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44 Cards in this Set
- Front
- Back
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Clorthalidone
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thiazide - Na/Cl symporter blocker in DCT - increased water secretion. Used in HF (afterload reducing drug) and HPTN.
SE: hyperglycaemia, hypokalaemia, hyponatremia, hyperuricaemia, hypercalcaemia |
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Probucol
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Cholesterol-reducing drug
MOA unclear. Thought to relate to prevention of oxidation of LDL |
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Thyroxine
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increases LDL R in liver (decreases LDL - fat)
SE: metabolic action |
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Low Molecular Weight Heparin
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blocks Factor X action - stops coagulation from occurring.
EXPENSIVE but has a longer half life and can be brought home with patient (hospital vs patient at home costs) SE: haemorrhage, thrombosis, osteoperosis, hypoaldosternism, hypersensitivity reactions |
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Warfarin
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coumarin/coumadin
Vit K antagonist (which is a cofactor for factors II, VII, IX and X). - anticoagulant Delayed affect as need to wait for loss of factors for this to occur (wait 2 weeks, so give heparin and warfarin at the same time, wait awhile before patient can return home) MAIN IS TO DECREASE INCIDENTAL THROMBUS FORMATION SE: haemorrhage, necrosis of soft tissue |
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Protamine
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Heparin antidote
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Verapamil
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Cardioslective Calcium Channel blocker. Blocks Calcium channels and decreases contractions of myocytes -> decreased HR, decreased BP
Is a CLASS IV dysrhythmic. Used more for SVT (as blocks AV nodes) SE: AV block, bradycardia, hypotension, headache, oedema, HF |
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Minoxidil
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Potassium channel opener
Activates ATP-activated K channels, opens potassium channels and leads to hyperpolarisation of membranes, leading to decreased vasoconstriction --> vasodilation Used in HPTN emergencies and resistant HPTN SE: reflex tachycardia, hypertrichosis, hirutism, cardiac/CNS toxicity, peripheral oedema |
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Aspirin
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NSAID
Blocks COX enzyme irreversibly, stopping the formation of TXA2 and PGs Selective to platelets due to irreversible blocking --> stops platelet aggegration. Stops pain due to blocking PG (which cause pain) SE: haemorrhage, GI effects, resistance |
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Dipyridamole
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Anti-platelet aggregation/PDE Inhibitor
1. Adenosine uptake block. Maintain adenosine action to prolong cAMP elevation 2. Stops PDE from catabolising cAMP --> increased cAMP to stop platelet aggregation SE: headache |
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Clopidogrel
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anti-platelet aggregation
ADP R antagonist. Inhibit ADP-mediated activation of glycoprotein IIb/IIIa --> decrease platelet crosslinking. Decrease incidental thrombus formation DON'T combine with statins, as is also used to metabolise - impedes drug activity SE: haemorrhage, headache, flu-like symptoms, diarrhoea (not major SEs) |
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Digoxin
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Anti-arrhythmic (stops SVT) and cardiac glycoside
Activate mAChR-linked K channels in the AV node via hyperpolarise cells. Block Na/K ATPase, increase Na in cell and thus stop Ca from being released --> increased contractility SE: if too high K, leads to bradycardia (AV node block) If too low K, Na/K ATPase binding more strongly --> delayed after-depol --> tachycardia Nausea, altered colour perception, headache |
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Breytlium
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Class III K channel blocker
Block K channels in heart, slow rate of K efflux, prolong relative refractory period --> AP duration First choice treatment for re-entry tachycardia. SE: promiscuous drug. pulmonary and CNS toxicity, deposition of drugs crystals in eye, skin IS ALSO AN ADRENERGIC NEURON BLOCKER |
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Amiloride
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Epithelial Na Channel Blocker
Blocks Na channels in the DCT and CD --> decreased Na reabsorption leads to increased water loss. K sparing as Na loss leads to change in electrical gradient between basolateral and luminal membranes (K loss driven by electrochemical gradient). SE: hyperkalaemia, renal failure, headache, nausea, diarrhoea, vomiting, impotence |
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Osmotic Laxative
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Causes water movement into colon to allow passing through
