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Pharmacology
Final 2008 -new info
| Question | Answer |
|---|---|
| Hemostasis | prevention of blood loss following damage to a vessel |
| blood clotting involves | platelet adhesion, activation, and aggregation |
| thrombus | platelet plug and fibrin |
| normal blood vessels have a what preventing platelets from adhearing | endothelial layer |
| platelets activate acording to what hormones | ADP, seratonin, thromboxaine A2 |
| thrombosis | pathological formation of a thrombus in the absece of bleeding |
| arterial thrombus | "white" thrombus -made up of platelets and leukocytes associated with rupture of artheroscrlotic plaque in artery, very few red blood cells |
| Venous thrombus | associated wtih stasis of blood, platelets only a minor component |
| Drugs afect hemostasis and thrombosis by affecting | platelet function, blood coagulation, and fibrin degredation |
| platelet adhesion | von willebrand factor on sub-endothelium binds to GP1b receptors on platelet |
| platelet activation | secretion of granule contents, (ADP, 5-HT), synthesis of thomboxane A2, these increase the expression of GP2b and GP3a receptors |
| platelet aggregation | fibrinogen binds to adjacent platelets causing crosslinking |
| Use of anti platelet drugs | primary and secondary prevention of arterial thrombosis in pts a high risk for MI or stroke, during baloon angioplasty or stent placement |
| Low dose ASA | cardioprotective effect, irreverssible inhibitor of TXA2 (lesser effect on endothelial cox due to ability to sythesize more) |
| ADP receptors on platelets | p2y1 receptor and p2y12 receptor, both must be activated in order to aggregate |
| p2y1 receptor | on platelet, involved with ADP, Gq linked leading to aggregation |
| p2y12 receptor | on platelet involved with ADP, cAMP linked activation results in reduced cAMP |
| p2y12 receptor antagonist | ticlopidine and clopidrogel, 7-10 days to see affect, may give loading dose, bleeding, thrombocytopenia, thrombotic thrombocytopenia purpura, effects additive wtih ASA |
| ticlopidine (ticlid) | p2y12 receptor antagonist, 2.4% of people get severe neutropenia and fatal agranlocytosis can occur (early in therapy) |
| clopidrogrel (plavix) | p2y12 receptor antagonist |
| GP2b and GP3a receptor antagonist | only used acutely, not chronically, by injectioninfused during coronary angioplasty or stent placementADR: bleeding and thrombocytopenia |
| abciximab (reopro) | GP2b/GP3a receptor antagonist recombinant, most effective, treatment limited to once due to fatal thrombocytopenia after first time, remains bound to platelets long after cleared, |
| Aggrastat | peptide, complete with fibrinogen for receptor, GP2b/GP3a receptor antagonist |
| integrilin | peptide, complete with fibrinogen for receptor, GP2b/GP3a receptor antagonist |
| dipyridamole | blocks cellular uptake of ADP, also inhibits PDE3, ADR: headache |
| Aggrenox | additive benifit with ASA in stroke (dipyridamole) |
| Pentoxifylline | used for peripheral vascular disease, rheuological modulator that changes the shape of RBC's to get around artherscroltic areas |
| cilostazol | PDE3 inhibitor, contraindicatied in HF pts. Indicated for peripheral vascular disease pts |
| Anagrelide | potent PDE3 inhibitor, also inhibits the maturation of megakaryocytes, indicated for people with thrombocytoTHEMIA |
| Drug eluting stents | taxol and sirlimus, stents are coated in anti cancer drugs to prevent restenosis |
| anticougulants | treat or prevent thrombosis, work against clotting cascade |
| heparin | a family of sulfated glycosaminoglycan proteins, MW 5000-30000, for tertiary complex between antithrombin 3 and thrombin 2a causing inhibition of thrombin activity, also inhibiting factor Xa, monitor with ptt |
| heparin antidote | protamine sulfate, too much can lead to bleeding via inhibition of fibrinogen and platelets |
