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Endocrine-pathology

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drnieves's version from 2017-06-21 13:26

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Question Answer
Cushing syndromeIncreased cortisol
Exogenous cortisolResult in decrease ACT and bilateral adrenal atrophy.
Decrease ACTH causesPrimary adrenal adenoma, hyperplasia or carcinoma.
Paraneoplastic ACTH secretionSmall cell lung cancer, bronchial carcinoids
Cushing syndromeHTN, weight gain, moon facies, truncal obesity, buffalo hump, striae, osteoporosis, hyperglycaemia, amenorrhea, immunosuppression.
Primary hyperaldosteronismexcessive aldosterone secretion s a result of bilateral nodular hyperplasia of zone glomerulosa or aldosterone producing adrenal adenoma.
HTN, low plasma renin activity, hypokalemia, metabolic alkalosisHyperaldosteronism
Familial retinoblastoma2 hit mutation of Rb gene. Increased risk of sarcomas.
Adrenal insufficiencyInability to produce mineralocorticoids/ glucocorticoids.
Weakness, fatigue, orthostatic hypotension, muscles aches, weight loss, GIT, sugar or salt cravingsAdrenal insufficiency
Adrenal insufficiency dxSerum electrolytes, morning/random serum cortisol and ACTH.
Metyrapone stimulationMetyrapone blocks last step of cortisol synthesis (11- deoxycortisol to cortisol).
1ry adrenal insufficiencyLoss of gland function. Hypotension, hyperkalemia, metabolic acidosis, hyperpigmentation.
Acute adrenal crisisSudden onset. Shock
Chronic adrenal insufficiency (addison)Adrenal atrophy or destruction.
Waterhouse Friedrichsen syndromeacute 1ry adrenal insufficiency due to adrenal haemorrhage with septicaemia, DIC, endotoxic shock.
2RY adrenal insufficiencyDecreased ACTH
Tertiary adrenal insufficiencyChronic exogenous steroid use, precipitated by abrupt withdrawal.
CretinismDue to maternal hypothyroidism, thyroid agenesis/dysgenesis, I deficiency, dyshormonogenetic goiter.
Cretinism sxPot bellied, pale, puffy faced with protruding umbilicus, protuberant tongue, poor brain development.
Diabetic ketoacidosis
Hyperplasia of zone fasciculata/ reticularisACTH overproduction
Hyperplasia of zone glomerulosaConn syndrome
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