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pharm of IBD


what is the goal of treatment of inflammatory bowel disease? reduce inflammation and subsequently induce and maintain clinical remission
the agent chosen for treatment depends on: acute flare or maintenance of remission, location of lesions, severity of disease
name some factors which are involved in inflammation cytokines (TNF alpha), T cells, AA metabolites (PGs, LTs), growth factors, oxygen radicals
what is the mainstay therapy for treatment of inflammatory bowel disease? reduce inflammaiton
COX breaks down Arachidonic acid to what? prostaglandins
5-lipoxygenase breaks down arachadonic acid to what? Leukotrienes
these drugs act as topical anti-inflammatory agents in the treatment of inflammatory bowel disease 5-ASA derivatives
how do 5-ASA derivatives work? they block cyclooxygenase and 5-Lipoxygenase
NSAIDS also block AA metabolism. Are they effective in the treatment of IBD? no
what is the mechanism of action of 5-ASA derivatives? unknown
what are some other possible means of producing anti-inflammatory effects? inhibition of IL1 and TNF alpha production, inhibition of Tcell proliferation, ihibition of antibody production by B cells, inhibition of migration of inflammatory cells into the bowel wall.
what percent of the 5-ASA derivative will be absorbed in the upper GI system and metabolized? ninety percent
to prevent upper GI absorption of the 5-ASA derivatives, what are three pharmacological options? give the medication rectally (mesalamine rectal suppository, mesalamine rectal enema), create a delayed (pH) or sustained (time) released preparation (mesalamine), conjugate the 5-ASA to a carrier that will be released in the colon
what are the 5-ASA derivatives that will be released into the colon? sulfasalazine, olsalazine, balfasalazine
the carrier of this drug is sulfapyridine sulfasalazine
the carrier of this drug is another molecule of 5-ASA olfasalazine
the carrier of this drug is an inert molecule balfasalazine
there is this type of bond between a 5-ASA derivative and its carrier Azo bond
the bactera that have the enzyme needed to lceave the azo bond are only present in the...that's why agents prepared this way are only effective after reaching the.... colon....cecum
which drugs are only work once they get to the cecum sulfasalazine, olsalazine, balsalazide
pentasa starts working in the... stomach
asacol starts working in the... small intestine
the azo bond starts to get cleaved once you get to the cecum and large intestine
for patients to mild to moderate Ulcerative colitis or Chron's disease, what is the first drug of choice used to induce remission? what is the second drug of choice? 5-ASA derivatives (sulfasalazine, mesalamine), second drug of choice is antibiotics, especially fistulizing CD, or steroids if they have UC.
what is the drug of choice to induce remission for severe and/or steroid resistant or dependent Ulcerative colitis or Chrons disease? what is the second choice drug? first line is steroids (severe disease). Second line is methotrexate, cyclosporine, or infliximab.
what is the drug of choice to maintain remission of mild to moderate UC or CD. what is the second drug of choice? first line: 5ASA derivative (sulfasalazine, esalamine). second drug of choice is methotrexate, AZA/6-MP, or infliximab.
in severe and/or steroid resistant or dependent UC or CD, what is the first drug of choice to maintain remission? what is the second drug of choice? first: methotrexate, AZA/6-MP or infliximab
what are some dose dependent side effects of sulfasalazine and why do these complications occur? nausea, vomitting, headache, epigastric pain, malaise, male infertility. they occur because of the sulfa molecule
what are some idiosyncratic adverse effects that occur with sulfasalazine? fever, rash, hemolytic anemia, agranulocytosis, pulmonary complications, hepatitis, pancreatitis, folic acid deficiency
what are some adverse effects of mesalamine/olsalazine/balsalazide headache, dyspnea, rash, diarrhea (especially olsalazine)
bottom line: these specific drugs are considered the drug of choice for induction of remission for mild to moderate CD or UC. the 5-ASA derivatives: sulfasalazine and mesalamine.
these drugs reduce recurrent disease in patient swith UC and all patients with UC should be on a maintenance 5-ASA derivative. aminosalicylates
this class of medicaitons has questionable efficacy in maintenance therapy for Crohns disease 5-ASA derivatives
what antibiotic class does ciproflaxaci belong to? fluoroquinolone
what is the mechanism of action of ciproflaxacin (fluoroquinolone) inhibition of DNA gyrase and topoisomeraase 4.
what is the mechanism of action of the antibiotic metronidazone exact MOA is unknownn, disrupts DNA and inhibits nucleic acids synthesis.
what is the MOA of the antibiotic rifixamin? inhibits DNA dependent RNA polymerase; reduces urease producing bacterial flora; decreases ammonia production
what is the MOA of antimicrobials in reducing inflammation associated with IBD? unclear
if bacteria are considered pro-inflammatory molecules, what is the theory of anti microbial use in IBD? they diminish the presence of bacterially mediated antigenic trigger, reduce the bacterial load of the gut, alters the composition of the gut microflora, directly suppress the intestinal immune system (metronidazole)
what is the bottom line of antimicrobial use in IBD? they have a role to induce remission during a flar of mild to moderate CD. they are considered esepeically useful for fistulizing chrohns disease and crohns associated with perianal fissures.
antimicrobials are not effective for what? inducing remission in ulcerative colitis!!
are antimicrobials considered an effective maintenance therapy? no
you have an ulcerative colitis patient that is placed on sulfasalazine in an attempt to induce remission. after three weeks of therapy this patient continues to have 5-6 bloody stools per dya and abdominal pain. what can you do for this patient? you use corticosteroids, because the 5-ASA derivatives are considered the drug of choice for remission of induction in mild to moderate CD or UC, but this treatment has failed.
are antimicrobials effective in inducing remission in UC? NO
what are the corticosteroids that may be used in IBD? prednisone, methylprednisolone, hydrocortisone, budesone
these corticosteroids are oral only prednisone, budesonide
this corticosteroid is oral or IV methylprednisolone
this corticosteroid can be given oral, rectal enema, or rectal foam hydrocortisone
what drug sare primarily used to treat flares of UC and CD? corticosteroids
oral corticosteroids are primarily used to treat what kind of flares in IBD? mild to moderate flares
IV steroids are used to what? induce remission in moderate to severe IBD
this corticosteroid is a pH dependent ileal releaase oral glucocorticoid that is not available for systemic absorption (10%) but provides topical anti-inflammatory effects. budesonide
what is the bottom line for corticosteroid use? they are used to induce remission in mild to moderate CD or UC that have failed induction with 5-ASA. they are considered first line agetns to induce remission in patients with moderate to severe disease. they are NOT used for maintenance therapy!!
why are corticosteroids not good for maintenance therapy in IBD? steroid man. udedesonide is not systemically absorbed but its effects wane and disappear over a priod of approximately 12 months.
give the classification of disease base don steroid responsiveness: clincally response in 1-2 weeks, remian in remission when agent is rapered over weeks/months steroid responsive
give the classification of disease base don steroid responsiveness: clinical response in 1-2 weeks , relapse with attempts at tapering steroid dose steroid dependent
give the classification of disease base don steroid responsiveness: no clinical response to steroids, steroid unresponsive
what types of drugs do you use in patients that remain symptomatic with 5-ASA derivatives and glucocorticoid use? immune modulators
which immune modulator drugs are thiopurine analogues? 6-mercaptopurine and azathioprine
which drugs are immune modulating agents? cyclosporine, methotrexate, 5-mercaptopurine, azathioprine
this immune modulator is a pro drug that is converted to that active metabolite 6-mercaptopurine in the body. azathioprine
what is the mechanism of action of 6-mercaptopurine and azathioprine? inhibition of purine synthesis needed for proliferation of leukocytes and lymphocytes. it competes with guanine and hypoxanthine. it also inhibits T lymphocytes.
how do immune modulators work in treating IBD? they play an importnat role in the inflammatory cascade. the immune modulators disrupt the immune response and inhibit T cell proliferation resulting in decreased inflammation
what is the MOA of methotrexate as an immune modulator? inhibits dihydrofolate reductase, which is responsible for the conversion of dihydrofolate to tetrahydrofolate. this is a critical step in the synthesis of purines and pyrimidines. methotrexate thus blocks DNA synthesis in lymphocytes in IBD.
what is the MOA of cyclosporine as an immune modulator it is a calcineurin inhibitor, which is responsible for dephosphorylation of the nuclear factor of activated T cells. this results in movement of nuclear factor into the nucleus where expression of genes for IL2 and other inflammatory cytokines is stimula
the basic MOA in which immune modulators work in IBD is by.. inhibiting T cell proliferation.
how long is the onset of effect in AZA/6-MP and what is its use? 3-6 months, use is ofr UC or CD maintenance
how long is the onset of effect in MTX? and what is its use? several weeks, used in CD to induce remission and maintenance.
how long is the onset of effect in cyclosporine and what is its use? 1-2 weeks, use is to induce remission in UC or CD.
which immune modulators are good for inducing remission in steroid dependent or steroid unresponsiveness UC or CD. methotrexate and cyclosporine
these immune modulators are not good agents to induce remissiondue to the length of time taken to achieve the benefit. it can be used to maintain remisison in moderate to severe CD or UC or mild to moderate disease that is not responsive to the 5-ASA s 6-MP and and azathioprine
what are some adverse effects of immune modulators? there are many: allergic reactions, pancreatitis, myelosuppression, nausea, hepatotoxicity, malignancy. you have to monitor their liver chemistries and blood coutns throughout therapy.
List the biologic responsive modifiers infliximab, adalimumab, certolizumab pegol
what role does TNF alpha pllay in the inflammatory cascade? List some things it does. macrophage activation, phagosome activation, differentiation of monocytes into macrophages, recruitment of neutrophils and macrophages, stimulation of release of inflammatory cytokines, upregulatoin and expression of endothelial adhesion molecules
the coupling of this drug to PEG may reduce antigenicity and prolong the half life of this medication certolizumab
this is a chimeric/mouse human monoclonal antibody inflixumab
this is fully human monoclonal antibody adalimumab
Antigen binding fragment of human monoclonal antibody coupled to polyethelyne glycol certolizumab
what is the mechanism of action of biologic response modifiers? they block the actions of TNF alpha.
what is the clinical utility of biologic response modifiers? induction of remission in steroid dependent or steroid unresponsive moderate to severe CD or UC, maintenance of remission in moderate to severe CD or UC, maintenance of remission in mild to moderate IBD that is not responsive to 5-ASA preparations.
what are some adverse reactions of biologic response modifiers? injection site reactions, rash, infusion reactions, neutropenia, infection, demyelinating disease, heart failure, hepatotoxicity, malignancy
what is the biggest problem with prescribing biologic response modifiers? they are extremely expensive.
Created by: aferdo01