Module 7: Digestive System Disorders

GERD

Gastroesophageal reflux disease

Development of GERD

Return of stomach contents into the esophagus due to lower esophageal sphincter relaxation or gastroparesis, leading to heartburn and dyspepsia. Long-term inflammation can result in fibrosis and precancerous lesions.

Dyspepsia

Indigestion

Factors increasing GERD likelihood

Infancy, increased intra-abdominal pressure, smoking, certain foods, lupus

Peptic ulcer

Breakdown in the protective mucosal lining of the lower esophagus, stomach, or duodenum

Melena

Black-foul smelling stools

Complications of peptic ulcers

Hemorrhage, perforation, penetration, gastric/duodenal outlet obstruction

Pathophysiology of peptic ulcers

H. pylori penetration and NSAIDs inhibiting prostaglandin synthesis

Duodenal ulcers

• Caused by H. pylori & chronic use of NSAIDs

• occur with greater frequency than other types of peptic ulcers

• tend to develop more in younger people, and in males

Differences between duodenal and gastric ulcers

Pain pattern, age affected, chronicity

Treatments for peptic ulcers

Eradicate H. pylori, antacids, proton pump inhibitors, H2 receptor antagonists, surgery

crohn’s disease

inflammatory disease of the intestine, thought also to be unregulated response against bacteria

Ulcerative colitis

chronic inflammatory disease of colon

Tenesmus

Urge to defecate even if the colon is empty

Toxic megacolon

Abrupt increase in colon diameter

Celiac disease

Malabsorptive disease where the mucosa fails to absorb digested nutrients

Development of celiac disease

T cell immune reaction to gluten damaging small intestine villi

Clinical manifestations of celiac disease

Failure to thrive, abdominal pain and bloating, diarrhea with fatty stools, malabsorption

Portal hypertension

High blood pressure in the portal venous system

Ascites

Fluid accumulation in the peritoneal cavity due to portal hypertension or decreased serum protein

Ascites treatment

Paracentesis (drainage of fluid from abdominal cavity using a needle); caution to avoid shock; reoccurs if liver issue persists

esophageal varices

varicose veins on the esophageal wall

caput medusa

collateral veins form varices on abdominal wall

Hepatic encephalopathy

toxins remain in bloodstream and reach the brain

• clinical manifestations include personality changes, coma

Asterixis

Flapping of hands

Icterus

• technical term for jaundice

• green/yellow tinge to the skin caused by hyperbilirubinemia

• yellow discolouration occurs first in the sclera of the eye, and then the skin

Light feces and dark urine in jaundice

Poor liver function prevents bilirubin reaching intestines; bilirubin in bloodstream darkens urine

Jaundice occurrence

First in the sclera of the eyes

Splenomegaly in liver disorders

Due to portal hypertension, affects blood cell numbers

Acute hepatitis

Liver inflammation caused by viral strains A, B, C, D, E

Viral strains in hepatitis

A, B, C, D, E

Infection routes of HAV vs

Ingestion vs. body fluids

Liver damage in acute hepatitis

Destruction of hepatocytes, scarring, hyperplasia of hepatic macrophages

Determining hepatitis virus type

Specific antibody assay

Stages of acute viral hepatitis

Prodromal, icteric, convalescent

Chronic hepatitis

Persistent liver inflammation post-acute HBV, HCV infection; can lead to cirrhosis, liver cancer

Cirrhosis

scarring of the liver tissue

Hepatotoxin

Toxins causing liver damage

Disorders from cirrhosis

Hepatomegaly, splenomegaly, ascites, portal hypertension, encephalopathy, varices

Liver alterations in cirrhosis

Metabolism and structure changes due to channel blockage

Cirrhosis "treatment"

Managed but not cured; includes rest, nutrition, complications management, possible transplant

Liver failure

Reduced liver function affecting synthesis and metabolism

Clinical manifestations of liver failure

Result from acute or chronic diseases

epistaxis

nose bleeding

chronic pancreatitis

Prolonged, progressive, and irreversible destruction of the exocrine and endocrine pancreas leading to malabsorption, weight loss, and diabetes mellitus.

Inflammatory cytokines

Released into the bloodstream due to pancreatic damage, causing systemic effects like nausea, vomiting, and anorexia.

Chronic alcohol abuse

Most common cause of chronic pancreatitis

Pancreatic cancer

Risk factor for developing chronic pancreatitis

hematemesis

• vomitting of blood, bright red or “coffee ground”

cholelithiasis

formation of gallstones

cholecystitis

inflammation of the gallbladder - if gallstones obstruct the outlet to the gallbladder

gastroparesis

slowing of food movement from the stomach