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From Flashcardlet big > Cardiac pharmacology > Flashcards

Cardiac pharmacology Flashcards

1
Q

What are pharmacological properties of clopidogrel

A

Class of drug: Platelet ADP (adenosine diphosphate) receptor antagonist

Clopidogrel irreversibly modifies the platelet ADP receptor thereby directly inhibiting the binding of ADP and subsequent ADP-mediated activation of the glycoprotein IIb/IIIa complex.

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2
Q

What are the pharmacological properties of heparin

A
  1. inactivates factor Xa
  2. inhibits conversion of prothrombin to thrombin
  3. prevents fibrin formation from fibrinogen
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3
Q

More details of heparin physiology

A

Acts near the end of the coagulation cascade
The first target is thrombin (Factor II) –by activation Anti-Thrombin III (AT III) to a form > 1000times more potent
also targets Xa, XIIIa, XIa
Full dose does not completely suppress thrombin
Heparin comes pork intestine or beef lung* different*

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4
Q

What are differences between UF heparin and low moelecular weight heparin

A

a) longer half-life, about 12 hours compared to 90 min
b) does not require monitoring
c) greater anti-factor Xa activity
d) lower incidence of thrombocytopenia and osteoporosis

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5
Q

What is advantage LWMH

A 
↓ heparin resistance
↓ inhibition of platelet function
↓ incidence of HIT 1 vs 5 %
↓ risk of bleeding
↑ bioavailability
↑ half life
No need for monitoring
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6
Q

What are pharmacological properties of warfarin

A

Coumadin derivative that interferes with vitamin K metabolism.
Vit K is a co-factor in the hepatic production of Factors II, VII, IX, and X.

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7
Q

What are pharmacological properties of glycoprotein IIb/IIIa blockers

A

Inhibit platelet aggregation by binding to the glycoprotein IIb/IIIa receptors on platelets thereby preventing these receptors from linking to other platelets by fibrinogen cross-bridges.

examples

1) Abciximab
2) tirogibran
3) eptifibatide

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8
Q

Pharmacological properties of fibrinolytics

A

convert plasminogen to plasmin which in turn degrades fibrin-containing thrombi.

Two categories

a) non-specific thrombolytic agents
b) fibrin-specific

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9
Q

Pharmacological properies of Transexamic acid

A

lysine analogue anti-fibrinolytic agent
Binds to plasminogen, therby inhibiting fibrinolysis
possible renal function and graft patency issues

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10
Q

Pharmacological properties of statins

A

competitively inhibit hepatic HMG-CoA reductase, which is involved in last step of cholesterol synthesis

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11
Q

What are pharmacological properties of beta blockers

A

Bind to beta adrenoreceptors to produce negative inotropic and chrontropic effects, thereby reducing myocardial oxygen demand.

cardiomyocyte membrane stabilizing effect, thereby acting as an anti-arrhythmic agent

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12
Q

What are pharmacological properties of calcium channel blockers

A

inhibit calcium influx during phase 2 of cardiac action potential (plateau phase) thereby reducing cardiac contractility and the propagation of cardiac electrical impulses

also relax vascular smooth muscle, dilating coronary and peripheral arteries

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13
Q

What are pharmacoloical properties of ACE inhibitors

A

Prevent conversion of inactive angiotensin I to active angiotensin II, thereby reducing the release of aldosterone by the adrenal cortex.

ARBs have similar mechanism as ACE but do not break down bradykinin which is thought to be responsible for the cough

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14
Q

What are pharmacological properties of nitrates

A

smooth muscle relaxants that

1) coronary vasodilation and reduced coronary spasm
2) peripherally vasodilate
3) reduce preload and afterload, thereby reducing myocardial oxygen demand

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15
Q

What are pharmacological mechanism of nitroprusside

A

relaxes arterial smooth thereby reducing systemic and pulmonary afterload

use for aortic dissection

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16
Q

What are pharmacological properties of dopamine

A

Dopaminergic and adrenergic receptor agonist ug/kg/min

Good for low cardiac output and post MI

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17
Q

What are pharmacological properties of dobutamine

A

synthetic inodilator that activates B1 adrenergic receptors and has moderate B2 (vasodilaton)

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18
Q

what are pharmacological properties of adrenaline

A

A potent alpha 1 agonist producing increased myocardiac contractility and increased heart rate. At low doses it does B2 vasodilation.

will cause metabolic acidosis

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19
Q

What are pharmacological properties of noradrenaline

A

Potent alpha 1 agonist producing systemic vasoconstriction and beta 1 increasing myocardial contracility

