Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Medicine > peptic ulcer diseases > Flashcards

peptic ulcer diseases Flashcards

1
Q

histological layers of the gastric wall?

A 
epithel
lamina propria
muscularis mucosa
sub mucosa
musculris externa
circular
longditual 
serosa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

cells that line the stomach’s glands

A 
foveola- surface mucus 
neck mucus 
parietal
endocrine
cheif
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

parietal cells acid production inducing receptors

A

gastrin (g cells, antrum, endocrine)
achetylcholin (vagus)
histamine (entrochromaffin like cells, paracrine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

which cells responsable for the gastric mucin layer?

A

foveolar cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

most potent acid production inducer in parietal cells

A

histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what stimulates acid prduction in parietal cells (phase wise)

A

chephalic- vagus
gastric- amino acids and distention
small intestine- distantion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

which cell produce pepsin and due to what stimuli?

A

chief cells
gastrin (g cells, antrum, endocrine)
achetylcholin (vagus)
histamine (entrochromaffin like cells, paracrine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

in what PH does pepsin seize to work?

A

greater than 4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

which cell produce histamin and due to what stimuli

A

entero-chromaffin like cells

due to gastrin secreted by G cells (endocrine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

by which cell does G cell regulate negatively ?

A

D cells, somatostatin (paracrine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

to which stimuli does G cell regulate possitivly?

A

food in antrum

achetycholin (vagus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

which cell produce secretin and to what stimuli?

A

s. cells

acidic food in the deodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what do secretin do?

A

increase secrition of bicabonate at pancrease
inhibit gastric motility
decrease bile secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what stimulate CCK release (and from where?)

A

I-cells

indigested FF+ AA in deodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what does CCK do?

A

increase bile secretion

increase pancreatic enzymes flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

pre-epithelial mechanism for mucosal integrity?

A

mucus- bicarbonate

surface active phospholipids layer

17
Q

epithelial cells mechanism for mucosal integrity?

A

tight junctions
ion pumps
cell renewal

18
Q

post-epithelial cells mechanism for mucosal integrity?

A

mucosal blood flow (PGE2, PGI2 vasodialition)

19
Q

which system operates the gastric emptying while fasting?

A

migratory motor complex (every 90min)

20
Q

what does the vaso-vagal reflex do when food enters the stomach?

A

receptive relaxition and accomodition of fundus

later on, perylstasis

21
Q

what is the differance between erosion and ulceration?

A

ulcer involves the sub-mucosa

22
Q

favored area of peptic ulcers?

A

antrum and body of stomach

1st part of deodenum

23
Q

peptic ulcers empidemiology?

A

g.ulcers represent malignancy whilst d.ulcers do not

bening g.ulcers locate typically distal to antrum

H.pyloric associated g.ulcers associate with chronic gastritis

NSAIDS -dont cause chronic gastritis

24
Q

peptic ulcers epidemiology?

A

g.ulcers less common than d.ulcers
M>F
60’s

25
Q

location at which H.pylori is found?

A

deep parts of the mucus layer of the stomach

between epithel layer to mucus layer

26
Q

toxins H.pylori produce?

A

cag A

vaculating cytotoxin a

27
Q

trasmission of H.pylori?

A

oral-oral
facal-oral
usually occurs in first decade of life

28
Q

what can antral predominant gastritis caused by H.pylori

deteriorate to?

A

asymptomatic H.infection
or
dudenal ulceration (HCL production is up)

29
Q

what can non-atrophic pangastritis cause by H.pylori

deteriorate to?

A

asymptomatic H.infection

B-cells lymphoma

30
Q

what can corpus (body) predominant atrophic gastritis cause by H.pylori deteriorate to?

A

asymptomatic H.infection
gastric ulcers
gastric cancer

31
Q

location at which H.pyloric induced gastritis produce most HCL?

A

antral > non-atropic > adenocarcinoma

32
Q

clinical outcomes of H.pyloric inflammation response?

A

d.ulcer
B-cell lymphoma
non cardia gastric adenocarcinoma

33
Q

non invasive H.pyloric tests?

A

serology (not for iradication, after first possitive test all shall be positive ever on)

urea breath test

stool antigen

34
Q

which test wont be used to check for H.pyloric eradication?

A

serology, after first possitive test all shall be positive ever on

35
Q

H.pylori treatment?

A

PPI+ amoxicillin+clarithromicin+metronidazole (10-14 days)

PPI+ Bismuth + tetracyclin + metronidazole (10-14 days)

Medicine (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions