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Gen Med: GI > Diseases of the stomach > Flashcards

Diseases of the stomach Flashcards

1
Q

What is dyspepsia?

A

Impaired digestion

Epigastric pain or burning, early satiety or postprandial fullness

Dyspepsia must be distinguished from heartburn (pyrosis)

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2
Q

What is the etiology 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 are the dz of the stomach?

A

Gastroparesis
Gastritis
Peptic ulcer disease
Gastric neoplasms

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4
Q

Define gastroparesis?

A

Delayed gastric emptying w/o evidence of mechanical obstruction

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5
Q

What are the sxs of gastroparesis?

A

1 PP fullness persisting for hours

2. Nausea, vomiting, early satiety, bloating

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6
Q

What are the 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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7
Q

What is the gold standard test for dx gastroparesis?

A
  1. Scintigraphic gastric emptying test
  2. Isotope tagged meal permits pictures to be taken as the meal passes through the stomach and the GI tract
  3. 4 hr test
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8
Q

What are the nonmedical tx options for gastroparesis?

A
  1. Freq. small meals

2. Avoid excess fat & dietary fiber

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9
Q

What meds are used for gastroparesis?

A
  1. 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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10
Q

What is gastritis?

A
  1. Inflammation, irritation, or erosion of the lining of the stomach
  2. Can occur
    A. Suddenly (acute)
    B. Gradually (chronic)
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11
Q

What are the causes of gastritis?

A
  1. Helicobacter pylori infection
  2. NSAIDs
  3. Severe illness/stress
  4. ETOH
  5. Smoking
  6. Cocaine
  7. Autoimmune disorders
  8. Radiation therapy
  9. Crohn’s disease
  10. CMV
  11. Candida
  12. Pernicious anemia
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12
Q

What can H. pylori infections lead to?

A
  1. Bacteria infection in mucous lining of the stomach

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

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13
Q

What are the sxs 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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14
Q

What dx studies are used for gastritis?

A 
1. ↓ Hct 
A. If significant bleeding 
2. +/- Iron deficiency anemia
A. If bleeding is chronic
3. Upper endoscopy
A. Bx
B. Identifies source of bleeding
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15
Q

What are the ddx for gastritis?

A
  1. Erosive gastritis
  2. PUD
  3. Esophageal varices
  4. Mallory Weiss tear
  5. Gastric AV malformations
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16
Q

What is the rx for stress induced gastritis?

A 
1. Pts w/risk factors for bleeding
A. Coagulopathy
B. 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)
5. Early enteral tube feeding may ↓ risk of GI bleed in ICU pts
6. 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
7. Endoscopy for clinically significant bleeding
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17
Q

What is the treatment for NSAID induced gastritis?

A

1.D/C NSAID
2. Give lowest effective dose if have to give NSAID
3. Administer NSAID w/ meals
4. Oral PPI x 2-4 weeks:
omeprazole (Prilosec)
lansoprazole (Prevacid)
pantoprazole (Protonix)
esomeprazole (Nexium)
dexlansoprazole (Dexilant/Kapidex)
rabeprazole (Aciphex)
naproxen/esomeprazole (Vimovo)

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18
Q

What is the treatment for ETOH 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

What is the most common etiology of nonspecific gastritis?

A
  1. H pylori most common
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20
Q

What are the sxs of acute H. pylori gastritis?

A
  1. Nausea, abd pain, no fever

2. epigastric pain

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21
Q

What are the sxs of chronic H. pylori infection?

A
  1. After acute sx’s resolve, majority progress to chronic state w/ diffuse mucosal inflammation
    A. Most asymptomatic w/mild inflammation
    B. ~15% have inflammation in antrum only w/↑ gastrin secretion
    C. ~ 1% have inflammation in gastric body → ↑ risk gastric ulcers & gastric cancer
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22
Q

What are the complications of H. pylori infections?

