1. hypertension
1.1. demographics
1.1.1. 50 million Americans affected
1.1.1.1. 28-31% of adults
1.1.1.2. 90-95% have primary
1.1.1.3. more common in SE USA and african-americans
1.1.2. onset b/w ages 20 and 50
1.1.3. two types
1.1.3.1. primary (95%)
1.1.3.2. secondary
1.1.4. most common cause of heart failure
1.1.5. associated with other problems
1.1.5.1. arteriosclerosis (hardening of muscles, endothelium): small
1.1.5.2. 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"
1.3.2.1. asymptomatic until organ damage
1.3.2.2. damages target organs
1.3.2.2.1. heart
1.3.2.2.2. eyes
1.3.2.2.3. brain
1.3.2.2.4. kidneys
1.3.3. very damaging
1.3.3.1. heart failure
1.3.3.2. myocardial infarction
1.3.3.3. stroke
1.3.3.4. a-fib
1.3.3.5. aortic dissection
1.3.3.6. peripheral artery disease
1.3.4. algorithm to predict IHD mortality
1.3.4.1. Baseline 115/75
1.3.4.2. Each 20/10 increase = 2x risk
1.3.5. multifactorial condition
1.3.5.1. increased SNS
1.3.5.2. increased renal NaCl/water reabsorption
1.3.5.3. increased RAA activity
1.3.5.4. decreased vasodilation
1.3.5.5. 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
1.5.1.1. history and physical
1.5.1.2. labs/diagnostics
1.5.1.2.1. urinalysis
1.5.1.2.2. blood chems
1.5.1.2.3. cholesterol
1.5.1.2.4. 12-lead ecg
1.5.2. treatment
1.5.2.1. ideal bp ranges
1.5.2.1.1. <140/<90 (standard)
1.5.2.1.2. <130/<80 (CKD/DM)
1.5.2.2. lifestyle modification
1.5.2.2.1. weight loss
1.5.2.2.2. reduce alcohol
1.5.2.2.3. reduce sodium
1.5.2.2.4. regular activity
1.5.2.2.5. DASH diet
1.5.2.3. medications
1.5.2.3.1. thiazides (initial)
1.5.2.3.2. additional PRN meds
1.5.2.3.3. may be combo therapy
1.5.2.3.4. must maintain lifestyle modification
1.6. nursing process
1.6.1. assessment
1.6.1.1. history
1.6.1.2. risk factors
1.6.1.3. s/s target organ damage
1.6.1.4. pertinent social/financial factors
1.6.2. treatment goals
1.6.2.1. understanding process
1.6.2.2. understanding treatment plan
1.6.2.3. participation in self-care
1.6.2.4. no complications
1.6.3. interventions
1.6.3.1. education
1.6.3.2. support adherence
1.6.3.3. consultation/collab
1.6.3.4. follow-up
1.6.3.5. control > care
1.6.3.6. lifestyle changes
1.6.3.7. lifelong process
1.6.4. gerontological care
1.6.4.1. noncompliance
1.6.4.2. family role
1.6.4.3. understanding therapy
1.6.4.3.1. reading instructions
1.6.4.3.2. monotherapy
1.7. complications
1.7.1. emergency
1.7.1.1. BP >180/120
1.7.1.2. Must be lowered immediately
1.7.1.3. Risk for target organ damage
1.7.1.4. treatment goals
1.7.1.4.1. reduce by 25% during first hour
1.7.1.4.2. reduce to 160/100 over 6 hours
1.7.1.4.3. gradual reduction to normal over days
1.7.1.5. exceptions to standard
1.7.1.5.1. ischemic stroke
1.7.1.5.2. aortic dissection
1.7.1.6. treated with IV vasodilators
1.7.1.6.1. sodium nitroprusside
1.7.1.6.2. nicardipine
1.7.1.6.3. fenodopam mesylate
1.7.1.6.4. enalprilat
1.7.1.6.5. nitroglycerin
1.7.1.7. frequent BP/CV monitoring
1.7.2. urgency
1.7.2.1. BP = very high
1.7.2.2. No evidence of immediate/progressive damage
1.7.2.3. treatment
1.7.2.3.1. close BP/CV monitoring
1.7.2.3.2. assess for potential damage
