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UWM Patho II Exam 4
GI Disorders Part 3
| Question | Answer |
|---|---|
| Alcoholic Hepatitis | 1.U.S. More common 2.Acute illness follows drinking binge No symptoms RUQ pain hepatomegaly jaundice malaise anorexia Fulminant liver failure - very quick death, jaundice->encephalopathy in 2 wks AST/ALT ratio: > 1.5 (*ALT > AST in viral hepatit |
| Pathophysiology of Alcoholic hepatitis | Hepatocyte swelling (ballooning) and necrosis Mallory bodies (cytokeratin intermediate filaments) Fatty change |
| Alcoholic cirrhosis: | Develops in 15% of alcoholics Micronodular cirrhosis Most common disease requiring liver transplantation in adults |
| Stage of Alcoholic Hepatitis: Fatty Liver | Deposits of fat cause liver enlargement Strict abstinence can lead to a FULL RECOVERY |
| Stage of Alcoholic Hepatitis: Liver Fibrosis | Scar tissue forms Recovery is possible, but scar tissue remains |
| Stage of Alcoholic Hepatitis: Cirrhosis | Growth of connective tissue destroys liver cells The damage is IRREVERSIBLE |
| Cirrhosis | (Hardened Liver) Definition: end-stage liver disease characterized by disruption of the liver architecture by bands of fibrosis that divide the liver into nodules of regenerating liver parenchyma |
| Etiology of Cirrhosis | Alcohol,Chronic viral hepatitis,Biliary tract disease,Hemochromatosis (fam hx cirrhosis, Fe overload),Drugs or toxins, tylenol!,Wilson disease (low serum ceruloplasmin and Cu accum in hepatic cells),a1-antitrypsin deficiency (pts may also have COPD) |
| Mechanism of Cirrhosis | Fibrosis (formation of scar tissue) is produced by the Ito cell (aka, hepatic stellate cells) in response to liver damage, impairs the liver's ability to function and obstructs the flow of blood through the portal vein |
| Cirrhosis Manifestations: Liver size and Spleen size | Liver size Can be enlarged, normal, or shrunken. Splenomegaly Due to congestion of the red pulp as a result of portal hypertension |
| Cirrhosis Manifestations:Fluid accumulation and rupture | Ascites in the peritoneal cavity ->flank dullness (needs about 1500 ml to detect flank dullness). Caput medusa (↑ portal hypertension → the umbilical vein may open → ↑ blood into abdominal wall veins through the periumbilical veins → caput medusa) |
| Cirrhosis Manifestations:Breath and esophagus | Fetor hepaticus Sweet pungent smell in breath due to increased dimethylsulfide due to severe portal-systemic shunting. Esophageal varices Dilated, twisted veins to form at the lower end of the esophagus (the most common cause of death in cirrhosis) |
| Cirrhosis Manifestations: Issues with bleeding | Hematemesis is the vomiting of fresh red blood Hemorrhoids varicosities or swelling and inflammation of veins in the rectum and anus |
| Portal-Systemic Anastomosis | Also known as a portacaval anastomosis. Is a specific type of anastomosis occurs between the veins of portal circulation and those of systemic circulation |
| Cirrhosis Manifestations: Manifestations due to increased sex hormone | Spider angioma from i/c in estrogen,Palmar erythema due to altered sex hormone metabolism, Gynecomastia from i/c estradiol Hypogonadism - impotence, infertility,↓ libido, and testicular atrophy |
| Cirrhosis Manifestations: Manifestations due to decreased synthesis | Hypoalbuminemia & edema due to ↓ synthesis of albumin or globulin Bleeding diathesis due to ↓ synthesis of clot factors & thrombocytopenia, Infection due to dysfunction of immune system caused by ↓ synthesis of complements |
| Cirrhosis Manifestations: Manifestations due to decreased detoxification | Jaun cell necrosis r/d liver's ability to metabolize & excrete bilirubin -> buildup in blood,may cause normal, mod. high or high bilirubin. Hepatic encephalopathy cells → changed LOC & asterixis |
| Cirrhosis Manifestations: Other Miscellaneous | Jaundice, Itching, Asterixis, Clubbing, Other Weakness, fatigue, anorexia, weight loss |
| Other consequences of Cirrhosis | Hepatorenal syndrome Acute renal failure without visible gross or microscopic abnormalities of kidneys Liver cancer |
| Diagnosis: | AST and ALT are elevated, with AST > ALT.Alkaline phosphatase - Usually slightly elevated. Bilirubin - May elevate as cirrhosis progresses. ↓ Albumin – ↑ PTT & ↑ PT, ↓ Na Thrombocytopenia Leukopenia and neutropenia,Coagulation defects |
| Treatment and prognosis | Cirrhosis is usually progressive. Formation of scar tissue (fibrosis), once formed, remains indefinitely. No cure exists for cirrhosis, poor prognosis Liver transplantation Liver biopsy (gold standard for diagnosis of cirrhosis) |