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20
Q

How does Milrinone work

A

Inhibition of phosphodiesterase enzyme, which normally converts to cAMP to inactive 5 -AMP

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21
Q

What are pharmacoligcal properties of milirinone

A

Acts as an inodilator by reducing systemic and pulmonary vascular resistance as well as having moderate positive inotropic effects

phosphodiesterase- 3–inhibitor

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22
Q

What are pharmacological properties of digoxin

A

Inhibits the action of the sarcolemmal membrane Na-K-ATPase thereby inhibiting the sodium pump.This results in a greater influx of sodium and development of bound intracellular calcium producing weak inotropic effect.

prolongs the atroventricular node refractory period and conduction, as well as stimulating vagal function thereby slowing down the ventricular rate

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23
Q

What are the pharmacological properties of amiodarone

A

increases the action potential duration throughout the cardiac conduction system, thereby reducing the excitability of both atrial and ventricular myocytes

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24
Q

What are the pharmacological properties of loop diuretics

A

loop diuretics inhibit water and electrolyte reabsorption from the ascending limb of henle

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25
Q

List 2 source of Nitric oxide and the effects of NO on endothelium

A

Source of NO
Active byproduct of nitrates and NA nitroprusside
Inhaled NO

The effects of NO on endothelium
	reduced cytosolic CA+
	reduce platelet aggregation
	increase cGMP
	increase guanylate cyclase
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26
Q

What is the mechanism of nitrate intolerance

A 
Reduced bioconversion to NO 
Desensitization of  guanyl cyclase
increased vasopressin and catecholamines
Renin-angiotensive system activation 
Increased production of endothelin-1
increased superoxide anion production
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27
Q

What are usual doses of inotropes that maybe required to come off CPB for difficult wean are

A

Milrinone: 50u/KG loading dose, then 0.5u/kg/min infusion

Epinephrine -0.01-to0.1u/kg/min

NE is 0.01 to 0.03 u/kg/min

Dopamine 5 to 15 u/kg/min

Dobutmaine 5 to 15 u/kg/min

Phenylephrine 40 to 70 u boluses every few minutes

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28
Q

List 5 effects on the vascular endothelium from Nitric Oxide

A

Vasodilation
inhibits vascular smooth muscle growth
inhibits platelet aggregation and adhesion
inhibits neutrophil adhesion

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29
Q

List indications for nitric oxide

A

pulmonary hypertension post-heart transplant
pulmonary hypertension post repair of congential heart lesion—VSD
pulmonary hypertension following mitral valve repair
treat acute right heart failure/dysfunction
massive acute PE
ARDS
following lung transplantation

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30
Q

What are toxic byproducts of NO

A

Nitric dioxide
methemoglobin
peroxynitrite
nitrate

31
Q

What is mechanism of Abciximab (Reopro)

A

Non-competitive monocolonal antibody against GIIB/IIIa which inhibits platelet aggregation

The bleeding time is prolonged for 12 -48 hours

Risk of bleeding is very high

32
Q

How does Eptifibatide (Integrilin) and Tirofioban (Aggra stat) work

A

Competitive binders of GIIbIIIa, BT is prolonged for 8 hours

for urgent surgery wait a few hours.

33
Q

What is Vaughn-Williams Classification

A

Class I = sodium
Class II = beta blockers
Class III = Prolong reploraization (think K)
Class IV = Calcium channel

34
Q

How do Fibrates work?

A

Increase HDL

Reduce HDL

35
Q

How do Resins work

A

Reduced LDL and Increase HDL

36
Q

Describe mechanisms of amiodarone toxicity

A

Direct injury: high affinity of amiodarone to lung tissue and its long half life, it accumulates in the lung causing direct cell injury. Alternation of the lipid bilayer, release of toxic O2 radicals and chronic inflammation– pulmonary fibrosis

Indirect: (immune-mediated) injury: hyper sensitivity reaction leading to acute inflammation and severe pneumonitis resembling BOOP. Mediated by CD8-T cells and IgG antibodies.

Treatment of cessation of amiodarone and steroids

37
Q

Describe the mechanism of action of amiodarone, half life and usually loading dose

A

has all 4 classes of action in VW classification

Reduces SA node automaticity, AV node refractoriness, and ventricular and atrial automaticity

35-45% is absorbed when given orally

The elimination half life is 40 to 60 days

38
Q

Name side effects of amiodarone

A 
Corneal deposits causing halos and blurred vision
Hyperthroidism and hypothyroidism
Acute hypersensitivity pneumonitis
Interstitial pneumonitis
Hepatitis (watch for increase in GGT) 
Bradycardia and AV block 
Hearing loss
Blue-Gray skin
Hypotension when given IV
39
Q

