N444: Test 3

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N444: Test 3 by Mind Map: N444: Test 3

1. hypertension

1.1. demographics

1.1.1. 50 million Americans affected 28-31% of adults 90-95% have primary more common in SE USA and african-americans

1.1.2. onset b/w ages 20 and 50

1.1.3. two types primary (95%) secondary

1.1.4. most common cause of heart failure

1.1.5. associated with other problems arteriosclerosis (hardening of muscles, endothelium): small atherosclerosis (accumulations in intima): medium/large

1.2. pathophysiology

1.2.1. causes increased force to be exerted on vascular walls

1.2.2. vessel damage, plaque buildup, lipid infiltration, and calcium accumulation

1.2.3. also causes strain on left ventricle

1.3. characteristics

1.3.1. +140/+90 mmHg

1.3.2. "silent killer" asymptomatic until organ damage damages target organs heart eyes brain kidneys

1.3.3. very damaging heart failure myocardial infarction stroke a-fib aortic dissection peripheral artery disease

1.3.4. algorithm to predict IHD mortality Baseline 115/75 Each 20/10 increase = 2x risk

1.3.5. multifactorial condition increased SNS increased renal NaCl/water reabsorption increased RAA activity decreased vasodilation insulin resistance

1.3.6. remember: catapres

1.4. risk factors

1.4.1. smoking

1.4.2. obesity

1.4.3. sedentary

1.4.4. dyslipidemia

1.4.5. DM

1.4.6. microalbuminuria

1.4.7. gfr <60

1.4.8. older age

1.4.9. family history

1.5. management

1.5.1. assessment history and physical labs/diagnostics urinalysis blood chems cholesterol 12-lead ecg

1.5.2. treatment ideal bp ranges <140/<90 (standard) <130/<80 (CKD/DM) lifestyle modification weight loss reduce alcohol reduce sodium regular activity DASH diet medications thiazides (initial) additional PRN meds may be combo therapy must maintain lifestyle modification

1.6. nursing process

1.6.1. assessment history risk factors s/s target organ damage pertinent social/financial factors

1.6.2. treatment goals understanding process understanding treatment plan participation in self-care no complications

1.6.3. interventions education support adherence consultation/collab follow-up control > care lifestyle changes lifelong process

1.6.4. gerontological care noncompliance family role understanding therapy reading instructions monotherapy

1.7. complications

1.7.1. emergency BP >180/120 Must be lowered immediately Risk for target organ damage treatment goals reduce by 25% during first hour reduce to 160/100 over 6 hours gradual reduction to normal over days exceptions to standard ischemic stroke aortic dissection treated with IV vasodilators sodium nitroprusside nicardipine fenodopam mesylate enalprilat nitroglycerin frequent BP/CV monitoring

1.7.2. urgency BP = very high No evidence of immediate/progressive damage treatment close BP/CV monitoring assess for potential damage medications: fast-acting and PO

2. gi disorders

2.1. lab tests

2.1.1. blood cbc electrolytes cea levels

2.1.2. stool ova and parasites culture c. diff fecal fat fobt "guaic" blue = +

2.1.3. ultrasound non-invasive must be NPO for 8 hrs before identifies fluid masses hematoma fat tissue any barium swallow >> AFTER ultrasound

2.1.4. x-rays plain films (abnormalities) mass stricture obstruction upper gi (barium swallow) scans for preparation post-procedure small bowel follow through traces UGI >> duodenum, small bowel lower gi (barium enema) indications contraindicated preparation post-procedure care nursing care

2.1.5. mri contraindications preparation NPO 6 hours prior remove all metal + dental plates instruct patient

2.1.6. ct 3-D cross sections With or without contrast PO or IV NPO for 2-4 hrs before Need large bore IV access scans for 5 sec at a time HR and RR may cause artifacts, blurriness need to lie flat and still

2.1.7. gastric analysis measures acid output preparation NPO for 8-12 hours before must avoid certain things procedure NG tube placement remove and discard stomach contents sample q15 min for 1 hour >> lab

2.1.8. gastric acid stimulation same prep as gastric analysis no tobacco or meds for 1-2 days prior procedure SQ med >> gastric secretions stimulated sample q15 min for 1 hr

2.1.9. pH monitoring to diagnose GERD direct correlation b/w reflux and chest pain preparation NPO for 6 hours before hold all meds affecting secretions for 1-3 days procedure probe into nose near LES connected to monitoring device worn for one day

2.1.10. endoscopy egd/ercp preparation procedure post-procedure discharge teaching proctosigmoidoscopy visualization indications contraindications preparation post-procedure discharge teaching colonoscopy purposes prepration procedure post-procedure discharge education

