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157 Cards in this Set
- Front
- Back
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When is ADH released |
-high osmolality
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ADH locations |
-released from hypothalamus -stored in posterior pituitary |
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what is released by the adrenal cortex |
-corticosteroids -mineralocorticoids -androgens |
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what is released by the adrenal medulla |
-END |
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Pancreas secretes: |
-insulin from beta cella -glucagon from alpha cells |
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glucose range: |
70-120 |
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glucagon |
-released when glucose levels are low -stimulates glycolysis and gluconeogenisis in liver |
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counterregulatory hormones: |
-epinephrine -glucagon -growth hormone -cortisol |
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growth hormone location and function |
-anterior pituitary gland -plays role in protein, fat, and carb metabolism |
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cortisol location and function |
-natural corticosteroid -adrenal cortex -promotes metabolism -increases glucose by stimulating hepatogluconeogenesis -inhibits protein synthesis -stimulates lipolysis |
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how much beta cell insulin production is present in DM 1 |
-10-20% |
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DM 2: 4 major metabolic abnormalities |
1. insulin resistance 2. pancreas loses ability to produce insulin as well 3. inappropriate glucose production from liver 4. alteration in production of hormones and adipokines |
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when is gestational diabetes detected |
24-28 weeks of gestation |
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when does gestational diabetes resolve |
6 weeks post partum |
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secondary diabetes causes: |
-cushings (cortisol) -hyperthyroidism (increases gluconeogenesis) -pancreatitis -parenteral nutrition (dextrose in solution) -cystic fibrosis -hemochromatosis (thyocemia major tranfusions) -thiazides, penytoin, atypical antipsychotics |
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prediabetes is characterized by: |
-impaired fasting glucose -impaired glucose tolerance |
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A1C |
AKA: glycosylated hemoglobin D: >6.5% PD: >5.7 |
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Fasting plasma glucose |
D: >126 PD: >100 -must have 2 positives |
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random glucose measurement: |
D: >200 + symptoms |
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2 hour oral glucose tolerance test |
D: >200 PD: >140 use 75 g of glucose |
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DKA |
-DM 1 -low insulin causes cell starvation -body starts to break down fat which releases ketones -causes metabolic acidosis and dehydration -glucose >250 -E imbalance is priority |
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DKA care (saline) |
-half normal saline .45% or .9% -once glucose is <200, D5 |
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HHS |
-DM 2 -life threatening -glucose >600 -increase in serum osmolality -can mimic stroke -requries greater fluid replacement than DKA due to more frequent voiding |
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DKA/HHA management: |
-accucheck every 1-2 hours -LOC ->30ml/hr urine output -cardiopulmonary status due to hypocalcemia -give bicarb is PH <7 |
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hypoglycemia CM |
-can mimic stroke or drunkness -confusion and irritability -weakness, tremors, and hunger -diaphoreses -visual disturbances -common in elderly and pts on beta blockers |
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Hypoglycemia treatment is alert: |
-15-20 g of simple carb -avoid fat food -recheck sugar in 15 min and repeat every 15 min until glucose is >70 -check glucose again 45 min after treatment |
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Hypoglycemia treatment if not alert |
-administer 1 mg of glucagon IM or subcut -ingest a complex carb acute care: 25-50 ml of 50% dextrose IV push |
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Cushing's causes |
-prolonged corticosteroid administration -ACTH secreting tumor -cortisol secreting neoplasm -excess secretion of ACTH from a malignant growth outside adrenals and pituitary |
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Cushing's CM: |
-hyperglycemia -hypokalemia -osteoporosis -HTN -anxiety or euphoria |
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treatment of cushings: pituitary tumor |
