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Gen Med: GI > Diseases of the Stomach > Flashcards

Diseases of the Stomach Flashcards

1
Q

What is Dyspepsia?

A
  1. Impaired digestion
  2. Epigastric pain or burning, early satiety or postprandial fullness
  3. Dyspepsia must be distinguished from heartburn (pyrosis)
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2
Q

Causes of Dyspepsia?

A 
Food or drug intolerance
Functional dyspepsia- no obvious organic cause 
GERD
Peptic Ulcer Dz (PUD)
H. pylori infection
Biliary Tract Dz
Gastroparesis
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3
Q

What is Gastroparesis?

A

Delayed gastric emptying w/o evidence of mechanical obstruction

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4
Q

Signs & Symptoms of Gastroparesis?

A

PP fullness persisting for hours

Nausea, vomiting, early satiety, bloating

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5
Q

Causes of Gastroparesis

A
  1. Idiopathic (50%)
  2. DM
  3. Postsurgical
    A. Incidental injury to vagus nerve
  4. Meds
    A. Narcotics, CCB, dopamine agonists, clonidine, antichol.
  5. Connective tissue Dz
    A. Scleroderma
  6. Neurologic dysfunction
    A. MS
    B. Parkinson’s Dz
    C. Brainstem stroke/tumor
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6
Q

What is the gold standard for diagnosing gastroparesis?

A

Scintigraphic gastric emptying test

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7
Q

What is Scintigraphic gastric emptying test?

A
  1. Isotope tagged meal permits pictures to be taken as the meal passes through the stomach and the GI tract
  2. 4 hr test
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8
Q

Treatment for Gastroparesis

A
  1. Freq. small meals
  2. Avoid excess fat & dietary fiber
  3. Prokinetic meds improve movement of food through stomach
    A. metoclopramide (Reglan)
    B. erythromycin
    C. dicyclomine (Bentyl)
    D.phenobarbitol/hyoscyamine/atropine/scopolamine (Donnatal)
    E. hyoscyamine (Levsin)
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9
Q

What is gastritis?

A

Inflammation, irritation, or erosion of the lining of the stomach

Can occur

  • Suddenly (acute)
  • Gradually (chronic)
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10
Q

Causes of gastritis

A 
Helicobacter pylori infection               
NSAIDs
Severe illness/stress
ETOH
Smoking
Cocaine
Autoimmune disorders
Radiation therapy
Crohn’s disease
CMV
Candida
Pernicious anemia
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11
Q

What is H. Pylori?

A
  1. Bacteria infection in mucous lining of the stomach

2. W/out Tx, can lead to ulcers, & stomach cancer

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12
Q

Signs & Sx’s of Erosive Gastritis

A
  1. Epigastric pain
  2. Hematemesis
    A. “Coffee ground” emesis or bloody vomitus
  3. Melena
  4. Anorexia
  5. Nausea
  6. Eructations
  7. Bloating
  8. Early satiety
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13
Q

Diagnostic Studies for Gastritis

A 
1. ↓ Hct 
A. If significant bleeding 
2. +/- Iron deficiency anemia
A. If bleeding is chronic
3. Upper endoscopy
Bx Identifies source of bleeding
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14
Q

DDx for Gastritis

A 
Erosive gastritis
PUD
Esophageal varices
Mallory Weiss tear
Gastric AV malformations
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15
Q

Treatment for stress induced gastritis

A 
1. Pts w/risk factors for bleeding
A. Coagulopathy
- Plt  < 50,000 or INR > 1.5
2. ICU pt
3. Mechanical ventilation
4. Prophylactic Tx
A. IV H2 receptor antagonists 
- cimetidine, ranitidine, famotidine, nizatidine
B. Oral sucralfate (Carafate)
C. Oral PPI + bicarbonate (Zegerid)
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16
Q

Treatment for continuous bleeding in gastritis

A
  1. Early enteral tube feeding may ↓ risk of GI bleed in ICU pts
  2. If bleeding occurs, Tx w/
    A. Continuous infusions of PPI
    - IV Pantoprazole (Protonix) 80 mg bolus, then 8 mg/h
    B. Oral sucralfate
    - 1 gm q 4-6 hrs
  3. Endoscopy for clinically significant bleeding
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17
Q

Treatment for NSAID induced gastritis

A
  1. D/C NSAID
  2. Give lowest effective dose
  3. Administer NSAID w/ meals
  4. Oral PPI x 2-4 weeks
    A. omeprazole (Prilosec)
    B. lansoprazole (Prevacid)
    C. pantoprazole (Protonix)
    D. esomeprazole (Nexium)
    E. dexlansoprazole (Dexilant/Kapidex)
    F. rabeprazole (Aciphex)
    G. naproxen/esomeprazole (Vimovo)
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18
Q

