GI tract

  1. What is Dysphagia? What are the common pathophysiologies?
    • Difficulty swallowing (initiating swallowing), Sensation that swallowed food get "stuck", pain when swallowing.
    • 3 pathophysiologies: neuromuscular in coordination, altered peristaltic, LES (lower esophagal sphincter) dysfunction.
  2. What is type I dysphagia? causes? CM?
    • Upper GI problem. problems in delivery of food/fluid into esophagus.
    • Causes: R/T neuromuscular incoordination/disorder (stroke pt), normal sequence is altered or absent.
    • CM: May cough and expel the ingested food/fluids, aspirate when attempting to swallow, worse with liquids than solids.
  3. What is dysphagia type II? Causes? CM?
    • Problems in transport of bolus down esophagus. Food gets to the esophagus, but it doesn't get down to the stomach)
    • Causes: Weakening of the muscularis layer of GI tract. Food gets stuck there, causes a outpouchings of one or more layers (diverticula).
    • Disorder of the smooth muscle function, peristalisis is not working well (achalasia).
    • Structural interference of esophageal peristaltic activity, narrower of the esophagus. Maybe bc of a tumors, neoplasms, strictures within or in.
    • Abnormal peristaltic activity.
    • CM: Sensantion food is "stuck" behind sternum.
    • Initially with solid food, may progress to liquid.
  4. What is dysphagia type III? causes? CM?
    • problems in bolus entry into stomach.
    • Causes: lower esophageal dysfunction or lesion obstruction. Often times tumors.
    • CM: Tightness or pain in subternal area during swallowing.
  5. What are the most common etiologies of dysphagia?
    • Fibrosis
    • compression
    • diverticulum
    • congenital atresia
    • congenital tracheoesophageal fistula
    • neurologic damage to cranial  nerves V, VII, IX, X, and XII.
    • achalasia.
    • Look at slide 12 on GI for drawing.
  6. What is dyspepsia?
    • Feeling of epigastric discomfort. symptoms usually increase in times of stress.
    • Present w heartburn, indigestion, epigastric distress.
    • Symptoms profile does not differentiate b/t GERD, PUD (peptic ulcer disease) , and Non-ulcer dyspepsia.
  7. What type of pain is visceral? somatic? referred?
    • Visceral: diffuse, poorly located, burning.
    • Somatic: Sharp, intense, well organized.
    • Referred: Distant from the source but in same dermatome.
  8. What are the types of diarrhea?
    • Osmotic : increased amount of poorly absorbed solute. It moves too fast, not enough time to absorb.
    • Secretory: Due to toxins that stimulate the intestine. (lots of cramping w the diarrhea)
    • Exudative: (mucus,blood, protein) results from the inflammatory process.
    • Motility disturbances: A result of decreased contacct time with absorptive surfaces if interstinal lumen. (Often times could be neurologic, peristalisis could be too fast)
  9. What are the etiologies of diarrhea?
    • Bacterial: campylobacter, salmonella, shingella, E. Coli.
    • Viral infection: Norwalk virus (cruises),
    • Food intolerances: Lactosintolerance.
    • Parasites: Giardia, Cryptosporidium.
    • Reaction to meds: Antacids containing magnesium, bc MG irritatest the gut.
    • Intestinal disease: inflammatory bowl disease, i.e
    • Finctional bowel diorders: IBS, the only disease w/o a defined pathology.
  10. what are the common disorders of the mouth and esophagus?
    • Stomatitis/oral infections
    • Gastroesophageal Reflux Disease (GERD)
    • Hiatal Hernia.
  11. What is stomatitis? Cause?
    • Inflammation of the oral mucosa.
    • Common cause: Candida albicans (oral Thrush)
    • usually seen in immunosupress ppl (chemo, radiation therapy, etc.
  12. what is GERD? etiologies? pathophysiology? CM?
    • Back flow of acidic gastric content through the LES (lower esophageal sphincter). It is an inflammation caused by reflux of highly acidic material.
    • One of the most prevalent GI disorders.
    • GERD --> esophagitis --> Barret esophagus, which is a pre-cancerous condition.
