adult gi Flashcards
(211 cards)
gastroesophageal reflux disease
upper gastrointestinal disease caused by reflux of gi contents into esophagus; relaxation of lower esophageal sphincter
gastroesophageal reflux disease
relaxation of lower esophageal sphincter
gerd: causes
- fatty foods, caffeinated bevs, chocolate, citrus, tomatoes
- stress
- body habitus
- gastric anatomy
gerd: effects
- esophageal stricture
- esophagitis, erosion, ulceration
- aspiration
- barrett’s epithelium
barrett’s epithelium
COLUMNAR epithelium instead of normal SQUAMOUS cell that develops in lower esophagus when healing from gerd (exposed to acid, pepsin)
considered premalignant, associated with increased risk of CANCER after prolonged disease.
gerd: manifestations/dx
not much objective, rely on patient report: dyspepsia, regurgitation, dysphagia, odynogphagia
crackles (aspiration)
odynophagia
painful swallowing
barrett’s esophagus: interventions
- esophagectomy
- ablative therapy: radiofrequency, photodynamic, cryotherapy
esophagectomy
remove esophagus, reanastemose stomach to what’s left of upper esophagus.
because stomach stretched and in the thoracic cavity, exposed to pressures from lungs. HIGH RISK OF ASPIRATION.
hiatal hernia
protrusion of stomach through diaphragm
high risk for aspiration
hiatal hernia: effects
gerd, impaired esophageal emptying, volvulus
volvulus
obstruction of bowel caused by twisting of bowel
hiatal hernia: manifestations
s: chest pain, breathlessness, worse when lying down
o: belching, dysphagia
hiatal hernia: eating habit modification
more frequent small meals closer together = easier to manage
esophageal varices
dilation of esophageal and gastric veins
- high risk of bleeding, associated with cirrhosis (liver failure, blood backs up into portal veins then into mesoteric veins, then vessels in esophagus)
hiatal hernia: nursing implications (3)
- caution with ng tube placement
- monitor vitals: slow downward trend (HR higher, BP lower)
- hypovolemic shock, signs of bleeding in stools (extreme situation)
gastritis
inflammation of stomach lining!
- acute v chronic
gastritis: causes
- increased acid production
- decreased protective mechanism
- exposure to irritants (chemical ingestion, bleach)
- meds/therapies (chemo, radiation)
- h. pylori
gastritis: compromised protective mechanisms
- mucus
- bicarb (acids go wild)
- blood flow
- prostaglandins (pivotal in production of mucus & bicarb)
pivotal in production of mucus, bicarb in stomach
prostaglandins
acute gastritis: effects
localized;
- thickened, irritated rugae
- mucosal necrosis in isolated area
- edema, swelling
healing, regeneration usually within a few days
chronic gastritis: effects
diffuse/generalized;
- gastric atrophy
- impaired absorption
gastritis: manifestations
s: anorexia, nausea, dyspepsia, cramping
o: epigastric pain, vomiting, hematemesis, melena
dyspepsia
indigestion, heartburn following meals