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Flashcards in Exam 3/Final Deck (166)
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1
Q

GERD etiology and clinical manifestations

A
  • most common upper GI disorder in the U.S.
  • no identifiable cause
  • relaxation of LES/Reflux of gastric contents into lower esophagus
    Clinical Manifestations:
  • dyspepsia
  • regurgitation
  • belching (eructation)/Flatulence(gas)
  • Chronic GERD- dysphagia
  • Other: atypical chest pain, cough, wheeze, asthma
2
Q

GERD diagnostic studies

A
  • 24 hr esophageal pH monitoring: gold standard
  • esophogogastroduodenoscopy (EGD)
  • biopsy & cytologic specimens to differentiate carcinoma from Barrett’s esophagus (precursor to cancer)
3
Q

Risk factors for GERD

A
  • hiatal hernia
  • obesity
  • pregnancy
  • high fat, spicy foods
  • chocolate, caffeine, alcohol
  • nitrates, Ca channel blockers, estrogen
  • presence of NG tube
4
Q

lifestyle modifications for GERD

A
  • nutritional therapy: avoid milk products at night, late snacks or meals, caffeine, alcohol, citrus fruits, chocolate, high fat foods
  • weight reduction
  • stress management
  • eat upright
5
Q

drug therapy for GERD

A
  • H2 receptor blockers
  • proton pump inhibitors
  • antacids
6
Q

prevention for GERD

A
  • avoid factors that cause reflux
  • HOB > 30 degrees
  • decrease intra-abdominal pressure
  • stay upright for 2hrs after eating
  • no eating 3hrs before bed
  • drug therapy
7
Q

complications of GERD

A
  • ulcers
  • increased risk of esophageal cancers
  • strictures
8
Q

Hiatal hernia & clinical manifestations

A
opening of diaphragm where esophagus passes through becomes enlarged & part of stomach tends to come into lower portion of thorax
- can be incarcerated or rolling 
CM:
- heartburn, dysphagia, regurgitation
- 50% pts asymptomatic
9
Q

Nissen Fundoplication

A
  • laparoscopic anti-reflux surgery
  • reinforces the valve between esophagus & stomach
  • wrap upper portion of stomach around esophagus
  • outcomes: symptom free, significant improvement in condition
  • common complication: post-op bleeding
10
Q

Gastritis

A
  • inflammation of gastric mucosa
  • chronic or acute
  • can lead to PUD, polyps (precancerous overgrowth of tissue), cancer
  • prevention: eat well, moderate alcohol, moderate caffeine, stop smoking, cautious use of aspirin, other NSAIDS, and corticosteroids, manage stress
11
Q

peptic ulcer disease

A
  • erosion of mucus membrane of stomach
  • types: gastric, duodenal, stress
  • develop in an acid environment
  • mucosal barrier is impaired: HCl, mucosa, tissue damage, cellular destruction, inflammation.
  • majority of ulcers associated with h.pylori
12
Q

clinical manifestations of PUD

A
  • dyspepsia
  • epigastric pain or tenderness
  • black tarry stools
  • n/v
13
Q

diagnostic studies for PUD

A
  • h & p
  • EGD
  • IgG anti H. pylori antibody
  • CBC
  • nuclear medicine scans (bleeding scan)
  • FOBT
  • gastric biopsy
14
Q

causative factors of PUD

A
  • H. pylori (90% of cases)
  • NSAIDS
  • risk factors for gastritis
15
Q

PUD collective care

A

treatment goals
- reduce degree of gastric acidity- enhance mucosal defense mechanisms & minimize harmful effects on mucosa
requires many weeks of therapy; pain disappears after 3 to 6 days
healing may take 3-9 weeks
- should be assessed by means of x-rays or endoscopic examination
drugs that aggravate the condition are removed
smoking cessation
TLC as best we can do; different for every patient
stress reduction

16
Q

PUD dietary modifications

A
  • avoid: foods that cause symptoms e.g. caffeine, alcohol, spicy foods, hight fat foods & cream. No smoking/tobacco
  • non-irritating or bland diet, 6 small means in acute phase
  • avoid foods high in roughage (bulk, fiber)
  • milk products and protein can neutralize gastric activity (milk can also increase gastric acid production & can aggravate ulcers)
17
Q

PUD drug therapy

A
  • antacid H2 receptor blockers, proton pump inhibitors, antibiotics
18
Q

PUD complications: most serious

A

Hemorrhage: most serious complication
- assessment focus: changes in v/s, increase in amt of redness of aspirate (NGT) signals massive UGI bleeding; increased amt blood gastric contents; may have decrease in pain b/c blood helps neutralize acidic gastric contents
- watch for s/s of hypovolemia & shock
Nursing implications: lab tests, goals of care, interventions, evaluation of outcomes of care.
Perforation: surgical emergency

19
Q

PUD complication: gastric outlet obstruction

A
- overtime, edema, inflammation & pylorospasm associated with active ulcer formation causes digestive tract to become narrowed & obstructed
CM:
- abdominal bloating
- n.v
(can also be an emergent situation)
0 NG tube to decompress stomach
20
Q

PUD surgical interventions

A

Partial gastrectomy: removal part of the stomach
Vagotomy
- cutting the vagus nerve to reduce gastric secretions
- used when ulcers not controlled by other means
- all meds have failed
- done with partial gastrectomy
Pyloroplasty
- relieve narrowing of pyloric channel
- allows stomach contecnts to enter into duodenum more readily

21
Q

Dumping syndrome

A
  • result of surgical removal of large portion of stomach & pyloric sphincter
  • vasomotor symptoms that occur after eating
  • early dumping syndrome (w/i 30 min of eating): vertigo, tachy, sweating, pallor
  • late dumping: 90min-3hrs after eating. excessive amt of insulin released–>hypoglycemia
    Prevention: smaller meals, avoid liquids with meals, low moderate carbs, no milk, sweets, or sugars
22
Q

Obesity: criteria

A

most common nutritional problem

  • 50% of Americans are overweight, 15% obese
  • overweight= BMI b/t 25-29.99
  • obesity= BMI > 30
  • extreme obesity BMI > 40 (surgery considerations)
  • high risk for complications: DMII, HTN, CAD, stroke, PAD, OSA, depression, chronic back pain, early osteoarthritis, obstructive sleep apnea
23
Q

