Upper GI problems Flashcards
causes of nausea
GI issues
CNS issues
CV issues
pregnancy
endocrine/metabolic stuff
med side effects
anesthesia
chemo
psych
motion
pathophysiology of pukine
chemoreceptor trigger zone in brainstem responds to stimuli from dugs, toxins, and motion and activates ANS
SNS = tachycardia, tachypnea, diaphoresis
PNS = relaxes LES, increases gastric motility, increases saliva
Stimuli from GI tract, kidney, heart, or brain send impulses to vomiting center in medulla
Goal when treating vomiting
-Identify and treat cause
Watch for
-anorexia/weight loss
-fluid and electrolyte imbalance
-acidosis/alkalosis
-hypovolemia
-circulatory issues
What do these types of vomit mean:
1. partially digested
2. fecal odor and bile
3. bile
4. bright red blood
5. coffee ground
- gastric outlet obstruction or delayed gastric emptying
- obstruction below pylorus –> EMERGENCY
- obstruction below ampulla of vater
- active bleeding (varices, ulcer, cancer)
- gastric bleeding (gastritis or gastric ulcer)
Nursing interventions for vomiting
NPO
IV fluids
NGT (aspiration)
Monitor I/O, VS –> dehydration
Psychosocial/environmental comfort
Oral cancer causes
unknown, but risks are:
-tobacco
-alc
-sun
-pipe stem or other irritation
-HPV (get the shot)
-STDs
Oral cancer symptoms
vague –> usually delayed treatment
sore throat, dysphagia, slurred speach, salivaion issues, toothache
leukoplakia and erythroplakea = precancerous lesions
oral cancer diagnosis
biopsy is main one
oral exfoliative cytology = scraping
toludine blue test is screening
oral cancer treatment
Surgery: BE CAREFUL —> HEAD BLEEDS A LOT!!
radiation
chemo
palliative –> 80% die w/in 5 yrs
nutritional
PEG tubes
GERD primary factor
incompetent LES allows acid to come up and inflame mucosa
food, drugs, obesity, smoking, and hiatal hernia or mucosal damage all affect LES pressure
Manifestations of GERD
Heartburn (pyrosis) (can spread to jaw)
Dyspepsia (abdominal pain)
Regurgitation
Resp issues (wheezing, coughing, throat irritation)
Complications of GERD
esophagitis
-ulceration leads to scar tissue, stricture, and dysphagia
Barrett’s esophagus
-metaplasia of cells; increase risk for cancer
Aspiration leading to asthma, bronchitis, or pneumonia
Dental erosion
Gerd nursing interventions
low fat, small meals w/o caffeine, alc, or tobacco
-upright 2-3 hrs after meals
-no tight clothes
-no food hrs b4 bed
-weight loss
Drugs for GERD
PPIs and H2
-PPIs are more effective, but H2 are cheaper
-risk of infection with PPIs bc of alkaline environment that they create
PPIs
-stop HCl secretion
-good for treating esophagitis
-take b4 1st meal
-if you take it too long, bad for bone density kidney, vet B12, magnesium, dementia
H2 receptor blocks
takes 1 hr to work –> lasts 12 hrs
-take with antacid
Antacids
neutralize acid
-take 1-3 hrs after meal and bedtime
-increases Na+, so careful if old, cirrhosis, htn, or kidney issues
Nissen Fundoplication
tie LES tighter
Hiatial hernia
hernia @ LES
-can be sliding (not too bad) or paraesophageal (serious)
Esophageal cancer tumors
appear as ulcers
often advanced
metastasis to liver and lungs
manifestation of esophageal cancer
progressive dysphagia
swallowing pain
weight loss
regurgitation
hemorrhage, perforation, obstruction
Eosiophilic Esophagitis
-Allergic reaction
-manifests as heartburn, dysphagia, food impaction, nausea, vomiting, weight loss
-treat with PPIs and corticosteroids
Esophageal strictures
Usually from GERD
-dysphagia, regurgitation, weight loss
-treat by dilating with balloon –> careful of rupture
Achalasia
lower 2/3 of esophagus wont peristalsis
manifests as dysphagia, globus sensation or chest pain; nighttime regurgitation, halitosis, can’t eructate, weight loss
treat with endoscopic dilation or Heller myotomy
-also botulinum, nitrates, and CCBs
Gastric ulcer risk factors
H pylori
NSAIDs –> don’t take on empty stomach
bile reflux
corticosteroids and anticoagulants
stress
alc, caffeien, tobacco
Duodenal ulcer risk factors
COPD, cirrhosis, pancreatitis, hyperparathyroidism
pretty much always H pylori –> take antibiotics
H pylori
causes 80% gastric ulcers and 90% duodenal ulcers
from oral-oral or oral-fecal transmission
lives a long time
produces urease
Diagnostic study for peptic ulcers
Endoscopy!