2.2. gerd

2.2.1. characteristics backflow of contents g/d >> esophagus some backflow is normal 3 causes of excessive reflux increases with aging

2.2.2. manifestations pyrosis dyspepsia post-meal nausea regurgitation dysphagia more saliva esophagitis may mimic s/s of ??? need a good history GI cocktail

2.2.3. diagnostics endoscopy barium swallow ambulatory pH monitoring

2.2.4. education avoid triggers low-fat diet, weight loss no smoking or excessive alcohol elevate HOB or upper bodies stop eating 2 hrs before bed progression if untreated

2.2.5. management drugs antacids h2-receptor antagonist proton-pump inhibitors prokinetic agents surgery nissen fundoplication last-ditch effort

2.3. hiatal hernia

2.3.1. process enlarged opening in diaphragm where esophagus moves part of stomach moves into lower thorax

2.3.2. females > males

2.3.3. two types sliding (1) 90% of cases upward displacement slides in and out of thorax manifestations management paraesophageal (2) rest of cases stomach pushes through diaphragm beside esophagus subclassified by degree of herniation (II-IV) manifestations same management/surgery as GERD risk for stomach torsion (emergency surgery)

2.4. gastritis

2.4.1. mucosal inflammation/autodigestion

2.4.2. progressive problem decrease functionality of parietal cells lose source of IF (pernicious anemia)

2.4.3. two types acute rapid onset usually caused by poor diet aggravated by ingestion of strong acid or base causes manifestations management chronic prolonged inflammation other causes manifestations management

2.4.4. risk factors drugs diet microbes environment pathologies stress NG tube placement autoimmune atrophic gastritis

2.4.5. diagnostics endoscopy ugi radiography biopsy specimens for h. pylori serum antibodies breath urine, feces gastric tissues

2.4.6. collaborative cause treat n/v NPO fluids rest antiemetics watch for hemorrhage frequent vs test vomit for blood drug therapy reduce irritation symptom-relief treat the cause lifestyle modification diet alcohol smoking medical follow-up

2.5. peptic ulcer disease

2.5.1. erosion of mucosa >> excavation h. pylori aspirin nsaids corticosteroids lipid-soluble cytotoxic agents

2.5.2. risk factors excessive hcl diet chronic use of NSAIDs alcohol, smoking family history

2.5.3. manifestations dull, gnawing pain mid-epigastric burning heartburn/vomiting (possible)

2.5.4. treatment medications lifestyle changes surgery*

2.5.5. types gastric break in mucosal barrier variable causes characteristics duodenal penetrate through mucosa into muscle usually caused by h. pylori hypersecretion of hcl pain 2-3 hours after meal acute superficial, minimal inflammation short duration when cause removed chronic wall erosion with fibrous tissue formation long duration (continuous or intermittent) four times > acute erosion

2.5.6. diagnostics endoscopy + biopsy h. pylori tests x-rays urea breath test stool antigen test barium contrast studies gastric analysis lab analysis CBC for anemia urinalysis liver enzymes serum amylase determination r/t pancreatic fxn stool exam for blood

2.5.7. collaborative care treatment goals reduce gastric acidity enhance mucosal defense mechanisms minimize harmful effects on mucosa ambulatory care clinics may stop aspirin, nonselective nsaids medical regimen rest, diet modification medications no smoking, alcohol long-term follow up stress management

2.5.8. drug therapy h2-receptor antagonist result in zantac or pepcid proton pump inhibitors block ATPase (r/t hcl secretion) more effective than h2-receptor antagonists nexium or prilosec antibiotics clear up h. pylori need combo therapy treatment for 10-14 days antacids adjunct therapy take on empty stomach (20-30 min onset) take after meals for long duration (3-4 hrs) cytoprotectants protection for tract accelerate ulcer healing carafate or cytotec

2.5.9. nutritional therapy protein neutral food stimulates hcl carbs/fats least stimulating to hcl not neutral foods to avoid hot, spicy pepper alcohol carbonated beverages tea, coffee broth

2.5.10. complications hemorrhage most common assessment findings nursing care perforation/penetration erosion into peritoneal cavity w/o warning causes leakage of contents into cavity manifestations nursing care gastric outlet obstruction process manifestations collaborative care

2.5.11. gerontology increased use of nsaids 1st appearance = frank gastric bleed or low hematocrit similar treatment to young want prevention of gastritis and PUD

2.6. stress ulcers

2.6.1. in gastroduodenal mucosa

2.6.2. occurs in patients who are physically stressed

2.6.3. preceded by shock decreased blood flow duodenal reflux large amounts of pepsin + ischemia and acid >> ideal condition

2.7. gastric surgeries

2.7.1. gastroenterostomy body of stomach & jejunum neutralizes hcl by alkaline regurg from duodenum into stomach