1.7.2.3.3. medications: fast-acting and PO
2. gi disorders
2.1. lab tests
2.1.1. blood
2.1.1.1. cbc
2.1.1.2. electrolytes
2.1.1.3. cea levels
2.1.2. stool
2.1.2.1. ova and parasites
2.1.2.2. culture
2.1.2.3. c. diff
2.1.2.4. fecal fat
2.1.2.5. fobt
2.1.2.5.1. "guaic"
2.1.2.5.2. blue = +
2.1.3. ultrasound
2.1.3.1. non-invasive
2.1.3.2. must be NPO for 8 hrs before
2.1.3.3. identifies
2.1.3.3.1. fluid
2.1.3.3.2. masses
2.1.3.3.3. hematoma
2.1.3.3.4. fat tissue
2.1.3.4. any barium swallow >> AFTER ultrasound
2.1.4. x-rays
2.1.4.1. plain films (abnormalities)
2.1.4.1.1. mass
2.1.4.1.2. stricture
2.1.4.1.3. obstruction
2.1.4.2. upper gi (barium swallow)
2.1.4.2.1. scans for
2.1.4.2.2. preparation
2.1.4.2.3. post-procedure
2.1.4.3. small bowel follow through
2.1.4.3.1. traces UGI >> duodenum, small bowel
2.1.4.4. lower gi (barium enema)
2.1.4.4.1. indications
2.1.4.4.2. contraindicated
2.1.4.4.3. preparation
2.1.4.4.4. post-procedure care
2.1.4.4.5. nursing care
2.1.5. mri
2.1.5.1. contraindications
2.1.5.2. preparation
2.1.5.2.1. NPO 6 hours prior
2.1.5.2.2. remove all metal + dental plates
2.1.5.2.3. instruct patient
2.1.6. ct
2.1.6.1. 3-D cross sections
2.1.6.2. With or without contrast
2.1.6.2.1. PO or IV
2.1.6.2.2. NPO for 2-4 hrs before
2.1.6.2.3. Need large bore IV access
2.1.6.3. scans for 5 sec at a time
2.1.6.3.1. HR and RR may cause artifacts, blurriness
2.1.6.3.2. need to lie flat and still
2.1.7. gastric analysis
2.1.7.1. measures acid output
2.1.7.2. preparation
2.1.7.2.1. NPO for 8-12 hours before
2.1.7.2.2. must avoid certain things
2.1.7.3. procedure
2.1.7.3.1. NG tube placement
2.1.7.3.2. remove and discard stomach contents
2.1.7.3.3. sample q15 min for 1 hour >> lab
2.1.8. gastric acid stimulation
2.1.8.1. same prep as gastric analysis
2.1.8.2. no tobacco or meds for 1-2 days prior
2.1.8.3. procedure
2.1.8.3.1. SQ med >> gastric secretions stimulated
2.1.8.3.2. sample q15 min for 1 hr
2.1.9. pH monitoring
2.1.9.1. to diagnose GERD
2.1.9.2. direct correlation b/w reflux and chest pain
2.1.9.3. preparation
2.1.9.3.1. NPO for 6 hours before
2.1.9.3.2. hold all meds affecting secretions for 1-3 days
2.1.9.4. procedure
2.1.9.4.1. probe into nose near LES
2.1.9.4.2. connected to monitoring device
2.1.9.4.3. worn for one day
2.1.10. endoscopy
2.1.10.1. egd/ercp
2.1.10.1.1. preparation
2.1.10.1.2. procedure
2.1.10.1.3. post-procedure
2.1.10.1.4. discharge teaching
2.1.10.2. proctosigmoidoscopy
2.1.10.2.1. visualization
2.1.10.2.2. indications
2.1.10.2.3. contraindications
2.1.10.2.4. preparation
2.1.10.2.5. post-procedure
2.1.10.2.6. discharge teaching
2.1.10.3. colonoscopy
2.1.10.3.1. purposes
2.1.10.3.2. prepration
2.1.10.3.3. procedure
2.1.10.3.4. post-procedure
2.1.10.3.5. discharge education
2.2. gerd
2.2.1. characteristics
2.2.1.1. backflow of contents
2.2.1.1.1. g/d >> esophagus
2.2.1.1.2. some backflow is normal
2.2.1.2. 3 causes of excessive reflux
2.2.1.3. increases with aging
2.2.2. manifestations
2.2.2.1. pyrosis
2.2.2.2. dyspepsia
2.2.2.3. post-meal nausea
2.2.2.4. regurgitation
2.2.2.5. dysphagia
2.2.2.6. more saliva
2.2.2.7. esophagitis
2.2.2.8. may mimic s/s of ???
