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Med Surg 1 > care of pt. with stomach disorders > Flashcards

care of pt. with stomach disorders Flashcards

1
Q

gastritis patho

what is it caused by

A
  • Inflammation of gastric mucosa
  • Erosive versus nonerosive
  • Acute gastritis usually heals after several months, chronic gastritis does not
  • Often caused by long-term NSAID use
  • Can be caused by H. pylori
  • Chronic gastritis is associated with an increased risk of gastric cancer
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2
Q

gastris health promotion and maintenance

A
  • Eat a well- balanced diet
  • Regular exercise
  • Stress-reduction techniques
  • Limit foods and spices that cause gastric distress
  • Avoid alcohol, tobacco
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3
Q

acute gastritis

A
  • rapid onset of epigastric pain and dyspepsia

- epigastric burning sensation referred to as heart burn

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4
Q

acute gastritis accompanied by

A
  • gastric bleeding

- Hematemesis- vomiting blood or melena (dark, “tarry” sticky stool

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5
Q

chronic gastritis assessment

A

may have few symptoms unless ulceration occurs
- nausea, vomiting, upper abdominal discomfort, periodic epigastric pain may occur after a meal, some patients have anorexia

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6
Q

gastritis diagnosis tools

A
  • egd via endoscope with biopsy is gold standard diagnostic tool
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7
Q

acute gastritis treating

A
  • treated symptomatically and with supportive care because the healing process is spontaneous and occurs within a few days
  • Eliminate causative factor, which usually results in pain and discomfort being reduced
  • A blood transfusion and fluid replacement may be given if bleeding occurs
  • Drugs that block and buffer gastric acid secretions
  • Consider Nutrition and Drug Therapy
  • Nutrition
  • Drug therapy
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8
Q

food to avoid in gastritis

A
  • avoid caffeine
  • highly acidic foods
  • spicy foods
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9
Q

chronic gastritis treatment

A
  • causative agent
  • may require b12 for prevention or treatment of pernicious anemia
  • H.Pylori infection
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10
Q

peptic ulcer disease

A
  • occurs when mucosial defenses become impaired epithelium not protected from effects of acid and pepsin
  • many caused by h.pylori
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11
Q

three types of peptic ulcers

A
  • duodenal
  • gastric
  • stress ulcer
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12
Q

peptic ulcer disease common route H.pylori infection transmission

A

oral-to-oral or fecal-to-oral contact

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13
Q

conditions favoring the development of duodenal ulcers

A
  • normal gastric acid secretion
  • delayed stomach emptying with increased diffusion of gastric acid back into stomach tissues
  • increased stomach emptying
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14
Q

conditions favoring gastric ulcers

A

favoring the development of duodenal ulcers, which are normal diffusion of acid back into stomach tissues with increased secretions of gastric acid and increased stomach emptying.

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15
Q

complications of ulcers: Hemorrhage

A
  • Occurs more often in patients with gastric ulcers and in older adults
  • Patients have a second episode of bleeding if underlying infection with H. pylori remains untreated or if therapy does not include H2 antagonist
  • Massive bleeding = vomiting bright red or coffee- ground blood (hematemesis)
  • Minimal bleeding from ulcers = minimal occult bleeding in a dark, ”tarry” stool (melena), melena may occur with gastric ulcers, more common with duodenal ulcers
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16
Q

complications of ulcers: perforation

A
  • Occurs when the ulcer becomes so deep that the entire thickness of the stomach or duodenum is worn away
  • The stomach or duodenal contents can then leak into the peritoneal cavity
  • Patients can experience sudden, and sharp pain, peritonitis infection, severe illness within hours, bacterial septicemia and hypovolemic shock, paralytic ileus
17
Q

what kind of emergency is peptic perforation

A

surgical emergency and can be life threatening

18
Q

ulcers of complications: pyloric (gastric outlet) obstruction (blockage)

A
  • Occurs in small percentage of patients and manifests with vomiting caused by stasis and gastric dilation
  • Obstruction occurs as the pylorus (the gastric outlet) and is cased by scarring, edema, inflammation, or a combination of these factors
  • Symptoms of obstruction include abdominal bloating, nausea, and vomiting
  • With persistent vomiting, metabolic alkalosis may occur due to loss of large quantities of acid gastric juice in the vomitus
  • Hypokalemia may also occur from the vomiting or metabolic alkalosis
19
Q

complications of ulcers: intractable disease

A

May develop from complications of ulcers, excessive stressors in the patient’s life, or an inability to adhere to long-term therapy

