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Pharmacology > GI: IBS and IBD Drugs > Flashcards

GI: IBS and IBD Drugs Flashcards

1
Q

Lubriprostone (amitiza)

  • class
  • MOA
  • indication
  • OOA
  • SE
  • drug-drug interactions
A

Secretory Agent (chloride chanel activator)

MOA: activates Cl- channels–>increases fluid secretion in the intestinal lumen–>eases passage of stool with LITTLE electrolyte change
*increases weekly BMs

IND:

  • IBS-C
  • chronic constipation

OOA: 24 hours

SE:

  • N/V
  • dyspepsia
  • HA
  • dizziness
  • hypotension

*Very little drug-drug interactions bc drug is quickly absorbed in stomach + jejunum

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2
Q

Linaclotide (Linzess)

  • class
  • MOA
  • indication
  • SE
  • do not use in?
A

Secretory Agent

MOA:
peptide agonist of cyclic GMP–>enhancing Cl- and HCO3- secretion into the lumen–>incrs water secretion–>increasing motility

IND:
*IBS-C

SE: 
*diarrhea 
*abdmon pain 
*flatulence 
*HA 
*abdominal distention 
DO NOT USE in PT <17 YO
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3
Q

IBS vs IBD

A

irritable bowel syndrome vs inflammatory bowel disease

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4
Q

list the drug classes to tx IBD

A
  • 5-aminosalicylates
  • Corticosteroids
  • Biologic Agents–TNF-alpha inhibitors, Alpha-4 integrin inhibitors, IL-12/23 inhibitor
  • Immunomodulators
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5
Q

MOA of 5-aminosalicylates

A
  1. exact MOA unknown
  2. anti-inflammatory + immunosuppressive properties effects via multiple mechanisms
    - ->inhibition of cytokine synthesis
    - ->inhibition of leukotriene and prostaglandin synthesis
    - ->scavenging of free radicals
    - ->inhibition of T-cell proliferation, activation and differentiation
    - ->impairment of leukocyte adhesion and function
  3. act locally in intestine
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6
Q

what is the first line agent for UC

A

5-aminosalicylates

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7
Q

Distribution patterns of CD vs UC

A

UC: continuous involvement of colon–beginning w/ rectum.

CD: affect any portion of the GI tract from mouth–anus—noncontinuous fashion and is characterized by transmural inflammation.

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8
Q

what layer does UC affect

A

limited to mucosal layer

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9
Q

what are the two compounds found in the 5-ASA agents

A

Azo and Mesalamine

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10
Q

Sulfasalazine

  • class
  • chemical composition
  • MOA…. also works primarily where?
  • indications
  • SE
  • routes of admin
A
  • 5-ASA (azo compounds)
  • prodrug w/ 5-ASA linked to sulfapyridine

MOA:

  • 5-ASA linked to Sulfapyridine is cleaved by gut bacteria–> to produce 5-ASA aka Mesalamine + Sulfapyradine
    • works primarily in the colon
  • inhibits transport of reduced folic acid across cell membranes

Indications: UC–induction and maintenance of remission
have to give with folate**

SE:

  • Nausea
  • HA
  • fever
  • rash
  • RARE–life threatening agranulocytosis

PO route only

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11
Q

which causes more SE: Sulfasalazine or Mesalamine

WHY

A

Sulfasalazine
because its composition is 5-ASA + Sulfapyridine— when the gut bacteria cleave the drug–>5-ASA and Sulfapyridine

Sulfapyradine is the reason for the SE

Mesalamine is unliked 5-ASA so it has less SE

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12
Q

which drug can cause agranulocytosis

A

Sulfasalazine

used in tx for IBD

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13
Q

which drug do you need to give with folate

A

Sulfasalazine—- 5-ASA for IBD
and
methotrexate

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14
Q

Mesalamine

  • class
  • chemical composition
  • MOA…. also works primarily where?
  • indications
  • SE
  • routes of admin
A

5-ASA within a protective coat
*mostly absorbed in SI

MOA:
1. exact MOA unknown

  1. anti-inflammatory + immunosuppressive properties effects via multiple mechanisms
    - ->inhibition of cytokine synthesis
    - ->inhibition of leukotriene and prostaglandin synthesis
    - ->scavenging of free radicals
    - ->inhibition of T-cell proliferation, activation and differentiation
    - ->impairment of leukocyte adhesion and function
  2. act locally in intestine

Indications: UC– both induction and maintenance of remission
*Mainstay for UC FIRST LINE **

SE:

  • less SE than Sulfasalazine
  • HA
  • dyspepsia

Routes of admin

  • PO
  • rectal–>FIRST LINE
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15
Q

Pharmacokinetics for 5-ASA agents

  • incr and decr absoprtion with?
  • contraindicated with?
A

drugs increase absorption with more severe dz and has decreased absorption in decreasing pH evi (EX if PPI or H2 blocker also taken)

contra with sulfa allergy

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16
Q

SE for 5-ASA agents *mainly for Sulfasalazine

A

Blood dyscrasias– abnormalities in blood (anemia)

Nephrotoxicity

Hepatitis

SJS

Reversible male infertility

Inhibition of folate absorption

17
Q

what happens if you take a PPI, H2 rec antag and/or antacid with a 5-ASA agent ?

A

may increase systemic absoprtion and premature release of 5-ASA b4 reaching the site of action

*these drugs are pH dep

18
Q

Corticosteroids w/ IBD mainly used for?

