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34 Cards in this Set
- Front
- Back
Thiazides |
diuretics used for hypertension to lower BP. Inhibits the Na+ and Cl- reabsorption in the kidney. (distal tubule) usually well tolerated but... hypotension= dizziness, loss of potassium loss of Na+= loss of water= decrease in BP |
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Cilazapril |
ACE inhibitor. Inhibits angiotensin 1-->2 decrease in production of AGT2= vasodilation, increased Na+ excretion, fewer activation of AT1 and AT2 receptors= decrease in aldosterone (Na retention) increase in bradykinin concentration. (vasodilator, involved in inflammation) = cough used for hypertension. cough, hypotension, rash, angiodema |
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Losartan |
Angiotensin 2 receptor blocker . Blocks the AT receptors= no bradykinin accumulation= no coughs. still have positive effects of AT2 receptors. - vasodilation - increased Na+ excretion Used for hypertension Generally well tolerated |
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Glyceral Trinitrate (GTN) |
Nitrate. breaks down to release nitric oxide (NO) - NO is a vasodilator - Causes Vasodilation to coronary arteries which supply the heart. - Not specific vasodilation NO--> Guanylate cyclase enzyme activity--> increase in cyclic CGMP levels--> activate CGMP dependent protein kinase--> smooth muscle relaxation Used for acute angina attacks effects: hypotension, headaches, dizziness |
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Propanolol- |
Non selective beta blocker. Reduces sympathetic activity. by being a non selective antagonist for Beta 1 and 2 receptors. Lipophilic so CAN pass through BBB Blocks B1 receptors in kidney. (renin release X) Blocks B1 and 2 receptors in the heart Blocks B2 receptors in the lungs Used for: Hypertension, angina and anxiety Adverse effects: CNS effects, Fatigue and poor exercise tolerance, worse lipid profiles, bronchoconstriction |
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Metoprolol |
Selective Beta Blocker Selective antagonist for Beta 1 receptors. Used for: arrythmias-->atrial fibrillation and tachcardia, angina, ypertension Lipophillic and can pass through BBB Adverse effects: fatigue, CNS effects, poor exercise tolerance |
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Atenolol |
Selective beta 1 receptor Used for: arrythmias, angina, hypertension Hydrophobic so cannot pass through BBB Adverse effects: Fatigue, poor exercise tolerance |
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Vepramil and Diltiazem |
Non selective Calcium Channel blocker Blocks L type Voltage gated Calcium channels. (blocks the pores) - Cardiac and vessel selectivity - Prevents Ca2+ ions from moving through Reduce HR, conduction velocity, and heart contraction Used for: Angina, arrthrias, hypertension Adverse effects: flushing, GI effects, Hypotension, bradycardia |
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Nifedipine |
Vessel specific selective CCB Blocks L type voltage gated Ca2+ channels on smooth muscle. (stabilizes inactive channels) - Vessek sekectivity - prevents depolarization from occuring - relaxation of smooth muscle= vasodilation Does not directly affect HR or contraction Used for hypertension. (esp elderly with stiff vessels) Adverse effects: DO NOT USE ALONE WITH ANGINA. causes tachycardia (elevated HR) because BP will decrease, increased force of contraction, Dramatically increase myocardial O2 demand. Use nifedipine with Beta blockers |
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Aspirin |
Antiplatelet Inhibits cox 1 at low dose and prevents thromboxane formation= platelet aggregation prevented, reduced recruitment of further platelets, reduced clot formation At high dose inhibits COX 2 which prevents production of Prostacyclin and promotes dilation Used for: reducing risk of developing clot, post treatment for angina, stroke. MI CAN get gastric bleeding |
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Heparin |
Anticoagulant ( IV administration ) Promotes the binding of heparin to AT3+ Factor 10 or + thrombin both needed for the coagulation cascade. and prevents production of fibrin because fibrinogen--> fibrin needs thrombin. (factor 10 needed to produce prothrombin-->thrombin) Used for: MI, stroke, deep vein thrombosis Adverse effects: haemorrhage Reversal therapy: Protamine sulphate. Heprain binds this instead of AT3 |
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Warfarin |
Anticoagulant (oral administration) Prevents reduction of vitamin K epoxide reductase. (reduced form of VK is the active version) Prevents Vitamin K from activating clotting factors Reduces formation of fibrin Used for: MI, stroke Adverse effects: Low therapeutic index, risk of hemorrhage Reversal therapy: Vitamin K administration (slow) Fresh frozen plasma (fast) |
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Alteplase |
Fibrinolytic Breaks down the clot after it has formed. Converts plasminogen to plasmin. Plasmin then breaks down the fibrin Used for: MI, Stroke If outside therapeutic window: High risk of haemorrhage= excessive bleeding |
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Indomethacin |
Acetic acid NSAID Potent anti inflammatory agen. Most adverse effects in NSAIDS. because more selectivity for COX 1 (COX 1 produces PGE1,2 and PGI2 which protects against gastric ulcers ) COX 1 inhibited= more gastric side effects |
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Ibuprofen |
Propionic acid NSAID class Analgesic and anti inflammatory effects. Widely used for inflammatory pain. Weaker than other NSAIDS Fewer Adverse effects: has reversible binding like aspirin. May have GI disturbances |
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Diclofenac |
Acetic Acid NSAID class Most potent/ powerful NSAID Higher affinity for toxins Powerful analgesic effects= Pain reliever for inflammation Adverse effects: GI upset, Headache |
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Paracetamol |
Simple analgesics (not considered NSAID) Weak inhibitor of COX 1 and COX 2 Analgesic and antipyretic - Pain reliever and prevent fever - No anti inflammatory effects Mechanism not fully determined Irak administration Quite safe. Large regular intake causes kidney damage |
