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This Concept Map, created with IHMC CmapTools, has information related to: Adrenal, Adrenal Cortex Adrenal Insufficiency -hypofcn PRIMARY CHRONIC AC INSUFF (ADDISON DZ) - WHITE WOMEN -progressive destruction of cortex -at least 90% compromised ᢒ%-AUTOIMMUNE adrenalitis, TB, or METS -others: lymphomas, amyloid, sarcoid, hemochromotosis, fungi, ad hemorr AI ad'itis-60-70%-1/2 w/ just ad -or other AI -DM-I, Hashimoto, etc. =Polyglandular syndromes -HLA-B8 or DR-3 -irreg shrunken glands -LYMPHOID INFILTRATE in cortex INFX-TB-granulomatous changes METS-common place for mets -LUNG, BREAST ->enlarged adrenals, obscured CLINICAL-fatigue, weakness ->GI-anorexia, N/V/D, wt loss -hyperpigmentation (ACTH on mels) -sun-exposed, pressure pts -hyperK+, hypo Na+, hypoTN -small heart (hypovol), HYPERCORTISOLISM (CUSHING SYNDROME) -mostly due to exogenous steroids OR -primary hypothal-pit dz->ACTH ᡪ% of endogenous -Cushing DZ if pituitary -WOMEN-20s-30s-no mass effect ->nod hyperplasia->high cortisol -dexamethasone-LD-no suppression -HD-suppression -adrenal adenoma, CA, hyperplasia -ACTH-indep-15-30% of endog -adenoma=CA-adults, more CA in kids -CA makes more cort -if unilateral-other ad will atrophy -30-60yo for both - CAs bigger -totally dexa-insensitive -ectopic ACTH by nonendocrine CA -*LUNG - SMALL CELL CA - SCC -Carcinoid tumors -Thyroid medullary CA, panc islet cell ->bilat hyperplasia->rapid course -totally dexamethasone-insensitive MORPH CLINICAL -Early-HTN, wt gain -Later-truncal obesity, buffalo hump, moon facies -atrophy of fast-twitch mm -prox mm weakness -GNG induced, hyperglycemia, glucosuria, ploydipsia -loss of collagen, resorbed bone -osteoporosis -fragile skin, reddish striae -mood swings, psychosis, Adrenal Cortex Adrenogenital Syndromes CONGENITAL AD HYPERPLASIA-AR -enzyme deficiency -steroidogenesis channeled into other steroids -lack of cortisol->more ACTH ->hyperplasia ->virilization -rarely involves only aldosterone, Adrenal Cortex Adrenocortical Hyperfcn (Hyperadrenalism) HYPERCORTISOLISM (CUSHING SYNDROME) -mostly due to exogenous steroids OR -primary hypothal-pit dz->ACTH ᡪ% of endogenous -Cushing DZ if pituitary -WOMEN-20s-30s-no mass effect ->nod hyperplasia->high cortisol -dexamethasone-LD-no suppression -HD-suppression -adrenal adenoma, CA, hyperplasia -ACTH-indep-15-30% of endog -adenoma=CA-adults, more CA in kids -CA makes more cort -if unilateral-other ad will atrophy -30-60yo for both - CAs bigger -totally dexa-insensitive -ectopic ACTH by nonendocrine CA -*LUNG - SMALL CELL CA - SCC -Carcinoid tumors -Thyroid medullary CA, panc islet cell ->bilat hyperplasia->rapid course -totally dexamethasone-insensitive, Adrenal Cortex Adrenocortical Hyperfcn (Hyperadrenalism) SECONDARY HYPERALDOSTERONISM -due to activation of RAAS -increased renin -due to CHF, dec'd renal perfusion, hypoalbuminemia, pregnancy, Adrenal Cortex Adrenal Insufficiency -hypofcn PRIMARY ACUTE AC INSUFFICIENCY 1. Crisis - in chronic ACI + extra stress -gland can't respond to stress 2. Rapid w/drawal of exo steroids ->crisis 3. Massive adrenal hemorrhage -in newborns after prolonged delivery -anticoag Tx -post-surgical pts w/ DIC -plus bacteremic infx=W-F syndrome, Adrenal Cortex Adrenocortical Neoplasms CARCINOMAS -USUALLY FCNAL -at any age ->virilism, etc. -primary look like mets -often