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IMF-024-02-0001-en	Why does a large acute iodine load have different effects in normal, autonomous and autoimmune thyroid tissue?	In normal physiology it temporarily suppresses organification and release, but autonomous tissue uses the substrate to produce excess hormone, and susceptible autoimmune glands may become hypothyroid.	Integrated Medical Foundations; chapter 24, TTS module 2; https://theisegoria.github.io/medical-textbook/integrated-medical-foundations-expanded-english.md; module SHA256 at export: f8b90b7ae886e295c8eaa5a468be71e76d32cec610a9036b39930a4c69f11f75; editorial review pending	imf lang::en chapter::024 module::024-02 review::pending
IMF-024-02-0002-en	Why should thyroid-stimulating hormone not be rechecked too soon after a levothyroxine dose change?	Hormone and feedback turnover are slow, so it takes weeks to reach a new steady state; testing early provokes repeated dose changes and oscillation.	Integrated Medical Foundations; chapter 24, TTS module 2; https://theisegoria.github.io/medical-textbook/integrated-medical-foundations-expanded-english.md; module SHA256 at export: f8b90b7ae886e295c8eaa5a468be71e76d32cec610a9036b39930a4c69f11f75; editorial review pending	imf lang::en chapter::024 module::024-02 review::pending
IMF-024-02-0003-en	Why do thionamides help Graves-type synthesis-driven disease but not destructive thyroiditis?	Thionamides block synthesis, which drives hyperthyroidism, whereas destructive thyroiditis causes thyrotoxicosis by releasing stored hormone that thionamides cannot stop.	Integrated Medical Foundations; chapter 24, TTS module 2; https://theisegoria.github.io/medical-textbook/integrated-medical-foundations-expanded-english.md; module SHA256 at export: f8b90b7ae886e295c8eaa5a468be71e76d32cec610a9036b39930a4c69f11f75; editorial review pending	imf lang::en chapter::024 module::024-02 review::pending
IMF-024-02-0004-en	Why is thyroid storm defined clinically rather than by hormone level, and in what order is it treated?	It is severe decompensation, not a hormone threshold; treatment blocks adrenergic effects, then new synthesis, then hormone release after synthesis blockade, then peripheral conversion and the trigger.	Integrated Medical Foundations; chapter 24, TTS module 2; https://theisegoria.github.io/medical-textbook/integrated-medical-foundations-expanded-english.md; module SHA256 at export: f8b90b7ae886e295c8eaa5a468be71e76d32cec610a9036b39930a4c69f11f75; editorial review pending	imf lang::en chapter::024 module::024-02 review::pending
IMF-024-02-0005-en	How do inherited adrenal enzyme defects cause adrenal hyperplasia and varied clinical signs?	Cortisol deficiency raises adrenocorticotropic hormone, causing hyperplasia, while precursors are redirected so mineralocorticoid and androgen output rise or fall by block, giving salt loss, hypertension, virilisation or undervirilisation.	Integrated Medical Foundations; chapter 24, TTS module 2; https://theisegoria.github.io/medical-textbook/integrated-medical-foundations-expanded-english.md; module SHA256 at export: f8b90b7ae886e295c8eaa5a468be71e76d32cec610a9036b39930a4c69f11f75; editorial review pending	imf lang::en chapter::024 module::024-02 review::pending
IMF-024-02-0006-en	Why does central adrenal failure usually preserve aldosterone?	Central failure removes adrenocorticotropic drive to cortisol, but aldosterone remains under renin-angiotensin regulation; hence hyperkalaemia, salt craving and high renin are more typical of primary disease.	Integrated Medical Foundations; chapter 24, TTS module 2; https://theisegoria.github.io/medical-textbook/integrated-medical-foundations-expanded-english.md; module SHA256 at export: f8b90b7ae886e295c8eaa5a468be71e76d32cec610a9036b39930a4c69f11f75; editorial review pending	imf lang::en chapter::024 module::024-02 review::pending
IMF-024-02-0007-en	Why does a patient with adrenal failure need planned stress dosing and parenteral rescue during illness?	Illness normally increases cortisol, a response the patient cannot mount, and vomiting can prevent oral absorption, so injected rescue therapy is required.	Integrated Medical Foundations; chapter 24, TTS module 2; https://theisegoria.github.io/medical-textbook/integrated-medical-foundations-expanded-english.md; module SHA256 at export: f8b90b7ae886e295c8eaa5a468be71e76d32cec610a9036b39930a4c69f11f75; editorial review pending	imf lang::en chapter::024 module::024-02 review::pending