-transsphenoidal resection and/or radiation -stabilize glucose and BP preop -increase dietary protein preop -monitor fluid loss (clear can be cerebral) -runny nose is concerning -nasal packing for 2 days -minimize coughing and sneezing |
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treatment of cushings: adrenocortical tumor/hyperplasia |
-adrenalectomy or drug therapy -unilateral or bilateral (uni causes hormone imbalance and hypertrophy of opposite side) -may require steroid therapy post op -monitor F & E 24-48 hrs postop -mitotane, camaconsole, and antifungals for non surgical candidates |
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what drugs are used in treatment of cushing when pt is not a candidate for adrenolectomy |
-mitotane -comacanozole -antifungals |
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treatment of cushings: ACTH-secreting tumor |
-surgical removal or radiation -most common is lung and pancreatic cancer -complete pneumonectomy, lobectomy, wedge resection for lung cancer -pancreatectomy, whipple in pancreatic cancer |
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Cushings post op care |
-risk for hemorrhage in adrenolectomy -manipulation of glandular tissue may release hormones into circulation so monitor vitals -BP, F& E may be unstable due to hormone fluctuation -high doses of corticosteroids administered Iv during and several days after -avoid infection |
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Addisons disease |
-all 3 classes of corticosteroids are decreased |
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addisons disease causes |
-AIDS -Fungal infections (ketoconazole) -metastatic cancer -latrogenic (cushings treatment) -adrenalectomy |
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Addison's disease CM |
-progressive weakness and fatigue -weight loss (low sodium adn water) -skin hyperpigmentation (bronze) -hypotension, hyponatremia, hyperkalemia, hypoglycemia -N/V/D -not present until 90% of cortex is destroyed |
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Addisonian crisis |
-life threatening! -acute phase of adrenal insufficiency |
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addisonian crisis causes |
-stress -sudden withdrawl of steroids -pituitary gland destruction -after adrenal gland surgery |
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Adisonian crisis CM |
-hypotension & tachy -dehydration w/hyponatremia, hyperkalemia, and hypoglycemia -fever -weakness and confusion |
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addison's disease treatment |
-daily glucocorticoid replacement: 2/3 in morning, 1/3 in late afternoon -daily mineralocorticoid in the morning (fludrocortisone) |
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Addisons disease: assess the following frequently: |
-vitals, fluid volume deficit, E imbalance, daily weight |
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Adissons disease patient teaching |
-life long therapy -double dose with minor stress -triple dose for major stress -medic alert bracelet -100 mg IM hydrocortisone emergency kit |
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pheocromocytoma |
-rare -tumor of the adreanl gland produces excessive catecholamines (ENd) -results in severe hypertension -negative feedback fails |
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Catecholamines |
-released in trauma and blood loss to constrict vessels and increase BP and perfusion E: dilates pupils and increases HR and respirations |
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Pheocryomocytoma CM: |
-severe episodes of HTN -pounding headache -tachycardia -profuse sweating (catacholemine release) -anxiety -palpitations (tachy) |
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Pheocryomocytoma treatment: |
- surgical removal of tumor -sympathetic blockers preop (Orthostatic hypotn) to decrease catecholamine excess symptoms (minipress, cardura) -metyrosine to diminish catecholamine if no surg -monitor triad symptoms -emotional support |
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SIADH |
-too much ADH -occurs when ADH is released despite normal or low plasma osmolality |
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SIADH CM: |
-fluid retention -serum hypoosmolality -dilutional hyponatremia -concentrated urine w/normal or increased intravascular volume and normal renal function -GFR increase but water is being reabsorbed in loop of henle -low urine output -V/cramps/muscle twitching/seizure/confusion/HA |
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SIADH causes: |
-malignant tumor -CNS disorder (CVA, head injury) -drug therapy (tegretol, diabenese, opioids, thiazides, tricyclic antidepressants) |
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Which medications can cause SIADH |
-tegretol -diabenese -opioids -thiazides -tricyclic antidepressants |
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SIADH and head injury |
-watch urine I&O -ADH increased BP with can increase intracraneal pressure -dark urine is a sign |
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SIADH treatment |
