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Pharmacology > Inflammatory Bowel Disease > Flashcards

Inflammatory Bowel Disease Flashcards

1
Q

What are the two types of IBD?

A
  • CUC

- Crohn’s disease

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2
Q

What is pathology of IBD?

A

uncontrolled immune mediated inflammatory responses

  • increased IL, 1,6,8 and TNF-alpha
  • downregulation of TNF-beta, IL-2, 10
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3
Q

Difference between CUC and Cronh’s?

A

CUC: mucosal layer only, involves colon, bloody diarrhea ad abdominal pain

Cronh’s: transmural inflammation, involves small bowel and terminal ileum, skip lesions, intra abdominal abscess and fistulas

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4
Q

Pharmacotherapy tx for CUC and Crohn’s is based on what?

A

site of action

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5
Q

These non biological DMARDS work on what part of GI system?

Sulfasalazine/Azulfidine, sulfasalzine-DR/Azulfidine DR, Balsalazide/Colazal, Olsalazine-Dipentum

A

-colon

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6
Q

Which non biological DMARDS work in the rectum?

A
  • Mesalamine suppository-Canasa

- Mesalamine enema- Rowasa

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7
Q

Mesalamine CR/Pentasa works where in the GI tract?

A
  • small intestine

- colon

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8
Q

Mesalamine ER/Apriso, mesalamine DR/Asacol HD, mesalamine DR/Delzicol, tx IBD in what location?

A
  • distal terminal ileum

- proximal colon

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9
Q

What is the difference between Sulfasalazine/Olsalazine/Balsalazide vs Mesalamine?

A

Sulfasalazine/Olsalazine/Balsalazide have an azo compound with 5-ASA that prevent its absorption in small intestine
-in the terminal ileum or colon the bacteria cleave the AZO compound releasing the active 5-ASA-only works in terminal ileum and colon

-Mesalamine does not have azo compound and therefore can be absorbed in the small intestine

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10
Q

T/F Mesalamine is packaged in different ways to allow for different segments of the small or large bowel to be targeted

A

TRUE

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11
Q

What is MOA of 5-ASA?

A
  • modulates inflammatory mediators derived from cyclooxygenase and lipooxygenase pathways
  • inhibits the activity of nuclear factor-kB to stop production of inflammatory cytokines
  • scavenges reactive oxygen species
  • blocks function of NK cells, mucosal lymphocytes, and macrophages
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12
Q

T/F 5-ASA undergoes N-acetylation in gut and liver into a metabolite

A

True

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13
Q

What is the clinical use of 5-ASA?

A
  • it is used as first line tx for CUC

- no proven efficacy in Crohn’s but can be used as first line tx for colon or distal ileum

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14
Q

What are ADE of mesalamine?

A

N/V/, HA

-higher doses can cause interstitial nephritis

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15
Q

What is ADE of Olsalazine?

A

diarrhea

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16
Q

What is ADE of Sulfasalazine?

A

sulfapyradine metabolite causes N/V, HA, rash, anemia, pneumonitis, liver toxicity, lymphoma

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17
Q

What should you monitor for Olsalazine, Sulfasalazine, and Balsalazide?

A

CBC
Folate
Liver function test
oligospermia

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18
Q

What is MOA of glucocorticoids?

A
  • blocks production of inflammatory cytokines TNF-alpha, IL-1, IL-8
  • reduces expression of cell adhesion molecules
  • block gene transcription of NO synthase, phospolipase A2, cycloxygenase-2, NF-k
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19
Q

T/F Budesonide has a controlled release formulation that is released in colon and distal ileum where it is absrobed

A

True

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20
Q

Which steroid has enema, suppository formulations and topical tx in the rectum and sigmoid colon

A

Hydrocortisone

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21
Q

What are the clinical uses of steroids?

A

mod to severe IBD

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22
Q

T/F Doses above 60 mg of steroids are better at tx IBD

A

False-higher doses not proven effective

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23
Q

T/F In severe IBD, IV steroids are used

A

True

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24
Q

T/F In Rectal and sigmoid IBD, topical/rectal formulations are used due to lower systemic absorption

A

True

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25
Which oral budesonide is used for Crohn's?
Entocort | -site of action: terminal ileum, ascending colon
26
Which oral budesonide is used for CUC?
Uceris | site of action: ascending, descendning, and transverse colon
27
T/F Budesonide is useful in achieving remission in IBD
False- it is less effective but used because it has less adverse effects
28
Which drug is used at maintaining remission?
5-ASA or immunosuppressives
29
What are ADE of steroids?
``` hyperglycemia dyslipidemia osteoporosis HTN acne psychosis ```
30
What should you monitor if taking steroids?
BP, fasting lipid panel, glucose, vitamin D, bone density
31
How do abx help control IBD?
- control infection - reduce flares - suppress GI immune system - heal fistulas in Crohn's
32
What is a risk of using abx in IBD?
risk of c. difficile infection
33
T/F oral vancomycin is used to c. difficile infection
True
34
T/F Metronidazole/Flagyl can be used to treat severe CUC and c. diff
True
35
Pouchitis is treated with what abx?
Cipro, Rifaximin, Fidaxomicin
36
Which drugs are immunomodulators used to tx IBD?
- Azathioprine - 6-mercatopurine - MTX - cyclosporine
37
What is MOA of cyclosporine?
- blocks activation and proliferation of T-helper cells by blocking IL-2 - blocks cytotoxic production via blockade of IL-3, IL-4,, TNF-alpha, and interferon
38
What is clinical use of cyclosporine?
severe CUC pts that are hospitlaized | -salvage therapy for Crohn's fistula
39
What are ADE of cyclosporine?
``` parathesia hypertrichosis tremor HTN Nausea gingival hyperplasia ```
40
Which drugs are purine analogs?
- Azathioprine | - 6-mercatopurine
41
What is MOA of purine analogs?
- Block the pathway for purine synthesis | - Metabolites are incorporated into replicating DNA and halt replication
42
What is 1/2 life of purine analogs?
Azathioprine and 6-MP have a serum half-life of less than 2 hours
43
What is bio availability of purine analogs?
- Azathioprine (80%) | - superior to 6-MP (50%)
44
T/F -Azathioprine is rapidly converted to 6-MP
6-Mercaptopurine undergoes biotransformation via competing catabolic enzymes--xanthine oxidase and thiopurine methyltransferase
45
What is clinical use of purine analogs?
- induction and maintenance of remission of Ulcerative colitis and Crohn disease - Allows for dose reduction or elimination of steroids in the majority of patients
46
Adverse Effects & Monitoring of purine analogs?
bone marrow depression hepatic toxicity Increased risk of lymphoma complete blood count and liver function tests is required in all patients
47
Drug Interactions with Azathioprine and 6-MP?
ALLOPURINOL: reduces xanthine oxide catabolism of the purine analogs, potentially increasing active 6-thioguanine nucleotides -severe leukopenia
48
What is MOA of methotrexate?
- inhibition of dihydrofolate reductase enzyme important in the production of thymidine and purines - may interfere with the inflammatory actions of interleukin - may stimulate increased release of adenosine, an endogenous anti-inflammatory autacoid - may stimulate apoptosis and death of activated T lymphocytes
49
What are routes of MTX?
oral, sub Q, IM
50
What are the clinical uses of MTX?
-Used to induce and maintain remission in patients with Crohn disease
51
What are ADE of MTX?
permanent peripheral neuropathy when used for prolonged periods - bone marrow depression, alopecia, mucositis, - pt with psoriasis experience liver damage
52
What supplement needs o be given if pt is taking MTX?
folic acid
53
Two biologic anti-adhesion agents | natalizumab and vedolizumab
TX IBD | IV infusion
54
Four anti-TNF agents | infliximab, adalimumab, certolizumab, and golimumab
TX IBD | subQ except for infliximab=IV infusion
55
Infliximab, adalimumab, and vedolizumab are approved for both ulcerative colitis and Crohn disease
true
56
Certolizumab and natalizumab are approved only for Crohn disease.
true
57
Golimumab is only approved to treat ulcerative colitis
true
58
What is MOA of Infliximab or Adalimumab or Golimumab
- bind to membrane-bound TNF - prevent the cytokine from binding to its receptors - Fc portion of the human IgG1 region promotes antibody-mediated apoptosis
59
T/F Certolizumab has same MOA as infliximab?
False: without an Fc portion, lacks antibody-mediated apoptosis properties
60
What are ADE of anti-TNF
- infection due to suppression of Th1 inflammatory response ( reactivation of TB, sepsis, fungal infection) - risk of serious infection with concomitant use of steroids - delayed serum sickness (lupus like syndrome develops, myalgia, arthralgia, fever, rash - development of antibodies to the antibody - increase risk of lymphoma when you use immunomodulators in combination
61
What can you add to tx for IBS to reduce the chance of developing antibodies to infliximab
6-mercaptopurine or MTX
62
What are integrins?
adhesion molecules on surface of leukocytes that bind selectins on surface of vessel endothelium -allows WBC to move through vessel wall and into tissue
63
Natalizumab and Vedolizumab are what type of drug class?
Anti-integrins | -IgG4 antibody blocks alpha 4 subunit and blocks integrins on circulating WBC
64
What is the clinical use of anti-integrin therapy/Natalizumab?
mod to severe Crohn's | -use when all other tx has failed
65
What are ADE of anti-integrin therapy/Natalizumab?Monitor?
infusion rxn small risk of opportunistic infection Monitor: PMI, brain MRI, mental status
66
What is the difference between Natalizumab and Vedolizumab?
Vedolizumab is selective to the gut - this can help prevent JC virus and PMI - can be used in both CRonh's and CUC
67
What is Stelara/ Anti-IL 12/23, MOA?
Ustekinumab | -antibody that blocks IL-12 and IL-23 receptors on NK cells, T cells and APC
68
What is ADE of Stelara?
nasopharyngitis SCC antobody development

Pharmacology (47 decks)

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