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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