Gastritis Flashcards

1
Q

sign of past ulcers in stomach?

A

radial scarring

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2
Q

are there normally inflammatory cells in the lamina propria of the stomach?

A

No.

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3
Q

2 ways that stomach protects itself from it’s own acid:

A

bicarbonate mucous ‘gel’ layer

hydrophobic monolayer

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4
Q

5 things that damage stomach mucosal barrier:

A
H/Pylori
aspirin
NSAIDS
bile
alcohol
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5
Q

What is the role of prostaglandins in stomach mucosal barrier? 4 things

A

inhibit acid secretion
stim bicarb, mucous
increase blood flow
modify inflam

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6
Q

Acute gastritis lasts how long usually?

A

a few days

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7
Q

How long does it take for stomach to heal? why?

A

24-48 hours due to constant regeneration

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8
Q

does H pylori heal spontaneously after progressing to chronic?

A

Nope./

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9
Q

Shock or sepsis can do what to stomach?

A

acute gastritis

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10
Q

neutrophils with erosion?

A

not much bro.

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11
Q

Chronic superficial gastritis bacterial infections you see more what?

A

plasma cells

eosinophils

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12
Q

All people in ICU are put on what?

A

proton pump inhibitors

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13
Q

When does an erosion become an ulcer?

A

once it goes below the muscularis mucosae

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14
Q

defining feature of chronic ulcer?

A

fibrosis in the deep layers

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15
Q

acute Ulcers in proximal duodenum from what?

A

severe burns/trauma

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16
Q

acute Ulcers in gastric and duodenum from what? called what?

A

intracranial injury. Cushing ulcers.

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17
Q

proximal duodenal ulcers are called what?

A

Curling ulcers

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18
Q

if you get subactue gastric ulcer with erosion of artery, what clinical manifestation do you see?

A

haemetemesis

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19
Q

What are the 3 main types of chronic gastritis?

A

autoimmune (rarer)
H.Pylori
Chemical

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20
Q

What happens in Autoimmune gastritis?

A

destruction of acid secreting tubules of parietal cells

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21
Q

No parietal cells also mean no intrinsic factor which means?

A

decreased B12 absorption and defiency

22
Q

What is spared in autoimmune gastritis?

A

antrum of stomach

23
Q

no parietal cells>hypergastriaemia>linear/nodular hyperplasia> increased risk of?

A

carcinoidosis

24
Q

How else can B12 be interfered with in autoimmune gastritis?

A

IF-Ab secretion complexes with B12 preventing absorption

25
Q

What are ECL cells?

A

neuroendocrine cells

26
Q

Chemical chronic gastritis caused by?

A

reflux of bile/alkaline

long term aspirin/NSAIDS

27
Q

What happens to mucosa in Chemical chronic gastritis?

A

disruption of mucus layer

epithelial desquamation

28
Q

what does epithelial desquamation mean in Chemical chronic gastritis?

A

foveolar hyperplasia with elongation of gastric pits

vasodilation and oedema

29
Q

erosions and ulcers in Chemical chronic gastritis?

A

yes

30
Q

H. pylori is linked to 2 things:

A

peptic ulcers

gastric cancers

31
Q

where do H. pylori find their niche?

A

below the mucus bicarb gel layer of stomach

32
Q

Why are H. pylori good at surviving in stomach?

A

motile
have adhesins
have urease

33
Q

Acute H. pylori infections bring what kind of immune response?

A
neutrophilic gastritis
acute inflam (IL-8)
34
Q

What happens to parietal cells after Acute H. pylori infection?

A

transient hypochlorhydria up to 4 months

35
Q

What do antibodies do with Acute H. pylori infection?

A

helps but not curative

36
Q

high infection of Acute H. pylori infection means what 2 things?

A

low rate of clearance

persists for life when established

37
Q

H.Pylori in intercellular junctions?

A

yes when it’s bad

38
Q

H.Pylori for cancer sequence

A
normal
chronic gastritis
atrophic gastritis
intestinal metaplasia
dysplasia
adenocarcinoma
39
Q

in gastric cancer, there are no more specialized cells in walls of stomach, they are replaced by

A

lyphoid follicles with germinal centres

40
Q

in antrum predominant H.Pylori gastritis what happens to acid and results?

A

chronic inflam, polymorphs
H. Pylori colonisation
increased acid
duodenal ulcer

41
Q

in pan-gastritis predominant H.Pylori gastritis what happens to acid and results?

A

reduced acid
chronic inflam, intestinal metaplasia>adenocarcinoma
gastric ulcer

42
Q

What is MALT?

A

mucosa associated lymphoid tissue

43
Q

When do you get B-cell lymphoma of MALT?

A

in H. Pylori chronic pangastritis

44
Q

92% of duodenal ulcer is caused by?

A

H-pylori

45
Q

25% of gastric ulcer is caused by?

A

NSAIDS

46
Q

where is the most common site of peptic ulcer?

A

D1 and antrum

47
Q

3 other common places for peptic ulcers?

A
  1. oesophagus at squamocolumnar junction
  2. gastroenterostomy stoma
  3. Meckel’s diverticulum if H-pylori infected
48
Q

4 layers of chornic peptic ulcer floor?

A
  1. fibrin exudate
  2. narrow zone of fibrinoid necrosis
  3. granulation tissue
  4. fibrosis: endarteritis/hypertrophied nerves
49
Q

4 complications of peptic ulcers

A

perforation (peritonitis/septicaemia)
haemorrhage (haematemesis)
penetration (into adjacent organ)
stenosis (pyloric canal and obstruction)

50
Q

what happens to the muscosal folds with gastric carcinoma?

A

obliterated

51
Q

diffuse-type gastric carcinoma (linitis plastica) looks like?

A

stomach is sharply punched out, no glands for cells and is discohesive.

52
Q

Signet-ring cell carcinoma

A

form of gastric adenocarcinoma