GI - Crohn's and Colitis Flashcards

1
Q

what does IBS stand for

A

irritable bowel syndrome

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

does IBS come with inflammation

A

no

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

what does IBD stand for

A

inflammatory bowel disease

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

what are 2 types of IBD

A

ulcerative colitis and crohns disease

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

what is the major difference with IBD and IBS

A

IBD has inflammation, IBS does not

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

how do IBS epithelial cells function appear

A

to be normal

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

which subset of population gets more IBS

A

women before 35

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

is IBS chronic

A

yes

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

what are 5 possible causes of IBS

A

food sensitivities, stress, bacterial infection, hormones, alteration of 5-HT reuptake into neurons

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

what does increased GI motility lead to

A

diarrhea

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

what does decreased GI motility lead to

A

constipation

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

how do you generally try to treat IBS

A

symptomatically

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

what are 3 symptom treatments for IBS

A

diet, stress, laxatives/antidiarrheals

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

what drug do you use for constipation dominant IBS

A

lubiprostone

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

what is lubiprostone used for

A

drug for constipation dominant IBS

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

what is the mechanism of lubiprostone

A

binds to EP4 receptors, increase cAMP, activate CFTR (Cl-), stimulates fluid secretion

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

what is the structure of lubiprostone

A

analogue of PGE1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what does lubiprostone do to transit of gut contents

A

speeds up

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

how does lubiprostone speed up gut (physically, not like receptor stuff)

A

increases fluid in stool to stretch gut and speed it up

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what happens when lubiprostone activates EP4 receptors

A

increase cAMP and activate epithelial Cl- channels (CFTR) to stimulate fluid secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

how does Cl- channel activation stimulate water secretion

A

Cl- movement creates an osmotic gradient, H2O and other electrolytes flow passively from the ECF into the lumen through channels

21
Q

why is lubiprostone selective for the gut

A

because it is poorly absorbed

22
Q

what is ulcerative colitis

A

inflammatory disorder causing ulcers in the lining of rectum and colon

23
Q

where do ulcers form in ulcerative colitis

A

where inflammation leads to cell death (cells die in mucosa)

24
Q

what is the main symptom in ulcerative colitis and why

A

diarrhea because colon inflammation in colon causes frequent emptying

25
Q

which layer gets cell death in ulcerative colitis

A

in mucosa (closest to lumen)

26
Q

what is the diff with ulcerative colitis and crohns disease

A

in crohns, inflammation is deeper in intestinal wall and occurs in other parts of GI tract (SI, mouth, esophagus, stomach)

27
Q

does ulcerative colitis associate with increase cancer risk

A

yes

28
Q

does crohns associate with increase cancer risk

A

yes

29
Q

how do you treat UC and crohns

A

long term anti-inflammatories and immunosuppressant drugs

anti-diarrheals for symptoms

30
Q

why do you use anti-diarrheals for UC and crohns

A

for symptomatic relief, but it does not affect etiology of the disease (doesnt cure)

31
Q

what are glucocorticoids

A

potent anti inflammatory and immunosuppressant agents

32
Q

how does prednisolone work

A

binds to members of nuclear receptor superfamily, modifties gene transcription

33
Q

what stages of inflammation does prednisolone inhibit

A

all of them

34
Q

what is an example glucocorticoids

A

prednisolone

35
Q

how do you use prednisolone for mild UC

A

rectal enemas (local inflammation, systemic steroids is not ideal)

36
Q

how do you use prednisolone for severe UC and crohns

A

it is given orally

37
Q

what is the pro and con for using prednisolone

A

it can induce remission but long term use is nad

38
Q

what are aminosalicylates used for

A

maintenance of remission of both UC and crohns disease

39
Q

what is an example of aminosalicylates

A

sulfasalazine

40
Q

is sulfasalazine absorbed well in the drug

A

no

41
Q

what happens once sulfasalazine is in the colon and why

A

5-ASA is released in the colon by bacteria

42
Q

what are the 2 things that sulfasalazine breaks into

A

5-ASA and sulfapyridine

43
Q

what is a type of person that shouldnt take sulfasalazine + why

A

antibiotic allergies (cause sulfapyridine)

44
Q

what are 3 things that sulfasalazine does that is good

A
  • localized anti-inflammation
  • scavenges free radicals
  • inhibits prostaglandin synthesis
45
Q

what does sulfasalazine do to prostaglandin synthesis + why important

A

inhibit cause that can cause inflammation

46
Q

what is the mechanism of action of sulfasalazine

A

localized anti-inflammatory actions including scavenging of free radicals and inhibition of prostaglandin synthesis

47
Q

sulfasalazine cannot be used by persons with allergies to what?

A

sulphonamides, class of antibiotics

48
Q

what is mesalazine

A

just 5-ASA on its own

49
Q

what are biologicals

A

humanized antibodies targeting components of the inflammatory pathway

50
Q

what are 3 main targets for biologicals

A
  • TNF-alpha
  • anti-alpha4beta7 integrin on T-helper lymphocytes
  • anti-protein subunit of IL-12 and IL-23