Treatment for alcohol induced gastritis

A
  1. Tx empirically for 2-4 weeks (choice)
    A. H2 receptor antagonist
    B. PPI
    C. Oral sucralfate
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19
Q

H. Pylori Gastritis increases risk for what kinds of cancer?

A

↑ risk of gastric adenocarcinoma & primary B cell gastric lymphoma

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20
Q

H Pylori Gastritis Signs & Sx’s

A

Epigastric pain

21
Q

H. Pylori Gastritis Diagnostic Testing

A
  1. Serologic ELISA test for H pylori
    A. 80% specificity
  2. Urea breath test
  3. Fecal antigen immunoassay
    A. Above 2 tests excellent specificity & sensitivity (>95%)
    B. More expensive when compared to ELISA
    C. Must be off of PPI’s, abx wks prior to testing
22
Q

Treatment for H. Pylori gastritis

A
  1. Standard Triple Therapy x 10-14 days
    A. Oral PPI bid
    B. Clarithromycin (Biaxin) 500 mg po bid
    C. Amoxicillin 1 gm po bid or metronidazole (Flagyl) 500 mg po bid (if PCN allergic)
    OR
    D. Prevpac (lansoprazole/amoxicillin/clarithromycin) x 10-14 d
  2. Standard Quadruple Therapy x 10-14 days
    A. Used if pt tests (+) after standard triple therapy or previously on macrolide
    - Oral PPI bid
    - Bismuth subsalicylate (Pepto-Bismol) 500 mg po qid
    - Tetracycline 500 mg po qid
    - Metronidazole (Flagyl) 500 mg po tid
23
Q

What is PUD?

A
  1. Circumscribed lesions in mucosal membrane extending below epithelium
  2. Ulcers extend thru muscularis mucosae
  3. > 5mm in diameter
  4. PUD - any ulcer of upper digestive system
    A. Gastric ulcer
    B. Duodenal ulcer (5x’s more common)
  5. Assoc. w/ gastric malignancy
  6. M = F
24
Q

Duodenal ulcers are more common in what age group?

A

30 & 55 yrs

25
Q

Gastric ulcers are more common in what age group?

A

55 & 70 yrs

26
Q

Signs & Sx’s of PUD?

A
  1. Dyspepsia
    A. Acid-provoked:
    - Burning pain; epigastric hunger-like pain; relief w/food, antacids
    B. Food-provoked:
    - PP epigastric discomfort & fullness, belching, early satiety, nausea, & occasional vomiting
  2. Quality of pain:
    A. Burning, gnawing, or “hunger-like”
    B. Can be vague, dull, crampy
27
Q

Sxs of gastric ulcers?

A

Pain worsens w/food

Assoc w/nausea, anorexia

28
Q

Sxs of duodenal ulcers?

A

Sx’s occur 2-5 hrs PP, occur during night

Pain improves w/food

29
Q

Silent ulcers

A

NSAIDs

Elderly

30
Q

2 major causes of PUD

A
  1. NSAIDs
    A. COX-2 inhibitors safer
  2. Chronic H pylori infection
    A. Most important risk factor for duodenal ulcer
    B. Most common chronic bacterial infection in humans
31
Q

Pathophysiology of PUD

A 
1. Ulceration stems from 
A. Inhibition of prostaglandin synthesis
B. ↑ gastric acid & pepsin secretion
C. ↓ gastric mucosal blood flow
D. ↓ cytoprotective mucus production
32
Q

Risk of NSAID complications are greater with?

A
  1. W/in 3 months of starting therapy
  2. > 60 yr
  3. Hx of PUD
  4. NSAIDs in combination w/
  5. ASA, steroids or anticoagulants
  6. Alcohol
33
Q

Pathophysiology of H. Pylori ulcers?

A
  1. H pylori release toxin that destroys gastric & duodenal mucosa
    A. Reduces epithelium’s resistance to acid digestion
    B. Causes gastritis & ulcer disease
34
Q

Diagnostic Studies for PUD?

A
  1. Upper Endoscopy
    A. Most sensitive (90-95%) & most specific (95-100%)
    B. Bx to R/O cancer & H pylori
  2. Rapid Urease Test via endoscope on antral biopsy
    A. If H pylori suspected, RUT kit gives results w/in one hr
    B. MUST stop PPI/H2 antagonist 4 weeks prior to test
  3. Noninvasive testing
    A. Urea breath test
    B. Fecal antigen testing
    C. Serology- H pylori Ab
35
Q

What is a rapid urease test (RUT)?

A

Mucosal Bx from theantrum of thestomach, & placed into a medium containing urea & an indicator(phenol red).

The urease produced byH. pylorihydrolyzes urea to ammonia, raises thepHof the medium, and changes the color of the specimen from yellow (-) to red (+)

36
Q

What is a urea breath test?