Obesity: etiology

A
  • environmental & genetic factors
  • obesity affects several persons within a family
  • Leptin
24
Q

Special considerations after bariatric surgery

A
  • abdominal binder
  • position
  • SaO2 monitoring
  • SCDs or heparin
  • skin assessment
  • absorbant padding
  • removal or urinary catheter w/i 24 hrs
  • AOOB
  • ambulate ASAP
  • monitor abdominal girth
  • 6 small meals, prevent dehydration
  • observe for signs of dumping
25
Q

IBD: UC or Crohn’s

A
  • characterized by chronic recurrent inflammation
  • may be long periods of remission
  • episodes of acute exacerbations
  • debilitating
    (different from IBS: vasomotor. not an inflammatory process- char. by alternating diarrhea/constipation)
26
Q

IBD: Incidence

A
  • affects approx. 1 million Americans
  • evenly split b/t UC & Crohn’s
  • men and women equally affected
  • often family hx seen
  • American Jewish or European decent more often affected
  • steady increase among AA pop
27
Q

Ulcerative Colitis: overview

A
  • widespread inflammation, mainly rectum & rectosigmoid colon
  • 10-20 liquid, bloody stools/day
  • periods of remissions & exacerbations
  • can range from mild to severe or fulminant
  • inflammation limited to outermost layers of visera (as opposed to Crohn’s: transmural).
  • bleeding: key characteristic
28
Q

Ulcerative Colitis: incidence

A
  • can occur at any age; 15-25yr & 55-65
  • males & females equally affected
  • more common in American Jewish of European decent
  • cause unknown
  • tends to run in families but no research yet to support genetic link
29
Q

Ulcerative Colitis: assessment

A
  • family hx
  • tx
  • surgery
  • nutrition history
  • bowel patterns
  • timing of diarrhea
  • recent antibiotics
  • travel to tropical areas
  • recent NSAID use
  • extraintestinal symptoms: arthritis, mouth sores, vision, skin problems
  • psychosocial assessment
  • fever
  • ab. distention along colon (painful)
  • ab. tenderness
  • s/s peritonitis (board-like rigidity)
  • Hgb, Hct, platelets, WBC, C-reactive protein, ESR, electros albumin.
30
Q

Ulcerative Colitis: diagnostics

A
  • sigmoidoscopy or colonoscopy (gold standard)
  • CT
  • barium enema: radio opaque dye. look @ patterns of inflammation
31
Q

Ulcerative Colitis: drug therapy

A
  • Aminosalicylates: anti-inflammatory drugs (most common) e.g. sulfasalazine & oral formulations of mesalamine (long term option)
  • corticosteroids: prednisone & methylprednisone PO or PR (short term; increased risk for infection)
  • immune modifiers: may use to decrease to decrease steroid dosage
  • antibiotics: metronidazole, ampicillin, cipro (don’t use prophylactically)
  • biologic therapies: Infliximab (Remicade) IV monthly (newest), Monoclonal antibody: blocks TNF & allows time for remission
32
Q

Crohn’s Disease: overview

A
  • chronic, nonspecific IBD
  • unknown origin
  • can affect any part of GI tract
  • 5-6 loose stools/day, non bloody
  • most often seen in terminal ileum, jejunum & colon
  • lesions have cobblestone appearance w/sections of normal mucosa between lesions (skip lesions); unlike UC, transmural inflammation - increase risk for fistulas from erosion
33
Q

Crohn’s Disease: incidence

A
  • may occur in all ages
  • primarily disease of adolescents & young adults (15-35)
  • can also occur in people 70 or > & young children
34
Q

Crohn’s Disease assessment

A
  • CM may vary (based on extent of disease)
  • diarrhea
  • steatorrhea (fat) in stool
  • stools w/bright red blood rare
  • abdominal pain (RLQ)
  • if fever (may be low grade)–> fistulas, abscesses, severe inflammation
  • fatigue and weight loss
  • psychosocial impact
  • issues w/nutrition, malabsorption
35
Q

Crohn’s Disease: diagnostics

A
  • no single test to dx with certainty
  • labs- CBC, lytes, C-reactive protein, ESR, albumin, folic acid, vitamin B12 (cobalamin) levels (B12 for pernicious anemia & absorption problems). Osteoporosis.
  • x-rays: upper & lower GI barium studies
  • CT or abdominal ultrasound
  • endoscopy- sigmoid/colonoscopy
  • pathology tests- biopsies
  • exclude other known causes of intestinal inflammation
36
Q

Crohn’s Disease: drug therapy

A
  • similar to UC

- use corticosteroids with caution- may mask sx infection (e.g. sepsis, fistulas, abscesses).

37
Q

Crohn’s Disease complications

A
  • hemorrhage
  • perforation
  • abscess
  • toxic megacolon
  • malabsorption
  • fistulas
  • osteoporosis
  • bowel obstruction
  • extraintestinal: arthritis, hepatobiliary disease, oral/skin lesions, eye problems
38
Q

UC complications

A
  • hemorrhage
  • perforation
  • abscess
  • toxic megacolon
  • colorectal cancer
  • bowel obstruction
  • extraintestinal: arthritis, hepatobiliary disease, oral/skin lesions, eye problems
39
Q

IBD: Interventions

A
  • monitor for GI bleeding (may need blood products &/or surgery)
  • Nutrition therapy: NPO if severe (initially), TPN if severely ill & malnourished
  • if not NPO: elemental formulas, may be on low fiber diet, avoid foods that cause symptoms, alcohol, smoking
40
Q

IBD Surgery

A
  • colectomy
  • ileostomy- conduit (incontinent, continent)
  • ileoanal reservoir (J pouch)
41
Q

Colorectal Cancer: overview

A
  • 3rd most common cause of cancer deaths
  • insidious onset (difficult to diagnose)
  • need regular screening
  • solid tumor cancer (colon, rectum)
42
Q

Colorectal Cancer: risk factors

A
  • age > 50
  • personal history, polyps, colorectal cancer, IBD
  • family hx
  • Infections (H.pylori, HPV)
  • diet high in red meats & processed foods
  • physical inactivity
  • obesity
  • smoking
  • heavy alcohol use
43
Q

Colorectal Cancer: clinical manifestations

A
  • change in bowel habits, such as diarrhea, constipation, or narrowing of the stool, that lasts more than a few days
  • feeling need to have a bowel movement that is not relieved by doing so
  • rectal bleeding, dark stools, or blood in stool
  • cramping or abdominal pain
  • weakness & fatigue
  • unintended weight loss (red flag)
44
Q

