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64 Cards in this Set

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Cause of Parkinson's Dz
Loss of dopamine, degenerative changes in substantia nigra (makes dop). Severe shortage of dop vs. Ach. Most common in white males
Meds for Parkinson's dz
L-dopa, Sinemet (levadopa and carbidopa), Dop-agonists, anticholinergics, COMT inhibitors
Osteoarthritis (idiopathic and secondary)
Idiopathic: women, 65+, genetic trait
Secondary: more prevalent in men, results from trauma, wear and tear.
Characteristics of Osteoarthritis
Chronic degenerative cond. in which cartilage degenerates and new bone forms. Becomes fibrotic w/ limited movt. Ls, CS, proximal, and distal jts. of hands. Pain and stiffness relieved by rest
Mgt. of osteoarthritis
Palliative. NSAIDs first line, then COX-2 inhibitors. Moderation is key. ROM, water aerobics, parafin dip, firm mattress.
Nursing mgt. after THR
*keep in place to prevent popping out.
drains (no more than 200 cc in 8 hr), HOB <70 degrees, don't cross legs, bend at waist, use high toilet seat for 6-8 wks.
Rheumatoid arthritis char.
Systemic,autoimmune, women more than men, exacerbations and remissions, WBCs move into synovium, causes thick secretion, both sides at same time.
Medical mgt. of RA
Pain and inflammation relief, maintain or restore jt. function, control systemic involvement.
Fasting Blood Glucose levels
>126 Diabetes
110-126 Pre-diabetes
<110 Normal
Oral glucose tolerance test levels
>200 Diabetes
140-200 Pre-diabetes
<140 Normal
Steroids effects on [glu]
Increases
A1C levels
Measures BG over last 3 mos. Normal <6, Goal <7 ([glu]<150)
Insulin that is administered IV
Regular (short acting)
Somogyi Effect
Hypoglycemia at night w/ rebound hyperglycemia in AM. Caused by excessive insulin at night. Monitor BG b/w 2-4 am and at 7 am
Dawn Phenomenon
Rise in early morning BS (b/w 4-8 AM), caused by nocturnal elevation of GH or incr. insulin clearance. Increase insulin dose
Hyperglycemia symptoms
Hot, dry, GI (thirst, polyurea, dry skin, flushed, hunger, blurred vision, drowsiness)
Hypoglycemia symptoms
Cold, wet, CNS
Tx of DKA
Rehydration, insulin, K replacement, monitor BS
HHNKS S/S
hyperosmolar hyperglycemia nonketotic syndrome. S/S: similar to DKA except BS >600, ketones absent, no Kussmaul
Causes of goiter
Lack of iodine, inflammation or tumor.
Dx and Tx of goiter
Dx: palpate, T3, T4, and TSH normal
Tx: iodine replacement, TH, surgery for dyspnea, resp. support
Myxedema symptoms
End stage of uncorrected hypothyroidism, life-threatening. Caused by stress. Char: dry, waxy swelling w/ abnormal deposits of mucin around eyes, women in 60s, Tx w/ TH
Graves dz char. and clinical manifestations
Char: hyperthyroidism, goiter, exopthalmos. Autoimmune.
Manifestations: incr. metabolism, incr. sensitivity to stimulation by SNS
Thyroid storm char.
thyrotoxicosis, caused by stress. Severe hyperthyroidism, severe tachycardia, heart failure, shock, hyperthermia, n/v, febrile
Thyroid storm tx
Fever reduction, fluid replacement, elemination or mgt. of stressor, reduce TH
Thyroid ablation
Renders thyroid useless, use radioactive iodine
Post-op mgt. for thyroid surgery
Ca gluconate at bedside to mamage tetany
Tests for tetany
Chvostek's sign-twitching of facial muscles after tapping nerve in front of ear
Trousseau's sign-carpal spasms when arm compressed
Parathyroid function
Manage Ca levels (8-11 mg/dL)
Hyperparathyroidism manifestations
Stones: r/t decreased volume
Bones: osteoporosis, joint and bone pain, fractures
Moans: fatigue, weakness, memory loss
Groans: constipation, n/v, indigestion

Plyuria leads to polydipsia
*Too much PTH
Tx of hyperparathyroidism
Hydration w/ NS, Lasix (Ca release in urine), glucocorticoids (prevent Ca absorption in GI), cranberry juice to prevent stones, 3L fluid qd,
Hypoparathyroidism
Abnormally low Ca, too little PTH, can be Iatrogenic (acute, caused by tx) or Idiopathic (chronic autoimmune disorder)
Clinical manifestations of hypoparathyroidism
Positive chosteks and trousseau's signs, hyperactive deep tendon reflexes, numbness and tingling of fingers, mouth, and eyes.
