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Hannah MS2 GI > stomach > Flashcards

stomach Flashcards

1
Q

signs and sx of acute gastritis

A
  • neutrophils present
  • sx: N/V, epigastric pain
  • damage = superficial inflammation possibly leading to erosion or ulcer
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2
Q

___ is an important step in the diffuse type of gastric adenocarcinoma

A

loss of E-cadherin

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3
Q

does PUD relate to an increased risk of gastric cancer?

A

no but surgery of PUD with partial removal does

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4
Q

genetic causes of diffuse gastric adenocarcinoma

A

CDH1 mutation (decreased function) - suppose to encode E-Cadherin proteins

*mainly diffuse type

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5
Q

referred pain associated with both types of PUD

A

back, LUQ, and chest (if penetrating ulcer)

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6
Q

population associated with gastric adenocarcinomas

A

Japan, chile, costa rica, eastern europe

-also poor people and people with multifocal atrophy and intestinal metaplasia

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7
Q

2 types of non stress related GI lesions leading to gastric bleeding

A
  1. GAVE dz (watermelon stomach)
    - associated with cirrhosis and systemic sclerosis
  2. Dieulafoy lesions (unbranched large submucosal A. at the lesser curve GEJ, that with epithelial erosions (maybe by NSAIDs) can lead to bleeding
    - associated with NSAIDs, and other erosive causes
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8
Q

what is a MALToma and what is the histo characteristics

A

-extranodal marginal zone B cell lymphoma

histo: LYMPHOEPITHELIAL LESIONS (neoplastic lymphocytic infiltrate in gastric glands)
- markers: CD19 and CD20

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9
Q

what tumor arises from the interstitial cells of CAJAL

A

GIST tumors

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10
Q

3 types of stress related GI lesions that lead to gastric bleeding

A
  1. stress ulcer (seen in pts with shock, sepsis, severe trauma, and are in the ICU)
  2. curling ulcer (in proximal duodenum and due to burns)
  3. cushing ulcer ( increased intracranial pressure leads to increased alcid secretion–>ulceration–> increased risk of perforation and bleeding)
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11
Q

ulcer form from destruction of ____; and what are the components of an ulcer

A

the mucosa layer

mucosa- necrotizing debris (N)
submucosa- inflammation (I)
granulation tissue (G)
Fibrotic scarring (S)

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12
Q

MALToma is associated with what pathology

A

chronic H. pylori gastritis

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13
Q

how does increased intracranial pressure (as seen in a cushing ulcer) cause acute gastritis

A

(increases vagus stimulation–> increases Ach–>increases acid production–> acid damage)

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14
Q

hallmarks if gastric ulcer (GU)

A
  • MC on lesser curve of antrum
  • MCC is H.pylori, others are NSAIDS and bile reflux
  • sx: Pain that WORSENS with meals and at night, N/V, bloating, belching, wt. loss
  • posterior wall rupture = bleeding from LEFT. GASTRIC A.
  • *MUST RULE OUT MALIGNANCY
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15
Q

where are G cells located and what are there function

A

in the antrum and release gastrin (which stimulates parietal cells to secrete HCL acid)

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16
Q

function of PGE in the stomach

A

decrease acid
stimulate mucus and bicarb secretion
increase blood flow to barrier

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17
Q

what are the three types of polys associated with gastric adenocarcinoma

A
  1. fundic gland polyps (seen in syndromic FAP, or chronic PPI use)
  2. gastric adenomas
  3. inflammatory/ hyperplastic polyps (MOST COMMON)-pts 50-60 yo; can be caused by chronic H. Pylori gastriis
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18
Q

virulence factor of H. Pylori

A

urease (decreases acidity) , flagella, adhesions, CagA toxin

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19
Q

what type of gastric adenocarcinoma = signet ring cells and no precursor lesions, but does have desmoplasia with resulting thickening of stomach wall (linitis plastica)

A

diffuse type
*signet rings cells ( cells with nucleus pushed to side) diffusely infiltrate

desmoplasia = cancer + reaction to cancer

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20
Q

3 factors that increase stomach acidity

A

Ach
Gastrin
histamine

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21
Q

HISTO: antral mucosa= reactive gastropathy with dilated capillaries containing fibrin thrombi

