Hypothyroidism
- Causes (Primary): Chronic autoimmune thyroiditis (Hashimoto’s, most common), iatrogenic (thyroidectomy, radioiodine), iodine deficiency/excess, drug-induced (lithium, amiodarone, thionamides, interferon alfa, interleukin-2, tyrosine kinase inhibitors, checkpoint inhibitors), infiltrative disease (fibrous thyroiditis, hemochromatosis, sarcoidosis), transient forms (painless, subacute granulomatous, postpartum thyroiditis), congenital.
- Causes (Central): TSH or TRH deficiency (pituitary/hypothalamic disorders).
- Clinical Features:
- Slowed metabolism: fatigue, weakness, cold intolerance, dyspnea, weight gain, cognitive dysfunction, constipation, growth failure, bradycardia, delayed tendon reflex relaxation.
- Matrix accumulation: dry skin, hoarseness, edema, coarse skin, puffy facies, loss of outer eyebrows, enlarged tongue.
- Other: decreased hearing, myalgia, depression, menorrhagia, diastolic hypertension, pleural/pericardial effusions, galactorrhea.
- Diagnosis:
- TSH first-line; confirm with FT4/FT3 if abnormal. TSH alone unreliable in suspected pituitary disease.
- TPO antibodies: sensitive for autoimmune thyroiditis; useful in subclinical disease. Not needed routinely for overt hypothyroidism.
- Thyroglobulin antibodies: support autoimmune diagnosis; relevant when monitoring thyroglobulin in thyroid cancer.
- Ultrasound: for structural abnormality/nodules, not for uncomplicated hypothyroidism.
- Radionuclide scan: not used for autoimmune hypothyroidism.
- Subclinical Hypothyroidism:
- Retest TSH in 1-3 months if abnormal.
- TSH > 10 mIU/L: treat with levothyroxine.
- TSH 4-10 mIU/L with positive TPO antibodies: consider treatment.
- Symptomatic: trial of levothyroxine.
- Levothyroxine Administration: Empty stomach, 30-60 minutes before breakfast, or at bedtime (2+ hours after last meal). Avoid concurrent bile acid resins, calcium carbonate, ferrous sulfate, PPIs.
- Starting Dose: Partial replacement (25-50 mcg daily) for mild elevation, subclinical disease, cardiovascular disease, or older patients. Full replacement for overt hypothyroidism.
- Dose Adjustment: Every 4-8 weeks, guided by age-specific TSH targets:
- Age < 60: TSH 0.5-2.5 mIU/L
- Age ≥ 60: TSH 1-5 mIU/L
- Age > 80: TSH 4-6 mIU/L
- Overtreatment Risk: Atrial fibrillation, accelerated bone loss.
- Perioperative: Safe to withhold up to 7 days if euthyroid; treat hypothyroidism before elective surgery.
Specialist Referral Red Flags:
- Age ≤ 18 years
- Unresponsive to therapy
- Pregnant
- Cardiac disease
- Structural thyroid changes
- Other coexisting endocrine disease
Hyperthyroidism
- Aetiologies: Graves’ disease (TSH receptor antibodies), toxic adenoma, toxic multinodular goitre, factitious ingestion, drug-induced (amiodarone), postpartum thyroiditis, painful subacute thyroiditis.
- Diagnosis:
- Low TSH, elevated FT4/FT3.
- TRAb/TSI confirms Graves’ disease.
- Radionuclide scan if aetiology unclear:
- Diffuse uptake: Graves’ disease
- Focal uptake with suppression: toxic adenoma
- Multifocal uptake with suppression: toxic multinodular goitre
- Near-absent uptake: thyroiditis or exogenous hormone intake
- Antithyroid Drugs (Thionamides):
- First-line: Carbimazole. Both inhibit thyroid peroxidase.
- PTU used if carbimazole not tolerated, pre-conception/1st trimester, or thyroid storm (also blocks peripheral T4→T3 conversion).
- Initial dosing based on severity: Carbimazole 10-45 mg/day; PTU 100-450 mg/day.
- Titrate every 4-6 weeks using FT3/FT4 (TSH may remain suppressed). Halve dose if hormone levels halve.
- Continue 12-18 months for Graves’ disease to improve remission; do not stop abruptly.
- Beta-blockers: Propranolol/atenolol for rapid symptom control (palpitations, tremor, sweating); do not alter metabolic state. Diltiazem if beta-blockers contraindicated.
- Radioiodine: Severe/recurrent Graves’, severe hyperthyroidism in older patients, toxic adenoma/multinodular goitre, young patients with persistent high TRAb.
- Thyroidectomy: Severe/recurrent Graves’, toxic adenoma/multinodular goitre, thyroid cancer.