A

Urea breath testing—UBT is based upon the hydrolysis of urea by H pylori to produce CO2 & ammonia

Labeled carbon isotope is given by mouth; H pylori liberate tagged CO2 that can be detected in breath samples

False (-) results in pts taking antisecretory therapy, bismuth, or abx

  • Off PPI’s for 1-2 wks
  • Off abx for 4 wks
37
Q

Ddx of PUD

A 
1. GERD
A. Epigastric pain
2. Biliary tract disease
A. Intermittent abd pain, colicky
3. Perforated peptic/gastric ulcer
A. Severe epigastric pain
4. Acute pancreatitis
A. Epigastric pain, LUQ pain/tenderness, radiates to back
5. Acute cholecystitis
A. RUQ pain/tenderness, + Murphy’s
38
Q

Treatment for PUD

A 
1. PPI's
A. 1st line therapy
2. H2 receptor antagonists
3. Mucosal Defense Agents
A. Bismuth (Pepto Bismol)
- Antibacterial action against H pylori
B. Misoprostol (Cytotec)
- Prostaglandin analog that stimulates mucus and bicarbonate secretion (↓ proton pump)
- Used for ulcer prevention w NSAID
C. Antacids 
A. Commonly supplement anti-secretory agents during the first few days of treatment
39
Q

H. Pylori Tx

A
  1. Standard Triple Therapy x 14 days – 1st line
    PPI po bid
    Clarithromycin 500 mg po bid
    Amoxicillin 1 g po bid
    (PCN allergy, Metronidazole 500 mg po bid)
  2. Standard Quadruple Therapy x 14 days – 2nd line
    PPI po bid
    Bismuth 2 tabs po bid
    Tetracycline 500 mg po qid
    Metronidazole 500 mg po tid
40
Q

For patients with large ulcers (H. Pylori treatment continued)

A
  1. For pts with large ulcers
    A. Cont. PPI additional 2-4 weeks for duodenal ulcer
    B. Cont. PPI additional 4-6 weeks for gastric ulcer
  2. Confirmation of H pylori eradication approx 4-6 weeks after therapy completion
    A. Urea breath test
    B. Fecal Ag test- more widely available
    C. Endoscopy
    - If Abx resistance is suspected, endo w/Bx & culture
  3. Hold Abx & bismuth 4 wks prior to testing(retesting) & PPIs at least 2 wks
41
Q

Treatment NSAID-Induced Ulcers

A
  1. Stop NSAID
  2. PPI once daily → healing rates 80% at 8 weeks
  3. All pts with NSAID associated ulcers should undergo testing for concomitant H pylori infection
    - If (+) , standard triple therapy
42
Q

Prevention NSAID Induced Ulcers

A
  1. Weigh benefits NSAID therapy w/ risks GI & CV complications
  2. For all pts, NSAIDs should be prescribed w/ lowest effective dose possible for shortest period of time
  3. Misoprostol (Cytotec) 100-200 mcg po qid
    A. Reduces incidence of NSAID induced gastric & duodenal ulcers by 50-75%
    - Inhibits gastric acid secretion
    - Increases mucus and bicarb secretion
43
Q

Complications of PUD

A

GI Hemorrhage

~50% of all UGI bleeds are due to PUD
Clinically significant bleeding occurs in ~ 10% of pts
~ 80% stop bleeding spontaneously
~ 20% have more severe bleeding

44
Q

Most Common Causes of UGI Bleed

A 
Gastric and/or duodenal ulcers
Esophagogastric varices
Esophagitis
Severe or erosive gastritis/duodenitis
MWS
Polyps/cancers
45
Q

Risk Factors for bleeding PUD

A

H pylori
NSAIDs
Physiologic stress
Excess gastric acid

46
Q

Signs & Sx’s of a GI Hemorrhage

A
  1. Melena
  2. Hematemesis
  3. “Coffee ground” emesis or bright red blood w/ NG lavage indicates UGI bleed
  4. Assess for signs of hypovolemia
    A. Tachycardia, orthostatic hypotension
47
Q

Diagnostic Studies for GI Hemorrhage

A
  1. Hct may ↓
  2. ↑ BUN
    - Absorption of blood nitrogen from small intestine
48
Q

Diagnostic Testing for GI Hemorrhage

A
  1. Upper EGD
    A. Identify cause & location to stop bleeding, Bx for H pylori
    - Epi injection, heat coagulation or hemoclip application
  2. IV PPI’s
  3. If suspect perforated ulcer, stat CT abdomen/pelvis emergently
  4. Surgery if endoscopic measures fail
49
Q

Complications PUD

A 
1. Ulcer Perforation
A. Usually on anterior wall of stomach or duodenum
B. Results in chemical peritonitis
- Sudden severe abd pain
- Sick appearing
- Rigid & quiet abdomen
- Rebound tenderness
- Hypotension w/ bacterial peritonitis
C. Abd CT establishes Dx
D. CXR can help. How?
E. Laparoscopic perforation closure treatment of choice

Gen Med: GI (9 decks)

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