A

GAVE Disease

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22
Q

infiltrate seen with AI chronic gastritis

A

T/B cells and Macrophages

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23
Q

hallmarks of Chronic H.Pylori Gastritis

A
  • intraepithlial neutrophils and sub epithelial PLASMA cells
  • thickend rural folds
  • increased acid production
  • AB to H.Pylori
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24
Q

gastropathy key feature

A

no inflammatory cells

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25
Q

genetic cause of intestinal gastric adenocarcinoma

A

-increased WNT signaling–> LOF mutation in APC, GOF mutation in B catenin,

26
Q

NL damaging factors of gastric mucosa

A
  1. gastric acidity

2. peptic enzymes

27
Q

what are the two types of hypertrophic gastropathys and the basic principle of hypertrophic gastropathy

A
  1. Zollinger Ellis Syndrome (ZES)
  2. Menetrier DZ

= giant “cerebriform” enlargement of RUGAL FOLDS due to epithelial hyperplasia from excess growth factors **(hyperplasia WITHOUT inflammation) **

28
Q

what pathology is associated with MEN1 ? and what is MEN1?

A

ZES and therefore ZES caused Duodenal ulcers and carcinoid tumors

-MEN1 = the 3 P’s (pituitary tumor, pancreatic tumor, and increased PTH from hyperparathyroidism

29
Q

what cause impaired defenses of gastric mucosa:

A
  1. shock (decrease Blood flow)
  2. ischemia (decrease blood flow)
  3. NSAIDs (decrease PGE)

“SIN”

30
Q

ZES

A

location: fundus (pancreas or SI as well)
- gastrin secreting tumor that causes an increase in parietal cells (doubling of oxyntic mucosal thickness), and mucous neck cell hyperplasia, and increase endocrine cells (Gcells)
- sx: duodenal ulcer, chronic diarrhea, possible GI BLEED
- no increased risk of adenocarcinoma but increases risk of Carcinoid tumor
* *SEE neutrophils infiltrate
* *ASSOC WITH MEN1

31
Q

cause of acute gastritis

A

imbalance of protective barrier and defensive factors leading to acidic damage

32
Q

most common translocation associated MALToma

A

11;18 q21;q21

33
Q

most common cause of pernicious (B12 deficient) anemia

A

Autoimmune chronic gastritis

34
Q

what is the most common stomach malignancy

A

gastric adenocarcinoma

35
Q

complications of both types of PUD

A

iron deficiency anemia, hemorrhage (bleeding), perforation, and obstruction
*BLEEDING CAN BE LIFE THREATENING

36
Q

risk factors of acute gastritis

A
  1. severe burn (curling ulcer)
  2. NSAIDs
  3. Heavy alcohol
  4. chemo
  5. increased intracranial pressure (cushing ulcer)
  6. shock
  7. high altitudes (decreases oxygen)
37
Q

NL protective factors of the stomach barrier (and what produces them if applicable)

A
  1. mucus (from foveolar cells in cardia/antrum)
  2. bicarbonate (from foveolar cells)
  3. blood flow
  4. epithelial barrier
  5. epithelial regeneration
  6. prostaglandins (PGE2)
38
Q

prognosis of GIST tumor

A

related to:

  1. size
  2. mitotic index
  3. location
39
Q

cancers associated with AI chronic gastritis vs H.Pylori type

A

AI: Carcinoid Tumor, and adenocarcinoma

H.P: MALToma, and adenocarcinoma

40
Q

most common location of Chronic H.Pylori Gastritis

A

antrum

can extend to body and fungus but is PATHCY, where AI type is diffuse in this location

41
Q

what is the most common mesenchymal tumor of the abdomen

A 
GIST tumor (gastrointestinal stromal tumor) 
(1/2 of them occur in the stomach)
42
Q

unique hallmarks of AI chronic gastritis

A

-Ab vs Parietal cells and IF
-decrease pepsinogen I
-achlorydia (no acid production)
-Hypergastrinemia
-G-cell (endocrine) hyperplasia
-Rugal folds are lost
-DIFFUSE mucosal atrophy with intestinal metaplasia
-B12 deficient megaloblastic pernicious anemia
(leading to CNS disturbances of peripheral neuropathy and spinal cord lesions; as well as glossitis)

*demyelination of dorsal and lateral tracts

43
Q

similar to other forms of gastric dysplasia, ______ almost always occur on a background of chronic gastritis with atrophy and intestinal metaplasia

A

gastric adenomas

  • 50-60 yo
  • 3x male>female
  • risk is associated with size of lesion (if > 2cm significantly increased risk)
44
Q

injury factors that damage gastric mucosa

A
  1. H.pylori
  2. alcohol
  3. duodenal gastric reflux
  4. tabacco
  5. acid (hyperacidity; possibly from gastrinoma)
  6. NSAIDs

