After reading this note you will be able to describe the clinical approach to patients with thyroid excess or deficiency, list local aetiologies, interpret key investigations, grade severity and outline safe acute and definitive management – remembering to verify doses and local protocols against the Kenya MoH guideline and your hospital formulary.
Definition
- Hyperthyroidism – clinical syndrome caused by excess circulating thyroid hormones (T4, T3) leading to a hypermetabolic state.
- Hypothyroidism – clinical syndrome caused by insufficient thyroid hormone production, resulting in a hypometabolic state.
Anatomy and physiology you need
| Structure | Relevance |
|---|---|
| Thyroid gland (follicular cells) | Synthesise T4 & T3 from iodide; regulated by TSH |
| Hypothalamus‑pituitary axis | TRH → TSH release; feedback by T4/T3 |
| Peripheral deiodinases (type 1 & 2) | Convert T4 → active T3 in tissues |
| Thyroid hormone receptors (nuclear) | Mediate genomic effects on metabolism, heart, CNS |
| Iodine transport (NIS) | Essential for hormone synthesis; deficiency common in some Kenyan regions |
Causes and risk factors
| Condition | Hyper‑ / Hypothyroidism | Kenyan relevance |
|---|---|---|
| Graves’ disease | Hyper | Most common autoimmune cause |
| Toxic multinodular goitre | Hyper | Iodine‑deficient areas |
| Post‑radioiodine or surgery | Hypo | Iatrogenic |
| Hashimoto’s thyroiditis | Hypo | Autoimmune, prevalent in women |
| Subacute (de Quervain) thyroiditis | Hyper → Hypo | Viral, can follow malaria |
| HIV infection | Hyper (immune reconstitution) / Hypo (autoimmune) | High prevalence |
| Tuberculosis of thyroid | Hypo | Rare but reported |
| Antitubercular therapy (rifampicin) | Hyper | Enzyme induction ↑ hormone clearance |
| Malaria (severe) | Hyper | Cytokine surge may increase hormone release |
| Sickle cell disease (chronic hemolysis) | Hyper | Increased peripheral conversion |
| Rheumatic fever (post‑infective) | Hyper | Rare, autoimmune cross‑reactivity |
| Iodine excess (iodinated contrast, supplements) | Hyper | Common in urban centres |
| Iodine deficiency (soil, diet) | Hypo | Rural high‑altitude areas |
| Medications – amiodarone, lithium, interferon | Hyper / Hypo | Drug‑induced thyroid dysfunction |
Pathophysiology
Hyperthyroidism
Autoimmune stimulation (Graves) → ↑ TSH‑receptor antibodies → ↑ thyroid hormone synthesis & release → ↑ basal metabolic rate, ↑ β‑adrenergic receptor density → tachycardia, heat intolerance, weight loss.
Hypothyroidism
Destruction of follicular cells (autoimmune, infection, surgery) → ↓ T4/T3 output → loss of negative feedback → ↑ TSH (initially) → slowed metabolism, ↓ cardiac output, accumulation of mucopolysaccharides → non‑pitting edema, cold intolerance.
Arrows format:
Graves’ antibodies → ↑ TSH‑R activation → ↑ T4/T3 → ↑ metabolic demand → clinical hyperthyroidism
Thyroiditis → follicular damage → ↓ hormone release → ↓ metabolic rate → clinical hypothyroidism
Clinical features
| Domain | Key questions / findings | Why it occurs |
|---|---|---|
| General | Weight loss despite normal/increased appetite; heat intolerance; sweating; tremor; fatigue or paradoxical “restlessness”; insomnia; menstrual irregularities; libido change; change in bowel habit (more frequent). | Excess thyroid hormone accelerates basal metabolic rate, increases catecholamine sensitivity and alters gut motility. |
| Cardiovascular | Palpitations; dyspnoea on exertion; chest discomfort; history of atrial fibrillation; orthopnoea. | Thyroid hormone ↑ β‑adrenergic receptors → tachycardia, increased stroke volume, atrial ectopy; high output state may precipitate heart failure. |
| Ophthalmic | Grittiness, diplopia, lid lag, proptosis, periorbital oedema, dry eyes. | Auto‑immune orbital fibroblast activation (Graves’ ophthalmopathy) leads to extra‑ocular muscle swelling and glycosaminoglycan deposition. |
| Dermatologic | Warm, moist skin; fine hair; pretibial myxedema (non‑pitting induration). | Vasodilation and increased sweat gland activity; fibroblast stimulation in Graves’ disease. |
| Neurological / Psychiatric | Anxiety, irritability, tremor, hyperreflexia, fine motor clumsiness, difficulty concentrating, occasional psychosis. | ↑ sympathetic tone and direct central effects of T3/T4 on neuronal excitability. |
| Reproductive | Menstrual oligomenorrhoea or amenorrhoea; infertility; decreased libido. | Hormonal imbalance interferes with gonadotropin secretion and peripheral conversion. |
| Gastro‑intestinal | Increased frequency of bowel movements, occasional diarrhoea, nausea. | Accelerated GI motility from heightened metabolic activity. |
| Musculoskeletal | Proximal muscle weakness, especially in thighs; easy fatigability. | Catabolic effect of thyroid hormone on skeletal muscle proteins. |
| History of exposure | Recent iodine load (contrast, iodinated drugs, seaweed), family history of thyroid disease, prior radiation to neck, presence of autoimmune disease, HIV status, TB history, use of amiodarone, pregnancy. | Iodine excess can precipitate hyperthyroidism (Jod‑Basedow); autoimmune predisposition; infections (TB) can cause destructive thyroiditis; amiodarone releases iodine. |
Examination findings and rationale
- Tachycardia (≥100 bpm) – direct β‑adrenergic stimulation.