A

A. ↑ risk of gastric adenocarcinoma & primary B cell gastric lymphoma

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23
Q

What are the dx studies for H. pylori gastritis?

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
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24
Q

What is the included in the standard triple therapy for H pylori infections?

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
  2. Prevpac (lansoprazole/amoxicillin/clarithromycin) x 10-14 d
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25
Q

What is the included in the standard quadruple therapy for H pylori infections?

A
  1. Standard Quadruple Therapy x 10-14 days

A. Oral PPI bid
B. Bismuth subsalicylate (Pepto-Bismol) 500 mg po qid
C. Tetracycline 500 mg po qid
D. Metronidazole (Flagyl) 500 mg po tid

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26
Q

When is quadruple therapy used compared to quadruple therapy?

A

Used if pt tests (+) after standard triple therapy or previously on macrolide

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27
Q

What are the general characteristics of 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. M = F
28
Q

What is PUD asst with?

A

Assoc. w/ gastric malignancy

29
Q

What type of ulcers are more common in 30-55 yo?

A

Duodenal ulcers

30
Q

What type of ulcers are more common in 55-70 yo?

A

Gastric ulcers

31
Q

What percentage of ulcers are silent?

A

20% pts w/ulcer complications such as bleeding have no other sx’s

32
Q

What sxs may be present with 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
33
Q

What is the quality of the dyspepsia?

A

Burning, gnawing, or “hunger-like”

Can be vague, dull, crampy

34
Q

What are the sxs characteristics with gastric ulcers?

A
  1. Pain worsens w/food

2. Assoc w/nausea, anorexia

35
Q

What are the sxs characteristics with duodenal ulcers?

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

2. Pain improves w/food

36
Q

What group of ppl are silent ulcers more common in?

A
  1. NSAID users

2. Elderly

37
Q

What are the 2 major cause 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
38
Q

What is the general pathophys 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
39
Q

What is the prevalence of gastric and duodenal ulcers in NSAID induced PUD?

A
  1. 10-20% prevalence gastric ulcers

2. 2-5% prevalence of duodenal ulcers

40
Q

When are the risk of NSAID complications increased?

A 
1. W/in 3 months of starting therapy
A. > 60 yr 
B. Hx of PUD 
C. NSAIDs in combination w/ ASA, steroids or anticoagulants
D. Alcohol
41
Q

What is the pathophys of H. pylori PUD?

A
  1. H pylori release toxin that destroys gastric & duodenal mucosa
    A. Reduces epithelium’s resistance to acid digestion
    B. Causes gastritis & ulcer disease
42
Q

What dx studies are used for PUD?

A

1/ Upper Endoscopy
A. Most sensitive (90-95%) & most specific (95-100%)
B. Bx to R/O cancer & H pylori

  1. 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
  2. Noninvasive testing
    A. Urea breath test
    B. Fecal antigen testing
    C. Serology- H pylori Ab
43
Q

What is the Rapid Urease Test?

A
  1. Mucosal Bx from theantrum of thestomach, & placed into a medium containing urea & an indicator(phenol red).
  2. The urease produced byH. pylorihydrolyzes urea to ammonia, raises thepHof the medium, and changes the color of the specimen from yellow (-) to red (+)
44
Q

What is the urea breath test?

A
  1. Urea breath testing—UBT is based upon the hydrolysis of urea by H pylori to produce CO2 & ammonia
  2. Labeled carbon isotope is given by mouth; H pylori liberate tagged CO2 that can be detected in breath samples
45
Q

When may a false negative results occur in urea breath test?

A
  1. False (-) results in pts taking antisecretory therapy, bismuth, or abx
    A. Off PPI’s for 1-2 wks
    B. Off abx for 4 wks
46
Q

What are the DDX for 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
47
Q

What is the first treatment for PUD?

