GERD
reflux of gastric contents into lower esophagus
no single cause of the disease
incompetent Lower Esophageal Sphincter (LES) - gastric contents move from stomach to esophagus d/t decreased pressure in esophagus when supine, increased abdomen pressure
aggravated by foods, meds, nicotine
GERD: RF
- obesity
- cigarette/cigar smoking
- hiatal hernia (diaphragm becomes weekend and part of stomach is actually above diaphragm)
GERD: S/Sx
variable from person to person
- heartburn or pyrosis: most common sx (irritation of esophagus by gastric secretions, burning sensation, tightness of lower sternum radiating to throat or jaw)
- dyspepsia: pain or discomfort centered in upper abdomen area
- fullness, bloating
- N/V
- belching, regurgitation
- respiratory sx (wheezing, coughing, dyspnea)
- nocturnal coughing disrupting sleep
- throat irritation
- globus sensation
*GERD can mimic angina
GERD: Dx
Upper GI Endoscopy
-look for inflammation, scarring, and strictures
can do bx during endoscopy to look for Ca
GERD: Complications
esophagitis: inflammation of esophagus
- esophageal stricture is created with possible ulcers b/c of repeated irritation which causes scarring
barrett’s esophagus: precursor to esophageal Ca
- Sx: heartburn (GERD sx)
- monitor: every 2-3 years w/ endoscopy, bx, radiofrequency
respiratory complications: coughing, bronchospasms, laryngospasms, asthma, bronchitis, pneumonia
dental: erosion of posterior teeth from acid coming up
GERD: Interventions
Lifestyle modifications:
- stop smoking
- limit alcohol
- HOB elevated (wedge pillow)
- weight reduction if pt is overweight
Nutritional modifications:
- stay away from trigger foods
- avoid caffeine
- limit seasoning
- avoid late evening meals, nocturnal snacking
- small frequent meals w/ lots of fluids inbetween
- decrease fat content
- don’t lay down after eating
GERD: Meds
antacids (tums): offer quick short-lived relief
- most effective if taken 1-3 hours after meals and at bedtime
- neutralizes HCl acid
H2 Receptor Blockers: block action of histamine on H2 blockers to decrease HCl secretion
- ranitidine (Zantac)
- famotidine (Pepcid)
Proton Pump Inhibitor (PPI): decreases incidence of esophageal strictures or complications of chronic GERD, prevention of GERD by inhibiting proton pump secretion of HCl
-omeprazole (Prilosec)
sucralfate (Carafate): antiulcer, acts as a protective layer on the stomach
bethanechole (Urecholine): increase LES pressure, which promotes gastric emptying
GERD: Surgical Tx
laparoscopically
reserved for pt w/ complications
Hiatal Hernia
herniation of part of the stomach into the esophagus through an opening in the diaphragm
two types:
- sliding: most common
- paraesophageal or rolling: less common, more concerning
Hiatal Hernia: Etiology and Pathophysiology
weakened muscle in diaphragm and esophagogastric opening is structurally part of problem
increased intra-abdominal pressure (obesity, pregnancy, ascites, tumors, heavy lifting, etc)
Hiatal Hernia: Clinical Manifestations
similar to GERD
- heartburn (pyrosis)
- dyspepsia
- regurgitation
- respiratory symptoms
- chest pain
Hiatal Hernia: Complications
GERD esophagitis ulcers hemorrhage stenosis (narrowing of esophagus) strangulation aspiration
Hiatal Hernia: Dx
same as GERD
Barium swallow
Endoscopy
Hiatal Hernia: Intervention
conservative: reduce intraabdominal pressure (reduce weight, etc)
surgical: reduce hernia, optimize LES pressure, and prevent movement of gastroesophageal junction
- herniotomy
- herniorrhaphy
- fundoplication
surgery done laparoscopically
Gastritis
inflammation of gastric mucosa of the stomach - breakdown of normal gastric mucosa which protects stomach against auto-ingestion causing acid to diffuse back into the mucosa resulting in:
- tissue edema, destruction of capillaries
- loss of blood
- possible hemorrhage
one of most common problems
-can be acute or chronic
Gastritis: RF
- meds: ASA, NSAIDs, corticosteroids, iron supplements
- alcohol
- spicy foods
- H. Pylori Infection (probably acquired in childhood): triggers breakdown of mucosal barrier with eventual destructive effects
- autoimmune atrophic gastritis: a form of chronic gastritis, immune response that directly affects parietal cells, increases risk of stomach Ca
- bacterial, viral, fungal infections
- other gastric surgical procedures - feeding tube placement
- intense emotional responses (hypersecretion of HCl)
Acute Gastritis
Sx: anorexia, N/V, epigastric tenderness and feeling of fullness
in those who abuse alcohol, only sx may be hemorrhage
self-limiting lasting hours to days
body heals itself
Chronic Gastritis
loss of cells or decrease in fxn
sx are similar to acute
can lead to pernicious anemia (think B12 def)
Gastritis: Dx Studies
- endoscopy: bx used for definitive dx of gastritis
- detection of H. Pylori through breath, urine, serum, gastric secretion, stool tested
- CBC: to detect anemia
- stools: occult blood
Acute Gastritis: Interventions
- eliminating the cause and prevention for future problems
