Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
182 Cards in this Set
- Front
- Back
|
What is the mechanism of class IA drugs?
what do they effect |
Block fast Na and K channels
state dependnet blockade - they prefer active channels |
|
|
What are the class IA drugs?
|
Quinidine and Procainamide
|
|
|
What are extra effects of quinidine in addition to the class IA properties?
|
antimuscarinic which can speed up the HR.
and alpha1 block |
|
|
how is quinidine given
|
oral
|
|
|
What are the side effects of quinidine?
|
GI, cinchonism
(GI, tinnitis, CNS), hypotension, torsades do to the K channel block, IMPORTANT - inhances toxicity of Digitalis and hyperkalemia Muscles relaxing effect will erase AchEI on myesthenia |
|
|
How is procainamide different from quinidine?
|
no Muscarinic or Alpha block
-metabolized via N-acetyltransferase to NAPA, an active metabolite which prolongs the action potention duration -LUPIS LIKE SYNDROME |
|
|
What is the action of class IB drugs?, and which channels do they effect?
|
block both fast and slow Na channels
they favor tissues partly depolarized possibly vis ischemia |
|
|
What are the class IB drugs?
|
Lidocaine
|
|
|
How and when is lidocaine given
|
IV post MI, surgery, or due to digitalis.
cannot give orally due to first pass metabolism |
|
|
What are the adverse effects and cardiotoxicity of lidocain?
|
seizures in severe OD and it is the least cardiogenic of antiarrhythmics.
|
|
|
What are the class IC drugs?
|
Flecainide and Encainide
|
|
|
Whare do class IC drugs work?
|
very pure mechanism...only work on fast Na channels, and thus only on phase 0
|
|
|
What is the mechanism of Class II drugs?
|
Beta Blockers which decrease cAMP
|
|
|
What are the Class II drugs?and which are selective?
|
Propranolol (nonselective, the rest are selective for Beta1), Acebutolol, Metoprolol, esmolol, atenolol
|
|
|
What is esmolol used for?
|
in ER for acute SVT and theophylline OD because it is very short acting
|
|
|
What is the mechanism for Class III drugs?
|
K channel clockers and thus increase phase 3 and increasing action potential duration
|
|
|
What are the class III drugs?
|
Bretylium
Sotalol Amiodarone |
|
|
What are the uses of Bretylium?
|
backup for SVTs but can be proarrhythmatic and thus is not used much
|
|
|
What is unique about Sotalol?
|
it is two compounds in one drug. it is both a K channel blocker and a Beta1 blocker
|
|
|
What is unique about amiodarone?
|
mimics all antiarrhythmic drugs classes - blocks Na, Ca, and K channels and Beta receptors
|
|
|
What are the main side effects of amiodarone?
|
pulmonary fibrosis, corneal and skin deposits (smurf skin), thyroid issues, and phototoxicity, torsades, and decreases clearance of many drugs
|
|
|
What is the mechanism of class IV drugs?
|
Block Ca channels and thus decrease slope of phase 4 in the SA and AV nodes
|
|
|
What are the Class IV drugs
|
Verapamil
Diltiazem |
|
|
When are Class IV drugs used?
|
supraventricular arrhythmias - but not WPW
|
|
|
What are the adverse effects?
|
hypotension due to the Ca blockage in the vasculature, although it is cardioselective
|
|
|
What are the unclassified antiarrhythmics?
|
adenosine
|
|
|
What is the mechanism of adenosine?
|
it activates A-receptors which causes G coupled decrease in cAMP
and increase K efflux thus hyperpolarizing cells |
|
|
How is adenosine given and why?
|
IV due to short 30 sec.
|
|
|
Significance of Magnesium?
|
raising Mg levels to normals levels can prevent torsade in K channel blockers
|
|
|
What are the main side effects of amiodarone?
|
pulmonary fibrosis, corneal and skin deposits (smurf skin), thyroid issues, and phototoxicity, torsades, and decreases clearance of many drugs
|
|
|
What is the mechanism of class IV drugs?
