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Cindy Exam 9

Billroth I Distal stomach is removed and gastric remnant is anastomosed directly to the duodenum
Billroth II Distal stomach and proximal/duodenum are resected, open duodenal stump is sutured closed and the gastric remnant is anastomosed to the jejunum with an end to end or side to side anastomosis
Total Gastrectomy Entire stomach, distal esophagus, and proximal cuff is removed. Gastrointestinal tract is reconstructed with an esophagojejunostomy
Vagotomy Surgical interruption of gastric vagal nerve fibers, which are the parasympathetic nerves that stimulate gastric secretion and mediate gastric motility
Signs of Postprandial Dumping Syndrome Sweating, weakness, nausea, vomiting, diarrhea. LOW CARB. Sandostatin
Reactive Hypoglycemia High protein, low carb, with feeds containing glucose between meals. Admin insulin as ordered before meals.
S/S of Intraabdominal Infection and Septic Shock Abdominal tenderness, distention, tachycardia, tachypnea, fever, hypotension
S/S of Compromised Nutrient Absorption Diarrhea, flatulence, cramping, nausea, anorexia
S/S of Short Bowl Syndrome Steatorrhea, weight loss, malabsorption, malnutrition, and fluid and electrolyte imbalance
S/S of Listeriosis Fever, muscle aches, nausea, diarrhea. If spreads to nervous system: headache, stiff neck, confusion, loss of balance, and convulsions
Listeriosis and Pregnancy Pregnant women are at risk. May experience only mild flu-like symptoms, however, infection during pregnancy can cause premature delivery, infection of NB, or stillbirth. Blood test most reliable way to determine listeriosis in pregnancy
Salmonella Fecal-oral route, incubation period is 8 to 48 hours after ingestion. Symptoms: 3 to 5 days of fever, nausea, vomiting, cramping abdominal pain and diarrhea that may be bloody. Bacterium may localize in joints or bone. Diagnose with stool culture.
Crohn's Disease Chronic, inflammatory disease that can affect any are of the alimentary canal from mouth to anus. Affects 15-30 year olds. Autoimmune response. Characterised by normal bowl with diseased segments and lymph node enlargement
Initial S/S of Crohn's Malaise, anorexia, fever, abd. discomfort
Later S/S of Crohn's Increased abd. pain and diarrhea with frequent small-volume non-bloody stool without mucus or pus
Dietary Factors for Crohn's Chemical food additives, refined carbs, heavy metals, low fiber diet
Extraintestinal Manifestations with Crohn's Systemic involvement (joint problems), skin lesions, ocular disorders, and oral ulcers
Ulcerative Colitis Chronic inflammatory condition affecting the mucosa of the colon and rectum. Autoimmune. Characterized by usually the mucosa layer of the colon is involved, remissions and exacerbations, and crypt abscesses
Clinical Manifestations of Ulcerative Colitis Rectal bleeding and diarrhea, small frequent stool with blood, pus and mucous or high volume watery diarrhea
Systemic Manifestations of Ulcerative Colitis Skin lesions, eye lesions, joint abnormalities, and liver disease
Nsg Interventions for Ulcerative Colitis Do not administer diphenoxylate or codeine to patient with severe inflammation or signs toxic megacolon
E. histolytica (Cysts and Trophozoites) Amebic dysentery. Trophozoites die, cysts remain in warm environment. Humans who eliminate cysts are infectious. It feeds on bacteria in intestine or invades and ulcerates the mucosa of the large intestine
S/S of E. histolytica None to severe. Mild to mod: odiferous stool with mucous, cramping, flatulence, fatigue, weight loss. Severe: Frequent liquid stools with mucous and blood, high fever, abd. tenderness, vomiting
Complications of E. histolytica Appendicitis and bowel perforation
Extra Intestinal Amebiasis Without symptoms of intestinal infection (ex) amebic liver abscess, fever, pain and enlarged liver. If ruptures, death can result
Dx of E. histolytica Serial examinations of stool, sigmoidoscopy for ulcerations
Tx of E. histolytica metronidazole (Flagyl), diloxanide furoate (Entamide), tetracycline hydrochloride (Sumycin)
G. lamblia Protozoal parasite that causes superficial invasion, destruction, and inflammation of the mucosa in the small intestine. Trophozoite and cyst form. Humans = host. Beavers and dogs = reservoirs. Infects intestines causing diarrhea or malabsorption synd
Tx of G. lamblia tinidazole (Fasigyn), stools assessed for 2 weeks after therapy
Health Teaching for Parasitic Infections Avoid contact with stool, keep toilet areas clean, hand washing with antimicrobial soap after bowl movements, avoid rectal sexual contact, water analyzed
Acute Gastritis Temporary inflammation of gastric mucosa due to irritants (alcohol, aspirin, antiinflammatory drugs, corticosteroids, metabolic disorders, physiologic stressords like burns or traumas, reflux of bile salts, intense emotions
Mechanisms of Damage for Gastrtitis Reduced gastric blood flow, decreased mucus production, disruption of junctions between epithelial cells, inhibition of prostiglandins
Cushing's Ulcer Acute gastritis from an alteration in intracranial processes characterized by hypersecretion of gastric acid in response to extreme vagal stimulation
Ischemic Ulcer Actue gastritis induced by decreased gastric blood flow which may occur after major burns, trauma, or sepsis. Bleeding is major clinical manifestation that usually occurs 2 to 10 days after stress event
Chronic Gastritis Progressive disease that occurs primarily in the elderly
Type A (Fundal) Gastritis More severe, degeneration of the mucosa in both the body and fundus of the stomach. Associated with pernicious anemia and gastric malignancies. More common in women. Gastric function is reduced.
