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NUR 460 - Ch. 38: Portal Hypertension, Esophageal Varices, and Biliary Dyskinesia

by: ndp33

NUR 460 - Ch. 38: Portal Hypertension, Esophageal Varices, and Biliary Dyskinesia 460

Marketplace > Niagara University > Nursing and Health Sciences > 460 > NUR 460 Ch 38 Portal Hypertension Esophageal Varices and Biliary Dyskinesia

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These notes cover the following: portal hypertension, esophageal varices, and biliary dyskinesia. Ways to treat the disorders are included.
Nursing Concepts IV: Health of Maturing Adults / Chronic Disease
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This 3 page Class Notes was uploaded by ndp33 on Wednesday July 13, 2016. The Class Notes belongs to 460 at Niagara University taught by in Summer 2016. Since its upload, it has received 10 views. For similar materials see Nursing Concepts IV: Health of Maturing Adults / Chronic Disease in Nursing and Health Sciences at Niagara University.


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Date Created: 07/13/16
Chapter 38: -esophageal varices as a result of portal hypertension:  Esophageal varices area thin-walled veins in the esophagus that are prone to rupture, causing massive, life-threatening hemorrhage  Rupture can occur from increased P in vessel (even from coughing or trauma, such as from eating high-roughage food)  Slow and chronic bleeding can lead to melena (black or maroon, sticky, foul- smelling feces from digestion of blood)  Hemorrhage and vomiting from large volumes of dark-red blood occurs when varices ruptures -splenomegaly as a result of portal hypertension:  b/c splenic vein branches from portal vein  blood flow is obstructed through portal vein; and increasing pressure in splenic vein causes enlarged spleen -hepatic encephalopathy as a result of portal hypertension:  result of increased level of circulating neurotoxins (eg NH3; GABA; endogenous benzodiapepines, and fasle neurotransmitters)  sx incl asterixis (flapping tremor of hands when arms are outstretched, believed to be caused by accumulation of sub normally detoxified by liver, agitation, restlessness, and changes in mentation) -hepatorenal syndrome as a result of portal hypertension:  occurrence of azotemia (elevation of BYN) when other cause of renal failure have been excluded  renal vasoconstriction and decreasd renal blood flow  Type I is acute  Type II is chronic  Oliguria (diminished urine output); NA and H2O retention, hypotension, and peripheral vasodilation indicate a poor prognosis -treatment for ascites:  Spironolactone (Aldactone), a potassium-sparing diuretic, inhibits aldosterone action and increases reabsorption of K, at does of 100 mg /day  Treat the increased renin-agniotensin-aldosterone secretion  Fluid and Na restrictions; NA of no more than 400-800 mg /day; fluid b/t 800- 1000mL/day  Paracentesis: o Remove 1-2L fluid though vacuum tubing from peritoneal cavity, w/o increasing risk of f/e imbalance o 4-6L to reliev respiratory sx  Transjugular intrahepatic portosystemic shunt (TIPS) o Insert catheter into jugular vein, thorugh which han expandable stent is placed b/t hepatic vein and portal vein o Stent allows blood to flow from portal vein into hepatic vein, therefore bypassing liver and effectively reducing portal P -Treatment for hepatic encephalopathy:  Lactulose o Nonabsorbable synthetic disaccharide that casues contents of colon to become more acidic o Reduce ammonia levels in blood by creating NH$+ (nonabsorbable form of ammonia) that is absorbed and excreted in feces o Lactulose also reduces presence of bacteria in colon (that form ammonia when they digest protein stool) o 30mL of liquid 3-4x/day  Oxazepam (Serax) o Benzodiazepine o Treats marked agitation o 10-30 mg PO or through NG  Decrease H. pylori  Dietary protein restriction o During acute episodes o Reintroduce slowly to 60-80 g/day, preferably vegetable protein over animal protein -Surgery to treat esophageal varices:  Banding (Variceal ligation) o During endoscopy o Placement of tiny rubber bands on varices to occlude blood flow  Sclerotherapy o Inject varices with chemical agent that causes vessel to become sclerotic o Preferred for active bleeding, can see the obstruction  Balloon tamponade o Short-term when endoscopy or TIPS procedure can’t be performed immediately o Esophageal or Gastric balloon and lumen that opens into stomach is inserted through nose o Balloon is inflated once in stomach; P is applied to any bleeding vessels o Complications, though rare: aspiration, ulceration, and perforation of esophagus Treatmetn of biliary dyskinesis: laparoscopic v open cholecystectomy:  Laparoscopic: fewer complications, minimally invasive, shorter length of stay in hospital  Open procedure: patients with very large or infected gallbladder who are not candidates for laparoscopic procedure  T tube: o for when stones are located in common bile duct and an exploration of duct is done o T tube is placed in common bile duct to maintain patency, allowing bile to pass from liver into duodenum until edema from surgery diminishes -meds for biliary dyskinesia:  Ursodiol (Actigall) or chenodiol (Chenix) only effective if gallstones contain a high concentration fo cholesterol and are less than 1 cm in diameter  Drugs to reduce cholesterol content of stone, and dissolve gallstone  Tx < 6 months  Antibiotics if infection syspected  Questran to bind bile salts (if suspected) and excrete them in stool  Narcotic analgesic for pain during acute cholecystitis Ranson’s Criteria for Assessing Acute Pancreatitis Severity:  At onset of sx: o Age>55 o WBC>16K o Blood glucose >200 mg/dL o Serum lactase dehydrogenase (LDH) > 350 units/L o AST >250 units/L  During the following 48 hours: o Hematrocrit group of 10% or more o BUN increase of 5 or more o PaO2 < 60mmHg o Serum calcium < 8mg/dL o Base deficit > 4 mEq/L Estimated fluid sequestration > 6L


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