Exam 4- GI/Liver Flashcards
OSMOTIC DIARRHEA
ETIOLOGY: bacterial infection (e. coli), parasites, viral infection, drugs, celiac disease or UC, genetic d/o like congenital chloride diarrhea
- due to unabsorbed nutrients in the stool
- osmotic load causes fluid retention in the bowel
- seen with lactose intolerance and Zollinger Ellison syndrome and celiac disease
CLINICAL MANIFESTATION: stomach pain, bloating, nausea, watery bowel movement;
PATHOLOGY:occurs when too many solutes — the components of the food you eat — stay in your intestine and water can’t be absorbed properly. This excess water causes your bowel movements to be loose or more liquid than solid. Eating food that can’t be that can be absorbed and instead draw water into your intestine.
SECRETORY DIARRHEA
ETIOLOGY:
large volume: caused be excessive mucosal secretion of chloride- or bicarbonate rich fluid or inhibition of net sodium absorption. Usually caused by enterotoxins (E.coli), viruses (rotavirus), or exotoxins from overgrowth cdiff.
-increased water and electrolytes secretion by toxin or VIP in the intestinal lumen
Small volume: caused by IBD, UC, Crohns, colitis, fecal impaction
CLINICAL MANIFESTATIONS: stomach pain, bloating, nausea, watery bowel movement;
PATHOLOGY: large volume of feces caused by excessive amounts of water secretion. Occurs when your body secretes electrolytes into your intestine. This causes water to build up.
MOTILITY DIARRHEA
ETIOLOGY: diarrhea caused by resection of small intestine, surgical bypass of an area of the intestine, fistula formation between loops of intestine, irritable bowel syndrome, diabetic neuropathy, hyperthyroidism, and laxative abuse
CLINICAL MANIFESTATION: dehydration, electrolyte imbalance (hyponatremia, hypokalemia), metabolic acidosis, and weight loss, fever, cramping pain, and bloody stools, bloating, anal and perianal skin irritation.
PATHOLOGY: large volume of feces caused by excessive amounts of water secretion
DYSPHAGIA
Difficulty swallowing or perception of obstruction during swallowing
PATHOLOGY: mechanical obstruction of the esophagus or functional d/o that impairs esophageal motility.
- Functional dysphagia-caused by neural or muscular d/o that interfere with voluntary swallowing or peristalisis
- Mechanical dysphagia- can be intrinsic or extrinsic. Intrinsic is obstruction in wall of esophageal lumen. Extrinsic obstruction originate outside the esophageal lumen and narrow the esophagus by pressing inward on esophageal wall
EVALUATION: barium xray, swallow study, endoscopy, imaging scans, esophageal muscle test, fiber optic endoscopic evaluation of swallowing
TREATMENT:Medication, Swallowing retraining, Botulinum toxin, Dilation, Enteral feeding, Esophageal stent placement, Surgery, Treatment for specific swallowing disorders.
ACHALASIA
ETIOLOGY: It may be caused by an abnormal immune system response.
May be related to cell mediated and antibody mediated immune response against unknown antigen in myenteric neurons
-A motility d/or of esophagus d/t nerves fro swallowing being damanaged
CLINICAL MANIFESTATION: a backflow of food in the throat (regurgitation), chest pain, and weight loss, discomfort after swallowing, unpleasant taste, vomiting.
*discomfort 2-4 sec after eating=upper esophageal obstruction; discomfort 10-15 sec= lower obstruction
PATHOLOGY: Achalasia results from damage to nerves in the food tube (esophagus), preventing the esophagus from squeezing food into the stomach.
GERD
ETIOLOGY: reflux of acid and pepsin or bile salts from the stomach to the esophagus that causes esophagitis.