| heparin ADR | bleeding and hemmorageLong term, osteoporosis, LFT's, and hyperkalemia due to inhibition of aldosterone |
| Heparin induced thrombocytopenia (HIT) | 5-10 days after first exposure, binding to platelet factor 4, antibodies develop, pletelet number can be reduced by half, paradoxil thrombus may occur, significant mortality |
| LMWH | lower side of the heparins MW 1000-10000, binds to anti thrombin 3 complex however not large enough to inhibit thrombin so only inhibits factor Xa, can be giving out pt!, predictable response given based on body weight, less thrombocytopenia and bleeding |
| Lovenox | LMWH |
| enoxaparin | LMWH |
| fragmin | LMWH |
| innohep | LMWH |
| fondaparinox | factor Xa inhibitor, pentasaccaride based on heparins structure, less thrombocytopenia and bleeding |
| arixtra | factor Xa inhibitor, pentasaccaride based on heparins structure, less thrombocytopenia and bleeding |
| desirudin | thrombin inhibitor |
| thrombin inhibitor | based on hirudin (leach salivary peptide), predictable dose response, monitor with ptt, less antigentic, good for HIT pts |
| lepirudin | thrombin inhibitor, renal elimination |
| bivalrudin | thrombin inhibitor, renal elminiation |
| argatroban | thrombin inhibitor, p450 metabolized |
| Oral anticoagulants | inhibit the formation of complete clotting factors, via inhibiting vitamin K reducatase |
| warfarin | oral anticoagulant, onset of action around 48 hours, monitored by INR (2.5base), narrow theraputic index, bleeding hemmorage,teratogenic,antidote vit k |
| skin necrosis with warfarin | in protein c defficient individuals, actually causing initial thrombosis, 3-8 days after start of therapy, usualy in women |
| purple toe syndrome | extremly rare in individuals with artheriscrotic vessels, 3-8wks after starting therapy, discontinuation of warfarin stops pain but not discoloration |
| increasing warfarin effects | inhibiton of metabolism: cimmetidine (tagamet)inhibition of Vit K sythesis in gut: cephalosporinsIncreased degrdation of clotting factors: HypothyroidismDisplacement from plasma protein |
| reduction of warfarin effects | Vit K containing foodsDecreased degredation of clotting factors: hyperthyroidismIncreased metabolism: p45 inducers |
| Xigris | "specialty drug" recombinant active protein C, only approved in pts with severe sepsis, thought to inhibit some clotting factors -indirectly prolongs activation of tissue plasminogen activator |
| fibrinolysis | activation of plasminogen to plasmin to make fibrin into fibrin degradation products, action localized to thrombus due to circulating plasminogen inactivated by plasma inhibitors |
| fibrinolytic or thrombolytic drugs | increase conversion of plasminogen to plasmin, used to reopen an occluded areareduced mortality with MI -within 12 hourswith stroke -within 3 hours |
| streptokinase | fibrinolytic agent, older drug, use usualy limited to once due to formaton of anti streptococcal antibodies, binds to and activated plasminogenADR: fever, allergic reactions, hypotension (via kinins), bleeding and hemmorraging |
| urokinase | fibrinolytic agent, produced from human neonatal kidney cells, binds to and activated plasminogen, often administerd into IV line to break up clot, ADR: hypersensitivity, bleeding, hemmorage |
| recombinant tissue plasminogen activators | binds fibrin and activated fibrin bound plasminogen, supposively clot selective but due to high pharmacological dose this is lost |
| activase | fibrinolytic, recombinant, needs continuous infusion, not antigenic, bleeding intracranial hemorage, |
| TNKase | fibrinolytic agent, not antigenic, bleeding intracrania hemmorage, |
| Retavase | fibrinolytic agent, not antigenic, bleeding, intracrania hemmorage |
| prostanoids | autocoids, they act near to where they are being produced, effects via specific receptors |