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Coxibs |
COX 2 Inhibitor Targets inflammatory COX 2 while maintaining Gastroprotective COX 1 High therapeutic potential for inflammatory condition. Has the same side effects except no GI upset. If take highly potent COX 2 inhibitor= risk of getting heart attack |
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Corticosteroids (Preventer) |
Preventer!! Powerful Anti Inflammatory drug (more than NSAIDS) Reduces # of airways inflammatory cells and damage to airways epithelium Reduces Vascular permeability No immediate effect on bronchodilation 2 Routes of administration - Orally (prednisolone, Prednisone)- Bone degeneration, fat deposition - Inhalation(fluticasone) Goes through first pass metabolism in liver. very little in systemic circulation. Reduces Adverse reactions |
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Leukotriene receptor antagonists |
Anti inflammatory drug (preventer) Binding to Leukotriene GPCR has effects: - Decreases vascular permeability ( leukotrienes= Inflammatory mediators produced by immune cells - Vasodilation - Bronchodilation Less potent. Gets into systemic circulation much less. Reduces ADR |
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Lipoxygenase Antagonist |
Targets the enzyme upstream |
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Salbutamol |
SABA Beta 2 Agonist short acting Beta 2 Agonist. Acute inhalation treatment for bronchospasm. Prevents exercise induced asthma. Effects: relaxes airways, Bronchodilation. Used as required. lowest dose possible. only lasts 2-5 hours. Not nocturnal Adverse effects: Skeletal muscle tremor, Increase HR and force of contraction, Dilate peripheral vessels--> BP lowered, reflex tachycardia |
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Salmetrol |
LABA. Long acting B2 agonist - used for nocturnal asthma used as a prevention treatment. Also used with inhaled corticosteroids. Better control= Lower dose of corticosteroids. |
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Muscarinic Antagonists |
Atropine, Scopolamine, Hyoscine, Ipratropium - Blocks effects of parasympathetic NS stimulation of M3 receptor= Causing Bronchoconstriction - Atropine, Scopolamine and Hyoscine: 30 min to onset, 3-5 hours of duration, given with Beta 2 agonist All these used for asthma treatment For ipratropium--> for acute asthma treatment Adverse effects: Dry mouth, GI motility disorders, Cardiac effects, urinary retention, blurred vision |
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Theophylline |
Methylxanthines Treatment for COPD and asthma Phosphodiesterase inhibitor - Increase smooth muscle relaxation - Inhibits Phosphodiesterase 4 in lymphocytes and eosinophils - Improves asthma control Adenosine receptor antagonists - Bronchodilation - May be responsible for toxic |
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Tubocurarine |
Paralytic/ non depolarizing NMJ - Blocks AcH from binding to receptors. They are competitive inhibitors which blocks the ability of motor neurons to activate muscle - Prevents depolarization and hence no AP too. Can be reversed by addition of acetylcholinesterase inhibitor |
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Suxamethionium |
Paralytic/ Cholinergic depolarizing NMJ - Activates nicotinic acetylcholine receptor. Not hydrolyzed, Causing excessive depolarisation of muscle membranes which deactivate Na+ channels. - Much stronger and more persistent agonists than acetylcholine - Used to relax muscles and have anaesthesia effect |
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Spasmolytics- CNS |
Diazepam- Blocks GabA A receptor. Sedation. Baclofen- Blocks GABA B receptor, GPCR. Sedation but less than baclofen TIzamidine- Works on alpha 2 adrenoreceptors on motor neurons. drowsy, hypotension dry mouth Gabapentin- Voltage gated Ca2+ channels. Dizzy, sedation
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Spasmolytic- PNS |
Dantrolene- Interferes with Ca release--> reduce release from intracellular calcium stores-->interfering with muscle fibres= decrease skeletal muscle strength Indications: Muscle spasticity , malignant hyperthermia Adverse effects: Muscle weakness, sedation, rare hepatitis Botulinum Toxin (BOTOX) - Blocks release of AcH by slicing SNARE proteins. Snare proteins are necessary for transport of vesicles to the membrane for the release of ACh Indications: - Cosmetic purpose - Painful muscle spasms Adverse effects: - Muscle paralysis |
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Carbidopa |
Dopa decarboxylase inhibitor- Cannot pass through BBB. Inhibits conversion of L-dopa to dopamine. Use when L-dopa alone is producing irregular therapeutic control. Also reduces peripheral side effects of elevated dopamine-->Hypotension, GI discomfort |
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Apomorphine (dopamine agonist) |
Second line treatment. Subcutaneous injection. Prior to L-dopa effect kicking in. antiparkinsons effect approximately 5 min Short relief but good for rapidly treating. and although less effective it... - Lasts longer - lower risk of dyskinesia Adverse side effects: - Hallucinations - Nausea |
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Selegiline--> Enzyme inhibitor |
Monoamine oxidase inhibitor Specifically binds to B subtype. Reduces the breakdown of dopamine at synapse. Which increases the duration of action of dopamine in brain and increases activity of binding to receptor. Can be used as monotherapy in the early stages of parkinsons disease |
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Haloperidol |
Typical Antipsychotic Antagonist for type 2 Dopamine receptors. Can get parkinson disease like symptoms Also blocks - Muscarinic (constipation) , histamine (weight gain, drowsiness) and adrenergic receptors ( decrease BP, Dizzy and drowsy) Side effects: - Reduced dopamine receptor activation in prefrontal cortex - Reduced dopamine activity in nigostriatal pathway |
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Clozapine |
Second generation. Atypical antipsychotic - Inhibits both D1 and D2 receptor types for dopamine. also blocks serotonin (5- HT) receptors |