what symptoms have higher specificity for Graves disease☆pretibial myxedema, proptosis(Graves orbitopathy)
Graves ophthalmopathy are not mediated by thyroid hormone or adrenergic stimulation and ☆do not respond to beta blockers. However, they are immune mediated, the manifestation usually respond to glucocorticoid therapy.
fibroblasts stimulated by TRAb secrete excess amount of ☆glycosaminoglycans (eg hyaluronic acid) along with adipogenesis, which expand ground substance of retro-orbital tissues
→desiccation(eg a sense of ☆grittiness), tearing endocrinologyUWorldUWorld SIM2 HirotoShishido
endocrine hormones which uses IP3 pathywayGOAT HAG(hˈæg, A witch)
GnRH, ¥Oxytocin, ADH(V-1), TRH, Histamine(H-1), Angiotensin Ⅱ, Gastrin endocrinologyAmboss level4 HirotoShishido
lid laga sign of ophthalmopathy caused by spasm of the smooth muscle portion of the levator palpebrae superioris due to sympathetic overactivity (as in from Graves hyperthyroidism).
Evaluated by instructing the patient to follow the examiner's finger as it moves downwards. Lid lag is present if the sclera can be seen above the iris as the patient looks down. endocrinologyAmboss level4 HirotoShishido
hypothyroidism effect on lipidsdecreased LDL receptor expression, leading to decreased clearance of LDL with resultant increased blood LDL levels endocrinologyUWorld HirotoShishido
excess T4 supplementation suppresses TSH, which decreases iodine organification, resulting in diffuse atrophy of the thyroid follicles with decreased colloid endocrinologyUWorld HirotoShishido
what regulate the release of prolactinTRH→ ↑prolactin
dopamine→ ↓prolactin
(¥malignant PKU→ ↓dopamin→ hyperprolactinemia)
(☆hyperprolactinemia can be caused by the lesion in hypothalamus or pituitary lesion by the disruption of hypothalamic-pituitary axis) endocrinologyAmboss level4UWorld HirotoShishido
what degrade triglylerides during fasting☆hormone sentitive lipase
+ stress hormone(catecholamines, glucagons, ACTH)
- insulin endocrinologyUWorld HirotoShishido
patiromer
mechanism, clinical use, adverse effecta nonabsorbable cation exchange resin that binds colonic potassium in exchange for calcium, trapping potassium within the resin where it is then excreted in the feces.
often used for treatment of ★chronic hyperkalemia. (however, onset of action takes several hours, so it is not recommended as monotherapy in acute hyperkalemia)
GI disturbance, hypercalcemia, hypokalemia, hypomagnesemia
osmotic demyelination syndrome
etiology, manifestationiatrogenic correction of hyponatremia
→☆cerebral demyelinatiom
☆pons is commonly affected, but can occur to basal ganglia, or cerebral white matter
→spastic quadriplegia, pseudobulbar palsy, locked in syndrome, acute paralysis, dysarthria, dysphagia, diplopia
change in PTH for the patients with multiple myelomaosteolytic cytokines→
liberate calcium from bone→
hypercalcemia→
inhibits the release of PTH from parathyroid cells→
①increase urinary calcium excretion(☆hypercalciuria)
②reduce renal 1-alfa-hydroxylase→☆low 1,25 dihydroxyvitamine D endocrinologyhematologyUWorld HirotoShishido
treatment of congenital adrenal hyperplasiaadministering ☆low (ie, physiologic) doses of exogenous corticosteroids to suppress ACTH secretion
By removing excessive ACTH stimulation, exogenous corticosteroids can decrease androgen production by the adrenal cortex. endocrinologyUWorld HirotoShishido
hypothyroidism and T3synthetic T3 (liothyronine) is not recommended for the routine treatment of hypothyroidism, as it has a short half-life and patients can experience wide fluctuations in plasma T3 levels
