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NURS 5315 GI Module 9, exam 5 review notes
1. Upper GI organs: mouth, pharynx, esophagus, stomach, and duodenum
2. Lower GI organs: small intestine, large intestine, rectum and anus
3. Hepatoportal circulation: hepatic artery receives oxygenated blood from the inferior mesenteric, gas-tric, and
cystic veins. The hepatic portal vein receives deoxygenated blood from the inferior and superior mesenteric vein and splenic vein and delivers nutrients that have been absorbed from the intestinal system
4. Osmotic diarrhea: Caused by the presence of a nonabsorbable substance in the intestines. This pulls water by
osmosis into the intestinal lumen and results in large volume diarrhea. This is how mag citrate, lactulose and miralax work. Causes include: excessive ingestion of nonabsorbable sugars, tube feedings, dumping syndrome, malabsorption, pancreatic enzyme deficiency, bile salt deficiency, small intestine bacterial overgrowth or celiac disease
5. Secretory diarrhea: Results in large volume losses secondary to infectious causes such as rotavirus, bacterial
enterotoxins, or c-ditt.
6. Motility diarrhea: AKA short bowel syndrome. Results from resection of small intestine or surgical bypass of small
intestine, IBS, diabetic neuropathy, hyperthyroidism, and laxative abuse. Fatty stools and bloating are common in malabsorption syndrome. Complications include: dehydration, electrolyte imbalance, metabolic acidosis, weight loss and malabsorption.
7. Upper GI bleed: bleeding that occurs in the esophagus, stomach or duodenum commonly caused by bleeding
varices, peptic ulcers or Mallory-Weiss tear(tearing of esophagus from stomach) Characterized by frank, bright red or cottee ground emesis.
8. Lower GI bleed: Bleeding in the jejunum, ileum, colon or rectum from inflammatory bowel disease, cancer, diverticula
2 / or hemorrhoids. Hematochezia, or the presence of bright red blood in the stools, suggest what kind of bleed
9. Peptic Ulcer Disease: Is a break in the integrity of the mucosa of the esophagus, stomach or duodenum resulting
in exposure of the tissue to gastric acid. Risk factors include smoking, advanced age, NSAID use, ETOH, chronic disease, acute pancreatitis, COPD, obesity, socioeconomic status, gastrinoma, and infection with Helicobacter pylori. S&S: Epigastric pain is worse with eating, melena or hematemesis
10. Duodenal ulcers: most common and tend to develop in younger patients. S&S: epigastric pain that is
relieved by food. Patients may have melena(black and tarry stool) or hematemesis
11. Ulcerative colitis (UC): Inflammatory disease of the large instestine in persons 20-40y/o. Less common in
people who smoke. Has periods of remission and exacerbations. Characterized by inflammation and ulcerations that remain superficial and in the small intestine.
12. UC S&S: recurrent diarrhea, bloody stools, febrile, polyarthritis, uveitis, sclerosing cholangitis, erythema
nodosum and pyoderma gangrenosum
13. UC complications: fissures, hemorrhoids, perirectal abscess, toxic megacolon, colon perforation, and
colorectal adenocarcinoma. Increased risk of VTE and microthrombi, and colon cancer
14. Crohn's disease: Chronic inflammatory disorders that can attect any portion of the GI tract but most often in
the ileum and proximal colon. Attects persons in their 20-30s and of jewish decent. CARD15/NOD2 gene mutation commonly associated.
15. Crohn's disease risk factors: smoking, family history, Jewish decent, age less than 40, slight
predominance in women and altered gut microbiome.
16. Crohn's disease patho: includes trasmural involvement of the attected area(entire wall of intestine is
4 / Partial SBO causes diarrhea. Complete SBO causes constipation and increased bowel sounds
23. Large bowel obstruction: not as common and typically occurs 2nd to a tumor, but can also be
diverticulitis, inflammatory bowel disease and volvulus. S&S: hypogastric pain, abdominal distention and vomiting which will occur late
24. Portal Hypertension: Abnormally high blood pressure in the portal venous system caused by resistance to
portal blood flow. Commonly caused by fibrosis, obstruction from cirrhosis, thrombosis, or narrowing of hepatic portal vein. Most common S&S is vomiting blood from bleeding esophageal varices.