    • Etiology: Any condition or agent that alters closure strength of LES or increase abdominal pressure.
    • Pathophysiology: High pressure in the stomach forces contents into esophagus causing irritation, by the reflux, bc the stomach content is high in HCL.
    • CM: pain after eating, pain when lying down, Feel better when they sit up, sleeping with 3 pillows (also for hiatal hernia)
  13. What are hiatal Hernias? types? Etiologies? Pathophysiology? CM?
    • Defect in the in the diaphragm that allows a portion of the stomach to pass through the diaphragmatic opening into the thorax.
    • Types: sliding (most common) and paraesophageal.
    • Image Upload 1
    • Etiologies: Aging (most common cause), upper abdominal surgeries, etc
    • Patho: Defect in the diaphragm, increased intra-abdominal pressure.
    • CM: Heartburn, Chest pain, Dysphagia, GERD.
  14. what is Gastritis? Types? CM?
    • Inflammation of the stomach lining.
    • Types: Acute and chronic.
    • Acute: Presipitating by the ingestion of irritating substances especially alcohol and aspirin.
    • Chronic: Gastritis may lead to atrophy of the gastric lining and decreased production of HCL and intrincic factor -- H. Pylori usually a factor.
    • CM: anorexia, diarrhea, vomiting, and abdominal pain.
  15. What is gastroenteritis? CM?
    • Inflammation of stomach and small intestine. It is the GI flue - usually treated with supportive fluids and dont need anything.
    • CM: diarrhea, abdominal pain, nausea, vomiting, fever, and malaise.
  16. What is peptic ulcer disease? etiologies? pathophysiology? difference b/t gastric and duodenal?  CM?
    • It is the disorder of the upper GI tract caused by the action of acid and pepsin.
    • Ulcers usually found in the esophagus, stomach, or duodenum.
    • Etiologies: 70% of them H. pylori and NSAIDs.
    • Patho: Gastric and duodenal ulcer.
    • Gastric: Caused by the breakdown of protective mucous layer (treat with drugs to protect the mucousa linning)
    • Duodenal: Excess of secretion of acid (treat w drugs that block the formation of HCL, H2 inhibitors)
    • CM: melena is associated w upper GI, and red is Lower GI bleeds.
    • Duodenal ulcer: feel better when they eat or antiacids. gain weight.
    • Gastric: pain occurs in empty stomach, food doesn't relieve pain. loose weight.
  17. what is crohn's disease? etiology? patho? CM?
    • Chronic inflmmatory condition of the bowl. Affects proximal portion (can affect any part of the GI tract) of the colon or terminal ileum (ileocecal area- ileum attached to the colon- close to appendix). Melena
    • affects all the layers. Exacerbations and remissions.
    • Not associated with cancer.
    • Etiology: just abt anything, now thinking autoimmune.
    • patho: inflammatory lesions usually in the ileum, involved all layers, "skip" lesions, abscesses, cobblestone tissue generate scar tissue.
    • CM: Exacerbations and remissions. urge to defacate at nigh, hypoalbuminemia, which could cause edema.
  18. What is ulcerative colitis? patho?
    • Chronic inflammatory disease of the mucosa of the rectum and colon. Affects the mucosal layer. Associated with increased cancer risk after 7-10 yrs of disease. Exacerbation and remissions. Bloody diarrhea.
    • Patho: no "skip" lesions. lesions have hemorrhages and abscesses, and ulcer turn fibrotic.
  19. Differences and similarities of Crohn's and ulcerative colitis disease?
    • Similarities: Both are inflammatory conditions of the intestine. Both have exacerbations and remissions.
    • Diff: Crohn's can affect any part of the GI tract, while colitis only the colon.
    • Colitis affects the inner linning only, Crohn's affects all the layers.
    • Colitis linked with cancer, crohn's isn't.
    • Smoking help colitis, but not crohn's.
  20. Enterocolitis? types?
    • Pseudomembranous enterocolitis: Acute inflammation and necrosis of small and large intestine. (C. diff) manifested by diarrhea, pain, fever, rectal bleeding, and perforation.