2.2.2.8.1. need a good history
2.2.2.8.2. GI cocktail
2.2.3. diagnostics
2.2.3.1. endoscopy
2.2.3.2. barium swallow
2.2.3.3. ambulatory pH monitoring
2.2.4. education
2.2.4.1. avoid triggers
2.2.4.2. low-fat diet, weight loss
2.2.4.3. no smoking or excessive alcohol
2.2.4.4. elevate HOB or upper bodies
2.2.4.5. stop eating 2 hrs before bed
2.2.4.6. progression if untreated
2.2.5. management
2.2.5.1. drugs
2.2.5.1.1. antacids
2.2.5.1.2. h2-receptor antagonist
2.2.5.1.3. proton-pump inhibitors
2.2.5.1.4. prokinetic agents
2.2.5.2. surgery
2.2.5.2.1. nissen fundoplication
2.2.5.2.2. last-ditch effort
2.3. hiatal hernia
2.3.1. process
2.3.1.1. enlarged opening in diaphragm where esophagus moves
2.3.1.2. part of stomach moves into lower thorax
2.3.2. females > males
2.3.3. two types
2.3.3.1. sliding (1)
2.3.3.1.1. 90% of cases
2.3.3.1.2. upward displacement
2.3.3.1.3. slides in and out of thorax
2.3.3.1.4. manifestations
2.3.3.1.5. management
2.3.3.2. paraesophageal (2)
2.3.3.2.1. rest of cases
2.3.3.2.2. stomach pushes through diaphragm beside esophagus
2.3.3.2.3. subclassified by degree of herniation (II-IV)
2.3.3.2.4. manifestations
2.3.3.2.5. same management/surgery as GERD
2.3.3.2.6. risk for stomach torsion (emergency surgery)
2.4. gastritis
2.4.1. mucosal inflammation/autodigestion
2.4.2. progressive problem
2.4.2.1. decrease functionality of parietal cells
2.4.2.2. lose source of IF (pernicious anemia)
2.4.3. two types
2.4.3.1. acute
2.4.3.1.1. rapid onset
2.4.3.1.2. usually caused by poor diet
2.4.3.1.3. aggravated by ingestion of strong acid or base
2.4.3.1.4. causes
2.4.3.1.5. manifestations
2.4.3.1.6. management
2.4.3.2. chronic
2.4.3.2.1. prolonged inflammation
2.4.3.2.2. other causes
2.4.3.2.3. manifestations
2.4.3.2.4. management
2.4.4. risk factors
2.4.4.1. drugs
2.4.4.2. diet
2.4.4.3. microbes
2.4.4.4. environment
2.4.4.5. pathologies
2.4.4.6. stress
2.4.4.7. NG tube placement
2.4.4.8. autoimmune atrophic gastritis
2.4.5. diagnostics
2.4.5.1. endoscopy
2.4.5.2. ugi radiography
2.4.5.3. biopsy
2.4.5.4. specimens for h. pylori
2.4.5.4.1. serum antibodies
2.4.5.4.2. breath
2.4.5.4.3. urine, feces
2.4.5.4.4. gastric tissues
2.4.6. collaborative cause
2.4.6.1. treat n/v
2.4.6.1.1. NPO
2.4.6.1.2. fluids
2.4.6.1.3. rest
2.4.6.1.4. antiemetics
2.4.6.2. watch for hemorrhage
2.4.6.2.1. frequent vs
2.4.6.2.2. test vomit for blood
2.4.6.3. drug therapy
2.4.6.3.1. reduce irritation
2.4.6.3.2. symptom-relief
2.4.6.4. treat the cause
