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Pharm II Exam 4 > Inflammatory Bowel Disease Treatment > Flashcards

Inflammatory Bowel Disease Treatment Flashcards

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1
Q

What is UC?

A

mucosal inflammatory condition confined to rectum & colon

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2
Q

What is Crohn’s?

A

transmural inflammation from mouth to anus

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3
Q

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

A

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

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4
Q

Malaise & fever are uncommon in what form of IBD?

A

UC

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5
Q

What is the distribution of UC vs Crohn’s?

A

Crohn’s = discontinuous

UC = continuous

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6
Q

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

A

Crohn’s

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7
Q

What features are common in Crohn’s?

A 
Ileal involvement 
Strictures
Fistulas 
Granulomas 
Linear clefts 
Cobblestone appearance
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8
Q

What feature is common in UC?

A

Crypt abscesses

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9
Q

What is the goal of pharmacologic therapy for IBD?

A

Relieve the inflammatory process & induce remission

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10
Q

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

A

Reduce absorption of the parent drug from the small intestine

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11
Q

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

A

Terminal ileum & colon

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12
Q

What are examples of mesalamine compounds?

A

Pentasa

Asacol & apriso

Lialda

Rowasa (enema), canasa (suppositories)

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13
Q

What does pentasa act on?

A

small intestine

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14
Q

What does anacol & apriso act on?

A

distal ileum & proximal colon

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15
Q

What does lialda act on?

A

colon

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16
Q

What does rowasa & canasa act on?

A

rectum & sigmoid colon

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17
Q

5-ASA is derived from what 2 pathways?

A

Cyclooxygenase & lipoxygenase

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18
Q

What is the MOA of 5-ASA?

A

Interferes w/ production of inflammatory cytokines

Inhibit cellular functions

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19
Q

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

A

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)

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20
Q

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

A

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

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21
Q

How do you treat mod-severe active IBD?

A

Glucocorticoids

22
Q

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

A

Nope

23
Q

What is a con of glucocorticoids?

A

Not useful for maintaining remission

- Aminosalicylates or immunosuppressive agents should be used

24
Q

Purine antimetabolites have ___________ properties

A

immunosuppressive

25
Q

6-mercaptopurine undergoes biotransformation via…

A

competing catabolic enzymes - xanthine oxidase & thiopurine methyltransferase

26
Q

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

A

prolonged 1/2 life

27
Q

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

A

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

28
Q

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

A

Bone marrow depression

Hepatic toxicity

Increased risk of lymphoma

29
Q

Describe the drug interaction w/ allopurinol

A

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

30
Q

What has an important role in the pathogenesis of IBD?

A

Luminal bacteria

Fungi & viruses

31
Q

What is the role of abx on IBD?

A

Treats micro abscesses

Decreases bacterial translocation

Treats septic complications

Induces remission

32
Q

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

A

Mycobacterial infection

33
Q

What is the MOA of methotrexate?

A

Inhibit dihydrofolate reductase enzyme

Interfere w/ interleukin

Stimulate release of adenosine

Stimulate death of T lymphocytes

34
Q

What are ADEs of methotrexate?

A

Bone marrow depression

Alopecia

Mucositis

Peripheral neuropathy when used for prolonged periods

Hepatic damage in pts w/ psoriasis

35
Q

What reduces the risk of ADEs of methotrexate?

A

Folate supplementation

36
Q

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

A

Hepatic accumulation & toxicity

37
Q

What is the MOA of anti-tumor necrosis factor?

A

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

38
Q

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

A

Monoclonal antibodies to human TNF

39
Q

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

A

its receptors

40
Q

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

A

antibody-mediated apoptosis

41
Q

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

A

1/3

42
Q

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

A

May be due to development of antibodies to the TNF antibody

43
Q

What are ADEs of anti-tumor necrosis agents?

A

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
Q

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

A

lymphoma

45
Q

What are integrins?

A

Adhesion molecules on the surface of leukocytes

46
Q

Integrins may interact w/ what?

A

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

47
Q

What is the MOA of integrins?

A

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

48
Q

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

A

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

49
Q

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

A

acute infusion rxns

small risk of opportunistic infections

50
Q

What should you monitor w/ anti-integrin therapy?

A

Brain MRI, mental status, progressive multifocal leukoencephalopathy

Pharm II Exam 4 (14 decks)

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