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GI Problems
Pathophysiology 7 - GI Problems
| Question | Answer |
|---|---|
| what role(s) does the liver serve? | - bile production - metabolizes drugs and hormones - synthesizes proteins, glucose, clotting factors - stores vitamins, minerals, large amounts of glycogen - converts ammonia to urea - converts fatty acids to ketones |
| name the 4 layers of the GI wall | - mucosal layer - submucosal layer - muscularis externa - serosal layer |
| describe the function of the mucosal layer of the GI wall | - lubrication of inner surface - secretion of digestive enzymes - absorption of broken down products - protects by maintaining barrier |
| describe the submucosal layer of the GI wall | - blood vessels - nerves - structures to secrete digestive enzymes |
| describe the muscularis externa of the GI wall | - inner layer of circularly arranged smooth muscle cells and an outer layer of longitudinally arranged smooth muscle layers - these layers help move the contents through the GI tract |
| describe the serosal layer of the GI wall | - a serous membrane - outer most layer of organs - the visceral peritoneum |
| what is the mesentery | the double layer of peritoneum that encloses a portion or all of one of the abdominal viscera and attaches it to the abdominal wall. |
| what does the mesentery include | - blood vessels - nerves - lymphatic vessels - holds organs - stores fats |
| what is the omentum | -double-layered extension or fold of peritoneum that passes from the stomach to adjacent organs in the abdominal cavity or wall |
| describe the omentum | - contains fat and has a lot of mobility to follow the movements of the intestines |
| explain rhythmic movements | intermittent contractions that help to mix and move food along. |
| what GI organs do rhythmic movement | -esophagus - antrum of the stomach - small intestine |
| explain tonic movements | constant level of contraction or tone without regular periods of relaxation |
| what GI organs do tonic movements | - lower esophagus - upper region of stomach - ileocecal valve - internal anal sphincter |
| what is the enteric nervous system | - made up of the myenteric and submucosal plexuses. - located in the wall of the GI tract - |
| what is the myenteric plexus | (aka Auerbach plexus) is a linear chain of interconnecting neurons located between circular and longitudinal muscle layers |
| what is the submucosal plexus | (aka Meissner plexus) lies between the mucosal and muscle layers of the intestinal wall --- involved with controlling secretions, absorption and contraction of each segment of the intestinal tract |
| explain how the stomach churns food | - peristaltic fashion 3-5 contractions per minute (each lasting 2-20 seconds) - contraction of antrum pushes food towards the closed pyloric sphincter - larger particles are returned to the body of the stomach for further churning |
| what are segmentation waves | - slow contractions of circular muscle layer - contents are pushed forward and backward - chyme is mixed with digestive enzymes |
| what are peristaltic movements | - rhythmic movements designed to propel the chyme forward along the small intestine - contract then relax and always in one direction |
| name the two types of motility in the large intestine | - haustral churning - propulsive mass movements |
| what is haustral churning of the large intestine | - segmental mixing movement - occur in compartments called haustra - fill and expel contents in haustra - ensures the fecal mass are exposed to intestinal surface |
| what is the propulsive mass movement of the large intestine | - large segment of the colon (=> 20 cm) contracts as a unit - moves fecal contents forward - last about 30 seconds - followed by a 2-3 minute period of relaxation, then another contraction |
| what are the three main cells in the stomach necessary for digestion | - parietal cells - chief cells - g cells |
| what is diverticulosis | the herniation of mucosa and submucosa through the muscular layer of the colonic wall |
| what is diverticulitis | when the herniated mucosa of colon wall becomes inflamed or infected, which can cause left lower abdominal pain, fever, GI bleeding |
| irritable bowel syndrome symptoms | - recurrent abdominal pain/discomfort (relieved with defecation) - change in stool frequency and form - varying complaints of flatulence, bloating, nausea, anorexia, constipation, diarrhea, anxiety, depression |
