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DEMS unit 1 > Stomach > Flashcards

Stomach Flashcards

1
Q

HCl secretion importance

A

denatures proteins, protect from infection, absorption of Fe/B12

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2
Q

What triggers slowing in gastric emptying

A

decreased pH (acid), fatty acids and caloric density, increase in osmolality

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3
Q

Types of Gastritis

A

infectious, lymphocytic, Eosinophilic, gastritis associated with systemic disease

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4
Q

Autoimmune Atrophic Gastritis

A

autoimmune attack against parietal cells, IF

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5
Q

Causes of Infectious gastritis

A

Bacterial (H pylori, syphilis, TB)
Fungal (candidiasis, aspergillosis, histoplasmosis, mucormycosis)
Parasitic (giardia, cryptospyridia, etc)
Viral (CMV)

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6
Q

Peptic ulcer disease original hypothesis

A

thought to be all from stress-lifestyle –>increased acid

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7
Q

Helicobacter pylori

A

most common human bacterial infection, which is life-long for most–most asymptomatic
- makes urease enzyme to neutralyze stomach acid by creating ammonia from urea

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8
Q

Strain of H pylori associated with pathogenicity

A

CagA
- associated with duodenal and gastric ulcers

VacA– exotoxin, pores in membrane, inhibit T cells

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9
Q

H pylori risks

A

Gastric cancer
gastic lymphoma
atrophic gastritis
Peptic ulcer

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10
Q

Chronic gastritis

A

presence of mononuclear inflammatory (lymphocytes and plasma cells) cells within lamina propria

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11
Q

Progression of gastritis

A

Colonized mucosa –> superficial gastritis – gastric atrophy– intestinal metaplasia – dysplasia – gastric adenocarcinoma

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12
Q

Antral predominant infection associated with

A

acid secretion adn duodenal ulcer (DU)

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13
Q

Duodenal ulcer (DU)

A

gastric metaplasia in duodenum (H pylori colonize –>inflammation –> cell damage –>ulcer)

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14
Q

what is severity of body gastritis correlated with

A

acid secretion inversely correlates with severity of gastric body gastritis

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15
Q

Diagnosis of H pylori

A

Endoscopy Mucosal biopsy
- Histology, Rapid urease test

No mucosal biopsy required
- Blood antibody test, stool antigen test, urea breath test (not as common)

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16
Q

Treat H pylori infection

A
  • triple therapy (PPI + clarithromycin + amoxicilin 10-14 days)
  • Rescue quadruple therapy (PPI + metronidazole + tetracycline + bismuth)
  • Sequential therapy
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17
Q

when to treat H pylori

A

Peptic ulcer disease, gastric lymphoma, fam hx of gastric carcinoma, whenever diagnosed??

18
Q

Other causes of gastritis

A

Non H pylori infection – uncommon (CMV, Candidiasis, Aspergillosis, etc)

Eosinophilic (

- can have ulceration
- early satiety, nausea, vomiting
- increased eos in blood    - rare, cause unknown
19
Q

Thickened folds

A

H. pylori, neoplasia, Menetrier’s disease, lymphocytic infiltration, acid hypersecretory states

20
Q

Menetrier’s Disease

A

very very rare; increased mucous secretion, decreased acid; abdominal pain, weight loss, bleeding, hypoalbuminemia

21
Q

Non-inflammatory Epithelial cell injury also called…

A

Gastropathies

22
Q

Gastropathy

A

gastroduodenal injury in absence of significant inflammation

  • NSAIDs
  • Ethanol
  • Stress ulceration
  • Cocaine
  • Bile reflux
23
Q

ethanol gastropathy

A

similar to NSAID type injury; disrupts mucosa and increased acid secretion
- PUD with high concentration (>10%), high amounts of use, NSAID use

24
Q

GI side effets of NSAID use

A

heartburn, nausea, vomiting, abdominal pain; mucosal lesions - 20% in 3 months

GI complications– perforated ulcers or GI bleeding

25
Q

Gastric protective mechanisms

A

ALL PG dependent

  • mucous layer thickness
  • cell membrane hydrophobicity
  • bicarb secretion
  • mucosal blood flow
  • epithelial cell migration/proliferation
26
Q

Stress ulcers

A

ICU patients
- CNS injury (cushing’s ulcer), Burns (Curling’s ulcer), prolonged mechanical ventilation > 48 hours, coagulopathy
- fundus and body,
impaired mucosal protection, incerased acid secretion

27
Q

Peptic ulcer complications

A

abdominal pain, anemia, bleeding, acute bleed (hematemesis melena–black tarry smelly stool), perforation (5% lifetime), Gastric outlet obstruction-duodenal ulcer

28
Q

Treatment of Severe PUD -acute bleeding

A
  • IV resuscitation –>restore IV volume
  • acid suppression - PPI drip (improves clotting)
  • Endoscopy
  • Angiography- coils
    Surgery
29
Q

Treatment of severe PUD with perforation

A

Surgery

30
Q

Treat PUD

A

PPI therapy, H pylori test and treat, risk factor avoidance (NSAIDs, smoking, chronic PPI if NSAID needed for cardiac disease)

31
Q

Types of gastric neoplasms

A

polyps, adenocarcinoma, stromal tumors, neuro-endocrine tumors, lymphoma

32
Q

Gastric polyps

A

Hyperplastic, adenomia, fundic gland polyps (common-benign and unrelated o H pylori)

33
Q

Hyperplastic gastric polyps

A

found near gastritis ulcer; rare,malignant potential (>1 cm)

34
Q

Adenoma (gastric polyp)

A

Premalignant, FAP

35
Q

Fundic gland polyps

A

type of gastric polyp associated with chronic PPI use; benign and unrelated to H pylori

36
Q

2nd most common cancer world-wide

A

gastric Adenocarcinoma

37
Q

2nd most common cause of death from cancer world-wide

A

gastric adenocarcinoma

38
Q

Gastric cancer treatment

A

Surgery (endoscopic removal for stage 0), Chemo, Radiation

39
Q

GIST

A

distinct stromal tumor —most common in mesenchymal tumor of stomach (60%)

  • Leiomyomas NOT GISTs
40
Q

Treatment of GIST

A

Gleevec

41
Q

Prognosis of GIST compared to other stromal tumors

A

WORSE

42
Q

GISTs

A

cell of origin = interstitial cell of Cajal (pacemaker)

+ for c-kit (CD117) mutation in transmembrane receptor tyrosine kinase (RTK)

DEMS unit 1 (15 decks)

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