Type B (Antral) Gastritis More common and less limited to the antral area at the stomach. Causes: possible chronic reflux of bile and/or C. pylori
S/S of Chronic Gastritis Anorexia, fullness, n/v, epigastric pain, steatorrhea, gastric bleeding, pernicious anemia
Peptic Ulcer Disease Ulcerations in mucosal lining of lower esophags, stomach or proximal small intestine. Two most common types are duodenal and gastric
Duodenal Ulcers Occur between 40 to 60 years of age. Caused by increased level of gastric acid. Precipitating factors: type O blood, long standing anxiety, smoking, caffeine, alcohol, and irritating drugs
Pathophysiology of Duodenal Ulcers Inc. acidity erodes mucosal barrier, back diffusion of hydrogen ions into gastric epithelial cells, histamine released, inflammation which further stimulates acid production, mucosal edema, Heliobacter pylori bacteria. Pain/food relief pattern. Intermitt
Gastric Ulcers Antral area of stomach, chronic in nature. S/S: pain is not relieved by eating, fullness, nausea, vomiting, weight loss
Complications of Peptic Ulcers Perforation, penetration, obstruction, intractability, H. pylori?
Gastroenteritis Inflammation of the stomach and intestinal tact. Commonly caused by viral or bacterial infections and characterized by anorexia, nausea, vomiting, cramping pain, and diarrhea. Viral lasts 24-48 hours, bacterial 5-10 days and may require antibiotics
Appendicitis Inflammation of appendix. Caused by systemic infections, hardened stool, seeds or tumors. S/S LRQ pain, anorexia, n/v, low-grade fever. Comlications: perforation, abscess formation, peritonitis
Primary Peritonitis Infection caused by blood-born organisms from genital tract
Secondary Peritonitis Inflammation from contamination by GI secretions
Paralytic Ileus Result of peritonitis. Peristaltic inhibition due to gaseous distention, F&E disturbance (hypokalemia) and sympathetic stimuli
Clinical Manifestations of Paralytic Ileus Abd. pain, gradual or abrupt, from dull to intense, heneralized or localized, n/v, abd. distention, temperature, hypovolemia
Diverticulitis Inflamed sac like outpouching of the colon wall caused by herniation of the mucosal and submucosal layers through weak points in the colonic musculature. Usually in sigmoid. Progressive. Contrib. factors: low fiber diet, hypertrophy of colonic musc.
Complications of Diverticulitis Peritonitis, bleeding, fistula formation, ureteral obstruction, intestinal obstruction
Cholecystitis Inflammation of the gallbladder, associated with cholelithiasis or the presence of gallstones
Gallstones Cholesterol and pigmented stones
Cholesterol Stones Develop when there is an imbalance in cholesterol, bile salts, and phospholipids (lecithin). Imbalance occurs if there is biliary stasis and/or excess of factors promoting precipitation
Pigmented Stones Will develope when bilirubin and ionized Ca exceed their solubility levels and begin to precipitate. Conditions such as hemolysis and cirrhosis will predispose person (unconjugated bilirubin)
Cholecystis Develops when stones become impacted in the cystic duct. Stones that are dislodged pass through biliary ducts into the intestine or they stay in the gallbladder
Chronic Cholecystitis Repeated episodes of RUQ pain, dyspepsia, heartburn, and nausea after eating fatty food
S/S of Acute Cholecystitis RUQ pain, tenderness, anorexia, n/v, jaundice will occur if the common bile duct is obstructed by calculi
People at Risk Obesity, sedentary lifestyles, multiparidy, increased protein diet, and gastric bypass
Created by: mollyluvender