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ADH2/WK6
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GI Health History Components
• Changes, stool
• Age, gender, culture
• GI disorders or abdominal surgeries
• Medications, herbs, supplements
• Smoking or vaping history; chewing tobacco use
• Travel
• Nutrition
• Alcohol, caffeine intake
• Socioeconomic status
• Family history and genetic risk
• Current health problems
• Weight, and any changes in weight/appetite/intake
• Pain with PQRST mnemonic
GI Physical Assessment
RUQ, LUQ, LLQ ,RLQ (Assess each one)
Inspection (Look for symmetry, discoloration, wounds, bulging)
Auscultation (Active/hypo or hyper, important for surgery pts to see if they have passed gas) (also checking for vascular sounds called bruit over the abdominal aorta, if heard, don’t palpate and notify HCP immediately)
Palpation ( light feeling for the presence of normal organs or abnormal masses)
Percussion – performed by a health care provider
GI Psychosocial Assessment
• Recognize discussion may feel embarrassing for patient
• Ask about stressful events
• If patient has cancer, they may be experiencing the grieving process
GI issues lab Studies
Serum Tests (CBC, PT, Electrolytes, liver enzymes)
Urine Tests
Stool Tests ( Fatty stools, occult blood
GI issues Imaging Assessment
• X-rays
• Virtual colonoscopy( Done via CT scan)
• CT (quicker imaging) or MRI (good at finding abnormalities/ no metal/ some need antianxiety) - Both Preferred over X-ray
GI Diagnostic Assessments
• Endoscopy
• Esophagogastroduodenoscopy (EGD)
• Endoscopic retrograde cholangiopancreatography (ERCP)
• Small bowel capsule endoscopy (enteroscopy)
• Colonoscopy (traditional or virtual)
• Sigmoidoscopy • Flexible sigmoidoscopy (View large intestine through the rectum with a camera)
• Ultrasonography (may be endoscopic)
• Liver-Spleen scan
Peptic Ulcer Disease Characteristics
Occurs when mucosal defenses become impaired;
epithelium not protected from effects of acid and pepsin
Characterized by the erosion of the GI mucosa
Many caused by H.pylori infection (spread oral to oral, fecal to oral)
Types of Peptic Ulcers
Duodenal (most common), gastric, and stress ulcers (less common)
Duodenal Ulcers
Upper portion of the duodenum
Most common
Deep
Penetrate through mucosa and submucosa into the muscularis/muscle layer
Floor of ulcer is necrotic
High gastric acid secretion
Pain is common 2-3 hours after a meal, common to see pain at night because of this
Eating food can decrease pain
Melena - black tarry stools
Gastric Ulcers
Occurs in the Antrum of the stomach near acid secreting mucosa
Hydrochloric acid injures epithelium
Back diffusion of acid
Dysfunction of pyloric sphincter
pain increases with eating and is common 30 min - 1 hour after meals
Stress Ulcers
Acute
Occur after a medical crisis or trauma (sepsis head trauma)
NPO
Critically ill
Proton pump inhibitors (PPI’s) commonly used to prevent when in hospital
Complications of Ulcers
Hemorrhage (most serious) If recurring, it is most commonly caused by untreated H.pylori infection
Perforation (ulcer has made hole in stomach or intestinal lining) - Surgical emergency. can cause peritonitis can be life threatening
Pyloric obstruction
Intractable disease ( gastric cancer
Peptic Ulcer Disease: Risk Factors
NSAIDs (increase gastric acid secretion)
Other substances that alter gastric secretion (caffeine, all coffee, alcohol, smoking
Also check family history and living conditions
Peptic Ulcer Disease: Incidence and Prevalence
More than 15 million in the U.S.
Mortality rate has declined over past decades
Peptic Ulcer Disease: Assessment
History
Assess for causes and risk factors
History of H. pylori, GI surgeries
Drugs being taken
Physical Assessment/Signs and Symptoms (view picture on next slide)
Epigastric tenderness and pain (usually located midline between umbilicus and xyphoid process)
Dyspepsia most common complaint
Rigid, board-like abdomen with rebound tenderness and pain = peritonitis
Psychosocial Assessment - how the disease affects them
Peptic Ulcer Disease Diagnostic
Testing for H. pylori - done through blood, breath or stool (breath/stool more accurate)
Hemoglobin and hematocrit (usually low)
Occult blood in stool
Others -
EGD (most accurate means of diagnosing of ulcer giving visualization of the ulcer)
Nuclear medicine scan (checks for GI bleeding) - often done 1-2 days after treatment to check for improvement
PUD Triple Drug Therapy
Two antibiotics + proton pump inhibitor (PPI)
PPI- lansoprazole, Antibiotics- Metronidazole & Tetracycline or clarithromycin & amoxicillin for 10 to 14 days.
PUD Quadruple Therapy
PPI with bismuth and two antibiotics
Bismuth therapy often used in pt.’s who are allergic to PCN based meds
Be sure pts do not use NSAIDS as it can lead to an overdose.
Nutrition Therapy for PUD
Eating food can work as an antacid by balancing out stomach acid levels but only provides relief for 30-60 minutes, depending on ulcer and other factors.