-IV hypertonic solution, via pump slowly -Lasix for diuresis -800-1000 ml/day of fluid |
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SIADH nursing therapeutics: |
-assess v/s, I&O, s/s of hyponatremia (fluid status) and LOC (cerebral changes) -continuous cardiac assessment (increased work load on heart; CHF) -position bed <10 degrees -seizure precautions -hard candy to decrease thirst -supplemental sodium |
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Diabetes Insipidus |
-group of conditions associated with a deficiency of production or secretion of ADH or decreased renal response to ADH -increases urine output and plama osmolality |
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Diabetes insipidus Cm: |
-polydipsia and polyuria (5-20 L/day) -low specific gravity (highly diluted urine) -hyperosmolality of serum (water loss) -nocturia -weakness, wt loss, constipation -shock symptoms: (poor skin turgor, hypotension, tachycardia) -hypovolemic or cardiogenic shock |
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diabetes insipidus treatment: |
-maintain F&E balance -hormonal replacement (desmopressin acetate) -hypotonic saline IV -<3g sodium/day -drugs: pitressin, diapid, indocin, tegretol, diabenese |
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Drugs to treat diabetes insipidus |
-desmopressin acetate -pitressin -diapid -indocin -tegretol -diabenese |
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Diabetes nursing considerations and monitoring |
-adequate PO and IV hydration -monitor urine output for glucose (increases urine ouput and affects reabsorption in tubules) -I&O -daily weights |
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When is dialysis initiated? |
GFR <15 ml/min (creatinine clearance) |
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Why is glucose added to dialysate? |
-big enough not to pass through semipermeable membrane but will continue to attract water and pull it out of vasculature -solves fluid volume excess |
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Ultrafiltration |
-movement of fluid and solutes due to changes in pressure -increased in blood chamber -decreased in dialysate chamber -pushes ECF from blood into dialysate chamber |
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Inflow phase of pertioneal dialysis |
-10 min -2 L of dialysate infused and then tubing is clamped to avoid air entrance |
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Dwell phase of pertioneal dialysis |
-20-30 min -AKA equilibrium phase -diffusion and osmosis pushes dialysate past pertoneum and blood vessels -blood vessels around infusion area attract and enhance infusion |
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Drain phase of peritoneal dialysis |
-15-30 min -open clamp, and change pt position to drain -cloudy dialysate indicates infection! |
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complications of peritoneal dialysis |
-infection, peritonitis, abdominal pain, hernia -lower back problems due to pressure -bleeding and protein loss -pulmonary complication (distention) |
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AVFs |
-anastomosis between an artery and vein usualy in forearm -allows arterial blood flow into vein to strengthen it -takes 6 weeks - months to heal |
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AVGs |
-synthetic graft forms a bridge b/w arterial and venous blood supplies -2-4 weeks to heal -more likely than AVFs to become infected |
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complications of hemodialysis |
-hypotension (hang normal saline) -muscle cramps -blood loss -hepatitis -sepsis |
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Hep A prevention |
passive: -IG given 1-2 weeks after exposure for 6-8 weeks of immunity then booster 6-12 mos later active: -immunization and booster -0-1-6 mos |
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Hep B prevention |
Active: vaccination -Recombivax HB/Engerix @ 0-1-6 mos passive: -HGIB 24 hours post exposure then vaccine series |
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Preicteric phase of hepatitis |
-lasts 1-21 days -period of maximal infectivity |
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Icteric phase of hepatitis |
-lasts 2-4 weeks -jaudice -anorexia, N/D, HA, malaise, hepatomegdaly -itching, light colored stool, dark urine |
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Posticteric phase of hepatitis |
-lasts weeks to months (2-4 months) -jaundice and hepatomegdaly being to resolve |
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Fulminant hepatitis |
-complication of Heb B and D -severe impairment or necrosis of liver cells -can lead to liver failure and cirrhosis |
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Hepatitis Care and therapeutics |
-emphasis on rest and liver regeneration -high cal, protein, and carb, low fat, vitamin |
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Hepatitis medicines |