invade IVC, ad vein, lymphatics -METS common to nodes, lungs -NOT BONE, Adrenal Cortex Adrenocortical Hyperfcn (Hyperadrenalism) PRIMARY HYPERALDOSTERONISM ->Na+ retention, K+ secretion ->HTN, hyperK+ -suppresses RAAS -due to AC neoplasm, esp adenoma -CONN SYNDROME-adenoma in 1 ad -middle-aged WOMEN -LEFT>right, buried w/in gland -resemble fasciculata cells (not glom!) -or AC hyperplasia -resemble NL glom cells w/ some fasc GLUCOCORTICOID-SUPPRESSIBLE HYPERA. -familial-deranged zonation ->hybrid steroids + cort + aldost -influenced by ACTH, so suppress w/ dex, Adrenal Cortex Adrenal Insufficiency -hypofcn SECONDARY AC INSUFF -d/o of hypothal or pit -or exogenous steroids -no hyperpigmentation though -deficient CORTISOL, ANDROGENS -NL aldosterone-no ion changes -administer exogenous ACTH -big change MORPH-mod-marked reduction in size -medulla UNAFFECTED, Adrenal Cortex Adrenogenital Syndromes 21-HYDROXYLASE DEFICIENCY -most common CAH-90% -defective progesterone-> 11deoxycorticosterone -affects aldost & cortisol 3 Syndromes 1. salt-wasting-no aldost or cort -hyperK+->acidosis -hypoTN, CV collapse->death ->excess androgens->virilize -easily IDed in F, later in M 2. Simple Virilizing-subtotal def -enough aldost for salt -still too much androgen->vir -too little cort->hyperplasia 3. Nonclassic/Late-onset ad virilism -MOST COMMON -(-)Sx or mild hirsutism MORPH-hyperplastic in all 3 -hyperplasia of corticotrophs in Pit CLINICAL- FM-pseudoherm'ism in baby, oligomenorrhea, hirsutism, acne M-big external genitalia, precocious puberty, oligospermia Tx - exogenous glucocorticoids, Adrenal Cortex Adrenocortical Neoplasms ADENOMAS Functional or not-MOSTLY NOT -based on clinical findings -NOT morph MORPH-usually incidental at autopsy, Adrenal Cortex Other ADRENAL CYSTS -larger->flank pain -can be from old neoplasm ADRENAL MYELOLIPOMA -fat, hematopoietic cells -usually small -can be in tumors, hyperplasia ADRENAL INCIDENTALOMA -ASx, adrenal mass -nonsecreting cortical adenoma, HYPERCORTISOLISM (CUSHING SYNDROME) -mostly due to exogenous steroids OR -primary hypothal-pit dz->ACTH ᡪ% of endogenous -Cushing DZ if pituitary -WOMEN-20s-30s-no mass effect ->nod hyperplasia->high cortisol -dexamethasone-LD-no suppression -HD-suppression -adrenal adenoma, CA, hyperplasia -ACTH-indep-15-30% of endog -adenoma=CA-adults, more CA in kids -CA makes more cort -if unilateral-other ad will atrophy -30-60yo for both - CAs bigger -totally dexa-insensitive -ectopic ACTH by nonendocrine CA -*LUNG - SMALL CELL CA - SCC -Carcinoid tumors -Thyroid medullary CA, panc islet cell ->bilat hyperplasia->rapid course -totally dexamethasone-insensitive MORPH Pituitary-Crooke Hyaline Change -change no matter what cause Adrenal-exogenous-bilat atrophy -hyperplasia-mostly diffuse Pigmented micronod ad dz -in kids-lipofuscin in Zona Fasc, Adrenal Cortex Adrenocortical Hyperfcn (Hyperadrenalism) CLINICAL Hypokalemia-weakness, paresthesias, visual disturbances, tetany Hypernatremia-expande ECF Both can-> cardiac decompensation, Adrenal Cortex Adrenal Insufficiency -hypofcn WATERHOUSE-FRIDERICHSEN SYNDROME -CATASTROPHIC 1. bac infx - N. MENING septicemia, Pseudomonas, H. influen, staph, p'cocci 2. Rapidly progressive hypoTN, shock 3. DIC w/ PURPURA 4. Rapid AC insuff due to bilat ad hemorrh MORE COMMON IN KIDS -Adrenals become sacs of clotted blood -Death w/in hours-days if unTx