| what is Barrett esophagus | - squamous mucosa is gradually replaced by abnormal columnar epithelium - a major risk factor for developing esophageal adenocarcinoma |
| what are the two most common causes of peptic ulcer disease | - H. pylori infection - the use of ASA and other NSAIDs |
| what is the final product of heme breakdown | bilirubin |
| what are common causes of cirrhosis | - viral hepatitis - toxic reactions to drugs/chemicals - biliary obstruction - non-alcoholic fatty liver disease **** most commonly associated with alcoholism**** - metabolic disorders that cause deposition of minerals |
| what is nonalcoholic fatty liver disease | ***most common cause of chronic liver disease in Western world*** - associated with obesity and metabolic syndrome (DMII, hyperlipidemia) |
| what is cholelithiasis | gallstones |
| what are gallstones primarily made of | cholesterol |
| function of saliva | - lubricates food - eases swallowing - aids in breakdown of food |
| name enzymes in saliva and their function | - salivary amylase ----breakdown of carbohydrates - lipase -----breakdown fats |
| location and function of pharyngoesophageal sphincter | - upper esophagus - prevents air from entering in esophagus/stomach during breathing |
| location and functions of gastroesophageal sphincter | - lower esophagus - connects to stomach - prevents reflux of gastric contents |
| pyloric sphincter | controls emptying of stomach contents into the small intestine and prevents backflow of contents into stomach |
| sections of the small intestine | - duodenum - jejunum - ileum |
| function of small intestine | - majority of digestion/absorption occurs here |
| emulsification | - lipid digestion by water-soluble digestive enzymes (pancreatic enzymes and bile) |
| sections of the large intestin | - cecum - colon - rectum - anal canal |
| sections of the colon | - ascending colon - transvers colon - descending colon - sigmoid colon |
| function of large intestine | - reabsorb water - stores waste (until defecation) |
| largest visceral organ in the body, weighs about 3 lb | liver |
| gluconeogenesis in liver | - the synthesis of glucose from amino acids, glycerol, and lactic acid during times of fasting/increased demand |
| function of bile | dietary fat digestion and absorption, ----composed of bile salts from cholesterol |
| parietal peritoneum | - lines wall of abdominopelvic cavity |
| peritoneal cavity | potential space between parietal and visceral peritoneum, prevents friction between moving abdominal organs |
| interstitial cells of Cajal | - smooth muscle cells in stomach - act as pacemaker for stomach contraction |
| parasympathetic control of the GI tract comes from | Cranial nerve X (Vagus nerve) |
| sympathetic control of the GI tract comes from | thoracic chain of sympathetic ganclia |
| what is chyme | a creamy mixture formed by the stomach when it is full of food |
| when is chyme from the stomach emptied into the duodenum | between contractions |
| pyloric sphincter regurgitation leads to | gastric ulcers ------bile salts and duodenal contents which damage the mucosa of the antrum |
| rapid influx of gastric contents in duodenum leads to | damage of the duodenal mucosa |
| hormones that help regulate stomach emptying | - cholecystokinin (CCK) - glucose dependent insulinotropic polypeptide (GIP) both are released in response to composition of chyme |
| gastric retention | when stomach emptying is too slow (usually caused by obstruction of gastric atony (decrease in muscular tone)) |
| dumping syndrom | stomach contents emptying too fast |
| normal colonic transit time is | 24-48 hours |
| normal stool is made up of | 75% water and 25% solid mass |
| defecation is controlled by | the involuntary internal and voluntary external anal sphincters |
| site of secretion for CCK | duodenum and jejunum |
| stimulus for secretion of CCK | products of protein digestion and long-chain fatty acids |
| what is the function of CCK | - stimulates gallbladder - secretion of pancreatic enzymes - slows gastric emptying - inhibits food intake |
| site of secretion of Ghrelin | fundus of stomach |
| stimulus for secretion of Ghrelin | - Nutritional (fasting) and hormonal (decrease levels of growth hormone) |
| what is the function of Ghrelin | - stimulates secretion of growth hormone - act as an appetite-stimulating signal from stomach when an increase in metabolic efficiency is necessary |