Addison's dz
Hypofuncion of adrenal gland caused by abnormal function of adrenal cortex or long-term use of glucocorticoids. Slow onset w/ mild symptoms of weakness, ortho. hypotn, weight loss, axillary and pubic hair loss
Hallmarks of Addison's dz
Hypoglycemia, hyponatremia, hypovolemia, hypotension, hyperkalemia, hyperpigmentation
Tx of Addison's dz
Replace steroids, f/e replacement, 5 S's (Salt, sugar, steroids, support, search for cause)
Cushing's syndrome causes
Too much cortisol: prolonged use of corticosteroids,ACTH secreting pituitary tumor, Cortisol secreting neoplasm in adrenal cotex
Char. of Cushing's syndrome
Abdominal obesity w/ very thin arms (wasting of extremeties), moon shaped face, fat pad on back (buffalo hump), excessive facial hair
Tx of Cushing's
Discontinuation of steroid admin., surgical removal of tumor, radiation on inoperable tumors
SIADH clinical manif.
Too much ADH->excess fluid volume, hyponatremia, anorexia, n/v, tachycardia,
DI clinical manif. and tx
Too little ADH, 5-20 L urine output qd
Tx: surgery for pituitary tumor, meds (ADH replacement), IV fluids
Brain changes w/ Alzheimer's
Senile plaques, nerofibrillary tangles, enlarged ventricles, generalized atrophy
Stages of AD
Stage 1: (1-3 yrs) memory disturbances
Stage 2: (2-10 yrs) Palilalia and echolalia, motor disturbances (apraxia, pacing, wandering)
Stage 3: (8-12 yrs) All mental and speech abilities lost
Dementia vs. Delerium
Dementia-irreversible, slow onset, MMSE <20
Delirium-reversible, rapid onset, medication related, infection
Meds for AD
AChE inhibitors: memory
Vit. E and Selegiline
Ginkgo biloba
Anxyiolytics
Haldol
Antidepressants
NO CURE, JUST DELAY PROGRESSION
Hepatitis transmitted via fecal-oral route
A,E, and F
Hepatitis transmitted via blood
B, C, D, G
Prodromal stage of hepatitis virus
Highly transmissible, 1-5 days before onset of clinical stage. lethargy, irritability, myaligia, arthralgia, anorexia, n/v, abd pain, diarrhea, fever
Clinical stage of hepatitis
1-2 wks after prodromal stage, phase of actual illness, aka icteric stage, itching, indigestion, jaundice (can last up to two weeks), abd. pain, anorexia,
Recovery stage of hepatitis
bigins w/ resolution of jaundice, contiued fatigue, flatulence, abd. pain
Medical mgt. of hepatitis
Rest, antihistamines to relieve itching, emooients and lipid creams, maintain nutrition and fluid balance, vit. K for elevated PT, avoid hepatotoxic drugs (tylenol), get most nutrients early in day
These heps have a vaccine
HAV and HBV
Fulminant hepatitis
Rare, B,D, and E, massive hpatic necrosis, jaundice, encephalopathy, and ascites, mortality rate reaches 90%
Chronic hepatitis
liver inflamed longer than 3-6 mos, three types (B, C, and autoimmune), mainly occurs in males
Cirrhosis of the liver
Chornic, progressive, fibrosis (scarring) and nodule formation. Collapse of reticulin network, distortion of vascular bed
Risk factors for cirrhosis
Excessive ETOH, viral hepatitis (postnecrotic cirrhosis), use of drugs, hepatic congestion, ingesting same toxin daily
Causes of ascites
Portal htn, lowered plasma osmotic pressure, Na retention, cor pulmonale, plasma leaks from congested protal capsule into abd.
Mgt. of ascites
Correct f/e imbalance, paracentesis, administer albumin and diuretics, diet modifications (low Na, fluid restrictions), effective breathing patterns, maintain skin integrity
Hepatic encephalopathy
Severe liver dz, liver's inability to metabolize ammonia to form urea, NH3 a CNS depressant (from GI and kidneys when decr. K)
Manif. of hepatic encephalopathy and tx
Neurologic (mild confusion to deep coma), liver flap (asterixis)
Tx: demodialysis, neomycin (dec. NH3), induce osmotic diarrhea, laxative, low protein diet
Melena
Black, tarry stool passed w/ GI bleed
Manifestations of GI perforation
Abd. hard and tender, diminished bowel sounds
Ulcerative colitis s/s
Inflammation, ulcers BLEED and produce pus, thickening of colon, congestion, edema, absesses->necrotic, bleed. Abd. pain, bloody diarrhea, weight loss, anorexia, becomes more severe as dz progresses,
Crohn's dz manifestations
Inflammation of segments of GI tract, no bleeding, cobblestone appearance, stricture development, blockage of intestine, steatorrhea (smelly b/c not reabsorbing fats and bile salts), incr. WBC