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Clin Med- GI > Stomach and Duodenum Lecture > Flashcards

Stomach and Duodenum Lecture Flashcards

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1
Q

H pylori

NSAIDs

Idiopathic

…associated with?

A

Peptic ulcer disease

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2
Q

NSAIDs

Alcohol

Stress (associated with major medical illnessess)

H pylori

…associated with?

A

Gastritis

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3
Q

What does H pylori produce that makes it easy to test for?

A

Urease

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4
Q

What is the size for small vs large ulcers?

Why is this important?

A

less than 1 cm..small

larger than 1 cm…large

*importat for duration of treatment

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5
Q

What percentage of ulcers will recur if H pylori is not eliminated?

A

85%!!

(only half of those will have the typical signs/symptoms)

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6
Q

A break in the gastric or duodenal mucosa as a result of:

  • impaired normal mucosal defesnse factors (ie NSAIDs)
  • Defensive factors overwhelmed by aggressive luminal factors (acid, pepsin, infection)
A

Peptic ulcer disease

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7
Q

Greater than 5 mm in diameter, extend through muscularis mucosa

Location: duodenal bulb, pyloris, stomach

A

Peptic ulcer disease

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8
Q

500,000 new cases a year in USA

10-20% lifetime incidence in adults

A

Prevalence of ulcers

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9
Q

Decrease in H pylori thru successful treatment

Development of anti secretory drugs

A

Reason for decrease in # of ulcers since the 70’s

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10
Q

Most common location of uclers?

A

Duodenal ulcers are 5x more common than gastric

  • gastic antrum (60%)
  • lesser curvature (25%)
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11
Q

Is smoking a risk factor for ulcers?

A

YES

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12
Q

H pylori infection (gastric antrum)→ ↑acid→ gastric metaplasia in duodenal bulb→ further H pylori infection→ duodenitis→ mucosal breakdown → _______ ulcer.

A

duodenal ulcer

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13
Q

H pylori infection of stomach (body) → gastritis with chronic inflammation overwhelms defenses→ mucosal breakdown→______ ulcer.

A

gastric ulcer

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14
Q

________→ impaired defenses→mucosal breakdown→ gastric ulcer.

A

NSAIDs

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15
Q

Necessary cofactor for majority (75-90%) of duodenal/gastric ulcers; not associated with NSAID ulcers.

  • sprial, gram negative rod
  • urease production
  • spreads person to person (transmission unknown)
A

H pylori

(incidence is correlated with socioeconomic status and higher age)

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16
Q
A
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17
Q

May be associated with acute infectious syndrome: “gastroenteritis”,
nausea, abd pain x several days.

A

H pylori

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18
Q

Epigastric pain common (80-90%)

burning, gnawing, aching…“hunger like”

50% of pts have pain relief with eating and/or antacids with subsequent return in 2-4 hours

Nocturnal awakening with pain common

A

Peptic ulcer disease

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19
Q

caution*** if change in pain pattern!!!

change may indicate penetration or perforation

A

Peptic ulcer disease

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20
Q

Do you usually find something on physical exam in peptic ulcer disease?

A

No, often unremarkable

(must do rectal exam to test for occult blood, but often negative)

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21
Q

Why would you test Hgb/Hct in a PUD pt?

A

To look for signs of bleeding!

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22
Q

Best diagnostic tool for PUD?

A

Endoscopy!!

can test for H pylori via histology and/or rapid urease biopsy testing

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23
Q

Barium upper GI can be used as screening tool for dyspepsia

..why is this test limited?

A

Cannot distinguish between malignant and benign gastric ulcers

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24
Q

Fecal antigen test: indicates ACTIVE infection (95% S/S)

13C-urea breath test: indicates ACTIVE infetion (95% S/S)

A

Non invasive H pylori testing

(no longer use serologic blood test bc does not distinguish between old or active infections)