- meds: antacids, H2Rs, PPIs
- if severe and in ED or admitted:
- NPO, IV fluids
- antiemetics: ondansetron (Zofran), prochlorperazine (Compazine)
- NG tube: lavage irritating substances or empty stomach
- VS: monitor for hemorrhage, dehydration
- gradual reintroduction of foods
- stop smoking
Chronic Gastritis: Interventions
- eliminating causes: ETOH, meds
- H.Pylori tx
- meds: H2R’s or PPI’s to tx sx
- Cobalamin deficiency (B12) - B12 injections (lifelong)
- lifestyle modifications (stop smoking, small meals, avoid irritating foods)
- d/t increased Ca risk, need to be closely monitored
Peptic Ulcer Disease
- erosion of GI mucosa from HCl and pepsin
- susceptible areas of GI tract: lower esophagus, stomach, duodenum, post-op gastrojejunal anastomosis
Types:
- acute: superficial erosion and minimal inflammation
- chronic: erosion of muscular wall with formation of fibrous tissue; present continuously for long duration
can be classified by location: gastric or duodenal
Gastric Ulcer
Gastric: antrum
- more prevalent in females older than 50 YO
- increased obstruction
- RF: H.Pylori, NSAIDs, bile reflux
- increased mortality
- high recurrence
Duodenal Ulcers
1-2cm
- prevalent age 35-45YO
- etiology: H. Pylori
- high HCl secretion
- high risk: COPD, cirrhosis, pancreatitis, hyperparathyroidism, Zollinger-Ellison syndrome, CRF
- occur, disappear, recur
PUD: RF
- H. Pylori
- Medication-induced injury: NSAIDs especially w/ corticosteroids or anticoagulants
- Lifestyle factors: alcohol use, smoking, caffeine, psychologic distress, stress-related mucosal disease in upper GI bleed
PUD: Clinical Manifestations
Gastric: epigastric discomfort 1 to 2 hours after meal; burning or gaseous pain; food may worsen sx (perforation is first sx in some patients)
Duodenal: burning or cramplike pain in midepigastric or back; 2 to 5 hours after meal
Other: bloating, n/v, early satiety (may be silent especially with older adults b/c they take NSAIDs)
PUD: Dx
- endoscopy
- non-invasive H. Pylori: serology, stool, breath test
- other tests: barium contrast, secretin stimulation
- labs: CBC, liver enzymes, serum amylase
- stool: blood
EGD
esophagogastroduodenoscopy
directly visualizes the mucosal lining of the stomach with a flexible endoscope
ulcers/tumors can be directly seen and biopsies taken
PUD: Intervention
conservative care:
- adequate rest, no smoking or alcohol, stress management, dietary modifications
- pain management: no NSAIDs or ASA for 4-6wks unless administered with PPI, H2R’s, or misoprostol
- endoscopic evaluation and follow-up; 3-6 months for healing
drug therapy:
antibiotic therapy: H. Pylori 14 days of PCN
-bismuth alone or combined w/ tetracycline and metronidazole
Proton pump inhibitors
Cytoprotective drug therapy - sucralfate (works best in low pH; give 1 to 2 hours before or after antacid; binds with cimetidine, digoxin, warfarin, phenytoin, and tetracycline)
Nutritional therapy:
- avoid foods that cause distress or irritation
- avoid caffeine and alcohol
surgery is uncommon unless complications or cancer
PUD: Complications
hemorrhage: most common; duodenal
perforation: most lethal, GI contents spill into peritoneal cavity
- sx: sudden, severe abdominal pain, radiates to back and shoulders, no relief with food or antacids, abdomen rigid/boardlike, bowel sounds absent, n/v, respirations shallow, pulse increased and weak
gastric outlet obstruction: edema, inflammation, pylorospasm, or scar tissue can cause obstruction in distal stomach and duodenum
- stomach fills and dilates causing discomfort and pain; worse at end of day
- belching and vomiting (projectile) may provide some relief
- constipation and anorexia
Perforation from PUD: Tx
if untreated, bacterial peritonitis occurs in 6-12 hours
immediate focus: stop spillage and restore blood volume
- NGT for aspiration and gastric decompression
- IV fluids and blood; broad spectrum antibiotics
- Other: central line, PA catheter, ECG, urinary catheter
- small perforations: self-sealing; monitor for obstruction
- large perforations: surgery for closure, suctioning and lavaging of peritoneal cavity
Gastric Outlet Obstruction: Tx
decompress w/ NGT PPI or H2Rs pain management fluid and electrolyte replacement surgery or balloon dilation (loosen up stenosis that might be there)
NGT to suction
irrigate per policy
monitor I&O
reposition patient
IV fluids and replace electrolytes
Gastric residual (if less than 200ml after clamped for 8-12 hours, begin oral intake, progress to solids)
no relief or recurrence, then surgical intervention
PUD: Acute Care for Complications
for hemorrhage: monitor VS and NG aspirate
for perforation: notify HCP, frequent VS, no oral or NG intake, IV fluids, pain management, antibiotics; prepare for surgery if needed.
PUD: Gerontologic Considerations
- increased morbidity and mortality
- frequent use of NSAIDs (often for arthritis)
- first sx may be GI bleed or decreased Hct
- tx plan is similar with emphasis on teaching and prevention