| TXA2 | platelet aggregation and vasoconstriction |
| PGE2 | vasodilation, sensitation or norireceptors on nerve endings, central actions that mediate pain, hypothalmic thermoregulatory effect, increases mucus secretion in teh stomach, inflmattion, redness, edema, swelling, stiffness, pain, mainly found in WBC's |
| PGI2 | vasodilation, inhibition of platelet aggregation |
| COX | a family of isoenzymes |
| cox-1 | everywhere |
| cox-2 | constituent in the brain and kidneys, induceable in areas of inflamation |
| cox inhbitors | ASA (irreversible), non-acetylated salicylates (reversible), NSAIDS (reversible) |
| non-acetylated salicylates | weak inhibitors of cox (high dose required), may involve another unknown mechanism |
| dolobid | non-acetylated salicylates |
| diflunisol | non-acetylated salicylates |
| trilisate | non-acetylated salicylate |
| disalad | non-acetylated salicylate |
| salsalate | non-acetylated salicylate |
| NSAIDs | inhibit cox-1/cox-2, anti-inflammatory, analgesic, antipyretic (PGE3 in hypothalmic regulatory center), reduced risk of developing colon cancer, |
| ADR of COX inhibitors | lover levels of PGE2 reduces cytoprotective effect of the mucus lining in stomach, ulcers occur in 25% of pts. often requires drug that reduces stomach acid, prolonged bleeding time and brusing, can worsen preexisting edema, HF, or hypertension |
| furosemide | increases PGE2 which has a renal vasodilatory effect which = more pee |
| NSAID hypersensitivity rxns | Rhinitis, bronchoconstriction, angioedema, hypotension, shock, cross-sensitivity between ASA/NSAIDS in 1% population, 25% of allergy also have asthma & nasal polyps, associated with increased conversion of AA to leukotrienes, via 5 lipooxygenase |
| NSAID ADR | GI (nausea, constipation, diarrhea), dizziness, severe skin reactions, dermatitis, not to be used in 3rd trimester will close the ductus arteriousis "patent" = dead baby |
| ketorlac | prominant analgesic effects, can be used in place of opoid medications, may have effect on opiod receptors NSAID |
| Indomethacin | NSAID: 25-50% of pts will have severe frontal headaches, used IV to close ductus arteriousis with premature babies |
| ASA ADR | direct GI irritant, may cause iron deficiency anemia, not to be used in children under 16 due to reyes syndrome, salicylism, salicyate intoxication |
| salicylism | mild intoxication, headache, dizziness, sweating, tinnitus, reversible upon discontinueing |
| salicylate intoxication | central excitation, hyperplexia, death via respiratory failure (acute and chronic) |
| ASA with Cox-I | can interfear with the cardioprotective effect, if must take take, take ASA 2 hours prior to COXI |
| Cox-2 Inhibitors | Designed to only inhibit cox in inflamed tissue, however 5 fold incrase in MI/stroke, though there are alot less GI irritations occuring and does not effect platelets |
| diclofenac | moreselective for cox 2 then cox 1 NSAID |
| meloxicam | more selective for cox2 then cox 1 NSAID |
| celecoxib (celebrex) | least selective cox-2 inhibitor , only one still on the market reserved for pts that are intolerant of NSAIDS and not at risk for thromboembolic events |
| Off market Cox-2 inhibitors | Vioxx and bextra |
| Acetaminophen (tylenol) | analgesic and antipyretic effect, only weak inhibitor of cox-1 and cox-2, some evidence shows that it inhibits brain specfic cox isoenzyme overdose is bad 4g/day max |
| cysteinyl leukotrienes | LTC4, LTD4, LTE4 |
| cysteinyl leukotrienes cause | smooth muscle contraction (bronchoconstriction), incrased inflammatory cell acticity (eosinophil migration), incrased vascular permeability (edema), and increased bronchial and nasal secretions |
| Aspirin exacerbated respiratory disease | associated with cox inhibitors, more 5 lipooxygenase working, these pts are shown to have more LTC4 synthase activity |
