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NURS 3165 > elimation- GI disorders slides (quiz 2) > Flashcards

elimation- GI disorders slides (quiz 2) Flashcards

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1
Q

role of GI system/GI tract

A

Ingestion and propulsion of food
Digestion (physical and chemical breakdown of food into absorbable substances)
Absorption (transfer of the end products of digestion across the intestinal wall to the circulation)
Small bowel absorption of nutrients
Large bowel absorption of water
Elimination

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2
Q

exemplars of GI disorders

A

Nausea and vomiting
Constipation/Diarrhea
Infectious/Inflammatory Disorders (GERD, gastritis, peritonitis, gastroenteritis, peptic ulcer disease, GI bleed, ulcerative colitis, Crohn’s disease)
Cancers (oral, esophageal, gastric, colorectal)
Digestive disorders (celiac disease)
Diverticulosis, Diverticulitis

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3
Q

nausea

A

feeling of discomfort in the epigastric area with a conscious desire to vomit
related to slowing of gastric motility and emptying

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4
Q

vomiting

A

forceful ejection of partially digested food and secretions (emesis) from the upper GI tract
vomiting centre in the brainstem

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5
Q

nausea and vomiting occurs from

A

Occurs from:
GI disorders
Pregnancy
Infectious diseases
CNS disorders
Cardiovascular problems
Metabolic disorders
Side effects of drugs
Psychological factors

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6
Q

N/V clinical manifestations

A

Nausea – subjective
Vomiting – client becomes aware of the need
- can be accompanied by tachycardia, diaphoresis
- dehydration can occur rapidly if prolonged
- water, electrolytes are lost
- acid-base imbalances
- aspiration risk

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7
Q

N/V nursing management

A

Assessment – amount, colour, consistency of emesis, I/O, VS, signs of dehydration
IV fluids, replace electrolytes
NG tube
Clear fluids (room temp, warm tea)
Advance to dry toast, crackers
Drug therapy prn
Non-drug therapy

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8
Q

consipation

A

Decrease in bowel movements from normal
Bowel movements may be hard, difficult to pass, decreased in volume
Manifestations include - abdominal distension, bloating, nausea, headache, pain, increased flatulence, bloody stool, hemorrhoids

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9
Q

consitpation causes

A

Multiple causes – low fibre, low fluid intake, medications, inactivity, ignoring urge to defecate, environmental barriers to privacy, chronic laxative abuse, depression, stress, changes in normal routine, disorders of the colon (diverticulitis), endocrine and neurological disorders

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10
Q

consipation nursing mangement

A

Nursing management:
- assessment of normal pattern verses current pattern, amount, consistency, look for cause
- diet changes (increase in fibre)
- ensure adequate fluid intake
- ensure adequate activity as tolerated
- bowel protocol prn, ? laxatives

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11
Q

Diarrhea

A

Increase in stool frequency, increase in looseness of stool
Considered chronic if lasts for > 2 weeks
Manifestations include – explosive/watery stool, tenesmus, abdominal cramps, perianal skin irritation, fever, nausea/vomiting, dehydration, malaise

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12
Q

diarrhea causes

A

Causes – poor absorption of fluid in GI tract (celiac disease, inflammatory bowel disease, cystic fibrosis), increased fluid secretion into GI tract (infectious bacterial endotoxins, drugs, sorbitol), increased motility (irritable bowel, food poisoning)

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13
Q

*

diarrhea nursing management

A

Nursing management:
- assessment of normal pattern verses current pattern, amount, consistency, look for cause, I/O, VS, signs of dehydration
- IV fluids, replace electrolytes
- Drug therapy prn
- skin assessment, skin care

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14
Q

diarrhea - Clostridium diffcile

A
  • Most common cause of infectious diarrhea in the developed world, easily transmitted from patient to patient
  • 3 watery/loose diarrhea per day for 2 or more days (make sure no other cause)
  • Diagnosed through stool sample
  • Can progress to severe dehydration, pseudomembranous colitis, sepsis
    Treated with Metronidazole (Flagyl)
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15
Q

GERD (gastro esophageal relfux disease)

