Thyroid, Adrenal and Stress Physiology
Core concepts of thyroid hormone action, cortisol, catecholamines and the stress response for first-year medical physiology.
Keyboard Shortcuts
💡 Pro tip: Use keyboard shortcuts for faster studying!
Study Smart Tips for Thyroid, Adrenal and Stress Physiology
Master these concepts using proven study techniques that actually work:
Active Recall
Test yourself before flipping each card to strengthen memory retention
Spaced Repetition
Review difficult cards more frequently than easy ones
Multiple Sessions
Break study time into shorter, focused sessions
Explain Aloud
Verbalize answers to reinforce understanding
Questions Covered in This Set
10 cards to master
What does the Na⁺/I⁻ symporter (NIS) do?
Actively pumps iodide into thyroid follicular cells against its gradient across the basolateral membrane; iodide then exits apically via pendrin.
Role of thyroid peroxidase (TPO)
Oxidises iodide and attaches it to tyrosine residues of thyroglobulin (organification), then couples iodotyrosines to form T3 and T4.
Why is T4 called a prohormone?
The gland secretes ~20:1 T4:T3, but T4 has low receptor affinity; peripheral 5′-deiodinases (D1, D2) remove an outer-ring iodine to make active T3.
What produces reverse T3 (rT3) and when does it rise?
Inner-ring deiodinase D3 makes inactive rT3; in illness, starvation or after surgery D1 falls and D3 rises — euthyroid sick syndrome (low T3, high rT3, near-normal TSH, do not treat with levothyroxine).
Why does thyrotoxicosis look adrenergic despite normal catecholamines?
T3 upregulates cardiac β₁-adrenergic receptor expression → tachycardia, increased contractility, wide pulse pressure; β-blockers relieve symptoms.
How does thyroid hormone raise BMR?
T3 acts on nuclear TR to increase transcription of Na⁺/K⁺-ATPase and promote mitochondrial uncoupling → more heat and O₂ consumption (slow onset over days).
Lab pattern: primary hypothyroidism vs primary hyperthyroidism
Primary hypothyroidism = ↑TSH with ↓free T4 (Hashimoto's, iodine deficiency); primary hyperthyroidism = ↓TSH with ↑free T4 (Graves'). TSH moving the same way as T4 suggests a central/pituitary cause.
Adrenal cortex zones and their products (GFR — Salt, Sugar, Sex)
Zona glomerulosa → aldosterone (angiotensin II and K⁺ driven); zona fasciculata → cortisol (ACTH); zona reticularis → adrenal androgens DHEA/DHEAS (ACTH). Rate-limiting step: StAR-mediated cholesterol transport and desmolase cleavage.
Metabolic actions of cortisol
Increases hepatic gluconeogenesis (PEPCK, glucose-6-phosphatase), causes muscle/fat insulin resistance and hyperglycaemia, muscle proteolysis and limb lipolysis with truncal fat deposition.
Immune and permissive effects of cortisol
Anti-inflammatory: inhibits phospholipase A₂ via annexin-1, blocks NF-κB and cytokine transcription; causes neutrophilia with lymphopenia and eosinopenia. Permissive for catecholamines by upregulating α₁ receptors and PNMT.