SE: flatulence, abdominal distention, cramping |
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Adenosine
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Used for diagnosis of VT vs SVT
Activates A1/A3 R in AV node --> activate ATP -dependent K channels --> K efflux --> hyperpolarise cells and decreased AV node output. 3-6 second half life Caffeine intake affects dose (make sure to ask amount taken) |
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Neomycin
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Decrease fat
Given in large amounts as last resort drug, bind to cholesterol and bile salts in GI --> prevent reabsorption --> similar to ion exchange resins |
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Nicotinic Acid/Niacin
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Lower VLDL
Decreased VLDL production Increase formation from VLDL to LDL (consequently, to HDL) last resort (as poorly tolerated) SE: flushing, palpitation, impaired liver function, altered glucose tolerance, may trigger gout (hyperuricaemia) |
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Dexamethasone
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inhibit peripheral deiodination of TH (T4>T3)
Steroid drug --> antiinflammatory |
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-rinone
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PDE inhibitor in HF
Inhibits breakdown of cAMP --> encourage Ca channels to stay open for longer, increased contraction |
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Fish Oil
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need 250 grams of fish
meant to increase conversation of VLDL to LDL/HDL (debated) SE: high kilojoule preparations. Vit A and D toxicity, inhibit platelet aggregation |
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Fluticasone, Budesonide, Mometasone
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Glucocorticoids for asthma
MOA: activate glucocorticoid R --> migration of receptor complex to nucleus --> bind to glucocorticoid response element, decrease production of cytokines, decreased immune response --> decreased late phase response remodelling |
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-tidine
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H2 R antagonist
Antagonist histamine receptors at parietal cells --> block cAMP production and the activation of H/K ATPase, stops HCl production in stomach. SE: abdominal and gastric disturbances, constipation, diarrhoea, vomiting/nausea, possible increased risk of pneumonia |
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H1R antagonists
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anti-emetic/prokinetic
Blocks CBZ centres and stops vomiting and nausea |
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Procainamide
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Class Ia Na channel Blocker
Block Na channels, delay depolarisation rate K channel effects --> prolong repolarisation rate. Affects of automaticity due to K channel effects. SE: antimuscarinic (dry mouth, blurred vision, urinary retention), hypotension |
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Lignocaine
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Class Ib Na Channel blocker
Delay depolarisation rate by blocking Na channels Decreased automaticity due to Na leaky channel effect NOT ADVISED IN REENTRY TACHYCARDIA SE: drowsiness, numbness, GI disturbances, tremor, dizzy |
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Mexilitine
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Class Ib Na Channel Blocker
Delay depolarisation rate by blocking Na channels Decreased automaticity due to Na leaky channel effect NOT ADVISED IN REENTRY TACHYCARDIA SE: dizzy, drowsy, tremor, headaches, GI disturbances, paresthesias |
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Tocainide
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Class Ib Na Channel Blocker
Delay depolarisation rate by blocking Na channels Decreased automaticity due to Na leaky channel effect NOT ADVISED IN REENTRY TACHYCARDIA SE: dizzy, drowsy, GI disturbances, headaches, tremor |
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Encainide
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Class Ic Na Channel Blocker
Na channel blocker --> delay depolarisation rate. Small effects on K channels (increase hyperpolarisation time) Small effects as B-blocker --> increase effective refractory period SE: dizzy, visual disturbances, headache, life-threatening VTs |
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Flecainide
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Class Ic Na Channel Blocker
Na channel blocker --> delay depolarisation rate. Small effects on K channels (increase hyperpolarisation time) Small effects as B-blocker --> increase effective refractory period SE: dizzy, visual disturbances, headache, life-threatening VTs |
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-eplase
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Tissue-plasminogen activators
Activate Serine proteases --> catalyses conversion of plasminogen to plasmin. Leads to fibrinolysis. Clot-specific expensive, as made from rDNA inhibited by lipoprotein a SE: haemorrhage |
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-stigmine
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AChE inhibitor