2.4.6.5. lifestyle modification
2.4.6.5.1. diet
2.4.6.5.2. alcohol
2.4.6.5.3. smoking
2.4.6.6. medical follow-up
2.5. peptic ulcer disease
2.5.1. erosion of mucosa >> excavation
2.5.1.1. h. pylori
2.5.1.2. aspirin
2.5.1.3. nsaids
2.5.1.4. corticosteroids
2.5.1.5. lipid-soluble cytotoxic agents
2.5.2. risk factors
2.5.2.1. excessive hcl
2.5.2.2. diet
2.5.2.3. chronic use of NSAIDs
2.5.2.4. alcohol, smoking
2.5.2.5. family history
2.5.3. manifestations
2.5.3.1. dull, gnawing pain
2.5.3.2. mid-epigastric burning
2.5.3.3. heartburn/vomiting (possible)
2.5.4. treatment
2.5.4.1. medications
2.5.4.2. lifestyle changes
2.5.4.3. surgery*
2.5.5. types
2.5.5.1. gastric
2.5.5.1.1. break in mucosal barrier
2.5.5.1.2. variable causes
2.5.5.1.3. characteristics
2.5.5.2. duodenal
2.5.5.2.1. penetrate through mucosa into muscle
2.5.5.2.2. usually caused by h. pylori
2.5.5.2.3. hypersecretion of hcl
2.5.5.2.4. pain 2-3 hours after meal
2.5.5.3. acute
2.5.5.3.1. superficial, minimal inflammation
2.5.5.3.2. short duration when cause removed
2.5.5.4. chronic
2.5.5.4.1. wall erosion with fibrous tissue formation
2.5.5.4.2. long duration (continuous or intermittent)
2.5.5.4.3. four times > acute erosion
2.5.6. diagnostics
2.5.6.1. endoscopy + biopsy
2.5.6.2. h. pylori tests
2.5.6.3. x-rays
2.5.6.4. urea breath test
2.5.6.5. stool antigen test
2.5.6.6. barium contrast studies
2.5.6.7. gastric analysis
2.5.6.8. lab analysis
2.5.6.8.1. CBC for anemia
2.5.6.8.2. urinalysis
2.5.6.8.3. liver enzymes
2.5.6.8.4. serum amylase determination r/t pancreatic fxn
2.5.6.8.5. stool exam for blood
2.5.7. collaborative care
2.5.7.1. treatment goals
2.5.7.1.1. reduce gastric acidity
2.5.7.1.2. enhance mucosal defense mechanisms
2.5.7.1.3. minimize harmful effects on mucosa
2.5.7.2. ambulatory care clinics
2.5.7.3. may stop aspirin, nonselective nsaids
2.5.7.4. medical regimen
2.5.7.4.1. rest, diet modification
2.5.7.4.2. medications
2.5.7.4.3. no smoking, alcohol
2.5.7.4.4. long-term follow up
2.5.7.4.5. stress management
2.5.8. drug therapy
2.5.8.1. h2-receptor antagonist
2.5.8.1.1. result in
2.5.8.1.2. zantac or pepcid
2.5.8.2. proton pump inhibitors
2.5.8.2.1. block ATPase (r/t hcl secretion)
2.5.8.2.2. more effective than h2-receptor antagonists
2.5.8.2.3. nexium or prilosec
2.5.8.3. antibiotics
2.5.8.3.1. clear up h. pylori
2.5.8.3.2. need combo therapy
2.5.8.3.3. treatment for 10-14 days
2.5.8.4. antacids
2.5.8.4.1. adjunct therapy
2.5.8.4.2. take on empty stomach (20-30 min onset)
