NO SPECS (Graves' Ophthalmopathy)

Class	Feature
0	No signs or symptoms
1	Only signs (lid retraction, stare, lid lag)
2	Soft tissue involvement (periorbital oedema, chemosis)
3	Proptosis (Hertel exophthalmometer)
4	Extraocular muscle involvement
5	Corneal involvement
6	Sight loss (optic nerve)

Thyroid Cancer Types & Prognosis

Type	10-yr mortality	Overall 5-yr survival
Papillary	5%	96%
Follicular	10%	91%
Hürthle cell	15%	—
Medullary	20%	85%
Anaplastic	—	7%

Prognosis worsens: Papillary > Follicular > Hürthle > Medullary > Anaplastic.

Papillary vs Follicular Carcinoma

Feature	Papillary	Follicular
Focality	Multifocal (21–46%)	Unifocal
Spread	Lymphatic	Bloodstream
Blood-borne mets	Unusual	Common
Orphan Annie nuclei	Present	Absent
Capsular/vascular invasion	Absent	Diagnostic
Lymph node involvement	Common	Uncommon
Prognosis	Good	Worse

ATA Post-op Risk Stratification (WDTC)

Risk	RAI ablation	TSH goal
Low (intrathyroidal, no LVI, <5 micromets)	Not recommended	0.5–2.0 mU/L
Intermediate (microscopic ETE, aggressive histology/VI, >5 nodes)	Low-dose (30 mCi)	0.1–0.5 mU/L
High (gross ETE, distant mets, node >3 cm)	High-dose (100–150 mCi)	<0.1 mU/L

Thyroglobulin — tumour marker; should be undetectable post-total-thyroidectomy ± RAI; unreliable if anti-Tg antibodies present.

Compressive Thyroid Mass — Surgical Approach

Scenario	Management
Secondary toxic goitre (↓TSH, ↑FT₄) + retrosternal extension	Prepare the patient medically before resection
Unilateral neck swelling + tracheal shift	Lobectomy ± lymph-node dissection (according to FNA result)
Retrosternal extension	Resection of the involved gland according to suspected pathology
Scabbard trachea — poorly differentiated carcinoma	Isthmusectomy to release the trachea
Scabbard trachea — suspected tracheomalacia	Prepare for tracheostomy

Scabbard trachea = severe lateral tracheal compression → chest X-ray shows narrowing + lateral deviation of the tracheal air column. Possible underlying causes (all 3): Riedel's thyroiditis · poorly differentiated thyroid carcinoma · suspected tracheomalacia.

Retrosternal extension sign — large soft-tissue mass extending below the clavicles into the upper mediastinum on chest X-ray.

Pharmacology & Bone

7 entries

Antidiabetic Drug Classes

Class	Action	Key adverse effect
Biguanide (metformin)	↓ hepatic glucose production	GI, B12 deficiency, lactic acidosis; caution CKD 3B
Sulfonylureas (gliclazide)	↑ insulin secretion	Hypoglycaemia, weight gain
Meglitinides (repaglinide)	↑ insulin secretion (prandial)	Hypoglycaemia; safe in renal disease
TZDs (pioglitazone)	↑ insulin sensitivity	Weight gain, oedema/HF, fractures, bladder cancer
DPP-4i (gliptins)	↑ insulin, ↓ glucagon (glucose-dependent)	Weight-neutral, no hypo; ↑ HF (saxagliptin)
α-glucosidase inhibitors (acarbose)	Slows carbohydrate absorption	Flatulence, GI
SGLT2i (flozins)	Blocks renal glucose reabsorption	Genital infection/UTI, DKA, Fournier's, amputation (cana)
GLP-1 RA (semaglutide)	↑ insulin, ↓ glucagon, satiety	GI, ↓ weight, CV benefit; MTC/C-cell (rare)

Insulin Types

Type	Examples	Onset	Peak	Duration
Rapid	Lispro, aspart, glulisine	12–30 min	0.5–3 h	3–5 h
Short	Regular	30 min	2.5–5 h	4–24 h
Intermediate	NPH	1–2 h	4–12 h	14–24 h
Long	Glargine, detemir, degludec	3–4 h	No peak	≥24 h

Starting dose — T1DM 0.2–1 U/kg/day · T2DM 0.2–0.3 U/kg/day.

T2DM Therapy Step-Up

Monotherapy — Metformin + lifestyle (initial)
Dual — + 1 agent (SU, TZD, DPP-4i, SGLT2i, GLP-1 RA, or basal insulin) if A1C target not met after ~3 mo or A1C ≥9%
Triple — + 2 agents if not met after ~3 mo of dual therapy
Start insulin — suboptimal control despite max oral agents (A1C <7% not reached) or complications

Hyperparathyroidism Classification

Type	Ca	PO4	PTH	Setting
Primary	High	Low	High	Adenoma / hyperplasia
Secondary	Low/normal	High	High	CKD (compensatory)
Tertiary	High	High	Very high	Post-transplant (autonomous)

DEXA T/Z-score & FRAX

T-score — vs young healthy same-sex adult; defines osteoporosis (<−2.5; osteopenia −1 to −2.5)
Z-score — vs age + sex matched; flags secondary osteoporosis

FRAX (10-yr fracture probability)

Zone	Action
Red	Treat
Orange	Measure BMD
Green	Lifestyle advice + reassure

Parathyroidectomy Criteria (Asymptomatic PHPT)

Recommend surgery if any one:

Age <50
Serum calcium >1 mg/dL over upper limit of normal
Creatinine clearance <60
Osteoporosis (T-score <−2.5)
24-h urinary calcium >400 mg
Occult vertebral fracture / nephrolithiasis / nephrocalcinosis
Patient unable/unwilling for surveillance

Else surgery or surveillance both reasonable (annual Ca/creatinine + BMD every 1–2 yr).

Hypercalcaemic Crisis

Corrected calcium >3.5 mmol/L; precipitated by intercurrent illness (vomiting/diarrhoea) or diuretics
Features — fatigue/weakness, polyuria, confusion/coma, pancreatitis, CV instability, hypotension (poor-outcome predictors)
Aggressive rehydration — normal saline up to 200 mL/h; avoid diuretics
Pamidronic acid 60–90 mg IV over 4–24 h
Delay surgery until corrected calcium <3 mmol/L

Diabetes Therapeutics — Special Situations

Peri-operative

Poor peri-operative glycaemic control → poor surgical outcomes; aim HbA1c < 8.5% before elective surgery (unless emergency)
Hospitalised patients are switched from oral glucose-lowering agents to a basal-bolus insulin regimen during their stay

Diabetes + MI / IV contrast

Stop metformin before IV-contrast procedures (ideally 48 h before) — risk of contrast nephropathy/lactic acidosis
Stop metformin ideally for ~6 months following MI; use basal-bolus or premixed insulin
Patients with cardiovascular risk or renal disease → offer a GLP-1 analogue or SGLT-2 inhibitor

Ramadan / fasting

Risks: hypoglycaemia, hyperglycaemia, DKA, dehydration/thrombosis
Higher hypoglycaemia risk with insulin and sulfonylureas → change or dose-reduce; monitor glucose more frequently
Highest-risk (hypo history, insulin-treated, established complications) may be advised NOT to fast
Diet: low-GI foods at sohour, limit high-GI at iftar, hydrate 2–3 L/day; break the fast if hypo- OR hyperglycaemic

Gestational diabetes — therapeutics

Screen 24–28 wks (50 g GCT → if abnormal, 100 g 3-h OGTT); diet first (complex carbs, avoid large simple-carb meals); early insulin if diet fails; target near-nondiabetic glucose profiles (see GDM disease card)