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Pharmacology - Unit 4 - 10 > Unit 5 - Rx of Cardio > Flashcards

Unit 5 - Rx of Cardio Flashcards

1
Q

Cardiotonic drugs

A

Drugs increase the STRENGTH of heart.

Drugs for a FAILING heart (CHF)
– Heart becomes weaker as a pump.
– Over many years or rapidly in response to injury

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2
Q

Cardiotonic drugs

Goals for treatment

A

increase CO and pumping efficiency while reducing cardiac work (increase preload and decrease afterload)

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3
Q

*cardiac glycosides (digoxin)

MOA

A

MOA: increases contractility in the heart muscle

  • increases intracellular calcium ion concentration and increases the force of contraction
  • increases CO and relieves edema if present
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4
Q

*cardiac glycosides (digoxin)

S/E

A
  • narrow therapeutic window, long half life
  • development of arrhythmia - many kinds esp. ventricular
  • can induce AV block
  • GI
  • Visual: single color vision (yellow/green), halos around obj
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5
Q

*cardiac glycosides (digoxin)

A

also used to treat ATRIAL FLUTTER (has muscarinic effect on atria)

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6
Q

arrhythmia(s)

A
  • abnormal pacemaker activity: cell takes over the pacing of the heart at a rate that is diff from what it ought to be
  • ectopic pacemakers: cells generating impulse outside of the SA node
  • 1st cell to reach threshold will begin to pace the heart
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7
Q

4 classes of drugs for arrhythmias

A
  • Na+ channel blockers
  • calcium channel blockers
  • blocking beta receptors
  • K+ channel blockers
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8
Q

sodium channel blockers

A

delay upward spike –> will take longer to trigger the action potential.

delay phase 4 to spike of AP

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9
Q

calcium channel blockers

A

same MOA as above

increases intracellular calcium ion concentration and increases the force of contraction

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10
Q

blocking beta receptors

A

slows automaticity

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11
Q

potassium channel blockers

A

will cause the cell to take longer to get back to resting membrane potential and slows the HR.

Makes the whole AP process take longer

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12
Q

Class 1: Na+ channel blockers

A

Bind to channels in the inactive and active state, they prolong the period in which these channels don’t work

drugs will lengthen the time it takes for the channel to go back to the resting state

especially effective in sites of ischemia

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13
Q

Quinidine

A
  • Na+ channel blocker
  • not widely used, antimuscarinic effect
  • blocks open and active Na+ channels
  • stop an arrhythmia
  • chiefly a cardiac depressant
  • effective ORALLY
  • PROBLEM: potentil for generating arrhythmias due to lengthening of AP
  • S/E: cinchonism…similar to aspirin toxicity
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14
Q

Lidocaine

A

Na+ channel blocker

  • used for VENTRICULAR ARRHYTHMIAS (esp. v-fib)
  • effective w/ less tendency for cardiotoxicity
  • used IV, first pass metabolism
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15
Q

An antiarrythmic agent that is used for ventricular arrhythmias in emergency situations because it has a rapid onset and a short duration of action and does not have an anticholinerigc effect is:

A

lidocaine

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16
Q

In a patient with complete heart block, ventricular rate:

A

is decreased over its former rate

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17
Q

Which antilipemic agent inhibits the enzyme necessary for cholesterol synthesis?

A

statins

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18
Q

What class of drug is indicated for the control of blood pressure because it acts by inhibiting vasoconstriction and decreases fluid retention?

A

ACE inhibitor

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19
Q

Coumarin derivatives are:

A

anticoagulants

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20
Q

A cardiac glycoside is often indicated for a patient with congestive heart failure because it has the effect of increasing the force of contraction and decreasing the rate of contraction. This class of drug is said to have a(n) ______________ effect.

A

positive inotropic and negative chronomtropic

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21
Q

When there is a mismatch in oxygen supply and demand a patient may present with chest pain. To address the chest pain, a drug that relaxes smooth muscle, decreasing blood pressure and ultimately decreases the work of the heart would be prescribed. What class of drug can accomplish this goal?

A

nitroglycerine

22
Q

A major side effect of cardiac glycosides is:

A

ventricular tachycarida

23
Q

Atrial flutter is:

A

treated with a cardiac glycoside or an antiarrythmic agent since both are effective

24
Q

The antihypertensive agent(s) that shows an increased efficacy for African American patients is (are):

A

calcium channel blockers and diuretics

25
Q

*Amiodarone

A

K+ channel blocker
Na+ channel blocker

  • also blocks Ca+2 and beta-adrenergic receptors
  • effective in ORALLY suppressing arrhythmias
  • less likely to produce arrhythmias
  • very long half life, tendency to go crystalize in the tissue (pulmonary fibrosis is limiting side effect)
  • crystal formation in cornea
26
Q

Class 2: Beta adrenergic antagonists

A
  • SLOW the heart down and suppresses arrhythmias

- decrease catecholamine induced automaticity (epi or nor-epi)

27
Q

Class 3: Potassium channel blocker (sodalol) (adenosine)

A
  • prolongs AP and refractory period
  • if you lengthen the AP it takes longer to get back to resting potential and longer until cells can fire again
  • produces same arrhythmias as Quinidine.
28
Q

Class 4: Calcium channel blockers (verapamil)

A
  • works same way as Na+ channel blockers, they have a preference for open/active channels
    (BUT they work at SA and AV nodes, places where calcium currents are driving the current)
  • effective for atrial arrhythmias and circus movements
  • can weaken cardiac muscle for time
29
Q

