Professional Documents
Culture Documents
Upper GIT Disorders
Upper GIT Disorders
PEPTIC ULCER
A break in the mucous lining of the gastrointestinal tract when it comes in contact with gastric juice peptic ulcer occurs in any area of the gastrointestinal tract exposed to acid- pepsin secretions, including esophagus, stomach or duodenum.
RISK FACTORS
H. pylori infection
Low socioeconomic status Crowded, unsanitary living conditions Unclean food or water
Use of NSAIDs
Advance age History of ulcer
Cigarette smoking Family history of PUD Psychological stress, alcohol, caffeine consumption
PATHOPHYSIOLOGY MANIFESTATIONS
pain- gnawing, burning, aching or hungerlike located at the epigastric region sometimes radiating at the back pain occurs when the stomach is empty 2-3 hours after meals and in the middle of the night Relieved by eating
Occult or obvious blood in the stool hematemesis Weakness, dizziness orthostatic hypotention hypovolemic shock
sensation of epigastric fullness nausea and vomiting electrolyte imbalances metabolic alkalosis
OBSTRUCTION
PERFORATION
severe upper abdominal pain, radiating to the shoulder rigid boardlike abdomen absence of bowel sounds diaphoresis tachycardia fever
DIAGNOSTIC TESTS
Upper GI series using barium as a contrast can detect 80%- 90% of peptic ulcers. Gastroscopy- allows visualization of the esophagus, gastric and duodenal mucosa and direct inspection of ulcers. Tissue can be obtained for biopsy
MEDICATIONS
eradication of H. pylori combination of two antibiotics bismuth or proton pump inhibitors ( omeprazole, metronidazole and clarithromycin or bismuth subsalicylate, tetracycline and metronidazole medications that decrease gastric acid content include proton pump inhibitors and H2 receptor antagonist agents that protect mucosa sucralfate, bismuth, antacids and prostaglandin analogs
TREATMENTS
dietary management
Clients are encourage to maintain good nutrition, consuming balanced meals at regular intervals. alcohol intake smoking should be discourage as it slows the rate of healing and increases the frequency of relapses.
SLEEP PATTERN DISTURBANCES- night time ulcer pain, typically occurs between 1- 3 am, may disrupt the sleep cycle and result in inadequate rest.
the importance of taking the medications as prescribed ( bedtime dose) instruct the client to limit food intake after the evening meal, eliminating bedtime snacks. (stimulate the production of gastric acid and pepsin) encourage use of relaxation techniques
DEFICIENT FLUID VOLUME- bleeding can lead to hypovolemia and volume deficit, which can lead to decrease in cardiac output and impaired tissue perfusion.
monitor stool and gastric drainage ( vomitus or nasogastric tube)
Bright red with possible clots acute hemorrhage dark red or coffee ground blood has been in the stomach for a period of time hematochezia- stool containing blood and clots( acute hemorrhage melena black tarry stool ( less acute bleeding)
maintain IVF with volume and electrolyte solutions, administer whole blood or PRBC as ordered. insert NGT and maintain its position and patency( if ordered may irrigate with sterile normal saline until return flow is clear) monitor hgb and hct, serum electrolyte BUN and CREA. ( digestion and absorption of blood in the GI tract may result to elevated BUN and CREA. assess abdomen, including bowel sounds, distention, girth and tenderness. maintain bedrest with the head of bed elevated
DIVERTICULAR DISEASE
are saclike projections of mucosa through the muscular layer of the colon. diverticula may occur anywhere in the gastrointestinal tract affect the large intestine with 90% - 95% occurring in the sigmoid colon.
PATHOPHYSIOLOGY
DIVERTICULOSIS
presence of diverticula asymptomatic episodic pain ( usually left- sided), constipation or diarrhea, abdominal cramping, occult bleeding in the stools, weakness and fatigue complications include hemorrhage and diverticulitis
DIVERTICULITIS- inflammation in and around the diverticular sac. undigested food and bacteria collect in the diverticula , forming a hard mass ( fecalith) that impairs he mucosal blood supply, allowing bacterial invasion mucosal ischemia can lead to perforation, bacterial contamination and can lead to abscess formation or peritonitis.