|
Block Ca channels and thus decrease slope of phase 4 in the SA and AV nodes
|
|
|
What are the Class IV drugs
|
Verapamil
Diltiazem |
|
|
When are Class IV drugs used?
|
supraventricular arrhythmias - but not WPW
|
|
|
What are the adverse effects of class IV drugs?
|
hypotension due to the Ca blockage in the vasculature, although it is cardioselective
|
|
|
What are the unclassified antiarrhythmics?
|
adenosine
|
|
|
What is the mechanism of adenosine?
|
it activates A-receptors which causes G coupled decrease in cAMP
and increase K efflux thus hyperpolarizing cells |
|
|
How is adenosine given and why?
|
IV due to short 30 sec.
|
|
|
Significance of Magnesium?
|
raising Mg levels to normals levels can prevent torsade in K channel blockers
|
|
|
What are the sympathoplegics acting in the brain?
|
Methyldopa
Clonidine |
|
|
What is the mechanism of methyldopa
|
prodrug to methyl-NE which activates Alpha2 receptors thus decreasing vasomotor outflow and decreaseing resistance
|
|
|
What is unique about methyldopa?
|
positive coombs test
|
|
|
what is the mechanism of clonidine?
|
directly activates alpha2 receptors thus decreasing vasomotor outflow and decreaseing periferal resistance
|
|
|
What are some other uses of clonidine outside of cardiology?
|
used to treat dependency states in opioids and nicotine
|
|
|
what are the main adverse effects of clonidine?
|
rebound HTN on abrupt withdrawal
|
|
|
What are the adrenergic neuron blockers?
|
reserpine
guanethidine |
|
|
what is the mech of reserpine?
|
decreases NE loading into granules and thus decreases its release thus leading to decresed CO and periferal resistance
|
|
|
What is unique to reserpine?
|
blocks release of 5NT and dopamine in addition to NE in the brain and thus can cause depressoin
|
|
|
What is the mechanism of action of guanethidine?
|
decreases NE release from granules, bu tmust get to the granules via uptake1 and thus can be clocked by TCA
|
|
|
What are the adverse effects of guanethidine?
|
strong GI effects, orthostatic hypotension, and sexual dysfunction
|
|
|
What are the Alpha1 Blockers
|
Prazosin and the other "osins"
|
|
|
What is the mech of alpha blockers?
|
bloch alpha1 and thus dilate both arterial and venous vessels, with no change in renal blood flow
|
|
|
What is on effect that distinguishes alpha from beta blockers?
|
alpha blockers do not effect the plasma lipids
|
|
|
What are the beta blocker drugs?
|
propranolol and the "lols"
|
|
|
What is the mechanism of the beta blockers?
|
they decrease CO
|
|
|
Who respond best to beta blockers
|
white people and young people
|
|
|
how do lipids differ b/w partial beta1 agonists and full antagonists?
|
the lipds to not rise with partial agaonist whereas they do rise with the full beta blockers
|
|
|
What is something you must watch out for when taking someone off beta blockers
|
rebound hypertension
|
|
|
What are the direct acting vesodilators?
|
Hydralaxine
Nitroprusside Minoxidil Diazoxide |
|
|
What are the direct acting vesodilators?
|
Hydralaxine
Nitroprusside Minoxidil Diazoxide |
|
|
What are the direct acting vesodilators?
|
Hydralaxine
Nitroprusside Minoxidil Diazoxide |
|
|
What are the direct acting vesodilators?
|
Hydralaxine
Nitroprusside Minoxidil Diazoxide |
|
|
What are the direct acting vesodilators?
|
Hydralaxine
Nitroprusside Minoxidil Diazoxide |
|
|
what is the mechanism for hydralazine?
|
increases formation of NO/EDRF which leads to ARTERIOLAR dilation including hte coronary, renal and cerebral beds
|
|
|
what is the mechanism for hydralazine?
|
increases formation of NO/EDRF which leads to ARTERIOLAR dilation including hte coronary, renal and cerebral beds
|
|
|
what is the mechanism for hydralazine?
