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Gastrointestinal STEP 2 > Gastritis, ulcer, non-ulcer dyspepsia > Flashcards

Gastritis, ulcer, non-ulcer dyspepsia Flashcards

1
Q

gastritis - defnition

A

inflammation or erosion of the gastric lining that is sometimes called gastropathy

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2
Q

gastritis - is caused by

A
  1. alcohol 2. NSAID 3. H. pylori 4. Porta hypertension

5. Stress (burns, trauma, sepsis, multiorgan failure, uremia)

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3
Q

atrophiuc gastritis is associated with

A

vit B12 deficiency

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4
Q

gastritis often presents with

A

GI bleeding without pain. Severe erosive gastritis can present with epigastric pan
- NSAID or alcoholsim in the history is a clue

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5
Q

gastritis - physical findings

A

there are no unique physical findings for gastritis

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6
Q

gastritis - bleeding

A

almost any degree: from mild cofee-graound emesis to large vomiting to red blood , to black stool (melena)

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7
Q

corellation of manifestations with volume of bleeding

A

cofee-ground emesis: 5-10 ml
heme (quaic) positive stool: 5-10 ml
melena: 50-100 ml

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8
Q

Gastritis - definitive diagnosis

A

only with upper endoscopy

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9
Q

Gastritis - anemia - diagnosis

A

no specific blood tests

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10
Q

Gastritis - radiologic studies

A

such as uppe GI series are NOT SPECIFIC ENOUGH

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11
Q

gastritis - capsule endoscopy

A

not appropriate for upper GI bleeding if endoscopy is one of the choices

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12
Q

in gastritis, also test fo

A

H. pylori –> this organism should be treated if it is associated with gastritis

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13
Q

tests for H. pylori - types (which is the most accurate)

A
  1. endoscopic biopsy (The most accurate)
  2. serology
  3. Urea C13 or C14 breath testing
  4. H. pylori stool antigen
    If endoscopy, there is no point in doing other test
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14
Q

H. pylori - endocopic biopsy - advantages

A

The most accurate test for H. pylori

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15
Q

H. pylori - endocopic biopsy - disadvantages

A

invasive

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16
Q

H. pylori - serology - advantages

A
  1. low cost
  2. easily excludes infection if it is negative
  3. no complications ore procedures required
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17
Q

H. pylori - serology - disadvantages

A

Low specificity –> a (+) test does not easily tell difference between current and previous infection

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18
Q

H. pylori - Urea C13 or C14 breath - advantages

A
  1. (+) only in active infection

2. non-invasive

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19
Q

H. pylori - Urea C13 or C14 breath - disadvantages

A

requires expensive equipment in office

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20
Q

H. pylori - stool antigen - advantages

A
  1. (+) only in active infection

2. non-invasive

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21
Q

H. pylori - stool antigen - disadvantages

A

Requires stool sample

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22
Q

gastritis - treatment

A

treat with PPI

H2 blockers, sucralfate and liquid anntiacids are not as effective

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23
Q

Sucralfate inert substance (aluminium hydroxide complex) that coats stomach

A 
inert substance (aluminium hydroxide complex) that coats stomach
NEVER CORRECT
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24
Q

stress ulcer prophylaxis is indicated in

A
  1. mechanical ventilation
  2. Burns
  3. Head trauma
  4. Coagulopathy
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25
Q

how to distinguish definitely gastric and duodenal ulcers

A

no way wothout endoscopy

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26
Q

Peptic ulcer disease (PUD) is most commonly caused by

A

H. pylori

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27
Q

2nd MCC of PUD

A

NSAID: inhibition of the production of the protective mucus barrier in the stomach
(inhibit prostagladins which produce mucus)

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28
Q

Less common causes of PUD

A
  1. Burns
  2. Head trauma
  3. CROHN DISEASE
  4. gastric cancer
  5. Gastrinoma (Zollinger-Ellison syndrome)
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29
Q

alcohol and tobacco - PUD

A

they do not cause –> but they delay the healing

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30
Q

PUD - presentation

A
  • recurrent episodes of epigastric pain hat is described as dull, sore, gnawing
  • Bleeding
  • tenderness and vomiting are UNUSUAL
    CANNOT ANSWER PUD BASED ONLY ON SYMPTOMS
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31
Q

PUD - bleeding?

A

although is the MCC of upper GI bleeding, the majority of ulcers do not bleed

32
Q

PUD - tenderness and vomiting

A

unusual

33
Q

duodenal vs gastric ulcers regarding sympoms

A
  • duodenal is more often improved with eating
  • gastric is more often worsened by eating
    YOU CANNOT definitively distinguish duodenal, gastric and non ulcer dysplasia without endoscopy
34
Q

PUD - diagnosis

A

there is no way to diagnose withou endoscopy or barium studies

35
Q

PUD - most accurate tests

A

Upper endoscopy

36
Q

PUD - radiologic testing such as Upper GI series

A

can detect ulcers, but cannot detect the presence of either cancer or H. pylori

37
Q

PUD - cancer: epidemiology / diagnosis

A

cancer is present in 4% of thise with gastric ulcer but none o thise with Duodenal ucler
The only method to diagnose gastric ca is endoscopy

38
Q

duodenal vs gastric ulcer regarding H. pylori

A

Duodenal: 80-90%
gastric: 50-70%

39
Q

PPIs in PUD

A

responds in 95% of cases, but will ecure unless H. pylori is eradicated in those who are infected

