- obesity - cigarette/cigar smoking - hiatal hernia (diaphragm becomes weekend and part of stomach is actually above diaphragm)

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

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

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

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

Upper GI Dysfunctions Flashcards by Kaitlin Hobbs

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

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GERD: RF

obesity
cigarette/cigar smoking
hiatal hernia (diaphragm becomes weekend and part of stomach is actually above diaphragm)

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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

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GERD: Dx

Upper GI Endoscopy
-look for inflammation, scarring, and strictures

can do bx during endoscopy to look for Ca

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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

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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

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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

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GERD: Surgical Tx

laparoscopically

reserved for pt w/ complications

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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

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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)

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Hiatal Hernia: Clinical Manifestations

similar to GERD

heartburn (pyrosis)
dyspepsia
regurgitation
respiratory symptoms
chest pain

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Hiatal Hernia: Complications

GERD
esophagitis
ulcers
hemorrhage
stenosis (narrowing of esophagus)
strangulation
aspiration

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Hiatal Hernia: Dx

same as GERD

Barium swallow
Endoscopy

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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

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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

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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