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Hannah MS2 GI > stomach > Flashcards

stomach Flashcards

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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
genetic cause of intestinal gastric adenocarcinoma
-increased WNT signaling--> LOF mutation in APC, GOF mutation in B catenin,
26
NL damaging factors of gastric mucosa
1. gastric acidity | 2. peptic enzymes
27
what are the two types of hypertrophic gastropathys and the basic principle of hypertrophic gastropathy
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
what pathology is associated with MEN1 ? and what is MEN1?
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
what cause impaired defenses of gastric mucosa:
1. shock (decrease Blood flow) 2. ischemia (decrease blood flow) 3. NSAIDs (decrease PGE) "SIN"
30
ZES
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
cause of acute gastritis
imbalance of protective barrier and defensive factors leading to acidic damage
32
most common translocation associated MALToma
11;18 q21;q21
33
most common cause of pernicious (B12 deficient) anemia
Autoimmune chronic gastritis
34
what is the most common stomach malignancy
gastric adenocarcinoma
35
complications of both types of PUD
iron deficiency anemia, hemorrhage (bleeding), perforation, and obstruction *BLEEDING CAN BE LIFE THREATENING
36
risk factors of acute gastritis
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
NL protective factors of the stomach barrier (and what produces them if applicable)
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
prognosis of GIST tumor
related to: 1. size 2. mitotic index 3. location
39
cancers associated with AI chronic gastritis vs H.Pylori type
AI: Carcinoid Tumor, and adenocarcinoma H.P: MALToma, and adenocarcinoma
40
most common location of Chronic H.Pylori Gastritis
antrum | can extend to body and fungus but is PATHCY, where AI type is diffuse in this location
41
what is the most common mesenchymal tumor of the abdomen
``` GIST tumor (gastrointestinal stromal tumor) (1/2 of them occur in the stomach) ```
42
unique hallmarks of AI chronic gastritis
-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
similar to other forms of gastric dysplasia, ______ almost always occur on a background of chronic gastritis with atrophy and intestinal metaplasia
gastric adenomas - 50-60 yo - 3x male>female - risk is associated with size of lesion (if > 2cm significantly increased risk)
44
injury factors that damage gastric mucosa
1. H.pylori 2. alcohol 3. duodenal gastric reflux 4. tabacco 5. acid (hyperacidity; possibly from gastrinoma) 6. NSAIDs "HAD TAN"
45
where is gastric wall thickening "leather bottle" and diffuse rugal flattening seen
diffuse type of gastric carcinoma
46
what population do you see GIST tumors in
- 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
pathogenesis of autoimmune chronic gastric
-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
hallmarks of duodenal ulcer (DU) (most common ulcer)
- 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
even though the most common site of a carcinoid tumor is in the small intestine, what are associated pathology with gastric carcinoid tumors
AI chronic gastritis, ZES (MEN1), and phi use -all these factors increase G cells (endocrine cells)
50
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
intestinal type (most common type) -other risks = intestinal metaplasia from chronic and AI gastritis, nitrosamines, blood type A, male
51
Menetrier Disease
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
what are precursor lesions of gastric adenocarcinomas
gastric dysplasia and adenomas
53
what is the carney triad
1. Gastric GIST 2. extra- adrenal paragangliomas 3. pulmonary chondroma seen in young girls
54
solitary chronic mucosal ulcerations
Peptic ulcer disease (PUD)
55
two branches/causes of chronic gastritis
1. Autoimmune Chronic gastritis | 2. H.pylori Chronic gastritis
56
benign vs malignant ulcer in PUD
``` benign = sharp punched out margins malignant= heaped up margins ```
57
risk factors of PUD
cigarette smoking, H.Pylori, and NSAIDS
58
GAVE Disease
-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
when is gastric adenocarcinoma usually dx and where does it metastasize
- 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
what genes are associated with GIST
GOF mutation in KIT gene | mutation in PDGFRA
61
-intraepithlial neutrophils and sub epithelial PLASMA cells = hallmark off
H.pylori Chronic gastritis
62
what is intestinal metaplasia
loss of parietal cells with increased goblet cells

Hannah MS2 GI (10 decks)

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