| site of GLP-1 release | distal small intestine |
| stimulus for GLP-1 release | high-carb meal |
| function of GLP-1 | - augments insulin release - suppresses glucagon release - slows gastric emptying - decreases appetite and body weight |
| site of GIP release | small intestine (mainly jejunum) |
| stimulus for GIP release | high-carb meals |
| function of GIP release | augments insulin release |
| site of secretin release | duodenum |
| stimulus for secretin release | - acid (pH < 3) or chyme entering duodenum |
| function of secretin | inhibition of gastric acid secretion |
| function of colonic microogranisms | - vitamin synthesis (vitamin k) - absorption of calcium, magnesium, and iron - protects against invading pathogens |
| what is diarrhea | -excessively frequent passage of loose or unformed stools |
| what is acute diarrhea | last for 2 weeks or less, |
| cause for acute diarrhea | infectious organisms |
| non-inflammatory diarrhea | - non-bloody stool - cramps - bloating - nausea - vomiting |
| common causes on non-inflammatory diarrhea | - S. aureus - E. coli - Cryptosporidium parvum - Vibrio cholerae - Giardia |
| inflammatory diarrhea | - fever - bloody stool - lower abdomen cramps - urgency - tenesmus (difficulty/inability to void) |
| causes of inflammatory diarrhea | - Shigella - Salmonella - Yersinia - Campylobacter (toxins associated with the following) - C. difficile - E. coli O157:H7 infection |
| what is chronic diarrhea | when the symptoms of diarrhea last 4(+) weeks |
| four major causes of chronic diarrhea | - presence of hyperosmotic luminal contents - increased intestinal secretory processes - inflammatory conditions - infections processes |
| what is factitious diarrhea caused by | overuse of laxatives or excessive intake of laxative type foods |
| what is osmotic diarrhea | water is pulled in to the bowel from hyperosmotic contents. this water is not reabsorbed |
| an example of an individual with osmotic diarrhea | lactose intolerance |
| what is secretory diarrhea | increased secretions of bowel OR excess bile acids remain in intestinal contents |
| what is chronic inflammatory diarrhea | associated with inflammatory diseases such as ulcerative colitis and Crohn disease |
| what is chronic infectious diarrhea | protozoans (Giardia, E. histolytica, Cyclospora), usually someone who is immunocompromised |
| how is motility/diarrhea diagnosed | - based on symptoms (freq. stools with history of recurrent illness) - medication use - travel - potential exposure to intestinal pathogens |
| in general, treatment for motility/diarrhea | most instances do not require treatment |
| treatment for infants, small children, and elderly with diarrhea | electrolyte and fluid replacement |
| name some medications that can help treat diarrhea | - diphenoxylate (Lomotil) - loperamide (Imodium) - Bismuth subsalicylate (Pepto-Bismol) |
| mechanism of diphenoxylate (Lomotil) and loperamide (Imodium) in diarrhea | GI motility and stimulation of water and electrolyte absorption |
| mechanism of bismuth subsalicylate (Pepto-Bismol) | - inhibits intestinal secretions - works to decrease frequency of unformed stools |
| is it ok to use antidiarrheal medication with bloody stool, high fever, or signs of toxicity | no |
| in cases of diarrhea, when should one use antibiotics | only once the pathogen has been identified |
| name the three categories of constipation | 1) normal transit constipation 2) slow-transit constipation 3) defecatory disorders |
| what is normal transit constipation | the perceived difficulty in defecation. however, defecation will usually occur after increased fluid and fiber intake |
| what is slow-transit constipation | - infrequent bowel movements caused by changes in colonic motor function |
| give one example of slow-transit constipation | Hirschsprung disease -----defect where there is an absence of ganglion cells in the distant bowel (pregnancy is another example) |
| what are defecatory disorders | constipation disorders that are due to a lack of muscle coordination in the pelvic floor/anal sphincter |
| compare and contrast Crohn disease and Ulcerative colitis based on type of inflammation | Crohn disease - Granulomatous Ulcerative colitis - Ulcers and exudative |
| compare and contrast Crohn disease and ulcerative colitis based on the level of involvement | Crohn disease - primarily submucosal Ulcerative colitis - primarily mucosal |
