DIGESTIVE SYSTEM DISORDERS - MODULE 7

What is gastroesophageal reflux disease (GERD) and how does it develop?

• return of stomach contents into the esophagus

• caused by:

  • relaxation of the lower esophageal sphincter

  • gastroparesis (slowed stomach emptying)

    • increasing gastric volume and pressure

• reflux can occur in healthy individuals

  • stomach contents are usually cleared within minutes

What are the clinical manifestations and complications of GERD?

• heartburn

  • burning sensation beneath the sternum

• dyspepsia

  • indigestion

• frequent reflux

  • causing esophagitis

• long-term inflammation

  • can lead to fibrosis and precancerous lesions

What factors increase the likelihood of GERD?

• infancy

  • positional factors and reduced sphincter tone

• increased intra-abdominal pressure

  • obesity

  • pregnancy

• smoking

• foods and drinks that relax the lower esophageal sphincter (LES)

  • fats

  • coffee

  • alcohol

• lupus

  • connective tissue problems increasing the risk of GERD

What is peptic ulcer disease (PUD)?

• breakdown of the protective mucosal lining

  • lower esophagus

  • stomach

  • duodenum

• ulcers can be:

  • single or multiple

  • acute or chronic

  • superficial (erosions) or deep

What are the complications of peptic ulcer disease (PUD)?

• hemorrhage

  • hematemesis (vomiting blood)

    • bright red or coffee-ground appearance

  • melena (black, foul-smelling stools)

• perforation

  • ulcer erodes through the wall

  • contents enter the peritoneum

• penetration

  • ulcer erodes into another organ

    • e.g. liver

• gastric/duodenal outlet obstruction

  • caused by edema or scarring

How does Helicobacter pylori (H. pylori) cause peptic ulcers?

• stomach acid maintains the mucin layer

  • keeping it in a spongy, gel-like state

  • preventing H. pylori from penetrating

• H. pylori releases urease

  • neutralizing stomach acid

  • liquefying the mucin layer

• H. pylori penetrates the mucin layer

  • reaching epithelial cells

  • causing inflammation

How do NSAIDs contribute to peptic ulcer disease?

• prostaglandins normally:

  • inhibit stomach acid secretion

  • stimulate mucus and bicarbonate secretion

• NSAIDs inhibit prostaglandin production

  • decreasing mucus and bicarbonate secretion

  • increasing stomach acid production

• reduced protection of the stomach lining

  • making it vulnerable to injury from acid and enzymes

What are gastric ulcers and what causes them?

• commonly develop in older adults

  • ages 55–65

• about ¼ as common as duodenal ulcers

• major causes:

  • H. pylori infection

  • chronic NSAID use

What are the clinical manifestations and characteristics of gastric ulcers?

• intermittent epigastric pain

  • pain in the upper abdomen

  • frequently occurs immediately after eating

• more chronic than duodenal ulcers

  • requiring longer treatment

What are duodenal ulcers and what causes them?

• most common type of peptic ulcer

• commonly develop in:

  • younger people

  • males

• major causes:

  • H. pylori infection

  • chronic NSAID use

What are the clinical manifestations of duodenal ulcers?

• chronic intermittent epigastric pain

  • pain in the upper abdomen

• pain begins 2–3 hours after eating

  • when the stomach is empty

• pain is rapidly relieved by:

  • eating food

  • taking antacids

How is peptic ulcer disease treated?

• eradicate H. pylori

  • antibiotics

• reduce stomach acidity

  • antacids: e.g. calcium carbonate

  • proton pump inhibitors (PPIs):

    • interfere with hydrogen ion secretion from parietal cells

  • H2 receptor antagonists:

    • block histamine action, reducing HCl secretion

• surgical treatment

  • minimally invasive resection if ulcers are bleeding or have perforated the GI wall

What is ulcerative colitis?

• a chronic inflammatory disease of the colon

• causes ulceration of the colonic mucosa

  • most common in the rectum and sigmoid colon

  • usually begins in the rectum and spreads continuously

• cause is unknown

  • may involve a loss of normal tolerance to gut bacteria

  • this leads to an unregulated immune response

• risk factors

  • age: 20–40 years

  • family history

How does ulcerative colitis develop?