Colorectal Cancer: diagnostics

A
  • CBC: look for bleeding
  • FOBT
  • colonoscopy: gold standard
  • flexible sigmoidoscopy
  • double contrast barium enema
  • CT or MRI
45
Q

Colorectal Cancer: Collaborative Care

A
  • surgery- primary treatment
  • radiation- usually palliative
  • adjuvant chemotherapy after surgery (5-fluorouracil IV with other drugs)
  • -common s/e: diarrhea, mucositis, leukopenia, mouth ulcers, peripheral nueropathy
  • TNM criteria
46
Q

Colorectal Cancer: Surgical Intervention

A
  • tx depends on location & extent of cancer
  • if metastasis has occurred, tumor is removed for palliative reasons
  • colon resection with permanent or temporary colostomy
  • if below the sigmoid or rectum- approx 75% of tumors result in a colostomy
47
Q

Ostomies

A
  • performed to relieve bowel obstruction
  • opening in abdominal wall for excretion of waste
  • involves construction of a stoma
  • Ileostomy- brings ileum to abdominal wall (liquid to semi solid stools, may use incontinent or continent procedures)
  • sigmoid colostomy: descending or sigmoid colon to the surface of abdominal wall (firm stool, sometimes no appliance is worn)
  • temporary colostomy (inflammation): transverse colon emergency surgery, soft to fairly firm stool.
48
Q

Ostomies: Interventions

A
  • consult with the ET wound therapist re: best place for stoma to be placed
  • assessment of stoma: should be pink, red with slight edema, pale, white/blue–>ischemia, black brown–>necrosis
  • skin care around stoma site
  • assess for s/s infection
  • fluid & electrolyte balance
  • body image disturbance
  • assess stoma q8h for color
  • mild swelling first 2-3 wks
  • clear pouch to observe drainage, color, consistency
  • diet teaching- few diet restrictions, control gas & odor
  • psychological concerns
  • sexuality
49
Q

Ostomies: stoma care

A
  • colostomy irrigation for sigmoid colostomy to regulate elimination
  • 500-1000mL of warm tap water
  • hang 18-24inches above the stoma (about shoulder height)
  • apply irrigating sleeve & place bottom end in toilet
  • lubricate cone & insert tip gently
  • allow irrigation solution to flow slowly 5-10 min
  • if cramping occurs, stop
  • clamp & remove, allow 30-45 min for fecal returns
50
Q

Hepatitis: Overview

A
  • inflammation of the liver associated with a broad spectrum of clinical manifestations from asymptomatic infection to hepatic necrosis
51
Q

Hepatitis: Etiology

A
  • typically caused by viruses
  • may be toxin induced (drugs, alcohol, chemicals, & autoimmune)
  • pathophysiologic changes in various types of viral hepatitis are similar
  • acetaminophen: self medicating for months.
52
Q

Hepatitis: A

A
  • mode of transmission primarily fecal-oral
  • usually thru ingestion of contaminated foods/liquids
  • prevalent in underdeveloped countries, overcrowding, & poor sanitation
  • infected food handler can spread disease
  • can contract by consuming water or shellfish from contaminated water
  • commonly spread person to person, rarely by blood transfusion
  • worldwide- usually among children and young adults (5-14)
  • low mortality
  • mild to severe symptoms or none at all
53
Q

Hepatitis: B

A
  • mode of transmission is primarily thru blood
  • parenteral needle sticks, permucosal
  • oral route- saliva or breast feeding
  • sexual activity thru blood, semen, saliva, or vaginal secretions
  • wound exudate
  • world wide, mostly young adults 20-49 y/o
  • mortality can be as high as 10% with another 10% developing chronic hepatitis
  • main cause of cirrhosis & liver carcinoma
  • 100x more infectious than HIV
54
Q

Hepatitis: C

A

Mode of transmission:
- blood or blood product transfusion
- IV drug users, renal dialysis patients & personnel
- Can be transmitted via intercourse
- can be through contaminated piercing and tattooing tools
Occurrence:
- common in all age groups
- most common form of post-transfusion hepatitis
- maybe seen sporadically or in epidemic proportions

55
Q

Hepatitis: Clinical Manifestations

A
  • assessment findings are consistent for different types of hepatitis (vary based on type/individual)
  • signs & symptoms progress over several stages
  • Pre-Icteric phase
  • Icteric phase
  • Post Icteric or Recovery phase
56
Q

Hepatitis: Assessment findings

A

Various for the different stages

  • constipation & diarrhea
  • fatigue, malaise
  • hepatomegaly
  • RUQ pain
  • clay-colored stools, dark urine
  • pruritis
57
Q

Hepatitis: Diagnostics

A

Hematology:
- increased ALT, AST, alk phosphatase, LDH, bilirubin, & ESR
- prothrombin time prolonged
- Leukocytosis
- Bilirubin- direct, indirect & total (increase in icteric phase)
- antibody testing (for specific viruses)
Urine Chemistry
- increase urobilinogen, mild proteinuria, mild bilirubinuria
- clearing toxin from blood
Get good med history: acetamenophen history (often hidden in other products. should not consume more than 4g/day.)

58
Q

Hepatitis: Collaborative Management

A

Monitoring level of activity: bed rest
Diet:
- small, frequent, palatable meals as tolerated
- may need parenteral & enteral feedings
- Na restrictions in presence of edema
- high caloric diet, moderate protein and fat
- all alcoholic beverages are strictly prohibited.
- vitamins
Management of pruritis
- alkaline soaps restricted, emollients & liquid creams prescribed
- antihistamines & tranquilizers if used administer with caution

59
Q

Hepatitis: pharmacotherapy

A
  • parenteral Vit K: reversal agent for Warfarin/Coumadin. for prolonged PT, if hepatic failure will not respond to Vit K may require transfusions
  • antihistamines: relief of pruritis
  • antiemetics: nausea (avoid Compazine)
  • immune globin: for close personal contacts of pts w/ HAV
  • Hepatitis B immune globin (HBIG): recommended for individuals exposed
  • Interferon alpha
  • HAV vaccine: for potential exposure to HAV–> traveling
  • HBV vaccine: immunization of health care workers or anyone at risk for exposure to blood products
  • corticosteroids: to control sx & decrease abnormal liver function
  • recombinant interferon: antiviral agent that inhibits viral replication
60
Q

