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19 Cards in this Set
- Front
- Back
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Il-2 is the most important factor in ________ proliferation. While all the 1st generation immunosuppressants generally inhibit T cell proliferation, the production of IL-2 is specifically blocked by the 2nd generation drugs _______ and ______. Another 2nd generation drug, _______, blocks proliferation by halting translation leading to the Il-2 receptor.
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Il-2 is the most important factor in _T-cells_ proliferation. While all the 1st generation immunosuppressants generally inhibit proliferation, the production of IL-2 is specifically blocked by the 2nd generation drugs _cyclosporin_ and _FK506_. Another 2nd generation drug, _rapamycin_, blocks proliferation by halting translation leading to the Il-2 receptor.
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Cyclosporin : ________ :: ________ : FK506bp
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cyclophilin, FK506
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Things to know about Etanercept:
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-fusion protein (Ab + TNFreceptor)
-rheumatoid arthritis Tx -parenterally given -resistance via host Ab (methotrexate helps delay) -exacerbates MS |
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the link between TNF and MS
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TNF receptor 1 = inflammation
TNF receptor 2 = re-myelination after injury/disease |
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Why are mast cells and basophils part of both the adaptive and non-specific immune systems?
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Adaptive: membrane bound IgE
Nonspecific: can be triggered by complement |
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Azothiprine
mech of action? toxicity? |
works via the salvage pathway to inhibit purine synthesis
infection |
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mycophenylate
mech of action? toxicity? |
blocks the de novo synthesis of GMP (and therefore iNOS)
infection |
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Leflunomide
mech of action? toxicity? |
Blocks thymidine pyrimidine synthesis; blockage of lymphocytes: B > T
diarrhea |
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methotrexate
mech of action? toxicity? |
irreversibly binds DHF reductase, inhibiting de novo purine synthesis
infection |
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3rd generation drugs Etancept and Inflix: what are their mechs and toxicities?
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Etancept: fusion pt (IgG + TNFR2)
Inflix: anti-TNF Ab Toxicities: Unmask latent infection + MS exacerbation |
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3rd generation: Natalizumab
mech? toxicity? |
mech = anti VLA4 (adhesion molecule), blocks leukocyte diapedesis into brain
toxicity: unmasks "JC" virus |
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immune changes mediated by glucocorticoids (txn and cell count)
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1. decreased inflammatory cytokines
2. decreased COX2 3. decreased adhesion molecules 4. lymphopenia (mono/leukocytes trapped in lymph nodes, can't access tissues 5. neutraphilia (high blood count b/c they can't access tissues) |
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Glucocorticoid toxicities (5)
Hints: (2) decreased strength (1) minerals! (1) COX2 inhibitor (1) feedback |
1. hypokalemia from excess Na+/H20 retention (stems from other mineral corticoids)
2. bone resorption 3. muscle catabolism 4. adrenalcortical insufficiency (negative feedback) 5. peptic ulcers (COX2 inhibition) |
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PInositol gives rise to arachidonic acid. AA can either go down one of two pathways, each of which is named for the initial enzyme.
Name the enzymes and the major downstream products. |
Cyclooxygenase pathway
prostaglandins thromboxanes prostacyclins Lipoxygenase Pathway LTB4 LT(C/D/E)4 |
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Matching
1. Leukotriene production 2. Prostaglandin production 3. Thromboxane production a. Macrophages b. PMN c. Basophil/Mast d. Platelets |
Matching
1. Leukotriene production: PMN, Basophil/Mast 2. Prostaglandin production: Macrophages 3. Thromboxane production: Platelets |
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Aspirin (salicylate) mech of action:
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O-acetylate active site of COX
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Main concerns with aspirin (and all NSAIDs to a degree)
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1. gastric irritation
2. prelonged clotting time 3. GFR changes 4. CNS effects |
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Describe the balance between PG and TX production
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PG inhibits clotting; TX promotes clotting
(both effects mediated via changes in platelet aggregation) |
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para-amino-phenol: what and why important
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metabolite of acetominphen
thought to act centrally to decrease pain and fever |