25. Ascites: accumulation of fluid in the peritoneal cavity and is a complication of portal hypertension. Cirrhosis
is most common cause. S&S: abdominal distension, increased abd girth, weight gain and in large volumes dyspnea, increased respiratory rate, peripheral edema, dilutional hyponatremia and may develop peritonitis.
26. Hepatic Encephalopathy: due to ammonia accumulation. Ammonia causes the neurons to swell
which leads to cerebral edema and IICP. Triggers for this include: ETOH abuse, infection, GI bleed, portal vein thrombosis, sedatives, volume depletion, constipation, electrolyte imbalances and diuretics. Asterixis AKA liver flap is most common sign.
27. Jaundice: not a disorder but a manifestation. It is the yellowing of skin and other tissues. Visible when bilirubin
reaches 2.5-3mg/dL.
28. Non-obstructive jaundice: Increase in the amount of indirect(unconjugated) bilirubin typically from RBC
hemolysis. Caused from ABO or RH incompatibility, sickle cell anemia, in newborns, and hepatocellular damage from hepatitis, cirrhosis or cancer. Total bili levels are elevated, direct bili is low and indirect bili is high
29. Obsructive jaundice: Occurs when the liver can conjugate bilirubin fine but there is an obstruction of
outward flow to the intestines. Most commonly caused by obstruction in the biliary tract. Hallmark sign is gray stools
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30. Alcoholic Cirrhosis: The change of healthy liver parenchyma to fibrotic scar tissue which is nonfunction-ing.
The injury results in cellular necrosis, inflammation and regeneration which leads to fibrosis. The fibrotic changes compress the blood vessels and develop portal hypertension.
31. Effects of cirrhosis: Decreased clotting factors, decreased synthesis of albumin, ascites, decreased detox of
medications, hormones and toxins, jaundice, esophagel and gastric varices, anemia, hematemesis/cottee ground emesis, black stools, splenomegaly, portopulmonary syndrome(pulmonary arterial vasoconstriction and vascular remodeling), hepatopulmonary syndrome, hepatorrenal syndrome
32. Hepatopulmonary syndrome: Pulmonary complication of portal hypertension causing Intrapul-
monary arteriovenous dilation and R to L shunt causing hypoxemia
33. Hepatorenal syndrome: renal failure caused by severe renal vasoconstriction or decreased perfusion
34. Autoimmune Hepatitis: Autoimmune inflammatory liver disease that is triggered by infection or drugs.
There may be no symtpoms and persons respond to immunosuppressive drug therapy with remission within 24 hours. Relaspes are common with treatment withdrawal
35. Hepatitis A: Incubation-30 days. Transmission-Fecal oral route. Period of communicability-up to 1 week
after onset of jaundice. Chronic carrier-no. Age-children and young adults. Vaccine-yes. Prevention-hand washing, and vaccine. IG availabe-yes. Household contacts treated
36. Hepatitis B: Incubation-60-180days. Transmission-blood and body fluids. Period of communicabiltiy-as long
as they are positive for HBsAg. Chronic carrier-yes. Age-any. Vaccine-yes. Prevention-vaccine, no kissing, safe sex. IG available-yes. Household contacts treated
37. Hepatitis C: Incubation-35-72 days. Transmission-Blood and body fluids. Period of communicability-indef-
7 / age, female gender, oral contraceptives, native american ancestry, ileal disease, low HDLs, malabsorption disorders and hypertriglyceridemia.
47. Gallstones S&S: May not cause any S&S if they are small. Some can pass into the common bile duct and
cause an obstruction which will cause painful spasms and contraction of the bile duct in the RUQ area called biliary colic. Pain is also felt in the back, right should or right scapula. N/V.
48. Cholecystitis: inflammation of the gallbladder from obstruction in biliary tract. S&S: precipitated by a fatty meal,
GERD, positive murphy's sign and rebound tenderness. Lab abnormalities include leukocytosis, increased alkaline phosphatase and direct bilirubin.
