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scc med/surg 2

s/s of rapid hypoglycemia tachy, tremors, diaphoretic, dilated pupils, pale, clammy
s/s of prolonged hypoglycemia  restlessness, difficulty thinking, trouble speaking, visual disturbances, paresthesia change in LOC, convulsions
BS levels for mild, moderate, severe hypoglycemia < 70 mg/dL -Mild <55mg/dL -Moderate <40mg/dL-Severe
Sz precautions- suction device, padded side rails, oral airway, o2 use, anything that could harm or strangle
HgA1c norm <5% /7% in DM
differnece between DKA & HHS HHS-hyperosmolality 350, DM2,older adults,slow Insidious Onset, HYPERNATREMIA, BS >1000, incr glucose production DKA- DM1,young,quick onset, ketones formed, aidosis, kussmaul respirations, HYPERKALEMIA fruity breath,330 osmolality,BS avg.675
comparison of DKA & HHS Insulin deficiency in production & reaction; dehydration, hyperglycemia, osmotic diuresis, fluid volume deficit, electrolyte imbalance, tachy, hypotension
DKA & HHS interventions 1.montior respiratory status 2.Redhydrate (bolus hypertonic) 3. establish K+ levels 4. administer insulin (bolus; then insulin drip)
normal plasma osmolality 275-295 ml osmol/kg
ADH effects vasoconstriction distal & collecting tubules reabsorb water
Diabetes Insipidus neurogenic patho trauma to pos. pituitary or hypothalamus from surgery/trauma; more common pituitary can’t release ADH ↓ release ADH → free H2O loss Low urine osmolality w/ hi serum osmolality (r/t hypernatremia), decr in urine specific gravity 4-40 L/24hrs Sudden
Diabetes Insipidus nephrogenic patho adequate ADH but kidneys not responding to it (or extreme H20 intake/2ndary DI) impaired renal conservation collecting ducts & distal tubules unresponsive to ADH slow onset HYPOKALEMIA/HYPERCALCEMIA
s/s DI XS poliuria>3L/24hr sometime 4-6L s/s if awake-polydipsia/if unconscious signs of hypovolemia- tachy, hypotension, dry mucous, wt loss
DI labs Low urine osmolality < 100 mOsm/kg H20 w/High serum osmolality > 295 mOsm/kg H20 Decr. urine specific gravity < 1.005 Elevated serum Na+ > 145 mEq/L Decreased plasma volume (xs urine low BP)
DI interventions Volume replacement r/t hypovolemia I & O, wt. Q Day VS Qhr monitor Hemodynamics, urine Sp. Gr., Neuro's Hypotonic D5W or isotonic NS Hormone replacement Exogenous ADH- help kidneys reserve water Desmopressin- most common- then Monitor for fluid xs
SIADH Patho Too much ADH; Problem of stimulation of hypothalamic/pituitary system or both malignant &,Non malignant,CNS disorders,Meds Secretion of adh unrelated to plasma volume feedback system not working properly
S/S SIADH s/s of H2O intoxication CNS - ICP, Weak, confused, Sz, coma GI- decr motility r/t low Na, n/v anorexia, muscle cramps Cardio -pulm artery & central venous pressure incr , wt gain, incr BP Resp - s/s fluid overload, advent lung sounds, pink frothy sput
labs for SIADH hynatremia, hypo-osmolality, hi urine Na+, hemodilution
Adrenal gland medulla- where?, releases?affects? inner layer-secretes cathecomline-epihephrine, norepinephrin, dopamine- incr metabolic rate,incr. insulin levels,fight/flight
Adrena gland cortex- where?, releases?, affects? outer-glucocorticoids-CORTISOL-help w/stress, suprress inflammation, incr BS, regulate metabolism of carbs, fats, protein, synthesis protein; ALDOSTERONE- Na & h20 retention; MINERALCORTICOIDS- K+ retention/excretion; ANDROGENS- growth & development