A
  • Most common acid-related GI disorder
  • Reflux of acidic gastric contents into the lower esophagus when supine or increased intra-abdominal pressure
  • Due to several factors affecting the defences of the lower esophagus
  • Common cause is hiatal hernia (herniation of a portion of the stomach into the esophagus)
  • Results in esophageal irritation and inflammation and can progress to erosion of esophageal mucosa
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16
Q

GERD nursing mangement

A
  • Diagnosis by barium swallow, endoscopy/biopsy
  • Elevate HOB
  • Encourage weight loss if overweight, smoking cessation
  • Avoid foods that aggravate – high fat foods (slow gastric emptying), chocolate, coffee, tea, peppermint (decrease LES pressure), milk products (increases acid secretion), orange juice, tomato-based
  • Small frequent meals, avoid late night meals
  • Drug therapy
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17
Q

gastritis

A
  • Inflammation of gastric mucosa
  • May be acute or chronic, diffuse or local
  • Breakdown in gastric mucosal barrier
  • Stomach tissue unprotected from acid/pepsin
  • Tissue edema, capillary wall breakdown, possible hemorrhage
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18
Q

gastritis risk factors

A
  • NSAIDS, Aspirin, Corticosteroids
  • Alcohol, spicy food
  • Smoking
  • Burns
  • Renal failure
  • Sepsis
  • Psychological stress
  • NG tube
  • Microorganisms
  • Helicobacter pylori (autoimmune chronic gastritis linked to
    H. pylori)
  • Mycobacterium
  • Cytomegalovirus
  • Syphilis
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19
Q

actue gastritis clinical manifestation

A
  • Anorexia
  • Nausea
  • Vomiting
  • Epigastric tenderness
  • Feeling of fullness
  • Hemorrhage
  • Common with alcohol abuse
20
Q

chronic gastritis clinical manifesations

A
  • Symptoms are similar to acute gastritis
  • Loss of intrinsic factor if acid-secreting cells are lost or nonfunctioning
  • Essential for absorption of cobalamin (vitamin B12)
21
Q

gastritis diagonistics

A
  • Endoscopic examination with biopsy - necessary for definitive diagnosis (rule out gastric cancer)
  • Breath, urine, serum, stool, and gastric tissue to detect presence of H. pylori
  • CBC - Confirm presence of anemia
  • Occult blood test
  • Serum antibody tests for parietal cells and intrinsic factor
22
Q

gastris nursing mangement

A
  • Acute Gastritis – eliminate cause, prevent/avoid triggers
  • Supportive care for nausea, if vomiting – NPO, fluids, rest, antiemetics
  • NG tube for severe symptoms
  • Watch for hemorrhage, monitor vital signs
  • Chronic Gastritis – lifestyle changes - diet, alcohol, smoking
  • Acute and Chronic – drug therapy
  • Chronic – antibiotics if H. pylori, cobalamin supplements
23
Q

peritonitis

A
  • Inflammation of the peritoneum
  • Due to trauma or rupture of an organ, causing leakage of chemical irritants or bacteria into the peritoneal cavity
  • Abdominal pain, rebound tenderness, abdominal wall rigidity/guarding
  • Medical management focused on eliminating the cause, preventing infection and/or complications
  • Nursing management includes pain control, nausea and vomiting control (NG maintenance), managing/monitoring hemodynamic status (fluid replacement, vital signs)
24
Q

gastroenteritis

A
  • “stomach flu” but is not the flu
  • Inflammation of gastric mucosa and small intestine – can be due to bacteria (food poisoning), virus (norovirus), parasite
  • Nausea, vomiting, abdominal cramping, distension, diarrhea, fever, elevated WBCs, blood/mucus in stool
  • Usually self-limiting, more of a concern in elderly and chronically ill
  • Supportive care for symptoms until resolved
25
Q

peptic ulcer disease (PUD)

A
  • Erosion of GI mucosa resulting from digestive action of HCl acid and pepsin
  • Any portion of GI tract in contact with gastric secretions is susceptible
  • Gastric and/or duodenal most common
  • Acute – usually superficial, short duration
  • Chronic – more common, continuous or intermittent for months, more likely muscular wall erosion with fibrous tissue formation
26
Q

peptic uclers stages

A

Peptic ulcers, including an erosion, an acute ulcer, and chronic ulcer. Both acute and chronic ulcers may penetrate the entire wall of the stomach