IMF-024-02-0008-en	How does glucocorticoid excess produce proximal weakness, thin skin and bone loss?	Protein catabolism causes proximal weakness and thin skin, while bone formation falls and resorption rises.	Integrated Medical Foundations; chapter 24, TTS module 2; https://theisegoria.github.io/medical-textbook/integrated-medical-foundations-expanded-english.md; module SHA256 at export: f8b90b7ae886e295c8eaa5a468be71e76d32cec610a9036b39930a4c69f11f75; editorial review pending	imf lang::en chapter::024 module::024-02 review::pending
IMF-024-02-0009-en	In primary aldosteronism, why can potassium be normal, and what confounds the aldosterone-renin screening ratio?	Intake and kidney adaptation compensate for potassium loss; posture, sodium, potassium, medicines, kidney function and assay conditions all affect the ratio.	Integrated Medical Foundations; chapter 24, TTS module 2; https://theisegoria.github.io/medical-textbook/integrated-medical-foundations-expanded-english.md; module SHA256 at export: f8b90b7ae886e295c8eaa5a468be71e76d32cec610a9036b39930a4c69f11f75; editorial review pending	imf lang::en chapter::024 module::024-02 review::pending
IMF-024-02-0010-en	Before surgery for a catecholamine-secreting tumour, why is alpha blockade established before beta blockade and volume restored?	Alpha blockade first avoids unopposed vasoconstriction, and chronic vasoconstriction has reduced circulating volume, which often needs restoring before surgery.	Integrated Medical Foundations; chapter 24, TTS module 2; https://theisegoria.github.io/medical-textbook/integrated-medical-foundations-expanded-english.md; module SHA256 at export: f8b90b7ae886e295c8eaa5a468be71e76d32cec610a9036b39930a4c69f11f75; editorial review pending	imf lang::en chapter::024 module::024-02 review::pending
IMF-024-02-0011-en	How does kidney failure lead to secondary hyperparathyroidism?	Failing kidneys retain phosphate and activate less vitamin D, and fibroblast growth factor 23 rises early but also lowers active vitamin D, so the parathyroid is stimulated and may become partly autonomous.	Integrated Medical Foundations; chapter 24, TTS module 2; https://theisegoria.github.io/medical-textbook/integrated-medical-foundations-expanded-english.md; module SHA256 at export: f8b90b7ae886e295c8eaa5a468be71e76d32cec610a9036b39930a4c69f11f75; editorial review pending	imf lang::en chapter::024 module::024-02 review::pending
IMF-024-02-0012-en	Why can calcium replacement fail in severe magnesium deficiency, even though mild deficiency stimulates parathyroid secretion?	Magnesium is needed for parathyroid hormone release and action; severe deficiency paradoxically suppresses secretion and causes resistance, so calcium may not work until magnesium is corrected.	Integrated Medical Foundations; chapter 24, TTS module 2; https://theisegoria.github.io/medical-textbook/integrated-medical-foundations-expanded-english.md; module SHA256 at export: f8b90b7ae886e295c8eaa5a468be71e76d32cec610a9036b39930a4c69f11f75; editorial review pending	imf lang::en chapter::024 module::024-02 review::pending
IMF-024-02-0013-en	How does the parathyroid hormone level split the differential diagnosis of hypercalcaemia?	Elevated or inappropriately normal levels point to primary hyperparathyroidism, tertiary disease, lithium or familial calcium-sensing variants; suppression favours malignancy, vitamin D pathways, granulomas, medicines or immobilisation.	Integrated Medical Foundations; chapter 24, TTS module 2; https://theisegoria.github.io/medical-textbook/integrated-medical-foundations-expanded-english.md; module SHA256 at export: f8b90b7ae886e295c8eaa5a468be71e76d32cec610a9036b39930a4c69f11f75; editorial review pending	imf lang::en chapter::024 module::024-02 review::pending
IMF-024-02-0014-en	Why can denosumab not simply be stopped when treatment ends?	Denosumab suppresses resorption through a reversible antibody pathway, so abrupt discontinuation can cause rebound turnover and vertebral fractures; a planned subsequent antiresorptive strategy is essential.	Integrated Medical Foundations; chapter 24, TTS module 2; https://theisegoria.github.io/medical-textbook/integrated-medical-foundations-expanded-english.md; module SHA256 at export: f8b90b7ae886e295c8eaa5a468be71e76d32cec610a9036b39930a4c69f11f75; editorial review pending	imf lang::en chapter::024 module::024-02 review::pending