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the loss of fat in the stool. Stool is light colored and soft
occurs from an irritation to the lining of the stomach, small intestine, or large intestine by a pathogen or toxin. The disease can occur from a virus, bacteria, parasite, or chemical toxin. Gastroenteritis is transmitted from person to person or can be a water or foodborne illness
pain in the parietal peritoneum
Dark, black, sticky stool
Bright red blood in stool=lower GI or hypermotility
Esophageal varices are engorged varicose veins that develop in the lower third of the esophagus because of portal vein hypertension in the liver. Cirrhosis of the liver is the major cause of esophageal varices. Portal vein hypertension, which occurs in liver disease, is the cause for the development of esophageal varices. Alcoholic and viral cirrhosis of the liver are the major diseases associated with esophageal varices
Upper GI Bleeding (UGIB)
The presence of bleeding in the esophagus, stomach, or duodenum. associated with a rupture, tear, or perforation in the esophageal or gastric lining, resulting in blood loss. An acute UGIB can quickly develop into hypovolemic shock. A chronic bleed is the result of a small tear or opening in the GI tract that causes a gradual, small amount of blood loss. A chronic bleed causes complaints of fatigue, low hemoglobin, and low iron levels. Slow UGIB often leads to iron deficiency anemia. The stool contains blood in chronic blood loss, a condition referred to as melena. Classic symptoms of UGIB include hematemesis, melena, and occult blood
Lower GI Bleeding
Bleeding of the large intestine
LES not relaxed-causes difficulty swallowing
Esophageal Cancer Risk Factors
Males, Age over 65, Caucasian-adenocarcinoma, African Americans- Squamous Cell, Squamous Cell: Alcohol (whisky), Tobacco. Adenocarcinoma: Barrett's Esophagus, Chronic GERD, Tobacco use. Susceptible gene loci on chromosomes 5q11, 6p21, 10q23, 12q24, and 21q22. Food containing nitrosamines. Achalasia
Esophageal Cancer Patho
Chronic irritation of the epithelial cells that line the esophagus causes chronic cellular injury. In GERD, a metaplastic change often occurs at the lower esophagus, called Barrett's esophagus. From metaplasia, over time, the cells become dysplastic and gradually turn into adenocarcinoma
Esophageal Cancer Manifestations
Difficulty swallowing. Heartburn. Weight loss. Change in eating pattern. Sore throat.
GERD and Risk factors
Reflux of acid, pepsin and bile salts from the stomach up into the esophagus
RF: Alcohol, chocolate, coffee, fatty meals, medications (anticholinergics, betaangonsists, calcium channel blockers, nitrates, & hormones such as progesterone), nicotine, obesity, pregnancy
the LES is weak and allows the contents of the stomach to reflux up into the esophagus. The stomach contents are acidic; when refluxed upward, they irritate the esophageal squamous epithelium
Obesity, pregnancy, smoking, alcohol, fatty foods, and coffee. Some medications, such as calcium antagonists, anticholinergics, NSAIDs, and bisphosphonates. Factors for Candida esophagitis include antibiotic use, radiation therapy or chemotherapy, hematologic malignancies, and acquired immune deficiency syndrome (AIDS). Esophageal stasis, alcoholism, malnutrition, and advanced age
occurs as a result of an irritation to the squamous epithelium, the protective lining of the esophagus. The body responds to the injury by initiating the inflammatory process
Hiatal Hernia Type 1
Sliding (direct), is most common, can easily protrude above the diaphragm when the person is lying supine. When the person stands, the hernia slides back into the abdominal cavity.
Hiatal Hernia Type 2
Paraesophageal (rolling); the protrusion of only the fundus part of the stomach into the thorax while the gastroesophageal junction stays below the diaphragm. This type of hernia is less common and has a higher risk for complications because the fundus of the stomach pushes into the thorax cavity and remains above the diaphragm. This leads to the potential for gastritis, ulcer formation, or strangulation of the herniated portion of the stomach.
