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My DEMS I > Stomach > Flashcards

Stomach Flashcards

1
Q

Describe the epidemiology, pathophysiology, and treatment of H. pylori infection

A

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2
Q

Identify the causes of gastritis

A

Infectious
lymphocytic
eosinophilic
gastritis assoc w/ systemic disease

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3
Q

Describe peptic ulcer disease pathogenesis

A

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4
Q

Explain peptic ulcer disease treatment

A

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5
Q

List the 5 most common types of gastric neoplasms

A

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6
Q

Gastric emptying is slowed in response to:

A
  • decrease in pH (acid)
  • fatty acids and caloric density
  • increase in osmolality
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7
Q

Autoimmune Atrophic Gastritis

A
  • autoimm attack against parietal cells, IF
  • Achlorhydria
  • pernicious anemia (B12 low, IF absent)
  • biopsies:atrophy, loss of parietal cells, intestinal metaplasia
  • Risk of gastric carcinoid tumor
  • Gastric cancer risk higher:
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8
Q

Infectious gastritis

A

Bacterial: H. pylori, syphilis, tuberculosis

Fungal: candidiasis, aspergillosis, histoplasmosis, mucormycosis

Parasitic: giardia, cryptospyridiosis, anisakiasis, strongyloidiasis

Viral: CMV

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9
Q

H. Pylori

A
  • most common human bacterial infection
  • infection lifelong for most
  • 15% weight urease (Urea–>ammonia, neutralizaes H+)
  • corkscrew into mucus
  • CagA pathogenicity island/effector protein (injected into host cells, type IV secretion system; decreased cell ahdesions, assoc w/ ulcers DU and GU)
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10
Q

VacA of H. pylori

A

exotoxin, makes pores in membrane

inhibits T cells

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11
Q

Consequences of H. pylori

A
  • PUD (1-10%)
  • atrophic gastritis
  • gastric cancer (0.1-3%)
  • gastric lymphoma (
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12
Q

What does chronic gastritis look like?

A

mononuclear inflammatory (lymphocytes and plasma cells) cells within the lamina propria

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13
Q

What augments risk of progression from superficial gastritis to gastric atrophy and adenocarcinoma?

A

presence of genes like CAG island and vacA encoding virulence factors in H. pylori

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14
Q

H. pylori infection and duodenal ulcer

A

ANTRAL predominant infection–> acid secretion and DU (gastric metaplasia in duodenum; H. pylori colonize duodenum–> inflammation–> cell damage–> ulcer)

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 (prepyloric biopsy, high sens/spec)
  • rapid urease test: sens 90%, spec 95%

No mucosal biopsy:

  • blood antibody test (sens 85%, spec 79%; positive with prior infection)
  • ***stool antigen test (sens/spec 95%)
  • urea breath test-Ammonia (sens/spec 95%)
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16
Q

Treatment of H. pylori infection

A

Triple therapy:
PPI+clarithromycin+ amoxicillin 10-14 days
test for H pylori stool antigen

Rescue quadruple therapy: PPI+metronidazole + tetracycline + bismuth

When?
PUD
Gastric lymphoma
FH of gastric carcinoma
?whenever diagnosed?
17
Q

Other causes of gastritis

A

Non-H pylori infection uncommon
Immunosuppressed: CMV, candidiasis, aspergillosis, strongloides

Eosinophilic:
can have ulceration
early satiety, nausea, vomiting
increased eos in the blood
rare, cause unknown
18
Q

thickened gastric folds

A

H pylori
Neoplasia
Menetrier’s Disease: VERY rare, inc mucus secretion, decreased acid, abd pain, wt loss, bleeding, hypoalbuminemia

lymphocytic infiltration
acid hypersecretory states (gastrinoma– ZE syndrome)

19
Q

Gastropathies

A 
(non inflammatory epithelial cell injury)
-gastroduodenal inj in absence of signif inflammation:
NSAIDs
Ethanol
Stress 
Ulceration
Cocaine
Bile Reflux
20
Q