|
increases formation of NO/EDRF which leads to ARTERIOLAR dilation including hte coronary, renal and cerebral beds
|
|
|
What is unique about hydralazine?
|
metabolized by N-acetyltransferse and thus can present as SLE - just like procainamide
|
|
|
what is the mechanism for hydralazine?
|
increases formation of NO/EDRF which leads to ARTERIOLAR dilation including hte coronary, renal and cerebral beds
|
|
|
What are the direct acting vesodilators?
|
Hydralaxine
Nitroprusside Minoxidil Diazoxide |
|
|
What is the mech of nitroprusside
|
releases NO that increases cGMP which leads to ARTERIOLAR AND VENULAR dilation
|
|
|
What are the direct acting vesodilators?
|
Hydralaxine
Nitroprusside Minoxidil Diazoxide |
|
|
What is unique about hydralazine?
|
metabolized by N-acetyltransferse and thus can present as SLE - just like procainamide
|
|
|
When in nitroprusside used?
|
such a good dilator that it is drug of choice in severe hypertensive crisis
|
|
|
what is the mechanism for hydralazine?
|
increases formation of NO/EDRF which leads to ARTERIOLAR dilation including hte coronary, renal and cerebral beds
|
|
|
What is unique about hydralazine?
|
metabolized by N-acetyltransferse and thus can present as SLE - just like procainamide
|
|
|
What is unique about hydralazine?
|
metabolized by N-acetyltransferse and thus can present as SLE - just like procainamide
|
|
|
What is the mech of nitroprusside
|
releases NO that increases cGMP which leads to ARTERIOLAR AND VENULAR dilation
|
|
|
what is the mechanism for hydralazine?
|
increases formation of NO/EDRF which leads to ARTERIOLAR dilation including hte coronary, renal and cerebral beds
|
|
|
When in nitroprusside used?
|
such a good dilator that it is drug of choice in severe hypertensive crisis
|
|
|
What is unique about hydralazine?
|
metabolized by N-acetyltransferse and thus can present as SLE - just like procainamide
|
|
|
How id nitroprusside given and what are ide effects
|
IV and prolonged used causes cyanide poisoning
|
|
|
What is the mech of nitroprusside
|
releases NO that increases cGMP which leads to ARTERIOLAR AND VENULAR dilation
|
|
|
what is the mechanism for hydralazine?
|
increases formation of NO/EDRF which leads to ARTERIOLAR dilation including hte coronary, renal and cerebral beds
|
|
|
What is unique about hydralazine?
|
metabolized by N-acetyltransferse and thus can present as SLE - just like procainamide
|
|
|
What is unique about hydralazine?
|
metabolized by N-acetyltransferse and thus can present as SLE - just like procainamide
|
|
|
What is the mech of nitroprusside
|
releases NO that increases cGMP which leads to ARTERIOLAR AND VENULAR dilation
|
|
|
What is the mech of nitroprusside
|
releases NO that increases cGMP which leads to ARTERIOLAR AND VENULAR dilation
|
|
|
What is the mech of minoxidil?
|
it is a prodrug that gets sulfated and then opens K channels, thus hyperpolarizing the cell and thus causing vasodilation
|
|
|
When in nitroprusside used?
|
such a good dilator that it is drug of choice in severe hypertensive crisis
|
|
|
What are two unique effects of minoxidil?
|
pulmonary HTN
and hypertrichosis (hair growth) |
|
|
When in nitroprusside used?
|
such a good dilator that it is drug of choice in severe hypertensive crisis
|
|
|
How id nitroprusside given and what are ide effects
|
IV and prolonged used causes cyanide poisoning
|
|
|
How id nitroprusside given and what are ide effects
|
IV and prolonged used causes cyanide poisoning
|
|
|
What is the mech of minoxidil?
|
it is a prodrug that gets sulfated and then opens K channels, thus hyperpolarizing the cell and thus causing vasodilation
|
|
|
What is the mech of minoxidil?