| compare and contrast Crohn disease and ulcerative colitis based on the extent of involvement | crohn disease - has skip lesions ulcerative colitis - the damage is continuous |
| compare and contrast crohn disease and ulcerative colitis based on diarrhea | diarrhea is COMMON with BOTH diseases |
| compare and contrast crohn disease and ulcerative colitis based on rectal bleeding | crohn disease - rare ulcerative colitis - common |
| compare and contrast crohns disease and ulcerative colitis based on the occurrence of fistulas | crohn disease - common ulcerative colitlis - rare |
| compare and contrast crohns disease and ulcerative colitis based on the appearance of strictures | crohn disease - common ulcerative colitis - rare |
| compare and contrast crohn disease and ulcerative colitis based on the perianal abscesses | crohn disease - common ulcerative colitis - rare |
| compare and contrast crohn disease and ulcerative colitis based on development of cancer | crohn disease - uncommon ulcerative colitis - relatively common |
| list a few things that occur with both ulcerative colitis and crohn disease | - results from inflammatory cells and mediators - characterized by remissions and exacerbations - has systemic manifestations |
| how does both ulcerative colitis and crohn disease exacerbations present themselves | - diarrhea - fecal urgency - weight loss |
| what are some systemic manifestations of both ulcerative colitis and crohn disease | - arthritis - inflammatory conditions of the eyes - skin lesions - stomatitis - autoimmune anemia - hypercoagulability - sclerosing cholangitis |
| what is crohn disease | an inflammatory response that can affect any part of the GI tract, but mostly in the terminal ileum and cecum |
| crohn disease affects what type of people | mostly women in their 20 and 30s |
| what are skip lesions in crohn disease | multiple lesions that are interspersed between normal segments of bowel, gives the affected bowel a "cobblestone" appearance |
| clinical manifestations of crohn disease | - exacerbations and remissions - diarrhea (less bloody than ulcerative colitis) - abdominal pain - weight loss - fluid/electrolyte disorders - malaise - low-grade fever |
| complications due to crohn disease | - fistulas (tube-like passages...most common) - abdominal abscesses - intestinal obstruction |
| what are fistulas | tub-like passages that form connections between different sites in the GI tract |
| fistulas can be problem because they cause | - malabsorption - bacterial overgrowth - diarrhea - can become infected and cause abscesses |
| crohn disease diagnosises | - intestines need to be visualized ---- small bowel capsule endoscopy ---- colonoscopy - stool cultures (to r/o infection) - CT scans (r/o inflammatory mass or abscesses) |
| treatment of crohn disease | - stop inflammatory response - promote healing - adequate nutrition - prevent/treat complications - medications - possible surgical intervention |
| types of medication used for crohn disease | - inflammation surpression ----- corticosteroids ----- immunosuppressants ----- immunomodulators |
| when would surgery be performed for crohn disease | - damaged bowel - drainage of abscess - fistula repair |
| ways nutrition would be used to treat crohn disease | - high in calories - high in vitamins - high in protien - avoid fatty foods |
| what is ulcerative colitis | an inflammatory condition of the colon, more common in US and western world |
| lesions in ulcerative colitis form | crypts of Lieberkuhn |
| clinical presentation of ulcerative colitis | - relapsing bouts of diarrhea (containing blood and mucous) - mild abdominal cramping - fecal incontinence - anorexia - weakness - fatigue |
| four types of ulcerative colitis severity | - mild - moderate - severe - fulminant |
| patients with fulminant ulcerative colitis are at risk for | developing toxic megacolon |
| what is toxic megacolon | dilation of the colon with signs of systemic toxicity (d/t vast inflammatory response) |
| diagnosis of ulcerative colitis | - sigmoidoscopy/colonoscopy - biopsy - negative stool cultures |
| treatment of ulcerative colitis depends on | extent and severity of symptoms |
| treatment of ulcerative colitis is geared toward | control of acute manifestations and prevention of recurrence |
| those with mild to moderate ulcerative colitis are able to control the disease by | avoiding - caffeine - lactose - highly spicy food - gas-forming foods - fiber supplements (avoid diarrhea) |
| what medications are used to help treat ulcerative colitis | - corticosteroids - immunomodulators - immunosurppressants |
| when is surgery required for those with ulcerative colitis | when someone does not respond to medications and conservative treatment |
| why is it important that people with ulcerative colitis have more frequent colonoscopies and biopsies | they are at a higher risk of developing colon cancer |
| what is GERD | the contents of the stomach backflows into the esophagus, |
| causes of GERD | - transient relaxation of weak lower esophageal sphincter - incompetent lower esophageal sphincter - hiatal hernia - delayed gastric emptying (increased gastric volume/pressure) |
| clinical presentation of GERD | - heartburn after eating - belching - chest pain - dysphagia - bloating/early satiety - laryngitis - chronic cough - sour taste in mouth - dental erosion - reflux associated asthma |
| name some ALARMING GERD symptoms that would require further testing | - weight loss - persistent vomiting - dysphagia - odynophagia - evidence of blood in stool |
| what id dysphagia | difficulty swallowing |
| what is odynophagia | painful swallowing |
| chronic reflux esophagitis can cause | mucosal injury, hyperemia, and inflamation |
| complications of chronic reflux esophagitis | strictures and barrett esophagus |
| what are strictures | narrowing of the esophagus |
| barrett esophagus is a major risk factor for developing which cancer | esophageal adenocarcinoma |
| how is GERD diagnosed | - review of history of patient symptoms - trial of PPI for days (positive if symptoms improve) - other optional tests include ----- ambulatory esophageal pH monitoring ----- upper endoscopy (EGD) |
| possible triggers for GERD and these should be avoided | - alcohol use - smoking - intake of specific foods ---- coffee/caffeine ---- chocolate ---- mints ---- citruc fruit ---- acidic/spicy food ---- fats - lying down immediately after eating - large meals close to bedtime |
| most effective drug for treating GERD | proton pump inhibitors (PPIs) - omeprazole |
| how do PPI help prevent GERD | inhibit gastric proton pump (regulates the final pathway for acid secretion) |
| other drug classes that help with GERD but might not be as effective. | - histamine-2 receptor (H2)- blocking antagonists ----- Zantac - antacids (immediate relief) |
| how do H2-blocking antagonists help prevent GERD | inhibit gastric and acid production |
| what is peptic ulcer disease | a group of ulcerative disorders in the upper GI track that are exposed to acid-pepsin secretions |
| name the two most common forms of peptic ulcer disease (of the two which is more common) | duodenal (5X more common) and gastric ulcers |
| of the two types of peptic ulcers, which is more common in men and which is more common in women | duodenal ulcers - men between 30 and 60 gastric ulcers - middle aged and older men and women |
| how does H. pylori cause PUD | causes inflammation and stimulates the release of cytokines that contribute to mucosal damage |
| how does NSAID-induced cause PUD | inhibits prostaglandin synthesis; this is drug dose dependent and life-threatening complications can occur without warning |
| risk factors for PUD | - advanced age - prior history of PUD - multiple NSAID use - NSAID concurrent with Warfarin - corticosteroid drugs - smoking - alcohol use - stress |
| clinical presentation of PUD | - chronic, upper abdominal pain - dyspepsia - epigastric tenderness |
| gastric ulcer abdominal pain is worsened by | eating |
| duodenal ulcers, abdominal pain is worsened by | emptying of stomach, eating may relieve the pain |
| most common complication for PUD | gastroduodenal bleeding |
| evidence of a bleeding peptic ulcer | - hematemesis (blood in vomit) - melena (dark, tarry stools) |
| what is perforation in PUD | when an ulcer erodes through all the layers of the stomach or duodenum wall |
| what is peritonitis | when GI contents enter the peritoneum |
| presentation of peritonitis | - abdominal pain radiating into back - severe night distress - inadequate pain relief from eating food or after taking antacids |
| how does a perforated ulcer appear on an e-ray | as air under the diaphragm |
| how is PUD diagnosed | - endoscopy (visualize/diagnose ulcer) - biopsies (for H. pylori and exclude malignancies) - hx evaluate for ASA of NSAID use - lab studies (eval. anemia and occult blood in stool) - barium radiography (only for those unable to undergo endoscopy) |