Hiatal Hernia Type 3
The esophageal hiatus is the opening in the diaphragm that allows the esophagus and vagus nerve to connect with the stomach. With age, the opening within the diaphragm weakens and widens, and the stomach is able to protrude upward through the aperture into the thorax
mechanical blockage of the lumen of the bowel
Functional Obstruction (paralytic Ileus)
failure of intestinal motility (esp after abd surg)
mechanical causes (like adhesions or hernias)
Chronic (partial) obstruction
tumors or inflammatory disorders of large bowel
Small Bowel Obstruction (SBO) Patho
Tumor, adhesions, hernia, or inflammation can cause obstruction. A partial obstruction decreases the flow of intestinal contents through the bowel. A complete obstruction prevents passage of all contents and fluid through the bowel.
Small Bowel Obstruction Manifestations
Abdominal Pain, Abdominal Distention, nausea, vomiting, Diarrhea (if partial obstruction). Hyperactive bowel sounds.
Large Bowel Obstruction Patho
These obstructions can be caused by mechanical, vascular, or neurogenic disorders and can be complete or partial. The bowel dilates proximal to the obstruction. Causes include diverticular disease, volvulus, hernia, and neoplasm.
Large Bowel Obstruction Manifestations
Acute or chronic colicky lower abdominal pain, distention, tenderness, and rigidity caused by buildup of pressure and gas proximal to obstruction. Abdominal Tenderness, High pitched bowel sounds (partial), lack of bowel sounds (complete)
an inflammation in the lining of the stomach. It can be caused by a number of medications and factors such as infection, allergy, acute stress, bile reflux, alcohol abuse, radiation, and direct trauma.
Symptoms: heartburn, nausea, epigastric pain
also known as nonerosive gastritis, is associated with an underlying disease or severe infection. The presence of the H. pylori bacterium is the most common cause of chronic gastritis, which usually affects the fundus of the stomach. It is different than acute gastritis because it causes atrophy of the glandular stomach lining, a condition called atrophic gastritis.
Symptoms: pain, nausea, weight loss, anorexia and hematemesis
ulcerations/erosions in the lower esophagus, stomach, or duodenum commonly caused by H. pylori infection.
Risk factors: NSAIDS, Alcohol, smoking, age, chronic diseases, type O blood, psychological stress.
Upper portion of duodenum, near pyloric sphincter, single erosion. Risks: H. pylori, alcoholic cirrhosis, hyperthyroidism
Manifestations: pain relief when eating, pain increases 2-3 hours after eating, nocturnal epigastric pain
Stomach ulcers occur when the thick layer of mucus that protects your stomach from digestive juices is reduced. This allows the digestive acids to eat away at the tissues that line the stomach, causing an ulcer.
RF: smoking, alcohol, stress, spicy foods
Pain when eating, vomiting, dark blood in stool
Rapid gastric emptying because of removal of part of the stomach.
Phase 1: abdominal pain, diarrhea, diaphoresis.
Phase 2: gastric fullness, symptoms of hypoglycemia.
Condition caused by narrowing of the appendix lumen from obstruction. Inflammation of the wall of the appendix develops. Inside the appendix, there is development of a medium for bacterial growth.
RF: Trauma, low fiber diet, family history
Inflammation of the peritoneal membrane. Infection of peritoneum commonly caused by rupture of organs into the peritoneal cavity. Abdomen
RF: Peritoneal dialysis
anywhere mouth to anus
patho: a chronic, transmural inflammatory process of the bowel that often leads to fibrosis and obstructive symptoms;
RF: genetic, before 30
S/S: abdominal pain, blood in feces, weight loss bc malabsorption
mucosal layer of large intestine
Patho: inflammation of large bowel, PSEUDOPOLYPS in intestine
Abdominal pain, chronic diarrhea with blood, weight loss bc malabsorption
Patho: hypersensitivity reaction to gluten, a by-product of wheat, barley, and rye. A gluten-derived peptide called gliadin damages the intestinal mucosa
Abdominal pain, bloating, diarrhea
Irritable Bowel Syndrome (IBS)
Patho: Modification in GI motility that is linked to alteration in central nervous system-directed motor function of the bowel. Enhanced visceral sensitivity exists, as well as no inflammation.
Colicky abdominal pain lasting 6 months or more
Asymptomatic, diverticule out-pouching present
inflammation of diverticuli, risk for perforation
Patho: Weakness in bowel wall musculature, which allows protrusion of small outpouchings or sacs called diverticula. Diverticula can become infected (called diverticulitis) or inflamed or can fill with intestinal contents and cause an obstructive mass.
