Chapter 41 Flashcards
Acute Gastritis
Common causes of acute gastritis include:
NSAID use: Inhibition of prostaglandin synthesis reduces the protective mucosal barrier.
◦Helicobacter pylori (H. pylori) infection: Bacteria colonize the gastric mucosa, causing inflammation.
◦Physiologic stress: Severe illness or trauma can lead to stress ulcers.
◦Other contributing factors: alcohol, digitalis, metabolic disorders (e.g., uremia
Acute Gastritis: Pathophysiology
Acute gastritis involves injury to the protective gastric mucosal barrier. This can be due to:
◦Direct damage from substances like NSAIDs or alcohol.
◦Inflammation triggered by H. pylori.
◦Ischemia from stress, leading to decreased blood flow
Chronic Gastritis: Type A
Type A chronic gastritis (autoimmune/fundal) involves:
◦Loss of T-cell tolerance.
◦Production of autoantibodies to parietal cells.
◦Diminished secretion of acid and intrinsic factor.
◦Increased risk of pernicious anemia due to decreased vitamin B12 absorption
◦Elevated plasma levels of gastrin due to impaired feedback inhibition
Chronic Gastritis: Type B (H. pylori)
Type B chronic gastritis (nonimmune/antral) is primarily associated with H. pylori infection. It can also be linked to chronic use of alcohol, tobacco, and NSAIDs. It is characterized by:
◦High hydrochloric acid secretion (initially).
◦Increased risk of duodenal ulcers.
◦Potential progression to pangastritis (inflammation of the entire stomach)
Duodenal Ulcers: Key Factors
Key factors in the pathophysiology of duodenal ulcers include:
◦Increased acid and pepsin concentrations in the duodenum.
◦Often associated with increased gastrin and stomach acid due to H. pylori in the antrum.
◦Decreased duodenal bicarbonate production.
◦H. pylori activates immune cells and releases inflammatory cytokines, damaging the mucosa.
Gastric Ulcers: Key Defect
The primary defect in the pathophysiology of gastric ulcers is an abnormality that increases the mucosal barrier’s permeability to hydrogen ions
Gastric Ulcers: Contributing Factors
Contributing factors to the development of gastric ulcers include:
◦Chronic gastritis, limiting the mucosa’s ability to secrete protective mucus.
◦Decreased prostaglandin synthesis (e.g., from NSAIDs).
◦Damage from reflux of bile and pancreatic enzymes.
◦H. pylori infection (present in 60-80% of cases).
◦Back-diffusion of acid into the gastric mucosa, leading to further damage and histamine release.
SRMD: Ischemic Ulcers
Ischemic stress ulcers develop due to:
◦Events like hemorrhage, trauma, burns, heart failure, or sepsis.
◦Shock, anoxia, inflammation, and sympathetic responses causing ischemia of the stomach and duodenal mucosa.
◦Disruption of the mucosal barrier.
◦Burns can lead to specific ischemic ulcers called Curling ulcers
SRMD: Cushing Ulcers
Cushing stress ulcers are associated with:
◦Severe brain trauma or brain surgery.
◦Decreased mucosal blood flow.
◦Hypersecretion of acid caused by overstimulation of the vagal nuclei.
◦Damage to the mucosal barrier, leading to erosions and ulceration.
Ulcerative Colitis: Location and Layer
In ulcerative colitis:
◦Inflammation begins in the large intestine, starting in the rectum and potentially extending proximally.
◦Lesions are continuous and limited to the mucosal layer.
◦Skip lesions are not present.
Ulcerative Colitis: Mechanisms
The pathophysiology of ulcerative colitis involves:
◦Inflammation starting at the base of the crypts of Lieberkühn.
◦Decreased mucin secretion, increasing mucosal permeability.
◦Triggering of an inflammatory response with activation of T cells and dendritic cells.
◦Production of pro-inflammatory cytokines.
Crohn Disease: Location and Layer
In Crohn disease:
◦Inflammation begins in the intestinal submucosa.
◦Involvement is transmural (affects the entire intestinal wall).
◦Characterized by discontinuous involvement or “skip lesions” that can occur anywhere from the mouth to the perianal area.
Crohn Disease: Key Features
Key pathological features of Crohn disease include:
◦Inflamed areas mixed with uninvolved areas.
◦Noncaseating granulomas.
◦Formation of fistulas.
◦Deep penetrating ulcers.
◦The distal small intestine and proximal large colon are most commonly involved.
IBS: Contributing Factors
While the exact pathophysiology of IBS is unknown, several factors are thought to contribute:
◦Infection.
◦Alterations in gut microbiota.
◦Immune activation.
◦Serotonin dysregulation.
◦Psychological stress.
◦Abnormal gut function and motility.
◦Diet.
IBS: Visceral Hypersensitivity
A key pathophysiological feature of IBS is visceral hypersensitivity or hyperalgesia, which may originate in either the peripheral or central nervous system and is related to dysregulation of the brain-gut axis.
Portal Hypertension: Cause
Portal hypertension is caused by prolonged elevation of pressure in the portal vein. This often results from increased resistance to blood flow through the liver, commonly due to cirrhosis.
Portal Hypertension: Consequences
Consequences of portal hypertension include:
◦Development of varices (distended collateral veins) in the esophagus, stomach, abdominal wall (caput medusae), and rectum (hemorrhoidal varices).
◦Impaired mucosal defenses in the stomach and esophagus, increasing the risk of erosion, ulceration, and bleeding.
◦Potential for life-threatening hemorrhage from ruptured varices
Ascites: Causes and Mechanisms
Ascites in liver disease is primarily due to:
◦Increased portal hypertension.
◦Splanchnic vasodilation.
◦Increased capillary permeability.
◦Renal retention of sodium and water.
◦Translocation of gut bacteria contributing to inflammation
◦Cirrhosis is the most common cause
Hepatic Encephalopathy: Toxin Accumulation
Hepatic encephalopathy results from the accumulation of toxins in the brain because the diseased liver cannot adequately remove them. The most hazardous substance is ammonia from intestinal protein digestion
Hepatic Encephalopathy: Mechanisms
The pathophysiology of hepatic encephalopathy involves:
◦Liver dysfunction and shunting of blood around the liver.
◦Accumulated toxins altering cerebral energy metabolism.
◦Interference with neurotransmission.
◦Ammonia metabolism to glutamine in the brain, causing osmotic disturbances and astrocyte edema.
◦Disruption of the blood-brain barrier leading to vasogenic edema.
◦Increased GABA levels.
Jaundice: Hemolytic
Hemolytic jaundice (prehepatic) is caused by excessive destruction of erythrocytes, leading to increased unconjugated bilirubin that exceeds the liver’s conjugation capacity.
Jaundice: Obstructive (Cholestatic)
Obstructive (cholestatic) jaundice is caused by obstruction to the passage of conjugated bilirubin from the liver to the intestine. This can be intrahepatic (within the liver) or extrahepatic (outside the liver, e.g., due to gallstones or tumors). The predominant bilirubin in this type is conjugated bilirubin.
Jaundice: Hepatocellular
Hepatocellular jaundice results from the failure of liver cells (hepatocytes) to conjugate bilirubin and/or excrete it into the bile. Both conjugated and unconjugated bilirubin levels are increased. This can be caused by hepatitis or biliary cirrhosis.
Cirrhosis: Key Process
Cirrhosis is an irreversible inflammatory, fibrotic liver disease where normal liver tissue is replaced by scar tissue