20
Q

peptic ulcer disease diagnostic assessment

A
  • Testing for H. pylori using a urea breath test, the stool antigen test, or serologic blood test
  • Hemoglobin and hematocrit
  • Occult blood in stool
21
Q

peritonitis infection

A

inflammation of peritoneum of blood

22
Q

bacterial septicemia

A

infection in blood stream

23
Q

paralytic ileus

A

muscle of intestines not moving

24
Q

Peptic ulcer disease history

A
  • Assess for causes and risk factors
  • History of H. pylori, GI surgeries (especially partial gastrectomy)
  • Drugs being taken, specifically corticosteroids, chemotherapy, and NSAIDs
  • Any radiation treatments
  • History of GI upset, pain and its relationship to eating and sleeping pattern
25
Q

peptic ulcer disease physical assessment s/s

A
  • epigastric tenderness and pain

- rigid, board-like abdomen with rebound tenderness and pain= peritonitis

26
Q

peptic ulcer diagnostic test

A
  • Testing for H. pylori using a UREA BREATH, THE STOOL ANTIGEN test, or serologic blood test
  • Hemoglobin and hematocrit
  • Occult blood in stool
  • EGD- Most accurate way- direct visualization
  • rapid urease test- can confirm a quick diagnosis
  • nuclear medicine scan
27
Q

peptic ulcer disease prioritize hypotheses

A
  • Acute pain or persistent pain due to gastric and/or duodenal ulceration
  • Potential for upper GI bleeding due to gastric and/or duodenal ulceration or perforation
28
Q

peptic ulcer managing pain: drug therpay

A

Primary purpose is 1) pain relief 2) eliminate H. pylori infection 3) heal ulcerations 4) prevent recurrence

Treatment regime:

  • Proton pump inhibitor (PPI),
  • antibiotics,
  • Bismuth therapy
29
Q

peptic ulcer managing pain: nutrition

A
  • No evidence that dietary restriction reduces gastric acid secretion or promotes tissue healing
  • Bland diet may assist in relieving symptoms
  • Avoid alcohol and tobacco and
  • Avoid bedtime snacks
30
Q

managing upper GI bleed from peptic ulcer disease: nonsurgical management

A
  • Remember – active GI bleeding is a life-threatening emergency!
  • Monitor and manage hypovolemia, electrolyte imbalances, H + H levels, vital signs, and oxygen saturation
  • Nasogastric tube placement and lavage- requires the insertion of a large-bore NGT with installation of a room-temperature solution in volumes of 200 to 300 mL
  • Endoscopic therapy- can assist in achieving homeostasis during an acute hemorrhage by isolating the bleeding artery to embolize (clot) it
31
Q

managing upper GI bleed from peptic ulcer disease: surgical managemt

A
  • Used to treat patients who do not respond to medical therapy or other nonsurgical interventions
  • Treat a surgical emergency that develops as a complication of PUD, such as perforation
  • Two surgical options: minimally invasive surgery vs. conventional open surgery
  • Minimally invasive surgery (MIS)- via laparoscopy may be used to remove a chronic gastric ulcer or treat hemorrhage from perforation
32
Q

home care considerations for peptic ulcer disease

A
  • Assess gastrointestinal and cardiovascular status
  • Assess nutritional status
  • Assess medication history
  • Assess patient’s coping status
  • Assess patient’s understanding of illness and ability to adhere to the therapeutic regimen
33
Q

peptic ulcer evaluating outcomes

A
  • Does not have active PUD or H. pylori
  • Verbalizes pain control or relief
  • Adheres to drug regimen, lifestyle changes
  • Does not experience upper GI bleed, or is managed quickly if GI bleed occurs
34
Q

dumping sydrome

A

A postgastrectomy condition that refers to a group of vasomotor symptoms that occur after eating.

35
Q

dumping syndrome risk factor

A

believed to occur as a result of the rapid emptying of food contents into the small intestine, which shifts fluid into the gut, causing abdominal distention.

36
Q

dumping syndome symtoms

A

Observe for early manifestations of this syndrome, which typically occur within 30 minutes of eating. Symptoms include vertigo, tachycardia, syncope, sweating, pallor, palpitations, and the desire to lie down. Report these manifestations to the surgeon, and encourage the patient to lie down. Monitor the patient for late symptoms.

37
Q

dumping sundrome diet

A

teach the patient to eat a high-protein, high-fat, low-to moderate-carbohydrate diet Acarbose may be used to decrease carbohydrate absorption. A somatostatin analog, octreotide, 50 mcg subcutaneously two or three times daily 30 minutes before meals, may be prescribed in severe cases.

8 ounces or more per day: fish, poultry, beef, pork, veal, lamb, eggs, cheese, peanut butter,Potato, rice, pasta, starchy vegetables,White bread, rolls, muffins, crackers, and cereals (small amount),Two or more cooked vegetables Diet jelly, diet syrups, sugar substitutes

Med Surg 1 (25 decks)

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