Hepatitis: Problems & Interventions

A

Fatigue related to decreasing metabolic energy production due to liver dysfunction

  • diet history
  • encourage small frequent feedings, refer to dietician
  • provide bed rest of at least 90 minutes before & after exercise
  • avoid activity immediately after meals
  • keep frequent objects within reach
  • administered acid suppression therapy, antiemetic, etc.
  • knowledge deficit
  • risk for impaired skin integrity
  • ineffective protection
61
Q

Cirrhosis: overview

A
  • chronic disease in which normal configuration of liver is changed resulting in cell death
  • when new cells are formed, resulting scaring causes disruption of blood & lymph flow
  • pathological changes over years, structural changes gradually lead to total liver dysfunction
  • manifestations are related to hepatocellular necrosis & portal hypertension
  • portal hypertension, esophageal varices—> scar tissue a big problem. .
62
Q

Cirrhosis: types

A

Alcoholic (Laennec’s)
- long term ETOH use: 5 or > per day for 10-15 yrs
- scar tissue surrounds portal areas
Post Necrotic Cirrhosis
- associated with hx viral hepatitis or hepatic damage from drugs or toxins
- broad bands of scar tissue as a result of previous acute viral hepatitis
Biliary
- develops when ducts that carry bile out of liver become inflamed & blocked
- exact cause unknown, but may be related to problem with immune system

63
Q

Cirrhosis: complications

A
Portal hypertension
- increased venous pressure in portal circulation
- splenomegaly
- esophageal varices: vomiting copious amounts of blood
- systematic hypertension
- "caput medusae": veins
Peripheral edema & ascites
Hepatic encephalopathy
Risk of GI bleed
breathing: displaced diaphragm
64
Q

Cirrhosis: diagnostics

A
  • decreased RBC, WBC, & platelets
  • increased bilirubin, alk phos, AST, ALT
  • decreased albumin levels esp in ascites
  • Na: normal to low
  • K: reduced
  • glucose decreased r/t impaired glucogenesis
  • coagulation: increased PT
  • urine testing: increased bilirubin
  • barium swallow to verify presence of active bleeding
  • angiographic studies to view patency of portal veing
65
Q

Cirrhosis: collaborative care

A
  1. rest
  2. avoidance of alcohol & anticoagulants
  3. Management of ascities
    - low Na
    - diuretics
    - paracentesis
    - peritoneovenous shunt
    - respiratory support
  4. Sengstaken-Blakemore tube
66
Q

Bell’s Palsy: overview

A

Peripheral Facial Nerve Paralysis (CN VII)

  • benign, unilateral
  • cause unknown, evidence caused by herpes simplex virus
  • flaccidity of affected side of face with drooping mouth
  • Recover w/i a few weeks or months
  • s/s: increased pain, inability to close the eyes, loss of taste, decreased chewing, drooping of mouth, fever, tinnitus
67
Q

Bell’s Palsy: medications

A
  • Prednisone: steroid. decreases inflammation.

- Zovirax: antiviral

68
Q

Bell’s Palsy: nursing interventions

A
  • pain, moist heat, protect face, good nutrition (chew on the unaffected side, oral hygeien), dark glasses, artificial tears, change in facial appearance
69
Q

Trigeminal Neuralgia: overview

A
  • involving maxillary & mandibular branches (opthalmic usually spared)
  • chronic pain syndrome
  • unknown etiology (nerve compression, herpes, jaw, and tooth infections)
  • terrible pain. “suicide disease”
70
Q

Trigeminal Neuralgia: clinical manifestations

A
  • abrupt onset of excruciating facial pain
  • burning, knifelike pain, electric shock: effected kips, gums, cheek, forehead or side of nose
  • intense twitching, grimacing, blinking, eye tearing
  • attacks are brief, 2-3 seconds, unilateral
  • course is unpredictable & cyclical
  • precipitating stimuli- chewing, brushing teeth, hot or cold air, touch or tickle
  • poor nutrition & hygiene, withdrawal, excessive sleep
71
Q

Trigeminal Neuralgia: diagnostics

A
  • MRI, CT, scan, lumbar puncture to R/O other problems

- complete neurological assessment

72
Q

Trigeminal Neuralgia: drug therapy

A
  • anti-seizure medications- Dilantin, Tegretol

- stabilize neuronal membrane

73
Q

Trigeminal Neuralgia: surgical and nursing interventions

A
  • focus to relieve pain- injections into trigeminal nerve roots
  • history of pain
  • environmental management- room temperature, draft free
  • patients perform own facial care
  • hygiene, oral hygiene
  • limit conversation during acute periods
  • assess nutritional status
74
Q

Guillain- Barre Syndrome: Etiology & Pathophysiology

A
  • cause unknown
  • ascending muscle weakness…flaccid paralysis w/o muscle atrophy, symmetric (alteration in myelin sheaths)
  • acute inflammatory process directed at peripheral nerves
  • destruction of the myelin
  • muscles undergo denervation & atrophy
75
Q

Guillain- Barre Syndrome: clinical manifestations

A

respiratory compromise/paralysis & infection
- frequent respiratory assessment
- chest PT, sputum cultures
- paralytic ileus, DVT, PE
loss of bowel and bladder fx
- intermittent catheterization, prevent UTI
sensory paraesthesias/paralysis
- cranial nerves- dysphagia, diplopia, facial weakness
ANS dysfunction: labile BP, cardiac dysrhythmias
weakness of lower extremities: distal muscles more affected

76
Q

Guillain- Barre Syndrome: treatment

A
  • no cure
  • plasmapheresis
  • immunogloblin therapy
77
Q

Multiple Sclerosis: overview

A
  • chronic, autoimmune disease affecting myelin sheath & conductive pathway of CNS
  • one of the leading causes of neurological disability in young adults
  • periods of exacerbations & remissions (as severity & duration progresses, exacerbations more frequent
  • relapsing-remitting most common of 4 types
  • major concern–> long time to diagnose
  • unknown cause
  • research on biral, immunologic, genetic, & environmental factor
  • tends to occur b/t 20-40 y/o
  • women 2x
78
Q

Multiple Sclerosis: assessment

A
  • often presents like other neuro diseases (dx difficult)
  • early symptoms vague & nonspecific (vision, mobility, & sensory changes)
  • ask if factors aggravate symptoms: fatigue, stress, overexertion, temp extremes, hot bath or shower.
79
Q

