Cushings Disease

WHAT:hyperfunctioning of adrenal gland cause increased production of cortisol, high levels cause immunosupression RISK FACTORS: endogenous ( adrenal hyperplasia, adenocorticoid neoplasm, pituitary tumor secreting ACTH, Tumors secret ACTH, women 25-50 y/o ) Exogenous ( cortisol Tx for another disorder such as fibrosis, allergies, chemo, organ transplant, autoimmune disease, asthma) DIAGNOSTICS: Dexamethasone suppression ( 24 urine tests shows cortisol excretion and no suppression indicates Cushings) Increased Na. Decreased K and Ca. Increased glucose. Elevated levels urine free cortisol. Elevated plasma cortisol S&S: decreased immune function/Inflamm response, HTN( from Na and water retention) Change in fat distribution( moon face, trunk obesity, buffalo hump) fractures, impaired glucose tolerance, brushing/petechiae. Muscle wasting NI: Diet change ( decrease Na and increase K and Ca and protein) Daily weights, ck I&O, safe environment, prevent infection, Risk for adrenal crisis ( with abrupt withdrawal of steroids, HypoTN, hyperK, and pain, weakness , weight loss,--taper meds gradually , Tx w/glucocorticoids

ADDISON'S DISEASE/ ADDISON CRISIS

WHAT: adenocorticoid insufficiency from damaged/dysfunctional adrenal gland cause decreased aldosterone and cortisol, Crisis is emergency RISKS: Disease(idiopathic autoimmune dysfunction, TB) Crisis ( sepsis, trauma, stress, adrenal
hemorrhage, steroid withdrawal )

LABS: increased K and Ca. Decreased Na Increased BUN. Decreased glucose. Decreased cortisol. ACTH stimulation test( ACTH infused and cortisol levels don't rise) S&S: disease slow crisis fast. Hyper pigmentation. Weakness. N/V. Dizziness. Ortho HypoTN. Dehydration. HypoNA/hypoCa. HyperK. Hypoglycemia NI: increase corticosteroids during times of stress, Ck for fluid defects /hypoNa ( give saline to restore fluids) give hydrocortisone bolus (continuous infusion/ or periodic) Tx hyperK ( give sodium polystyrene --Kayexalate, insulin, Ca , glucose and Na Bicarb ) Tx hypoGlycemia ( give
food and supplemental glucose)

Cushing , Hypercortisolism
WHAT : exaggerated action of glucocorticoids , excessive secretion of cortisol from adrenal cortex, CAUSE: nitrogen/carbs/mineral metabolism altered, increase in ttl body fat from slow turn over of fatty
acids cause truncal obesity, buffalo hump, moon face , increased tissue protein breakdown , increased urine nitrogen, decreased muscle mass, thin skin fragile capillaries , bone density loss, decreased Inflamm and immune response ( corticosteroids kill lymphocytes, shrink organ containing these sites like liver and
spleen , and lymph nodes) , acne, hirutism, clitorla hypertrophy, oligomenorrhea

RISK FACTORS: Endogenous ( Bil adrenal hyperplasia , pituitary adenoma increasing production of
ACTH( when over secretion Of ACTH cause hyperplasia of adrenal cortex in Bil adrenal glands and excess of hormones secreted form here--pituitary Cushing, tissue causing prob is pituitary ) Malignances( adrenal Cushings --when prob cause by adrenal cortex , usuall occur in only one gland for tumor )

Exogenous ( Use of ACTH or steroids for -- asthma, autoimmune, organ transplant, cancer chemo, allergic response, chronic fibrosis--known as Cushings syndrome) Women, LABS: high blood cortisol , increased saliva cortisol ( obtained at midnight, put cushion in check next salovary gland , Norm is less than 2.0, ) increase urine cortisol levels( elevated in 24 h collection , so is Ca, K and glucose) , ACTH ( high in pituitary Cushing, steroids causing Cushing have low ACTh levels) Dexamethasone suppression testing ( give med and test 24 urine collection, if no levels u are good) Increased glucose/Na, decreased lymphocyte/Ca/K S&S:

Moon face/buffalo hump/ truncal obesity/ weight gain, HTN/TAchy ( Na and water retained) Increase DVT'S risk, dependent edema( water and Na reabsorbed) capillary fragility ( brushing,petechiae) muscle atrophy( nitrogen and minerals lost, increase fall risk) , osteoporosis( fractures, loss height, slow bone healing ) , thinning paper skin, Striae( due to destructive affect of cortisol on collagen) increased pigmentation ( w/ectopic or pituitary production of ACTH) increase infection risk, decreased immune ( less lymphocytes/immunoglobulins--antibodies) decrease Inflamm response ( less eosinophils, increase neutrophils but activity reduced) acne, fine hair over face, High Blood sugar/Hyperglycemia ( liver stimulated to convert glycogen into glucose and insulin receptors less sensitive , so glucose don't move as easily into tissues, muscle mass loss increase sugar also) NI: fluid Vl overload care ( prevent Vl overload form worsening,mck S&S--increased pulse/ JVD/crackles
in,units , increased edema, reduced output, overload increase risk for HF, pulmonary edema and skin breakdown-- ck round bony and O2 tubes, change position q2, ck wight and I&O, restrict Na , low Na diet, Ckmspecific gravity--overload shown by less than 1.005, Radiation Tx-- from pituitary tumors , ck neurologic status, HA, elevated BP, chang pupil size/reaction

MEDS-- amnioglutethimide-Elipten and metyrapone-Metopirone decrease cortisol production , cyprohepatidine-Perilactin interferes w/ACTH production

surgery ( hypophysectomy--removal of pituitary gland for disease caused by too much ACTH, pituitary tumor,
Adrenalectomy--removal of adrenal gland ; PRE-- correct Na , K and electrolyte prior, Tx glucose levels prior, high calorie high protein diet , give glucocorticoids b4 and during surgery to prevent adrenal crisis from sudden drop in cortisol levels ; POST-- Ck for shock-- hypoTn/rapid weak pulse/ decreased output due to insufficient cortisol replacment , ck weight, I&O, electrolyte levels, Bil adrenalectomy must have glucocorticoid replacment for life , if unilateral must have replacment till left over gland increases hormone production )

RISK FOR INJURY ( raise bed rails,mgive assistance with OOB, change position q2, avoid activities cause skin
trauma, monitor for bleeding/take precautions , monitor for falls and fall risks, maintain safe environment )

NUTRITION ( high calorie diet, increased Ca and Vit D , milk cheeses, yogurt, green veggies, , avoid alcohol GI PROTECTION ( GI bleed is common , cortisol inhibits mucus that protects stomach lining, increase HCL production decrease GI blood flow, give antacids 1 hr post eating, give H2 blockers-Tagamet/Zantac/Pepcid/Nexium, decrease smoking,Malcolm, NSAID,aspirin

IINFECTION PROTECTION POTENTIAL FOR ADRENAL INSUFFICENCY( most at risk is Cushings from glucocorticoid therapy,
these med prevent body from producing CRH which stimulate the production ofACTH from pituitary , without normal levels of SCTH adrenal glands atrophy and stop production of corticosteroids so pt depends Sony on medication, if med is stopped atrophied adrenal gland can't produce cortisol

Addison's ADRENAL GLAND HYPOFUNCTION WHAT: Decreased adrenalcorticoid steroids due to lack of ACTH from pituitary system or direct adrenal dysfunction , Symptoms can occur fast with stress, adrenal crisis can cause fast life threatening complications CAUSE: loss of aldosterone and cortisol action , low cortisol cause decreased glucogenesis--make glucose from proteins , depletion of liver and muscle glycogen, globular filtration rate and gastric acid production decrease , decreased urea nitrogen excretion, anorexia and weight loss, hyperK, hypoNa, HypoVl, acidosis , TYPES: Primary ( autoimmune, TB, Cancer, fungal lesion, AIDS, hemorrhage, adrenalectomy, drugs and toxins) Secondary ( cessation of high dose steroids, pituitary tenor, Sheehans syndrome/postpartum pituitary necrosis, hypophysectomy, high dose pituitary radiation, whole brain radiation) LABS: ACTH and MSH elevated ( in primary insufficency, MSH cause pigmentation changes) Hypoglycemia, HyperK, , HypoNa, HypoVl, increase Ca, Increased bicarb2330, increase BUN10-20. Decreased cortisol ACTH stim test ( ACTH o.25-1g given IV and cortisol levels checks q30 min and 1hr intervals , primary insufficency cortisol responses absent , in secondary it is increased S&S: hypoglycemia , anorexia, weight loss, decreased body/auxiliary/pubic hair ,muscle weakness, fatigue, joint/muscle pain, N/V, bowel,changes, salt craving, vitiligo hyper pigmentation ( primary autoimmune ) anemia, HypoTn, HypoNa, HyperK, hyperCa NI: promote fluid balance , Ck fluid defecit, prevent hypoglycemia ( shakiness/tremor/sweating/nervousness/tachy/pallor/hunger/nausea, give carb, glucagon, IV access,) weigh daily, I&O, monitor dysrhytmia /postural hypoTn , ck HEMOCONCENTRARION ( increase H&H , BUN)