Antiviral agents: Interferon -reduces replication of virus -also is antiprolipherative for tumors & cirrhosis Adefovir dipivoxil (Hepsera) -slows progression of chronic HBV by interfering with virus replication |
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Jaundice therapy |
-monitor occurance -small, frequent feedings -avoid hot/cold foods -2500-3000 ml fluids per day |
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Pancreatic functions: |
Exocrine: digestive -enzymes release into duodenum to break down protein, fat, and starch Endocrine: -insulin (beta) and glucagon (alpha) |
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Grey Turner's Sign |
-pancreatitis -bruising on flanks |
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Cullen's sign |
-pancreatitis -bruising in periumbilical area |
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Acute pancreatitis CM: |
-decreased or absent bowel sounds (worry about paralytic ilius) -risk for hemorrhage -low grade fever and leukocytosis due to inflammation -possible jaundice -shock (hypotension, tachycardia) |
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Acute pancreatitis complications |
-pseudocyst -pancreatic abscess -plueral effusion, ARDS, pneumonia, atelectasis -hypotension -hypocalcemia: tetany |
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pseudocyst |
-pancreatitis -palpable epigastric mass w/N/V -usually resolves on its own -watch for peritonitis if it ruptures into duodenum -percutaneous catheter to drain |
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pancreatic abscess |
-abdominal mass -leukocytosis and high fever -prompt surgical drain to prevent sepsis |
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Hyocalcemia: tetany |
-pancreatitis -due to calcium binding to necrotic tissue -watch for muscle contractions/twitching, numbness and tingling around lips and fingers -Chvostek's sign (facial twitching) -Trousseous sign (BP cuff and hand contraction) |
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Acute Pancreatitis Care: |
-pain releif -prevent or alleviate shock (F&E) -rest to prevent pancreatic secretion -prevent and treat infection |
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Pain relief for acute pancreatitis |
-IV morphine -antispasmodics (dicyclomine C/I: Para ilius) -carbonic anhydrase inhibitors (diamox Scitozolamide to decrease secretions) -antacids -PPI (decrease HCl) -fetal position or head at 45 degrees |
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Reduction of pancreatic secretions: |
-NPO, NG suction -enteral nutrition after pancreatitis gets better -then small, frequent high carb and low fat meals -supplemental vitamins |
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Correction of F&E imbalance in acute pancreatitis |
-aggressive hydration (lactated ringers: isotonic) -monitor for hypocalcemia and hypomagnesemia -possible metabolic acidosis (give O2 and check glucose) |
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Preventing/treating shock in acute pancreatitis |
-due to hypovolemia -tranellemburg position (feet up, head down) -plasma or plasma volume expanders (dextran or albumin) |
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Acute Cholecystitis |
-sudden onset -pain >1 hr -95% have gallstones |
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Chronic cholecystitis |
-repeated attacks of pain when stones block cystic duct -causes scarring and thickening of gallbladder wall |
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Acalculous cholecystitis |
-rare (5-10%) with high mortality rate -older and critically ill pts -bile stasis causes it |
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Cholelithiasis CM |
-severe to no symptoms -pain <1 hr -spasms -tachycardia and diaphoresis |
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Total obstruction |
-stone obstructs bile duct and impedes flow from pancreas and bile from galbladder |
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Total obstruction CM: |
-obstructive jaundice and pruritis -dark amber urine -clay-colored stool and steatorrhea -fatty food intolerance -bleeding tendency (vit K deficiency) |
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Acute Cholecystitis CM |
-Murphy's sign -indigestion, pain, and tenderness in RUQ - scapula -N/V, restlessness, diaphoresis, and tachycardia -abdominal rigidity -leukocytosis, |
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Chronic cholecystitis CM |
-hx of fat intolerance -flatulence -dyspepsia -heartburn |
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Cholecystitis complications |
-gangrenous cholecystitis -subphrenic abscess -pancreatitis -cholangitis -biliary cirrhosis -fistula -rupture choledocholithiasis |
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subphrenic abscess |
-cholecystitis complication -infection of fluid between the diaphragm and liver -associated with peritonitis |
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fistula in cholecystitis |
-abnormal connection between gall bladder and portion of the gut |