Multiple Sclerosis: clinical manifestations

A
  • fatigue & weakness
  • abnormal reflexes (absent or exaggerated)
  • visual disturbances (impaired, diplopia, nystagmus)
  • motor dysfunction: weakness, tremors, incoordination
  • sensory dysfunction: parasthesias, impaired vibration & position
  • impaired, slurred speech
  • urinary dys: hesitancy, frequency, urgency, UTI
  • neurobehavioral: depression, emotional lability
80
Q

Multiple Sclerosis: diagnostics

A
  • no specific procedure diagnostic of MS
  • collective results of variety of tests: abnormal CSF, two attacks separated in time & space, MRI consistent with MS
    (rule out acute meningitis, other neuro problems)
81
Q

Multiple Sclerosis: nursing interventions

A
  • promote motor function
  • minimize fatigue
  • optimize sensory fx
  • maintain urine elimination (straight cath, voiding schedule)
  • normalize family processes
  • promoting sexual functioning
82
Q

Multiple Sclerosis: collaborative care

A

Acute attacks:
- corticosteroids
- immunosuppressive agents
Chronic symptom mgmt:
- treatment of spasticity
- control of fatigue
- treatment of depression with antidepressants & counseling
- bladder mgmt w/anticholinergics & intermitted cath
- bowel mgmt: stool softeners, bulk laxatives, suppositories
- multidisciplinary rehab approach
- dystonia
Educate: hand washing, avoid crowds/children, oral hygiene

83
Q

Amyotropic Lateral Sclerosis: overview

A
  • progressive weakness

- lower neuron signs: atrophy, fasciculations (muscle spasms, tremors)

84
Q

Amyotropic Lateral Sclerosis: patho

A
  • unknown cause
  • degeneration of the upper & lower neurons
  • progressive loss of voluntary muscle contraction
  • death often occurs within 3 years of dx due to resp failure
85
Q

Amyotropic Lateral Sclerosis: clinical manifestations

A
  • progressive weakness & muscle wasting
  • progressive difficulty swallowing
  • drooling, regurgitation through the nose of liquids
  • difficulty speaking & ultimately breathing
86
Q

Amyotropic Lateral Sclerosis: diagnostic evaluation

A
  • electromyography- evaluate degeneration & muscle atrophy
  • nerve conduction studies (EMG): how nerves are innervated/how muscles are responding
  • PFT
  • barium swallow
87
Q

Amyotropic Lateral Sclerosis: collaborative mgmt

A
  • baclofen to control symptoms
  • valium to control fasciculations
  • antidepressants
  • sleeping pills
  • feeding gastronomy
  • mechanical ventilation when necessary
88
Q

Amyotropic Lateral Sclerosis: nursing interventions

A
  • maintaining respiration
  • optimizing mobility
  • nutritional requirements (high calorie, small frequent feedings)
  • minimize fatigue
  • maintain social interaction
  • prevent aspiration & infection (speech therapist, chest PT)
89
Q

Meningitis: patho

A
  • droplet spread- close proximity
  • inflammation of the meninges
  • pathogenic organisms cross the BBB & enter CNS
  • viral usually self-limiting; bacterial may be life threatening
  • usually infectious in nature. if suspected, isolate for 24hrs. after that, no longer infectious.
90
Q

Meningitis: clinical manifestations

A
  • severe headache, fever, n/v
  • classic: nuchal rigidity, Kernig’s & Brudzinski’s signs
  • photophobia symptoms of increased ICP
  • LOC, seizures, rash (enterovirus)
91
Q

Meningitis: complications

A
  • cranial nerve dysfunction
  • hemiparesis, dysphasia, hemianopsia
  • cerebral edema–> seizures, bradycardia
  • severe headache- assess for stroke. worst headache ever in life?
92
Q

Meningitis: lab assessment

A
  • CSF analysis by lumbar puncture most significant
  • CT scan
  • CBC with differential (increased WBCs to indicate an infectious process)
  • serum electrolytes: may have dilutional decrease Na r/t SIADH (inappropriate ADH levels)
93
Q

Meningitis: nursing interventions

A
  • follow ABCs
  • v/s, neuro checks (Glasgow coma scale, AMS), lungs, skin
  • reduce fever- fever increases cerebral edema (cooling blankets, tylenol, sponge baths)
  • manage fluid balance (I&O)
  • enhance cerebral perfusion
  • reduce pain
  • optimal LOF: rehab, passive to active ex.
  • prevention: Meningococcal vaccine for at risk pts (not recc for everyone- children, teenagers, young adults)
94
Q

SCI: overview

A
  • occurs following trauma
  • significant contributing factor to morbidity and mortality in the US
  • alcohol has been found to play a major factor in 25% of cases
  • mostly males, aged 15-35
95
Q

SCI: common causes

A
primary:
- trauma: MVA, falls, violence
- results from fractured or displaced vertebra
- can also occur from spinal tumors
secondary (worsens primary)
- hemorrhage
- ischemia
- hypovolemia
- neurogenic shock (hemodynamic instability, bradycardia, warm skin)
- can experience concurrent shocks
96
Q

SCI: assessment

A
  • ABCs: if cervical, high risk for respiratory compromise (C3-C5 innervate phrenic nerve)
  • check intra-abdominal bleeding or bleeding around fracture
  • LOC (Glasgow)
  • spinal shock occurs as concussion response: often lasts < 48 hrs but can last weeks. (immediacy of traumatic event leads to total loss of neuro function. decrease inflam to hopefully improve prognosis)
97
Q

SCI: assessment by systems

A
  • Respiratory: above C4 requires mechanical ventilation, below C4 edema/hemorrhage affects phrenic nerve- resp insufficiency
  • Cardio: any lesion above T6 greatly decreases SNS–> bradycardia. vasodilation=hypotension.
  • urinary: atonic bladder=retention. foley, straight cath
  • GI: hypomotility leads to paralytic ileus, gastric distension (NG tube to relieve pressure), stress ulcer risk
  • integumentary: skin breakdown
  • PV problems: DVT (Doppler), PE, numbness, tingling, impaired sensation
98
Q

