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Most abundant TRACE mineral-used in synthesis of hemoglobin, myoglobin and enzyme iron |
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2nd most abundant trace mineral. important in protein metabolism and synthesis, in nucleic acid metabolism, and in stabilization of cell membranes. functions as a cofactor for more than 200 enzymes and is essential to numerous cellular metabolic functions. |
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Low amounts in breastmilk. Need to determine water content before supplementing. |
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Most abundant MAJOR mineral. Makes up 99% of skeleton. Half of bone mineral accretion occurs during adolescence. |
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seiZure, hyperacusis, microcytic anemia, neuropathy |
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alopecia, dermatitis (skin/tin) |
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MEGAloblastic anemia, neuropathy, and big bad things |
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not Able to drive at night |
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30-40% of body weight, Potassium, Proteins, organic anions, phosphate |
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20-25% body weight, sodium, chloride |
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ECF: Plasma Volume effected by... |
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age, dehydration, anemia, polycythemia, heart failure, decreased plasma albumin, abnormal plasma osmolality |
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ECF: Interstitial Fluid altered by... |
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(Every Prostitute Loves Nookie) Edema Protein-losing enteropathy Liver failure Nephrotic syndrome |
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Main EXTRAcellular cation & is restricted to ECF. Adequate amounts needed to maintain intravascular volume |
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Renin is released when there is... |
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-decreased perfusion of kidneys -decreased delivery of sodium to distal nephron -increased beta 1 adrenergic agonists |
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-provides 20% of caloric needs -quantity sufficient to prevent ketoacidosis and breakdown of protein |
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-Serum Sodium <135 mEq/L -diarrhea & consume a hypotonic fluid (H2O) -Volume depletion stimulates secretion of ADH, preventing water excretion -correct at 12mEq/L over 24 hr |
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Hypernatremic dehydration |
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-Serum Sodium >150 mEq/L -irritable & lethargic, fever, hypertonicity, hyperreflexia -Correct at 1/2 mEq/L per hour |
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TPN-total parenteral nutrition |
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Short bowel syndrom is the most common indication for long-term. May be caused by a congenital gastrointestinal anomaly or acquired after necrotizing enterocolitis |
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-Sepsis -Electrolyte abnormalities -Hyperglycemia -Azotemia -CHRONIC: liver disease, cirrhosis, and liver failure, requiring liver/small bowel transplant |
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Congenital Hypothyroidism |
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-1/400 -caused by dysgenisis of thyroid -picked up on newborn screening |
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-Counteracts PTH -decreases serum calcium -increases calcium deposition in the bone, and decreases calcium absorption |
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-secreted from parathyroid gland if calcium is decreased -mobilizes calcium from bone, and increases calcium absorption from the kidney -increased serum calcium stimulates vit D. secretion |
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-ionized calcium <4.5 or total calcium <8.5 -neuromuscular irritability; muscle cramps, spasms, and weakness; parethesis; seizure like activity |
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hypocalcemia-palpation of facial nerve results in spasm of ipsilateral cheek |
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hypocalcemia-BP cuff 3 to 5 mins carpal spasm |
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causes decreased calcium but DOES NOT cause rickets |
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causes of hypoparathyroidism |
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-congenital malformations -surgical procedures -autoimmune |
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-secrete PTH, but is inactive -have decreased serum calcium but elevated serum phosphate -Albright (autosomal dominant form of this disorder) |
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-decreased bone mineralization in children -symptoms include poor linear growth, bowing of legs, painful weight bearing, and rachitic rosary |
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Hormones produced by adrenal glands |
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-mineralocorticoid aldosterone -cortisol -sex steroids |
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secondary adrenal insufficiency |
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CRH or ACTH deficiency (corticotropin-releasing hormone or adrenocorticotropic hormone) |
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Most common form of congenital adrenal hyperplasia |
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-1/12000 white children -impairs production of 17-OH progesterone to cortisol -get increase ACTH, which than stimulates other sex hormones -causes virilization of external female genitalia |
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-in females can range from labiosacral folds to clitromegally or phallus -male infants usually have normal external genitalia -75% of pts have aldosterone deficiency |
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biochemical changes seen in congenital adrenal hyperplasia |
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-elevated serum 17-OH progesterone -decreased serum cortisol and aldosterone levels -elevated testosterone levels |
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-virilization, salt retention & hypokalemia -get buildup of deoxycorticosterone, which is a potent mineralocorticoid |
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-destruction of adrenal cortex -primary adrenal insufficiency -lack of glucocorticoids & mineralocorticoids |
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-hyperpigmentation -salt craving -hypotension -fasting hypoglycemia |
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Treatment for Addison's disease |
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replacement with hydrocortisone |
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-usually the result of exogenous glucocorticoid administration -can have endogenous increase in glucocorticoids from adrenal adenoma, carcinoma, or adrenal hyperplasia |
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