• inflammation causes edema and thickening of the colon wall

• destruction of the mucosa causes:

  • bleeding and pain

  • an urge to defecate, even when the colon is empty (tenesmus)

• common symptom: frequent bloody diarrhea (1–10+ bowel movements per day)

What are the complications of ulcerative colitis?

• fluid loss, bleeding, and inflammation can cause dehydration, weight loss, anemia, and fever

• increased risk of colon cancer

• severe cases can cause toxic megacolon

  • sudden increase in colon diameter over one to several days

  • may lead to colon rupture

What are the treatments of ulcerative colitis?

• anti-inflammatory drugs

• IV fluids for dehydration and malnutrition

• surgical removal of the colon and anus

  • requires a colostomy bag

What is Crohn’s disease?

• chronic inflammatory disease of the intestine

• thought to involve an unregulated immune response against bacteria

• affects both the small and large intestines

• rectum is seldom involved

How does Crohn’s disease affect the intestinal wall?

• inflammation begins in the submucosa

• neutrophils and macrophages cause tissue injury

• granulomas develop in the intestinal wall

• lesions have a cobblestone appearance

• inflammation affects the full bowel wall, from mucosa to serosa

• inflammation may occur in patches called skip lesions

What are the risk factors and long-term changes of Crohn’s disease?

• bowel becomes thickened and inflexible over time

• risk factors:

  • family history

  • age 20–30

  • slightly more common in women

What are the symptoms of Crohn’s disease?

• may remain asymptomatic for years

• most common symptom: diarrhea

  • less commonly bloody than in UC

• may also cause:

  • tenesmus

  • weight loss

  • abdominal pain, usually in the lower right quadrant

• can occur sporadically

What are the complications and treatments of Crohn’s disease?

• absorption problems can cause:

  • electrolyte imbalances

  • anemia

  • vitamin B12 deficiency if the ileum is involved

• complications:

  • toxic megacolon (less common than in UC)

  • fistulas

  • abscesses

  • intestinal obstruction

• treatment: similar to ulcerative colitis

What is celiac disease?

• a malabsorption disease where the intestinal mucosa cannot absorb digested nutrients

• also called:

  • sprue

  • gluten-sensitive enteropathy

How does celiac disease develop and how is it treated?

• T-cell mediated immune disorder

• gliadin triggers an intense immune reaction

• inflammation damages the small intestinal villi

  • interferes with absorption of macro and micronutrients

• usually in infants but can occur at older ages

• treated by a gluten free diet

What are the common symptoms of celiac disease?

• childhood: failure to thrive

• abdominal pain and bloating

• diarrhea with fatty stools

What complications can result from nutrient malabsorption in celiac disease?

• low calcium: osteoporosis, seizures, and tetany

• low iron: anemia

• general malnutrition: short stature in children

• during pregnancy:

  • miscarriage

  • neural tube defects due to low folic acid

  • other nutrient deficiencies

What is portal hypertension?

• very high blood pressure in the portal venous system

• occurs when blood flow through the portal venous system or vena cava is obstructed

• causes include:

  • hepatic vein thrombosis

  • severe RHF

  • alcoholic cirrhosis

What are the complications of long-term portal hypertension?

• ascites: fluid buildup in the peritoneal cavity

• splenomegaly: enlarged spleen

• portosystemic shunts: alternate blood flow pathways

  • can cause esophageal varices (enlarged veins)

What is ascites, and what causes it?

• ascites: fluid buildup in the peritoneal cavity

• caused by:

  • portal hypertension

  • decreased serum protein production by the liver

• low capillary osmotic pressure causes fluid to leave the blood and enter tissues, then the abdominal cavity

What are the symptoms and treatment of ascites?

• 15 L of fluid can collect in the abdomen

• fluid pushes against the diaphragm, causing breathing difficulties

• treatment: paracentesis

  • drains abdominal fluid using a needle

• ascites will return if the underlying liver problem is not fixed

What are portosystemic shunts?

• diversion of blood through the IVC to bypass the liver

• blood goes through collateral veins

• example: blood bypasses the liver through esophageal veins

How do esophageal varices develop?

• normally, esophageal veins drain into the:

  • hepatic portal vein

  • inferior vena cava

• portal hypertension increases resistance to blood flow into the portal system

• collateral veins develop between esophageal veins and the IVC

• blood backs up and bypasses the liver

• increased pressure causes the veins to swell and distend, forming varices

What are the complications of esophageal varices?

