Lecture 12 Flashcards
jaundice, alchoholic liver injury, cirrhosis (59 cards)
What factors make the gastrointestinal tract (GIT) an adverse environment?
Bacteria, acid, chemicals, chemical reactions, and toxins.
How does the lining of the GIT respond to its adverse environment?
It constantly regenerates and combats damage.
Where do peptic ulcers typically form?
In the stomach.
Where do duodenal ulcers form, and how common are they?
They form in the duodenum and are more common than peptic ulcers.
What are some damaging forces that contribute to ulceration?
Gastric acidity, peptic enzymes, H. pylori infection, NSAIDs, alcohol, smoking, delayed gastric emptying, and host factors.
What are some of the stomach’s defensive mechanisms against ulceration?
Surface mucus secretion, bicarbonate secretion, mucosal blood flow, epithelial regenerative capacity, and elaboration of prostaglandins.
What can cause acute gastritis and peptic ulceration?
NSAIDs, alcohol, Helicobacter pylori infection, loss of epithelial cells, decreased mucus secretion, vasodilation, and edema of the lamina propria.
What characterizes chronic gastritis and peptic ulcers?
Often linked to Helicobacter pylori infection (infecting 40% of the Western population, though only 15% develop ulcers) or chemical causes.
How does Helicobacter pylori contribute to ulcer formation?
It attaches to the gastric epithelium, thins the mucus layer through its toxins and inflammation, allowing gastric acid to damage the epithelial cells and underlying tissue.
What are the histological features seen in H. pylori infection?
Presence of neutrophils and lymphocytes indicating inflammation, with damage to the gastric mucosa.
How do NSAIDs lead to mucosal injury and bleeding?
They inhibit COX enzymes, leading to reduced mucosal blood flow, decreased mucus and bicarbonate secretion, impaired platelet aggregation, and increased leukocyte adherence, all of which impair mucosal defenses.
What specific effects does COX-1 inhibition by NSAIDs have on the stomach lining?
Reduced mucosal blood flow and decreased mucus and bicarbonate secretion, compromising the stomach’s defenses.
What are the effects of COX-2 inhibition by NSAIDs?
Reduced angiogenesis and impaired healing, which can worsen mucosal injury in the stomach.
What is the role of proton pump inhibitors in ulcer management?
They block hydrogen/potassium ATPase (gastric proton pump) to reduce stomach acid production.
How do H₂ receptor antagonists aid in ulcer management?
they block acid production by inhibiting histamine action on parietal cells.
What compensatory mechanism can occur with chronic proton pump inhibitor use?
G cell hyperplasia, which increases gastrin to stimulate acid production as a response to reduced acidity.
What are the primary functions of the liver?
Synthesis, metabolism, detoxification, bilirubin conjugation, enzyme production (ALT, AST), albumin production, and clotting factor production.
What are some treatment options for ulcers?
Antibiotics, proton pump inhibitors, H₂ receptor antagonists, and antacids.
What is G cell hyperplasia, and when is it commonly found?
G cell hyperplasia is an increase in the number of G cells, typically seen in chronic proton pump inhibitor use as a compensatory mechanism.
What is bilirubin conjugation?
It is the process where bilirubin, a pigment from red blood cell breakdown, is conjugated with glucuronic acid in the liver, making it water-soluble and excretable in bile.
What role does the liver play in bilirubin metabolism?
The liver conjugates bilirubin with glucuronic acid, making it water-soluble for excretion.
How is bilirubin excreted from the body?
Conjugated bilirubin is excreted into the bile, then into the intestine, and eventually leaves the body through feces and urine.
summary of bilrubin metabolism
“Silly Tired Lizards Swim By River, Kissing Frogs”
S - Senescence (Breakdown of red cells in macrophages)
T - Transport (Unconjugated bilirubin bound to albumin, transported to the liver)
L - Liver Conjugation (Uptake by the liver and conjugation with glucuronic acid)
S - Secretion (Conjugated bilirubin is secreted into bile, goes to intestine)
B - Bacterial Action (In intestine, bacteria convert it to urobilinogen)
R - Reabsorption (Some urobilinogen is reabsorbed and recirculated)
K - Kidney Excretion (Urobilinogen excreted in urine as urobilin)
F - Fecal Excretion (Some urobilinogen oxidized to stercobilin, excreted in feces)
What is jaundice, and what causes it?
jaundice is a yellowing of the skin and eyes due to the deposition of free bilirubin. Causes include hepatic diseases (e.g., hepatitis, drug-induced injury) and bile duct obstruction.