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25
Must D/C PPI _____ days before H pylori retest or can have false negative
**7-14** days
26
Gastric or duodenal ulcer?: More likely to be malignant Take longer to heal Require longer length of treatment
Gastric ulcers!
27
inactivate the H+ K+ ATPase or “proton pump” in stomach. Short T1/2 but ≈24 hr pump inactivation allows 1-2x daily Rx mostly oral agents **inhibit \>90% acid secretion.**
Proton pump inhbitors (PPIs)
28
Benefit of H2 drugs over PPIs?
H2 cheaper!! (but not as good)
29
over 90% of **duodenal** ulcers heal in **4 wks** over 90 of **gastric** ulcers heal in **8 weeks**
PPIs
30
If you are trying to eliminate H pylori..how does the dosing work?
Twice daily while eradicating H pylori (if need to continue after H pylori is gone, then go to once daily)
31
Omeprazole Lansoprazole (Esomeprazole and pantoprazole availble IV)
PPIs
32
Esomeprazole Pantoprazole ...only 2 PPIs availble in this form
IV
33
**inhibit histamine mediated gastric acid secretion.** Suppress nocturnal\> waking/post meal acid secretion. Less effective than PPI, but most ulcers heal (85-90% efficacy) **over 6-8 weeks.**
H2 receptor antagonists
34
anti bacterial vs H pylori enhances mucosal defenses
Bismith (ie pepto bismal)
35
Difficult to eradicate; requires **“triple” therapy** or more- 2/3 antibiotics plus PPI± bismuth. Several antibiotic regimens. 10-14 day course “triple Rx”: successful eradication ∼70-75%
H pylori eradication
36
**PPI** 2x daily (**omeprazole** dose: 40 mg 2x/d) **Clarithromycin**\* 500 mg 2x daily **Amoxicillin** 1 gram 2x daily **\*\*TRIPLE THERAPY**
Used to eradicate H pylori (Metronidazole, Tetracycline may be used instead of Clarithro bc of **abx resistance**)
37
38
1. PPI 2x daily (omeprazole 40 mg dose) 2. Bismuth subsalicylate: 2 4x/day 3. Tetracycline 500 mg 4x/day 4. Metronidazole 500 mg 3x/day **Successful eradication \>90%** _\*\*10-14 day course!!_
Quadruple treatment for eradicating H pylori
39
PPI 2xd Days 1-5: Amoxicillin 1 gram 2x/d Days 6-10: Clarithromycin 500mg and metronidazole 500 mg, both 2x/d (quadruple Rx and 3 antibiotics for eradicating H pylori) **success rate?**
Over 90%
40
For post H pylori treatment If the ulcer is less than 1 cm, what now?
No further treatment needed
41
Post H pylori tx If ulcer is larger than 1 cm or complication What is the tx for a **duodenal** ulcer and for a **gastric** ulcer?
Duodenal ulcer: continue PPI once a day for 2-4 weeks Gastric ulcer: contine PPI once a day for 4-6 weeks **must wait until this tx is done until you can retest for H pylori**
42
If an ulcer recurs, what must you rule out?
H pylori! (check to make sure eradicated) NSAIDs! (must get pt hx..they should NOT be on NSAIDs)
43
Once H pylori is gone, what is the reinfection rate?
Less than 0.5% a year.. very low!
44
Non-selective ______ inhibit COX-1 and 2. Anti-inflam/pain effects via inhibition of COX-2. Inhibition of gastric COX-1→↓prostaglandin synthesis→ impair gastric mucus/HCO3 secretion and other
NSAIDs (COX2 is responsible for pain and inflammation, COX1 is responsible for gatric mucus production)
45
46
Can you use selective COX2 dugs (like Celecoxib) to avoid ulcers?
VERY LOW DOSES AND VERY SHORT DURATION ..these drugs lead to decrease in production of prostacycline, which **increases risk of MI, stroke, etc.**
47
Tx for NSAID ulcers?
**discontinue NSAID!!** PPI therapy for 4 weeks (duodenal) or 8 weeks (gastric)
48
Is H pylori a cofact with NSAID ulcers?
NO..but if present, must eradicate
49
Can you give prophylaxis PPIs for NSAID use patients?
YES, if high risk
50
Caused by: **-Non compliance with meds** - Cigarettes (retard healing) - NSAIDs (including low dose ASA) **-Failure to eradicate H pylori** **-**Malignancy
Causes of refractory ulcers (uncommon) \*refractory= not healing while on medical Rx
51
**BLEEDING\*** Penetration/Perforation Gastric outlet obstruction
Ulcer complications
52
50% of upper GI bleeding is from.....
ULCERS
53
6-10% mortality **Presents with: Hematemesis and/or melena.** Hematochezia unusual unless massive bleeding.
Bleeding ulcers
