UCF Pathophysiology II Exam 1 (Chapter 35 + 36 + 38)

GI Tract Functions

- Provides nutrients for for the body with repulsive and mixing movements.

- Secretion of digestive juices.

- Absorption of nutrients.

Atresia

Condition where an orifice or passage of the body is abnormally closed or absent.

Fistula

Abnormal passage way or tube between two body parts that are not normally joined together.

Stenosis

Abnormal narrowing of a passage in the body.

Mouth and Salivary Glands

- Food broken down and moistened by saliva.

- Point of entry for nutirents.

Pharynx

Transport of food to the esophagus and protection of the airway from aspiration of food particles.

Esophagus

- Movement of food to the stomach by peristaltic waves. The lower esophageal sphincter (LES) prevents reflux of stomach contents.

- Mucous glands are scattered throughout the submucosa.

Stomach

- Reservoir for food, mixing, and initial digestion of proteins; secretion of hydrochloric acid, instrinsic factor, and gastrin. The pyloric sphincter prevents reflux of intestinal contents.

- Parts include cardiac region, fundus, and antrum.

Small Intestines

Digestion and absorption of nearly all nutrients in the duodenum and jejunum; absorption of bile salts in the terminal ilium. The brush border contains numerous digestive enzymes. The enzymes secretin and cholecystokinin are secreted by intestinal mucosa.

Large Intestines

Reabsorption of water and storage of feces. Feces are delivered to the rectum for defecation

Pancreas

The pancreas delivers digestive enzymes and bicarbonate to the duodenum.

Gallbladder

Delivers bile salts to the duodenum.

How does the autonomic nervous system influence gastrointestinal motility?

Sympathetic nervous system activity is generally inhibitory to GI motility and secretion. Parasympathetic nervous system (vagus nerve) activity generally enhances motility

Gastrin

Peptide hormal which stimulates secretion of gastric acid by the parietal cells of the stomach and aids in GI motility. Secreted by G cells.

Cholecystokinin

Secreted by I cells of the jejunum. It's secretion is stimulated by the introduction of HCl, amino acids, or fatty acids into the stomach or duodenum. Stimulates the gallbladder to contract and release stored bile into the intestine.

Gastric Inhibitory Peptide

Secreted by mucosa of upper portion of small intestine in response to the presence of fat; decreases stomach motility.

How do segmental and propulsive movements influence the digestive and absorptive functions of the small intestine?

Segmental and propulsive movement mixes the chyme and digestive enzymes to enhance digestion and spreads out the chyme along the intestinal mucosa to aid absorption

Digestion of carbohydrates

- Mouth, stomach, and small intestines.

- Salivary/Pancreatic Amylase

Digestion of fats

- Occurs in small intestines.

- Emulsification (bile salts breakup large fat glops into droplets)

- Lipase

Digestion of proteins

- Pepsin

- Pancreatic Proteases

- Begins in Stomach

4 Potential pathologies for disorders of the GI tract?

- Problems with innervation

- Obstruction of tube

- Deficient digestion / absorption

- Problems with blood supply

Common manifestations of GI disorders?

Can manifest in dysphagia, esophageal (heartburn), abdominal pain, vomiting, intestinal gas, or alterations in bowl movements.

Stomatitis

Oral infection. Inflammation of the oral mucosa. Inflammation can be caused by pathogens, trauma, chemical irritants, chemotherapy, radiation, nutritional deficiency.

Acute Herpetic Stomatitis

The cold sore. Caused by herpes simplex virus. Manifest in tinging/itching, vesicles, and remains latent. Treatment is through acyclovir, steroids.

Gastroesophageal Reflux Disease (GERD)

Backflow of gastric contents into esophagus through the lower esophageal sphincter (LES). Inflammation caused by a reflux of highly acidic material. The extent and severity of damage to the esophagus reflects the frequency, duration, volume, and acidity. Can be caused by fatty foods, caffeine, large amounts of alcohol, anything that alters closure strength of LES, cigarette smoking, highly active vagus nerve, etc. Manifests in heartburn, regurgitation, chest pain, or dysphagia. Treated through suppressing gastric acidity, histamine blockers, proton pump inhibitors.

Barrets Esophagus

Complication from GERD. Intestinal metaplasia of a normally squamous esophageal mucosa. The presence of goblet cells in the esophageal mucosa is diagnostic. Single most common risk factor for esophageal adenocarcinoma. 10% of GERD patients get it.