27
Q

destroyers of mucosal barrier

A
  • Helicobacter pylori (produces enzyme urease -
    mediates inflammation, mucosa becomes vulnerable)
  • Aspirin and NSAIDs (inhibit syntheses of prostaglandins - cause abnormal permeability)
  • Corticosteroids (decrease mucosal cell renewal)
  • Lifestyle factors (stress, caffeine, smoking, alcohol)
28
Q

PUD risk factors

A
  • Physiological stress ulcer – surgery or trauma
  • Duodenal ulcers - 35 to 40, genetics, blood grp O
    • H. pylori in 90-95%
    • increased risk if COPD, cirrhosis, chronic pancreatitis, hyperparathyroidism, chronic renal failure, Zollinger-Ellison syndrome, smoking, alcohol
  • Gastric ulcers - > women, older adults (> 50)
    • risk factors include H. pylori, medications (Aspirin, NSAIDS), smoking, bile reflux
29
Q

pud clinical manifestation

A
  • Gastric ulcers – burning or gaseous pain 1-2 hours after a meal, high in epigastrium
  • Duodenal ulcers – mid-epigastric burning or cramp-like pain, 2-5 hours after meals, tendency to occur, then disappear, then occur again
30
Q

PUD- diagonstics

A
  • To determine presence and location of ulcer
  • Endoscopy with biopsy, can identify H. pylori and rule out gastric cancer
  • Non-invasive tests for H. pylori: blood test, urea breath test, stool antigen test
  • Barium contrast tests
  • X-ray studies
  • Gastric analysis for HCL acid
  • CBC, urine analysis, liver/pancreas enzymes, stool examination (blood)
31
Q

pud - medical/collborative mangement

A
  • Adequate rest, elimination of smoking and alcohol, stress management
  • Drug therapy
  • Dietary modifications – irritating food and beverages avoided or eliminated from diet, six small meals a day
  • Aim is to reduce gastric acidity and enhance mucosal defence mechanisms
32
Q

nursing mangement

A
  • Nursing assessment
  • Teach diet/lifestyle modifications, early signs and symptoms of exacerbation, take ulcerogenic drugs with food or milk
  • Manage nausea, vomiting, pain
  • May be NPO with NG insitu, provide mouth care and nares care
  • Monitor I/O, may administer fluids
  • Teaching regarding drug therapy
33
Q

pud complications

A
  • Hemorrhage/Upper GI bleeding
    • most common PUD complication
    • develops from erosion of granulation tissue found at base of ulcer during healing and/or….
    • develops due to ulcer through a major blood vessel
  • Other causes of GI bleeding include gastric cancer, esophagitis, gastritis, bleeding disorders (liver failure, leukemia), medications, polyps, colorectal cancer, hemorrhoids
34
Q

GI bleeding nursing mnagement

A
  • Vital signs hourly or more – monitor for signs of hypovolemic shock
  • Closely monitor I/O – assess bowel movements, emesis, NG drainage
  • Provide physical and emotional rest
  • Make sure has IV access – may receive IV fluids, blood transfusion
  • Keep NPO
  • Monitor lab results – Hgb and Hct q 4-6h
35
Q

perforation with PUD

A

Perforation
- most lethal complication
- ulcer penetrates serosal surface with spillage of contents into peritoneal cavity
- sudden dramatic onset of severe abdominal pain, shock symptoms, rigid and boardlike abdomen, no bowel sounds, nausea/vomiting
- bacterial peritonitis may occur within 6 to 12 hours

36
Q

perforation nursing management

A
  • Monitor for signs of septic shock
  • NPO, manage NG tube, continuous aspiration
  • IV access, administer IV fluids, IV antibiotics, possible blood transfusion
  • Monitor I/O, central venous pressure
  • Monitor for EKG changes if cardiac history
  • Administer pain medication
  • Post-op care after laparoscopic or open surgical repair
37
Q