2.5.8.4.3. take after meals for long duration (3-4 hrs)
2.5.8.5. cytoprotectants
2.5.8.5.1. protection for tract
2.5.8.5.2. accelerate ulcer healing
2.5.8.5.3. carafate or cytotec
2.5.9. nutritional therapy
2.5.9.1. protein
2.5.9.1.1. neutral food
2.5.9.1.2. stimulates hcl
2.5.9.2. carbs/fats
2.5.9.2.1. least stimulating to hcl
2.5.9.2.2. not neutral
2.5.9.3. foods to avoid
2.5.9.3.1. hot, spicy
2.5.9.3.2. pepper
2.5.9.3.3. alcohol
2.5.9.3.4. carbonated beverages
2.5.9.3.5. tea, coffee
2.5.9.3.6. broth
2.5.10. complications
2.5.10.1. hemorrhage
2.5.10.1.1. most common
2.5.10.1.2. assessment findings
2.5.10.1.3. nursing care
2.5.10.2. perforation/penetration
2.5.10.2.1. erosion into peritoneal cavity w/o warning
2.5.10.2.2. causes leakage of contents into cavity
2.5.10.2.3. manifestations
2.5.10.2.4. nursing care
2.5.10.3. gastric outlet obstruction
2.5.10.3.1. process
2.5.10.3.2. manifestations
2.5.10.3.3. collaborative care
2.5.11. gerontology
2.5.11.1. increased use of nsaids
2.5.11.2. 1st appearance = frank gastric bleed or low hematocrit
2.5.11.3. similar treatment to young
2.5.11.4. 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
2.6.3.1. decreased blood flow
2.6.3.2. duodenal reflux
2.6.3.2.1. large amounts of pepsin
2.6.3.2.2. + ischemia and acid >> ideal condition
2.7. gastric surgeries
2.7.1. gastroenterostomy
2.7.1.1. body of stomach & jejunum
2.7.1.2. neutralizes hcl by alkaline regurg from duodenum into stomach
2.7.2. vagotomy
2.7.2.1. eliminates acid-secreting stimulus to gastric cells
2.7.2.2. decreases responsiveness of parietal cells
2.7.3. pyloroplasty
2.7.3.1. widens exit of pylorus
2.7.3.2. facilitates emptying of stomach contents
2.7.4. gastrectomy
2.7.4.1. removal of all or part of stomach
2.7.4.2. general PACU care
2.7.4.3. fluids, electrolytes, IV antibiotics
2.7.4.4. s/s complications
2.7.4.4.1. peritonitis
2.7.4.4.2. localized infection
2.7.4.4.3. paralytic ileus
2.7.4.4.4. abdominal distension
2.7.4.4.5. increased or absent bowel sounds
2.7.5. other surgeries
2.7.5.1. billroth 1
2.7.5.1.1. gastric resection
2.7.5.1.2. gastroduodenostomy
2.7.5.2. billroth 2
2.7.5.2.1. gastric resection
2.7.5.2.2. gastrojejunostomy
2.7.6. nursing care
2.7.6.1. post op
2.7.6.1.1. NG tube
2.7.6.1.2. acute gastric dilation r/t closed NG tube
2.7.6.2. nutrition
2.7.6.2.1. B12, folic acid, iron
2.7.6.2.2. impaired ca++ metabolism
2.7.6.2.3. reduced ca++ and vit d absorption
2.7.6.3. complications
2.7.6.3.1. dumping syndrome
