Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Clin Med- GI > Stomach and Duodenum Lecture > Flashcards

Stomach and Duodenum Lecture Flashcards

1
Q

H pylori

NSAIDs

Idiopathic

…associated with?

A

Peptic ulcer disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

NSAIDs

Alcohol

Stress (associated with major medical illnessess)

H pylori

…associated with?

A

Gastritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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

A

Urease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Greater than 5 mm in diameter, extend through muscularis mucosa

Location: duodenal bulb, pyloris, stomach

A

Peptic ulcer disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

500,000 new cases a year in USA

10-20% lifetime incidence in adults

A

Prevalence of ulcers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Most common location of uclers?

A

Duodenal ulcers are 5x more common than gastric

  • gastic antrum (60%)
  • lesser curvature (25%)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Is smoking a risk factor for ulcers?

A

YES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

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

A

duodenal ulcer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

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

A

gastric ulcer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

________→ impaired defenses→mucosal breakdown→ gastric ulcer.

A

NSAIDs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

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

A

H pylori

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

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

change may indicate penetration or perforation

A

Peptic ulcer disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

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

A

To look for signs of bleeding!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Best diagnostic tool for PUD?

A

Endoscopy!!

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Must D/C PPI _____ days before H pylori retest or can have false negative

A

7-14 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Gastric or duodenal ulcer?:

More likely to be malignant

Take longer to heal

Require longer length of treatment

A

Gastric ulcers!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

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.

A

Proton pump inhbitors (PPIs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Benefit of H2 drugs over PPIs?

A

H2 cheaper!! (but not as good)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

over 90% of duodenal ulcers heal in 4 wks

over 90 of gastric ulcers heal in 8 weeks

A

PPIs

30
Q

If you are trying to eliminate H pylori..how does the dosing work?

A

Twice daily while eradicating H pylori

(if need to continue after H pylori is gone, then go to once daily)

31
Q

Omeprazole

Lansoprazole

(Esomeprazole and pantoprazole availble IV)

A

PPIs

32
Q

Esomeprazole

Pantoprazole

…only 2 PPIs availble in this form

A

IV

33
Q

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.

A

H2 receptor antagonists

34
Q

anti bacterial vs H pylori

enhances mucosal defenses

A

Bismith (ie pepto bismal)

35
Q

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%

A

H pylori eradication

36
Q

PPI 2x daily (omeprazole dose: 40 mg 2x/d)

Clarithromycin* 500 mg 2x daily

Amoxicillin 1 gram 2x daily

**TRIPLE THERAPY

A

Used to eradicate H pylori

(Metronidazole, Tetracycline may be used instead of Clarithro bc of abx resistance)

37
Q
A
38
Q
  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!!

A

Quadruple treatment for eradicating H pylori

39
Q

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?

A

Over 90%

40
Q

For post H pylori treatment

If the ulcer is less than 1 cm, what now?

A

No further treatment needed

41
Q

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?

A

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
Q

If an ulcer recurs, what must you rule out?

A

H pylori! (check to make sure eradicated)

NSAIDs! (must get pt hx..they should NOT be on NSAIDs)

43
Q

Once H pylori is gone, what is the reinfection rate?

A

Less than 0.5% a year.. very low!

44
Q

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

A

NSAIDs

(COX2 is responsible for pain and inflammation, COX1 is responsible for gatric mucus production)

45
Q
A
46
Q

Can you use selective COX2 dugs (like Celecoxib) to avoid ulcers?

A

VERY LOW DOSES AND VERY SHORT DURATION

..these drugs lead to decrease in production of prostacycline, which increases risk of MI, stroke, etc.

47
Q

Tx for NSAID ulcers?

A

discontinue NSAID!!

PPI therapy for 4 weeks (duodenal) or 8 weeks (gastric)

48
Q

Is H pylori a cofact with NSAID ulcers?

A

NO..but if present, must eradicate

49
Q

Can you give prophylaxis PPIs for NSAID use patients?

A

YES, if high risk

50
Q

Caused by:

-Non compliance with meds

  • Cigarettes (retard healing)
  • NSAIDs (including low dose ASA)

-Failure to eradicate H pylori

-Malignancy

A

Causes of refractory ulcers

(uncommon)

*refractory= not healing while on medical Rx

51
Q

BLEEDING*

Penetration/Perforation

Gastric outlet obstruction

A

Ulcer complications

52
Q

50% of upper GI bleeding is from…..

A

ULCERS

53
Q

6-10% mortality

Presents with: Hematemesis and/or melena.

Hematochezia unusual unless massive bleeding.

A

Bleeding ulcers

54
Q

5% of emergency admissions

80% stop spontaneously

10% patients die
(rebleeding increases mortality rate by 10x)

A

Peptic ulcer bleeding

55
Q

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.

A

Bleeding ulcers

56
Q

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.

A

Tx for bleeding ulcers

57
Q

Is H pylori eradication essential in preventing ulcer re bleeding?

A

YES

58
Q

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.

A

Ulcer perforation

59
Q

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.

A

Erosive and hemorrhagic gastritis

60
Q

UGI bleeding: hematemesis, “coffee ground” emesis, melena
usually self-limited.

Dx often requires endoscopy: DDx: bleeding peptic ulcer, esophageal varices, mallory-weiss tear.

A

Erosive or hemorrhagic gastritis

61
Q

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.

A

Stress gastritis/ulcers

62
Q

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.

A

Prophylaxis for stress gastritis/ulcers

63
Q 
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.

A

NSAID gastritis

64
Q

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.

A

Alcohol gastritis

65
Q

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).
A

H pylori gastritis

66
Q

Gastric adenocarcinoma

B cell gastric lymphoma

..associated with?

A

H pylori gastritis

67
Q

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

A

Zollinger-Ellison Syndrome

68
Q

How do you dx Zollinger-Ellison syndrome?

A

Check gastric levels…WILL BE VERY HIGH!!!

(pernicious anemia also will have high gastric levels tho)

69
Q
A
70
Q

How do you do distinguish between Zollinger-Ellison and pernicious anemia as the cause of HIGH GASTRIN LEVELS?

A

Zollinger-Ellison will have low pH

Pernicious anemia will have high pH

(use NG tube to determine)

71
Q

Gastrin levels over 500 pg/ml plus pH under 3

A

Zollinger-Ellison Syndrome

72
Q

If isolated primary tumor: PPI + resection.

If metastasis: PPI in high dose to decrease basal acid output.

Prognosis: good for isolated tumor.

A

Tx for Zollinger-Ellison

Clin Med- GI (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions