IBD Flashcards

1
Q

what is ibd

A

chronic inflammatory disorder of the Gi tract

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2
Q

what is indeterminate colitis

A

features of both crohns and ulcerative colitis

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3
Q

what is ulcerative colitis

A

disease confined to bowel wall
rectum then progresses proximally up the splenic flexure then the transverse colon and so on
only in terminal ileum, colon, and rectum

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4
Q

CD and UC pathophysiology

A

genetic predisposition with infectious and immunological responses

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5
Q

what is crohns disease

A

extensive destruction of bowel wall, invasion of adjacent tissues
any part of GI tract

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6
Q

crohns signs and symptoms

A

RLQ tenderness, painful with masses

diarrhea with low grade fever

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7
Q

ulcerative colitis signs and symptoms

A
rectal bleeding(very few things cause this so prob UC if present with this) and diarrhea
no masses or specific tenderness
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8
Q

goals of therapy for crohns

A

control acute flares
induce remission
maintain remission
avoid or manage ocmplications

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9
Q

non drug therapy for crohns

A

NSAIDS - increased risk of ulcers, worsens inflammation
stop smoking helps as much as drug therapy
avoid foods that trigger
ensure proper nutrition many people wont feel like eating
may have to avoid dairy because the inflammation can cause the lactase enzyme to be shed and produce lactose intolerance

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10
Q

non drug therapy for UC

A

avoid constipating drugs - can cause the colon to expand and lose the ability to regulate your fluid balance
smoking helps

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11
Q

surgery in crohns

A

reserved for strictures and obstructions as theres an increased risk of recurrence at surgical site

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12
Q

ulcerative colitis surgery

A

cured with colectomy

some post op issues

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13
Q

examples of aminosalicylates

A

sulfasalazine

5ASA (mesalamine)

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14
Q

aminosalicylates MOA

A

prostaglandins
decreased cytokines
free radical scavenging

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15
Q

sulfasalazine AE

A

fever, fatigue, headache, diarrhea, dyspepsia
allergic reactions - SJS
hemolysis, agranulocytosis, thrombocytopenia

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16
Q

mesalamine products to target different sites

A

asacol: released in terminal ileum
pentasa: released in small bowel, can open the capsules (increased diarrhea)

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17
Q

aminosalicylate forms

A

oral, enema, suppository

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18
Q

aminosalicylate 5ASA dosing possibility

A

can give any of the qid 5ASA tablets or capsules as a single daily dose

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19
Q

can you give 5ASA in a patient with an ASA allergy

A

yes

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20
Q

how long to assess clinical response to aminosaliccylates

A

4-8 weeks

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21
Q

lowest dose that can be used for aminosalicylate

A

2g/day

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22
Q

if fail 4.8g of one agent what do you do

A

dont switch to diff 5ASA, pick a different agent

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23
Q

aminosalicylate efficacy in UC

A

remission in some
decrease relapse rate in half the patients
most effective in more distal disease

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24
Q

aminosalicylate efficacy in CD

A

benefit is in the colon not ileal disease

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25
Q

corticosteroid suppository used for

A

proctitis

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26
Q

corticosteroid enema used for

A
left sided (sigmoid/rectum) disease 
for uncontrolled UC
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27
Q

when would you use topical corticosteroids

A

mild-mod left sided UC not controlled with 5ASA

budesonide MMX in mild=mod right side colonic and ileal disease

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28
Q

when do you use systemic corticosteroids

A

treatment for mod-severe UC and CD

good for flares

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29
Q

onset of systemic corticosteroids

A

few days to a week
if fail 1 week have to use big guns
reevaluate in 2 weeks

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30
Q

is there long term use of systemic corticosteroids

A

yes but many problems with long term use, not good to prevent relapse long term
patinets just cant get off them

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31
Q

efficacy of azathioprine and 6mercaptopurine

A

induce and maintain remission
heals fistulas
allows elimination of steroids

32
Q

onset of azathioprine/6mercaptopurine

A

1 month for improvement

3 to see if actually working

33
Q

how does azathioprine and 6mercaptopurine work

A

induces t cell apoptosis

34
Q

describe the break down of sulfasalazine

A

the diazo bond is cleaved by bacteria into sulfapyridine (responsible for the AE) which is rapidly absorbed into circulation form the colon

35
Q

aminosalicylates are not the same as

A

cox 2 inhibitors

36
Q

why is it so important to ensure adherance to aminosalicylates

A

once you go beyond this the next drugs have big time toxicity so want to keep on 5ASA as long as possible

37
Q

problem with buesonide MMX

A

maintaining remission wiht it alone

38
Q

what is thiopurine methyltransferase

A

major regulator of 6 TG concentration

39
Q

____ TPMT activity leads to preferential metabolism of 6 TG (increase efficacy and toxicity)`

A

low

40
Q

how is thiopurine methyltransferase enzyme activity determined

A

genetically

polymorphism

41
Q

exmplain azathioprine breakdown

A

breaks down into 6mercaptopurine then into thioinsinic acid

TPMT breaks that into 6methylmercaptopurine or it breaks down into thioguanine metabolite

42
Q

explain TPMT testing

A

becoming the standard of care

17 mutant allelles but only tests for the most common 3

43
Q

problem with TPMT testing

A

patients with a recent blood transfusion willhave other peoples RBC so may seem like they have normal TPMT when its actually low
have to wait 3 months for the RBC to die???

44
Q

can you rely on the TPMT testing to predict who will have severe myelosuppression from azathiopirine

A

no

STILL HAVE TO DO BLOOD TESTS REGULARLY to ensure myelosuppresssion doesnt happen

45
Q

very important drug interaction to remember

A

azathiopurine and allopurinol

46
Q

SE of AZA 6MP

A
neutropenia
atypical infection  
pancreatitis - first 6 weeks watch for ab or back pain and vomiting 
skin rash 
small increase in maignancies
47
Q

do you need PJP prophylaxis when on AZA

A

not unless also on high dose steroids

48
Q

CBC monitoring for aza

A

weekly for first month then every 2 weeks for month 2 and 3 then every month

49
Q

what do you ask someone getting a drug that needs blood work

A

when theyre getting blood work done not if

50
Q

methotrexate is used fr

A

CD similar results to aza somewhat faster onset but still need a month trial
not used in UC except if refractory to aza

51
Q

methotrexate contraindicated in

A

pregnant women

52
Q

AE of methotrexate

A

neutropenia
atypicla infections
liver dysfunction
pneumonitis

53
Q

dosing with immunomodulator methotrexate

A

no set dosing

54
Q

cyclosporine use

A

severe active UC refusing surgery or have bad surgical risks limited to 6 months use
to brudge patients to aza

55
Q

if a patient fails on methylprednisolone and refuses surgery we use

A

anti TNF

56
Q

how does infliximab work

A

antibody that binds to tumor necrosis factor and induces t cell apoptosis

57
Q

infliximab used for

A

severe active or fistulizing CD
active UC
best data for remission in fistulizing crohns

58
Q

dosing of infliximab and time for response

A

3 doses at 0,2,6 weeks

see a response in the first week

59
Q

how long do people stay on infliximab

A

data for up to 1 year but some people on it indefinitely although we are still learning how long its efficacy and safety lasts

60
Q

what to do if not responding to induction doses of infliximab

A

no benefit in continuing into maintenance therapy with the same agent

61
Q

what to do if not responding to the first anti tnf agent

A

evidence of benefit in trying another one though response is lower than in the anti TNF naive

62
Q

infliximab SE

A

nausea
URT infections
GI pain
infections - impairment of IS, TB reactivation, too rapid closure of fistulas
allergic reactions
infusion related reactions - headache, flushing, dizzy

63
Q

infliximab long term issues

A
infections - tuberculosis 
malignancies
lupus like syndrome 
demyelinatin - optic neuritis, MS 
pancytopenia
hepatic
lymphomas in young people - hepatosplenic T cell lymphomas cases were fatal 
leukemias 
new onset psoriasis
64
Q

impact of antibody formation to murine component of infliximab

A

loss of response

need to increase dose or frequency

65
Q

ways to prevent infliximab antibody formation

A

intermittent use increase risk of antibodies so use continuously i guess
dont start on infliximab unless patient agrees to go on aza
pretreat with steroids if just starting treatment

66
Q

anti TNF questions for the pahrmacist

A

have they previously been exposed to antiTNF
are pretreatment steroids required
mantoux test or chest xray (to test for TB), baseline LFT and hepatitis viral studies been performed

67
Q

antidiarrheals for supportive therapy

A

loperamide and codiene - cna use prior to sports to decrease ileostomy drainage
stop temporarily whrn CD deteriorates quickly
never use in severe disease as increases risk of toxic megacolon
cholestyramine for bile salt diarrhea

68
Q

drugs for inducing remssion in UC

A
aminosalicylates with mild-mod
corticosteroids
cyclosporine 
antiTNF
vedolizumab
69
Q

drugs for maintaining remission in UC

A

aminosalicylates with mild-mod disease
AZA,6MP, maybe MTX
anti TNP
vedolizumab

70
Q

monitoring UC therapy

A

scoring systems of disease activity
rectal bleeding and diarrhea, frequency of stools/day
anemia, low albumin, increased ESR, fever, ab pain - serious
fever new ab pain - see doctor
adherence very important - esp with 5ASA

71
Q

drugs for inducing remission in crohns

A

corticosteroids

anti TNFs

72
Q

drugs for maintaining remission in crohns

A
aminosalicylate?
budesonide?
aza, 6MP, methotrextae 
antiTNF
metronidazole, ciprofloxacin sometimes in ileal or colonic 
never use cyclosporin
73
Q

monitoring crohns therapy

A

heterogenous features
heal fistula, decrease in diarrhea and ab pain
weight, hemoglobin, endoscopic features
frequency of needing support therapy - ex loperamide
frequency of missing school or work

74
Q

whats the main treatment for mild - mod UC

A

5ASA

75
Q

difference between crohns and ulcerative colitis

A

crohns: occurs in the colon and lower SI commonly but can affect entire GI tract, can comprise multiple separate areas of inflammation, can form fissures
UC: affects only sigmoid colon and rectum, continuous patch of inflammation, damages inner lining of intestinal wall