Addisons Disease patho Decr corticosteroids/ dysfunction in hypothalamus or adrenal gland LOW CORTISOL L/T hypoglycemia LOW ALDOSTERONE L/T low blood volume Decr K+ excretion (hyperkalemia) Reabsorption of hydrogen ions acidosis Incr Na+ and H2O excretion (hyponatremia)
Addisons cause Primary-idiopathic Secondary- abrupt steroid stop
s/s Addisons Disease confusion, fatigue, hi K+, Hi BS, muscle spasms, hypotension, hyperpigmentation, hyponatremia, GI imbalance, wt loss, hypovolemia
Addisons Disease Tx fluid balance Freq check wts, vs I&O’s,dysrhythmia labs- Na+, K+,pH (acidosis) Cortisol, aldosterone,Mineralocorticoid replace Meds-Solucortex,flucortisol, hydrocortisone h2 blockers/ K+ d5ns / diet restrict (k+)/ ECG/ IV glucose(hypoglycemia)/ fre
Cushing’s Disease patho Produce too much steroids- xs secretion of cortisol/glucocorticoids from adrenal Altered nitrogen, mineral,fat metabolism redustributed fat decr in muscle mass D/T tissue protein breakdown hi BS liver stimulated to make glucose & insulin receptors de
Cushing's Disease cause Primary-D/T adrenal or pituitary tumor Secondary- (little release of ACTH) Disorders of the pituitary or hypothalamus Iatrogenic- (most common cause) Long-term steroid therapy, xs cortisol levels
Cushing’s Disease s/s buffalo hump, moon face, decr muscle mass, capillary bleeding, decr bone density at risk for fx, high BS,acne, lenugo, hypervolemia, edema, incr hr/BP r/t cardiac hypertrophy, trunkal obesity, emotional
Cushings Disease LAbs Na incr, K+ decr, BS norm - incr, Ca decr, bicarb decr, BUN norm
Addison's Labs Na decr,K+ incr, BS norm-decr, Ca incr, Bicarb incr, BUN incr
Pheochromocytoma patho, causes Catecholamine-producing tumor on adrenal gland tumors store & release epi & norepi causes-=Triclycic, theophylizine, aged cheese , red wine
Pheochromocytoma s/s recurrent episodes w/ severe super HA, diaphoertic, flushed, htn, angina, gi symptoms, n/v, cramping, heat intolerance, wt loss, tremors, easily go into htn crisis
Pheochromocytoma diagnosis/ treatment Test 24 hr urine to measure catecholimines;Lab and radiography-ct or MRI- to confirm tumor Surgery Monitor BP Hydration and diet
Chronic Renal Failure patho Insidious, progressive, irreversible destruction of kidneys Continues until nephrons are replaced with scar tissue Abnormal urine production hyperosmole Electrolyte /Metabolic abnormalities Isothenuria ↑ BUN and ↓urine output/Risk for fluid overload
Chronic Renal Failure cause infection dm, htn, kidney damage/trauma
Chronic Renal Failure stages At risk => 90 ml/min Mild CKD =60-89 ml/min Moderate CKD=30-59 ml/min Severe CDK=15-29 ml/min ESKD=< 15 ml/min
Chronic Renal Failure s/s Hypertension Hyperlipidemia Health failure Pericarditis Anemia Halitosis and stomatitis Anorexia, n/v from uremia Peptic ulcer disease
Peritonitis types Primary peritonitis-Common with cirrhosis Secondary peritonitis-Surgical peritonitis, gastric/intestinal ruptures appendix, perforated peptic ulcers, IBD
Peritonitis patho Inflammatory response L/t massive fluid shifts (peritoneal edema) & adhesions as the body attempts to wall off the infection; hypovolemia-> shock
peritonitis s/s acute severe distress pain, sudden onset, rebound tenderness, muscular rigidity, guarding, spasm, restlessness, n/v, anorexia, fever, altered bowel habits
Created by: cbohannan