    • Necrotizing enterocolitis: Occurs in premature infants characterized by diffuse patchy intestinal necrosis with sepsis, bowel ichemia manifested by admonial distention. High mortality rate 60-80%!
  21. What is appendicitis? patho? CM?
    • Inflammation of the veriform appendix.
    • Most common cause of emergency surgery in the abdomen.
    • 10 to 30 yrs.
    • Affects men more than women.
    • etiopathic.
    • Patho: Obstruction, inflammation and bacterial invasion.
    • Gangrene can develop if ruptured.
    • CM: Visceral umbelical pain that becomes localized to the RLQ within 24 hrs. elevated WBC.
  22. What is divericulosis? etiology? when does it become diverticulitis? CM?
    • Out pouching of the walls of the colon. Usually assymptomatic. Most ppl don't know they have unless colonostomy.
    • If the pouches become inflamed or infected and cause symptoms, then it becomes diverticulitis.
    • CM: constipation, LL-sided abdominal pain, rectal bleeding, diarrhea, elevated WBC, maybe asymptomatic, signs of peritonitis.
  23. What are motility disorders?
    • Disorders that affect peristalisis.
    • IBS (irritable bowel syndrome).
    • Volvulus.
    • Intussusception.
  24. What is Irritable bowel syndrome (IBS)? Treatments?
    • It is a chronic functional disorder with no identifiable pathology. usually Dx after complaining abt interchangable diarrhear and constipation for at least 3 months.
    • It is the only pathology that is funcional in nature (we don't know why it happens), we don't have a pathology for it.
    • Usually pts don't have the CM at night.
    • Tx: SSRIs (selective seratonin reuptake inhibitors)- common drug is ventols.
  25. What is intestinal obstructions? What are the types? What are the main differences?
    • It is a partial or complete blockage of the small or large intestine (small is most common). This causes inability of the content to progress through the bowel.
    • There are 2 types: Mechanical and functional.
    • Mechanical: Caused by condition that decrease the patency of the bowel (adhesions, hernia, tumors, volvulus, etc)
    • Functional: caused by neurogenic or muscular impairment that hinders peristalisis (abdominal surgery, or opiods)
    • Main differences: Mechanical there are bowel sounds initially above the site of obstruction, in functional bowel sounds are absent.
  26. What is a intussusception?
    • Telescoping/invagination of a portion of bowel into adjacent (usually distal) bowel causing intestinal obstruction.
    • Most common in males from 6-12 months.
    • Signs and symptoms: Increased bowel sounds abdominal pain.
    • Image Upload 2
  27. What is a volvulus?
    • It is a twisting of bowel on itself causing intestinal obstruction and blood vessel compression (ischemia/gangrene, necrosis, and perforation).
    • It is a medical emergency.
  28. What are the main malabsorption disorders? what is it? Causes? CM?
    • Celiac disease.
    • Dumping Syndrome.
    • Short Bowel Syndrome.
    • Failure of small intestine to absorb or normally digest one or more dietary constituents.
    • Causes: Crohn's disease, celiac disease, tropical sprue, any surgical alterations.
    • CM: in general diarrhea, passage of inappropriately processed intestinal contents, abdominal pain.
  29. what is Celiac disease? CM?
    • Known as Sprue - causes malnutrition.
    • Inflammation and atrophy of intestine with sever malnutrition.
    • Familial intolerance to gluten.
    • Usually Dx young age.
    • More females than males.
    • Increase for intestinal malignancy.
    • CM: everything related to malnutrition, FTT (failure to thrive)
    • Tx: take them off gluten a see if they get better.
  30. What is dumping syndrome? CM?
    • dumping of the stomach to the small intestine bc of lost of pyloric regulation of gastric emptying.
    • Usually occurs after beriatric or gastric surgery, also in pt who had the stomach removed bc of cancer. 
    • CM: Diarrhea and abdominal pain.
    • The main problem is rapid absorptions of glucose leads to an excessive rise in plasma insulin and rebound hypoglycemia.
  31. Neoplasm of GI tract? Warning sign? Risks? Prognosis? Treatment?
    • stomach cancer is very rare. but the other ones are common, colon cancer is the most.
