cardio pharm

Question 1

diabetic nephropathy

Answer 1

ACE inhibitors and ARBS are protective

Question 2

calcium channel blockers

Answer 2

block voltage dependant L-type calcium channels of cardiac and smooth muscle –> reduce muscle contractility

Vascular smooth muscle: amolidipine = nifedioine > diltiazem> verapamil

Heart: verapamil> diltiazem > amlodipine = nifedipine

Question 3

dihydropyridines (amlodipine and nifedipine) are used for?

Answer 3

HTN, angina (including prinzmetal), raynaud

Question 4

non-dihydropyridines (diltiazem, verapamil) are used for?

Answer 4

HTN, angina, atrial fibb/flutter

Question 5

Nimodipine a calcium channel blocker is used for?

Answer 5

subarachnoid hemorrhage (prevents cerebral vasospasm)

Question 6

Calcium channel blockers side effects

Answer 6

cardiac depression, AV block, peripheral edema, flushing, dizzyness, hyperprolactinemia and constipation

Question 7

Class IV antiarryhthmics - Ca2+ channel blockers:

Verapamil and diltiazem

Answer 7

-slow the rise of the action potential on nodal cells (Ica phase 0)
-prolongue the repolarization at the AV node
… decrease in conduction velocity, increase in ERP and an increase in PR interval

used:
prevention of nodal arrhthmias (SVT), rate control in a fibb

side effects: constipation, flushing, edema, CHF, AV block, sinus node depression

Question 8

Hydralazine

Answer 8

increases cGMP–smooth muscle relaxation. Vasodilates arterioles> veins; decreases after load

use: HTN, CHF, first line with pregnancy with methyldopa, frequently coadministered with a beta blocker to prevent reflex tachycardia
tox: compensatory tach (contraindicated in angina/CAD), fluid retension, nausea, headache, angina can cause lupus like syndrome

Question 9

hypertensive emergency

Answer 9

nitroprusside, nicardipine, clevidipine, labetalol, fenoldopam

Question 10

nitroprusside

Answer 10

short active increases cGMP –> NO–> vasodilation, can cause cyanide toxicity as it release CN

Question 11

Fenoldopam

Answer 11

Dopamine D1 receptor agonist - coronary, peripheral, renal, splanchnic vasodilation –> decrease BP and increase naturesis

Question 12

Nitrogylcerin, isosorbide dinitrate

Answer 12

-vasodilate increase NO via cGMP increase
dilate veins» arteries decrease preload
use: angina, acute soronary syndrome and pulmonary edema

toxicity: reflex tach (treat with a beta blocker), hypotension, flushing, headahce

Monday disease in industrial exposure:
development of tolerance for the vasodilating action during the work week, loss of tolerance over the weeknd. on monday exposure–> tach, dizzy, headache

Question 13

Mg

Answer 13

effective in torsades de pointes and digoxin toxicity

Question 14

Cadiac gycoside: digoxin

Answer 14

75% bioavailabilty
20-40% protein bound
t1/2 = 40 hours
urinary excreted

mech: inhibits na/k/atpase leads to less Na out of cell and a build up of Na in the cell, so less Na wants to enter the cell to kick out the Ca in the Na/Ca exchanger

increase in the intracellular Ca –> positive inotropy.
It also stimulates the vagus nerve –> decrease the HR

treat: CHF, increase contractility; a fibb (decreases conduction at the AV node and depression of the SA node)

Question 15

digoxin antidote

Answer 15

slowly normalize K, cardiac pacer, anti digoxin Fab fragments, Mg

Question 16

Digoxin toxicity

Answer 16

cholinergic (stimulates vagus) - nausea, vomiting, diarrhea, blurry yellow vision
ECG- increase PR, decreases QT, ST scooping, T-wave inversion, arrhythmia, AV block

Can lead to hyperkalemia
factors predisposing to toxicity:
renal failure, hypokalemia (permits digoxin to bind at the K+ binding site on ?Na/k/atpase since less competition), verapamil and miodarone, quinidine (decreases digoxin clearance; diplaces digoxin from tissue binding sites)

Question 17

HMG CoA reductase inhibitors:
lovastatin
pravastatin
simvastatin
atorvastatin
rosuvastatin

Answer 17

decrease LDL
Increase HDL
Decrease TG’s
-inhibit hmgcoa conversion to mevalonate a cholesterol precurser

side effects: hepatotoxicity (increase LFTS)
rhabdomyolysis, espeically when used with vibrates and niacin

Question 18

Niacin (vitamin B3)

Answer 18

decrease LDL
Increase HDL
Decrease TG

Inhibit lipolysis in adipose tissue (decrease VLDL to IDL and LDL); reduces hepatic VLDL synthesis

side effects:
red flushed face, which is decreased with aspirin
cause:
hypergycemia, may see acanthosis nigricans
hyperuricemia (exacerbate gout)