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Main diagnostic study for cholecystitis |
-US |
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Cholecystitis diagnostic studies
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-UC -ERCP -percutaneous transhepatic cholangiography (PTC) |
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ERCP |
-endoscopic retrograde cholangiopancreatography -combines endoscopy and flouroscopy -IV meds to relax, Spray for gagging, mouth gaurd -2-3 hours long -can remove stone during |
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PTHC |
Percutaneous transhepatic cholangiography -radiologic technique that injects dye into bile duct |
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Cholecystitis drug therapy |
-pain management -antispasmodics (anticholinergics) -fat soluble vitamins -bile salts |
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Transhepatic biliary catheter |
-surgical procedure for cholecystitis -catheter is inserted into bile duct to relive obstruction |
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How much weight gain in what time is too much? |
more than 2kg/day or 5 lbs/week |
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Urine studies |
-urinalysis -creatinine clearance -culture and sensitivity |
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Urinalysis |
-first morning void is more concentrated -examine within 1 hour |
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creatinine clearance |
-24 hour urine sample -discard first void and save last -clean pt first |
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urine culture and sensitivity |
-clean catch/midstream |
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Renal blood studies |
-BUN -Creatinine -BUN/Creatinine ratio -Electrolytes |
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Blood electrolyte levels in kidney disease |
-too much water = dilutional hyponatremia -hypokalmia or hyperkalemia -hypocalcemia and hyperphosphatemia -low bicarb |
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Radiologic procedures and imaging studies for renal system |
-Kidneys, ureters, bladder (KUB) -Intravenous pyelogram (IVP) -renal US and CT -renal arteriogram -renal biopsy |
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IVP |
-Intravenous pyelogram -injects dye and takes an xray to look at shape of kidneys and ureters -cautious use in kidney impairment (dye) -acetylcystine may be given before |
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Renal arteriogram |
-similar to cardiac cath -monitor vitals, bleeding, and pedal pulses |
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renal biopsy |
-bedrest 24 hours -may have flank pain, hypotension -check vitals and for hemorrhage -avoid heavy lifting 5-7 days post biopsy |
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UTI CM: |
-dysuria, urgency/frequency, and hematuria -suprapubic discomfort -cloudy urine -flank pain and chill/fever in upper UTI older adults: cognitive impairment and decrease in other symptoms |
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Uncomplicated UTI ABT |
-1-3 days -bactrim |
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Complicated UTI ABT |
-cipro or floxacin -7-14 days |
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Upper UTI ABT |
-14-21 days |
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Phenazopyridin |
Pyridium -urinary analgesic -may cause orange urine -long term can cause hemolytic anemia |
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Pyelonephritis w/fever meds |
-NSAIDs and Antipyretics |
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Acute poststreptococcal glomerulonephritis |
-7-21 days after infection of skin or throat -antigen complexes attack glomeruli - |
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Glomerulonephritis CM: |
-hematuria and proteinuria -WBC in urine -Elevated BUN and creatinine |
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Acute poststreptococcal glomerulonephritis CM: |
-generalized body edema (Na and H2O retention) -HTN (aldosterone) -oliguria and hematuria -abdominal or flank pain |
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Glomerulonephritis treatment: |
-rest -Low protein diet (if problem with protein urea) -antiHTN and diuretics -watch for hyperkalemia in ace inhibitors -watch for hypokalemia or hyperkalemia in diuretics |
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Nephrolithiasis risk factors |
-increased calcium in urine -warm climate (dehydration) -large intake of dietary protein -sedentary occupation/immobility -increased juice/tea intake -family hx of sones/gout |
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Nephrolithiasis CM: |
-abdominal and flank pain -hematuria -N/V and midle shock with cool moist skin (pain) -S/S of UTI |
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Nephrolithiasis diagnostic studies |
-Urinalysis -IVP -US -cystoscopy -BUN/serum creatinine |
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ESWL |
