Inflammatory Bowel Disease Treatment Flashcards Preview

Pharm II Exam 4 > Inflammatory Bowel Disease Treatment > Flashcards

Flashcards in Inflammatory Bowel Disease Treatment Deck (50):
1

What is UC?

mucosal inflammatory condition confined to rectum & colon

2

What is Crohn's?

transmural inflammation from mouth to anus

3

What does therapy for UC or Crohn's depend on?

Anatomic location, the severity, responsiveness, goal of therapy, & drug toxicity

4

Malaise & fever are uncommon in what form of IBD?

UC

5

What is the distribution of UC vs Crohn's?

Crohn's = discontinuous

UC = continuous

6

Aphthous or linear ulcers are common in which form of IBD?

Crohn's

7

What features are common in Crohn's?

Ileal involvement
Strictures
Fistulas
Granulomas
Linear clefts
Cobblestone appearance

8

What feature is common in UC?

Crypt abscesses

9

What is the goal of pharmacologic therapy for IBD?

Relieve the inflammatory process & induce remission

10

What is the action of azo compounds (end in "salazine")?

Reduce absorption of the parent drug from the small intestine

11

Azo compounds: Where are high concentrations of active drug made available?

Terminal ileum & colon

12

What are examples of mesalamine compounds?

Pentasa

Asacol & apriso

Lialda

Rowasa (enema), canasa (suppositories)

13

What does pentasa act on?

small intestine

14

What does anacol & apriso act on?

distal ileum & proximal colon

15

What does lialda act on?

colon

16

What does rowasa & canasa act on?

rectum & sigmoid colon

17

5-ASA is derived from what 2 pathways?

Cyclooxygenase & lipoxygenase

18

What is the MOA of 5-ASA?

Interferes w/ production of inflammatory cytokines

Inhibit cellular functions

19

What is the efficacy of 5-ASA on UC vs Crohn's?

UC: induces & maintains remission, considered 1st line for mild-mod disease

Crohn's: efficacy unproven (many still use as 1st line for mild-mod disease involving the colon or distal ileum)

20

What is the action of the controlled-release oral formulation of budesonide?

Releases in the distal ileum & colon, where it is absorbed

21

How do you treat mod-severe active IBD?

Glucocorticoids

22

Have higher doses of glucocoricoids been shown to be more efficacious?

Nope

23

What is a con of glucocorticoids?

Not useful for maintaining remission
- Aminosalicylates or immunosuppressive agents should be used

24

Purine antimetabolites have ___________ properties

immunosuppressive

25

6-mercaptopurine undergoes biotransformation via...

competing catabolic enzymes - xanthine oxidase & thiopurine methyltransferase

26

Active 6-thioguanine nucelotides are concentrated in cells resulting in...

prolonged 1/2 life

27

Prolonged kinetics of 6-thioguanine nucelotide results in a delay of...

17 weeks before onset of therapeutic benefit from oral azathioprine or 6-MP

28

What are ADEs of azathioprine & 6-mercaptopurine (purine analogs)?

Bone marrow depression

Hepatic toxicity

Increased risk of lymphoma

29

Describe the drug interaction w/ allopurinol

Reduces xanthine oxide catabolism of the purine analogs --> increased active 6-thioguanine nucleotides

30

What has an important role in the pathogenesis of IBD?

Luminal bacteria
Fungi & viruses

31

What is the role of abx on IBD?

Treats micro abscesses

Decreases bacterial translocation

Treats septic complications

Induces remission

32

What has been hypothesized to have a role in the development of Crohn's?

Mycobacterial infection

33

What is the MOA of methotrexate?

Inhibit dihydrofolate reductase enzyme

Interfere w/ interleukin

Stimulate release of adenosine

Stimulate death of T lymphocytes

34

What are ADEs of methotrexate?

Bone marrow depression

Alopecia

Mucositis

Peripheral neuropathy when used for prolonged periods

Hepatic damage in pts w/ psoriasis

35

What reduces the risk of ADEs of methotrexate?

Folate supplementation

36

Those on methotrexate & who have renal insufficiency, are at increased risk for what?

Hepatic accumulation & toxicity

37

What is the MOA of anti-tumor necrosis factor?

Dysregulation of helper T cell type 1 response & regulatory T cells

38

What is an example of anti-tumor necrosis factor therapy?

Monoclonal antibodies to human TNF

39

Anti-tumor necrosis agents prevent the cytokine from binding to...

its receptors

40

Anti-tumor necrosis agents: the Fc portion of human IgG1 promotes...

antibody-mediated apoptosis

41

What fraction of pts will eventually lose response despite higher doses or more frequent injections of anti-tumor necrosis agents?

1/3

42

What causes the loss of response in anti-tumor necrosis agents?

May be due to development of antibodies to the TNF antibody

43

What are ADEs of anti-tumor necrosis agents?

Infection

Risk of serious infections increased w/ concomitant coricosteroids

Antibodies to the antibody (less likely in concomitant therapy w/ immunomodulators)

Delayed serum sickness-like rxn

44

Concomitant treatment w/ anti-TNF agents & immunomodulators may increase the risk of what?

lymphoma

45

What are integrins?

Adhesion molecules on the surface of leukocytes

46

Integrins may interact w/ what?

Selectins (another class of adhesion molecules, on the surface of the vascular endothelium)

47

What is the MOA of integrins?

Allows circulating leukocytes to adhere to the vascular endothelium & move through the vessel wall into the tissue

48

What is anti-integrin therapy (natalizumab) used for?

Mod-severe Crohn's who have failed other therapies through a carefully restricted program

49

What are ADEs of anti-integrin therapy (natalizumab)?

acute infusion rxns

small risk of opportunistic infections

50

What should you monitor w/ anti-integrin therapy?

Brain MRI, mental status, progressive multifocal leukoencephalopathy