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Year2 GI Exam I > IBD Tx > Flashcards

IBD Tx Flashcards

1
Q

What drug classes are used in IBD

A 
5 aminosalicylic acid preparations
corticosteroids
immunosuppressants
Anti TNF alpha Ab
alpha4 integrin monoclonal Ab
Antibiotics
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2
Q

What are the drug classes used in IBS

A 
laxatives
anti diarrheal agents
prokinetic agent
serotonin antagonist
antiaspasmodic agents (Anticholinergics)
antidepressents
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3
Q

UC affects what areas of GI

A

affects rectum and colon, mucosal and submucosal layers

superficial inflammation

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4
Q

complications UC

A

hemorrhoids, anal fissures, perirectal abscesses
toxic megacolon
colorectal carcinoma

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5
Q

what is toxic megacolon

A

segmental or total colonic distention of greater than 6 cm with acute colitis and signs of systemic toxicity

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6
Q

describe ulcers in CD

A

deep and elongated with nodular submucosal thickening

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7
Q

UC or CD has higher risk for fistula formation

A

CD

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8
Q

complications of CD

A

small bowel structures, fistulas, bleeding,nutritional deficiencies and extra-intestinal manifestations

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9
Q

What drugs are amiosalicylates used for IBD

A

sulfasalazine, olsalazine, balsalazide, various forms mesalamine

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10
Q

MOA aminosalicylates

A

uncertain. maybe modulates inflammatory medioators derived from cyclooxygenase and lipooxygenase

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11
Q

describe metabolism sulfasalazine, balsalazide and olsalazine

A

decrease absorption of parent drug in small intestine

high [ ] of active drug in terminal ileum or colon

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12
Q

describe the delayed or extendened release forms of msealamine

A

coated in special resins, pH sensitive film or ethylcellulose that release drug slowsly thorugh GI tract or only in terminal ileum and colon

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13
Q

what are the rectal formulations of mesalamine

A

rowasa and canasa

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14
Q

therapeutic use for aminosaliclyates

A

1st line for mild to moderate UC

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15
Q

effectiveness of aminosalicylates is determined how

A

by drug reaching site of active disease
suppositories useful in UC or CD rectum or distal colon
if proximal colon use axo and mesalmine formulations

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16
Q

adverse effects aminosalicylates

A

dose related: nausea, GI upset, HA, arthralgias, myalgias, bone marrow suppression, malaise
nephrotoxicity
lupus like syndrome, pancreatitis, hepatotoxicity

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17
Q

what are the glucocorticoids used for IBD

A

prednisone, budesonide, hydrocortisone

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18
Q

MOA glucocorticoids

A

inhibit production inflammatory cytokines TNFa and IL-1 and IL-8
reduce expression inflammatory cell adhesion molecules
inhibit gene transcription NO synthase, PLA2, COX-2, NFkB

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19
Q

therapeutic use glucocorticoids

A

mod- severe IBD
higher dose treat active disease
once responding, taper dose
hydrocortisone enemas used to maximize colonic tissue effects and minimize absorption

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20
Q

What is budesonide

A

potent synthetic analog of prednisolone with high affinity for glucocorticoid receptor
rapid first pass metabolism, low oral bioavailability and controlled release formulation that releases drug in distal ileum and colon

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21
Q

adverse effects glucocorticoids

A

insomnia, behavioral changes, acute peptic ulcers
fluid and electrolyte abnormalities, metabolic changes, HTN, hyperglycemia, increased susceptibility to infections, osteoporosis, myopathy, behavioral disturbances, cataracts, growth arrest

22
Q

what are the purine analogs

A

azathioprine, 6 mercaptopurine

23
Q

MOA purine analogs

A

inhibits purine NT synthesis
azathioprine is converted to 6 MP which coverts to active metabolites that suppress inosinic acid synthesis, B cell and T cell function, Ig production and IL-2 secretion

24
Q

PK of purine analogs

A

delay of 17 weeks before onset therapeutic benefit from oral azathioprine of 6 MP in IBD

25
Q

therapeutic use purine analogs

A

induction and maintenance of remission of UC and CD
for patients who need long term glucocorticoid therapy to control active disease, purine analogs, allow dose reduction or elimination of steroids in the majority,
d/t delay onset limited short time but effective long term

