Lecture notes

Nurs 208 Gastrointestinal Pathophysiology Terms and Objectives

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Module
NURS 208

Institution
San Diego State University

This is a comprehensive and detailed note on Gastrointestinal Pathophysiology ;Terms and Objectives for Nurs 208. *Essential!! *Precise!! *For you!!

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Uploaded on August 19, 2024
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nurs 208
university
pathophysiology
san diego
university
state
fall
summer
spring
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2025
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gastrointestinal
san diego state university
gastrointestinal pathophysiology

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Gastrointestinal Pathophysiology

Key Terms
1. Bilirubin: byproduct of the destruction of aged RBCs (which are absorbed and destroyed by
macrophages called Kupffer cells)
2. Jaundice: bilirubin being detoxified by the skin over time, yellow pigmentation of the skin
caused by ↑ levels of bilirubin in the bloodstream.
-cause: extrahepatic obstruction of blood flow, intrahepatic obstruction, excessive hemolysis of
RBCs
3. Hemolytic jaundice: excessive hemolysis (destruction) of RBCs. Metabolism of the heme
component of destroyed RBCs exceeds the conjugation ability of the liver -> ↑ unconjugated
bilirubin
-usually when blood is given that is not your own -> liver tries to break it down constantly
-causes blood transfusion reaction, sickle cell crisis, hemolytic anemia
4. Complement: system of proteins activated or increase the activity of immune response, or
destroy pathogen (p 138)
5. Hemolytic anemia (p 514) premature destruction of RBC.
6. Hepatitis: infection of the liver caused by a strain of the hepatitis virus. All types can cause
hepatic cell necrosis, Kuppfer cell hyperplasia, and infiltration of liver tissues by phagocytes ->
obstruct big flow and impair hepatocyte function
7. Cirrhosis: irreversible inflammatory fibrotic liver disease, slows the flow of blood back to the
heart. most common cause of ascites. Continued heavy drinking of alcohol
8. Liver cancer: risk factors are obesity, cirrhosis, alcohol abuse, infection with Hep. B,C,D. It
invades the hepatic and portal veins and often spreads to the heart and lungs. Patients with
cirrhosis, jaundice, and lack of appetite -> Hepatocellular carcinoma. Obstruction of the tumor ->
portal hypertension and ascites
9. Physiologic jaundice: frequent problem in healthy newborns caused by lack of bilirubin
maturation and conjugation. immature liver cannot remove the bilirubin quickly enough. Vitamin
K isn’t adequately produced leaving intracranial hemorrhage to result
10. Vitamin K: helps you clot, administered to newborns to prevent stroke
11. Portal hypertension: abnormally high BP in the portal venous system caused by resistance
to blood flow. In an attempt to equalize the pressure between the 2 systems, collateral vessels
develop (hemorrhoids and esophageal varices). Normal is 3 mm Hg, PH is 10 mm Hg or more
-Hepatic portal vein- returns blood to your heart on the right side. back up of blood in the
hepatic portal vein -> portal hypertension (congestion in the liver) -> poor functioning heart and
inflamed liver -> not gonna make bile -> can’t get the necessary nutrients

, 12. Ascites: accumulation of fluid in the peritoneal cavity -> ↓ fluid for normal physiological
functions. because without albumin it won’t help fluid stay in the correct spaces. Other organs
are squashed. DONT GIVE MEDS (wont be effective) not good auto-regulation
-treatment: tap the fluid, then give with IV fluids and little food
13. Hydrostatic pressure: mechanical force of fluid pushing against cellular membranes
14. Oncotic pressure: movement of water being dictated by albumin, so it doesn't leaks out
15. Ammonia: toxic to living cells, produced when proteins are broken down
16. GI bleed: poor ability to clot secondary to liver impairment. Symptoms: hematemesis
(vomiting of blood), melena (dark, tarry stools), hematochezia (frank bleeding from the rectum).
(pg 909) Occult bleed: slow, chronic blood loss -> iron deficiency anemia
17. Barrett’s Esophagus: columnar rather than squamous epithelium in the lower esophagus.
Manifestation of adenocarcinoma development in Esophageal cancer.
18. GERD: gastroesophageal reflux disease - reflux of acid and pepsin or bile salts (alkaline)
from the stomach into esophagus that causes esophagitis
19. H. Pylori: bacteria in the stomach -> can cause duodenal and peptic ulcers and acute
gastritis when infected; H. pylori mucosal infection underlies gastric and duodenal ulcers and
gastric cancer. H. pylori that carry the CagA gene that produces VacA is associated with gastric
adenocarcinomas.
20. Pepsinogen: converts to pepsin (pH = 2) which is an enzyme that breaks down protein and
forms polypeptides in the stomach
21. Pancreatitis: acute- due to obstruction to the outflow of pancreatic enzymes by stones
obstructing the bile or pancreatic duct. Also caused by alcohol, drugs or viral infection. enzymes
(activated trypsin activates chymotrypsin, lipase, elastase) get activated and released -> auto
digestion of pancreatic cells and tissues -> inflammation
chronic- progressive fibrotic destruction of the pancreas. Mostly caused by chronic alcohol
abuse. Toxic metabolites and release of inflammatory cytokines -> destruction of acinar cells
and islets of Langerhans
22. Amylase: enzyme that initiates carbohydrate digestion in the mouth and stomach (typically
elevated when the patient has pancreatitis)
23. Lipase: fats (pancreatic enzymes) -> fat necrosis (typically elevated when the patient has
pancreatitis)
24. Trypsin: proteolytic (protein digesting) enzymes
25. Cholecystitis (inflammation in the gallbladder): acute or chronic; gallstones lodged in the
cystic duct and blocks the bile duct -> bile is being backed up -> gallbladder becomes distended
and inflamed -> ↓ blood flow -> ischemia, necrosis and perforation

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Nurs 208 Gastrointestinal Pathophysiology Terms and Objectives

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