Thionamide Safety Red Flags:
- Agranulocytosis: rare, life-threatening, usually early in therapy — stop drug immediately if fever/infection.
- Severe liver injury with PTU; PTU contraindicated in children.
- Vasculitis (ANCA-positive) associated with PTU.
Thyroid Nodules
- Initial Evaluation: Check TSH.
- TSH normal/high → thyroid ultrasound.
- TSH low → thyroid scintigraphy.
- ACR TI-RADS Risk Stratification:
- TR1 (Benign): ~0% malignancy risk, no biopsy, no follow-up.
- TR3 (Mildly suspicious): ~5% malignancy risk, biopsy if ≥ 2.5 cm, follow-up USS at 1, 3, 5 years.
- TR5 (Highly suspicious): >20% malignancy risk, biopsy if ≥ 1 cm, yearly USS for 5 years.
Thyroid Disease & Pregnancy
- TSH Target Ranges:
- 1st trimester: 0.1-2.5 mIU/L
- 2nd trimester: 0.2-3.0 mIU/L
- 3rd trimester: 0.3-3.0 mIU/L
- Hypothyroidism Risks: Premature birth, low birth weight, miscarriage, impaired fetal neurocognitive development.
- Hyperthyroidism: Low TSH in 1st trimester often due to elevated hCG (gestational, self-limiting, usually no treatment needed). Differentiate from Graves’ disease via positive TRAb. Radionuclide scans contraindicated in pregnancy.
- Pre-existing Hypothyroidism: Optimize levothyroxine to preconception TSH < 2.5 mIU/L. Increase dose 25-30% at 4-6 weeks gestation. Monitor TSH every 4-6 weeks in 1st trimester, then at 30 weeks if stable.
- Postpartum: Reduce thyroxine to pre-pregnancy dose; recheck TSH at ~6 weeks postpartum.
- Postpartum Thyroid Dysfunction: Affects 1 in 20 women; autoimmune follicle destruction.
- Hyperthyroid phase (3-6 months postpartum): self-limiting, manage with beta-blockers; thionamides not indicated.
- Hypothyroid phase (6-12 months postpartum): treat with thyroxine if symptomatic or planning conception.
- 20-40% risk of permanent hypothyroidism within 10 years.
- Iodine Supplementation: 150 µg daily for pregnant, planning, or breastfeeding women.
Pregnancy Prescribing Red Flag: Avoid combination T4/T3 therapy in pregnancy.
Thyroiditis
- Subacute (de Quervain) Thyroiditis: Possibly viral. Pain radiating to ears/jaw, fever, malaise. Transient thyrotoxicosis → hypothyroidism → euthyroidism.
- Diagnosis: Markedly elevated ESR, near-absent uptake on nuclear scan.
- Treatment: Aspirin, ibuprofen, or indometacin for pain. Prednisolone (40 mg daily, tapering over 2-4 weeks) for severe/persistent cases. Antithyroid drugs ineffective. Thyroxine if hypothyroid phase persists/symptomatic.
- Painless Postpartum Thyroiditis: Managed as per postpartum thyroid dysfunction above.
Primary Adrenal Insufficiency (Addison’s Disease)
- Causes: Most commonly autoimmune adrenal cortex atrophy; also infection, metastatic cancer, drugs.
- Clinical Features: Fatigue, anorexia, weight loss, postural hypotension, hyperpigmentation, dizziness/syncope, decreased axillary/pubic hair (females), vitiligo (10-20% of autoimmune cases).
- Electrolytes: Hyponatraemia and hyperkalaemia common.
- Diagnosis:
- 8 AM serum cortisol (low), plasma ACTH (elevated).
- Definitive: short Synacthen stimulation test.
- Supportive: elevated plasma renin, electrolyte abnormalities.
- Adrenal autoantibodies (not initial). CT reserved for anatomy after biochemical confirmation.
- Corticosteroid Replacement: Hydrocortisone (glucocorticoid) and fludrocortisone acetate (mineralocorticoid).
- Non-pharmacological: Increased dietary salt, education on early crisis signs, sick day/stress dose adjustment, medical alert bracelet, osteoporosis prevention (baseline DEXA, weight-bearing exercise).
- Monitoring: Annual review of well-being and glucocorticoid excess/deficiency signs; serum sodium, potassium, plasma renin (upper-normal indicates optimal mineralocorticoid dose); BMD every 2 years. ACTH not useful for dose titration.
Adrenal Crisis — Medical Emergency:
- Precipitants: acute illness, surgery, trauma, abrupt glucocorticoid cessation.
- Features: nausea, vomiting, abdominal pain, severe hypotension/shock, drowsiness, confusion; can mimic sepsis.
- Labs: hypoglycaemia, hyponatraemia, hyperkalaemia, hypercalcaemia, raised urea/creatinine.