2.7.6.3.2. reflux gastropathy
2.7.6.3.3. delayed gastric emptying
2.7.6.3.4. afferent loop syndrome
2.7.6.3.5. recurrent ulceration
2.8. inflammatory bowel disease
2.8.1. two types
2.8.1.1. ulcerative colitis
2.8.1.1.1. inflammatory
2.8.1.1.2. exacerbations/remissions
2.8.1.1.3. two stages
2.8.1.1.4. manifestations
2.8.1.1.5. diagnostics
2.8.1.1.6. complications
2.8.1.1.7. drugs
2.8.1.1.8. diet
2.8.1.2. crohn's disease
2.8.1.2.1. chronic, non-specific
2.8.1.2.2. progressive, recurrent
2.8.1.2.3. "skip lesions"
2.8.1.2.4. etiology
2.8.1.2.5. manifestations
2.8.1.2.6. diagnostics
2.8.1.2.7. drug therapy
2.8.1.2.8. complications
2.8.2. management
2.8.2.1. inflammation
2.8.2.2. immune
2.8.2.3. bowel rest
2.8.2.4. quality of life
2.8.2.5. complications
2.8.3. nutrition
2.8.3.1. PO fluid
2.8.3.2. low-res, high protein, high cal
2.8.3.3. supplemental iron, vitamins
2.8.3.4. lactose intolerance
2.8.3.5. no cold food or smoking (increase motility)
2.8.3.6. TPN PRN
2.8.4. medications
2.8.4.1. sedatives, antidiarrheals, antiperistaltics
2.8.4.2. aminosalycilates (inflammation)
2.8.4.3. corticosteroids (severe cases)
2.8.4.4. immunomodulators (severe dz)
2.8.4.5. monoclonal antibodies
2.8.5. surgeries
2.8.5.1. crohn's dz
2.8.5.1.1. strictureplasty
2.8.5.1.2. small bowel resection
2.8.5.1.3. total colectomy and ileostomy
2.8.5.1.4. transplant
2.8.5.1.5. (all are non-curative)
2.8.5.2. ulcerative colitis
2.8.5.2.1. total colectomy = cure
2.8.5.2.2. surgical excision (qol)
2.8.5.2.3. protocolectomy w/ileostomy
2.8.5.2.4. IPAA (rectum preserved)
2.8.6. nursing care
2.8.6.1. elimination
2.8.6.2. pain
2.8.6.3. fluid intake
2.8.6.4. I/Os
2.8.6.5. optimal nutrition
2.8.6.6. rest
2.8.6.7. reduce anxiety
2.8.6.8. skin breakdown
2.8.6.9. complications
2.9. diverticular disease
2.9.1. etiology
2.9.1.1. constipation
2.9.1.2. obesity
2.9.1.3. lack of fiber
2.9.2. pathophysiology
2.9.2.1. increased ILP >> outpouching
2.9.2.2. walls are weak from diet
2.9.2.3. bacteria becomes trapped (-itis)
2.9.2.4. may be exacerbated by poor blood supply/nutrition
2.9.3. manifestations
2.9.3.1. acute (appendicitis pain)
2.9.3.2. chronic
2.9.3.2.1. severe constipation
2.9.3.2.2. pain
2.9.3.2.3. distension
2.9.3.2.4. flatulence
2.9.3.2.5. obstruction
2.9.3.3. general
2.9.3.3.1. constipation
2.9.3.3.2. LLQ pain
2.9.3.3.3. s/s peritonitis
2.9.3.3.4. elevated WBC
2.9.3.3.5. occasional rectal bleeding
2.9.4. diagnostics
2.9.4.1. x-ray with barium
2.9.4.2. upper gi
2.9.4.3. barium enema (rupture risk!!!)