| Accolate | LT receptor antagonist |
| Zafirlukasr | LT receptor antagonist |
| Singulair | LT receptor antagonist |
| Motelukast | LT receptor antagonist |
| LT receptor antagonist | inhibit LT's to being to LT receptor, chronic use in asthma, pt variablility in response, greater effect on pts who make more LTADR: headache, stomach pain, thrist, behavior related changes, agitation, insomnia, aggression, depression *preferd drug |
| Zyflo | 5 lipooxygenase inhibitor, reduce formation of LTS, heterogenity in pt response, ADR: Increased LFT's in about 5% pts, off market now but Zyflo CR now marketed |
| Uric acid | made via purine metabolism (xanthine oxidase), filterd by the glomerulus and reabsorbed via the proximal tubule |
| over producer vs underexcreter | given a 24 hr purine restricted diet and urine test, if high at the end = overproducer |
| tophaceous gout | gout of the tissues |
| urolitiasis gout | gout in the form of calculi (stones) in urine |
| uric acid precipitate | needle like crystalls in joints leading to pain/inflamation, large toe most likely |
| treatment of acute gout | releave pain and inflamation, NOT ASA!, NSAIDS (indomethacin high dose 3days/ lower 7days), colchicine |
| treatment of chronic gout | reduce serum uric acid concentrations, reduce recurrent attacks |
| colchicine | reduces the activity of the luekocytes, inhibits phagocytosis of urate cystals, must be given within 48 hours or useless, taken every 3 hours until pain releeaved, diarrhea has occured or max dose (8mg) has been reached |
| colchine ADR | diarrhea, dose dependant bone marrow suppression and neutropenia (can be fatal), metabolized via 3a4 and eliminated via Pglycoprotein into bile |
| colchine drug interactions | 3a4 substances (simvastatin = myopathy and rhabomyolysis), pglycoprotein inhibitors (verapamil, eryhromycin, and diltiazem) |
| under excreters therapy for gout | allopurinol or uricosuric drugs |
| over producers therapy for gout | allopurinol |
| therapy for chronic gout occurs when | when the pt has gotten over their acute attack completely |
| during first 6 months of chronic gout therapy | coadminister with nsaids or colchine (increased incident of attacks) |
| allopurinol | inhibits xanthine oxidase, useful for over producers and underexcreters ADR: hypersentitiity dermitis reversible upon discontinuation, can desensitize if neccisarym can be life thretening, decrease dose in renal infufficiency |
| allopurinal drug interactions | warfarin, azathioprine and 6 mercaptopurine (these 2 metabolized by xanthine oxidase) also immunosuppressants so very important |
| uricosuric drugs | block the transporter responsible for reabsorption of uric acid in the proximal tubule, DONT use in over producer =kidney stones, adjust dose with impaired renal function |
| uricosuric ADR | uric acid stones, increase fluid intake to prevent |
| uricosuric drug interactions | same drug as penacillins and cephalosporins |
| probenicid | uricosuric drug |
| sulfinpryrazole | uricosuric drug, can decrease the platelet aggregation causing bleeding |
| neurochemistry | presence, release, mimicry |
| presence | the ability to measure the levels of a compount in the body |
| lesions | cutting the neuron, this will significanly diminish or completely abolisn NT's from this site |
| release | most NT;s are CA+ mediated |
| EDTA | Calcium chelating agent, this will increas the NT in the area |
| mimicry | normal endogenous NT effects should be the same if we administer them exogenously |
| Falk-hillorp technique | NE = greenEPI+DA = greenSeratonin = yellow |
| NE orginates where in the CNS | locus cerolus |
| NE orginates where and goes to where | locus cerolus - hypothalmus, cortex, cerebellium, brainstem |
| amphetamines | arousal |
| beta blockers | wierd ass dreams |
| antidepressants | mood happyness |