Teach pt to avoid irritating foods like spicy foods, alcohol, tabacco, caffeine
Complementary and Integrative Therapies for PUD
Stress relievers - meditation, yoga, hypnosis
Managing upper GI bleeding for PUD
Nonsurgical management - monitoring for any pt changes
Remember – active GI bleeding is a life-threatening emergency!
Surgical management - treat pts that have emergencies (perforations) or that do not respond to treatment
PUD Transition Management
Home care management - ensure they know proper meds and treatment plan.
Self-management education - help to understand needed lifestyle modifications, notice condition changes and what to do if they occur, and teach risk factors
Health care resources
Magnesium Hydroxide
Antacid
Give after meals and at bed time
Take with a full glass of water
Don’t give other drugs within 1-2 hours
Can cause hypermagnesemia especially in renal impaired patients
Can cause diarrhea
Aluminum Hydroxide
Antacid
give one hour after meals and at bed time
H2 Blockers
Promote ulcer healing and prevent their return.
Examples Famotidine (Pepcid), nizatidine (Axid only given orally), cimetidine (tagemet)
Best at suppressing nocturnal acid production
Famotidine
H2 blocker
Give with or before meals
Mucosal Barrier Fortifiers
Protect the stomach mucosa
Coats stomach
Examples - Sucralfate (carafate), Bismuth (peptdo/no aspirin)
Give one hour before meals, 1 hour after meals, and at bedtime
PPI
Cause profound reduction of stomach acid
Examples - Omeprazole (prilosec), lansoprazole, pantoprazole
Dont crush capsules.
Some can be given IV if pt cant take by mouth
Antimicrobials (antibiotics)
Treat H.pylori infection
Examples erythromycin, amoxicillin, tetracycline, and metronidazole
Cholecystitis Pathophysiology
Inflammation of the gallbladder can be Acute vs. chronic
Acute Cholecystitis
stone obstructs cystic duct (most common), gallbladder neck or common bile duct.
Often caused by Gallstones (cholelithiasis) - often made of cholesterol, bilirubin, bile salts
Begins with attack of biliary colic may occur with tachycardia, pallor, diaphoresis, and extreme exhaustion. pain can radiate to right shoulder
Pain lasts longer than the colic
Anorexia, nausea, vomitins
Chronic Cholecystitis
caused by Repeated bouts of acute cholecystitis or Persistent irritation of the gallbladder wall by stones
may have slowly developing symptoms and may not seek medical attention till severe. Symptoms include: Jaundice, clay-colored stools, and dark urine from biliary obstruction.
Cholecystitis: Etiology and Genetic Risk
Familial or genetic tendency
American Indian, Mexican Americans, or Caucasian
Obesity
Women
Increases serum cholesterol & lipids
Four F’s - Fat, Forty, Female, and Fertile
Cholecystitis: Incidence and Prevalence
Usually occurs in affluent countries
American Indians 60-70%
Caucasian adults 15%
Cholecystitis History Assessment
Inquire about diet and foods and what occurs when they eat certain foods
Cholecystitis Physical Assessment/Signs & Symptoms
Abdominal pain
RUQ- radiates to right shoulder or scapula
Blumberg sign- severe (Rebound tenderness upon deep palpation, usually preformed by provider)
Late signs= jaundice, clay colored stool, dark urine, steatorrhea(fatty stools)
Cholecystitis Lab Assessment
Increases in -
WBC
Alkaline phosphatase
AST
LDH
Serum bilirubin levels (can be done directly or indirectly)
Cholecystitis Diagnostic assessment
X-rays
Ultrasound
ERCP - view the gallbladder and view the patency of the bowel and pancreatic ducts. done endoscopically
MRCP - magnetic resonance imaging (MRI) to create detailed images of the biliary tract (bile ducts), pancreas, and gallbladder
Cholecystitis Nonsurgical management
Avoid fatty foods
Hold food for any NV. An antemetic may be ordered. NG tube may be placed for severe NV. Assess hydration status
Opioid analgesic
Ketorolac - Toroidal, potent analgesic
Urosodiol and Chenodiol- Oral bile acid dissolution (dissolve gallstones) facilitate bile digestion, combines bile salts to fecal matter for excretion.
Extracorporeal shock wave lithotripsy (ESWL) - breaks up stones through sound waves. Pt’s often have drainage bag after to drain bile, check patency and position bag lower than catheter
Laparoscopic cholecystectomy (Lap chole)
Treatment of choice for cholecystitis
Minimally invasive
Low risk of complications
Pt. recovery is quicker
Post op pain is less severe
Risk that the surgery may be converted to laparotomy during the procedure
Traditional Cholecystectomy
Abdominal laparotomy
Severe obstruction - reason to do this instead of laparoscopy
Drainage tube- Jackson-Pratt (JP) drain (has a suction component to remove bile)
Drainage tube- T- tube (common bile duct exploration surgery) keep bag low to for bile to be collected.
Cholecystitis transition management/ care coordination
Eat nutritious foods
Avoid excessive intake of fatty foods
Weight reduction if needed
Report any repeated abdominal or epigastric pain / vomiting or diarrhea that may occur weeks to months after surgery. Possible signs of PCS (post-cholecystectomy syndrome)