Cardiac Drugs- Pharmacology

Card Set Information

Author:
ThomasStrugnell
ID:
233950
Filename:
Cardiac Drugs- Pharmacology
Updated:
2013-09-11 21:15:09
Tags:
UTAS2016
Folders:

Description:
pharmacology for cardiac drugs
Show Answers:

Home > Flashcards > Print Preview

The flashcards below were created by user ThomasStrugnell on FreezingBlue Flashcards. What would you like to do?


  1. Propanolol,Carvedilol
    • non-selective β blockers: Act on both β1 adrenoreceptors on cardiac muscle and β2 adrenoreceptors on smooth muscle. Inhibiting cardiac muscle contraction and increasing smooth muscle contraction
    • Indications: Hypertension, arrhythmia, heart failure, MI, angina
    • ADR: nausea, hypotension, bradycardia
  2. Metoprolol, Atenolol, Bisoprolol, Nebivolol
    β1 selective blockers only bind to β1 adrenoreceptors on cardiac muscle

    • Indications: Hypertension, arrhythmia, heart failure, MI, anginaADR- nausea, hypotension, bradycardia
    • ADR: nausea, hypotension, bradycardia
  3. Prazosin
    • α1 antagonists bind to α1 receptors,
    • inhibiting the binding of catecholamines without causing an increase in catecholamine release. Normally the catecholamine’s would bind and stimulate an up regulation of phospholipase C which would increase levels of both inositol
    • triphosphate and diacylglycerol leading to an influx of calcium. The influx of calcium then leads to smooth muscle contraction (vasoconstriction). However the blocking of catecholamines instead prevents this pathway resulting in the relaxation of smooth muscle.
    • Indications: Hypertension
    • ADR: Hypotension, Dizziness, Headaches
  4. Methyldopa, Clonidine
    • Noradrenalin release occurs under a negative feed back cycle controlled by its own concentration at pre-synaptic α2 receptors in the central nervous system. α2 agonists act to ‘speed up’ the response of the negative feed back cycle. By acting like catecholamines and binding to the α2 receptor, it is able to inhibit the activity of adenylate cyclase, leading to decreased cAMP levels. This then decreases the possibility of calcium channels opening resulting in the decreased exocytosis of the catecholamines.
    • Indications: Hypertension
    • ADR: Hypotension, Dizziness
  5. Nifedipine, Felodipine, Amlodipine
    • Dihydropyridines:Calcium channel blockers: L-type (slow) calcium channels. Mainly affect smooth muscle allowing for reduction of peripheral resistance without significant cardio depression. No negative inotropic effect observed due to baroreflex mediated increase in sympathetic tone.
    • Indications: Angina, Arrhythmia, Hypertension
    • ADR: AV block, Hypotension, Bradycardia, Arrhythmia, Oedema, Headache
  6. Verapamil
    • Non-Dihydropryidines: Calcoum channel blockers: This is the most commonly used
    • calcium blocker. It predominantly affects the atrioventricular node, and is capable of reducing ventricular response rates to supraventricular arrhythmias (as well as interrupting AV node re-entry circuits). It is much less active as a vasodilator then Dihydropyridines and is generally considered an antiarrhythmic rather than an antihypertensive.
    • Indications: Angina, Arrhythmia, Hypertension
    • ADR: AV block, Hypotension, Bradycardia, Arrhythmia, Oedema, Headache
  7. Diltiazam
    • Non-Dihydropyridines / Benzothiazepines: Calcium channel blockers:Affects the calcium influx of both smooth and cardiac muscle. Also depresses the SA pacemaker and AV nodal conduction
    • Indications: Angina, Arrhythmia, Hypertension
    • ADR: AV block, Hypotension, Bradycardia, Arrhythmia, Oedema, Headache
  8. Glycerol Trinitrate
    • In endothelial cells, GTN perfuses straight
    • across the membrane of and into smooth muscle cells. It is also converted to nitric oxide (NO). ‘NO’ diffuses into small muscle cells and stimulate guanylate cyclase which up regulates cGMP and then pKG. pKG regulates calcium concentration and causes changes in the degree of phosphorylation of smooth muscle proteins and ultimately to de-phosphorylation of myosin light chains.  At low doses, the main effect is within veins with little effect on arterioles. Venous relaxation leads to decreased central venous pressure and thus decreased preload. However any reduction in stroke output is compensated by reflex tachycardia and thus there is no change in mean arterial pressure.

    • Large doses cause arterioles to dilate and
    • thus arterial pressure drops.  Further more coronary flow increase occurs and there is an overall decrease in arterial pressure and cardiac output.
    • Indications: Angina, AMI, Hypertension
    • ADR: Tolerance, headaches, anxiety, hypotension, AF, vomiting, nausea, diarrhoea
  9. Enalapril, Captopril, Fosinopril, Lisinopril
    • Angiotensin converting enzyme (ACE) inhibitors;
    • ACE is a membrane bound endothelial enzyme responsible for the conversion of angiotensin I to angiotensin II which then continues down the renin angiotensin pathway. ACE inhibitors block the conversion of AI to AII. This results in a lowering of arteriolar resistance, and an increase in venous capacity (decreased cardiac output, stoke volume and increased natriuriesis). Renin will increase in concentration
    • in the blood due to a negative feedback loop, and so to will AI.
    • Indications: Hypertension, Heart failure, Chronic renal failure
    • ADR: Hypotension, Cough, dizziness, Fatigue, Nausea, Renal impairment
  10. Candesartan, Irbesartan, Losartan
    • Angiotensin
    • II receptor Blockers (ARBs): These drugs are AT-1 receptor antagonists meaning they block the activation of angiotensin II AT1 receptors. Blockage of these receptors directly causes vasodilation, reduces secretion of vasopressin
    • and reduces the production and secretion of aldosterone. This results in a reduction to blood pressure.
    • Indications: Hypertension, Heart failure, Chronic renal failure
    • ADR: Hypotension, Cough, dizziness, Fatigue, Nausea, Renal impairment
  11. Mannitol
    Osmotic Diuretic:This type of diuretic inhibits the reabsorption of water and sodium. It is pharmacologically inert and increases the osmolarity of blood and renal filtrate. They work by expanding the extracellular fluid and plasma volume, therefore increasing blood flow to the kidneys. The renal proximal tubule is the primary site of action. Normally water molecules follow sodium out of the proximal tubule, resulting in sodium and water reabsorption. When osmotic diuretics are introduced, they hold onto water molecules in the tubule. Since the luminal membrane is quite leaky to sodium, this causes a high back leak of sodium into the tubule.
  12. Acetazolamide
    • Carbonic Anhydrase Inhibitor:
    • These drugs suppress the activity
    • of carbonic anhydrase. Carbonic anhydrase
    • is largely responsible for converting carbon dioxide and bicarbonate ions. This means it helps regulation of acid levels and water content as well as the removal of carbon dioxide from the body. When carbonic anhydrase inhibitors are used, they typically work by reducing they body’s uptake of bicarbonate ions. They also decrease salt absorption. This has the effect of lowering fluid
    • levels in the body hence their use as diuretic agents.
  13. Hydrochlorothiazide, chlorthalidone, Bendrofluazide, Indapamide
    Thiazides and related diuretics: These diuretics control hypertensionin part by inhibiting reabsorption of sodium and chloride ions from the distal convoluted tubules in the kidneys by blocking the thiazide sensitive sodium/chloride symporter. They also increase calcium reabsorption at the distal tubule.
  14. Frusemide, Ethacrynic Acid, Butetanide, Piretanide
    • Loop Diuretics: These act on the ascending loop of Henle in the kidney. They act on the sodium/potassium/chloride symporter in the
    • thick ascending limb of the loop of Henle to inhibit sodium and chloride reabsorption. This is achieved by competing for the chloride-binding site.
  15. Spirinolactone, Amiloride, Triamterene
    • Potassium Sparing Diuretics:
    • These are competitive antagonists
    • that either compete with aldosterone for intracellular cytoplasmic receptor
    • sites or directly block sodium channels. The former prevents the production of
    • proteins that are normally synthesized in reaction to aldosterone. These
    • mediator proteins are not produced and so stimulation of potassium exchange
    • sites in the collection tubules does not occur. This prevents sodium
    • reabsorption and potassium and hydrogen ion secretion.
  16. Quinidine
    • Class 1a antiarrhythmic:By blocking sodium channels, class Ia drugs slow the rate of depolarization thereby increasing the duration
    • of the action potential. They have an intermediate rate of dissociation and also cause an additional blockage of the potassium rectifier channel resulting in increased refractoriness and thus delayed repolarization. The conduction
    • rate through normal and ischemic muscle is reduced and they affect almost all cardiac cells.
    • Indications: ventricular arrhythmias 
    • ADR: Pro-arrhythmic, Drowsiness, Hypotension, Bradycardia
  17. Lignocaine
    • Class 1B anti arrhythmic: 
    • These drugs bind to activated and inactivated sodium channels. They have a fast rate of dissociation. They are particularly effective at reducing the action potential in ischemic cells.
    • Their principle action is at the purkinje fibres, ventricular muscles and ectopic foci. Atrial muscles, sinoatrial and atrioventricular nodes are not affected. They slow the rate of depolarisation.
    • Indications: Myocardial infarction, Ventricular tachycardia, AF
    • ADR: Pro-arrhythmic, Drowsiness, Hypotension, Bradycardia
  18. Flecainide
    • Class 1C antiarrhythmic:     
    • Slow the rate of depolarization without affecting the action potential duration. They have a very slow rate of dissociation and are extremely pro-arrhythmic. There is potential for them to cause a slight prolongation of the refractory period. The result is a dramatic slowing of cardiac conduction via the sinoatrial and atrioventricular nodes, accessory pathways and atrial/ventricular fibres.
    • Indications: Atrial fibrillation prevention, suppress ventricular ectopic beats
    • ADR: Pro-arrhythmic, Drowsiness, Hypotension, Bradycardia
  19. Amiodarone, Sotalol
    • Class III drugs Antiarrhythmics
    • block potassium channels. This lengthens phase 3 of the action potential thus prolonging it. They also possess class I and II actions in that they slow down the SA and AV nodes conduction and also reduce excitability of atrial and ventricle cells.
    • Indications: Reverting back to sinus rhythm, VT and AT, Wolff-parkinson-white syndrome
    • ADR: Torsade's de pointes, bradycardia, hypotension, worsening arrhythmias, hyperthyroidism, corneal micro deposits in eye.
  20. Digoxin
    • Competes with the potassium in the sodium/potassium ATPase pump. By preventing this exchange of sodium and potassium, high levels of intracellular sodium occur. High intracellular sodium levels cause increased sodium and calcium exchange causing
    • a build up of intracellular calcium. A build up of intracellular calcium results in increased myocardiocyte contractility and excitability. The indirect effect is to increase vagal tone, slowing SA and AV node depolarization. It also slows the conduction velocity of the heart especially at the AV node.
    • Indications: AF, SVT, Heart failure
    • ADR: Bradycardia, Arrhythmia, confusion nausea, vomiting, visual disturbances
  21. Atropine
    • Completely inhibits the binding of Ach to muscarinic receptors in the parasympathetic and central nervous systems. This usually results in an increased heart rate, inhibition of smooth muscle contractions in the GI tract and genitourinary systems and also inhibits some glandular secretion.
    • Indications: Ach inhibitor for asystole, Bradycardia, excess sweating, salivation, vomiting, diarrhoea
    • ADR: Tachycardia, fever, visual disturbances, vomiting
  22. Adenosine
    • Adenosine acts at the A1 adenosine receptors and A2 receptors at the AV node. It causes an
    • increased potassium efflux and decreased cAMP induced calcium influx hence slowing down conduction at the atrioventricular node.
    • Indications: SVT
    • ADR: dyspnoea, chest pain, headache, nausea, Dizziness
  23. Adrenaline
    • Adrenalin acts to stimulate adrenergic nerves. To a variable degree it acts on both the alpha and beta-receptor sites of the sympathetic receptor cells (mostly it effects the beta receptors of the heart, vascular and smooth muscle). When given by rapid intravenous injection, it results in a rapid rise in systolic blood pressure by directly stimulating
    • cardiac muscle, which increases the strength of ventricular contraction. This causes increased heart rate and constriction of the arterioles in the skin, mucosa, and splanchnic areas of circulation.
    • Indications: anaphylaxis, sepsis
    • ADR: Palpitations, tachycardia, Arrhythmia, Anxiety, Hypertension, Acute pulmonary oedema
  24. Isoprenaline
    • Isoprenaline is a relatively selective beta2 adrenergic bronchodilator. Its stimulation of
    • beta-adrenergic receptors stimulates intracellular adenyl cyclase, the enzyme which catalyses the conversion of ATP to C-AMP. Increased C-AMP levels are associated with relaxation of bronchial smooth muscle and inhibition of release of mediators of intermediate hypersensitivity from cells, especially mast cells.
    • Indications: Heart block, Asthma, Chronic Bronchitis
    • ADR: Tachycardia, Cardiac Dysrhythmias
  25. Noradrenaline/ Dopamine
    • Noradrenaline activates alpha I receptors, causing phospholipase C to produce IP3 which
    • increases intracellular calcium via interactions with the sarcoplasmic reticulum. It also activates beta I receptors stimulating adenyl cyclase to produce cAMP and hence increase PKA levels which increase the probability of
    • calcium channels opening in myocytes and hence contraction occurrence increases. In smooth muscles the binding of beta I receptors results in a decrease in contractility.

    • Dopamine has different effects at different levels;
    • At low doses it is a vasodilator  
    • At medium doses it is a positive inotrope/chronotropic    
    • At high doses it is a
    • vasoconstrictor
    • Indications: Shock, Acute heart failure
    • ADR: anxiety, palpitations, headache, hypertension
  26. Dobutamine
    • Dobutamine is a direct acting inotropic agent whose primary activity results from stimulation
    • of the beta adrenoceptors of the heart while producing a mild chronotropic, hypertensive, and vasodilative effect.
    • Indications: inotropic support during acute heart failure and cardiogenic shock due to an MI or open heart surgery.
    • ADR: Tachycardia, Ventricular ectopic activity, Nausea, Palpitations
  27. Activated protein C
    • Activated protein C is an anticoagulant, which inactivates factors five and eight. This prevents
    • generation of thrombin and has additional anti-inflammatory actions including blocking monocyte production of cytokines and tumor necrosis factor and blocking cell adhesion.
    • Indications: severe sepsis in adults
    • ADR: Sever haemorrahage
  28. Gemfibrozil, Nictonic acid
    Triglyceride Lowering: Fibrates- these drugs activate the transcription factor PPAR-alpha that is found in the nuclei within the liver and brown adipose tissue (to a lesser degree). It is a transcription factor that up regulates expression of proteins involved in lipid metabolism;    