| EPI | made from NE via PNMT, inhibitory, in brain stem -partially controlls respiration |
| Dopamine | many theraputic indications within the CNSA-8 -tuberoinfuridubular -prolactin releaseA-9 -nigrostraiatal - parkinsons -onvoluntary movementA-10 mesolimbic -schizophrenia |
| Dopamine acts as | inhibitory, mood, milk, movement, eMesis |
| Seratonin precursers | 5HT, 5-OH-TRP and L-TRP |
| 5HT | orginates in the raphe -goes to hypothamus, brainstem, cortex, functions on apitite, respiration, BP, sleep, temp regulation, mood, pain |
| fenfluramine | part of Fen-Phen, increases the release of 5HT, anorexant agent, |
| TRP | used to be available as a dietary suppliment till the japs tried to kill us, now only 5-OH-TRP available, analgesic effects, and inhibitory |
| AcH | via choline through CAT, metablolized by cholinesterases, involved in memory (alzhiemers disease) |
| other NT's | monoamines, AA;s, peptides, other |
| AA NT | Gaba (via glutamate) , glycine, glutamate, aspartate -50% of CNS NT's |
| GABA | made from glutamate, via GMD, broken down by GABAT into inactive cmpds, poorly understood in the perophery, A-ion channel B- GPCR, C-ion channel, highest concentrations in cortex, brain stem, spinal cord, and stiatta |
| drugs that effect gaba-A receptors | ethanol, pheobarbitol, benzodiazepines, |
| bicucilline | gaba - a receptor antagonist |
| picrotoxin | increased excition, block gaba-a channal |
| allyglcione | preventing sythesis of gaba -prevents GAD -convulsant |
| gabacone | inhibits gabaT -anticonvulsant |
| 4-methyl gaba | reuptake inhibitor -anticonvulsant |
| GHB | approved for narcolepsy through one pharmacy, works on gaba-b receptor, induces sleep schedule 1 and 3 drug, also works on ghb receptor but effect not know, |
| GHB precursers, | GBL and 1-4BD |
| baclofen | agonist at gaba-b receptors, skeletal muscle relaxant, induces sleep |
| Extasy | with sildinafil = sextasty, deletetion of seratonin = seratonin syndrome, dehydration due to high body temp, genetic disposition for certain reaction bruxism |
| bruxism | clenching of the teeth, why people on E use passifiers |
| cataplexy | paralysis of the body before a narcoleptic pts falls asleep, 75%, usualy via excitation |
| glycine | neither D or L, inhibitory, glycine A receptor, cl channel, involved in BP and seizure control , highlevels in brain and spinal cord |
| how to make glycine! | thr or SER via STHM makes glycine past the BBB |
| stirmychrine | convulsant, agonst at the glycine A receptor |
| glycine B receptor | part of a larger receptor NMDA receptor, excitatory, |
| glutamate | excitatory, NMDA receptor, involved in neuronal cell death, looking for an antagonist for stroke victums! |
| NMDA receptor | glycine B receptor is an allosteric modulator of this receptor, glutamate works a ton better with it |
| PCP | activates glutamate recptor, causes nystagmus |
| dextromethorphan | causes nystagmus via metabolites |
| peptide NTs | beta endorphins, met-enkaphelin, tev-enkaphalin, morphine like, works via not letting substance P out! no more pain.. yay |
| morphine | works presynapticly to decrease substance p , does not cross the BBB, made in the CNS |
| CCK- cholesytokinin | involved in fat absorption, modulater of dopamine release, onvolved involved in myostriatal dopamine -may be selective for parkinsonts?!?!?!?! |
| NO | very short t1/2 = 5 seconds, involved in learning and memory, help in alzheimers?, through NOS can be made from L-arg, |
| scopalamine | antimuscarinic agent, can induce amnesia with a coctail of other drugs, anti nausal drug |
| CO | may be a NT? -tiny ammount neccisary in the CNS |
| endocannabinoids | make you hungry... fatty acid derivatives, CB-1 and CB-2 receptors, agonists makes one hunggieee |
| CB-1 receptor antagonist, | decrease food intake, marketed in europe |
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