- Afib on pulse – atrial electrical instability from high catecholamine tone.
- Warm, moist skin with flushed appearance – peripheral vasodilation.
- Fine tremor of outstretched hands – enhanced neuromuscular excitability.
- Thyroid bruit – increased vascularity in Graves’ disease.
- Diffuse goitre, smooth, soft, non‑tender – hyperplastic follicular activity.
- Lid lag & stare – sympathetic over‑activity; exophthalmos if Graves’.
- Pretibial non‑pitting oedema – mucopolysaccharide deposition in Graves’.
- Hyperreflexia with clonus – central sensitisation.
- Weight loss despite normal/increased intake – catabolic state.
Differential diagnosis
| Condition | Points toward it | Distinguishing features |
|---|---|---|
| Graves’ disease | Diffuse goitre, ophthalmopathy, bruit, young female, family autoimmunity | Positive TSH‑receptor antibodies; scintigraphy shows uniform uptake |
| Toxic multinodular goitre | Older patient, palpable nodules, no ophthalmopathy, endemic iodine deficiency | Scan shows patchy uptake; TSH‑R antibodies negative |
| Toxic adenoma | Single palpable nodule, suppressed TSH, unilateral uptake on scan | Same as above but single hot nodule |
| Subacute (de Quervain) thyroiditis | Recent viral prodrome, painful tender thyroid, transient hyperthyroidism | Low radioactive uptake; ESR ↑; resolves spontaneously |
| Painless (autoimmune) thyroiditis | Post‑partum or early pregnancy, painless goitre, transient hyperthyroidism | Low uptake; anti‑TPO antibodies positive |
| Drug‑induced (amiodarone, lithium) | Recent start of offending drug, iodine excess | Low uptake; drug history key |
| Factitious thyrotoxicosis | Access to thyroid hormone, weight‑loss intent | Suppressed TSH with normal/low uptake; high serum T4 with low T3 |
| Thyrotoxic crisis (storm) | Acute decompensation, fever, delirium, heart failure | Severe tachyarrhythmia, high fever, precipitating event |
Investigations
| Test | What it answers | Interpretation |
|---|---|---|
| TSH | Primary vs secondary cause | Suppressed → primary hyperthyroidism; normal/high → secondary |
| Free T4 & Free T3 | Hormone excess severity | Elevated free T4/T3 confirms thyrotoxicosis |
| TSH‑receptor antibodies (TRAb) | Autoimmune Graves’ disease | Positive → Graves’; negative → other causes |
| Anti‑TPO / anti‑TG antibodies | Autoimmune thyroiditis | Positive in painless thyroiditis, Hashimoto’s |
| Radioactive iodine uptake (RAIU) scan | Etiology (diffuse vs nodular) | Uniform high uptake → Graves’; patchy → toxic multinodular; low uptake → thyroiditis |
| Thyroid ultrasound | Nodule characterization, vascularity | Diffuse increased flow in Graves’; solitary hot nodule in toxic adenoma |
| ESR / CRP | Inflammatory thyroiditis | Elevated in subacute thyroiditis |
| CBC, electrolytes, LFTs, renal panel | Baseline for therapy safety | Detect anemia, hepatic/renal impairment before antithyroid drugs |
| ECG | Cardiac involvement | A‑fib, tachyarrhythmias, QT changes |
| Chest X‑ray (if dyspnoea) | Heart size, pulmonary congestion | Helps assess heart failure in storm |
| Serum cortisol (if storm) | Adrenal reserve | Low cortisol worsens crisis; may need replacement |
Diagnosis and severity
- Confirm thyrotoxicosis – suppressed TSH with elevated free T4 and/or free T3.