Hiatal Hernia

Defect in diaphragm when a portion of the stomach passes through the diaphragmatic opening into the thorax. Risk increases with age and is more common in women. Manifestations are similar to GERD (chest pain, dysphagia, heartburn. (Two types: sliding, and rolling, or mixed)

Sliding Hernia

Portion of stomach and gastroesophageal junction slip up into thorax above diaphragm.

Paraesophageal (Rolling) Hernia

Part of the greater curvature of stomach rolls through the diaphragmatic defect.

Gastritis

Inflammation of the stomach.

Acute Gastritis

Precipitated by ingestion of irritating substances (alcohol, aspirin, etc). Manifest in anorexia, nausea, vomiting, etc. Hemorrhage.

Chronic Gastritis

Helicobacter pylori is nearly always a factor. Complications include peptic ulcer disease, atrophic gastritis, gastric adenocarcinoma, etc. No hemorrhage.

Gastroenteritis

Inflammation of the stomach and small intestines.

Acute Gastroenteritis

Direct infection of tract by pathogenic virus or bacterial toxin. May be caused by imbalance in normal bacterial flora by introduction of unusual bacteria.

Chronic Gastroenteritis

Usually a result on another GI disorder.

Peptic Ulcer Disease

Implies that acid is the cause of aggravation. Disorders of the upper GI tract caused by action of acid and pepsin. Include injury to the mucosa of esophagus, stomach, or duodenum. Caused by H. pylori, NSAIDS, stress, alcohol, smoking, spicy food, etc.

Dull, burning, aching pain. Nausea, vomiting coffee ground emesis. Epigastric pain in middle of the night. Food relieves pain (duodenal).

Can be treated different ways depending on cause: antibiotics, H2 antagonist, protein pump inhibitors, sucralfate, smoking cessation, etc.

Inflammatory Bowel Disease

Chronic, relapsing inflammatory bowel disorder of unknown origin. Can be related to immune response (CD4 cells), genetic susceptibility (specific MHC class II alleles, associations with non-HLA genes), and environment.

Treatment: Broad spectrum antibiotics, immunosuppressive agents, surgery.

Crohns Disease

3-5/100,000-person population. Occurs at any age. Peaks between 2nd and 3rd decades of life. Females more than males. 3-5x more amount Jews than non-Jews. Crohns crosses borders (affects any level of digestive tract). Has "skip lesions" which is just back and forth areas of lesions and areas of no lesions. Will typically start in mucosa and will usually result in edema.

Ulcerative Colitis

7/100,000-person population. Occurs at any age. Peaks between 20-25 years of age. No particular sex affected more. Familial association, around 20% have associated relatives. Limited to mucosa and submucosa. Typically, beings in rectum and extends proximally continuously. High risk of carcinoma development.

Appendicitis

Inflammation of the vermiform appendix. Possible causes are due to obstruction of lumen with stool & foreign bodies, etc. Causes ischemia, increase intraluminal pressure, infection, etc. Epigastric and RLQ pain (McBurney's point, rebound tenderness). Most serious complication is peritonitis. Manifestations include nausea, vomiting, fever, diarrhea. Treatment is through immediate surgical remove of appendix. Antibiotics with fluid and electrolyte replacement.

Irritable Bowel Syndrome

Motility Disorder. Spasms of muscles in the large intestine with increased sensitivity = "Gut reaction to your environment". Manifests in diarrhea or constipation, abdominal cramping pain, mucus in stool, nausea, etc.

Malabsorption Disorders

Failure of small intestine to absorb or normally digest one or more dietary constituents. Caused by enzyme abnormalities, infection, mucosal dysfunction, etc. Manifests in diarrhea, passage on inappropriately processed intestinal contents, abdominal pain.

Celiacs Disease

Type of malabsorption disorder. Also called SPRUE or NON-tropical SPRUE or Gluten Sensitive Enteropathy. Sensitivity to gluten, a heat protein. Leads to inflammation and atrophy of intestinal villi. Impaired nutrient absorption. Also, in oat, barley or rye. Progressive atrophy of mucosa. Relieved by gluten withdrawal.

Neoplasms of the GI tract

Warning signs for cancer of the GI tract include black, tarry, bloody, or pencil shaped stool and a change in bowel movements. Risk factors include low-fiber, high-fat diet, polyps, and chronic irritation or inflammation.

