B6.076 Endocrine Myopathies Flashcards by Lauren Sinik

hypothyroid myopathy pattern

slow, progressive proximal weakness
fatigue
cramps

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neuro tests of hypothyroidism

EMG often normal
carpal tunnel seen on nerve conduction studies
length-dependent peripheral neuropathy may be seen

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lab findings in hypothyroidism

TSH high
T3 low
T4 low

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thyroid stimulation loop

decreased T3 and T4 in the blood stimulate…
hypothalamus to release TRH which stimulates…
pituitary to release TSH which stimulates….
thyroid to release T3 and T4 which inhibits….
hypothalamus

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type 1 fibers

slow twitch
oxidative
low strength, low fatigability

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type 2a fibers

fast twitch a
oxidative & glycolytic
high strength, moderate fatigability

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type 2x fibers

fast twitch x
glycolytic
high strength, high fatigability

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what is a muscle core

zones of myofibrillar disarray lacking in oxidative and phosphorylase enzyme activity

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risk to parathyroid glands during thyroid surgery

at risk of trauma, devascularization, or removal

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pathological changes with parathyroid removal

decreased PTH
inability to maintain serum Ca
decreased 1,25 vit D
reduced intestinal C absorption
abnormal mobilization of Ca from bone
high urinary Ca excretion
--->>> hypocalcemia

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changes in phosphate in hypoparathyroidism

increased serum phosphate

proximal tubular effect of PTH to promote phosphate excretion is lost

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why does hypoparathyroidism have a prolonged latency period

may have decreased parathyroid reserve, not complete dysfunction
increased stress on glands may precipitate symptoms (pregnancy for example)

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Chvostek sign

tap on facial nerve anterior to the ear

twitching of ipsilateral facial muscle is a positive test

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Trousseau sign

inflate BP cuff over systolic BP for 3 min

painful carpal muscle contractions and spasms are a positive test

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what do Chvostek and Trousseau signs indicate

latent tetany secondary to hypocalcemia

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pathophys of hypertension in Cushing

increased R-A-A
increased mineralocorticoid activity
increased sympathetic nervous system
increased vasoconstriction

pathophys of atherosclerosis in Cushing

dyslipidemia
inflammation
insulin resistance
impaired glucose tolerance
DM
visceral obesity

cardiac remodeling in Cushing

LVH
changes in wall thickness
myocardial fibrosis

pathophys of cardiac arrhythmias in Cushing

hypokalemia

thrombosis diathesis in Cushing

increased VIII, vWf, platelets, fibrinogen, and PAI-1

cause of obesity in Cushing

unclear
increase in appetite
lipogenic effects of hyperinsulinemia caused by cortisol excess

cause of striae in Cushing

subQ fat deposition which stretches the skin and ruptures the subdermal tissues

major causes of Cushing

ACTH secreting pituitary adenoma
ectopic ACTH production
functioning adrenocortical adenoma / carcinoma
long term high dose exogenous glucocorticoid intage (iatrogenic)

p-a axis

hypothalamus releases CRF which stimulates….
anterior pituitary to release ACTH which stimulates….
adrenal cortex to release cortisol which increases….
blood glucose, blood pressure, amino acids & inhibits hypothalamus

how to demonstrate pathologic hypercortisolemia

free cortisol in 24 hour urine | overnight 1 mg dexamethasone suppression test

steps in diagnosis of Cushing etiology

1. demonstrate pathologic hypercortisolemia 2. distinguish ACTH independent disease from ACTH dependent disease 3. determine anatomic localization of the ACTH source

free cortisol 24 hour urine

outpatient most sens and spec screening for Cushing rarely normal in Cushing

overnight 1 mg dexamethasone suppression test

lack of normal suppression by exogenous corticosteroid of adrenal cortisol production in normal individuals: cortisol < 5 in Cushing: cortisol > 10

how to differentiate pituitary or ectopic ACTH secretion

high dose dexamethasone suppression test

anatomic localization of ACTH methods

MRI thin section CT IPSS CSS

rhabdo findings on biopsy

marked type 2 atrophy

changes in myoglobin with rhabdo

increases rapidly following muscle injury and cleared quickly through renal excretion normal level within 24 hours

changes in CK with rhabdo

rises 2-12 hours after onset of muscle injury | peaks at 3-5 days after injury and declines over 6-10 days

results of unaccustomed physical exercise that can lead to increased intracellular Ca

sarcolemmal and SR injury increased cellular permeability to sodium failure of energy production (Na+/K+ ATPase and Ca2+ATPase dysfunction)

results of increased intracellular Ca

activation of Ca-dependent proteases and phospholipases destruction of myofibrillar, cytoskeletal, and membrane proteins muscle contraction

symptoms of rhabdo

leakage in circulation: Ca, K, P, urate, aldolase, myoglobin, CPK, lactate dehydrogenase, aspartate transaminase renal failure blood clotting cardiac arrhythmias

CYP3A4 relationship to statins

oxidizes statins allowing their excretion | many drugs inhibit this CYP, reducing oxidation and resulting in greater bioavailability

fibrate relationship to statins

inhibits phase 2 metabolism of statins (normally responsible for further metabolism of the statin for excretion out of the body) fibrates cause oxidized statins to stay in the body and exert their inhibitory effect