hyperthyroidism

hyperthyroidism

Pathological state of excess thyroid hormone. Distinguish hyperthyroidism (increased endogenous synthesis) from thyrotoxicosis (any cause of excess hormone, including leak/exogenous).

pathophysiology & aetiology

Differentiation relies on Radioactive Iodine Uptake (RAIU).

high RAIU (>25%)

Increased de novo synthesis.

• graves’ disease (Autoimmune stimulation of TSH-R).
• toxic multinodular goitre (TMNG).
• Toxic Adenoma (Hot nodule).
• hCG-mediated (Gestational, Choriocarcinoma, Molar pregnancy).
• TSH-secreting pituitary adenoma (Rare).

low RAIU (<1%)

Release of pre-formed hormone or exogenous source.

• Thyroiditis (Subacute, Silent, Postpartum): Inflammatory leak.
• Iatrogenic/Factitious: Exogenous Levothyroxine ingestion.
• Iodine-induced (Jod-Basedow Effect): Amiodarone Type 1 (can be variable), Contrast dye.
• Struma Ovarii: Ectopic production (uptake is in pelvis, not neck).

clinical features

• General: Weight loss despite increased appetite, heat intolerance, diaphoresis.
• CV: Tachycardia (resting HR >90), atrial fibrillation (especially elderly), widened pulse pressure.
• Neuro: Fine tremor, anxiety, hyperreflexia, proximal myopathy.
• Ocular: Lid lag/retraction (sympathetic overactivity—seen in any thyrotoxicosis).
  • Graves’ Specific: Proptosis, chemosis, diplopia (extraocular muscle oedema).
• Derm: Pretibial myxoedema (Graves’), onycholysis (Plummer’s nails).

ophthalmopathy

True ophthalmopathy (orbitopathy) is specific to Graves’ disease. If proptosis is present, the diagnosis is Graves’ regardless of the RAIU result.

diagnosis

biochemical screening

1. TSH: Best initial screen. Suppressed (<0.01 mIU/L) in primary hyperthyroidism.
2. fT4 & fT3: Elevated.
   • T3 Toxicosis: Suppressed TSH with normal fT4 but high fT3 (common in early Graves’ or hot nodules).

biotin interference

Biotin (Vit B7) >30 µg/day interferes with streptavidin-biotin immunoassays.

• Effect: Falsely $\downarrow$ TSH, Falsely $\uparrow$ fT4/fT3.
• Result: Mimics Graves’ disease biochemically in a euthyroid patient.
• Action: Stop Biotin 72h prior to bloodwork.

determining aetiology

• TSH Receptor Antibodies (TRAb/TSI):
  • Specificity >99% for Graves’ disease.
  • Highly cost-effective; avoids radiation.
• Radioactive Iodine Uptake (RAIU) & Scan:
  • Distinguishes “High” vs “Low” uptake aetiologies (see above).
  • Scan patterns:
    • Diffuse homogeneous: Graves’ disease.
    • Patchy/Multiple hot spots: toxic multinodular goitre.
    • Single hot spot (rest suppressed): Toxic Adenoma.
• Thyroid Doppler Ultrasound:
  • Use when RAIU contraindicated (pregnancy, breastfeeding).
  • Graves’: Increased vascularity (“Thyroid Inferno”).
  • Thyroiditis: Decreased vascularity.

management: general principles

Management depends on the aetiology.

• Graves’ disease: Antithyroid drugs (Methimazole), Radioactive Iodine (RAI), or Surgery. See Graves’ disease for detailed protocols.
• toxic multinodular goitre: Radioactive Iodine or Surgery are definitive. ATDs are for stabilization.
• Thyroiditis: Supportive (Beta-blockers). ATDs are ineffective.

management: toxic nodular disease (TMNG/TA)

• Pathophysiology: Autonomous function. Will not remit spontaneously.
• First Line: RAI or Surgery.
• ATDs: Used only for stabilization prior to definitive therapy or in elderly/comorbid patients with limited life expectancy.

management: thyroiditis

• Phases: Thyrotoxic $\to$ Euthyroid $\to$ Hypothyroid $\to$ Recovery.
• Treatment: Supportive.
  • Beta-blockers: Propranolol/Atenolol for palpitations/tremor.
  • Pain (Subacute): NSAIDs (first line) or Prednisone (severe).
  • Do NOT use ATDs: (No increased synthesis to block).

special situations

thyroid storm

Life-threatening decompensation (Burch-Wartofsky Score >45).

1. Beta-Blocker: Propranolol 60–80mg PO q4-6h (blocks adrenergic drive + T4→T3).
2. Thionamide: PTU preferred (blocks T4→T3). Load 500-1000mg.
3. Inorganic Iodine: Lugol’s or SSKI. Give >1 hour AFTER PTU (prevent Jod-Basedow fueling).
4. Steroids: Hydrocortisone 100mg IV q8h (blocks T4$o$T3, adrenal support).
5. Supportive: Cooling, fluids, treat precipitant.

hyperthyroidism in pregnancy

• hCG-mediated: Transient TSH suppression in T1. No Tx needed.
• Graves’: High risk of fetal complications.
  • T1: Propylthiouracil (risk of aplasia cutis/choanal atresia with MMZ).
  • T2/T3: Switch to Methimazole (liver safety) or continue PTU.
  • Target: Keep maternal fT4 in high-normal range (prevent fetal hypothyroidism).
  • Antibodies: Check TRAb at 18-22 weeks (crosses placenta $\to$ neonatal Graves’).

amiodarone-induced thyrotoxicosis (AIT)

• Type 1 (Jod-Basedow): Iodine load on underlying autonomous nodule/Graves. High vascularity. Tx: High dose MMI.
• Type 2 (Destructive): Direct toxic effect. Low vascularity. Tx: Prednisone.
• Mixed: Often requires both MMI + Prednisone.