MEDS: Cortisone ( 25-5o mg, take w/meals, can cause GI irritation) Hydrocortisone ( 20-50, ck for too much med--rapid wieght gain/round face/fluid retention-Cushing syndrome) Prednisone (5-10, report diarrhea/vomit/fever) Fludrocortisone--florinef( .05-0.2 , maintain electrolyte balance Na/K, ck Bo, report edema , weight gain , SE HTN, Na related fluid retention , m

ADDISION CRISIS: life threatening when need for cortisol/aldosterone is greater than supply, occur in response to stress--surgery, trauma,msevere infection, more severe than chronic problem , Na levels fall fast and K rises fast , sever hypTn occurs from blood Vl depletion occurring with loss of aldosterone ; TX--Hormone relpacment--start IV NS/5%dextrose in NS, give hydrocortisone Na succinate--Solucortef 100-300 mg or Dexamethasone 4-12 mg IV bolus, Inffuse added 100 mg hydrocortisone bynIV drip over 8 hr, give hydrocortisone 50 mg IM q12 h, Intiate H2 blocker--ranitidine IV for ulcer prevention, --HyperK TX--insulin 20-50 u w/dextrose in NS to move K into cells, give K binding and excreting resin-Kayexalate , loop diuretic, K restriction, Ck i&O, ck HR and rhythm for HyperK- slow HR,peaked T wave --Hypoglycemia Tx--- IV glucose, admin glucagon, IV access, ck Bs q1 h )

Pheochromocytoma WHAT: catechoamines producing tumor from adrenal medulla , occur as single lesion in one adrenal gland , usually benign,tumor produce, store and relase epi and nor-epi that stimulate adrenergic receptors RISKS: women, 40-60, LABS: 24 h urine collection ( shows vanillylmandelic acid a product of catechoamines production / metanephrine and catechoamines are elevated ) Clondine suppressing tests S&S: intermittent episode of HTN or , attacks lasting min to hours w/ severe HA, palpitation, profuse diaphoresis , flushing, apprehension, sense mending doom, pain on chest or abd w/ nausea/v , HTN crisis ( from increased abd pressure, defecation and and visors abd palpations m meds such as tricyclics, glucagon, metroclopramide, naloxone, foods high in tyramine-- aged cheese red wines ) heat intolerance, wight loss tremors NI: Surgery ( removal of one or both adrenal glands , post Surgery ck adequate perfusion , Nutriton needs and comfort measures ) HYN is hallmark of disease and most common complication post surgery ( Ck BP ,keep. UFC on same arm, get ortho BP, ) Don't smoke, drink alcohol or stand up too fast, do not pal plate abd b/c can release catechoamines and make HTN crisis, Diet high in calories , Vit and minerals, Hydration PRE surgery, stabilize BP w/adrenergic blocking agents like. Phenoxybenzamine PRE surgery , HTN crisis in Surgery give beta blockers

hyperaldosteronism WHAT: increased secretion of aldosterone causing mineralcorticoid excess TYPES: Primary --Conns syndrome ( excessive secretion of aldosterone from adrenal glands , from benign adrenal tumor, ) secondary ( high levels angiotensin 2 increase aldosterone levels from renal hypoxemia, thiazides diuretics

CAUSE: renal tubukes reabsorb Na , and excrete K and hydrogen ions, give HyperNa, HypoK, metabolic acidosis , Na retention increase BV cause increased BP which can cause strokes, and kidney damage LABS: low K, High Na, low plasma renin levels, high aldosterone, metabolic alkalosis( increased hydrogen ion loss) low specific gravity S&S: hypoK, elevated BP, HA, fatigue muscle weakness, nocturnal, loss stamina, polyuria, paresthesias ( if secret hypoK) visual changes ( due to HTN) NI: Surgeyr ( early stage of disease, removal of 1or both adrenal glands, NO GO if abnormal K levels, K supplement PRE surgery ,unilateral removal may need glucocorticoid replacment , this med is used life long if bilateral removal, steroids given PRE surgery to pevent adrenal crisis) MEDS : sprinolactone ( K sparing diuretic, control hypoK/HTN, ck for hyperK in renal fail pt, no increase dietary K , hypoNa SE ck for dry mouth, thirst, lethargy drowsiness, other SE--gynecomastia, HA, rash urticaria, ED) Aldosterone antagonist, Low Na diet, increase K ( great leafy veggies, canteloupe , apple ,orange )

SIADH WHAT: vasopressin ( ADH) secrets even when osmoalrity is low ( normal levels usually inhibit ADH production ) aka Schwartz Bartter syndrome, feed back mechanism regulating SDH don't work , CAUSE: water to be retained causing dilution. And hypoNa, expand extra cellular fluid Vl, increase glomerular filtration, inhabit release of renin and aldosterone , more Na is loss in urine increasing hypoNa RISKS: cancer of lung, Pancratic/duodenal/ GU carcinoma, Thynina, Hodgkins/Non Hodgkins , viral/bacterial PNA, TB, pneumothorax, chronic lung disease, my closes, PEEP, trauma, infection, stroke, SLE, MEDS( exogenous ADH, chlopropamide, carbamazepine, opioids, tricyclics , anesthetics LABS : low Na. Increased osmoalrity High urine Na. Elevated specific gravity s&S: anorexia, N/V, weight gain,water retention, hypoNa( <115 cause neuro changes, HA, lethargy, disorientation, change in LOC, seizures, decreased DTR, tachy ( due to increased fluid Vl) hypothermia ( CNS prob) NI : restrict fluid intake( may be as low as 500-600 ml/24, dilute tube Feedings with saline, mix meds w/saline not water, Ck I&O, daily weight , frequent oral rinsing, , replace lost Na, block ADH, provide safe environs tw/seizures( MEDS: diuretics especially if HF occurs, cause greater Na loss Hypertonic saline ( 3% Na chloride , give w/caution cause can add to fluid overload and HF, use saline solution instead of water ) Demeclocycline (Declomycin) ( PO only , antibiotic , SE--candidiasisCk mouth/mouth care/rinse tooth brush w/10% bleach /increase yogurt intake

COMPLICATION : fluid Vl overload( bounding pulse, JVD, crackers, increased edema, reduced output) , HF , pulmonary edema

Diabetes Insipidus WHAT: water metabolism problem from too little ADH ( decrease in synthesis or inability of kidney to respond to ADH) cause excretion of large Vl of urine, distal kidney tubules and collecting ducts don't reabsorbed water leading to polyuria and dehydration

CAUSE: dehydration from massive water loss increase plasma osmoalrity that stimulates opmore ephors to give thirst sensation TYPES : Nephrogenic ( inherited disorder, renal tubules don't respond to ADH cause poor water reabsorption by kidney ) Primary ( defect in hypothalamus/pituitary gland cause lack of ADH production/release) Drug related ( from lithium, and demeclocycline , interfere w/response to ADH LABS: low specific gravity ( <1.005), greater than 4 l urine in output ( 4-30L /day) S&S: dehydration, hypoTN, decrease pulse pressure, tachy, weak pulses, hemoconcentration ( increased H&H/BUN). increased urine output ( dilute low specific gravity) poor turgor, dry membranes, neurologic prob ( increased sensation, irritability, decreased LOC, hyperthermia, ataxia ) NI: early detection of dehydration, maintain hydration ( i&O, daily weight, urine specific gravity, increase fluids to match output ) permanent Di need life long Desmopressin/vasopressin therapy , meds can induce water retention cause fluid overload, water Tox ) MEDS: chlopropamide-Diabinese ( increase action of existing ADH, for partial defecit , stimulate production of ADH) Desmopressin acetate--DDAVP ( for severe ADH defecit, synthetic form of vasopressin PO or intranasal, SE of intranasal-- ulcer of membrane , allergy, , chest tightness, pulmonary inhalation

Hyperpitutarism WHAT: over secretion of hormones from pituitary tumors or hyperplasia( tissue overgrowth) TYPES : Prolactin Secretion( PRL)( most common, excessive amounts inhibit gonadotropins, sex hormones, cause glactorrhea, amenorrhea, infertility) Growth hormone (GH) ( result in gigantism/acromegaly that is gradual w/slow progression, changes in soft
tissue that can be reversible and skeletal changes that are Permanent, over secretion starts b4 puberty and after closure of the growth plates in bone during puberty causing rapid growth in length of bones and increased skeletal thickness , skin hypertrophy, enlargement of organs, bone thining/bone cell overgrowth occur slowly, degeneration of joint cartilage and hypertrophy of ligaments/vocal cords/eustachian tubes common, nerve intrapment from hyperplasia and myelin loss in peripheral nerves, GH blocks insulin causing hyperglycemia )

ACTH ( overproduction of gluco and mineralcorticoids cause Cushings) S&S of GH --- change in ring/hat/shoe size , fatigue lethargy, backache, arthralgias, HA, change in vision, increase lip/nose size, prominent brow ridge , increase in head/hand/feet, folding of scalp skin, coarse facial features, protrusion of lower jaw, deepening of voice, tufting of finer tips, sleep apnea, PRL--- difficult sex function, menstural irregularities, decreased libido, dyspareunia, impotence, increased body fat

NI: MEDS: bromocriptine (Parodel), cabergoline ( Dostinex), pergolide(Permax) (

dopamine agonis stimulate dopamine to inhibit release of pituitary hormones, decrease tumor size, used especially after surgery/radiation when hormone levels remain high, SE-- orth hypoTn, gastric irritation, n/abd cramps, constipation, cardiac Dysrhtymias , coronary artery spasms , CSF leakage, call dr if chest pain of watery nasal discharge, take med w/food , stop med if preggo)

octerotide ( SAndostatin)--

Somostatin analogue for acromegaly , GH receptor blocker, inhabit GH relase

from neg feedback , must be injected weekly , SE--gallbladder disease

radiation ( not useful in immediate acut management SE--hypopituatarism, optic nerve damage, vision probs Surgery--hypophysectomy--removal of pituitary gland and tumor PRE-- decrease hormone levels , relive HA, reverse sex dysfunction, body change/organ enlarg/visual change not reversible, must have nasal packing for 2-3 day post, must breathe thru mouth, mustache/drip pad must be worn under nose, do not brush teeth, cough, sneeze, blow nose, or bend froward b/c will open muscle graft , increase ICP, delay healing OP-- general anesthesia and in sitting position, gland removed and muscle graft taken to prevent CSF leakage, nasal packaging inserted and mustache dressing applied POST-- CK neuro status q1hr , change in vision, Chng mental staus/LOC, ck decreased muscle strengths ,Ck fluid balance Ck complications-- transient diabetes insipidus--output greater than input, CSF leak, infection, increased ICP;, oral rinse/lube jelly to lips, cough deep breathe, Ck for meningitis-HA,fever,nuchal rigidity, if removal occur lifelong Tx thyroid and glucocorticoid replacment is for life, prevent bowel straining--eat high fiber, increase fluidsstoolsoftner, No bending at waist b/c can increase ICp bend at knees, then lower body, Nubness and decreased sense smell normal for 3-4 month after surgery

COMPLICATION : CSF leak --Ck for halo sign--light yellow color at edge of clear dressing indicate CSF, report postnatal drip-could be CSF, elevate HOB, Ck nasal drainagepresence of glucose could indicate CSF, persist an sever HA my be CSF leak intonsinus area, , most leaks resolve w/bed rest, if leak persists may have spinal tap to decrease CSF pressure, coughing after surgery increase pressure at incision and lead to leak

Hypopituatrism WHAT: defecit in one or more anterior pituitary hormones causing metabolic and sexual dysfunction TYPES: Selective ( only 1hormone affected). panhypopiuitarism( defecit in all hormones ) CAUSED BY: pituitary tumors( compress and destroy pituitary tissue) Malnutrion/anorexia , Shock/severe HypoTn ( reduce BF to pituitary gland causing hypoxia and infarction) Head trauma/brain tumor and infection / radiation or surgery of head and neck /AIDS, Postpartum Hemorrhage ( most common cause of infarction caus edecreased
hormone secretion--Sheehans Syndrome-- glam usually inlarges and when HypoTn occurs from hemorrhage ischemia and necrosis of gland develop , usual happens immediately post surgey)

GH deficit: can occur form decreased production , fail of liver to produce somatomedins, fai, of cells to respond, defecit in kids cause short stature , growth retardation , defecit in adults cause osteoporosis , bone destructive activity, increase risk for fractures, decrease muscle strength , increase cholesterol levels

Gondatropin defecit: loss or change in secondary sex characteristics , ammenorhea, infertility, low estrogen levels, breast atrophy , loss bone density , decreased hair, TSH defecit: hypothyroidism -fat , cold intolerance , ACTH defecit: decrease cortisol. Pale, malaise/lethargy, Ha, hypoglycemia, HypoNa, decreased pubic hair ACH defecit: Diabetes Insipidus--increased output , low specific gravity <1.005, hypoVL, hypoTn, dehydration, increased thirst, LABS: injecting agents known to stimulate secretion of hormones then measuring response , insulin injection is supposed to increase GH and ACTH but w/decreased function levels remain unchanged NI: MEDS: Tetaoterone implacemt ( replace IM , start high cause increase dick, libido, muscle mass, bone size, bone strength, increased hair and deep voice, avoid w/prostate cancer may cause boobies, acne,mbaldness, prostate enlargement Estrogen replacment ( risk for HTn and thrombosis