2.9.4.4. CT/US
2.9.4.5. colonscopy or sigmoidoscopy after attack
2.9.5. management
2.9.5.1. drugs
2.9.5.1.1. broad spec antibiotics
2.9.5.1.2. mild analgesics
2.9.5.1.3. anticholinergics (reduce hypermotility)
2.9.5.2. bedrest
2.9.5.3. 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
2.10.3.1. mechanical
2.10.3.2. functional
2.10.3.3. partial
2.10.3.4. complete
2.10.4. variable severity
2.10.5. acute cases
2.10.5.1. adhesions
2.10.5.2. distension
2.10.5.3. inflammation
2.10.5.4. electrolyte imbalance
2.10.5.5. hemodynamic stability
2.10.5.6. corrective surgery
2.10.6. nursing management
2.10.6.1. assessment
2.10.6.2. NG tube
2.10.6.3. I/Os
2.10.6.4. perfusion/oxygenation
2.10.6.5. fluid/electrolytes
2.10.6.6. hemodynamic status
2.10.6.7. pre-op and post-op care
2.11. liver problems
2.11.1. two blood sources
2.11.1.1. hepatic artery (oxygenated)
2.11.1.2. hepatic portal vein (nutrient-rich)
2.11.2. hepatitis
2.11.2.1. causes
2.11.2.1.1. viral infection targets hepatocytes
2.11.2.1.2. other viruses (CMV, Epstein-Barr)
2.11.2.1.3. drug toxicity, alcohol abuse, autoimmune
2.11.2.2. types
2.11.2.2.1. a) fecal-oral
2.11.2.2.2. b) blood or body fluids
2.11.2.2.3. c) blood products
2.11.2.2.4. d) blood serum
2.11.2.2.5. e) fecal-oral
2.11.2.3. manifestations
2.11.2.3.1. prodromal period (flu)
2.11.2.3.2. classic sx (A/N/V, fatigue)
2.11.2.3.3. abdominal pain, fever
2.11.2.3.4. dark urine, light stools
2.11.2.3.5. jaundice (25%)
2.11.2.3.6. inflammation >> obstruction >> cholestasis, ob. jaundice
2.11.2.3.7. complement system activated
2.11.2.4. diagnostics
2.11.2.4.1. AST, ALT labs
2.11.2.4.2. high results
2.11.2.4.3. bilirubin in urine
2.11.2.4.4. low albumin
2.11.2.4.5. anemia
2.11.2.4.6. prolonged PT time
2.11.2.4.7. biopsy
2.11.2.4.8. physical assessment
2.11.2.5. collaborative care
2.11.2.5.1. home health
2.11.2.5.2. supportive therapy
2.11.2.6. assessment
2.11.2.6.1. weight loss
2.11.2.6.2. fatigue
2.11.2.6.3. pruritis
2.11.2.6.4. RUQ pain
2.11.2.6.5. low grade fever
2.11.2.6.6. lethargy
2.11.2.6.7. lymph node swelling
2.11.2.6.8. jaundice
2.11.2.6.9. splenomegaly, hepatomegaly
2.11.2.6.10. dark urine
2.11.2.7. nutrition
2.11.2.7.1. high carb and protein
2.11.2.7.2. low fat
2.11.2.7.3. good cals and fluids
2.11.2.7.4. sodium restriction
2.11.2.7.5. no alcohol
2.11.2.7.6. supplements
3. vascular diseases
3.1. overview
3.1.1. pvd
3.1.1.1. pad
3.1.1.1.1. sites
3.1.1.1.2. causes
3.1.1.1.3. types
3.1.1.2. pvd
3.1.1.2.1. lower extremities
3.1.1.2.2. types
4. cardiac disorders
4.1. structural
4.1.1. valvular disorders
4.1.1.1. mitral valve
4.1.1.1.1. prolapse
4.1.1.1.2. regurgitation
4.1.1.1.3. stenosis
4.1.1.2. aortic valve
4.1.1.2.1. regurgitation
4.1.1.2.2. stenosis
4.1.2. valve repair
4.1.2.1. valvuloplasty
4.1.2.1.1. commissurotomy
4.1.2.1.2. annuloplasty
4.1.2.1.3. leaflet repair
4.1.2.1.4. chordoplasty
4.1.2.2. valve replacement
4.1.2.2.1. anesthesia and bypass
4.1.2.2.2. can be mechanical (long-term anticoagulants) or biologic (less durable)
4.1.2.2.3. xenografts < homografts < autografts
4.1.3. cardiomyopathy
4.1.3.1. s/s of heart failure
4.1.3.1.1. dyspnea, fatigue
4.1.3.1.2. fluid retention
4.1.3.1.3. nausea r/t poor GI perfusion
4.1.3.1.4. chest pain, palpitations
4.1.3.1.5. cardiac arrest w/HCM