Beta Antagonist

(beta blocker)

Nonselective sympathetic beta antagonist - decrease BP

Beta-1 antagonist

Cardioselective (decrease BP)

Alpha-2 agonist

Sympatholytic and indirect (stop NE release)

Alpha-1 antagonist

(causes vasodilation)

all alpha-1 antagonist

-these vasodilate (for tx of hypertension and BPH)

Beta blockers

(sympathetic antagonist for Beta-1 and Beta-2)

A thiazide. It works on the distal tubule.

-Blocks NaCl co-transporter, so salt stays in urine, and hence you pee more. 

Side effects: hypokalemia and hypouricemia

Loop diuretic

-act on thick, ascending limb to prevent NaCl reabsorption, specifically from a Na/K/2Cl transporter. 

Side effects: hypokalemia and hyperuricemia

Potassium sparing diuretic.

-antagonist at the mineralocorticoid receptor. they block aldosterone from having an effect. normally aldosterone would increase Na/K ATPase, which promotes sodium reabsorption. Instead, we're blocking aldosterone from binding to MR receptor. so it's an MR antagonist.

Potassium sparing diuretic

Blocks Na channels on the lumen. 

alpha-2 agonist

-Works on solitary nucleus. It reduces sympathetic nervous system activity

Nonselective beta blocker. decreases BP. 

-Direct acting

Selective for Beta-1 antagonist. 

-Cardioselective beta-blocker

Alpha-1 antagonist

-vasodilate

Alpha-1 antagonist

-vasodilate

-oral drug. selective arterial dilator. 

-keeps potassium channels open

highly effective vasodilator. 

-used for severe hypertension

-lots of side effects: hypertrichosis

-keeps potassium channels open

-used in emergency situations. and is too efficacious with too many side effects for outpatient use. 

-it's a IV nitrate drug.

-it's dinitrated to nitric oxide (a vasodilator) and acts to hyperpolarize the neuron by keeping K channels open. 

Non-cardioactive and relax smooth muscles but have little effect on cardiac output

-all end in -dipine

Shorter acting Dihydropyridines (CCBs) at 4 hours. 

-increased risk of MI

These are inhibiting the conversion of angiotesin I to angiotensin II at ACE.

-end in -pril

-Side effects: due to bradykinin (less metabolism with ACE inhibitors) such as dry cough, angioedema; also hyperkalemia, and reduced kidney function (good for diabetic)

Inhibits the conversion of angiotensinogen to angiotensin I by blocking the enzyme renin.

So they're a renin-inhibitor

Low molecular weight heparin

-less efficacy

Only oral anticoagulant

-It prevents the synthesis of clotting factors by inactivating Vitamin K epoxide reductase . 

-slower than heparin. 

prevents bile acid reabsorption, so it gets eliminated!

-therefore you need to increase LDL receptors to get more LDL in the liver cells to make more cholesterol for bile!

inhibit HMG-CoA reductase

-ergo preventing cholesterol synthesis

Simvastatin/Ezetimibe

-combo drug

-it produced greater reductions in LDL than simvastatin alone, but no different in coronary atherosclerotic plaque.

These dilate veins (reduce preload and oxygen demand)  and dilate arteries (increase oxygen supply via coronary arteries) more than resistance arteries.

Note: high tolerance and toxic effects of headache, flushing/sweating and hypotension

Nitroglycerin is very effectively metabolized when given orally due to first pass effects. you can avoid this by giving nitroglycerine sublingually. This is because blood supply in mouth is different than hepatoportal system that shunts right to the liver. 

Note: there are also sprays &transdermal patches

-Use cardioactive CCBs when by themselves

-Use non-cardioactive when used with beta blockers.

Note: they should not be used when unstable or with people who have a history of acute MI.

Best for classic angina. They decrease oxygen demand by decreasing heart rate and decreased contractile force. 

Note: may precipitate vasospasm in people with variant angina

These dilate veins (reduce preload and oxygen demand)  and dilate arteries (increase oxygen supply via coronary arteries) more than resistance arteries.

Note: high tolerance and toxic effects of headache, flushing/sweating and hypotension

Nitroglycerin is very effectively metabolized when given orally due to first pass effects. you can avoid this by giving nitroglycerine sublingually. This is because blood supply in mouth is different than hepatoportal system that shunts right to the liver. 

Note: there are also sprays &transdermal patches

-Use cardioactive CCBs when by themselves

-Use non-cardioactive when used with beta blockers.

Note: they should not be used when unstable or with people who have a history of acute MI.

Best for classic angina. They decrease oxygen demand by decreasing heart rate and decreased contractile force. 

Note: may precipitate vasospasm in people with variant angina