Pud complications - gastric outlet obstruction

A

Gastric outlet obstruction
- narrowed pylorus sphincter due to edema, inflammation, pylorospasm, scar tissue formation
- overtime hypertrophy of stomach wall, stomach dilates and becomes atonic
- increasing pain through the day, vomiting
- distended upper abdomen, dehydration, constipation, loud peristalsis

38
Q

gastric outlet obstruction nursing managament

A

Nursing management:
- Manage NG tube, to continuous aspiration then intermittent, then clamped
- Follow NG clamping regimen based on NG output
- IV access for IV fluids, electrolyte replacement
- NPO with NG, NG out then advance to clear fluids
- Endoscopy or surgery may be necessary

39
Q

PUD surgical therapy

A
  • Uncommon because of antisecretory agents
  • Indications for surgical interventions
  • Unresponsive to medical management
  • Concern about gastric cancer
  • Billroth I and II
  • Vagotomy – severing of vagus nerve, can be total or selective
  • Pyloroplasty – enlargement/opening of pyloric sphincter, commonly done after vagotomy
40
Q

oral/oropharyngeal cancer

A
  • > 50
  • Squamous cell most common
  • Predisposing factors: tobacco use, excessive alcohol, poor dental care, chronic irritation
  • Manifestations include leukoplakia, erythroplakia, persistent sores, dysphagia
  • Diagnosed by biopsy
  • Treated by surgery, chemotherapy, radiation
  • Nutritional support needed
41
Q

esophageal cancer

A
  • Aggressive, rare but poor survival rate
  • Squamous cell or adenocarcinoma
  • Risk factors include smoking, alcohol, GERD, Barrett’s esophagus
  • Can have hemorrhage from erosion
  • Diagnosed by barium swallow, endoscopy
  • Treated by surgery, chemotherapy, radiation
  • Palliative care management
42
Q

gastric cancer

A
  • Low incidence in Canada
  • Adenocarcinoma, diagnosed by endoscopy/biopsy
  • Predisposing factors include repeated irritant exposure, atrophic gastritis, pernicious anemia, polyps, achlorhydria
  • Manifestations include anemia, PUD, indigestion, pallor, weakness, fatigue, weight loss, pain, nausea/vomiting
  • Treated by surgery, possible chemotherapy, radiation if not surgical candidate
43
Q

post- op complications of total/partial gastrectomy

A

Dumping syndrome (15-30 minutes post meal):
- bolus of hypertonic fluid into intestine, fluid into bowel
- weakness, sweating, palpitations, dizziness, abdominal cramps, urge to defecate
Postprandial hypoglycemia (2 hours post meal):
- bolus of CHO into small intestine
- increases blood sugar and insulin release
- hypoglycemia: sweating, weakness, mental confusion, palpitations, increased heart rate, anxiety
Should rest after meals, low CHO diet

44
Q

colorectal cancer

A
  • Common, most begin as adenomatous polyps
  • Etiology unknown, strong genetic link
  • Manifestations show late – change in bowel schedule, rectal bleeding
  • If normal risk recommended fecal occult blood test (FOBT) or fecal immunochemical test (FIT) every 2 yrs
  • If family history colonoscopy every 5 years
  • Surgery only cure, may or may not have ostomy, chemotherapy and radiation likely if positive lymph nodes
45
Q

celiac disease

A
  • 1:133 Canadians; many undiagnosed
  • Easily confused with IBD and IBS
  • Screening for specific antibody tissue transglutaminase, definitive diagnosis by biopsy and diet (gluten-free and symptoms resolve)
  • Autoimmune response; gluten (wheat, barley, rye) causes inflammation of GI tract
  • Flatulence, abdominal distension, foul-smelling diarrhea, steatorrhea
  • Malabsorption of nutrients – low iron/folate (anemia), low calcium/vitamin D (osteoporosis, osteopenia), low vitamin K and B12
46
Q

Diverticulosis/Diverticulitis

A
  • Milder manifestations with diverticulosis – abdominal discomfort/pain, nausea
  • Manifestations with diverticulitis include abdominal pain, fever, chills, nausea and vomiting, elevated WBC
  • Diagnosis by CT, barium enema, colonoscopy
  • Complications – perforation, peritonitis, abscess, fistula formation, obstruction, bleeding
  • Prevention – Metamucil

NURS 3165 (8 decks)

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