Please enable JavaScript.
Coggle requires JavaScript to display documents.
Cardiac medications (Beta blockers (LOLS, Three groups 1st generations-…
Cardiac medications
Beta blockers
-
Three groups 1st generations- Non selective causing more side effects , 2nd generations cardioselective in high doses can still cause side effects and 3rd generations Have additional dilation effects.
-
B blockers prevent the binding of noradrenalin to b1 which ;eads to decrease in intracellular Ca concerntrations. Causes decreased contractility of the heart (negative introaphy). Reduced HR and reduced conduction
-
Nitrates
-
Nitrates causes vasodilation within the coronary arteries resulting in reduced vasospasm and restoring blood flow. It also vasodilates systemic arteries and veins causing decrease in preload and after load which decreases work of heart.
Side effect is a headache due to vasodilation within the head and decreased bp- postral drop or falls
Nitrates convert into NO which act on enzyme in vascular system called guanlaucyclase which produces cyclic g mp which acts on Ca channels- reduces Ca entering the cells which results in smooth muscle dilation
Asprin
Blood thinner, Works by deactivating cyclol oxygenase (COX). COX acts on arachidonic acid and converts it into prostaglandins (inflammatory mediators). Aspirin stops COX which stops formation of prostaglandins and reduced inflammation
COX converts arachonidonic acid and turns it into thromboxane 2 which regulates clumping actopm of platelets. Stops clumping of platelets meaning blood becomes thinner
-
anti platelets
-
Stops platelet aggregation. Normally ATP binds to receptors on platelet surface which results in the release of anisnotral triphphate which causes the release of Ca ions. The increased Ca concentration activates glycoprotein receptors on membrane. Fibrogen binds to glycoprotein receptos on two separate platelets resulting in aggregation.
-
anti coagulants
Warfrin
Vitamin K inhibitor. Bonds to vit K reductase in the liver cells and inhibits the activity. Results in decrease in preduction of vit K which leads to deactivation of t-glutamyl carboxylase. This supresses the production of clotting factors.
-