54
5% of emergency admissions 80% stop spontaneously 10% patients die (rebleeding increases mortality rate by 10x)
Peptic ulcer bleeding
55
Gastric lavage/emesis: BRB vs “coffee grounds”. PE: vital signs, postural changes, palor etc. dependent on amount of blood loss. Lab: decrease Hgb, Hct (will drop further with volume expansion); check PTT, INR and platelets; BUN may be increased from digested blood.
Bleeding ulcers
56
Volume expansion (isotonic fluids); transfuse when needed. Endoscopy identifies site, stability of bleeding site; also used to stop bleeding when necessary (theromocoag, vasoconstricters, clips/staples, etc.). IV PPI or high dose oral PPI- decrease re-bleeding, need for transfusion or repeat interventions, including surgery.
Tx for bleeding ulcers
57
Is H pylori eradication essential in preventing ulcer re bleeding?
YES
58
5% incidence in ulcer patients. Anterior wall of stomach or duodenum. Results in chemical peritonitis- severe, generalized abdominal pain, rigid abd, rebound, ↑WBC, free air on KUB/upright. Laparoscopic perforation closure carries ↓morbidity compared to laparotomy with vagotomy, antrectomy.
Ulcer perforation
59
Etiologies: ETOH, NSAIDS; stress from underlying severe medical/surgical disease (common in ICU patients). Symptoms: Often asymptomatic; anorexia, N&V, “dyspepsia”; initial presentation may be GI bleeding.
Erosive and hemorrhagic gastritis
60
UGI bleeding: hematemesis, “coffee ground” emesis, melena usually self-limited. Dx often requires endoscopy: DDx: bleeding peptic ulcer, esophageal varices, mallory-weiss tear.
Erosive or hemorrhagic gastritis
61
Superficial erosions common and develop quickly in **critically ill/ICU patients;** bleeding in up to 6% with ↑ associated mortality. Pathophys: ↓gastric mucosal blood flow. Risk factors for bleeding: trauma, burns, sepsis, shock, hypotension, **respiratory failure/mechanical ventilation, coagulation problem**, ARF, CNS injury.
Stress gastritis/ulcers
62
IV H2 blockers ↓bleeding incidence by 50% or more in high risk patients. PPI- Oral/NG\* (omeprazole suspension) or IV (expensive) are better than H2 blocker→↓bleeding Goal: gastric pH\>4 Improve hemodynamics where possible. Enteral feedings when indicated; ↓risk of bleeding.
Prophylaxis for stress gastritis/ulcers
63
``` Very common (25-50% incidence) in patients on chronic NSAIDs; most unrecognized because no Sx. ``` Dyspepsia in 5-10% of patients with NSAID gastritis. If on NSAIDS with Sx, empiric Rx is reasonable: D/C NSAID; PPI for 2-4 wks.
NSAID gastritis
64
Excessive ETOH intake→nausea, dyspepsia, emesis, hematemesis (usually minor UGI bleeding.) Responds to H2 receptor blocker, PPI or sucralfate therapy- 4 week course. DDX of UGI bleeding in alcoholics includes PUD and esophageal varices from portal hypertension→more significant bleeding.
Alcohol gastritis
65
Non-erosive, non-specific picture. **Usually asymptomatic**; unlikely cause of dyspepsia. Co-factor for PUD Associations: 1. Gastric adenocarcinoma 2. B-cell gastric lymphoma (mucosa associated lymphoid tissue lymphoma or MALToma).
H pylori gastritis
66
Gastric adenocarcinoma B cell gastric lymphoma ..associated with?
H pylori gastritis
67
Tumor (**gastrinoma**) that **hyper secretes gastrin** VERY low pH..ulcers develop (often recurrent) Tumor found in: pancreas, duodenum, lymph nodes 2/3 are malignant Often mets to liver, slow growth
Zollinger-Ellison Syndrome
68
How do you dx Zollinger-Ellison syndrome?
Check gastric levels...WILL BE VERY HIGH!!! (pernicious anemia also will have high gastric levels tho)
69
70
How do you do distinguish between Zollinger-Ellison and pernicious anemia as the cause of HIGH GASTRIN LEVELS?
Zollinger-Ellison will have low pH Pernicious anemia will have high pH (use NG tube to determine)
71
Gastrin levels over 500 pg/ml plus pH under 3
Zollinger-Ellison Syndrome
72
If isolated primary tumor: PPI + resection. If metastasis: PPI in high dose to decrease basal acid output. Prognosis: good for isolated tumor.
Tx for Zollinger-Ellison

Clin Med- GI (8 decks)

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