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Interference to Nutritional Needs Due to Degeneration and Inflammation. Biliary disorders. Cholecystitis Acute Cholelithiasis Acalculous cholecystitis Calculous cholecystitis Pathophysiology Abnormal metabolism of cholesterol and bile salts Decreased gallbladder-emptying rates
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Interference to Nutritional Needs Due to Degeneration and Inflammation
Biliary disorders • Cholecystitis • Acute • Cholelithiasis • Acalculouscholecystitis • Calculouscholecystitis • Pathophysiology • Abnormal metabolism of cholesterol and bile salts • Decreased gallbladder-emptying rates • Changes in bile concentration or bile stasis w/in gallbladder • Cholangitis • Ascending • supporative
Chronic cholecystitis • Repeated episodes • Complications of pancreatitis and cholangitis • S/S: jaundice, pruritus, clay-colored stools, dark urine • Risk factors: Genetic relationship, cholesterol-lowering meds, age (>60), type I DM, rapid wgt loss, low-calorie or liquid protein diets, etoh abuse, white women, Native Americans, Mexican American, pregnancy (to name but a few-your book has more) • Assessment – see key features of cholecystitis chart 63-1 • Lab tests: nothing specific for gallbladder disease, tests look for ruling out other diseases.
Interventions • Diet therapy (see table 63-1) • Drug therapy – pain, antiemetics • PercutaneousTranshepaticBiliaryCatherization • Under fluoroscopy • Used for inoperable situations or for unstable high risk surgical candidates • Surgery – laparoscopic most common now • Same day surgery • Short recovery period • Back to normal activities in 1-3 weeks • Traditional method for cholecystectomy • Far greater chance for complications • Need for T-tube, JP drains (see chart 63-2 and 3) • Slower recovery • May require home visits by RN • Risk for postcholecystectomy syndrome
Pancreatitis • Acute • Necrotizing form dangerous, high mortality • Understand endocrine and exocrine functions of the organ (great chart pg 1403, figure 63-2) • Complications • See table 63-2 • Why might you see these problems occur? Understand the pathophysiology of what happens. • Risk factors – etoh most common followed by obstruction • Physical assessment • Jaundice • Cullen’s sign • Turner’s sign • No bowel sounds • Rigid abdomen = perforation, peritonitis
Labs • Amylase – when is it helpful, accurate to dx? • Lipase – more specific, more accurate. • Other tests to dxbiliary obstruction (note that these don’t indicate pancreatitis) • Tests done to identify fat necrosis • Interventions • Nonsurgical • Resting the bowel, TPN • Meds: pain control, give gi tract chance to rest • Comfort measures • ERCP – when is this done? • Surgical • Laparoscopic cholecystectomy
Chronic • The acute form done over and over and over again • Type is defined by why the patient gets the attack • Calcifying pancreatitis – etoh • Obstructive pancreatitis – guess • Does the chronic form of the disease have the same manifestations as the acute form? What is the same, what is different? • How is your nursing care changed when dealing with the chronic form vs the acute form? • See chart 63-8 for prevention of exacerbations
Peptic Ulcer Disease • Term includes both gastric and duodenal ulcers • Too much acid, violation in integrity of mucous coating over stomach wall, H. pylori • What are those things that cause acid to be secreted? These are the things you need to teach your patient about re: change in lifestyle. • Complications • Hemorrhage • How can you tell an upper gi bleed from a lower gi bleed? An old bleed from a fresh one? • Perforation • Pyloric obstruction – not common • Intractable disease
Risk factors • Nsaid usage, theophylline (when is this used?), steroids (remember these pesky little buggers?) • Genetics • H. pylori • Caffeine products, lots and lots of them • Physical assessment – see chart 59-4 • Dyspepsia (another word for your vocab.) • Pain: upper epigastrium with localization to L of midline relieved with food; R of epigastrium 90 min. to 3 hours after eating. • Exacerbating foods, meds. • Vomiting • Orthostatic bp changes • Labs • H&H
Dx tests • EGD • IgG serologic testing • Urea breath test • Stool test • Interventions – see chart 59-5 • Drug therapy – what are the differences btwn these? • Antibiotics • Proton pump inhibitors • H2 receptor antagonists • Prostaglandin analogues • Antacids • Mucosal barrier fortifiers • Diet therapy • Alternative medicine
Nonsurgical management • Endoscopic therapy • Acid suppression (didn’t we already cover this?) • Add somatostatin to your med list • NG tube (what’s the difference btwn using this for an ulcer vs to treat pancreatitis?) • Saline lavage • Management of perforation • Management of obstruction • Surgical management • Gastrectomy • Gastroenterostomy • Vagotomies • Dumping syndrome – see diet table 59-2 • Reflux gastropathy • Delayed gastric emptying • Afferent loop syndrome • Recurrent ulceration
You had care of the surgical patient back in Nursing 2. If you need to review that material to refresh it, you had best do so. • See chart 59-7 for home care assessment • What do you need to teach this person now that they have had surgery? • Can you figure out how all of these diseases are linked? If so, you will know how I will approach teaching this material in class.