SCI: collaborative care

A
  • immobilization/stabilization
  • drug therapy for specific dys.
  • HR- bradycarida: anticholinergics/ Atropine, temp. pacemaker
  • TEDS, ROM, DVT assessment
  • Methylprednisolone: administered early can increase neuro fx
  • fluid maintenance
  • respiratory
  • temp control
  • bowel/bladder
  • psychological needs
99
Q

Autonomic Dysreflexia: overview

A
  • overactivity of ANS- abrupt onset of excessively high BP (usually caused by distended bladder or fecal impaction)
  • at risk if injury above T5
  • occurs suddenly without warning
  • life threatening- CVA, seizures, death
  • stimulus introduced below injury sends nerve impulses to the spinal cord, travel upward until blocked by lesion: impulses don’t reach brain, action by SNS
  • narrowing of vessels & increased BP> 200/100
  • h/a, slow pulse, blotchy skin, restlessness, nausea, cold&clammy
100
Q

Autonomic Dysreflexia: priority nursing interventions

A
  • 1st: sitting position
  • notify HCP
  • loosed tight-fitting clothing
  • assess & treat cause e.g. distended bladder or fecal impaction
  • room temp should not be too cool
  • monitor BP q10-15min
  • nitrates or hydralazine as ordered
101
Q

transfusion reactions: febrile

A
  • chills
  • increased HR
  • fever
  • decreased BP
  • tachypnea
  • bacterial or allergy related
102
Q

transfusion reactions: hemolytic

A
  • apprehension
  • headache
  • chest pain
  • low back pain
  • increased HR
  • low BP
  • tachypnea
  • hemoglobinemia
  • sense of impending doom
  • ABO, Rh incompatibility
103
Q

transfusion reactions: bacterial

A
  • chills
  • increased HR
  • fever
  • low BP
  • tachypnea
  • shock
104
Q

transfusion reactions: circulatory overload

A
  • HTN
  • bounding pulse
  • distended jugular veins
  • dyspnea
  • restlessness
  • confusion
105
Q

DM Type I

A
  • autoimmune disorder–> beta cells destroyed
  • onset usually < 30y/o but can happen at any age
  • etiology viral infection
  • At risk if HLA-DR, HLA-DQ (tissue specific antigens)
  • usually not obese
  • insulin dependent
  • PO agents ineffective
106
Q

DM Type II

A
  • progressive disorder pancreas makes < insulin over time, resistance occurs
  • Etiology unknown
  • peaks in 50s, may occur earlier
  • 60-80% obese
  • insulin therapy req’d for 20-30%
  • oral agents effective for most
  • most common
107
Q

Metabolic Syndrome

A
  • group of symptoms/diseases
  • metabolic factors that increase risk for type II DM & CV disease
  • abdominal obesity (visceral)
  • hyperglycemia
  • HTN
  • dyslipidemia
  • health promotion: teach about lifestyle changes to improve health (primary prevention), screening for increased BP, BG
  • children at great risk
108
Q

DM: Acute Complications

A
  • DKA: caused by lack of insulin & ketoacidosis
  • HHS: caused by lack of insulin profound dehydration. more common, particularly in elderly.
  • hypoglycemia: caused by too much insulin or too little glucose
109
Q

DKA

A
  • lack of insulin & ketoacidosis
  • ketones from fat breakdown
  • not eating, infection, fever, not taking insulin
  • check urine for ketones
  • concern for K depletion
110
Q

HHS

A
  • caused by lack of insulin, profound dehydration

- more common, particularly in elderly (concern for fluid overload, complicate a heart problem)

111
Q

DM: Chronic Complications

A

Macrovascular
- CV disease: MI leading cause of death for pts with DM
- Cerebrovascular disease: stroke
Microvascular: retinopathy, neuropathy, nephropathy, male erectile dysfuntion

112
Q

Erectile Dysfunction

A
  • inability to achieve or maintain erection for sexual intercourse
  • organic (physiological) vs. functional (psychological)
  • assessment: medical, social, sexual hx; complete physical; duplex doppler ultrasonography test
113
Q

DM: assessment

A
High risk factors:
- age (especially in Type II)
- gestational DM (type III. at risk for II)
- wt & wt change (I will lose weight, II will gain)
Symptoms
- fatigue, 3Ps
major & minor infections
changes in vision or sense of smell
114
Q

normal fasting glucose

A
  • less than 100mg/dl
  • older adults: levels increase 1mg/dl per decade
  • > 126mg/dl diagnostic of DM even in older adults (one time test not necessarily diagnostic)
115
Q

normal glucose tolerance test

A
  • s metabolized to assess for gestational diabetes

- hard to administer: drink dextrose

116
Q

normal glycosylated hemoglobin test

A
  • 4%-6%
  • levels >8% indicate poor diabetic control
  • tests over 3 months- the lifespan of a RBC
117
Q

DM: urine tests

A
  • ketone bodies
  • glucose
  • tests for kidney function: urine albumin excretion, creatinine clearance (assess GFR)
118
Q

Insulin therapy

A
  • rapid, short, intermediate, long acting
  • mixing insulins
  • insulin pumps
  • IV drip 100 units regular insulin/100mL 0.9%NS for DKA & HHS (extreme situations)
119
Q

DM: education

A
  • foot care (injury most common cause leading to hospitalization)
  • full foot assessment
  • wound care (slow healing–>complications)
  • manage chronic neuropathic pain (anticonvulsants, TCA’s)
  • pt education re: hypoglycemia & treatment (elderly at higher risk!!)
120
Q

Hyperthyroidism

A
  • sustained increase in synthesis & release of thyroid hormones by thyroid gland
  • women more than men, 30-50
  • Grave’s disease: autoimmune disease of unknown etiology. diffuse thyroid enlargement & excessive thyroid secretions
121
Q

Clinical manifestations of hyperthyroidism

A
  • increased metabolism & sensitivity to SNS
  • CV (tachycardia, increased SBP, dysrhythmias; at risk for hypoxia & ischemic states)
  • goiter
  • exophthalmos–>visual losses
  • muscle weakness
  • fatigue
  • heat intolerance
  • GI: loose stools, bouts of diarrhea
  • hair loss, skin changes
  • weight loss w/ increased appetite
122
Q

diagnostic care: hyperthyroidism

A
  • H&P, ECG

- lab findings: low TSH, high free thyroxine (T4) levels.