RISK FACTORS: vomiting, coughing, lifting, bending, obesity, or pregnancy
CLINICAL MANIFESTATION: heartburn chronic cough, asthma attacks, laryngitis, sinusitis, and upper abdominal pain within 1 hr of eating. Symptoms worsen when person lays down
PATHOLOGY: abnormalities in lower esophageal sphincter function, esophageal motility, and gastric motility or emptying can cause GERD
UPPER GI BLEED
ETIOLOGY: bleeding from the esophagus, stomach, or duodenum
RISK FACTORS: helicobacter pylori infection, NSAIDs, aspirin, selective serotonin reuptake inhibitors, and other antiplatelet and anticoagulant medications
CLINICAL MANIFESTATION: frank red blood in emesis or coffee ground color stool
PATHOLOGY:cause by esophageal or gastric varices, tear eso-gastric junction, cancer, andiodysplasias, peptic ulcers, severe retching
LOWER GI BLEED
ETIOLOGY: bleeding from the small intestine, colon, or rectum
RISK FACTORS: age, overuse of NSAIDs, chronic constipation leading to hemmorhoids, family hx like IBD, bleeding d/o of family hx of bleeding d/o
CLINICAL MANIFESTATION: bright red blood in stool, abd cramps or pain, faintness/dizziness, paleness, SOB
PATHOLOGY: caused by polyps, inflammatory bowel disease, diverticulosis, cancer, vascular extasias, or hemorrhoids
PYOLRIC OBSTRUCTION
ETIOLOGY: is a result of any disease process that causes a mechanical impediment to gastric emptying. Can be due to a mechanical cause or motility d/o
RISK FACTORS: PUD, gastrointestinal tumors, pancreatitis
CLINICAL MANIFESTATION: nausea, nonbilious vomiting, epigastric pain, early satiety, abdominal distention, and weight loss
PATHOLOGY:
can be congenital or acquired. Acquired caused by peptic ulcer disease or tumor near the pylorus. Duodenal ulcers are more likely than gastric ulcers to obstruct the pylorus. Ulceration causes obstruction resulting from inflammation edema, spasm, fibrosis or scarring. Tumor caused obstruction by growing into the pylorus.
INTESTINAL OBSTRUCTION
ETIOLOGY: is a blockage that keeps food or liquid from passing through your small intestine or large intestine (colon). Can be SBO or LBO
RISK FACTORS: hernias, crohns, abd/joint/or spine surgery, swallowing a foreign body, decrease blood supply to small bowel, abnormal growth of tissue in or next to small intestine, tumors, cancer
CLINICAL MANIFESTATION:constipation, vomiting, inability to have a BM or pas gas, swelling of abd.
PATHOLOGY: Ingested fluid and food, digestive secretions, and gas accumulate above the obstruction.
ILEUS
ETIOLOGY:the motor activity of the bowel is impaired, usually without the presence of a physical obstruction.
RISK FACTORS: electrolyte imbalance involving potassium and calcium, hx of intestinal injury or trauma, hx of crohns or diverticulitis, sepsis, PAD, exposure to radiation near abd
CLINICAL MANIFESTATION: distended abd, fullness, gas, abd spasms, constipation, diarrhea, n/v
PATHOLOGY:Caused by Bacteria or viruses that cause intestinal infections (gastroenteritis)
3 ULCERATIVE DISEASE
- gastric ulcers
- duodenal ulcers
- stress r/t mucosal ulceration
DUODENAL ULCERS
ETIOLOGY:a peptic ulcer that develops in the first part of the small intestine (duodenum)
RISK FACTORS: alcohol abuse, H pylori infection (90%), hx radiation therapy, NSAIDs (ibuprofen, naproxen, or asprin), stress, severe illness, tobacco use
CLINICAL MANIFESTATION: belching, burning stomach or upper abd pain that may be severe, fullness, loss of appetite, n/v
PATHOLOGY:stomach acid damages the lining of the digestive tract: H pylori decrease mucosal protection and increases gastric acid secretion
STRESS RELATED MUCOSAL ULCERATION
ETIOLOGY: acute form of erosive, inflammatory peptic ulcer that tends to accompany the physiologic stress of severe illness; multisystem organ failure, or major trauma, including severe burns or head injury.