    • WS: Black, tarry, bloody, or pencil-shaped stool and a change in bowel habits.
    • Risks: Low fiber, hih-fat diet, polyps, and chronic irritation or inflammation. Family history is probably the most important.
    • Prognosis: If found early, prognosis could be really good.
    • Tx: perfect scenario, remove the tumor and not follow w chemo.
  32. Esophageal Cancer? Risk factors? prognosis?
    • RF: ppl w GERD (Barrett esophagus).
    • Prognosis: Poor prognosis bc o the amt of lymph nodes around the area.
  33. Gastric carcinomas? Risk factors? CM?
    • Seen in men >30, 5 yr survival rate 10%.
    • Aspirin has a protective effect.
    • RF: H. pylori infections are highly correlated with gastric cancer. and all the others.
    • CM: anorexia, weight loss, and GI bleeding.
  34. What are colonic polyps? importance?
    • Any protrusion into the GI lumen.
    • I: they are major precursor lesion in development of colon cancer!
    • Tx: take each polyp out, if there is a section w lots of polyps, then take the section out to avoid scare tissue formation.
  35. Colon cancer? Risk factors? CM?
    • 2nd cause of death, after lung cancer.
    • RF: age, after 40.
    • high fat, low fiber diet.
    • Polyps.
    • Chronic irritation or inflammation.
    • Heriditary.
    • CM: Rt side (ascending colon) black tarry stools.
    • Lt side (descending) abdominal cramping, "ribbon" or pencil-shaped stools, blood or mucus in stool.
    • Rectum: change in bowel movements, constipation/diarrhea alterations, dull ache in rectum/sacral region.
  36. Gallstones? Causes? patho? CM?
    • Most of the time they are "silent" asymptomatic.
    • rapid weigh loss can increase the risk.
    • 95 % are associated w the cystic duct.
    • Causes: obesity, oral contraceptives, family history, hyperlipidemia.
    • Patho: Gallstones (chol n calcium)  obstruct the cystic duct, inflammation occurs, ischemia occurs bc of the pressure against the walls, pain is the result of ischemia.
    • CM: Very specific, after eating a heavy meal in fats, Rt shoulder pain, heartburn/belching/bloating, clay-colored stools.
  37. What is pancreatitis? types/patho? CM?
    • Inflammation of the pancreas. Usually happens when a gallstone gets stuck in the sphincter of Oddi, causing the digestive enzymes to stay in the pancreas and start auto digest it.
    • Types: Acute and chronic.
    • Acute: inflammation of the pancreas due to digestive enzyme autodigestion.
    • Chronic: Associated w chronic alcohol abuse leading to calcification with obstruction.
    • CM: Both manifest pain in the ULQ radiating to the back. (acute: tachy, hypo, fever, jaundice, etc) (chronic:malabsorption, weight loss, constipation, etc)
  38. Pancreas Cancer? Risk factors? CM?
    • Difficult to dx.
    • Survival rate 1 yr.
    • RF: smoking cigarretes, obesity, etc
    • CM: Jaundice, malabsorption, weight loss. Usually pts go to clinic w jaundice complain.
  39. what are the common liver diseases?
    • Hepatocellular failure - Jaundice.
    • Portal hypertension - Gastroesophageal varies.
    • Portal Systemic Encephalopathy.
    • Ascites.
    • Hepatitis.
    • Cirrhosis.
  40. what are the functions of the liver?
    • Digestive organ: Bile salt secretion for fat digestion.
    • Processing and storage of fats, carbohydrates, and proteins absorbed by the intestines.
    • Processing and storage of vitamins and minerals.
    • Hematologic organ: Temporary storage of blood.
    • Removal of billirubin from bloodstream.
    • Hematopoiesis in certain disease states.
    • Synthesis of blood clotting factors.
    • Endocrine organ: Metabolism of glucocorticoids, moneralcorticoids, and sex hormones.
    • Regulariong of carbohydrates, fat, and protein metabolism.
    • Excretory organ: Excretion of bile pigment. 
    • excretion of cholesterol via bile.
    • Urea synthesis.
    • Detoxification of drugs and other foreign substances.