|
it is a prodrug that gets sulfated and then opens K channels, thus hyperpolarizing the cell and thus causing vasodilation
|
|
|
What are two unique effects of minoxidil?
|
pulmonary HTN
and hypertrichosis (hair growth) |
|
|
What are two unique effects of minoxidil?
|
pulmonary HTN
and hypertrichosis (hair growth) |
|
|
What is the mech of diazoxide?
|
direct K channel opening and thus hyperpolarization
|
|
|
What is the mech of diazoxide?
|
direct K channel opening and thus hyperpolarization
|
|
|
how is each direct acting vasodilator given?
|
hydralazine - oral
nitroprusside - IV minoxidil - oral Diazoxide - IV |
|
|
how is each direct acting vasodilator given?
|
hydralazine - oral
nitroprusside - IV minoxidil - oral Diazoxide - IV |
|
|
How id nitroprusside given and what are ide effects
|
IV and prolonged used causes cyanide poisoning
|
|
|
What is the mech of minoxidil?
|
it is a prodrug that gets sulfated and then opens K channels, thus hyperpolarizing the cell and thus causing vasodilation
|
|
|
What is the mech of nitroprusside
|
releases NO that increases cGMP which leads to ARTERIOLAR AND VENULAR dilation
|
|
|
What is the mech of diazoxide?
|
direct K channel opening and thus hyperpolarization
|
|
|
What is the mech of nitroprusside
|
releases NO that increases cGMP which leads to ARTERIOLAR AND VENULAR dilation
|
|
|
When in nitroprusside used?
|
such a good dilator that it is drug of choice in severe hypertensive crisis
|
|
|
When in nitroprusside used?
|
such a good dilator that it is drug of choice in severe hypertensive crisis
|
|
|
How id nitroprusside given and what are ide effects
|
IV and prolonged used causes cyanide poisoning
|
|
|
How id nitroprusside given and what are ide effects
|
IV and prolonged used causes cyanide poisoning
|
|
|
how is each direct acting vasodilator given?
|
hydralazine - oral
nitroprusside - IV minoxidil - oral Diazoxide - IV |
|
|
What is the mech of minoxidil?
|
it is a prodrug that gets sulfated and then opens K channels, thus hyperpolarizing the cell and thus causing vasodilation
|
|
|
What is the mech of minoxidil?
|
it is a prodrug that gets sulfated and then opens K channels, thus hyperpolarizing the cell and thus causing vasodilation
|
|
|
What are two unique effects of minoxidil?
|
pulmonary HTN
and hypertrichosis (hair growth) |
|
|
What are two unique effects of minoxidil?
|
pulmonary HTN
and hypertrichosis (hair growth) |
|
|
What is the mech of diazoxide?
|
direct K channel opening and thus hyperpolarization
|
|
|
What is the mech of diazoxide?
|
direct K channel opening and thus hyperpolarization
|
|
|
What are two unique effects of minoxidil?
|
pulmonary HTN
and hypertrichosis (hair growth) |
|
|
When in nitroprusside used?
|
such a good dilator that it is drug of choice in severe hypertensive crisis
|
|
|
How id nitroprusside given and what are ide effects
|
IV and prolonged used causes cyanide poisoning
|
|
|
What is the mech of diazoxide?
|
direct K channel opening and thus hyperpolarization
|
|
|
how is each direct acting vasodilator given?
|
hydralazine - oral
nitroprusside - IV minoxidil - oral Diazoxide - IV |
|
|
What is the mech of minoxidil?
|
it is a prodrug that gets sulfated and then opens K channels, thus hyperpolarizing the cell and thus causing vasodilation
|
|
|
how is each direct acting vasodilator given?
|
hydralazine - oral
nitroprusside - IV minoxidil - oral Diazoxide - IV |
|
|
What are two unique effects of minoxidil?
|
pulmonary HTN
and hypertrichosis (hair growth) |
|
|
how is each direct acting vasodilator given?