Also can do serology, stool, or breath test for H pylori
how to treat peptic ulcers
PPI to reduce acid secretions
antibiotics to eliminate H pylori –> penecilin or metronidazole
Cytoprotective drugs given 1-2 hrs before or after antacids protect mucosa
Complications of PUD
hemorrhage, perforation, gasatric outlet obstruction
Hemorrhage is most common, but perforation is most lethal - if untreated, bacterial peritonitis w/in 6-12 hrs
Stomach cancer
-often metastasized when diagnosed
-a/w H pylori, autoimmune inflation, repeated irritant exposure
-spreads by direct extension –> liver and adjacent tissue
manifestations of stomach cancer
Anemia!
GI stuff: weight loss, pain, indigestion, early satiety
Late: ascites
Gastric surgery complications
Hemorrhage
Dumping syndrome - lasts 1 hr –> weakness, sweating, dizziness, cramping –> chyme bolus causes pushes fluid into bowel causing hypovolemia
Postprandial hypoglycemia = variant of dumping syndrome –> caused by carb bolus resulting in excess insulin
Bile reflux gastritis (after fixing or removing pylorus) –> bile damages gastric mucosa –> administer cholestyramine
most serious complication post op gastric surgery
anastomosis leak
-tachycardia, dyspnea, fever, ab pain, anxiety, restlessness
-requires immediate treatment to prevent sepsis and death
Why use NGT post op for gastric surgery?
For decompression –> reduces pressure to suture and decreases edema and inflammation
**aspirate for blood –> reporet if more than 75 cc/hr
**irrigate
**should change to dark yellow-green in 36 to 48 hrs
nutrition post gastric bypass
wound healing vits: C,D,K,B
give meds for pernicious anemia
soft, bland, low fiber, high complex carbs, high prot
no fluid with meals –> chew a lot
no simple sugars, lactose, or fried food
-avoid extreme temps
-avoid hypoglycemia
Gastritis
basically peptic ulcer but without to ulcer
-tissue edema, loss of plasma thru capilaries, possible hemorrhage
caused by same stuff as PUD - emphasis on corticosteroids
More causes of gastritis
alc and spicy food
H pylori
radiation and smoking
autoimmune issues, hiatal hernia, physical stress, renal failure, sepsis , shock
Manifestations of acute and chronic gastritis
acute:
anorexia, nausea/vomiting, epigastric tenderness, hemorrhage
chronic:
similar to acute or asymptomatic –> possibly pernicious anemia
care for acute gastritis
fix the cause
rest, NPO, IV fluids, antiemetics, watch for dehydration
possibly NGT to watch bleeding and lavage
monitor for bleeding
Drugs: PPIs or H2 receptor
chronic gastritis
fix cause
antibiotics for H pylori
cobalamin for pernicious anemia
small frequent meals
no smoking
take meds
melena
black tarry stools from upper GI bleed
Reasons for upper GI bleeds
PUD usually
Stress related mucosal disease
Chronic esophagitis, Mallory Weiss tear, or esophageal varices
Upper bleed diagnostic studies
endoscopy
angiography
labs
-cbc –> hgb and hct
-bun –> GI tract bacteria breakdown prot
-PTT, liver enzymes, electolytes, ABGs
vomit and stool for gross or occult blood
What constitutes a massive GI bleed
more than 1500 ml blood loss
25% intravascular volume
Assess for shock - monitor I/O
What to watch for with massive GI bleed
shock
O2 status –> give no matter what
perforation and peritonitis –> tense, rid
hypovolemia
Drug therapy for massive GI bleed
PPI - IV bolus then infusion
Antacids - after acute phase
Acute care
NGT management
lavage
watch for withdrawal if alcoholic