- Do not delay treatment for lab results.
- Immediate IV isotonic saline (e.g. 1L 0.9% NaCl over 1 hour).
- Urgent IV hydrocortisone: 100 mg bolus, then 50 mg IV every 6 hours.
- Vasopressor (norepinephrine) if hypotension persists after fluids/steroids.
- Arrange urgent hospital admission.
Cushing’s Syndrome
- Clinical Features:
- Appearance: facial plethora, buffalo hump, central obesity with thin limbs (“lemon with matchsticks”).
- Skin: purple striae >1 cm, thin skin, easy bruising.
- Musculoskeletal: proximal muscle weakness.
- Females: hirsutism, acne, amenorrhea/oligomenorrhoea.
- Associated: hypertension (often resistant), early-onset osteoporosis, diabetes, decreased libido, depression, insomnia.
- When to Test: Unusual findings for age, multiple progressive features, unexplained severe features, adrenal incidentaloma.
- Diagnostic Tests:
- Low suspicion: one of late-night salivary cortisol (x2), 24-hour urinary free cortisol (x2), overnight 1 mg dexamethasone suppression test.
- High suspicion: two of the above.
Phaeochromocytoma
- Clinical Features: Classic triad — paroxysmal hypertension with throbbing headache, palpitations, sweating. Also anxiety, pallor, rising chest/throat tightness, angina.
- Investigations:
- Plasma free metanephrines/normetanephrines (recommended screening).
- Urine total metanephrines (alternative).
- Series of three 24-hour urine free catecholamines (elevated VMA).
- Abdominal CT/MRI for localization after biochemical confirmation.
Primary Aldosteronism (Conn’s Syndrome)
- Causes: Aldosterone-producing adenomas, bilateral adrenal hyperplasia.
- Clinical Features: Hypertension, often with hypokalemia (normokalemia also common). Hypokalemia symptoms: weakness, cramps, paraesthesia, polyuria, polydipsia.
- Screening Indications: Hypertension with hypokalemia; severe (>150/100) or resistant hypertension; hypertension with adrenal incidentaloma, sleep apnea, or early-onset family history (<40 yrs); first-degree relatives of diagnosed patients; hypertension with atrial fibrillation.
- Case-Detection Testing: Morning seated sample; plasma aldosterone concentration (PAC) and plasma renin activity (PRA)/concentration (PRC). Suggestive: PAC ≥ 10 ng/dL AND PRA < 1.0 ng/mL/hour.
- Interfering Drugs: ACE inhibitors, ARBs, direct renin inhibitors affect PRA/PRC. Mineralocorticoid receptor antagonists usually discontinued 4-6 weeks before retesting.
- Confirmation Testing: 24-hour urine aldosterone/sodium/creatinine on high-sodium diet, OR fludrocortisone suppression test, OR saline suppression test.
Hypomagnesaemia
- Normal Range: 0.8-1.0 mmol/L. Depletion < 0.8; severe < 0.4 mmol/L.
- Causes: Malnutrition, GI losses (NG suction, diarrhoea, malabsorption, fistulae), kidney losses, drugs (diuretics, alcohol, aminoglycosides, cisplatin, amphotericin B, cyclosporin, PPIs), phosphate depletion, hungry bone syndrome, Gitelman syndrome.
- Clinical Features: Mild — asymptomatic. Moderate-severe — tetany, muscle weakness, arrhythmias (prolonged QT), neuropsychiatric changes, convulsions. Often coexists with hypocalcaemia, hypokalaemia.
- Treatment: Correct underlying cause.
- Mild: oral magnesium aspartate 1000-3000 mg daily in divided doses.
- Moderate-severe: IV magnesium chloride/sulfate 25-50 mmol in 500-1000 mL 0.9% NaCl over 12-24 hours. Goal serum magnesium > 0.4 mmol/L.
Hypermagnesaemia
- Normal Range: 0.8-1.0 mmol/L; hypermagnesaemia > 1.0 mmol/L.
- Causes: Excessive intake (antacids, enemas, IV infusion) usually with kidney impairment; decreased excretion (kidney failure, volume depletion); rhabdomyolysis; lithium.
- Clinical Features: Loss of deep tendon reflexes, muscle paralysis, impaired consciousness, respiratory depression, anorexia, nausea, flushing, hypotension, bradycardia/heart block, cardiac arrest. Often induces hypocalcaemia.
- Management: Stop magnesium therapy.
- Severe intoxication: IV calcium infusion (transient antagonism).
- Promote excretion with IV 0.9% NaCl (target urine output ≥ 60 mL/hr); add IV frusemide if needed.
- Dialysis if kidney impairment present.
Hypercalcaemia
- Normal Range: Total calcium 2.10-2.60 mmol/L.