49. Acute Pancreatitis: the escape of pancreatic enzymes into the surrounding area and into the pancreas.
Enzymes begin the digestive process of the tissues they touch which may lead to hemorrhaging.
50. Acute pancreatitis causes: ETOH, gallstones, PUD, abdominal trauma, hyperlipidemia, smoking,
some drugs, genetic factors, viral infections, autoimmune, ischemia, post ERCP, scorpion bite.
51. Acute pancreatitis S&S: abrupt post prandial pain, epifastric pain that radiates to the back and is worse
when lying down, n/v and if hemorrhaging occurs then persons will have signs of hypovolemic shock, fever, hypocalcemia, jaundice and a lot of fluid loss
52. Acute pancreatitis diagnosis and complications: 1 of 3: symptoms consistent with acute
pancreatitis, elevated lipase or findings consistent with acute pancreatitis on CT. Complications: ARDS, heart failure, renal failure, coagulopathies, sepsis, paralytic ileus and GI bleed
53. Esophageal cancer: not common. Related to chronic inflammation and metaplastic changes in the
esophagus. Do not show signs until later in the disease. 2 main symptoms are chest pain and dysphagia
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54. Colon cancer: Occurs in any portion of colon or rectum in persons over 50.. Casues age, high fat, low fiber
diets, smoking, obesity, family history, low levels of exercise, inflammatory bowel disease and gastrectomy. Commonly arise from polyps
55. Colorectal cancer signs and screening: S&S: pain, abdominal mass, anemia, occult bleeding,
obstruction, distention. Screening starts at age 50 and includes yearly test for occult blood, colonoscopy every 5-10 years, sigmoidoscopy every 5 years
56. Pancreatic cancer: Incidence increases with age and is more common in males and african americans.
Risk factors: ETOH use, family history, smoking, non O blood type, DM type 2, and chronic pancreatitis. K-ras mutation, a proto- oncogene is most common genetic alteration. Tumors arise from exocrine cells of pancreas ducts, called adenocarcinomas; tumors of the head of pancreas grow quickly and can obstruct the portal veins and common bile duct
57. pancreatic cancer: what S&S are jaundice, dull back pain, protein and fat malabsorption, lethargy, weight
loss, n/v, diabetes, changes in bowel patterns and pruritis
58. Cleft lip/palate: abnormalities that arise during embryonic development due to vit. B6, folic acid and B
deficiencies, smoking, ETOH ingestion during pregnancy, steroid or statin use, maternal hyperhomocysteinemia, diabetes and genetic mutations.
59. Pyloric stenosis: the pylorus is narrowed which slows the flow of food from stomach to deuodenum. most
common cause of intestinal obstruction in infancy. Usually causes vomiting after eating. Increase gastrin secretion in 3rd trimester has been linked to cause this. Other causes include deficiency in nitric oxide synthase containingneu-rons, abnormal innervation of myenteric plexus and presence of infantile hypergastrinemia and exposure to macrolide antibiotics
10 / Minimal: Abnormal psychometric testing, but do not have any S&S that are consistent with hepatic encephalopathy Nonspecific/covert Grade I: Oriented to time and space, but lack of awareness, anxiety, altered attention span, inability to perform simple addition or subtraction, may have impaired sleep patterns Nonspecific/covert Grade II: Disoriented to time, apathetic lethargic, dyspraxia, asterixis, personality changes, Obvious/overt S&S to hepatic encephalopathy Grade III: Obvious/overt S&S, D disoriented to space, semi-stuporous, but responsive to stimuli, obvious confusion, may have bizarre behavior Grade IV: Obvious/overt S&S, COMA, NO response to painful stimuli, @ risk for respiratory failure, as they cannot protect or maintain their airway
66. ammonia: end product of protein metabolism
67. cleft lip: what is an incomplete fusion on the nasomedial and intermaxillary process that fuses during the 4th
week of gestation
68. cleft palate: what is the failure of the primary palatal shelves or processes to fuse during the 3rd month of
gestation; can occur w or w/o the other type
69. hydrostatic
pressure excess oncotic pressure: When what exceeds it forces fluid out of mesenteric veins into the peritoneal cavity --> ascites
