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GI > stomach > Flashcards

stomach Flashcards

1
Q

R vagus

A

posterior wall

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2
Q

L vagus

A

anterior wall

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3
Q

layers of stomach

A 
mucosa
lamina propia/deep mucosa
submucosa
muscularis- inner oblique, middle circular, outer longitudinal
serosa
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4
Q

body/fundus is lined by what type of mucosa

A

oxytinic–>secretes acid

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5
Q

antrum/pyloris + mucosa

A

pyloric- gastrin

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6
Q

submucosa

A

deep connective tissue- colllagen/elastin

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7
Q

what makes up oxytinic cells

A 
surface mucous cells
mucous neck cells
parietal cells at neck
chief cells at base
endocrine cells- ECL (histamine), D cells-somato
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8
Q

3 fx of stoamch

A

reservoi
digeston
controlled emptyings

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9
Q

surface/ncek mucous cells

A

HCO3, mucous

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10
Q

parietal cells

A

H+

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11
Q

chief cells

A

lipases

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12
Q

antrum

A

g cells, surface and mucus, d cells

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13
Q

3 known parietal stimulants

A

Ach
gastrin
histamine

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14
Q

alkaline tide

A

HCO3- recycled from hcl generation and gose to surface mucosa to be usd to protec gastric ucosa

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15
Q

agents that disturb barrier of neutralization

A

weak acids
alcohol
NSAiDS
detergents

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16
Q

three pathways mediting response to a meal

A

endocrine- sensor villi
neurocrine neve stim
paracrine- histamine, CCk somato

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17
Q

what drives the cephalic phase

A

parasymp (vagus) secreting Ach and GRP

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18
Q

two things driving gastric phase

A

fundal distention–>mechanoR–>increase parietal cell secretion
vagally-mediatd arch (parietal and g cells)

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19
Q

low ph inhibits

A

gastrin

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20
Q

intestinal phase

A

mediated by chyme entry into duodenum around 1st hr post-meal–>slows gastric emptying and decreases acid secretion passively (decrease distention) and actively by inhibitors

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21
Q

aminoacids in small intestine

A

stimulate release of gastrin

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22
Q

secretin, Gip

A

inhibit gastric acid secretion

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23
Q

cells in isthus

A

suface mucous- insoluble visible mucous and HCO3- to form protective mucous gel neutralizatio zone

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24
Q

neck cells

A

ucous neck cells
parietal cells
stem cells

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25
Q

base cells

A

chief cells- pepsinogen & gastric lipase
ECL cells-histamine
D cells- somatostatin

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26
Q

SMS is inhibited by

A

vagal stim

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27
Q

duodenal gland cells

A

icell, s cell, Gip

28
Q

CCK

A

in response to AA and FAs

inhibits gastric emptying

29
Q

secretin

A

inhibits H+ secretion by parietal cells

promotes bicarb secretion by panc

30
Q

Gip

A

inhibits h+ secretion from gastric parietal cells

31
Q

when is hemorrhage most likely

A

posterior penetrating duodenal ulcer

32
Q

perforation

A

anterior penetrating duodenal or gastric ulcer

33
Q

gastric ulcers commonly

A

lesser curvature of stomach at junction of antrum and body or in pre-pyloric region of antrum

34
Q

duodenal main location ulcer

A

duodenal bulb

35
Q

jejunal ulcer often secondary to

A

zollinger-ellison syndrome

36
Q

tests for hyplori

A

bx-rapid urease test
urea breath test
serum Ab to H pylori
stool antigen test

37
Q

how do nsaids cause ulcers

A

pGE2 fro cox 1–>increase mucus secretion, increase mucosal blood flow, increase HCO3-

increase epitelial cell restitution and proliferation

38
Q

tx of ulcers

A

antacids
decrease acid production (h2ra, ppi)
increase mucosal protection (dec drugs, stop smoking, increase dissacharides, increase PGE2)
eradicate hplori

39
Q

SE NaHCO3

A

alkalosis, hyperNa

40
Q

CaCo3 SE

A

increase Ca–> more gastrin

41
Q

AlOH3 SE

A

constipating, binds to PO4 (bone pain), binds drugs

42
Q

MGOH2

A

cathartic

43
Q

what is diff about cimetidine vs rani, fom, & nizatidine (h2ra)

A

cimetidine interacts with CP450

anti-androgen–>gynecomastia, mental confusion

44
Q

best tx ulcers

A

ppi

45
Q

tx for hpylori

A

bismuth + tetra or metronidazole

amoxi/clarithomycin

46
Q

zonger ellison syndome

A

gastrinoma- lots of gastrin

diarrhea, steatorrhea due to low pH overload–>inact of lipases

main place is duodenal wall, bu also panc

47
Q

ZES gastrinomas often part of

A

MEN1 syndrome

48
Q

dx ZES

A

give secretin

49
Q

cushing ulcer

A

due to intracranial trauma

50
Q

posterior duo ulcers have potential to

A

perforate into pancreas–>pancreatitis

51
Q

important to bx gastric ulcer to rule out

A

carcinoma

52
Q

acute erosive gastritis

A

more advanced gastrics w/ erosion of tissue above muscularis

53
Q

curling ulcer

A

urns

54
Q

stress ulcer

A

extends to submucosa- burns ,shock, trauma

55
Q

stess ulcer tset

A

hemoccult + pos stools + visible change on EGF

56
Q

type a chronic gastritis

A

affects fundus and body, spares antrum

typically autoimmune

57
Q

type b chronic gastritis

A

typically secondary to h pylori infection

antrum predom

58
Q

types of gastric malignancies

A

carcinoma
lymphoma
neuroendocrine/carcinoid tumor
stromal tumor–intestinal cell of cajal

59
Q

types of gastric carcinomas

A 
intestinal type (from dysplasia of gastric cells)
diffuse type (de novo)
60
Q

px of gastric adenocarcinoa

A

early- does not penetrate muscularis

late- does

61
Q

diffuse tumor gies what sign

A

krukenberg- ovarian met, usually bilateral

signet ring

62
Q

other gastric adenocarcinoma distant sign

A

virchow’s
sister mary joseph sign
leser-trelat sign–explosive onset of multiple seb kertaoses

63
Q

TYPES of gastric lymphoma

A

chronic h pylori

b cell lymphoma of MALT lymphomas– can progress to NHL

64
Q

ealy vs late gastric lymphoma

A

early: t cell dep; h pylori–> t cells–> b cells
**need abx
later stages: t cell indep, t{11:18)

65
Q

gastric carcinoids

A

indolent edocrine tuors–ECL cells in oxytinic ucosa

66
Q

Gi stromal tumor

A

pacemaer cajal cells

pos for act mutation in ckit (CD117) and PDGFRa tyrosine kinase

GI (12 decks)

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