    • Enhance lipoprotein lipase,thereby increasing triglyceride uptake from the chylomicrons and VLDL
    • Inhibits peripheral lipolysis and decreases hepatic extraction of FFA, thus reducing hepatic triglyceride
    • production.
    • Inhibits synthesis of VLDL carrier apolipoprotein B causing a decrease in VLDL production.

    As a consequence of decreased triglyceride production the turnover and removal of cholesterol from the liver is accelerated and the excretion of cholesterol in the faeces is increased.

    • Ø  Nicotinic acid has also been used to decrease triglyceride
    • production. It is a vitamin that inhibits hepatic triglyceride production, VLDL
    • secretion, as well as increasing HDL synthesis.
  29. Atorvostatin, Simvastatin, Pravastatin, Fluvastatin
    • LDL lowering: Statins-Potent, specific reversible competitive inhibitors of HMG-CoA reductase, which is a rate limiting enzyme in cholesterol synthesis. HMG-CoA reductase inhibition
    • causes decreased hepatic cholesterol synthesis leading to increased synthesis of LDL receptors. This increase in turn results in a greater clearance of LDL. Reduced plasma LDL-c causes a small reduction in triglyceride and increased HDL.
  30. Cholestryamine
    • Absorption inhibitor: sequesters bile acids in the
    • intestine, preventing their reabsorption in the enterohepatic circulation.  Decreased absorption of exogenous cholesterol and increased metabolism of endogenous cholesterol into bile acids. It also causes increases in LDL removal from the body by increasing LDL receptor expression and also increasing triglyceride levels.
  31. Ezetimibe
    • Absorption Inhibitor: localizes at the brush border of the small intestine. It interacts with the intestinal mucosal transporter to inhibit cholesterol absorption to prevent and decrease delivery of intestinal cholesterol to the liver. The reduction of hepatic cholesterol stores leads to
    • an increase in clearance of cholesterol from the blood.
  32. Torcetrapib
    HDL increasing: Targets the cholesterol transfer protein to increase HDL levels
  33. Low Dose Aspirin
    • Anti-platelet: Alters balance between TXA2 (promotes aggregation) and PGI2 (inhibits aggregation) by acting mainly on COX-1 causing
    • it to irreversibly acetylate a serine residue in its active site, resulting in decreased TXA2 synthesis in platelets and prostacyclin synthesis in the endothelium.
    • Indications: AMI, Unstabole angina, prevention of stroke, Ischaemic heart disease, pain relief
    • ADR: GI bleeding, Haemorrhage, Allergic reaction, Gout, Hyperuricaemia
  34. Clopidogrel and Abciximab
    • Clopidogrel: Irreversibly binds platelet ADP
    • receptors, decreasing the release of calcium from the intracellular stores, which is required for GPIIb/IIIa receptor expression. 
    • Indications: Clotting, Ischaemia or other negative side effects have occured despite LDA therapy
    • ADR: Bleeding, anaemia, thrombocytopenia, diarrhoea

    • Abciximab
    • A monoclonal antibody which binds/ blocks the GPIIb/IIIa receptor thus preventing all pathways to platelet aggregation.
    • Indications: Bleeding, Diarrhoea, Anaemia, Thrombocytopenia
    • ADR: Development of antibodies
  35. Streptokinase, Tissue plasminogen activators
    • Thrombolytic agents 
    •     
    • Streptokinase- Binds plasminogen, exposing active site serine, causing plasmin activations. Derived from beta Haemolytic streptococci.

    Tissue plasminogen activators- TPAs activate plasminogen by converting it into plasmin, which splits fibrinogen and fibrin into their degradation products.

    • Indications: AMI, DVT, PE, Stroke
    • ADR: Bleeding, allergic reactions, Emboli
  36. Heparin/ LMWH
    • Heparin: activates and accelerates anti-thrombin III by binding and changing its conformation, resulting in enhanced thrombin inhibition of factors X and II (thrombin).
    •     
    • LMWH: are heparin fragments that bind, activate and accelerate anti-thrombin III action, however it only acts on factor X due to conformational binding.

    • Indications: High MI risk, DVT risk, PE risk, unstable angina
    • ADR: Bleeding, Hyperkalaemia, thrombocytopenia, osteoporosis
  37. Warfarin
    • Warfarin acts as a vitamin k antagonists, preventing the action and production of vitamin k reductase, thereby inhibiting the production of factors II, XII, IX, X and protein C and S.
    • Indications: stroke/DVT prevention, anticoagulation in AF and mechanical prosthetic heart valves
    • ADR: Bleeding, allergic reaction
  38. Rivaroxaban
    • Anti-coagulant 
    • Rivaroxaban inhibits factor X both the free and the pro-thrombin bound forms preventing thrombin production and limiting both the intrinsic and extrinsic pathways of the coagulation cascade.
    • Indications: Prophylaxis against thromboembolic disease in post surgical patients. 
    • ADR: Headache, nausea, vomiting

What would you like to do?

Home > Flashcards > Print Preview