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EXAM 2 - MED SURG II
Cirrhosis
| Question | Answer |
|---|---|
| Alcoholic Cirrhosis | in which the scar tissue characteristically surrounds the portal areas. This is most frequently caused by chronic alcoholism and is the most common type of cirrhosis. |
| Post necrotic Cirrhosis | in which there are broad bands of scar tissue. This is a late result of a previous bout of acute viral hepatitis. |
| Biliary Cirrhosis | in which scarring occurs in the liver around the bile ducts. This type of cirrhosis usually results from chronic biliary obstruction and cholangitis (bile duct infection) |
| Cirrhosis | a chronic liver disease characterized by fibrotic changes, the formation of dense connective tissue within the liver, subsequent degenerative changes, and loss of functioning cells. Cirrhosis is a late stage of fibrosis (scarring) of the liver caused by many forms of liver diseases and conditions, such as hepatitis and chronic alcoholism. |
| Hepatic Cirrhosis | The portion of the liver chiefly involved in cirrhosis consists of the portal and the periportal spaces, where the bile canaliculi of each lobule communicate to form the liver bile ducts. These areas become the sites of inflammation, and the bile ducts become occluded with inspissated (thickened) bile and pus. The liver attempts to form new bile channels |
| Antacids | alkaline substances that neutralize acids. |
| Aluminum Antacids | have low neutralizing capacity and often cause constipation. |
| Magnesium Antacids | have high neutralizing capacity and may cause diarrhea and hypermagnesemia. People with renal impairment should not take products that contain magnesium because magnesium can accumulate in the body and cause serious adverse effects. |
| Calcium Antacids | have high neutralizing capacity and rapid onset. The drugs may cause rebound acidity and hypercalcemia and so are not used for the treatment of peptic ulcer disease or GERD. |
| H2RAs | (e.g., cimetidine, famotidine, nizatidine, and ranitidine) inhibit secretion of gastric acid, decreasing the acidity of gastric juices. They are indicated for prevention and treatment of heartburn, peptic ulcer disease, GERD, esophagitis, GI bleeding due to stress ulcers, and hypersecretory syndromes such as Zollinger-Ellison syndrome. |
| PPIs | (e.g., omeprazole, esomeprazole, lansoprazole, pantoprazole, rabeprazole) bind irreversibility to the gastric proton pump to prevent the release of gastric acid from parietal cells into the stomach lumen. They are considered drugs of choice for treatment of heartburn, gastric and duodenal ulcers, GERD, esophagitis, and hypersecretory syndromes such as Zollinger-Ellison syndrome. |
| Treatment for Cirrhosis | usually symptomatic including antacids or H2 antagonists to decrease gastric distress and minimize the possibility of GI bleeding |
| Cirrhosis | Late stage of fibrosis (scarring) of the liver. It tries to repair itself, and scare tissue forms. As it progresses the more scar tissue forms, making it hard for the liver to function and leads to decompensated cirrhosis and it is life-threatening. |
| Cirrhosis Symptoms | Often has no signs or symptoms until liver damage is extensive. Symptoms then include fatigue, easy bleeding/bruising, loss of appetite, nausea, edema, weight loss, itchy skin, jaundice, ascites, spriderlike blood vessels on the skin, redness in the palms of the hands, for women absence or loss of periods not related to menopause, gynecomastia or testicular atrophy, hepatic encephalopathy |
| Decompensated Cirrhosis | decompensated result from failure of the liver to synthesize proteins, clotting factors, and other substances and manifestations of hypertension. Liver Enlargement, Portal Obstruction and Ascites, Infection & Peritonitis, Gastrointestinal Varices, Edema, Vitamin Deficiency & Anemia, Mental Deterioration. |
| Liver Enlargement | In the early stages of cirrhosis, the liver enlarges, and cells are loaded with fat. It is firm, and has a sharp edge noticeable upon palpation. Abdominal pain may be present. Later tension is placed on the Glisson Capsule (fibrous covering of the liver). Eventually the liver decreases in size, as scar tissue contracts the liver tissue, and the liver edge, if palpable, is nodular |
| Portal Obstruction & Ascites | late manifestations of cirrhosis—are caused partly by chronic failure of liver function and partly by obstruction of the portal circulation. Almost all of the blood from the digestive organs is collected in the portal veins and carried to the liver. Indigestion and altered bowel function result. Fluid rich in protein may accumulate in the peritoneal cavity, producing ascites. This can be detected through percussion for shifting dullness or a fluid wave. |
| Edema | Another late symptom of cirrhosis is edema, which is attributed to chronic liver failure. A reduced plasma albumin concentration predisposes the patient to the formation of edema. Although edema is generalized, it often affects the lower extremities, the upper extremities, and the presacral area. Facial edema is not typical. Overproduction of aldosterone occurs, causing sodium and water retention and potassium excretion. |
| Vitamin Deficiency & Anemia | Because of inadequate formation, use, and storage of certain vitamins (notably vitamins A, C, and K), signs of deficiency are common, particularly hemorrhagic phenomena associated with vitamin K deficiency. Chronic gastritis and impaired GI function, together with inadequate dietary intake and impaired liver function, account for the anemia that is often associated with cirrhosis. |
| Mental Deterioration | Additional clinical manifestations include deterioration of mental and cognitive function with impending hepatic encephalopathy and hepatic coma, as described previously. Serial neurologic assessment is indicated, including assessment of the patient’s general behavior, cognitive abilities, orientation to time and place, and speech patterns. |
| Cirrhosis Risk Factors | Drinking too much alcohol. Excessive alcohol consumption is a risk factor for cirrhosis. Being overweight. Being obese increases the risk of conditions that may lead to cirrhosis, such as nonalcoholic fatty liver disease and nonalcoholic steatohepatitis. Having viral hepatitis. Not everyone with chronic hepatitis will develop cirrhosis, but it's one of the world's leading causes of liver disease. |
| Cirrhosis Diagnosis | usually based on the presence of a risk factor for cirrhosis, such as alcohol use or obesity, and is confirmed by physical examination, blood tests, and imaging. |
| Cirrhosis Treatment | Low sodium diet and medication to help control ascites and swelling. Blood pressure meds to control portal hypotension. Upper endoscopy to look for varices that might bleed. Possible band ligation for those with varices that are bleeding/likely to bleed. trans jugular intrahepatic portosystemic shunt is placed into the vein to reduce blood pressure in the liver. Antibiotics for infections. Periodic blood tests and ultrasound exams looking for signs of cancer. |
| Liver Transplant | In advanced cases of cirrhosis, when the liver ceases to function, a liver transplant may be the only treatment option. Cirrhosis is one of the most common reasons for a liver transplant. Candidates for liver transplants have extensive testing to determine whether they are healthy enough to have a good outcome following surgery. |
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