pain it is usually left- sided and may be mild to severe and either steady or cramping. constipation or increase frequency in defecation nausea, vomiting and fever may occur abdomen is distended with tenderness and s palpable mass in the left lower quadrant resulting from inflammatory response
COMPLICATIONS
peritonitis abscess formation bowel obstruction( fistula formation and hemorrhage) severe or repeated episodes can lead to scarring and fibrosis of the bowel wall
Diagnostic tests
WBC count leukocytosis ( increase in the number of immature wbc) due to inflammation hemoccult or guaiac testing barium enema\abdominal x-ray CT scan sigmoidoscopy or colonoscopy
second- generation cephalosporin analgesic- causes less increase in colonic pressure stool softener
Dietary Management a high fiber diet is recommended- increases stool bulk , decreases intraluminal pressure and may reduce spasm. avoid foods with small seeds like popcorn, berries which could obstruct diverticula bowel rest is prescribed put patient on NPO with IVF and possibly TPN feeding is resumed initially clear liquid then soft, low roughage diet
pain
Ask the client to rate the pain using the pain scale, document level of pain and note for any changes in location or character of pain administer prescribed analgesics or PCA, use relaxation, positioning and distractions. maintain bowel rest and total body rest reintroduce oral foods and fluids slowly, providing a soft, low fiber diet with bulk forming agents
anxiety
assess and document the level of anxiety demonstrate empathy and awareness of the perceived threat to health attend to physical care needs spend as much time as possible to client encourage supportive family and friends to remain with the client assist client to use and identify appropriate coping mechanism involve the client and family in care decisions
CHOLELITHIASIS/ CHOLECYSTITIS
CHOLELITHIASIS is the formation of stones within the gallbladder or biliary tract system. Bile is formed by the liver and stored in the gallbladder. Bile contains bile salts, bilirubin, water, electrolytes, cholesterol, fatty acids and lecithin. In the gallbladder, some of the water and electrolytes are absorbed, food entering the intestine stimulates the gallbladder to contract and release bile through the common bile duct and sphincter of oddi in the intestine. The bile salts in the bile increases the solubility and absorption of dietary fats.
chronic cholecystitis result from repeated bouts of acute cholecystitis or from persistent irritation of the gallbladder wall by the stones. bacteria may be present asymptomatic complications include empyema a collection of infected fluid in the gallbladder, gangrene and perforation with resulting peritonitis or abscess formation
Diagnostic Tests
serum bilirubin elevated direct bilirubin may indicate obstructed bile flow in the biliary duct CBC- elevated may indicate infection and inflammation abdominal x-ray gall stones with a high calcium content serum amylase and lipase- possible pancreatitis related to common duct obstruction UTZ of the gallbladder- accurately diagnose cholethiasis
medications
ursodiol( actigall) and chenodiol ( chenix)- reduce the cholesterol content of gall stones, leading to gradual dissolution side effects diarrhea and hepatotoxic disadvantages long duration ( 2 years or more) and a high incidence of recurrent stone formation when treatment is discontinued. antibiotics
treatment
laparoscopic cholecystectomy ( removal of the gallbladder) cholecystostomy drain the gallbladder choledochostomy- remove stones and position a T tube in the common bile duct
dietary management
food may be eliminated during an acute attack NGT is inserted to relieve nausea and vomiting dietary fat intake may be limited
PANCREATITIS
inflammation of the pancreas, that involves self- destruction of the pancreas by its own enzymes through autodigestion. characterized by release of pancreatic enzymes into the tissue of the pancreas itself leading to hemorrhage and necrosis.
interstitial edematous pancreatitis- leads to inflammation and edema of pancreatic tissue. necrotizing pancreatitis inflammation , hemorrhage and ultimately necrosis of pancreatic tissue.
PATHOPHYSIOLOGY MANIFESTATIONS
ACUTE
Abrupt onset of severe epigastric pain and LUQ pain, may radiate to back nausea and vomiting, fever decrease bowel sounds, abdominal distention, rigidity tachycardia, hypotension,cold clammy skin possible jaundice
CHRONIC
recurrent epigastric and LUQ pain, radiates to the back anorexia, nausea, vomiting, weight loss Flatulence, constipation steatorrhea
Diagnostic Tests
UTZ can identify gallstones, pancreatic mass, pseudocyst( abnormal collection of fluid, dead tissue, pancreatic enzymes and blood that can lead to a painful mass in the pancreas) CT scan identify pancreatic enlargement, fluid collections Endoscopic retrograde cholangiopancreatography ERCP perform to diagnose chronic pancreatitis endoscopic UTZ percutaneous fine needle aspiration biopsydifferentiate from cancer
medications
narcotic analgesics antibiotics H2 blocker and proton pump inhibitor to neutralize or decrease gastric secretions synthetic hormone- octreotide( sandostatin) suppresses pancreatic secretion and may relieve pain
fluid and dietary management oral food and fluids are withheld during acute episodes NGT may be inserted IVF , TPN
surgery endoscopic transduodenal sphincterotomy- performed if the result of a gallstone lodge in the sphincter of oddi to remove the stone
NPO and maintain the patency of NGT- gastric secretions stimulate hormones that stimulate pancreatic secretion , aggravating pain. NGT decreases nausea, vomiting, and intestinal distention.
Imbalanced nutrition: less than body requirements monitor laboratory values weigh daily maintain stool charting monitor bowel sounds return of bowel sounds indicates return of peristalsis administer prescribed IVF to maintain hydration, TPN to provide fluids, electrolytes and kilocalories