Cardiovascular

BP = CO x SVR When there is increased peripheral resistance, blood flow is imposed by friction between the artery walls, blood pressure increases due to blood viscosity and diameter of the arteries. 2 + readings of 140/90 = pre hypertension. Primary / idiopathic / essential HTN - due to unknown causes

Due to other organ damage such as renal

Diet, smoking, alcohol, lack of exercise

Age, gender, family history

Genetic and environmental factors, Sympathetic nervous system stimulation, Excess adipose tissue = increased renin-angiotensin and aldosterone, insulin resistance, Na+ retention in the kidneys, Vasoconstriction - increased CO & SVR = HTN

ACE inhibitor Angiotensin II inhibitors A blocker B blocker Ca+ channel blockers Diuretics

Loop Thiazides Potassium sparing

Inhibits the action of epinephrine on the B1 receptors of the cardiac muscle to reduce contractility and reduce SVR = reduced BP

By inhibiting calcium ion channels it prevents calcium from entering the cardiac muscle and arteries, vasodilation can be accomplished by reducing contraction caused my Ca.

A potassium sparing diuretic, MOA inhibits NA/K exchange channel, increasing NA elimination and therefore H2O but sparing K

K sparing diuretic. MOA acts independent of aldosterone decreases water retention and Na in DCT

ACE inhibitors - inhibits enzyme ACE to prevent conversion of angiotensin I to II

B blocker - reduce the speed and force of heart contractions by blocking the effects of adrenergic (norepinephrine) receptors on the b1 receptors of the heart

Angiotensin II receptor blockers. Angiotensin II causes vasoconstriction.

Loop diuretic, blocks reabsorption of Na, K and H2O in the loop of henle therefore increasing urine output

Inflammatory cellular response leading to formation of fibro-fatty lesions (plaques) in the intimal layer of M&L arteries. Progressive accumulation of smooth muscle cells, lipids, and connective tissue.

Ischemic Heart Disease - narrowing of the arterioles due to atherosclerosis

Acute Myocardial Infarction - complete occlusion of a coronary artery with a thrombus. Cellular necrosis

Abnormal level of lipid concentration in the blood, imbalance of cholesterol, triglycerides, HDL and LDL

Focal accumulation of lipids in a vessel wall due to increased plasma lipoproteins, reaction to injury, proliferation of smooth muscle cells due to endothelial injury - inflammatory response. LDL accumulates -> macrophages phagocytise to create foam cells which builds up to progress to fatty streaks. Often accumulate at branch points.

Thrombus / emboli

Inhibit the enzyme HMG-CoA which is responsible for cholesterol production in the liver. Grapefruit juice contraindicated because of metabolism by cytochrome p450

A potassium sparing diuretic

Is a low molecular weight heparin