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20 Cards in this Set
- Front
- Back
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Adrenal Cortex: hormones
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Glucocorticoids: esp cortisol
Mineral Corticoids: esp Aldosterone Sex Steroids: estrogens and androgens |
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Cushing Syndrome: General
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*Due to exogenous glucocorticoids
* ACTH Dependent or Independent *Primary Hypothalamic-pit dz w/ hypersecretion of ACTH= pit gland w/ ACTH prod Adenoma * Primary Adrenocortical hyper/neoplasia *Ectopic ACTH secretion by nonendocrine neoplasms: small cell CA lung, medullary CA thyroid, panc tumor |
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Cushing syndrome: ACTH DEp vs Independent
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ACTH Dependent = cushing dz, ectopic corticotropin syndrome (ACTH secreting lung CA,etc)
ACTH Independent: adrenal adenoma, adrenal carcinoma, macronodular hyperplasia, primary pigmented nodular adrenal dz, McCune Albright Syndrome |
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Cushing Syndrome: Morphology
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MORPH: exogenous glucocorticoids: suppression of endogenous ACTH--> BL atrophy of adrenal cortices.
* inc ACTH by pit/ectopic: stim of adrenals--> BL hyperplasia, *Primary adrenocrortical neoplasm: benign or malig *pit gland: crooke's hyaline change= replacement of ant pit cells with basophilic cells from high levels of endo/exogenous glucocorticoids *hypothalamic-pit origin: arises from ACTH-secreting pit adenoma/ACTH cell hyperplasia |
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Cushing syndrome
Clinical Features |
HTN, weight gain, truncal obesity, moon face, buffalo hump, dec musc mass, hyperglycemia, glucosuria, polydipsia, cutaneous striae on abd, osteoporosis, inc risk infx, hirsutism, menstrual abnorm, mental disturb
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cushing syndrome: lab findings
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* inc 24hr free crotisol level
* loss of norm diurnal pattern of cortisol secretion * pit cushing syndrome: suppressible by HIGH dose of desamethasone * Adrenal cushing syndrome: low serum ACTH, sx NOT suppressible by high doses of dexamethasone * Ectopic Cushing: sx NOT suppressible by high dose dexamehtasone |
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Primary hyperaldosteronism
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*Na retention, K exretion, HTN, hypokalemia, NO inc renin levels
* usu casued by BL idiopathic hyperaldosteronism assoc w/ BL nodular hyperplasia adrenal glands (patho unclear) * other causes: adrenocortical neoplasms = CONN SYNDROME (single aldosterone secreting adenoma- adult women) & glucocorticoid remediable hyperaldosteronism (uncommoen cause of familial hyperaldosteronism) *MORPH: aldosterone secreting adenoma=usu solitary, small, bright yellow w/ uniform cells, if tx w/ spironolactone get SPIRONOLACTONE BODIES (laminated cytoplasmic inclusions). Adenoma do NOT suppress ACTH secretion. BL idiopathic hyperplasia= diffuse & focal. |
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Secondary Hyperaldosteronism
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* in response to activation of renin angiotensin syst. INCREASED PLAMSA RENIN.
* areteriolar nephrosclerosis & renal artery stenosis--> dec renal perfusion * arterial hypovolemia & edema--> heart fail, cirrhosis, nephrotic syndrome * preg: cause estrogen induced inc in plasm renin substrate |
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Hyperaldosteronism
Clincal |
* most common cause of secondary htn
*contrib to enothelial dysfxn by dec glc-6-P dehydrogenase levels--> reduces endoth NO synth --> oxidative stress * cardio prob, hypokalemia --> neuromusc manifest, weak, paresthesias, visual disturb, tetany |
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Adrenogenital Syndromes
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* produced by congenital adrenal hyperplasia
*defect in enz involved in cortisol synth * defect in 21-hydroxylase deficiency -->inc secretion of ACTH & testosterone synth *ACTH regulates adrenal formation |
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Adrenocortical insufficiency
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*Primary Adrenal dz
* dec stim of adrenal due to deficient ACTH * Patterns: primary acute adrenocortical insufficiency, primary chronic adrenocortical insufficiency (addisons), & secondary adrenocortical insufficiency |
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Primary Acute Adrenocortical Insufficiency
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* Rapid withdraw of Steroids/fail to inc steroids doses during periods of stress
* massive adrenal hemorrhae: newborns after difficult delivery w/ trauma & hypoxia * DIC * pt on anticoags *bactermic infx: waterhouse-friderichsen syndrome |
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Addison Dz
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* autoimmune adrenalitis: irreg shrunken glands
* tb, fungi = granulomatous inflam * met neoplasm: adrenal enlarged w/ infiltrating neoplasm *CLINIC: weakness, fatigue, NVD, wt loss, hyperpigment (inc ACTH precurser hormon stim melanocytes), hyperkalemia, hyponatremia, volume depletion, HoTN |
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Waterhouse-Friderichsen Syndrome
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Overwhelming infx caused by NEISSERIA MENINGITIDIS septicemia (aslo caused by pseudomonas, pneumococci, H influenza)
* rapid progressive, HoTN, shock, DIC, rapid developing adrenocortical insufficiency w/ massive BL adrenal hemorrhage * children *adrenals form sacs of blood, *Abrupt and devastating clinical course |
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adrenal medulla path
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pheochromocytoma
neuroblastoma MEN syndromes |
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pheochromocytoma
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* 30/40 yo w/ HTN, tachycardia, MI, CVA, inc urinary excretion of VMA
*well demarcated, well vascularized w/ fibrous tissue, hemorrhage, necrosis, cysts *rule of 10!! *divided into small nests = zellballen *25% have germline mutation * malig inc when assoc w/ SDHB, SDHC & SDHD: encode prot in Mito e- transport, loss of fxn= tumorigenesis *NO histo behavior that predicts clinical behavior. * Inc mets/agressive = inc mitoses, necrosis, spindle cell *benign tumors may met, may nuc pleomorphism, giant cells, mitotic figures, capsular invasion *aggressive tumors may have cell monotony *Malig dx based on METS |
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Neuroblastoma
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*common, solid childhood tumor, < 5yo. most in adrenal area or post mediastinum
* large, soft, necrosis, hemorrhage *small cells in solid sheets/nests, HOMER-WRIGHT PSEUDOROSETTES: cells gather around ephil fibrils *prod catecholamines, urinary VMA * met |
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Multiple endocrine neoplasm
Type 1 |
*wermer syndrome
*abnorm in parathyroid (hyperplasia &adenomas) , panc (gastrinomas,insulinomas, microadenomas), pit (prolactinoma, somatotropin secreting tumor) *cause: germline mut in MEN1 tumor suppressor gene, encode MENIN *clinic: hypoglycemia, peptic ulcer, nephrolithiasis |
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MEN 2A
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*sipple syndrome
*pheochromocytoma *medullary carcinoma of thyroid *parathyroid hyperplasia *linked to RET protooncogene |
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MEN 2B
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*medullary CA of thyroid, more aggressive than 2A
*pheochromocytoma * DOES NOT HAVE PRIMARY HYPERPARATHYROIDISM *ganglioneuromas of skin, resp tract, GIT *marfanoid habitus |
