Spring Drugs Flashcards
Mechanism of dapsone
Taken orally or applied topically ➡️ structural analog of paraaminbenzoic acid (PABA) that competes with PABA for binding to dihydropteroate synthetase prevents formation of dihydropteroate ➡️ inhibits folate synthesis ➡️ disrupts nucleic acid synthesis ➡️ decreased DNA synthesis ➡️ causes bacterial cell death
Mechanism of rifampin
Taken orally or inject intravenously ➡️ Binds with the beta-subunit of mycobacterial DNA-dependent RNA-polymerase ➡️ blocks bacterial RNA transcription ➡️ disrupts protein synthesis ➡️ causes bacterial cell death
Mechanism of clofazimine
Taken orally ➡️ binds to DNA ➡️ prevents reading of DNA template ➡️ causing bacterial cell death
Thought to generate cytotoxic oxygen radicals (H2O2) which is toxic to bacteria causing bacterial cell lysis
Mechanism of chloroquine on infected RBC
Oral administration ➡️ absorption in the gastrointestinal tract ➡️ chloroquine concentrates in the
acidic food vacuole of the malaria parasite and increases pH ➡️ chloroquine binds to heme ➡️ toxic heme cannot be polymerized to harmless hemozin ➡️ accumulation of toxic heme within the food vacuole of the malaria parasite ➡️ increased pH and accumulation of toxic heme
cause oxidative damage to plasmodial membrane and RBC membrane ➡️ lysis of malaria parasite
and red blood cell
Mechanism of primaquine
Oral administration ➡️ absorption in the gastrointestinal tract increased concentration in the plasma ➡️ converted to electrophilic intermediate ➡️ acts as an oxidation reduction mediator ➡️ generation of reactive oxygen species which can cause membrane damage (to parasite) OR can act by interfering with the mitochondrial electron transport (in the parasite) ➡️ prevention of replication of liver cell into merozoite-containing cells in liver ➡️ decreased parasitic load
Mechanism of pyrimethamine
Inhibition of dihydrofolate reductase ➡️ no formation of tetrahydrofolate ➡️ no purine synthesis of parasite ➡️ no DNA synthesis ➡️ increased parasitic death
Mechanism of chloroquine in blood
in blood: prevention of merozoite transformation into a trophozoite ➡️ decreased parasitic load
Mechanism of warfarin general
Oral administration ➡️ inhibits vitamin K epoxide reductase ➡️ decreased conversion/reduction of vitamin K epoxide to reduced vit K ➡️ decreased vit K ➡️ decreased gamma-carboxylation of glutamate residues of factor II, VII, IX, X, protein C and S ➡️ decreased binding to Ca2+ ➡️ decreased coagulation factor binding to neg charged phospholipid surface of platelet ➡️ decreased coagulation
Mechanism of unfractionated heparin
Heparin injected via IV into plasma ➡️ binds to Antithrombin III ➡️ induces conformational change ➡️ exposes active site ➡️ increased interaction of ATIII (1000x faster) ➡️ binds to coagulation factors free in plasma: IIa (thrombin), Xa, IXa
Mechanism of low molecular weight heparin
complex with antithrombin III ➡️ inactivate
factor Xa
Mechanism of aspirin
binds irreversibly to the active site of COX-1 ➡️ decreased conversion of arachidonic acid to prostaglandin G2 ➡️ decreased PGH2 ➡️ decreased synthesis of thromboxane A2 ➡️ shifts balance of chemical mediators to favor anti-aggregator effects of prostacyclin ➡️ preventing platelet aggregation ➡️ diminished ability of coagulation ➡️ suppression of platelet aggregation for life of platelet (7-10 days)
Mechanism of Clopidogrel (Plavix)
Irreversibly binds to P2y12 ADP receptors on platelets ➡️ decreased activation of GP IIb/IIIa receptors ➡️ decreased GP IIb/IIIa-fibrinogen-GP IIb/IIIa molecular bridges ➡️ decreased plate aggregation
Mechanism of Alteplase (t-PA)
rapidly activates plasminogen that is bound to fibrin in a thrombus or a hemostatic plug
Mechanism of Streptokinase
forms an active one-to-one complex with plasminogen ➡️ enzymatically active complex converts uncomplexed plasminogen to the active enzyme plasmin
complex also catalyzes the degradation of fibrinogen and clotting factors V and VII
Mechanism of Urokinase
directly cleaves the arginine–valine bond of plasminogen to yield active plasmin
Mechanism of loperamide
Activate presynaptic µ opioid Receptor in enteric nervous system ➡️ inhibit ACh release ➡️ decrease binding to M3 receptors ➡️ decrease Gqa activation ➡️ decrease PLC ➡️ decreased cleavage of PIP to IP3 and DAG ➡️
decreased Ca2+ released from ER d/t decreased IP3
and decreased PKC d/t decreased DAG decreased ➡️ decreased contraction of smooth muscle in intestine wall ➡️ decrease peristalsis ➡️ increase transit time in intestine ➡️ increase water absorption ➡️ decrease water excretion and diarrhea
Mechanism of diphenoxylate
Activate presynaptic µ opioid Receptor in enteric nervous system ➡️ inhibit ACh release ➡️ decrease binding to M3 receptors ➡️ decrease Gqa activation ➡️ decrease PLC ➡️ decreased cleavage of PIP to IP3 and DAG ➡️
decreased Ca2+ released from ER d/t decreased IP3
and decreased PKC d/t decreased DAG decreased ➡️ decreased contraction of smooth muscle in intestine wall ➡️ decrease peristalsis ➡️ increase transit time in intestine ➡️ increase water absorption ➡️ decrease water excretion and diarrhea
Mechanism of bismuth subsalicylate
Rapid dissociation of compound within stomach ➡️ absorption of salicylate ➡️ bismuth goes to intestine ➡️ coats mucosa of intestine ➡️ inhibits secretion of prostaglandin ➡️ decreased Gs activation ➡️ decreased AC ➡️ decrease cAMP intracellularly ➡️ decreased PKA ➡️ decrease stimulation of apical CFTR secretion channel ➡️ decreased secretion of Cl- into lumen ➡️ decreased Cl-/HCO3- exchanger on apical membrane with Cl- going in ➡️ decreased HCO3- secretion ➡️ decreased negative apical transmembrane potential ➡️ decreased secretion of Na+ ➡️ increase osmolarity intracellularly ➡️ increase water absorbed in intestine ➡️ decrease diarrhea
?Prostaglandin decrease peristalsis ➡️ increased colonic transit time ➡️ further increase in reabsorption of water
Mechanism of Aluminum hydroxide
Coats intestine ➡️ adsorbs (chemically bind to surface) intestinal toxins/microorganisms coating intestinal mucosa ➡️ sheds with bacteria out of body ➡️ increased clearing of bacteria ➡️ decrease stimulant of cause of diarrhea ➡️ decrease diarrhea
Mechanism of methylcellulose
Indigestible, hydrophilic colloids absorb water ➡️ forms bulky, emollient (make soft) gel ➡️ distends colon ➡️ promote peristalsis ➡️ increase excretion of bulky stools
Mechanism of Clindamycin
bind to the 50S subunit of ribosome ➡️ inhibiting translocation of the ribosome on the mRNA with only one ribosome (monosome) ➡️ insufficient translation of protein ➡️ prevent nucleic acid formation ➡️ cell death