123
Q

drug therapy: hyperthyroidism

A
  • mainstay of treatment
  • antithyroid drugs (inhibit synthesis of thyroid hormone)
  • potassium iodine (inhibits synthesis & release of thyroid hormone, decreases vascularity of thyroid gland): Lugol’s solution, SSKI, PTU, Tapazol
  • Beta-blocker: Propranolol/Inderal. some pts may need cardioselective. won’t directly affect TH, but will help w/anxiety s/s e.g. tachycardia
124
Q

radiation therapy: hyperthyroidism

A
  • radioactive iodine
  • destroys thyroid tissue, delayed response in 2-3 months
  • need to be on other meds in the meantime
  • not indicated in pregnancy
  • radiation precautions: radioactive material in body waste. private room/toilet, flush twice, washing clothes, avoid sharing utensils.
  • laxatives to clear contaminated stool from body
  • surgery if not responsive to this
125
Q

hyperthyroidism: nutrition

A
  • high calorie
  • may need increased proteins
  • avoid caffeine, high seasoned foods, etc (irritating, palp, anxiety)
126
Q

hyperthyroidism: assessment

A
  • health history
  • know clinical manifestations
  • determine patient’s knowledge of disease
  • problems: alt in O2, CV comp
    Goals: symptom relief, no serious complications, compliance, back to euthyroid state
127
Q

postop care following thyroidectomy

A
  • airway & O2 admin (tracheostomy set at bedside, check wall suction)
  • prevent postop complications: high fowlers w/pillow, hold head w/position changes. coughing, DB q2h &PRN- teach bracing.
  • monitor for s/s of parathyroid hormone disturbance (hypocalcemia manifested by tetany)
  • check incision site: bleeding, hematoma, swelling of soft neck tissues
  • watch for stridor (risk for swelling around airway)
128
Q

Thyrotoxicosis

A
  • complication of hyperthyroidism- thyroid storm
  • clinical manifestations: fever, tachycardia, increased SBP, agitation, abdominal pain, GI disturbances, delirium, coma (small increase can be indicative of a problem)
  • Interventions: ABCs, reduce fever, med therapy (immediate PTU, tapazol), treat dehydration
129
Q

Hypothyroidism

A

insufficient thyroid hormone, due to destruction of thyroid tissue or as a result of thyroid surgery &/or treatment for hyperthyroidism

  • can be idiopathic
  • possibly from treatment for head and neck cancer
130
Q

clinical manifestations of hypothyroidism

A
  • signs & symptoms of decreased metabolic rate
  • cool, pale yellowish dry skin (coarse), thick brittle nails, reduce hair growth, cold intolerance
  • dyspnea, hyopventilation
  • bradycardia, decrease CO & contractility, arrhythmias (a fib can be seen with both hypo and hyper), cardiomyopathy, CHF, pericardial effusion, anemia
  • weight gain, constipation, amenorrhea
  • neurocognitive symptoms
  • autoimmune: Hashimoto’s thyroiditis
131
Q

diagnostic studies: hypothyroidism

A
  • H&P, ECG (look for dysrhythmias)
  • lab findings: high TSH, low T3, T4
  • body telling self to give more hormone, but it’s not being used.
132
Q

drug therapy: hypothyroidism

A
  • thyroid hormone replacement (Levothyroxine), requires thyroid hormone levels monitoring for dosage adjustment
  • synthetic/exogenous TH replacement w/ narrow therapeutic index
  • start on low dose- check TSH levels
  • give on empty stomach in the morning
  • taking meds for the rest of life- difficult for people
133
Q

nursing management: hypothyroidism

A
  • assessment: hx, know CMs, pts knownedge of disease
  • prevention: resp. compromise, hypotension, support cognition, prevent myxedema coma (extreme hypothyroid state- med. emergency)
  • goals: symptom relief, maintain euthyroid state, positive self-image, compliance.
134
Q

interventions: hypothyroidism

A
  • patient/family teaching
  • acute care, monitor for complications such as myxedema (medical emergency): caused by long term hypothyroidism. could lead to coma. precipitated by infection, drugs, exposure to cold, trauma
135
Q

care of patients in myxedema coma

A
  • neuro assessment
  • mechanical ventilator
  • monitor core body temp
  • administer IV meds to treat paralytic ileus
136
Q

Cushing Syndrome

A
  • caused by excess of corticosteroids (hypercortisolism), particularly glucocorticoids, admin of exogenous corticosteroids
137
Q

clinical manifestations: Cushing Syndrome

A
  • wt. gain, trunk, face, cervical area, fat pads
  • glucose intolerance, protein wasting
  • osteoporosis, fragile skin
  • moon face, purple-red striae, hirsutism
  • hypertension, hypokalemia
  • immunosuppression
  • can have psychosis
138
Q

Cushing Disease/Syndrome collaborative care

A

Diagnostics: plasma ACTH level varies
TX dependent on cause
goal of normalizing hormone secretion
surgical removal or radiation for pituitary adenoma
adrenalectomy for adrenal tumores (pheochromocytoma) or hyperplasia
drug therapy when surgery is contra.
- find underlying cause

139
Q

Cushing Syndrome: management

A
  • identify risks: infection, imbalanced nutrition, skin integrity, imbalanced nut.
  • monitor v/s, weight, glucose, hormone & drug toxicity, complicating conditions (CV disease, diabetes, infection, thromboembolic events, pathologic fractures)
  • if indicated, prepare pt for surgery: hypophysectomy or adrenalectomy
  • preop: control HTN, hyperglycermia, hypokalemia
140
Q

post-op care: Cushing Syndrome

A
  • high risk for bleeding
  • v/s, f&e, i/o
  • morning urine levels of cortisol to evaluate effectiveness of surgery
  • ensure that corticosteroid dosage is tapered gradually
  • s/s hypocortisolism: vomiting, weakness, dehydration, hypotension
  • implement nursing measures to maintain skin integrity
141
Q

post-op nursing care after transsphenoidal hypophysectomy

A
Positioning: 
- maintain patent airway
- pts are mouth breathers
- HOB > 30 degrees
Watch for CSF leak
Neuro & pain assessment
Avoid coughing or sneezing
Monitor v/s, i/o, f&e
142
Q

superficial thickness burn

A
  • least damage;epidermis only part of skin that is injured

- desquamation (peeling of dead skin) occurs 2-3 days after burn

143
Q

partial thickness burn

A

-involves entire epidermis and dermis (varying depths)

