Hyperthyroidism Study Guide

📖 Core Concepts Hyperthyroidism: Over‑production of thyroid hormones (T₃, T₄) by the thyroid gland. Thyrotoxicosis: Any cause of elevated circulating thyroid hormone; hyperthyroidism is the most common cause. Graves’ disease: Autoimmune stimulation of the thyroid (TSH‑receptor antibodies) → accounts for 50‑80 % of U.S. cases. Subclinical hyperthyroidism: Suppressed TSH with normal free T₄/T₃; often asymptomatic but carries cardiovascular & bone risks. Thyroid storm: Acute, life‑threatening decompensation (fever, arrhythmia, altered mental status). 📌 Must Remember Lab hallmark: Low/undetectable TSH + high free T₄ and/or free T₃. Radioactive iodine uptake (RAIU): ↑ uptake in Graves, toxic nodules; ↓ uptake in thyroiditis. First‑line drugs: Methimazole (or carbimazole) – blocks iodine organification. Propylthiouracil – blocks organification and peripheral T₄→T₃ conversion (preferred in 1st‑trimester pregnancy). Beta‑blocker: Propranolol (non‑selective) controls tachycardia, tremor; its D‑isomer also ↓ T₄→T₃ conversion. Definitive therapy: Radioactive iodine (I‑131) → eventual hypothyroidism; thyroidectomy → risk of recurrent laryngeal nerve injury. Pregnancy: PTU first trimester; avoid excess iodine (seaweed, kelp). Complication risk: Atrial fibrillation, bone fractures, thyroid storm, ophthalmopathy (exophthalmos). 🔄 Key Processes Diagnostic Work‑up Draw TSH → if low → measure free T₄/T₃. If hormones high → order thyroid‑stimulating‑receptor antibody test (Graves) + RAIU scan. Antithyroid Drug Action (Methimazole/Carbimazole) Inhibit thyroid peroxidase → ↓ iodination of tyrosine residues on thyroglobulin → ↓ new hormone synthesis. PTU Dual Action Same peroxidase inhibition plus inhibition of 5′‑deiodinase → ↓ peripheral conversion of T₄ → T₃. Radioactive Iodine Ablation Patient ingests I‑131 → thyroid cells uptake → β‑radiation destroys over‑active follicles over weeks‑months → hypothyroidism → replace with levothyroxine. Thyroid Storm Management (stepwise) IV propranolol → control adrenergic symptoms. IV methimazole or PTU → block new synthesis. Iodine solution (e.g., Lugol’s) → block hormone release (given after antithyroid drug). IV hydrocortisone → reduce inflammation, support adrenal axis. 🔍 Key Comparisons Graves’ disease vs. Toxic Nodular Goiter Antibody profile: TSH‑R antibodies present in Graves only. RAIU pattern: Diffusely increased uptake (Graves) vs. focal “hot” nodule(s) (toxic nodules). Methimazole vs. Propylthiouracil Primary action: Both block iodination; PTU also blocks T₄→T₃ conversion. Safety in pregnancy: PTU → 1st trimester; Methimazole → 2nd/3rd trimester (less teratogenic). Beta‑blocker (Propranolol) vs. Other Symptom‑control Propranolol: Controls tachycardia, tremor, anxiety and modestly reduces T₃ via D‑isomer. Other agents (e.g., calcium channel blockers) → only heart‑rate control, no effect on hormone levels. ⚠️ Common Misunderstandings “All hyperthyroid patients need radioactive iodine.” – Not true; contraindicated in pregnancy, large goiters, or severe ophthalmopathy. “Low TSH always means Graves.” – Low TSH occurs in thyroiditis, drug‑induced, or exogenous hormone excess; antibodies and RAIU differentiate. “Weight loss is universal.” – 10 % of patients actually gain weight despite hyperthyroidism. 🧠 Mental Models / Intuition “Hormone traffic light”: Green = Normal TSH, T₄/T₃ → euthyroid. Red = Low TSH + high T₄/T₃ → hyperthyroid (pull the “stop” lever → treat). Yellow = Low TSH + normal T₄/T₃ → subclinical → monitor for complications. “Fire‑fighter analogy for storm”: Water (beta‑blocker) → calm the flames (adrenergic surge). Fire‑extinguisher (antithyroid drug) → stop new fuel (hormone synthesis). Blanket (iodine solution) → smother remaining sparks (release of stored hormone). 🚩 Exceptions & Edge Cases Iodine‑induced hyperthyroidism (e.g., seaweed binge) – may present with high RAIU but without antibodies. Amiodarone‑induced thyrotoxicosis – can be either type 1 (iodine‑excess) or type 2 (destructive thyroiditis); management differs. Pregnancy – normal physiologic rise in thyroid hormone; TSH reference ranges shift lower, making interpretation tricky. 📍 When to Use Which First‑line symptomatic control → non‑selective β‑blocker (propranolol). First‑line disease‑modifying therapy (non‑pregnant, mild‑moderate disease) → methimazole. Pregnant (1st trimester) or amiodarone‑type 2 → PTU (protects fetus, blocks peripheral conversion). Definitive therapy: Radioactive iodine → preferred for most adults without contraindications (pregnancy, large goiter, severe eye disease). Surgery → goiter causing compressive symptoms, suspicion of cancer, or intolerance to meds/RAI. Thyroid storm → aggressive combination (IV β‑blocker + IV antithyroid drug + iodine + steroids). 👀 Patterns to Recognize Cardiovascular cluster: Palpitations, tachycardia, atrial fibrillation → suspect hyperthyroidism when TSH low. Ophthalmopathy + diffuse RAIU → classic Graves. Transient hyperthyroidism after viral illness + low RAIU → subacute (de Quervain) thyroiditis. Weight loss with intact appetite + heat intolerance → metabolic hyperthyroid picture. 🗂️ Exam Traps “Low TSH + normal T₄/T₃ = euthyroid.” – Actually indicates subclinical hyperthyroidism; may still have clinical consequences. Choosing PTU for all patients – PTU has higher hepatotoxicity; methimazole is preferred except in early pregnancy or specific situations. Assuming iodine deficiency always causes hypothyroidism – Excess iodine can precipitate hyperthyroidism, especially in autonomous nodules. “Beta‑blocker alone cures hyperthyroidism.” – It only controls symptoms; does not address excess hormone production. “All Graves patients get eye disease.” – Only 30 % develop ophthalmopathy; risk rises after radioactive iodine unless steroids are given.