• enlarged veins that rupture easily

• resulting bleeding can cause:

  • hematemesis: vomiting blood

  • melena: black, tarry stools

• resulting severe hemorrhage can be life-threatening

What are other types of varices caused by portosystemic shunts?

• caput medusae: enlarged collateral veins on the abdominal wall

• hemorrhoids: enlarged collateral veins in the rectum

What causes hepatic encephalopathy?

• liver dysfunction allows toxins (e.g., ammonia) to remain in the bloodstream

• blood bypasses the liver, preventing toxins from being converted into urea

• toxins reach the brain and affect neurotransmission

What are the manifestations of hepatic encephalopathy?

• personality changes

• memory loss and confusion

• asterixis: flapping of the hands

• possible coma

What is jaundice (icterus)?

• yellow/greenish discoloration of the skin caused by hyperbilirubinemia

• bilirubin forms when RBCs are broken down

• the liver normally processes bilirubin and excretes it into bile

• yellow discoloration appears first in the sclera of the eyes, then the skin

What are the 3 causes of increased bilirubin in the blood?

1. too much RBC breakdown

2. liver dysfunction preventing bilirubin processing

3. processed bilirubin cannot be excreted into bile.

• bilirubin normally leaves the body through feces

• it can also pass into the urine when blood levels are high

What is splenomegaly, and what does it cause?

• splenomegaly: enlarged spleen caused by portal hypertension

• increased portal pressure diverts blood into the splenic vein

• blood cells take longer to pass through the enlarged spleen, increasing their removal

What are the effects of splenomegaly?

• blood cells take longer to pass through the enlarged spleen

• increased removal of blood cells causes:

  • anemia: low RBCs

  • thrombocytopenia: low platelets

  • leukopenia: low WBCs

What are the five types of viral hepatitis?

• HAV, HBV, HCV, HDV, HEV

• all can cause acute hepatitis

• HBV and HCV can also cause:

  • chronic liver disease

  • liver cancer

What happens to the liver during acute viral hepatitis?

• destruction of hepatocytes

• liver scarring

• increased growth of hepatic macrophages

• damage to intrahepatic bile ducts can cause:

  • bile obstruction

  • jaundice

• liver damage is more extensive with HBV and HCV

How is viral hepatitis transmitted, diagnosed, and prevented?

• transmission: body fluids

• co-infection can occur with HBV, HCV, HDV, and HIV

  • can cause faster progression of liver disease

• diagnosis: antibody tests for specific hepatitis viruses

• vaccines: available for HAV and HBV

What happens during the prodromal phase of acute viral hepatitis?

• begins about 2 weeks after exposure

• ends when jaundice develops

• symptoms:

  • fatigue, vomiting, headache

  • cough and low-grade fever

• very infectious during this stage

What happens during the icteric phase of acute viral hepatitis?

• lasts 2–6 weeks

• caused by liver damage

• manifestations:

  • jaundice

  • dark urine

  • clay-coloured stools

  • enlarged, tender liver

  • pain when the liver is palpated

What happens during the convalescent phase of acute viral hepatitis?

• healing and repair begin

• starts when jaundice and most symptoms resolve (about 6–8 weeks after exposure)

• liver may remain enlarged and tender

• liver function returns to normal about 4–14 weeks after onset

What is chronic viral hepatitis?

• ongoing liver inflammation after acute HBV or HCV infection

• virus remains in hepatocytes, causing a prolonged immune response

• continued immune activity leads to ongoing liver damage

• liver function tests remain abnormal for more than 6 months

• HBV/HCV surface antigens persist

What are the risks of chronic viral hepatitis?

increased risk of:

• cirrhosis

• liver cancer

What is cirrhosis, and what causes it?

• irreversible liver scarring (fibrosis) caused by damage and inflammation

• causes include:

  • HBV and HCV infections

  • excessive alcohol consumption

  • prolonged exposure to drugs or toxins like hepatotoxins

What are the major complications of cirrhosis?

• hepatomegaly: enlarged liver

• splenomegaly: enlarged spleen

• ascites: fluid buildup in the peritoneal cavity

• portal hypertension

• hepatic encephalopathy

• esophageal varices

How does cirrhosis affect the liver, and how is it treated?

