Home > Preview
The flashcards below were created by user
on FreezingBlue Flashcards.
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.
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.
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.
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.
What are the most common etiologies of dysphagia?
- congenital atresia
- congenital tracheoesophageal fistula
- neurologic damage to cranial nerves V, VII, IX, X, and XII.
- Look at slide 12 on GI for drawing.
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.
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.
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)
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.
what are the common disorders of the mouth and esophagus?
- Stomatitis/oral infections
- Gastroesophageal Reflux Disease (GERD)
- Hiatal Hernia.
What is stomatitis? Cause?
- Inflammation of the oral mucosa.
- Common cause: Candida albicans (oral Thrush)
- usually seen in immunosupress ppl (chemo, radiation therapy, etc.
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)
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.
- Etiologies: Aging (most common cause), upper abdominal surgeries, etc
- Patho: Defect in the diaphragm, increased intra-abdominal pressure.
- CM: Heartburn, Chest pain, Dysphagia, GERD.
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.
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.
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.
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.
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.
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.
- 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%!
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.
- 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.
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.
What are motility disorders?
- Disorders that affect peristalisis.
- IBS (irritable bowel syndrome).
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.
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.
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.
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.
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.
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.
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.
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.
Esophageal Cancer? Risk factors? prognosis?
- RF: ppl w GERD (Barrett esophagus).
- Prognosis: Poor prognosis bc o the amt of lymph nodes around the area.
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.
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.
Colon cancer? Risk factors? CM?
- 2nd cause of death, after lung cancer.
- RF: age, after 40.
- high fat, low fiber diet.
- Chronic irritation or inflammation.
- 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.
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.
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)
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.
what are the common liver diseases?
- Hepatocellular failure - Jaundice.
- Portal hypertension - Gastroesophageal varies.
- Portal Systemic Encephalopathy.
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.
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.
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.
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.
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.
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.
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.
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.
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,
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.