144
Q

full thickness burn

A
  • destruction of entire epidermis and dermis

- skin does NOT regrow

145
Q

resuscitation/early phase of burn injury

A
continues for 24-48 hrs
goals of management:
- secure airway
- support circulation- fluid replacement
- prevent infection
- maintain body temperature
- provide emotional support
146
Q

cardiovascular assessment: burns

A
  • hypovolemic shock common cause of death in early phase in patients with serious injuries
  • vital signs
  • cardiac status, especially in cases of electrical burn injuries
147
Q

kidney/urinary assessment: burns

A
  • changes related to cellular debris, decreased kidney blood flow
  • myoglobin released from damaged muscle, circulates to kidney
  • kidney fx, BUN, creatinine, serum sodium levels
  • urine color, odor, presence of particles/foam
148
Q

GI assessment: burns

A
  • changes in GI fx expected
  • decreased blood flow and sympathetic stimulation during early phase cause reduced motility, paralytic ileus (NG tube needed for decompression)
  • GI bleeding
  • risk for stress ulcer-> ischemia. Prophylactic PPI.
149
Q

vascular changes resulting from burn injuries

A
  • fluid shift: third spacing or capillary leak syndrome, usually occurs in 1st 12hr, can continue 24-36 hours
  • profound imbalance of fluid, electrolyte, acid-base; hyperkalemia and hyponatremia levels; hemoconcentration
  • fluid remobilization after 24hr, diuretic stage begins 48-72 hr after injury, hyponatremia and hypokalemia
150
Q

collaborative management: HIV/AIDS

A
  • assessment
  • history
  • physical assessment/clinical manifestations:
  • infections- opportunistic, protozoal (PCP), fungal (thrush), bacterial (TB, avium complex), viral (herpes)
  • malignancies- Kaposi’s sarcoma (skin- dark lesions), malignant lymphomas
  • endocrine complications
  • AIDS dementia complex
  • AIDS wasting syndrome
  • skin changes
151
Q

Priority patient problems: HIV/AIDS

A
  • potential for infection
  • inadequate oxygenation (esp if pneumonia)
  • pain: neuropathy. meds, increased viral loads
  • inadequate nutrition: wasting. need good reserves
  • diarrhea: opportunistic infection, s/e meds
  • reduced skin integrity
  • confusion: setting of dementia. risk for injury.
  • reduced self esteem
  • potential loss of social contact
152
Q

SIADH

A
  • ADH released despite normal or low plasma osmolality
  • common in older adults, specifically in patterns of malignancy (lung cancer)
  • self-limiting when caused by head trauma or drugs
153
Q

clinical manifestations/diagnostics: SIADH

A
  • fluid retention
  • dilutional hyponatremia
  • concentrated urine
  • normal renal fx
  • normal or increased vascular fluid volume
  • concern for pulmonary edema- resp. crisis
  • hyponatremia: neurological alterations
    Diagnostics:
  • Na < 134
  • serum osmolality < 280
154
Q

SIADH management

A
  • fix underlying problem
  • fluid restrictions: mainstay of tx. less than 1L fluid/day.
  • drug therapy: vasopressin antagonists, diuretics, hypertonic saline (caution)
  • monitoring response to therapy
  • preventing complications: from hyponatremia (neuro changes, seizures), fluid overload, pulmonary edema
  • daily weights
  • neuro checks: fatigue, irritability, glasgow coma scale
155
Q

DI

A
  • group of conditions associated with a deficiency of production of ADH or decreased response to ADH
  • Primary: lack of ADH r/t pituitary or hypothalamus defect
  • Secondary: tumors, head trauma, infections
  • Drug related: Lithium, declomycin
  • Nephrogenic: inadequate renal response to ADH
156
Q

CM/Diagnostics of DI

A
  • polydipsia, polyuria
  • serum osmolality > 295
  • fatigue, nocturia, wt loss
    Diagnostics:
  • ID underlying cause
  • 24 hours i/o: >4-5L in 24h
157
Q

Management of DI

A
  • meds (Desmopressin, Vasopressin, Diabinese)
  • adequate hydration
  • prevent dehydration
  • check urine specific gravity
  • daily weights
  • labs: elevated BUN and CC (BUN more so than CC), elevated Na
158
Q

Leukemias

A
  • cancers of WBCs or cells that develop into WBCs
  • WBCs not functional
  • invade and destroy bone marrow
  • can metastasize to liver, spleen, lymph nodes, testes, brain.
  • increase in immature blast cells- crowd out other blood cells
  • AML most common in adults
159
Q

Leukemias: complications

A
  • vulnerable to infection
  • thrombocytopenia
  • anemia secondary to bone marrow depression
160
Q

Lymphomas

A
  • cancers of the lymphocytes (B cells)
  • Hodgkin’s lymphoma- most cases adults. causes: viruses or chemicals
  • Non-Hodgkin’s lymphoma- more common over age 50. causes: genetic, viral, autoimmune, radiation, or toxins
  • can metastasize to almost any organ
161
Q

Leukemias/Lymphomas: risk factors

A
exact cause unknown
risk factors:
- ionizing radiation
- chemicals and drugs
- bone marrow hypoplasia
- genetic 
- immunologic
162
Q

diagnostics: leukemias/lymphomas

A
  • increase WBCs
  • decrease Hgb, Hct, platelets
  • increased bleeding times
  • bone marrow aspiration & biopsy:
    • apply site pressure 5-10 min
    • assess v/s
    • apply pressure dressing
    • chech s/s bleeding & infection x 24h
163
Q

Assessment: Leukemias

A
  • bone pain
  • joint swelling
  • enlarged liver & spleen
  • wt loss
  • fever
  • poor wound healing
  • signs of anemia (fatigue, pallor, high HR, DOE)
  • bleeding: ecchymoses, hematuria, bleeding gums
164
Q

Assessment: HL & NHL

A
  • enlarged lymph node: usually in neck with HL. generally spreads from 1 ln or single group in an orderly fashion, unlike NHL
  • fever
  • fatigue
  • infections
165
Q

Clinical manifestations of DIC

A

bleeding
- pallor, petechiae, hematomas, GI bleeding, hematuria, dizziness, headache, musculoskeletal changes
Thrombosis
- cyanosis, ischemia, pulmonary emboli, respiratory distress

166
Q

DIC nursing management

A
  • prevent septic shock: low bp, signs of hypoperfusion
  • early detection of bleeding
  • bleeding precautions
  • blood products
  • plasma volume expanders