26
Q

adverse effects purine analogs

A

dose related nausea vomiting bone marrow depression and hepatic toxicity
also HS: fever rash, pancreatitis, diarrhea, hepatitis
increase risk lymphoma with long term therapy

27
Q

drug interactions with purine analogs

A

allopurinol with 6MP

allopurinol inhbits the enzyme that metabolizes 6MP to inactive compound increasing toxic effects

28
Q

MOA methotrexate MTX

A

inhibits dihydrofolate reductase affecting lymphocyte and macrophage function
may stimulate release of adenosine, an endogenous anti-inflammatory autocoid
may also stimulate apoptosis and death of activated T lymphocytes

29
Q

therapeutic use of MTX

A

induction and maintenance of remission in patients with CD

Efficacy in UC uncertain

30
Q

adverse effects MTX

A

high doses may cause bone marrow depression, megaloblastic anemia, alopecia and mucositis

31
Q

what should you give with MTX

A

folate supplementation to decrease risk of adverse effects

32
Q

MOA cyclosporine

A

an inhibitor of calcineurin; cyclosporine is a potent inhibitor of cell-mediated immune responses

  • inhibits IL2 production form T helper cells
  • decreases recruitment of cytotoxic T cells and blocks other cytokines, including IL3 and 4, IFalpha and TNGa
33
Q

therapeutic use cyclosporine

A

IV infusion used to Tx severe UC that is unresponsive to IV glucocorticoids; may save patient from colectomy, but carries significant toxicity

34
Q

TNF levels in IBD

A

increased because key pro-inflammatory cytokine and mediator of intestinal inflammation

35
Q

Available TNFa Ab agents in IBD

A 
infliximab, adalimumab are Ab of IgG1 subclass
certolizumab- recombinant Ab that contains a Fab fragment conjugated to polyethylene glycol (PEG)
36
Q

what monoclonal Ab are fully humanized

A

adalimumab

37
Q

MOA TNFa Ab

A

all 3 Ab, bind soluble membrane bound TNFa with high affinity, preventing the cytokine from binding its receptors
suppreses cytokine release
lyses macrophages and T cells through Cā€™ fixation and Ab dep cytotoxicity

38
Q

therapeutic use of TNFa

A

acute and chronic Tx of mod-severe CD in patients who have inadequate response to conventional therapies

39
Q

median time to clinical response TNFa

A

2 weeks

40
Q

adverse effects TNFa

A

serious infections, Ab to Ab, delayed serum sickness like reaction
hepatic failure, lupus like syndrome, demyelinating disorders, hematologic reactions and new or worsening CHF
psoriatic skin rashes- resulting after drug discontinuation, lymphoma

41
Q

what serious infections can occur with TNFa

A

bacterial sepsis, TB, invasive fungal infections

42
Q

before starting on TNFa therapy what must you check for

A

TB infection because TB therapy needs to be initiated first

43
Q

What infecitons are more common with TNFa

A

URI(sinusitis, bronchitis, pneumonia) and cellulitis, risk of serious infection increases when taking concomitant glucocorticoids

44
Q

describe delayed serum sickness like reaction from TNFa

A

1-2 weeks post antiTNFa therapy

myalgia, arthralgia, jaw tightness, fever, rash, edema

45
Q

What are integrins

A

family of adhesion molecules on leukocytes that interact with selectins allowing leukocytes to enter vascular endothelium and into tissue

46
Q

what are the available anti-integrin agents

A

natalizumab, humanized IgG2 monoclonal Ab

47
Q

MOA natalizumab

A

prevent integrin binding to vascular adhesion molecules inhibiting subsequent migration into surround tissues

48
Q

therapeutic use of natalizumab

A

subset of patients with mod- severe CD

49
Q

why was natalizumab withdrawn in general.

A

lead to progressive multifocal leukoencephalopathy

50
Q

what is natalizumab still approved for

A

restricted use in patients with mod-severe CD who failed other Tx

51
Q

adverse effects natalizumab

A

acute infusion reactions and a small risk of opportunistic infections

Year2 GI Exam I (18 decks)

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