Recap Immune And Hemato Flashcards
Clopidrogrel MOA
Antiplatelet
Inhibit ADP binding to P2Y12 receptor
AAS MOA
Inhibit COX = less PG = less inflammation
Also blocks COX1 in platelets = less activation
Abciximab MOA
GP IIb/IIIa antagonist
No binding of fibrinogen or vWF
Tirofiban MOA
GP IIB/IIIa inhibitor (reversible)
Prevent fibrinogen binding
Alteplase MOA
Converts plasminogen to plasmin
—> lyses fibrin to fibrinogen
Streptokinase MOA
Produces activator complex: plasminogen —> plasmin
Tenecteplase MOA
Tissue plasminogen activator t-PA
Binds to fibrin clots —> cleaves Arg/Val bond = plasminogen—> plasmin
Thrombolytic
Nadroparin MOA
Binds to anti-thrombin III (ATIII) —> inhibition Xa
Antithrombotic
Warfarin MOA
Inhibits vit K ERC1 = no activation of vit K
Reduce clotting factors
Phytonadione MOA
Vitamin K
Cofactor to gamma glutamyl-carboxylase
= activation of factors: II, VII, IX, X
Procoagulant
Heparin MOA
Binds to antithrombin AT —> inactivates coag. factors
Enoxaparin MOA
Binds to anti-thrombin III (ATIII) = complex
= irreversible Xa inactivation
Acenocoumarol MOA
Inhibit vit K reduction = no carboxylation of coag.factors II, VII, IX, X
Folic acid MOA
Stimulate RBC, WBC, platelet production
Hydroxocobalamin MOA
DNA synthesis
Iron dextran MOA
Replenish iron stores
Famotidine MOA
H2 antagonist
Ranitidine MOA
H2 antagonist
Cyproheptadine MOA
H2 antagonist
5-HT antagonist
Cinnarizine MOA
Block Ca channels
Inhibit smooth muscle contraction
Misoprostol MOA
PGE1 analog —> PGE1R on parietal cells —> inhibit gastric acid secretion
Sucralfate MOA
Binds to + charged proteins in exudates —> protective coat in gastric mucosa
Metoclopramide MOA
D2 antagonist
Decrease LES pressure = more gastric emptying
More duodenal and jejunal motility
Domperidone MOA
D2 antagonist
Gastric muscle contraction —> prokinetic
Ondansetron MOA
Block 5-HT receptors in area postrema
Reduce vagus activity —> vomit center in medulla oblongata
Scopalamine butylbromide
Muscarinic receptor antagonist
For motion sickness
Aprepitant MOA
Substance P/ NK 1 receptor antagonist —> solitary nucleus and area postrema for CINV prophylaxis
Cinitapride MOA
5-HT agonist —> prokinetic and antiulcer
Mg Hydroxide MOA
React with HCl in stomach = neutralize
Pinaverium Bromide MOA
Block Ca channel
Inhibit GI smooth muscle contraction
Castor oil MOA
Anionic surfactant = less fluid absorption
Increase peristalsis
Butilhyoscine MOA
Block muscarinic receptors in GI and nicotinic
Spasmolytic for cramping
Cholestyramine MOA
Bile acid sequestrant —> feces excretion
Block cholesterol absorption
Sodium phosphate and citrate MOA
Increase fecal water content for more motility
Glycerin MOA
Draw water into intestine (hyperosmotic laxatives)
Loperamide MOA
Bind to opiate receptor —> inhibit Ach and PG release
—> reduce peristalsis
—> increase anal sphincter tone
Mesalazine MOA
Inhibit PG synthesis (COX) and interfere with leukotriene synthesis (lipooxygenase)
—> dampen inflammation
Octreotide MOA
Binds to somatostatin receptors - agonist
—> smooth muscle contraction in vessels
And less growth hormone (acromegaly, varices)
Pentoxifylline MOA
Increase erythrocyte ATP —> more RBC flexibility
Reduce plasma fibrinogen and platelet aggregation
Inhibit neutrophil activation
Plantago Psyllium MOA
Insoluble fiber, traps water in intestine
Bismuth MOA
Interacts with HCl and other anions to form bismuth salts
—> bactericidial and antimicrobial activity
= healing
Sibutramine MOA
Inhibit NE and 5-HT reuptake
Weight reduction
Dronabinol MOA
THC that binds to CB1 and CB2
—> increased appetite, reduce pain
Phentermine MOA
Increase in leptin and other mechanisms = appetite suppression
Rimonabant MOA
Selective CB1 blocker
Anti-obesity drug
Sennosides MOA
Metabolized by gut bacteria —> increase COX2
—> increase PGE2 —> less aquaporin 3 —> less reabsorption
= laxative
Tacrolimus MOA
Binds FK506-FKBP —> calcineurin inhibitor
= IL-2 downregulate
Sirolimus MOA
Binds to FKBP12 —> block mTOR —> stop between G1 and S
Cyclosporine MOA
Binds to cyclophilin —> calcineurin inhibitor
= IL-2 downregulation
Methotrexate MOA
Inhibit dihydrofolate reductase = folate antagonism
= less cell proliferation
Spermine inhibition
Adenosine release
Azathioprine MOA
Prodrug, purine analog
Inhibit purine synthesis = immunosuppression
Mycophenolate mofetil MOA
Prodrug, MPA inhibits IMPOH
Inhibit guanine synthesis = immunosuppression
Glucocorticoid MOA
Inhibit NF-kB
Inhibit cytokines, chemokines, AA metabolites, adhesion molecule
Glatiramer MOA
Induce peripheral Th2 to cross BBB
= CNS inflammation reduction
Elapegdemasa MOA
Supplement adenosine deaminase = more lymphocytes
(SCID treatment)
Perixafor MOA
CXCR4 antagonist = less binding of HSC to bone marrow
= mobilize progenitor cells
Trilaciclib MOA
CDK4/6 inhibition (kinase) = pause cell cycle
= prevent chemotherapy induces DNA damage
Pegademase MOA
Deaminates adenosine (toxic) —> inosine
Deficient adenosine deaminase replacement
(SCID treatment)
Allopurinol MOA
Inhibit xanthine oxidase —> less uric acid
Colchicine MOA
Binds to tubulin —> binds to microtubules —> stop elongation —> less monocyte and neutrophils —> less IL-1
= anti-mitotic and anti-inflammatory
(For gout flares)
Diclofenac MOA
COX1 and 2 inhibitor
Potent
Ketoprofen MOA
COX inhibitor
Meloxicam MOA
COX inhibitor
Methocarbamol MOA
Inhibit acetylcholinesterase —> CNS depression
(Acute muscle or bone pain)
Naproxen
COX inhibitor
(For CV history)
Piroxicam MOA
COX inhibitor
Sulindac MOA
COX inhibitor
Acemetacin MOA
COX inhibitor
Celecoxib MOA
COX 2 inhibitor
(For GI risk)
Acetaminophen MOA
COX inhibitor only in central tissues
Target heat-regulating centers in the brain
Natalizumab MOA
Binds to alpha 4 subunit of integrins
= prevent immune cell migration
(Crohn’s and MS)
Zolmitriptan MOA
5-HT agonist —> vasoconstriction and block pain signals
Rizatriptan MOA
5-HT agonist —> vasoconstriction —> block pain
Perphenazine MOA
Block D2 receptors in chemoreceptor trigger zone
—> prevent dopamine excess
—> reduce psychotic symptoms (halucinations)