Ethanol Gastropathy

A

Similar to early NSAID type injury
Disrupts mucosa
Increased acid secretion

PUD with high concentration (>10%), high amounts of use, NSAID use

21
Q

Gastric Protective Mechanisms

A 
All are PG dependent:
Mucous layer thickness
Cell membrane hydrophobicity
Bicarbonate secretion
Mucosal blood flow
Epithelial Cell migration/proliferation
22
Q

NSAIDs and GI SE

A

COX-1 (constitutive): PG–> E2 protection of gastric mucosa, I2 hemostasis
COX2 (inducible): PG–> pain, inflammation, and fever

Sx: heartburn, n/v, abd pain
Mucosal lesion: 20% in 3 months
GI complications: eg perforated ulcers or GI bleeding

(ulcer goes into submucosa)

23
Q

Peptic ulcer disease

A 
Lifetime prevalence 5-10%
Most asymptomatic
Depends on H. pylori
GU prevalence: male=female
DU prevalence: male>female
Increased incidence in COPD, cirrhosis, chronic renal failure, post-transplantation, smokers
Decreasing incidence of non-NSAID ulcers
24
Q

Assoc of H pylori with PUD

A

High prevalence of H. pylori in patients with PUD
H. pylori infection precedes ulcer
Cure of infection usually cures the ulcer

H. pylori proteins cause inflammation, apoptosis, disrupt cell adhesion…

25
Q

Stress ulcers

A 
ICU patients:
CNS injury (Cushing’s ulcer)
Burns (Curling’s ulcer)
Prolonged mechanical ventilation >48h
Coagulopathy

Fundus and body

Impaired mucosal protection

Increased acid secretion

26
Q

Peptic ulcer complications

A

-Abdominal Pain
-Anemia
Fe deficiency from chronic blood loss
Acute bleeding
-Bleeding in 30%
-Acute bleed
Hematemesis-vomiting blood
Melena-black tarry malodorous stool
Perforation 5% lifetime
Gastric Outlet Obstruction-Duodenal Ulcer

27
Q

Treatment of severe PUD

A

Acute Bleeding:
IV resuscitation–> restore intravascular volume
Acid suppression-PPI drip: Improves clotting
Endoscopy
Angiography-coils
Surgery

Perforation: Surgery

28
Q

Treatment for PUD

A

PPI therapy:
Ulcer Healing 4-8 weeks

H. pylori test and treat
Confirm clearance if H.pylori positive

Risk factor avoidance
NSAIDs, Smoking
Chronic PPI if NSAID necessary-cardiac disease

29
Q

Gastric polyps

A

Hyperplastic
found near gastritis-ulcer
rare malignant potential (>1cm)

Adenoma
Premalignant
FAP

Fundic gland polyps
chronic PPI use-benign
unrelated to H.pylori

30
Q

Gastric adenocarcinoma

A

2nd most common cancer worldwide/2nd most common cause of cancer death

31
Q

Gastric cancer treatment

A

Surgery
endoscopic removal for Stage O
Chemotherapy
Radiation therapy

32
Q

GISTs

A

stromal tumor that is the most common mesenchymal tumor of the stomach (60%). Leiomyomas, etc. are NOT GISTs
Prognosis (worse) and treatment (Gleevec) different than other stromal tumors

cell of origin: interstitial cell of Cajal (pacemaker)

Positive for c-kit (CD117) mutation in transmembrane receptor tyrosine kinase (RTK)
10-30% malignant (intra-abdominal spread or liver)
Treated with surgery, imatinib (small molecule RTK inhibitor)

33
Q

Gastric carcinoid

A 
Neuroendocrine Tumor
Annual 1:1,000,000
Found in fundus/body
Autoimmune atrophic gastritis:
-Hypochlorhydria
elevated gastrin-->stimulates ECL cells
antrectomy
ZE syndrome (gastrinoma) MEN1
-elevated gastrin-->stimulates ECL cells

Sporadic
More dangerous

34
Q

MALT lymphoma

(mucosa assoc lymphoid tumor)

A

Low grade B-cell lymphomas arise in gastric MALT stimulated by H. pylori infection.
Eradication of H. pylori can sometimes induce regression of lymphoma

My DEMS I (26 decks)

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