| treatment goals for PUD | - eradicate the cause and healing the uclesr |
| how to treat PUD with H. pylori negative patients | - d/c NSAID and ASA use - prescribe PPI (H2 antagonists and Sucralfate also work are less effective) - prostaglandin analogs (misoprostol) |
| how to treat PUD with H. pylori positive patietnes | - PPI plus 2 antibiotics |
| how do prostaglandin analogs work | - stimulate mucous and bicarb. secretion - modest inhibiting acid secretion |
| what is jaundice | a yellowish discoloration of the skin, which results from abnormally high levels of bilirubin in the blood |
| first place to examine if you suspect an individual of jaundice | sclera of the eyes |
| bilirubin is the final product of | RBC/heme breakdown |
| bilirubin is NOT soluble in _________________ but IS soluble in ________________ | plasma (requires plasma albumin for transport); bile |
| name the three categories of jaundice | - prehepatic - intrahepatic - posthepatic |
| what is the main cause of prehepatic Jaunice | excessive red blood cell destruction |
| list some disorders/diseases/conditions that can cause prehepatic jaundice | - hemolytic blood transfusion reaction - hereditary disorders of RBC - acquired hemolytic disorders - hemolytic disease of newborn - autoimmune hemolytic anemia |
| some hereditary disorders of RBCs that can cause prehepatic jaundice | - sickle cell anemia - thalassemia - spherocytosis |
| list some disorders/conditions/diseased that can cause intrahepatic jaundice | - decreased bilirubin uptake by liver - decreased conjugation of bilirubin - hepatocellular liver damage - drug-induced cholestasis |
| list a few diseases that lead to hepatocellular liver damage which leads to intrahepatic jaundice | - hepatitis - cirrhosis - liver cancer |
| main cause of posthepatic jaundice | obstruction of bile flow |
| list a few disorders/diseases/conditions that lead to posthepatic jaundice | - structural disorders of bile duct - cholelithiasis - congenital atresia of the extrahepatic bile duct - bile duct obstruction caused by tumor |
| what are the five major causes of jaundice | - excessive destruction of RBCs - impaired uptake of bilirubin by liver - decreased in conjugation of bilirubin - obstruction of bile flow in canaliculi of hepatic lobes OR extrahepatic bile products - excessive extrahepatic production of bilirubin |
| how would prehepatic jaundice present | - mild jaundice - elevated conjugated bilirubin - normal stool color - no bilirubin in urine |
| how would intrahepatic jaundice present | - elevated conjugated bilirubin - elevated unconjugated bilirubin - dark urine - elevated serum alkaline phosphate |
| list some drugs that can induce intrahepatic jaundice | - contraceptive use - estrogen use - steroids - isoniazid - rifampin |
| posthepatic jaundice is also called | cholestatic jaundice |
| how does posthepatic jaundice present | - elevated conjugated bilirubin - clay colored stools (d/t lack or bilirubin) - dark urine - elevated serum alkaline phosphatase - elevated aminotransferase - elevated bile acid in blood (pruritus) |
| describe how LFT labs would help dx jaundice | - help dx liver disease (signifies acute hepatocellular injury) * Alanine aminotransferase (ALT) * Aspartate aminotransferase (AST) -----both are elevated with liver disease |
| of the two (ALT and AST) which one is liver specific and which one is derived from organs other than the liver | alanine aminotransferase (ALT) is liver specific aspartate aminotransferase (AST) - derived from organs other than the liver |
| name 4 lab tests that measure hepatic excretory function | - serum bilirubin - gamma-glutamyltranserase (GGT) - 5'-nucleotidase - alkaline phosphatase |
| list two lab tests that measure chemicals between the liver cells and bile cells and are are released by disorders affecting bile ducts | - 5'-nucleotidase - alkaline phosphatase |
| which lab test help diagnose alcohol abuse and hepatorbiliary disease | gamma-glutamyltransferase (GGT) |
| what is cirrhosis | when functional liver tissue has been replaced by fibrous tissue |
| when does cirrhosis normally occur | end stages of chronic liver disease --- hepatitis --- toxic reactions to drugs --- biliary obstruction --- non-alcoholic fatty liver disease --- alcoholism --- other metabolic disorders |
| name two metabolic disorders that can cause cirrhosis | - hemochromatosis (iron deposition) - Wilson disease (copper deposition) |