Colon Cancer

Second only to lung cancer as a cause of cancer deaths.

Liver Anatomy

Largest organ of the body. Composed of structural until called liver lobules. Smooth muscle, no fibrous tissue.

Kuppfer Cells

Hepatic macrophages found in sinusoid walls. They remove debris such as bacteria and worn out blood cells from the blood as it flows past.

Functions of Liver

Metabolism of fats, proteins, and glucose; synthesis and secretion of bile salts; storage of vitamins and minerals; metabolism and detoxification of endogenous and exogenous substances; and urea synthesis.

Bilirubin

Bile pigment. Waste product of the heme portion of hemoglobin formed during the breakdown of senescent erythrocytes. Two types: conjugated and unconjugated.

Jaundice

Symptom where skin and sclera of eyes become yellow. Yellowing is associated with the accumulation of bilirubin in the skin, most often caused by liver and gallbladder disorders.

Pruritis

Bile salts deposit in the skin.

Unconjugated Bilirubin

Bilirubin that has not been processed in the liver. Is insoluble in water. Cannot be excreted in urine.

Conjugated Bilirubin

IS water soluble. Is non-toxic. Normally excreted in feces.

Prehaptic Jaundice

Results from acute or chronic hemolytic anemia.

Hepatic Jaundice

Results from disorders of bilirubin metabolism and transport.

Posthepatic Jaundice

Results from a compromised ability of the liver to excrete bilirubin.

Criglar-Najjar Syndrome

Cannot conjugate bilirubin, patients die early in life due to kernicterus (bilirubin deposition to the brain)

Gilberts Syndrome

Cannot get the bilirubin into the liver for conjugation, milder disease.

Dubin Johnson

Defective liver excretion of bilirubin into bile, cause grossly black liver.

AST

Liver enzyme, releases with injury to hepatocytes. Also associated with brain and heart tissues.

ALT

Liver enzyme, releases with injury to hepatocytes.

Alkaline Phosphatase

Bile ducts, released when biliary tree is obstructed, cells of bile ducts release Alk Phosphatase.

Portal Hypertension

Consequences include: GI varices, splenomegaly, ascites, hepatic encephalopathy.

Gastroesophageal Varices

Etiologies include: Portal hypertension, alcohol or postheaptic cirrhosis, increased blood flow etc.

Affects about hald cirrotic patients. Size is main determinant for risk of bleeding. Can manifest join hematemesis, anemia, shock, etc.

Treatment includes fluid resuscitation, nitroglycerin, vasopressin

Hepatic Encephalopathy

Complex neuropsychiatric syndrome from too much ammonia. Associated with hepatic liver failure or chronic liver disease.

Manifest in: dementia, psychotic symptoms. spastic myelopathy, etc

Treated through restricting dietary protein.

Ascites

Pathologic accumulation of fluid in the peritoneal cavity. Occurs with portal hypertension and hypoalbuminia. Can be treated through sodium restriction, diuretics, drainage, bed rest.

Hepatitis

Inflammation of the liver. Can be caused my multiple factors: viral infections, toxic agents, drugs, autoimmune response, etc.

Hepatitis A (HAV)

Fecal/Oral spread: Hygiene, drugs use, day care, food. Vaccine preventable.

Hepatitis B (HBV)

Sexually transmitted. 100x more infectious than HIV. Blood borne (sex, injection use, mother-child, etc). Vaccine preventable.

Hepatitis C (HCV)

Blood borne (injection needle use primarily). 4-5x more common than HIV. NOT VACCINE PREVENTABLE.

Hepatitis D (Delta Agent)

Depends on hepatitis b for replication. Defective virus that depends on Hb'sAg as it's envelope.

Hepatitis E

Fecal/Oral spread. Cause water borne epidemics. Developing countries. High mortality rate in expecting mothers.

Hepatitis G

Recently discovered. Parentally and sexually transmitted.

Acute Hepatitis Testing

- Increased AST and ALT (Usually AST is higher)

- Increased Alkaline Phosphatase

Chronic Hepatitis Testing

- Increased AST and ALT (Usually ALT is higher)

- Increased serum bilirubin

- Occasionally increased alkaline phosphatase.

Cirrhosis

Natural end stage irreversible disease of anything which chronically damages the liver. Can be alcoholic, biliary obstruction, acute or chronic hepatitis.