*what to avoid with corticosteroid use?

A

INDUCING remission

avoid longterm use can cause cushing’s dz

19
Q

which form of corticosteroids have less SE

A

rectal

  • foams
  • enema
20
Q

pros and cons of rectcal corticoids for tx of IBD

A

PROS: less SE than systemic agents
CONS: limited to left-sided dz of UC

21
Q

Budesonide forms for IBD

A

PO

rectal

22
Q

Hydrocortisone forms for IBD

A

PO
IV
Rectal

23
Q

Methylprednisolone routes for IBD

A

PO

IV

24
Q

list the corticosteroids used for tx of IBD

A

Budesonide
Hydrocortisone
Prednisone
Methylprednisolone

25
Q

List the three biologic agents for IBD

A
  1. Tumor Necrosis Factor inhibitors (Infliximab, Adalimumab, Certolizumab, Golimumab)
  2. Alpha-4 integrin inhibitors–Vedolizumab
  3. IL-12/23 Inhibitors (Ustekinaumab)
26
Q

TNF-necrosis factors

  • MOA
  • INDS
  • Contras
A

MOA:

  • monoclonal antibodies directed against TNF-alpha
  • TNF-alpha has several biologic activities that may be directly related to the pathogenesis of IBD

INDS

  • induction and maintenance of remission for IBD
  • usually second line agent for IBD who have failed 5-ASA, unresponsive to or dependent on corticoids or who present with more severe dz

Contra:

  • active infection
  • latent or untx TB
  • demyelinating dz (MS or optic neuritis)
  • HF
27
Q

use of biologics is associated with?

A

increase risk for infections

28
Q

what should be done before a PT is placed on biologic agent tx?

A

evaluated for TB

29
Q 
Alpha-Integrin Inhibitors 
MOA 
Pros to these agents 
INDs
SE
A

MOA: alpha-4 integrin inhibitors are monoclonal antibodies developed as gut-selective anti-integrin
*reduces leukocytes to the site of inflammation

Limited systemic immunosuppression-effect on GI tract

INDS:

  • moderate to severe CD and UC
  • refractory to TNF-alpha inhibitors

SE

  • HA
  • Arthralgia
  • Nausea
  • fatigue
  • MSK pain
30
Q

what are integrins

A

proteins involved in leukocyte migration to the gut

31
Q 
Ustekinaumab
*class
*MOA 
*INDS
SE
A

IL-12/23 inhibitor

MOA: cytokine inhibitors
*inhibit cytokine IL-12 and IL-23– which are involved in lymphocyte activation aka the inflammatory process

INDS:
*induction and maint of remission of CD in PTS refractory to or intolerant of TNF-alpha inhibitors, immunomodulators or corticosteroids

SE

  • HA
  • arthralgia
  • Infection
  • nausea
  • nasopharyngitis
32
Q

which drug can cause nasopharyngitis

A

Ustekinaumab—- IL-12/23 inhibitor

33
Q

List the immunomodulators

A

Methotrexate

Thiopurines

34
Q

Methotrexate

  • class of drugs
  • MOA
  • OOA
  • Absoprtion
  • metabolism
  • SE
  • contra
  • routes of admin
  • INDS
A

Immunomodulator

  • folic acid antagonist–inhibits DNA synthesis, repair and cellular replication– esp targeting actively proliferating tissues (esp psoriasis)
  • folate helps with DNA synthesis

MOA: inhibits cytokine production and purine nucleotide biosynthesis–>leads to immunosuppresive and anti-inflammatory effects

OOA: 3-6 weeks (for tx of RA)

*abs is variable and is decreased at higher doses—likely due to saturation

Metabolism: partially metabolized by intestinal flora

SE:

  • *Many serious SE
  • ->mucosal ulceration
  • ->nausea
  • ->Cytopenias (esp leukopenia)
  • ->liver cirrhosis
  • ->acute pneumonia-like syndrome
  • ->HA
  • ->Vomiting
  • ->abdominal discomfort
  • ->serum aminotransferase elevations
  • ->rash
  • ->tumor lysis syndrome
  • ->Malignant lymphomas
  • *BB warning
  • *

CONTRA IN PREGNANCY**

  • IM or SC
  • admin with folic acid supplement to reduce the incidence of GI adverse effects

Indications:
*maintenance of remission in CD— NOT FOR UC

35
Q

what tests should be done on PTs being treated with Methotrexate

A

LFTs
CBC
monitoring for signs of infection

36
Q

Azathioprine and Mercaptopurine

  • class of drug
  • inds
  • OOA
  • drug interactions
  • SE
  • monitor PT for?
  • special note about Azathioprine
  • routes of admin
A

Thiopurines

MOA: exert a glucocorticoid-sparing effect for IBD (both UC and CD)

INDs:
*for PTs who cannot maintain remission when glucocorticoids are withdrawn

OOA: slow acting–3 or more months*****

Drug interactions: allopurinol and Febuxostat (slows elimination of 6-MP)

SE

  • Nausea
  • anorexia
  • vomiting
  • bone suppression
  • hepatoxicity

Monitor PT for cytopenias (CBCs) and transaminitis (elevation of liver enzymes)

Azathiopurine–prodrug
*converted to 6-MP by compounds found in tissues and RBCs–>metabolized by the liver and gut –>induce immunosuppression by inhibiting protein and purine synthesis in lymphocytes

PO only

Pharmacology (28 decks)

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