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Flashcards in Upper GI Dysfunctions Deck (34)
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1
Q

GERD

A

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

2
Q

GERD: RF

A
  • obesity
  • cigarette/cigar smoking
  • hiatal hernia (diaphragm becomes weekend and part of stomach is actually above diaphragm)
3
Q

GERD: S/Sx

A

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

4
Q

GERD: Dx

A

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

can do bx during endoscopy to look for Ca

5
Q

GERD: Complications

A

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

6
Q

GERD: Interventions

A

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
7
Q

GERD: Meds

A

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

8
Q

GERD: Surgical Tx

A

laparoscopically

reserved for pt w/ complications

9
Q

Hiatal Hernia

A

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
10
Q

Hiatal Hernia: Etiology and Pathophysiology

A

weakened muscle in diaphragm and esophagogastric opening is structurally part of problem

increased intra-abdominal pressure (obesity, pregnancy, ascites, tumors, heavy lifting, etc)

11
Q

Hiatal Hernia: Clinical Manifestations

A

similar to GERD

  • heartburn (pyrosis)
  • dyspepsia
  • regurgitation
  • respiratory symptoms
  • chest pain
12
Q

Hiatal Hernia: Complications

A
GERD
esophagitis
ulcers
hemorrhage
stenosis (narrowing of esophagus)
strangulation
aspiration
13
Q

Hiatal Hernia: Dx

A

same as GERD

Barium swallow
Endoscopy

14
Q

Hiatal Hernia: Intervention

A

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

15
Q

Gastritis

A

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

16
Q

Gastritis: RF

A
  • 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)
17
Q

Acute Gastritis

A

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

18
Q

Chronic Gastritis

A

loss of cells or decrease in fxn
sx are similar to acute
can lead to pernicious anemia (think B12 def)

19
Q

Gastritis: Dx Studies

A
  • 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
20
Q

Acute Gastritis: Interventions

A
  • 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
21
Q

Chronic Gastritis: Interventions

A
  • 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
22
Q

Peptic Ulcer Disease

A
  • 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

23
Q

Gastric Ulcer

A

Gastric: antrum

  • more prevalent in females older than 50 YO
  • increased obstruction
  • RF: H.Pylori, NSAIDs, bile reflux
  • increased mortality
  • high recurrence
24
Q

Duodenal Ulcers

A

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
25
Q

PUD: RF

A
  • 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
26
Q

PUD: Clinical Manifestations

A

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)

27
Q

PUD: Dx

A
  • endoscopy
  • non-invasive H. Pylori: serology, stool, breath test
  • other tests: barium contrast, secretin stimulation
  • labs: CBC, liver enzymes, serum amylase
  • stool: blood
28
Q

EGD

A

esophagogastroduodenoscopy

directly visualizes the mucosal lining of the stomach with a flexible endoscope

ulcers/tumors can be directly seen and biopsies taken

29
Q

PUD: Intervention

A

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

30
Q

PUD: Complications

A

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
31
Q

Perforation from PUD: Tx

A

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
32
Q

Gastric Outlet Obstruction: Tx

A
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

33
Q

PUD: Acute Care for Complications

A

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.

34
Q

PUD: Gerontologic Considerations

A
  • 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