inhibits the enzyme AChE --> prolong ACh action in synapse --> allow repeated activation by ACh used in Alzhemier's and MG SE: increased PNS symptoms, muscle twitching |
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Succinycholine
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Depolarising neuromuscular blockers
AChR agonist --> desensitise muscles to ACh so won't respond Used adjacent to anaesthesia in artificial ventilation SE: muscle fasiculations, stimulate PNS, prolonged paralysis |
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non-depolarising neuromuscular blocker
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competitive antagonist for AChR --> stop ACh activation of muscles --> flaccid skeletal muscles and paralysis
Mainly in anaesthesia in conjunction with artificial ventilation SE: hypotension, increase HR, bronchospasms |
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Trimetaphan
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ganglionic blocker
Blocks ACh release from ganglions --> affects both SNS and PNS Cardio effects --> vasodilation, decreased arterial BP Used in anaesthetic procedures SE: postural hypotension, decreased secretions, decreased venous return, long-sightedness, hypothermia, decreased appetite, constipation (GI paralysis), impaired micturition |
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Pilocarpine
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Muscuranic Agonist
Activates mAChR by causing conformation change of the receptor --> activation of postsynaptic R Used for decrease CO, generalised vasodilation, SMOOTH muscle contraction, increase secretions, constriction of constrictor pupillae muscle in eye (GLAUCOMA and URINARY RETENTION) SE: increased bronchoconstriction, increased secretions, diarrohea, increased secretions and sweating. |
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Atropine, Pirenzipine
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mAChR Antagonist
blocks AChR --> stops PNS signalling decreased PNS effects and increases SNS effects Used in asthma and bronchitis SE: antimuscuranic (dried mouth, blurred vision, sedation, constipation, tachycardia, increased intraocular pressure (worsens glaucoma) and urinary retention |
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-terol
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B-agonist
activates B-adrenergic-R --> stimulate AdCy --> open Ca channels (in heart)/close Ca channels (in lungs) Used in asthma, cardiogenic shock, premature labour SE: tachycardia, dysrhythmia, peripheral vasodilation/oedema |
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Dobutamine
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Used in cardiogenic shock and HF
partial agonist Direct stimulation of B1 R in the SNS --> positive ionotropic actions SE: arrhythmia, HPTN, tachycardia, angina |
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Clonidine
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Centrally acting a2-agonist
Activates vasomotor centres in brain and leads to closing of Ca channels --> vasodilation Used in HPTN and HF SE: light-headed, dizzy, constipation, dry mouth, hypotension |
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Primidone
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Barbiturate
GABA channel modulator --> keeps GABA channels open longer --> increase GABA release which increase Ca channel block -> decrease NT release in brain. Inhibit spread of epileptic focus Used in EVERYTHING except absence seizures metabolised into phenobarb (using cyt P450) SE: sedation, depression, irritability, nystagmus, ataxia, megaloblastic anaemia |
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Phenobarbitone
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Barbiturate
GABA channel modulator --> keeps GABA channels open longer --> increase GABA release which increase Ca channel block -> decrease NT release in brain. Inhibit spread of epileptic focus Used in EVERYTHING except absence seizures SE: sedation, depression, irritability, nystagmus, ataxia, megaloblastic anaemiaBarbiturate GABA channel modulator --> keeps GABA channels open longer --> increase GABA release which increase Ca channel block -> decrease NT release in brain. Inhibit spread of epileptic focus Used in EVERYTHING except absence seizures SE: sedation, depression, irritability, nystagmus, ataxia, megaloblastic anaemia |
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Diazepam
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Benzodiazepine
GABA channel modulator --> increase frequency of GABA channels opening --> decrease Ca channel opening and decreased NT release. Inhibit spread of epileptic focus Used in ALL types (less effective in absence seizures) and first line for STATUS EPILEPTICUS SE: sedation, hypotonia, dysarthria, dizziness, anorexia, hyperphagia. Abuse potential |
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Valporate
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increase time of recovery for Na channels and limited capcity to inhibit thalamic Ca channels. Augment GABA production and impede metabolic breakdown (change RMP)
Used in most, ESPECIALLY ABSENCE SEIZURES SE: less than other drugs. alopecia, nausea, vomit, anorexia, sedation, ataxia, tremor, weight gain, foetal malformation |