• liver structure and metabolism become altered

• scarring blocks channels needed for normal liver function

• treatment focuses on:

  • rest and vitamin supplements

  • good nutrition

  • managing complications

  • stopping alcohol consumption

  • possible liver transplant

What is liver failure?

• most severe consequence of liver disease

• can result from acute or chronic liver disease

• liver cannot perform its normal synthetic and metabolic functions

• occurs when 80–90% of liver function is lost

What blood-related problems occur with liver failure?

• spleen dysfunction reduces blood cells, causing:

  • anemia: low RBCs

  • thrombocytopenia: low platelets

  • leukopenia: low WBCs

• loss of liver-made clotting factors causes:

  • purpura: 3–10 mm skin spots

  • petechiae: spots smaller than 3 mm

  • spider angiomas: radiating blood vessels on the skin

  • epistaxis: nosebleeds

• hemolysis: RBC destruction due to changes in membrane lipids

What neurological changes occur with liver failure?

hepatic encephalopathy causes:

• asterixis (flapping hands)

• confusion

• coma

What is hepatorenal syndrome?

• kidney failure associated with liver failure

• causes oliguria (reduced urine output)

• generally caused by decreased blood volume due to:

  • bleeding

  • fluid loss

  • vasodilation

How does poor steroid hormone metabolism affect the body?

• aldosterone: contributes to ascites

• sex steroids: can cause:

  • menstrual irregularities

  • loss of libido

  • gynecomastia (breast enlargement in males)

What are cholelithiasis and cholecystitis?

• cholelithiasis: formation of gallstones.

• cholecystitis: inflammation of the gallbladder, often when gallstones block the cystic duct

What causes gallstones to form?

• most gallstones are made of cholesterol.

• fewer are made of bilirubin and calcium.

• gallstone formation is favoured by:

  • abnormal bile composition: too much cholesterol in bile.

  • bile stasis: bile becomes stagnant due to obstruction.

  • gallbladder inflammation: causes excessive absorption of water and bile salts

What are the clinical manifestations of cholelithiasis?

• often asymptomatic.

• may cause abdominal pain and jaundice.

• pain occurs 30 minutes to several hours after eating a fatty meal.

What are the clinical manifestations and causes of cholelithiasis?

• often asymptomatic.

• may cause abdominal pain and jaundice.

• pain occurs 30 minutes to several hours after eating a fatty meal.

• caused by gallstones becoming lodged in the cystic or common bile duct.

• common bile duct obstruction: causes jaundice because bile backs up into the liver.

• cystic duct obstruction: causes cholecystitis (gallbladder inflammation)

What are the risk factors and treatments for cholelithiasis?

• risk factors:

  • obesity.

  • being female.

  • having several children.

  • contraceptive pills, because estrogen increases cholesterol excretion into bile.

• treatment:

  • endoscopic removal of gallstones.

  • gallbladder removal.

What is acute pancreatitis?

• a reversible inflammation of the pancreas.

• caused by premature activation of pancreatic digestive enzymes.

• common manifestation: ongoing abdominal pain.

• common causes:

  • gallstones.

  • alcohol abuse

How does acute pancreatitis develop?

• outflow of pancreatic digestive enzymes becomes obstructed, causing:

  1. accumulation of pancreatic secretions.

  2. premature activation of enzymes inside the pancreas.

  3. autodigestion (the pancreas begins digesting itself).

• this leads to:

  • vascular damage.

  • tissue necrosis.

  • edema.

  • inflammation

What can severe acute pancreatitis lead to?

• inflammatory cytokines are released into the bloodstream.

• this causes systemic effects, which may lead to:

  • renal failure.

  • respiratory distress syndrome

What is chronic pancreatitis?

• prolonged, progressive and irreversible destruction of the pancreas.

• affects the exocrine pancreas first, followed by the endocrine pancreas.

• most common cause: chronic alcohol abuse

What are the manifestations and complications of chronic pancreatitis?

• loss of pancreatic function and effects of chronic inflammation cause:

  • malabsorption.

  • weight loss.

  • diabetes mellitus.

• inflammatory cytokines enter the bloodstream, causing systemic effects:

  • nausea and vomiting.

  • anorexia.

• increases the risk of pancreatic cancer