40
Q

H. pylori eradication (treatment)

A

PPIs in combination with 2 antibiotics
1. best initial: PPIs with clarythromycin and amoxicillin (or metronidazole in allergy)
2. if no respinse: metronidazole and tetracycline
Adding bismuth to a change of antibiotics may aid in resolution of treatment-resistant ulcer

41
Q

H. pylori eradication (treatment) - best initial

A

PPIs + clarythromycin + amoxicillin (or metronidazole in allergy)

42
Q

H. pylori - confirmation of the eradication

A

1-2 months post-therapy –> retest with stool antigen or breath test

43
Q

patient with epigastric pain from confirmed ulcer that is not responded to antibiotics - next step

A

if duodenal –> confirm the persistence of the active infection (Urea, stool or endoscopy) –> switch antibiotics
if gastric –> repeat endoscopy to exclude cancer

44
Q

PUD - treatment of failure most often stems from

A
  1. nonadherence to medications
  2. alcohol
  3. tobacco
  4. NSAID
45
Q

differences between duodenal and gastric ulcer

A
  • Gastric is more often worsened by food
  • gastric is routinely biopsed (4% cancer)
  • routinely repeating the endoscopy to confirm healing is standard to gastric ulcer
46
Q

non-ulcer dyspepsia - definition

A

epigastric pain that has no identified etiology

with a normal endoscopy

47
Q

non-ulcer dyspepsia - diagnosis

A

only by endoscopy

48
Q

non-ulcer dyspepsia - pain is identical to

A

gastritis, PUD, gastric cancer, reflex

49
Q

non-ulcer dyspepsia - management

A

if under 45 –> treat empirically with PPIs and scope only if do not resolve
If over 55 –> endoscopy
45-55 –> unclear

50
Q

scope dyspepsia if

A
  1. over 55 age

2. alarm symproms

51
Q

alarm symptoms of dyspesia

A

dysphagia, weight loss, anemia

52
Q

non ulcer dyspepsia - etiology / best initiatl therapy

A

unknown

best initial therapy: PPIs

53
Q

MCC of epigastric pain

A

non ulcer dyspepsia

54
Q

non ulcer dyspepsia - H. pylori

A

No association
however, if symptoms not resolve, with initial therapy and H. pylori is present, you should try to treat it
no definite benefit to treating non ulcer dyspepsia with antibiotics to eradicate H. pyori
only 10% will expericne an improvement of symptoms after this

55
Q

when to suspect gastrinoma

A

patients with ulcers that are

1. large (more than 1-2cm), 2. recurrent after H. pylori eradication 3. distal in theduodenum 4. multiple

56
Q

gastrinoma - presntation

A

diarrhea because acid inactivates lipase

57
Q

gastrinoma - the most accurate test

A

once endoscopy confirms the presence of an ulcer, the most accurate test is by gastrin levels

58
Q

gastrinoma - gastrin levels

A
  1. high gastrin levels off antisecretory therapy (PPIs or H2 blockers) with high gastric acidity
  2. high despite a high gastric acid output
  3. persistent high gastrin levels despite injecting secretin
    any one of these 3 can be used to confirm the diagnosis –> the single most accurate test is always a functional test such as looking at the response of secretin
59
Q

gastrinoma - imaging - importance

A

once a diagnosis of gastrinoma is confirmed, the most important issue is to exclude metastatic disease

60
Q

gastrinoma - types

A
  1. CT
  2. MRI
  3. Somatostatin receptor scintigraphy (nuclear octreotide scan combined with endoscopic US
61
Q

gastrinoma - CT / MRI

A

poor sensitivity but are done first –> (-) does not exclude metastases

62
Q

gastrinoma - Somatostatin receptor scintigraphy (nuclear octreotide scan combined with endoscopic US

A

do these CT and MRI are normal –> to exclude metastasis

gastrinoma is associated wit ha massive increase of somatostatin receptors in the abdomen

63
Q

gastrinoma is aka

A

Zollinger- Ellison syndrome

64
Q

gastrinoma - treatment

A

local disease –> removed surgically

metastatic –> udresectable –> lifelong PPI to block acid production

65
Q

gastrinoma - MEN

A

MEN 1 (menin) : - pituitary tumors (prolactin or GH)

  • pancreatic endocrine tumors
  • parathyroid adenoma
66
Q

MEN 2A

A
  • Parathyroid huperplasia
  • medullary thyroid ca
  • pheochromocytoma
67
Q

MEN 2B

A
  • medullary thyroid ca
  • pheochromocytoma
  • mucosal neuromas (oral/intestinal ganglioneuromatosis)
  • marfanoid habitus
68
Q

diabetic gastroparesis - definition

A

long standing iabetes leads to gastric dysmotility

69
Q

the most important stimulant of GI motility

A

distention of the stomach and the intestines

70
Q

Gastroparesis?

A

autonomic neuroapty leading to dysmotility

71
Q

dysmotility?

A

from the inability to sense stretch in the GI

72
Q

diabetic gastroparesis - look for patient with … (symptoms)

A
  • diabetis with chronic abdominal discomfort, bloating, and constipation
  • also anorexia, nausea, vomiting, early satiety
73
Q

the most accurate test for diabetic gastroparesis

A

nuclear gastric emptying study (rarely needed)

74
Q

diabetic gastroparesis - treatment

A

erythromycin and metoclopramide –> increase GI motility

75
Q

diabetic gastroparesis - if it is clear diagnosis from the clinical picture

A

no need to do diagnostic testing, unless failure of therapy

Gastrointestinal STEP 2 (8 decks)

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