Pharm 2 Test

Front 1

What are the therapeutic uses of Quinidine and what is its class?

Back 1

Therapeutic Use: PAT, PSVT and Ventricular tachycardia

Quindine is a class Ia drug

Front 2

What are Adverse Effects of Quidinine?

Back 2

Cinchonism, hypotension (alpha-adrenergic blocking effect) and torsades de pointes. Also can cause nausea, vomiting and diarrhea

Front 3

How is Procainamide metabolized?

Back 3

Dependent on hepatic N-acetyltransferase and renal function. There are rapid(t1/2=2.5-3hrs) and slow(t1/2>5hrs) acetylators.

Also, 70% of procainamide is unchanged in the urine.

Front 4

What are adverse effects of Procainamide?

Back 4

Can cause SLE-like syndromes.
- Arthralgia, pericarditis, fever, weakness, skin lesions, lymphadenopathy, anemia and heptaomegaly
Also, causes GI nausea and vomitting, decreased renal functions may be prodysrhythmic, mental confusion and torsade de pointes

Front 5

What is the MoA of Lidocaine and what is its class?

Back 5

Inhibits the reentry mechanisms in ventricular tissue: suppresses spontaneous ventricular depolarizations

Front 6

What is special about Lidocaine, why would it be used after an MI?

Back 6

Works preferentially to block ischemic tissue and activate normal cardiac tissue

Front 7

How is lidocaine administered?

Back 7

IV administration only

Front 8

What class is flecainide and when should it be used?

Back 8

Class Ic. It should be used in the treatment of refractory life-threatening ectopic ventricular dysrhythmias cases because of marked cardiac depression and prominent prodysrhythmic effects

Front 9

What class is propranolol and what are its effects?

Back 9

Class II. It is a Beta antagonist: Lowers HR/CO (increasing ERP), lowers conduction in Atria, AV nodes and ventricles.

Front 10

What is propranolol used for?

Back 10

Excellent use for atrial flutter and fibrillation. PAT and digoxin-induced dysrhythmias

Front 11

What are adverse effects of propranolol?

Back 11

Hypotension, asytole, brochospasm with non-selective antagonists and rebound w/drawal effect due to recepto up-regulation

Front 12

What do Class III drugs do?

Back 12

Alters K+ flux during phase 3: increase ERP and APD

Front 13

What class of drug is amiodarone? And how is it useful?

Back 13

Class III.
purported less prodysrhythmic potential.

It is useful in refractory ventricular dysrhythmia

Front 14

What are the adverse effects of amiodarone?

Back 14

There is a 75% incidence rate in chronic, oral administration.

GI nausea and vomiting, pulmonary toxicity (10-17% pneumonitis/ARDS), photosensitivity and thyroid disorders/tumors

Front 15

What class of drug is verapamil and how is it used?

Back 15

It is a Class IV drug.
It is used with supraventricular tachycardia, angina and hypertension(need a higher dose for hypertension)

Front 16

What does verapamil do?

Back 16

It is a cardo depressant: decrease HR, SA automaticity and AV conduction, while increasing PR

Front 17

What do class IV drugs do?

Back 17

Class IV drugs are CCB (ca channel blockers). Affect slow inward Ca channels

Front 18

How should you use verapamil?

Back 18

If you want a rapid conversion administer it through IV.
If you want to maintain normal rhythms and prevent SVT administer drug orally.

Front 19

Is verapamil lipophilic or hydrophilic? Does that matter?

Back 19

It is lipophilic and can cross the BBB. Hemodialysis is ineffective in the event that you need to remove it.

Front 20

What are adverse effects of verapamil?

Back 20

GI constipation, hypotension, exacerbate CHF and AV heart block in combination with Beta Blockers

Front 21

What is adenosine used for?

Back 21

adenosine is comparable to verapamil, but it has a much SHORTER half-life. It is used to convert PAT, PSVT, WPW to NSR.

Front 22

What is the MoA for adenosine?

Back 22

It hyperpolarizes the membrane by opening K+ channels. It produces a complete AV nodal block--allows heart to "re-set" itself.

Front 23

How is Adenosine administered?

Back 23

Rapid bolus, close to the heart (brachial vein or jugular)

Front 24

What is digoxin used to treat?

Back 24

It treats chronic atrial fibrillation (but CCBs are clinically preferred at this time)

Front 25

What is the MoA of digoxin in CHF?

Back 25

Blocks Na/K ATPase

Front 26

What is the MoA of digoxin in Atrial Fibrillation?

Back 26

vagal stimulation effect resulting in a neg dromotropic effect at the AV node: prolonged ERP.
Slow ventricular rate by decreasing the number of P-wave depolarizations that reach the ventricles.

Sympathetic stimulation may over-ride this effect.

Front 27

What are the adverse effects of Digoxin?

Back 27

highly dysrhythmogenic due to the effects on plasma K+

Front 28

How can you overcome digoxin-induced ventricular dysrhythmia?

Back 28

Administer MgSO4 therapy: facilitates K+ distribution

Also, ClassIB and Class II agents appear to be affective.

Front 29

How can you manage Bradycardia?

Back 29

Atropine (vagal block to increase HR)
isoproterenol (Beta-1 stimulated increase in HR)
Pacemaker (morphologic AV nodal block)

Front 30

How can you manage a Sinus Tachycardia manually?

Back 30

Vagal stimulation through carotid sinus massage or Valsalva maneuver

Front 31

What causes Heart Failure?

Back 31

MI, chronic untreated hypertension, chronic dysrhythmia, CAD, etc.

Front 32

What characterizes Heart Failure?

Back 32

Reduction in SV(and CO) at any given end diastolic volume (EDV)

Front 33

How is the Frank-Starling curve affected by +/- inotropic agents

Back 33

+ inotropic increases contractility, while - inotropic decreases contracility

Front 34

Low Output congestive heart failure results from what?

Back 34

decreased contractile capacity

Front 35

What are the three main characteristic symptoms of CHF?

Back 35

ventricular hypertrophy, edema, and weak, rapid pulse(baroreflex activation)

Front 36

What is the goal of treatment with CHF?

Back 36

The goal is to reverse the three symptoms: ventricular hypertrophy, edema and weak, rapid pulse

Front 37

Clinical tx of CHF involves what tools?

Back 37

Diet and Na+ restriction
exercise
diuretics, AChEIs and vasodilators
positive inotropic agents

Front 38

Digoxin (digitalis) is found in what plant?

Back 38

foxglove

Front 39

Foxglove is classified as what type of agent?

Back 39

Cardiac Glycoside

Front 40

If a pt is in atrial fibrillation, what drug could you give that would inhibit the Na/K ATPase?

Back 40

Digoxin

Front 41

If you give Digoxin to your pt, what should you be worried about?

Back 41

prodysrhythmia

Front 42

What are some side effects that most pts will have with each dose of digoxin?

Back 42

nausea and vomiting caused by CTZ stimulation

Front 43

What are common side effects of Digoxin?

Back 43

enhanced morbidity/mortality when combined with diuretics (depletes the K+)
dysrhythmia, visual and neurological disturbances

Front 44

Why does digoxin cause nausea and vomiting?

Back 44

It stimulates the CTZ

Front 45

When you give digoxin to your pt, what should you always monitor?

Back 45

Electrolytes! Changes in K+ and Ca++ may lead to dysrhythmias

Front 46

Why does inhibiting Na/K ATPase cause greater contracitlity?

Back 46

The increase in intracellular NA causes an increase in Na/Ca exchange: More Ca++ is available for muscle fiber contraction.

Front 47

How can you correct for too much plasma digoxin?

Back 47

Administer Cholestyramine or digoxin immune Fab (binds to the free and bound cardiac glycoside where it is sequestered in extracellular fluid: renally eliminated.

Front 48

If you eliminate Digoxin, will there be lasting clinical effects?

Back 48

No

Front 49

What is the method of action for Isoproterenol?

Back 49

Beta-1 receptor: mediates increases in intracellular cAMP = elevations in Ca++

Increases membrane excitation and contraction

Front 50

What does isoproterenol do?

Back 50

It increases both the contracility and heart rate

Front 51

Should isoproterenol be used in preventive settings?

Back 51

No, it should only be used in acute situations

Front 52

What is the MoA of dopamine?

Back 52

It is an adrenergic agonist on peripheral receptors.

Front 53

Does Dopamine have different effects at different doses? What are those effects?

Back 53

Yes.
Low Dose: stimulates DA1 and DA2 receptors= vasodilation, especially in the renal bed (increase GFR, Urine output)

Moderate Dose: additional stimulation of Beta 1 receptors: increase contraction and slight increase in HR

High dose: additional stimulation of alpha 1 receptors causes peripheral vasoconstriction.

Front 54

Is Dopamine's metabolism slow or fast?

Back 54

Rapid action onset and metabolism by MAO/COMT

Front 55

When should you give Dobutamine?

Back 55

Use with short term management of heart failure following MI.

Front 56

How is dobutamine different from Dopamine?

Back 56

Dobutamine has a preferential increase in cardiac contractility w/o increasing HR

Front 57

Dobutamine's MoA is what?

Back 57

Less Alpha 1 effects and less Beta1 tachycardia

Front 58

How should you administer Dobutamine?

Back 58

continuous, short-term IV infusion. It will be eliminated by COMT and has a half life of 2 minutes.

Front 59

Name two phosphodiesterase inhibitors?

Back 59

Inamrinone and milrinone

Front 60

What does phosphodiesterases do?

Back 60

Metabolize cAMP

Front 61

What is the result of inhibiting phosphodiesterases

Back 61

results in elevated intracellular cAMP and ensuing increase in intracellular Ca++

Front 62

What is a phosphodiesterase inhibitor similar to?

Back 62

Beta 1 agonists

Front 63

When should you use phosphodiesterase inhibitors and what method of administration?

Back 63

You should it in acute settings only and with an IV administration.

Front 64

Where is the baroreflex and how is that info transmitted to the brain?

Back 64

Carotid sinus is the location and glossopharyngeal nerve transmits the information to the brain.

Front 65

What is essential hypertension?

Back 65

no clear cause or mechanism has been discovered for causing the hypertension.

clear genetic basis and usually found in middle age adults.

Front 66

What is secondary/non-essential hypertension?

Back 66

small number of adults who have hypertension for a specific reason: tumor, renal disease, etc.

They usually require surgery to adjust their blood pressure

Front 67

How do you dx hypertension?

Back 67

two or more readings with at least 4 wks apart.

Front 68

What are "normal" values of blood pressure?

Back 68

AHA: <140/90
WHO: <160/90

Front 69

Does hypertension require medical intervention?

Back 69

Yes--due to the pathological consequences.

Front 70

Treatment of hypertension depends on what qualities?

Back 70

Age, ethnicity, body-type, obesity, personality type

athletic/sedentary
etiology of HTN
rapidity of onset and severity
presence of other CV risks

Front 71

What is the first line of defense in HTN Tx?

Back 71

Modifications in lifestyle!

(lose weight, limit alcohol, increase activity, reduce NA+ <100mmol/6grams, maintain K+ 7grams, maintain Ca and Mg intake, stop smoking

Front 72

What should you consider when deciding to put your pt on HTN drugs?

Back 72

Cost to pt
life-long ordeal (usually)
dosage/drug class & side effects
pt compliance
ALWAYS consider Step-Care Therapy

Front 73

What must you consider with each drug for hypertension?

Back 73

the Baroreceptor reflex

Front 74

How will the baroreceptor reflex work?

Back 74

retains Na and H2O by the kidneys
increases peripheral vascular resistance, HR and CO (all sympathetically)

Front 75

How do antihypertensives work?

Back 75

MAP = CO x TPR

CO = HR x SV

Front 76

Name some diuretics

Back 76

Thiazides, loop diuretics, K+ sparing diuretics

Front 77

How do diuretics work?

Back 77

relatively unknown

May be due to a decrease in blood volume causing a decrease in CO

Front 78

How effective are diuretics?

Back 78

Have moderate monotherapy efficacy (20/10)
But augments antihypertensive effects of other drugs.

Front 79

What population has better efficacy with diuretics?

Back 79

African-Americans and eldery pts.

Front 80

How long does it take for diuretics to work?

Back 80

2-4wks, but their peak effect in 3-4 months

Front 81

Does increasing the dose of diuretics increase the efficacy?

Back 81

No, it does increase the severity of the side effects

Front 82

What are contraindications of diuretics?

Back 82

hyperlipidemia (elevates LDL and TG) and diabetes (may induce hyperglycemia)

Front 83

How does propranolol (Beta antagonists) help with HTN?

Back 83

Blocks Beta-Receptors:

In the heart: Decrease HR/contractility => decrease BP

In the Kidney: Decrease renin release => Ang II formation

Front 84

What is the efficacy of Beta-blockers with HTN?

Back 84

moderately good in monotherapy, but better in combination therapy

Front 85

Is there a population that responds poorly to beta-blocker therapy with HTN?

Back 85

smokers

Front 86

What are the side effects of Beta blockers?

Back 86

hyperlipidema, male sexual dysfunction, exacerbates asthma and CHF.

Diabetes: masks signs of hypoglycemia (dysrhythmia, tachycardia, tremor, diaphoresis) and could lead to coma or death

Front 87

What is a good drug to lower HTN in the presence of CHF? Why?

Back 87

Labetalol and carvedilol.

Block, Beta 1 and Beta 2, but also blocks alpha 1. This results in an vasodilation (which will decrease the afterload)

Front 88

What drug should you use in HTN emergencies?

Back 88

labetalol (IV only)

Front 89

What is the method of action with Clonidine?

Back 89

post-synaptic alpha 2 agonist in CNS: inhibits sympathetic outflow resulting in decrease HR/TPR

Pre-synaptic alpha 2 agonist in the periphery: decrease NE release from post-ganglionic nerve terminals

Front 90

What is the efficacy of clonidine?

Back 90

35/20 monotherapy (combination with a diuretic is common)

Front 91

How does alpha-methyldopa work?

Back 91

It is a centrally- acting sympatholytic.

Analog of DOPA, which is converted in CNS neurons to alpha-methylnorepinephrine.

Stimulates inhibitory alpha 2 receptors--acts as a false transmitter

Front 92

Your 30 year old female pt with chronic HTN needs to try drug therapy--which drug would you use?

Back 92

alpha-methyldopa

Front 93

What could be some side effects of alpha-methyldopa?

Back 93

positive direct Coombs test:
presence of auto-antibodies in RBCs.

This could result in frank hemolytic anemia

Also there is prominent sexual dysfunction, dry mouth and sedation.

Front 94

What are some peripherially acting sympatholytics?

Back 94

Prazosin, terazosin, doxazosin

Front 95

-zosin drugs act on what receptor?

Back 95

alpha 1 antagonist--they spare alpha 2(NE is not released)

Front 96

If you pt come into the office with HTN and you give them a -zosin drug--what might you expect as a pleasant side effect?

Back 96

lowering of the LDL, TG and total cholestrol.

Front 97

What would be some adverse effects of -zosin drugs?

Back 97

mild reflex tachycardia

Front 98

What is the efficacy of -zosin drugs?

Back 98

15/10 monotherapy and 25/15 with diuretic

Front 99

Verapamil can be used to treat supraventricular tachycardias with the heart...what else can verapamil and diltiazem be used to treat?

Back 99

HTN: It is a CCB which acts on the periphery to inhibit Ca release from the vascular smooth muscle and from the SR.

This causes direct
vasodilation

Front 100

What are the side effects and the effecacy of treating HTN with Verapamil?

Back 100

Side effects: cardio depressant--which may counter with a reflex tachycardia

efficacy: 30/20

Front 101

What is the efficacy of diltiazem in treating HTN?

Back 101

20/15

Front 102

How does nifedipine work?

Back 102

It is a CCB (dihydropyridine)

Front 103

Do you give nifedipine alone or with another drug? and why?

Back 103

Give with a beta blocker b/c of the prominent reflex tachycardia

Front 104

Which has better efficacy with treating HTN?
verapamil
diltiazem
nifedipine

Back 104

nifedipine

Front 105

What is the method of action with Hydralazine?

Back 105

direct vasodilation via cGMP.

increases intracellular cGMP
increase Ca sequestration (smooth muscle relaxant)
large effect on afterload with little effect on preload

Front 106

When would you want to use hydralazine?

Back 106

Because of the decrease in afterload, but little effect on pre-load you would use Hydralazine with CHF

(but recently it has been replaced with ACE inhibitors)

Front 107

What is negative about using hydralazine as a long term drug?

Back 107

It developes tachyphylaxis due to prominent baroreflex perturbation

Front 108

How could you prevent the tachphylaxis of hydralazine?

Back 108

Give with a beta-blocker and diuretic

Front 109

What are some adverse effects of hydralazine?

Back 109

SLE-like syndrome
palpitation, tachcardia
use limited to resistant, fulminant hypertension and management of hypertensive emergency

Front 110

If you have a hypertensive emergency in a CHF pt, what drugs should you consider?

Back 110

hydralazine

Front 111

IF you have a hypertensive emergency in a p, what drugs should you consider?

Back 111

labetalol

Front 112

What drug would you use for severe, refractory hypertension?

Back 112

Minoxidil

Front 113

What is the MoA of minoxidil?

Back 113

direct arteriolar vasodilation: stimulation of vascular smooth muscle K+ channel opening (results in membrane hyperpolariztion)

Front 114

What is a side effect of minoxidil?

Back 114

Tachyphylaxis (baroreflex mediated)

Front 115

What other drugs should you prescribe with minoxidil?

Back 115

Beta-blockers and diuretics

Front 116

what is the danger with sodium nitroprusside?

Back 116

extended continuous infusion may produce methemoglobinemia, cyanide poisoning and cell death.

Front 117

What is the MoA of sodium nitroprusside?

Back 117

Donates NO to cGMP mediated Ca sequestration.

It decreases BOTH after load and preload

Front 118

When and how would you use sodium nitroprusside?

Back 118

Parenterally infused agent used in hypertensive emergencies and the rapid management of CHF

Front 119

Name a few ACE inhibitors

Back 119

enalapril, captopril and linsinopril

Front 120

What is the efficacy of ACE inhibitors with monotherapy?

Back 120

25/30

Front 121

When is the maximium effect of ACE inhibitors occur?

Back 121

4-8wks after dosing

Front 122

Why would someone want to be removed from ACE inhibitor therapy?

Back 122

They develop a dry, peristent cough

Front 123

What group of people don't respond as well to ACE inhibitors?

Back 123

african americans

Front 124

What is the efficacy of ACE inhibitors?

Back 124

25/20

Front 125

When should you NEVER use Ace inhibitors?

Back 125

in pregnant women

Front 126

Why should you not use ACE inhibitors in pregnant women?

Back 126

ACE inhibitors can cross the placenta and cause neuronal defects

Front 127

What is ANG receptor blocker MoA?

Back 127

specific antagonist of ANG II at AT1 receptor on vascular smooth muscle.

Front 128

Is losartan okay to use in pregnancy?

Back 128

NO. it is an ANG receptor blocker.

Front 129

What are some names of ANG receptor blockers?

Back 129

Candesartan, losartan, irbesartan, valsartan


---sartan

Front 130

When does ischemia occur?

Back 130

when the work-load is greater than the oxygen supply

Front 131

How can you improve angina pain?

Back 131

improve oxygen (blood) delivery

decrease workload of the myocardium

Front 132

What is the Steal Phenomenon?

Back 132

the small vessel are already maximally dilated in chronic ischemic states (reactive hyperemia), so vasodilators do not improve the pt condition by producing coronary vessel dilation

They may direct blood flow to non-ischemic areas by dilating larger distal vessels

Front 133

What are good vasodilators to use in angina?

Back 133

non-endothelium-dependent:

NO-donators providing their own EDRF (endothelium-derived relaxing factor)

Front 134

What role does sodium nitroprusside play in tx of angina?

Back 134

use in emergency parenteral use only

reduce BOTH preload and afterload

Front 135

What is the MoA with nitroglycerin?

Back 135

NO stimulated increase in cGMP: Ca sequestration and vasodilation (preload and afterload)

Front 136

What can be a danger with Nitroglycerin?

Back 136

tachyphylaxis

Front 137

What is the fastest onset of action dose with nitroglycerin?

Back 137

sublingal (1-3 minutes), but some people have psychological relief within seconds

Front 138

What are some adverse effects of nitroglycerin?

Back 138

flushing of soft tissues and headache and sublingal burning sensation

headache and flushing pt will develop a tolerance

Front 139

What is EDRF?

Back 139

it is a soluble gas produced by vascular endothelial cells.

produces a potent cGMP-mediated vasodilation

Front 140

How are EDRF and angina possibly related?

Back 140

perhaps underproduction of EDRF could cause angina

Front 141

What is Endothelin?

Back 141

peptide produced by vascular endothelial cells that produce a potent receptor-mediated (ETa) vasoconstriction

Front 142

How are Endothelin and angina, vasospasm and hypertension possibly related?

Back 142

An overproduction of endothelin may cause angina, vasospasms or hypertension.