| Hepatocellular carcinoma (HCC) | S/S a known cirrhotic, ↑ abdominal girth, bloody ascites, sudden ↑↑ serum(GGT) and alkaline phosphatase (AP) Tendency for hematogenous spread and invasion of portal and hepatic veins Tumor marker:(AFP) |
| What is the most common Primary malignant tumor of the liver? (Asia and Japan > US) | Hepatocellular carcinoma (HCC) |
| What are the causes of Hepatocellular carcinoma (HCC)? | Cirrhosis (MC), hep B and C virus, alcohol, aflatoxin Bl |
| Cholangiocarcinoma (uncommon, < 10%) | Risk factors: Thorotrast (radioactive compound), Clonorchissinensis (liver fluke) Adenocarcinoma arising from bile duct epithelium Discovered late in the course, poor prognosis (average survival is 6 months) |
| Angiosarcoma | (a rare malignant vascular neoplasm) Associated with chemical carcinogens: vinyl chloride, thorotrast, and arsenic Aggressive tumors with a poor prognosis |
| Metastatic tumors to the liver | Most common tumor found within the liver Common primary sites: colon, breast, and lung Tend to occur as multiple well circumscribed masses |
| Gallstone | collections of solid crystals in the gallbladder or in the bile ducts Cholelithiasis (when stones are in the gallbladder) Choledocholithiasis (when stones are in the bile ducts) |
| What are the Three types of gallstones: | 1.Cholesterol stone: (80%, mostly cholesterol monohydrate) 2.Pigmented bilirubinate stones (20%, calcium salts and unconjugated bilirubin) 3.Mixed stones: Have both cholesterol and pigment components. Most common type. |
| What are the risk factors for cholesterol gallstones? | Female gender (estrogen related) Obesity Pregnancy Incidence increases with age Genetics (Native American Pima and Navajo Indians) Oral contraceptives and hormone replacement therapy (HRT) Crohn’s disease Cystic fibrosis Alcoholics |
| What are the risk factors for Pigmented bilirubinate stones? | 1) Chronic hemolytic anemia's 2) Cirrhosis 3)Bacteria 4)Parasites (Ascarisor Clonorchis [Opisthorchis] sinensis) |
| What are the 5 F's risk factors of cholesterol gallstones? | Female Fat Fertile Forty (near or above 40) Fair (Caucasians) |
| What is the Clinical presentation of gallstones? | Often silent and asymptomatic developing symptoms once the stones reach a certain size (>8mm) Fatty food intolerance Gallstone “attack”: Biliary colic: right upper quadrant (RUQ) pain due to impacted stones Nausea and vomiting may occur. |
| What is the Gold Standard test for gallstones? | Ultrasound |
| What are the complications of gallstones? | Cholecystitis (acute RUQ pain within 15-30min after eating) Pancreatitis Cholangitis (bacterial infection of the biliary tract) Choledocholithiasis: gallstones in the common bile duct causes jaundice and liver cell damage, is a medical emergency |
| What is the treatment for gallstones? | Do not require treatment for "silent" gallstones People with intermittent episodes of pain can try avoiding or reducing their intake of fatty foods Treat with cholecystectomy |
| What is Acute Pancreatitis? | an acute inflammation of the pancreas |
| What is the etiology of pancreatitis? | Gallstones (most common cause) Alcohol (most common cause of chronic pancreatitis) Other causes including Hypercalcemia, Drugs (e.g., diuretics such as furosemide, AIDS drugs DDI ), Shock, Infections, Trauma, Scorpion stings, etc |
| What is the mechanism of pancreatitis? | Pancreatic acinar cell injury results in activation enzymes and enzymatic destruction of the pancreatic parenchyma |
| What is the pathology of pancreatitis? | Hemorrhagic fat necrosis of pancreas and deposition of calcium soap |
| What are the clinical presentations of pancreatitis? | Stabbing epigastric abdominal pain radiating to the back Anorexia, nausea Shock of pancreatic (due to dehydration) Hypocalcemia (caused by loss of circulating Ca2+ into precipitated Ca2+ – fatty acid soaps) |
| What are the Lab tests used to diagnose pancreatitis? How is pancreatitis diagnosed? | Lab tests: ↑ serum amylase and lipase (higher specificity) Diagnosis: Signs and symptoms History of gallstones, gallbladder disease or alcohol consumption Lab findings and CT scan |
| How is pancreatitis treated? | Analgesics (mild) Hospitalization (moderate to severe) |
| What are the complications and prognosis of pancreatitis? | Complications: Local: Pseudocyst Systemic: Hypovolemic shock, acute respiratory distress syndrome (ARDS), or DIC Prognosis: Severe cases have a 30% mortality rate |
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czenecke
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