|
hydralazine - oral
nitroprusside - IV minoxidil - oral Diazoxide - IV |
|
|
What is the mech of diazoxide?
|
direct K channel opening and thus hyperpolarization
|
|
|
how is each direct acting vasodilator given?
|
hydralazine - oral
nitroprusside - IV minoxidil - oral Diazoxide - IV |
|
|
What are the direct acting vesodilators?
|
Hydralaxine
Nitroprusside Minoxidil Diazoxide |
|
|
what is the mechanism for hydralazine?
|
increases formation of NO/EDRF which leads to ARTERIOLAR dilation including hte coronary, renal and cerebral beds
|
|
|
What is unique about hydralazine?
|
metabolized by N-acetyltransferse and thus can present as SLE - just like procainamide
|
|
|
What is the mech of nitroprusside
|
releases NO that increases cGMP which leads to ARTERIOLAR AND VENULAR dilation
|
|
|
When in nitroprusside used?
|
such a good dilator that it is drug of choice in severe hypertensive crisis
|
|
|
How id nitroprusside given and what are ide effects
|
IV and prolonged used causes cyanide poisoning
|
|
|
What is the mech of minoxidil?
|
it is a prodrug that gets sulfated and then opens K channels, thus hyperpolarizing the cell and thus causing vasodilation
|
|
|
What are two unique effects of minoxidil?
|
pulmonary HTN
and hypertrichosis (hair growth) |
|
|
What is the mech of diazoxide?
|
direct K channel opening and thus hyperpolarization
|
|
|
how is each direct acting vasodilator given?
|
hydralazine - oral
nitroprusside - IV minoxidil - oral Diazoxide - IV |
|
|
What is a unique feature of diazoxide?
|
it decreases insulin release from the pancreus, which you may want for an insulin tumor
|
|
|
Which group of Calcium channel blockers works only on the vasculature?
|
dihydropyridines
|
|
|
in which groups do the calcium channel antagonists work well in?
|
blacks and elderly, as opposed to the beta blockers which mainly worked on whites and young people
|
|
|
What are the dihydropyridine drugs?
|
nifedipine
nimodipine |
|
|
what is the mech for nifedipine?
|
calcium blockage causes vasodilation and the reflex tachycardia can be dangerous
|
|
|
What is the mechanism and use of nimodipine?
|
it blocks cancium channels in the cerebral vasculature and is used in subarachnoid hemorrhage to prevent vasospasm
|
|
|
What is a unique effect of the dihydropyridines?
|
gingival overgrowth
|
|
|
What are the calcium channel blockers efects on lipids?
|
no change, in contrant to the beta blockers
|
|
|
Which receptor for angiotensin II are blocked by losartan?
|
AT-1 receptors
|
|
|
What are the ACE inhibitor drugs?
|
captopril and the other "-prills"
|
|
|
Which drugs are AT-1 receptor antagonists?
|
Losartan and the other "-artans"
|
|
|
What is the most common adverse effect of the ACE inhibitors?
|
dry cough which is not present with the AT-1 receptor antagonists
|
|
|
What are the cardio drugs which are teratogenic?
|
ACE inhib. and AT-1 receptor antagonists
|
|
|
do ace inhib affect plasms lipids?
|
no
|
|
|
Which drugs effect arteriolar tone?
|
diazoxide, hydralazine, minoxidil
|
|
|
Which drugs effect venular tone?
|
nitrates
|
|
|
Which drugs effect arteriolar and venular tone?
|
all excepts which effect only arteriolor or only venular (many)
|
|
|
What does orthostatic hypotention result from?
|
venular, not arteriolar, dilation
|
|
|
What do all Beta blocker names end with?