-Extracorporial shock wave lithotripsy -admits strong sound waves to break up kidney stone -pts will recieve general anesthetic |
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Percutaneous ultrasonic lithotripsy |
-small incision and percutaneous insertion of catheter for kidney stones -not too common |
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urinary diversions |
-ileal conduit -ureterostomy -nephrostomy |
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ileal conduits |
continent: pt self-catheterize every 4-6 hrs incontinent: urine continuously flows -mucous from irritation |
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Ureterostomy |
-ureter is brought through the abdominal wall and stoma is created -may need to catheterize to remain open |
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nephrostomy |
-catheter is inserted in renal pelvis and brought out to drain bag -temp or perm -uni or bi -ct or radiology for insertion -cath change every month |
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Prerenal failure causes |
-hypovolemia -decreased CO -decreased peripheral vascular resistance -decreased renovascular blood flow |
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hypovolemia and prerenal failure |
-commonly burns -fluid shifts and decreases BP, O2, and blood volume to nephron |
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Decreased peripheral vascular resistance in prerenal faillure |
-renal arterioles constict -decreased preload caused decreased CO -as peripheral resists, O2 is decreased to kidneys -dehydration is a cause |
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Decreased renovascular blood flow and prerenal failure |
-perfusion is decreased -decreases O2 supply to kidney tissues |
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Intrarenal failure causes |
-glomerulonephritis -prolonged ischemia -nephrotoxins -hemogobin from hemolyzed RBC -myoglobin from necrotic muscle cells -primary renal disease -thrombotic disorders and toxemia of pregnancy |
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Nephrotoxins in intrarenal failure |
-ex: ABT Gentomycin -causes crystal formation -ex: IV contrast |
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post renal failure causes |
-BPH -prostatic CA -calculi -trauma -extrarenal tumor |
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BPH in postrenal fialure |
-noncancerous enlarged obstructs fluid -urine backs up and causes hydronephrosis |
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Oliguric phase CM of ARF |
-oliguria and urinary changes -fluid volume excess (increased hydrostatic pressure causing reabsorption of filtrate) -metabolic acidosis (excess urea) -Na/K/Ca/P excess (HTN, arrhythmia, CHF) -hematologic disorders (decreased erythoro) -waste product accumulation -neurologic disorders (due to waste products) |
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Diuretic phase of ARF |
-increased urine output to 1-5 L/day -caused by osmotic diuresis due to increased urea in flitrate and innability to concentrate urine |
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recovery phase of ARF |
-filtration is reestablished -GFR increases -BUN and creatinine decrease |
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Cardiovascular CM of ARF |
-HTN & CHF (fluid overload) -atherosclerosis (hypercalcemia) -pericarditis (urea lodges in heart) -arrhythmia (hyperkalemia and Ca levels; tall peaked T wave) |
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Pulmonary CM of ARF |
-uretic lung (uretic crystals lodge in lung;mucus) -pulmonary edema (fluid retention) -uremic pleuritis -urine breath -pneumonia (mucus) -dyspnea and kousmall respirations (metabolic acidosis compensation) |
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Occular CM of ARF |
-hypertensive retinopathy -red eyes (uremic crystals and calcium deposits irritate eye) |
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Integumentary CM of ARF |
-pruritis & uremic frost -pigmentation changes (yellow-grey) -brittle, dry, scaly skin hair and nails -petechiae and ecchymosis (bluish) |
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Musculoskeletal CM of ARF |
-risk for fracture (hypocalcemia s/t vit d def) -osteomalacia (lack of mineralization from vit d def) |
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Nuerologic/psychological CM of ARF |
-poor concentration -fatigue -behavioral changes -emotional withdrawal and depression |
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GI CM of ARF |
-constant abdominal pain w/poss ulceration -stomatitis (crystalization) -metalic taste (waste products) -decreased appetite/malnutrition/anorexia -N/V -diarrhea (hyperkalemia) |
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ARF Collaborative care (including nutritional therapy) |
goal: preserve, treat CM, prevent complications, provide comfort -protein restriction with sufficient cals from carbs and fat -water restriction -sodium and potassium restriction |