S/S: chronic low LLQ episodic or steady pain
Period Prior to Jaundice (first phase)- nausea / vomiting, decreased appetite / weight loss, fever, fatigue, headache and joint pain, rt upper quadrant abdominal pain, enlarged spleen/liver/lymph nodes and rash and itching of the skin (urticaria). (2 weeks after exposure, but before jaundice)
Presence of Jaundice
Resolution of Jaundice. Symptoms typically diminish, but liver still may be tender or enlarged. (6-8 weeks after exposure)
Process involved in chronic hepatitis
occurs as a result of the progression of acute hepatitis. Hepatitis is considered chronic when inflammation and necrosis of hepatic tissue continues for 6 months or longer. Most cases of chronic hepatitis are from autoimmune diseases, drug toxicity, or progression of HBV or HCV.
Tests for liver/gall bladder disease
AST - elevated in alc liver disease
ALT - Elevated in liver disease
Bilirubin - elevated
Albumin - decreased indicates hepatic dysfunction
Liver normal function
Digestion of fats & cholesterol, vitamin absorption, production of bile-drains to duct, synthesize coag. factors, filters drugs, detox, excretes RBCs, protein synthesis, glucagon production
Alcoholic Liver Disease
Repeated alcohol abuse leads to steatosis, which is the replacement of hepatocytes with fat. Chronic ingestion of ethanol inhibits the oxidation of fatty acids in the liver. Fat accumulates in and around hepatocytes and disrupts the integrity of the organelles. Nuclear disruption causes death of the hepatocytes. With time, large areas of hepatocyte injury, necrosis, inflammation, and fibrosis develop. When the liver demonstrates fibrosis and scar tissue, the disorder is referred to as cirrhosis.
NonAlcoholic Fatty Liver Disease
linked to metabolic syndrome: insulin resistance, obesity, and hyperlipidemia. Infiltration of hepatocytes with fat (triglycerides) occurring in the absence of alcohol intake. Occurs in presence of obesity with high Chol, high Triglycerides, metabolic syndrome, and type 2 diabetes.
Store bile created from liver, releases bile used in fat digestion
Inflammation of the gallbladder; it is generally associated with cholelithiasis, biliary sludge, or bile stasis.
The formation of gallstones, also called calculi, caused by precipitation of substances contained in bile, mainly cholesterol and bilirubin. Gallstones irritate the inner walls of the gallbladder, causing inflammation; this is referred to as cholecystitis.
Abnormally high blood pressure in the portal venous system caused by resistance to portal blood flow. Dilated, superficial veins become visible around the umbilicus, a sign referred to as caput medusa. Prone to Rupture.
occurs because of one of three specific etiologies: excessive RBC hemolysis, hepatocellular injury, bile duct obstruction.
Abnormal accumulation of fluid in the abdominal peritoneal cavity. demonstrated by bulging flanks with shifting abdominal dullness with the patient in the supine position.
Severe cases of hepatocellular injury may progress to fulminant hepatic failure, which is acute liver failure complicated by hepatic encephalopathy—involvement of the brain. Hepatic encephalopathy is exhibited by lethargy, confusion, and, in extreme cases, stupor and coma.
a type of renal failure that occurs in approximately 10% of patients with cirrhosis. For unclear reasons, the kidney vessels undergo vasoconstriction; progressive impaired renal function then occurs. HRS is often seen in patients with a large amount of ascites
Transmission: fecal-oral, parenteral, sexual
Transmission: Blood products (parenteral), body fluids, sexual
A severe, life-threatening disorder associated with activated pancreatic enzymes secreted into the pancreatic tissue and surrounding tissue, causing inflammation and auto digestion
Usually mild and resolves quick
process of progressive fibrotic destruction, pain and weight loss
Cancer of the Pancreas
Neoplastic tumor that develops either in the head of the pancreas (most common) or the body or tail of the gland. Cancer of the head of the pancreas causes obstruction of the common bile duct, which causes backup of bile into the liver and backup of bilirubin into the bloodstream. This causes widespread destruction of the pancreas, with loss of pancreatic enzyme activity and metastasis to the liver
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