ACEIs? AT-1 antagonists? Vascular-selective CCAs? |
Beta blockers - "-olols"
ACEIs - "-prills" AT-1 antagonists - "-artans" Vascular-selective CCAs - "-dipines" |
|
|
What is the mechanism of cardiac glycosides?
|
inhibits cardiac membrane Na/K pump which increases Na inside cell and thus slows the Na/Ca exchange pump which normally pumps Ca out of cell and Na into cell. This increases Ca inside cell and therefore also in the Sarcoplasmic reticulum, which therefore releases more Ca on the action potential and increasing contractility
|
|
|
How does K blood levels effect digitalis?
|
K and digitalis competitively bind to the same receptor
|
|
|
What are the cardiac glycoside drugs?
|
digoxin and digitoxin and the digitalis leaf which is not used anymore
|
|
|
What is the main difference between digoxin and digitoxin?
|
the half life of digitoxin is much longer and therefore it is not used much. digoxin is cleared renally whereas digitoxin is cleared by the liver
|
|
|
What are the early and late signs of digitalis toxicity?
|
early- EKG abnormalities
later - CNS effects such as disorientation and hallucinations more severe- AV block, ventricular arrhythmias |
|
|
how do you treat digitalis toxicity?
|
balance electrolytes and give a class IB antiarrhythmic such as lidocaine or phenytoin
|
|
|
What are other drugs in heart failure besides digitalis?
|
Amrinone and milrinone
beta1 and beta2 abonists (dobutamine and dopamine) Carvdilol - Alpha and beta blocker; though not intuitively, it decreases remoldeling and increases survival |
|
|
What is the mechanism of amrinone and milrinone?
|
block phosphodiesterase which therefore blocks the breakdown of cAMP to AMP, thus increasing the effects of cAMP
Amiodipine - vascular selective CCA - increases survival and spironolactone (aldosterone receptor antagonist), when used with ACEIs increased survival |
|
|
what are hte adverse effects of amrinone and milrinone?
|
amrinone causes thrombocytopenia
milrinone actually decreases survival |
|
|
Which drug groups relieve angina due to vasospasm?
|
nitrates and CCAs
|
|
|
What is the pathway for the effects of NO
|
L-Arg to NO via NO synthase....NO activates guanylyl cyclase which produces cGMP with relaxes blood vessels vis dephosphorylation of myosin LC phosphate,, which prevents the interaction with actin
|
|
|
Which vessels do the nitrates mainly affect?
|
large veins, and arterioles only at very high levels
|
|
|
What are the nitrate drugs
|
nitroglycerin
isosorbide mono or dinitrate |
|
|
what are the adverse effects of nitrates?
|
tachyphylaxis
methemoglobinemia (more common with nitrItes |
|
|
What is the mechanism for sildenafil?
|
inhibits PDE 5 (found in the vessels supplying the corpora cavernosa) which would normally breakdown cGMP. this leads to increased cGMP and increased vasodilation
|
|
|
What is the mechanism for smooth muscle contraction?
|
Ca enters and binds to calmodulin and this complex binds to Myosin light chain Kinase, thus activating it. The activated myosin light chain kinase will PHOSPHORYLATE THE myosin light chain, thus allowing it to binds to actin and contract the muscle
|
|
|
do calcium channel blockers mainly effect arterioles or veins?
|
arterioles, because arterioles have more smooth muscle
|
|
|
What are the calcium channel blockers
|
mifedipine, verapamil, diltiazem, and bepridil
|
|
|
Where does nifedipine work?
|
vascular selective
|
|
|
where does verapamil work?
|
vascular and Ca channels in the heart
|
|
|
Where does diltiazem work?
|
vascular and Ca channels in the heart
|
|
|
where does depridil work?
|
Dilates coronary vessels (distinctive property) and also blocks cardiac Na/K channels
|
|
|
which of the beta blockers is equivalent to isosorbide dinitrate in treating classic angina?
|
carvedilol
|
|
|
What drugs are used in the treatemtn of unstable angina?
|
nitrates w/ beta blockers with oxygen
heparin, warfarin, and antiplatelets |
|
|
What is the last step in platelet aggregation and how is this treated?
|
crosslinking involving IIb/IIIa receptor. and the blocking of this receptor will inhibit platelet aggregation
|
|
|
What are the IIb/IIa receptor blockers?
|
abciximab, eptifibatide, tirofiban
|