- Identify cause – use TRAb, RAIU, antibodies, clinical clues (pain, nodules, drug exposure).
- Grade severity (based on clinical and biochemical parameters)
| Severity | Clinical hallmarks | Biochemistry |
|---|---|---|
| Mild | Weight loss <5 kg, HR 90‑110, no atrial fibrillation, no heart failure, mild tremor | Free T4 modestly ↑, T3 normal or mildly ↑ |
| Moderate | Weight loss ≥5 kg, HR >110, tremor, anxiety, mild dyspnoea, possible paroxysmal AF, goitre >2 cm | Free T4 ↑↑, T3 ↑ |
| Severe / Thyrotoxic storm | Fever >38 °C, HR >130, marked agitation or delirium, heart failure, high‑output cardiac failure, gastrointestinal upset, precipitating event | Very high free T4/T3, suppressed TSH, possible electrolyte derangements |
Severity guides urgency of immediate management (beta‑blockade, antithyroid drugs, iodine, steroids) and need for intensive monitoring (telemetry, electrolytes, cardiac output). The definitive plan (radio‑iodine ablation, thyroidectomy, long‑term antithyroid medication) follows once the patient is euthyroid or near‑euthyroid and the underlying aetiology is clarified.
Management
Immediate stabilisation
| Situation | Priority action | Rationale |
|---|---|---|
| Thyrotoxic storm (hyperthyroidism) | Give high‑flow oxygen, IV fluids, β‑blocker (non‑selective) and antithyroid drug (ATD) promptly | Reduces peripheral conversion of T4→T3, controls tachycardia and prevents cardiovascular collapse |
| Myxedema coma (severe hypothyroidism) | Secure airway, warm environment, IV glucocorticoids, and levothyroxine loading (IV) | Prevents adrenal crisis, restores thyroid hormone quickly, supports hemodynamics |
| Severe atrial fibrillation with rapid ventricular response | Rate control with β‑blocker or calcium‑channel blocker; consider electrical cardioversion if unstable | Prevents heart failure and thrombo‑embolism |
| Pregnancy with overt hyperthyroidism | Start PTU (first trimester) or methimazole (after first trimester) plus β‑blocker if needed | Minimises fetal exposure while controlling maternal disease |
Definitive (long‑term) treatment
Hyperthyroidism
- Antithyroid drugs (ATDs) – methimazole or propylthiouracil; chosen based on trimester, liver status, and risk of agranulocytosis.
- Radioiodine (I‑131) – single outpatient dose; preferred in non‑pregnant adults without severe ophthalmopathy.
- Surgery (total/near‑total thyroidectomy) – indicated for large goitre causing compressive symptoms, suspicion of malignancy, or when ATDs/RAI are contraindicated.
Hypothyroidism
- Levothyroxine – once‑daily oral replacement; titrate to achieve TSH in target range.
- Combination therapy (T4 + T3) – reserved for patients who remain symptomatic despite normal TSH on levothyroxine alone.
Monitoring & follow‑up
- Hyperthyroidism: check FT4/FT3 and TSH 4‑6 weeks after initiating ATD or after RAI; monitor CBC and liver enzymes for ATD toxicity.
- Hypothyroidism: re‑measure TSH 6‑8 weeks after dose change; adjust dose based on weight, age, cardiac status.
- Pregnancy: thyroid function every 4‑6 weeks; adjust therapy to keep TSH in trimester‑specific range.
- Post‑surgery: calcium and PTH on day 1–2; start levothyroxine when ready for oral intake.
Contra‑indications & safety
- ATDs: avoid in severe hepatic disease (propylthiouracil) and in patients with known agranulocytosis.
- Radioiodine: contraindicated in pregnancy, breastfeeding, and active ophthalmopathy.
- β‑blockers: caution in asthma, severe COPD, and decompensated heart failure.
- Levothyroxine: avoid overtreatment in elderly, cardiac disease, or after recent myocardial infarction.
Complications and prognosis
| Condition | Major complications | Typical prognosis (with treatment) |
|---|---|---|
| Hyperthyroidism (overt) | Thyrotoxic storm, atrial fibrillation, high‑output heart failure, osteoporosis, pretibial myxedema, Graves’ ophthalmopathy | Excellent if diagnosed early; storm mortality < 5 % with prompt care |
| Subclinical hyperthyroidism | Progression to overt disease, atrial fibrillation, reduced bone density in post‑menopausal women | Often stable; treat if TSH < 0.1 mIU/L or symptomatic |
| Hypothyroidism (overt) | Myxedema coma, dyslipidaemia, pericardial effusion, pregnancy loss, neurocognitive decline | Full reversal of symptoms with adequate levothyroxine; mortality low unless coma |
| Subclinical hypothyroidism | Progression to overt disease, dyslipidaemia, pregnancy complications | Treat if TSH > 10 mIU/L or symptomatic; many remain stable |
High‑yield exam points
- Look‑alike conditions:
- Thyrotoxic storm vs. septic shock – both have fever, tachycardia; skin warm, tremor, and history of thyroid disease point to storm.