HTN

A
  • CVD #1 killer in US
  • essential HTN: no identifiable cause that you can treat. Treatment aimed at symptoms
  • Sx are unnoticeable

risk factors: wt, sex, FHx, genetics

30
Q

Targets for treatment

A
  • CO: sympatholytics
  • Vascular resistance: sympatholytics, direct acting vasodilators, drugs that interfere w/ RAA system
  • fluid volume: diuretics (first line Rx)
31
Q

damage to cardiovascular system

A
  • hypertrophy to the heart
    1. heart is stretched and leads to remodeling cardiomyopathies
    2. bigger the heart, the more wall tension the heart has to generate to push blood against the pressure
  • vascular damage
    1. elevate pressure can damage the blood vessels
32
Q

Centrally acting sympatholytic (clonidine)

A
  • MOA: alpha-2 adrenergic agonist in the brain. Receptors are turned on it decreases sympathetic outflow (will see decrease in vascular resistance and decrease in CO)
  • Uses: HTN, when no other Rx work
  • S/E: sedation and depression (rebound HTN)

2nd or 3rd line Rx

33
Q

Centrally acting

guanefidine, reserpine

A

MOA: prevents release of nor-epi from nerve terminals
– Decrease vascular resistance and a decrease of CO
– 2nd line Rx

S/E: severe hypotension
– Reserpine can cross the BBB and can cause depletion of catecholamines, commonly causes depression

34
Q

Alpha (1) Blockers (prazosin)

A

MOA: block alpha receptors in peripheral arterioles. The arterioles dilate and BP falls.
– Drugs are very useful in lowering BP

S/E: 1st dose hypotension –> dizziness (postural hypotension)
– Drowsiness
– Fluid retention – tachycardia

35
Q

Beta Blocker (propranolol)

A

MOA: blocks beta adrenergic receptors, decreasing cardiac output and HR –> decreasing BP
– Decrease in vascular resistance and dilation arterioles

Indications: HTN, arrhythmias

S/E: decrease in contractility of heart, rebound HTN

Contraindications: asthma (b-2 receptors)

36
Q

Calcium channel blockers (verapamil)

A

MOA: blocks calcium channels in smooth muscle and cardiac muscle.

– Not all Ca++ channel blockers are the same; some work better for arrythmias (verapamil), some are better for the blood vessels (nifedipine)

S/E: decrease contractility in the heart

37
Q

ACE inhibitors

A

MOA: inhitbits angiotensin converting enzyme
– Decreases BP in practically everyone

Indications: HTN, also CHF

Adverse effects: common dry cough

C/I: pregnancy due to tendency toward renal stress, potential renal failure

38
Q

Angiotensin 2 receptor blocker

A

Same action as ACE inhibitor

  • No cough
39
Q

calcium channel blockers

A

MOA: cause vasodilation

Therapeutic uses: HTN, suptraventricular tachycardia, angina

Note: better antihypertensive agent for African Americans (in combo w/ diuretics)

C/I: not for patients w/ CHF

40
Q

Diuretics

A

Often first line therapy

If one drug only is being used, it is usually a diuretic

MOA: reduces hypervolemia
– Also appears to relax blood vessels

41
Q

Antihypotensive Agents (aka pressor)

A

These drugs increase BP

How?
– Increase peripheral resistance (alpha agonist)
– Increase CO (beta agonist)
– Increase (replace) fluid volume (whole blood)

Therapeutic uses: chronic symptomatic hypotension, acute hypotension, replace blood volume

42
Q

*Antianemic / Hemopoietic Drugs

A

Rx that replace missing factors for blood formation
– Iron, vitamin B12, folic acid (antinomic agents)

Therapeutic uses: treat anemias

43
Q

Drugs affecting Coagulation

A
  • Hemostatics
  • Anticoagulants
  • Thrombolytics
44
Q

*Hemostatics

A

speed UP blood clotting

– Used to treat hemorrhage

45
Q

*Anticoagulants

A

slow DOWN blood clotting, decrease risk of clotting

  • Work by blocking formation of thrombin and fibrin, decreases platelet aggregation
  • Therapeutic uses: venous thrombosis, prevent coronary thrombosis, any condition that results in blood remaining in heart after systole
46
Q

*Thrombolytics

A

drugs that dissolve clots

– MOA: cause plasminogen to convert to plasmin

– Therapeutic use: any clot

47
Q

Antilipemic Agents

A
  • Fibroic Acid Derivatives
  • Niacin
  • Bile sequestrant
  • Statins
48
Q

*Statins

A

MOA: inhibit enzyme for cholesterol synthesis
– Can greatly reduce LDL cholesterol (30- 40%)

Adverse effect:
– May negatively affect the liver
– Muscle pain, weakness

  • deplete CoEnzyme Q10, recommend supplement so minimize S/E
49
Q

*First line of therapy for CHF

A
  • ACE inhibitor - inhibit enzyme that converts angiotensin 1 to angiotensin 2
  • beta blockers also used for CHF
  • direct vasodilators
50
Q

arrhythmias

A

abnormal rate or rhythm

51
Q

Action Potential (AP)

A
  • depolarization - cell stimulated, Na+ channels open, Na+ rush in (inside + , outside -)
  • threshold - reached, then…
  • AP
  • re-polarization - K+ channels

Pharmacology - Unit 4 - 10 (7 decks)

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