“HAD TAN”

45
Q

where is gastric wall thickening “leather bottle” and diffuse rugal flattening seen

A

diffuse type of gastric carcinoma

46
Q

what population do you see GIST tumors in

A
  • MC 60 yo
  • uncommon in kids but associated with Carney triad in young girls (gastric GIST, paraganglioma, pulmonary chondroma)
  • assoc with neurofibromatosis type 1
47
Q

pathogenesis of autoimmune chronic gastric

A

-type 4 hypersensitivity reaction leading to CD4+ T-cell mediated destruction of parietal cells (H+/K+ ATPase) in the BODY and FUNDUS
(parietal cells make HCL and IF; i.e. make stomach acid and allow absorption of B12)

48
Q

hallmarks of duodenal ulcer (DU) (most common ulcer)

A
  • EGD= brunner gland hypertrophy (duodenal glands that secrete acid neutralizing factors in response to gastric acid entering SI)
  • most commonly due to H.pylori but can be caused by ZES (from increased acid secretion)
  • usually on anterior doudenum, but can be posterior and rupture leading tp bleeding from the GASTRODUODENAL A. or cause acute pancreatitis
  • sx: epigastric pain that IMPROVES with meals (bc of neutralizing secretions from Brunners gland),N/V, bloating, belching, wt. loss
49
Q

even though the most common site of a carcinoid tumor is in the small intestine, what are associated pathology with gastric carcinoid tumors

A

AI chronic gastritis, ZES (MEN1), and phi use

-all these factors increase G cells (endocrine cells)

50
Q

what type of gastric adenocarcinoma = bulky masses of a large irregular ulcer with heaped up margins, and most commonly presents at antrum lesser curvature (like a GU) * precursor lesions of flat dysplasia, adenoma, Menetrier, or polyps

A

intestinal type (most common type)

-other risks = intestinal metaplasia from chronic and AI gastritis, nitrosamines, blood type A, male

51
Q

Menetrier Disease

A

Location: body and fundus

  • diffuse foveolar (MUCUS) cell hyperplasia, and hyponatremia (leading to anasarca) due to increase TGFa
  • sx: wt loss, diarrhea, peripheral edema–> anasarca
  • NO GI BLEED
  • in kids it tends to follow a respiratory infection
  • in adults it increases the risk of ADENOCARCINOMA
52
Q

what are precursor lesions of gastric adenocarcinomas

A

gastric dysplasia and adenomas

53
Q

what is the carney triad

A
  1. Gastric GIST
  2. extra- adrenal paragangliomas
  3. pulmonary chondroma
    seen in young girls
54
Q

solitary chronic mucosal ulcerations

A

Peptic ulcer disease (PUD)

55
Q

two branches/causes of chronic gastritis

A
  1. Autoimmune Chronic gastritis

2. H.pylori Chronic gastritis

56
Q

benign vs malignant ulcer in PUD

A 
benign = sharp punched out margins
malignant= heaped up margins
57
Q

risk factors of PUD

A

cigarette smoking, H.Pylori, and NSAIDS

58
Q

GAVE Disease

A

-aka “watermelon stomach”
(nonstress source of UGIB)
(gastic antral vascular ectasia)

  • EGD: longitudinal stripes pf edematous red mucosa (made by ectatic mucosal vessels) alternating with severely injured paler mucosa
  • HISTO: antral mucosa= reactive gastropathy with dilated capillaries containing fibrin thrombi
  • ASSOC: Cirrhosis, systemic sclerosis
  • sx: occult fecal blood, iron def anemia
59
Q

when is gastric adenocarcinoma usually dx and where does it metastasize

A
  • usually dx in late stage when metastases has already occurred
  • sites: Virchow Node (Left supraclavicular LN);
    intestinal: Sister Mary Joseph LN (periumbical)
    diffuse: Irish LN ( left axillary) ; Krukenberg tumor (BL Ovary) , “Pouch of douglas” - aka rectouterine pouch (Blumer Shelf = palpable shelf during DRE of rectouterine pouch)
60
Q

what genes are associated with GIST

A

GOF mutation in KIT gene

mutation in PDGFRA

61
Q

-intraepithlial neutrophils and sub epithelial PLASMA cells = hallmark off

A

H.pylori Chronic gastritis

62
Q

what is intestinal metaplasia

A

loss of parietal cells with increased goblet cells

Hannah MS2 GI (10 decks)

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