- Symptoms (Bones, moans, stones, abdominal groans):
- Bones: bone pain, osteopenia/osteoporosis, muscle weakness.
- Moans: decreased concentration, lethargy, depression, confusion.
- Stones: nephrolithiasis, nephrocalcinosis, polyuria, polydipsia, renal insufficiency.
- Abdominal groans: anorexia, nausea, vomiting, constipation, pancreatitis, peptic ulcer disease.
- Causes: Most common — primary hyperparathyroidism, hypercalcaemia of malignancy. Less common — thiazides, vitamin D toxicity, sarcoidosis/granulomatous disease, severe hyperthyroidism, milk-alkali syndrome, renal osteodystrophy with tertiary hyperparathyroidism, adrenal insufficiency, familial hypocalciuric hypercalcaemia, prolonged immobilisation, and several rare paediatric/genetic causes.
- Diagnosis: Total calcium corrected for albumin; measure ionised calcium if albumin abnormal.
- Investigations: ESR, serum PTH, serum ACE (for sarcoidosis), alkaline phosphatase, chest X-ray, sestamibi scan, bone scan. Requires specialist referral.
Syndrome of Inappropriate ADH (SIADH)
- Causes: Cancers (small cell lung, lymphoma, kidney, pancreas), pulmonary disorders, intracranial lesions, drugs (carbamazepine, many antipsychotics).
- Diagnosis (Triad): Hyponatraemia, hypoosmolality, urine osmolality > 100 mosmol/kg.
- Management: Treat underlying disease (e.g. adrenal insufficiency, hypothyroidism, infection). Fluid restriction (< 800 mL/day) is the mainstay.
Male Androgen Deficiency
- Classification:
- Hypergonadotrophic (primary): testicular disorders — low testosterone, high LH/FSH. Causes: Klinefelter syndrome, cryptorchidism, orchidectomy, orchitis, cytotoxic/radiation damage, testicular torsion/trauma.
- Hypogonadotrophic (central): hypothalamic/pituitary disorders — low testosterone, low/normal LH/FSH. Causes: hyperprolactinaemia, pituitary tumours/surgery/radiotherapy, hemochromatosis, hypophysitis, idiopathic hypogonadotrophic hypogonadism (including Kallmann syndrome).
- Clinical Features: Most indicative — reduced libido, decreased spontaneous erections, hot flushes, reduced facial hair, gynaecomastia, loss of axillary/pubic hair, small testes (< 5 mL), low bone mass. Less specific — low energy/mood, disturbed sleep, reduced muscle bulk, increased BMI, mild anaemia. Normal adult testes: 15-25 mL.
- Diagnosis Criteria: Symptoms/signs + unequivocally low fasting early-morning testosterone (repeat on different day, 8-10 AM) + confirmed HPT axis dysfunction. Avoid testing during acute illness. Functionally low testosterone (obesity, diabetes, depression, opioid/glucocorticoid use) — treat underlying condition, testosterone therapy not recommended.
- Testosterone Replacement Therapy Goals: Relieve symptoms/signs of confirmed deficiency; not for isolated low libido/erectile dysfunction.
- Formulations:
- Transdermal: creams/gels/patches applied to trunk/proximal limbs each morning.
- Injectable: testosterone enantate/esters 250 mg IM every 2-3 weeks; testosterone undecanoate (Reandron) 1000 mg IM after 6 weeks, then every 10-14 weeks.
- Oral: rarely used, less effective.
- Monitoring: Symptom review at 3 months then annually; serum testosterone at 3-6 months; BMD at 12+ months. FBE at baseline, 3 months, then annually (polycythaemia risk, especially short-acting injectables). Assess baseline prostate/cardiovascular risk; discuss PSA screening limitations.
- Common Adverse Effects: Acne, modest weight gain, reduced spermatogenesis, increased truncal hair, temporal hair loss, gynaecomastia — generally reversible on cessation.
TRT Contraindications:
- Current prostate or breast cancer
- Desire for fertility (suppresses spermatogenesis)
- Elite athletes (prohibited substance)
- Specialist assessment required if history of curative treatment for prostate/breast cancer
Carcinoid Syndrome
- Clinical Features: Classic triad — skin flushing (especially face), diarrhoea with abdominal cramps, valvular heart disease (especially right heart). Also wheezing, telangiectasia, hypotension, cyanosis, pellagra.
- Common Tumour Sites: Appendix/ileum, stomach, bronchi.
- Diagnosis: 24-hour urinary 5-HIAA (end product of serotonin metabolism) is the most useful initial test.
- Putative Mediators:
- Flushing: kinins, histamine, kallikreins.
- Diarrhoea/cramping: serotonin.
- Valvular lesions: serotonin.