A
  1. PPIs
  2. Administer 30 mins before breakfast
  3. Inhibit >90% of 24 hr acid secretion
    Omeprazole/ Prilosec 20-40 mg po daily
    Lansoprazole / Prevacid 30 mg po daily
    Pantoprozole / Protonix 40 mg po daily
    Etc.
  4. 90% healing duodenal ulcers after 8 weeks Tx
48
Q

What is the second line treatment for PUD?

A
  1. H2 receptor antagonists
  2. Inhibits 50% - 80% of 24 hour acid secretion
    A. Cimetidine / Tagamet 800 mg po q hs
    B. Ranitidine / Zantac 300 mg po q hs
    C. Famotidine / Pepcid 40 mg po q hs
    D. Nizatidine / Axid 300 mg po q hs
49
Q

What mucosal defense agents can be used for PUD?

A
  1. Promote ulcer healing through mucosal defensive mechanisms
  2. Bismuth (Pepto Bismol)
    A. Antibacterial action against H pylori
  3. Misoprostol (Cytotec)
    A. Prostaglandin analog that stimulates mucus and bicarbonate secretion (↓ proton pump)
    B. Used for ulcer prevention w NSAID
  4. Antacids
    A. Commonly supplement anti-secretory agents during the first few days of treatment
50
Q

What is the effectiveness of triple and qyadruple therapy for H. pylori?

A

> 75% effective

51
Q

How long should pts with large ulcers from H pylori be treated w/ PPI after initial triple or quad therapy?

A

Cont. PPI additional 2-4 weeks for duodenal ulcer

Cont. PPI additional 4-6 weeks for gastric ulcer

52
Q

When should H pylori pts be assessed for eradication of H. pylori

A
  1. 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
53
Q

How long do pts have to be off abx, ppi, and bismuth prior to testing?

A

Hold Abx & bismuth 4 wks prior to testing(retesting) & PPIs at least 2 wks

54
Q

What should all pts with NSAID asst. ulcers be tested for?

A

concomitant H pylori infection

If (+) , standard triple therapy

55
Q

How can NSAID induced ulcers be prevented?

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%
    B. Inhibits gastric acid secretion
    C. Increases mucus and bicarb secretion
56
Q

What is a complication of PUD?

A
  1. 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

57
Q

What are the most common causes of UGi bleed?

A
  1. Gastric and/or duodenal ulcers
  2. Esophagogastric varices
  3. Esophagitis
  4. Severe or erosive gastritis/duodenitis
  5. MWS
  6. Polyps/cancers
58
Q

What are the risk factors for bleeding PUD?

A
  1. H pylori
  2. NSAIDs
  3. Physiologic stress
  4. Excess gastric acid
59
Q

What are the sxs of 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
60
Q

What are the dx studies for Gi hemorrhage?

A
  1. Hct may ↓
  2. ↑ BUN
    A. Absorption of blood nitrogen from small intestine
  3. Upper EGD
61
Q

Why is an upper EGD indicated for GI hemorrhage?

A
  1. Identify cause & location to stop bleeding, Bx for H pylori
    A. Epi injection, heat coagulation or hemoclip application
62
Q

What is the tx for GI bleed?

A
  1. IV PPI’s
  2. If suspect perforated ulcer, stat CT abdomen/pelvis emergently
  3. Surgery if endoscopic measures fail
63
Q

What is a complication of PUD?

A
  1. Ulcer Perforation
  2. Usually on anterior wall of stomach or duodenum
    A. Results in chemical peritonitis
64
Q

What are the sxs of ulcer perforation?

A
  1. Sudden severe abd pain
  2. Sick appearing
  3. Rigid & quiet abdomen
  4. Rebound tenderness
  5. Hypotension w/ bacterial peritonitis
65
Q

How can a perforated ulcer be diagnosed?

A
  1. Abd CT establishes Dx

2. CXR can help by showing air under diaphragm

66
Q

How is a perforated ulcer treated?

A

Laparoscopic perforation closure treatment of choice

Gen Med: GI (16 decks)

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