- Myxedema coma vs. severe sepsis – hypothermia, bradycardia, dry skin, and delayed reflexes favour myxedema.
- Commonest wrong first step:
- Giving iodine (e.g., Lugol’s solution) before an ATD in thyrotoxic storm – iodine can initially increase hormone release; ATD must precede.
- Typical bedside examiner questions:
- “What sign differentiates Graves’ ophthalmopathy from simple lid lag?” – Proptosis and restricted eye movements.
- “Why do you avoid β‑blockers in a patient with asthma presenting with thyrotoxicosis?” – Risk of bronchospasm; consider a selective β‑1 blocker or calcium‑channel blocker.
- “Explain the rationale for giving glucocorticoids in myxedema coma.” – Reduces peripheral conversion of T4→T3 and treats possible adrenal insufficiency.
Clinical case
Case: A 28‑year‑old Kenyan woman, 10 weeks pregnant, presents with a 3‑week history of heat intolerance, palpitations, weight loss of 4 kg, and a diffuse goitre. Examination shows tremor, fine hair, and a resting heart rate of 115 bpm. No ophthalmopathy.
Questions
- What is the most appropriate first‑line antithyroid drug?
Answer: Propylthiouracil – preferred in the first trimester to avoid methimazole‑related teratogenicity.
- Which additional medication should be added immediately and why?
Answer: A non‑selective β‑blocker (e.g., propranolol) – to control tachycardia and reduce peripheral conversion of T4 to T3.
- What is the target TSH range for this patient during pregnancy?
Answer: Keep TSH in the trimester‑specific reference (approximately 0.1–2.5 mIU/L in the first trimester).
Practice questions
Question 1
A 65‑year‑old man with known Graves’ disease presents with fever 39 °C, heart rate 130 bpm, altered mental status, and a palpable thyroid. What is the next best step?
A. Give high‑dose oral methimazole
B. Administer IV propranolol, glucocorticoid and start ATD
C. Immediate total thyroidectomy
D. Start broad‑spectrum antibiotics only
Answer: B. administer IV propranolol, glucocorticoid and start ATD
Explanation: This picture is classic thyrotoxic storm; rapid β‑blockade, steroids and ATD are essential before any other intervention.
Question 2
A 45‑year‑old woman on levothyroxine for primary hypothyroidism complains of persistent fatigue despite a normal TSH. Which is the most likely explanation?
A. Non‑adherence to medication
B. Coexisting iron‑deficiency anaemia
C. Inadequate absorption due to concurrent calcium supplement
D. All of the above
Answer: D. all of the above
Explanation: Fatigue with normal TSH can result from poor compliance, malabsorption (e.g., calcium, iron) or unrelated anaemia; each should be explored.
Question 3
A 30‑year‑old male with a toxic multinodular goitre is euthyroid after radioiodine therapy but develops new onset atrial fibrillation. What is the most appropriate management?
A. Restart antithyroid drug
B. Initiate rate‑control with a β‑blocker
C. Give high‑dose iodine
D. Immediate cardioversion without anticoagulation
Answer: B. initiate rate‑control with a β‑blocker
Explanation: Post‑RAI atrial fibrillation is usually rate‑controlled; anticoagulation decisions follow CHA₂DS₂‑VASc scoring.
Question 4
A 70‑year‑old man with known hypothyroidism presents with hypothermia, bradycardia, and a swollen tongue. Which investigation should be obtained first?
A. Serum cortisol
B. Serum TSH and free T4
C. Chest X‑ray
D. Blood cultures
Answer: B. serum TSH and free T4
Explanation: The presentation suggests myxedema coma; confirming severe hypothyroidism guides immediate levothyroxine therapy.
Question 5
Which of the following is a contraindication to the use of radioactive iodine in a patient with hyperthyroidism?
A. Age > 60 years
B. Presence of a large goitre causing dysphagia
C. Pregnancy
D. Mild ophthalmopathy
Answer: C. pregnancy
Explanation: Radioiodine crosses the placenta and can ablate the fetal thyroid; it is absolutely contraindicated in pregnancy.
Drafted with AI assistance from standard references and reviewed for structure. Check details against your lecture notes and the Kenya MoH guideline.