  41. Manifestation of liver dysfunction?
    • Impaired protein synthesis: bleeding (clotting factor deficiency), edema (hypoproteinemia-ascities, free fluids in the abdomen), Immune deficiency (susbtrate for antibody).
    • Accumulation of toxins and hormones: normally broken down in the liver. Feminization (excess of estrogens), poor metabolism of drugs, spider nevi (estrogen).
    • Inadequate bile synthesis: Increased bilirubin levels, Jaundice.
    • Inadequeate urea synthesis: increased blood ammonia levels (NH3), hepatic encephalopathy (confusion due to ammonia)
    • Release of marker enzymes into blood: AST (SGOT), ALT (SGPT).
    • Look at slide 154.
  42. What is Jaundice? pathogenesis?
    • The increased RBC breakdown. It results from impaired bilirubin metabolism. It is the green-yellow staining of the tissues by bilirubin. (sclera).
    • Most characteristic signs of liver disease.
    • Pathogenesis: Bilirubin is released into plasma and transported to liver by albumin. In liver bilirubin is bound.
    • 2 types of bilirubin: conjugated and unconjugated.
    • Unconjugated: lipid soluable not bound bolirubin.
    • Conjugated: bound bilirubin.
  43. What is hepatitis? Patho?
    • Inflammation of the liver parenchyma.
    • Each virus differs in mode of transmission, incubation period, degree of liver damage, and ability to create a carrier state.
    • May be acute or chronic.
    • Patho: causes hepatic cells necrosis, scarring, hyperplasia, and infiltration by mononuclear phagocytes.
    • Interpheres w the normal flow of the blood and bile.
    • Causes increased portal pressure.
    • Jaundice due to high bile in the blood.
  44. What is cirrhosis of the liver? Etiologies? cell failure vs portal vein?
    • It is irreversible en stage of many different hepatic injuries, which interfere w the hepatic blood flow and liver functions.
    • Etiologies: Chronic alcohol use (most common), biliary (obstruction in bile drainage), postnecrotic (viral, toxic hepatitis), cardiac ( RHF (right heart failure, liver congestion).
    • Cell failure: cause Jaundice, bleeding, low albumin-edema, immune deficient, estrogen excess, encephalopathy.
    • Portal hyperstension: Ascites, esophageal varices (varicous veins of the esophagus), hemorroids, anorexia.
  45. Biliary cirrhosis? Pathogenesis? CM?
    • End result of continuous, ongoing inflammation of bile ducts (cystic duct) caused by biliary obstruction with resultant backup of bile in the liver.
    • Pathogenesis: Scarring in the liver that eventually will cause portal hypertension.
    • CM: Need to know the whys. slide 154.
  46. what is ascites?
    • Pathologic accumulation of fluid within the peritoneal cavity that occurs in pts w advanced liver disease.
    • Usually complicated by portal hypertension and hypoalbuminemia.
    • Accumulation of sodium, water, and protein.
  47. what is portal hypertension? etiologies? CM?
    • Occurs when blood flow through the portal system is obstructed. This causes the blood to back up into the portal circulation and increase the pressure.
    • Etiologies: sluggish (slow moving blood) flow resulting in increased pressure in the portal circulation.
    • Congested venous drainage of much of the GI tract, abnormally HBP in the portal venous system.
    • CM: anorexia, varices, ascites.
    • *** major complication is hemorrhage.
  48. What is hepatic encephalopathy? CM?
    • Damage to the brain tissues, which occurs as a complication of cirrhosis of the liver due to much ammonia in brain tissue.
    • IT is a complex neuropsychiatric syndrome.
    • Could put the pt in stupor or coma.
    • CM: Asterixis "liver flap" its a classic sign (spastic jerking of hands held in forced extension) Dementia,
  49. what is esophageal varies? Causes? Importance?
    • like varicose veins, distended, tortous collateral veins that occurs from prolonged elevation of pressure.
    • Cause: increased pressure in portal veins.
    • Importance: Ppl usually died bc the varies rupture and pt can't clot bc no clotting factor.
Card Set
GI tract
Gastrointestinal disorders