Question 19

Bile acid resins :

cholestyramine, colestipol, colesevelam

Answer 19

decrease LDL
Slightly increase HDL
Slightly increase TG

Prevent intestinal reabsorption of bile acids; so the liver must use cholesterol to make more!

side effects: patients hate it tastes bad, GI discomfort, decreased absorption of fat soluble vitamins, you can also get cholesterol gallstones

Question 20

Cholesterol absorption blockers:

Ezetimibe

Answer 20

decrease LDL
Prevent cholesterol absorption at small intestine brush border

side effects: rare increase in LFTS
diarrhea

Question 21

Fibrates (gemfibrozil,clofibrate, bezafibrate, fenofibrate)

Answer 21

decrease LDL a bit
increase HDL a bit
Super decrease TG

Upregulate lipoprotein lipase, this will increase TG clearance. Activate PPAR-a to induce HDL synthesis

side effects: myositis (expeically with concurrent statins)
hepatotoxicity (increased LFTS)
cholesterol gallstones (esp with concurrent bile resins)

Question 22

Name the Antiarrhthmic Na channel blockers

Class 1A

Answer 22

Quinidine, Procainamide, Disopyriamide

The Queen Proclaims Disco pyramid partayyyy

Question 23

Name the Antiarrhthmic Na channel blockers

Class 1B

Answer 23

Lidocaine, Mexiletine

Question 24

Name the Antiarrhthmic Na channel blockers

Class 1C

Answer 24

Flecainide, Propafenone

Question 25

Name the Antiarrhthmic Beta blockers | Class II

Answer 25

Metoprolol, propanolol, esmolol, atenolol, timolol, carvediol

Question 26

Name the Antiarrhthmic K+ channel blockers | Class III

Answer 26

Amiodarone, Ibutilide, Dofetilide, Sotalol

Question 27

amiodarone toxicity

Answer 27

``` pulmonary fibrosis hepatotoxicity hypothyroidism/hyper 40% iodine by wt corneal deposits skin deposits (blue grey) resulting in photo dermatitis neurologic effects constipation bradycardia, heart block, CHF ``` it has Class i , ii,iii and iv effects! remember check PFT, LFT and TFT

Question 28

Antiarrhthmic Na channel blockers Class 1A: Quinidine, Procainamide, Disopyriamide

Answer 28

- decreases the slope of phase 0 - increased action potential - increased the ERP - Increase the QT interval (ventricle contraction) clinical use: atiral and ventricular ayyhythmias, espeically re-entrant and ectopic SVT and VT toxicity: Cinchonism (headahce, tinnitus with quinidine) reversible SLE syndrom with procainamide heartfailure with disopyrimide -thrombocytopenia -torsades de points due to increased QT interval

Question 29

Antiarrhthmic Na channel blockers | Class 1B: Lidocaine, Mexiletine, phenytoin

Answer 29

- decrease action potential duration, steeper slope of phase 3 - preferentially affect ischemic or depolarized purkinge and ventricular tissue. use: acute ventricle arrhthmia escially post MI, gigitalis induces arrhythmias tox: CNS stimulation/depression, cardiovascular depression

Question 30

Antiarrhthmic Na channel blockers Class 1C Flecainide, Propafenone

Answer 30

- prolongs refractory period at AV node - minimal affect on AP duration, slope at phase 3 is the same use: SVT, including AF, onyl as a last reost in VT tox: proarrhthmic, especially post-MI (contraindicated). Contraindicated in structural and ischemic heart disease

Question 31

Antiarrhthmic Beta blockers Class II Metoprolol, propanolol, esmolol, atenolol, timolol, carvediol

Answer 31

- decrease SA and AV nodal activity - decrease cAMP and thus PKA and thus less SR release of Ca - decrease Ca inward currents - decrease the slope of phase 4 depolarization in abnormal pacemaker cells - AV node is particularily sesistive, increase the PR interval note esmolol is very short acting

Question 32

Antiarrhthmic K+ channel blockers Class III: Amiodarone, Ibutilide, Dofetilide, Sotalol

Answer 32

- increase action potential - increase ERP - prolong repolariation slope of phase 3 decreases - increase QT interval use: a fibb, atrial flutter, v tach (amiodarone and sotolol) note sotolol- cause torsades de pointes and excessive B blockade ibutilide-torsades de points

Question 33

Antiarrhthmic Na channel blockers | Class 1A general:

Answer 33

``` slow or block conduction especially in depolarized cells. they decrease the slope of phase 0 (depolarization) and increase the threshold for firing in abnormal pacemaker cells. they are state dependent, selectively depress tissue that is frequently depolarized hyperkalemia cause increased toxicity for all class I drugs ```

Question 34

Antiarrhthmic Beta blockers | Class II toxicity

Answer 34

- impotence, exacerbation of COPD and asthma - bradycardia, AV block, CHF - sedation, sleep alterations - may mask the signs of hypoglycemia - metoprolol can cause dislipidemia - propanolol can exacerbate vasospasm in prinzmetal angina - contrain in cocaine users Treat overdose with glucagon