RISK FACTORS: immense physical stress like those pts in ICU; stress-related ulcer, H, pylori infection, NSAIDs
CLINICAL MANIFESTATION: upper abd pain/n/v, anemia, bloated, pain that varies with food intake
PATHOLOGY: COME ON SUDDENLY, USUALLY AS RESULT OF PHYSIOLOGICAL STRESS; changes in body’s pH; caused by mucosal ischemia
2 INTESTINAL DISEASES
- ulcerative colitis
2. crohn’s disease
CROHN’S DISEASE
ETIOLOGY: an idiopathic inflammatory d/o that is distinguished from UC in that it affects any part of the GI track from the mouth the anus and involves “skip lesions” with inflamed areas mixed with un-inflamed areas, non-caseating granulomas, fistulas, and deep penetrating ulcers
RISK FACTORS: family hx, cigarette smoking, Jewish ethnicity, urban residency, age less than 40 years, slight predominance in women, and altered gut microbiome
CLINICAL MANIFESTATION: irritable bowel; diarrhea, sometimes rectal bleeding if colon is involved; abd pain, diarrhea, weight loss, anemia, and fatigue
PATHOLOGY: inflammatory lesions begin in the intestinal submucosa and spread with discontinuous transmural involvement (skip lesions), mutations in Toll-like receptor, gene name CARD15/NOD2. overreact to normal flora of bacteria
5 TYPES OF LIVER INJURY/FAILURE
- Hepatitis A
- Hepatitis B
- Hepatits C
- Hepatitis D
- Hepatitis E
HEPTITIS A
ROUTE: fecal oral route; 4-6 week incubation period
RISK FACTORS: poor sanitation, lack of safe water, sexual contact with infected person
CLINICAL MANIFESTATION: fever, malaise, loss of appetite, diarrhea, nausea, abdominal discomfort, dark-coloured urine and jaundice
PATHOLOGY: acute infection; is caused by a picornavirus usually transmitted by the fecal-oral route
IMMUNITY: antibodies to HAV (anti-HA) develop within 4 weeks after incubation
**IgM increases»_space; IgG increases for several years which leads to immunity
HEPATITIS B
ROUTE: sexual intercourse, blood, perinatal (mother to baby); 6-8 week incubation period
RISK FACTORS: unprotected sex, IV drug uses, men with men, mother to infant, job that exposes you to blood
CLINICAL MANIFESTATION: fever, malaise, loss of appetite, diarrhea, nausea, abdominal discomfort, dark-coloured urine and jaundice
PATHOLOGY: can be acute or chronic (>6 months)the interaction of the virus and the host immune system, which leads to liver injury and, potentially, cirrhosis and hepatocellular carcinoma
HEPATISIS C
ETIOLOGY:Serum, sexual contact; 6-8 week incubation
RISK FACTORS: IV drug use; HIV; Hep B infection
CLINICAL MANIFESTATION: fever, malaise, loss of appetite, diarrhea, nausea, abdominal discomfort, dark-coloured urine and jaundice
PATHOLOGY: can develop into cirrhosis and then hepatocellular carcinoma.
Antibody: anti HCV IgG
HEPATITIS D
ETIOLOGY: occurs in people who are also infected with the hepatitis B virus.
RISK FACTORS: IVDU
CLINICAL MANIFESTATION: fever, malaise, loss of appetite, diarrhea, nausea, abdominal discomfort, dark-coloured urine and jaundice
PATHOLOGY: Hepatitis D virus is hepatotropic. Replication within hepatocytes results in cytotoxicity and direct liver damage. The virus depends on the viral coat of HBsAg molecules on HBV for replication
Antibody used for dx: anti-HD
HEPATITIS E
ETIOLOGY: co-infection with HBV, HIV; transmitted fecal oral route; MOST COMMON IN ASIAN AND AFRICAN COUNTRIES
RISK FACTORS: contaminated water supplies, poor sanitation, ingestion of undercooked meat and shellfish
CLINICAL MANIFESTATION: usually asymptomatic and resemble Hep A or it can progress to liver failure or chronic hepatitis
PATHOLOGY:
ANTIBODY: anti-HEV IgM
CHOLELITHIASIS
ETIOLOGY: hardened deposit within the fluid in the gallbladder aka gallstones that are hardened deposits of digestive fluid (cholesterol, excess bilirubin) with impaired contractility
RISK FACTORS: female, obese, pregnant, sedentary, high fat diet
CLINICAL MANIFESTATION: RUQ pain, indegestion, n/v, abd cramping–may have no signs
PATHOLOGY:
- *Cholesterol gallstones due to over secretion of cholesterol by liver cells and hypomotility.
- *Pigmented gallstones, high heme turnover, bilirubin higher concentration which crystallize and become stones
CHOLECYSTITIS
ETIOLOGY: inflammation of gallbladder
RISK FACTORS: obese, pregnancy, hormone therapy, older age, diabetes, Native American or Hispanic
CLINICAL MANIFESTATION: severe pain in RUQ, pain that spreads to your right shoulder or back, tender abd, nausea
PATHOLOGY: gallstones that block the gallbladder preventing biliary outflow