What is mechanism of amiodarone toxicity

A

Indirect (immune-mediated) –mediated by CD8 T-cells and IgGAb–hypersensitivity rxn leading to acute inflammation and severe
Direct: high affinity to lung tissue–injury mediated by phsolopodidosis in alveolar macrophages.type II cells, chronic inflammation
occurs in the 6 to 15% pts

40
Q

How do you diagnose amiodarone toxicity

A

a drop in 15% DLCO
High resolution CT and PFT
treatment is drug withdrawal and corticosteroid

41
Q

What is mechanism of Aprotinine

A

serine protease inhibitor that strongly inhibits plasmin.
Reducing the inflammatory reponse to CPB
Full Hammersmith dose is 4 Million KIU (allikrenin inhibitory units) as a loading dosease then 0.5 Million KIU/Hr

42
Q

Why would Aprotinin work

A

During CPB endothelial cells produce TPA which activates plasmin, a serine protease,
plasmin leads to clot lysis by degrading fibrin to fibrin degradation products

43
Q

What is dosing and drug treatment for Type B dissections

A 
Esmolol 
	500 ug/kg bolus over 1 minute
	50 o 200 ug/kg/min infusion  
	give another bolus of 500 ug/kg to achieve an acceptable SBP < 100
Nitroprussude 
	0.3 ug/kg/min infusion
44
Q

List 3 actions of amiodarone

A

decreased SA node automaticity
decreased AV node refractory time
decreased ventricular and atrial automaticity

45
Q

What are contraindications to nitrates

A

Angina caused by HOCM
Acute inferior myocardial infarction
with right ventricular involvement
fall in filling pressure may lead to hemodynamic and clinical deterioration
Glaucoma
no objective evidence to show any increase in intraocular pressure

46
Q

What is treatment of Torsade

A

Magnesium (stabilize the membrane)
Isopril (isoproternol)
pace at a faster rate (shorten the QT interval and avoid pause related initiation
Lidocaine (shorten the QT)

47
Q

What is nipride toxicity

A 
Excessive nipride  produces free cyanide radicals that cannot all bind with avilable methemaglobin 
Signs of toxicity: 
	tachyphylaxis
	elevated mixed venous Po2 
	metabolic acidosis 
	No cynanosis
48
Q

What are loop diuretics and side effects

A

act on tubular epithelial cells in thick ascending loop of Henle to inhibit Na, K, and 2Cl-

deafness (rare)

49
Q

Describe how Inotropes increase cardiac contractility

A

Increase the intracellular cyclic adenosine monophosphate (cAMP) levels. cAMP augments calcium influx into myocardial cells thereby increasing contractilty

50
Q

How do DA, NE, Epi effect cAMP levels

A

Stimulation of adnylate cyclase, which catayses the conversion of ATP to cAMP

51
Q

What are pharmacological properties of aprotinin

A

Anti-fibrinolytic agent

inhibits serine proteases including; plasmin, kallikren

side effects: renal dysfunction, graft patency

HMMERSMITH regime

BART-study killed it

52
Q

What are pharmacological properties of ARB

A

ARB are similar to ACE but do not break down bradykinin

TGF–can be used in those with family history of TAAA/Marfan

53
Q

What is difference between abicimab and Intergrellin and Aggra stat

A

Abicimab is a non-competitive monoclonal antibody against GP2b3A receptor which inhibits platelet aggregation. Need to wait 12 to 48 hours

Integrelline and Aggrastat are competitive binders. Bleeding time is only up for 8 hours. Can wait a few hours. Give platelets to over come.

54
Q

What are difference among calcium channel blockers

A

Non-dihydropyridine CCBs are considered to have negative inotropic and chronotropic effects. The dihydropyridine CCBs increase contractility and heart rate, therefore decreasing vascular resistance

Dihydropyridine reduce systemic vascular resistance and arterial pressure, but are not used to treat angina (with the exception of amlodipine, nicardipine, and nifedipine, which carry an indication to treat chronic stable angina as well as vasospastic angina) because the vasodilation and hypotension can lead to reflex tachycardia. Dihydropiridine calcium channel blockers can worsen proteinuria in patients with nephropathy

55
Q

How do ACE and ARB effect afterload

A

antagonizing the vasopressor effect of angiotensin, thereby decreasing the amount of work the heart must perform.

angiotensin directly affects cardiac remodeling, and blocking its activity can thereby slow the deterioration of cardiac function.

56
Q

How does spironalctone work for heart failure

A

The RALES trial showed that the addition of spironolactone can improve mortality, particularly in severe cardiomyopathy (EF < than 25%.)