2.7.2. vagotomy eliminates acid-secreting stimulus to gastric cells decreases responsiveness of parietal cells

2.7.3. pyloroplasty widens exit of pylorus facilitates emptying of stomach contents

2.7.4. gastrectomy removal of all or part of stomach general PACU care fluids, electrolytes, IV antibiotics s/s complications peritonitis localized infection paralytic ileus abdominal distension increased or absent bowel sounds

2.7.5. other surgeries billroth 1 gastric resection gastroduodenostomy billroth 2 gastric resection gastrojejunostomy

2.7.6. nursing care post op NG tube acute gastric dilation r/t closed NG tube nutrition B12, folic acid, iron impaired ca++ metabolism reduced ca++ and vit d absorption complications dumping syndrome reflux gastropathy delayed gastric emptying afferent loop syndrome recurrent ulceration

2.8. inflammatory bowel disease

2.8.1. two types ulcerative colitis inflammatory exacerbations/remissions two stages manifestations diagnostics complications drugs diet crohn's disease chronic, non-specific progressive, recurrent "skip lesions" etiology manifestations diagnostics drug therapy complications

2.8.2. management inflammation immune bowel rest quality of life complications

2.8.3. nutrition PO fluid low-res, high protein, high cal supplemental iron, vitamins lactose intolerance no cold food or smoking (increase motility) TPN PRN

2.8.4. medications sedatives, antidiarrheals, antiperistaltics aminosalycilates (inflammation) corticosteroids (severe cases) immunomodulators (severe dz) monoclonal antibodies

2.8.5. surgeries crohn's dz strictureplasty small bowel resection total colectomy and ileostomy transplant (all are non-curative) ulcerative colitis total colectomy = cure surgical excision (qol) protocolectomy w/ileostomy IPAA (rectum preserved)

2.8.6. nursing care elimination pain fluid intake I/Os optimal nutrition rest reduce anxiety skin breakdown complications

2.9. diverticular disease

2.9.1. etiology constipation obesity lack of fiber

2.9.2. pathophysiology increased ILP >> outpouching walls are weak from diet bacteria becomes trapped (-itis) may be exacerbated by poor blood supply/nutrition

2.9.3. manifestations acute (appendicitis pain) chronic severe constipation pain distension flatulence obstruction general constipation LLQ pain s/s peritonitis elevated WBC occasional rectal bleeding

2.9.4. diagnostics x-ray with barium upper gi barium enema (rupture risk!!!) CT/US colonscopy or sigmoidoscopy after attack

2.9.5. management drugs broad spec antibiotics mild analgesics anticholinergics (reduce hypermotility) bedrest colon resection for complications

2.10. intestinal obstruction

2.10.1. blockage preventing normal flow

2.10.2. usually in small bowel

2.10.3. types mechanical functional partial complete

2.10.4. variable severity

2.10.5. acute cases adhesions distension inflammation electrolyte imbalance hemodynamic stability corrective surgery

2.10.6. nursing management assessment NG tube I/Os perfusion/oxygenation fluid/electrolytes hemodynamic status pre-op and post-op care

2.11. liver problems

2.11.1. two blood sources hepatic artery (oxygenated) hepatic portal vein (nutrient-rich)

2.11.2. hepatitis causes viral infection targets hepatocytes other viruses (CMV, Epstein-Barr) drug toxicity, alcohol abuse, autoimmune types a) fecal-oral b) blood or body fluids c) blood products d) blood serum e) fecal-oral manifestations prodromal period (flu) classic sx (A/N/V, fatigue) abdominal pain, fever dark urine, light stools jaundice (25%) inflammation >> obstruction >> cholestasis, ob. jaundice complement system activated diagnostics AST, ALT labs high results bilirubin in urine low albumin anemia prolonged PT time biopsy physical assessment collaborative care home health supportive therapy assessment weight loss fatigue pruritis RUQ pain low grade fever lethargy lymph node swelling jaundice splenomegaly, hepatomegaly dark urine nutrition high carb and protein low fat good cals and fluids sodium restriction no alcohol supplements

3. vascular diseases

3.1. overview

3.1.1. pvd pad sites causes types pvd lower extremities types

4. cardiac disorders

4.1. structural

4.1.1. valvular disorders mitral valve prolapse regurgitation stenosis aortic valve regurgitation stenosis

4.1.2. valve repair valvuloplasty commissurotomy annuloplasty leaflet repair chordoplasty valve replacement anesthesia and bypass can be mechanical (long-term anticoagulants) or biologic (less durable) xenografts < homografts < autografts

4.1.3. cardiomyopathy s/s of heart failure dyspnea, fatigue fluid retention nausea r/t poor GI perfusion chest pain, palpitations cardiac arrest w/HCM