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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
Q

Which oral budesonide is used for Crohn’s?

A

Entocort

-site of action: terminal ileum, ascending colon

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26
Q

Which oral budesonide is used for CUC?

A

Uceris

site of action: ascending, descendning, and transverse colon

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27
Q

T/F Budesonide is useful in achieving remission in IBD

A

False- it is less effective but used because it has less adverse effects

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28
Q

Which drug is used at maintaining remission?

A

5-ASA or immunosuppressives

29
Q

What are ADE of steroids?

A 
hyperglycemia
dyslipidemia
osteoporosis
HTN
acne 
psychosis
30
Q

What should you monitor if taking steroids?

A

BP, fasting lipid panel, glucose, vitamin D, bone density

31
Q

How do abx help control IBD?

A
  • control infection
  • reduce flares
  • suppress GI immune system
  • heal fistulas in Crohn’s
32
Q

What is a risk of using abx in IBD?

A

risk of c. difficile infection

33
Q

T/F oral vancomycin is used to c. difficile infection

A

True

34
Q

T/F Metronidazole/Flagyl can be used to treat severe CUC and c. diff

A

True

35
Q

Pouchitis is treated with what abx?

A

Cipro, Rifaximin, Fidaxomicin

36
Q

Which drugs are immunomodulators used to tx IBD?

A
  • Azathioprine
  • 6-mercatopurine
  • MTX
  • cyclosporine
37
Q

What is MOA of cyclosporine?

A
  • 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
Q

What is clinical use of cyclosporine?

A

severe CUC pts that are hospitlaized

-salvage therapy for Crohn’s fistula

39
Q

What are ADE of cyclosporine?

A 
parathesia
hypertrichosis
tremor
HTN
Nausea 
gingival hyperplasia
40
Q

Which drugs are purine analogs?

A
  • Azathioprine

- 6-mercatopurine

41
Q

What is MOA of purine analogs?

A
  • Block the pathway for purine synthesis

- Metabolites are incorporated into replicating DNA and halt replication

42
Q

What is 1/2 life of purine analogs?

A

Azathioprine and 6-MP have a serum half-life of less than 2 hours

43
Q

What is bio availability of purine analogs?

A
  • Azathioprine (80%)

- superior to 6-MP (50%)

44
Q

T/F -Azathioprine is rapidly converted to 6-MP

A

6-Mercaptopurine undergoes biotransformation via competing catabolic enzymes–xanthine oxidase and thiopurine methyltransferase

45
Q

What is clinical use of purine analogs?

A
  • 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
Q

Adverse Effects & Monitoring of purine analogs?

A

bone marrow depression
hepatic toxicity
Increased risk of lymphoma
complete blood count and liver function tests is required in all patients

47
Q

Drug Interactions with Azathioprine and 6-MP?

A

ALLOPURINOL: reduces xanthine oxide catabolism of the purine analogs, potentially increasing active 6-thioguanine nucleotides
-severe leukopenia

48
Q

What is MOA of methotrexate?

A
  • 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
Q

What are routes of MTX?

A

oral, sub Q, IM

50
Q

What are the clinical uses of MTX?

A

-Used to induce and maintain remission in patients with Crohn disease

51
Q

What are ADE of MTX?

A

permanent peripheral neuropathy when used for prolonged periods

  • bone marrow depression, alopecia, mucositis,
  • pt with psoriasis experience liver damage
52
Q

What supplement needs o be given if pt is taking MTX?

A

folic acid

53
Q

Two biologic anti-adhesion agents

natalizumab and vedolizumab

A

TX IBD

IV infusion

54
Q

Four anti-TNF agents

infliximab, adalimumab, certolizumab, and golimumab

A

TX IBD

subQ except for infliximab=IV infusion

55
Q

Infliximab, adalimumab, and vedolizumab are approved for both ulcerative colitis and Crohn disease

A

true

56
Q

Certolizumab and natalizumab are approved only for Crohn disease.

A

true

57
Q

Golimumab is only approved to treat ulcerative colitis

A

true

58
Q

What is MOA of Infliximab or Adalimumab or Golimumab

A
  • 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
Q

T/F Certolizumab has same MOA as infliximab?

A

False: without an Fc portion, lacks antibody-mediated apoptosis properties

60
Q

What are ADE of anti-TNF

A
  • 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
Q

What can you add to tx for IBS to reduce the chance of developing antibodies to infliximab

A

6-mercaptopurine or MTX

62
Q

What are integrins?

A

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
Q

Natalizumab and Vedolizumab are what type of drug class?

A

Anti-integrins

-IgG4 antibody blocks alpha 4 subunit and blocks integrins on circulating WBC

64
Q

What is the clinical use of anti-integrin therapy/Natalizumab?

A

mod to severe Crohn’s

-use when all other tx has failed

65
Q

What are ADE of anti-integrin therapy/Natalizumab?Monitor?

A

infusion rxn
small risk of opportunistic infection
Monitor: PMI, brain MRI, mental status

66
Q

What is the difference between Natalizumab and Vedolizumab?

A

Vedolizumab is selective to the gut

  • this can help prevent JC virus and PMI
  • can be used in both CRonh’s and CUC
67
Q

What is Stelara/ Anti-IL 12/23, MOA?

A

Ustekinumab

-antibody that blocks IL-12 and IL-23 receptors on NK cells, T cells and APC

68
Q

What is ADE of Stelara?

A

nasopharyngitis
SCC
antobody development

Pharmacology (47 decks)

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