Eplerenone was shown in the EPHESUS trial[27] to have a similar effect, and it is specifically labelled for use in decompensated heart failure complicating acute myocardial infarction.

Antagonism of aldosterone will decrease the effects of sodium and water retention, the main mechanism of action is by antagonizing the deleterious effects of aldosterone on cardiac remodeling.

57
Q

What is role for nitrates in systolic heart failure

A

The combination of isosorbide dinitrate/hydralazine is the only vasodilator regimen, other than ACE inhibitors or angiotensin II receptor antagonists, with proven survival benefits

58
Q

What is role for BNP therapy in heart failure

A

Nesiritide, a recombinant form of B-natriuretic peptide, is indicated for use in patients with acute decompensated heart failure who have dyspnea at rest.
Promotes diuresis and natriuresis, thereby ameliorating volume overload.
BNP is elevated in heart failure, the peptide that is produced during CHF is dysfunctional or non-functional and thereby ineffective

59
Q

List exams of each of the VW class of antiarrythmics

A

Class I —Na+ channel (procainamide)
Class II—metoprolog
Class III most accurate to say prolong action potential duration * Soltalol
Class IV–verapamil

60
Q

What does Sotalol do and what is risk

A

Nonselective beta-blocker that also has K chalennl-blocking activity

risk of Torsade de Pointe

61
Q

What is quick action of Digoxin

A

Direct effect is to Inhibit Na_, K+ ATPase pump leading to decrease K+ inctracellular

the indirect effect is to stimulate the vagotonic effect on the AV now to slow it down.

62
Q

How does Adenosine work

A

Decreases AV node conductivity and breaks AV nodal reentrant tachycardia

63
Q

How does Epi work

A

alpha and beta1 effects but little beta2

both an inotrope and a vasopressor

64
Q

What is Levosimendan

A

Calcium sensitizer

used to treat decompensated heart failure

65
Q

How does Acetazolamide function

A

Diamox
alkalinzation of urine in the presence of metabolic alkalosis which is common with prolonged diuretic therapy
Acts in the proximal convoluted tubule to inhibit carbonic anhydrase, which reduced the destruction of bicarbonate ions.
Both Na+ and HCO3 reabsorption is diminished in the proximal tuble

66
Q

What is mechanism of action in HCTZ

A

Class of Benzothiazides
Act in the early distal convoluted tubules to decrease the electroneutral N+/Cl- costransport reabsorption of Na.
Enhanced action when combined with osmotic diuretic.

67
Q

How does Spironolactone (Aldactone) function

A

competitive antagonist of aldosterone
Late distal tuble
Decreases the electrogenic Na+ entry into cells (which is the driving

68
Q

What is mechanism of Mannitol

A

Osmotic diuretic
1) used for prophylazis and early treatment of ARF
2) enhancing the action of other diuretics by retaining water and solutes in the tubular lumen, therby providing the substrate for other diuretics to act.
It limits the reasbsortopm of water and dilutes the proximal tubular fluid which reduces the gradient for sodium and limits its reabsorption so that more is delievered to the distal portions of the nephron.

usually 25 to 50g is in the prime.

69
Q

List common herbs and the potential effects

A 
Ginger---potentiate ASA and warfarin
Ginkgo-- potentiate ASA and warfarin
Eichancea--decrease effect of steroids
Garlic----potentiate warfarin
Ginseng--decrease effects of warfarin
70
Q

What is methylene blue?

What is dose?

A

.

71
Q

What is penicillin G

A

Penicillin G is noted to possess effectiveness mainly against Gram-positive organisms

Bacteria constantly remodel their peptidoglycan cell walls, simultaneously building and breaking down portions of the cell wall as they grow and divide. β-Lactam antibiotics inhibit the formation of peptidoglycan cross-links in the bacterial cell wall; this is achieved through binding of the four-membered β-lactam ring of penicillin to the enzyme DD-transpeptidase

a synergistic effect with aminoglycosides, since the inhibition of peptidoglycan synthesis allows aminoglycosides to penetrate the bacterial cell wall more easily, allowing their disruption of bacterial protein synthesis within the cell

72
Q

What is Prostaglandin E1

A

Prostaglandin E1 (PGE1), known pharmaceutically as alprostadil, is a prostaglandin

maintaining a patent ductus arteriosus in newborns. This is primarily useful when there is threat of premature closure of the ductus arteriosus in an infant with ductal-dependent congenital heart disease, including cyanotic lesions

73
Q

What are the pharmacological properties of aspirin

A

Class: cyclo-oxygenase inhibitor

ASA inhibits platelet cyclo-oxygenase reducing the production of thromboxane A2 and effecting platelet adhesiveness

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