| which cancer is associated with cirrhosis | hepatocellular carcinoma |
| the most common cause of chronic liver disease in the Western world | nonalcoholic fatty liver disease |
| what other disease are normally associated with nonalcoholic fatty liver disease | - obesity - metabolic syndrome (DMII and hyperlipidemia) |
| best treatment for nonalcoholic fatty liver disease | lifestyle modification (diet/exercise/weight loss) |
| _______________ % of nonalcoholic fatty liver disease will progress to cirrhosis | 10-15% |
| clinical presentation of cirrhosis | (it ranges...most symptoms may not occur until disease is advanced) - hepatomegaly - hepatic failure - jaundice - abdominal pain - weight loss (sometimes masked by ascites) - weakness - anorexia - diarrhea |
| one of the late manifestations of cirrhosis includes portal hypertension which is | increased resistance to flow in the portal venous system |
| one of the late manifestations of cirrhosis includes esophageal varices which is | dilated veins |
| one of the late manifestations of cirrhosis includes caput medusae which is | distended and engorged superficial epigastric veins |
| complications to cirrhosis | - bleeding (d/t decreased clotting factors) - thrombocytopenia (d/t splenomegaly) - gynecomastia (d/t testicular atrophy) - spider angiomas - palmar erythema - encephalopathy with asterixis - neurological signs (d/t increased ammonia levels) |
| dx of cirrhosis | - thorough H+P - full panel blood test - upper GI endoscopy - ultrasound - CT scan - MRI - (most specific and most sensitive) liver biopsy |
| tx for cirrhosis | 1 - address underlying cause (hepatitis, alcholic liver disease) 2 - avoid ETOH, NSAIDs, and high dose acetaminophen 3 - adequate nutrition and regular exercise |
| if ascites occurs with cirrhosis, what should be done | - sodium restriction (<2g daily) |
| liver transplant should be suggested for patients with | - hepatocellular carcinoma - signs of decompensation cirrhosis |
| __________________________ remains the only curative treatment option for decompensated cirrhosis | liver transplant |
| function of gallbladder | store and concentrate bile. when food is in the intestine, organ contracts and releases bile into duodenum |
| bile contains | - bile salts - cholesterol - bilirubin - lecithin - fatty acids - water and electrolytes |
| what is cholestasis | a decrease in bile flow and reduced secretion of water, bilirubing, and bild acids by hepatocytes....instead these items accumulate in blood |
| intrahepatic cholestasis | - cholestasis caused by intrinsic liver disease |
| extrahepatic cholestasis | - cholestasis caused by an obstruction of large bile duct |
| what is cholelithiasis | gallstones |
| 80% of gallstones are made up of cholesterol, what is the other 20% made of | black/brown pigment stones composed of mucin glycoproteins and calcium salts |
| what two major factors contribute to the formation of gallstones | - abnormalities in bile composition (increased cholesterol) - the stasis of bile |
| risk factors for gallstone formation | - age (40's) - obesity - female gender (especially those with multiple pregnancies or taking contraceptives) |
| what is acute cholesystitis | diffuse inflammation of the gallbladder mostly (85%) due to obstruction of gallbladder outlet from gallstones |
| 85% of acute cholecystitis is due to gallstones, what is the other 25% from | - sepsis - severe trauma - infection of gall bladder |
| chronic cholecystitis occurs from | - chronic irritation by stones or multiple attacks of acute cholecystitis |
| clinical presentation of cholecystitis | (small stones <8mm in diameter and pass) - indigestion - biliary colic (larger stones, do not pass) - jaundice - biliary colic (RUQ and radiating to back) - mild fever - nausea - anorexia - vomiting |
| lab results with cholecystitis | - elevated WBC - mild elevations of ALT and AST - elevated alkaline phosphatase - elevated bilirubin |
| patients with chronic cholecystitis might be intolerant to | - fatty foods - belching - colicky pain |
| how is cholecystitis dx | - US is best method - cholecintography (highly accurate in diagnosis (HIDA) scan...cannot r/o other conditions) - CT scan |
| cholecystitis treatment | surgical removal (laparoscopic cholecystectomy) |
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kandriot
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