Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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*

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Pharmacological properties of statins

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are pharmacological mechanism of nitroprusside

A

relaxes arterial smooth thereby reducing systemic and pulmonary afterload

use for aortic dissection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are pharmacological properties of dobutamine

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are pharmacological properties of noradrenaline

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How does Milrinone work

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the pharmacological properties of loop diuretics

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
List 2 source of Nitric oxide and the effects of NO on endothelium
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 ```
26
What is the mechanism of nitrate intolerance
``` 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 ```
27
What are usual doses of inotropes that maybe required to come off CPB for difficult wean are
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
28
List 5 effects on the vascular endothelium from Nitric Oxide
Vasodilation inhibits vascular smooth muscle growth inhibits platelet aggregation and adhesion inhibits neutrophil adhesion
29
List indications for nitric oxide
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
30
What are toxic byproducts of NO
Nitric dioxide methemoglobin peroxynitrite nitrate
31
What is mechanism of Abciximab (Reopro)
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
How does Eptifibatide (Integrilin) and Tirofioban (Aggra stat) work
Competitive binders of GIIbIIIa, BT is prolonged for 8 hours for urgent surgery wait a few hours.
33
What is Vaughn-Williams Classification
Class I = sodium Class II = beta blockers Class III = Prolong reploraization (think K) Class IV = Calcium channel
34
How do Fibrates work?
Increase HDL | Reduce HDL
35
How do Resins work
Reduced LDL and Increase HDL
36
Describe mechanisms of amiodarone toxicity
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
Describe the mechanism of action of amiodarone, half life and usually loading dose
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
Name side effects of amiodarone
``` 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
What is mechanism of amiodarone toxicity
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
How do you diagnose amiodarone toxicity
a drop in 15% DLCO High resolution CT and PFT treatment is drug withdrawal and corticosteroid
41
What is mechanism of Aprotinine
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
Why would Aprotinin work
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
What is dosing and drug treatment for Type B dissections
``` 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
List 3 actions of amiodarone
decreased SA node automaticity decreased AV node refractory time decreased ventricular and atrial automaticity
45
What are contraindications to nitrates
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
What is treatment of Torsade
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
What is nipride toxicity
``` 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
What are loop diuretics and side effects
act on tubular epithelial cells in thick ascending loop of Henle to inhibit Na, K, and 2Cl- deafness (rare)
49
Describe how Inotropes increase cardiac contractility
Increase the intracellular cyclic adenosine monophosphate (cAMP) levels. cAMP augments calcium influx into myocardial cells thereby increasing contractilty
50
How do DA, NE, Epi effect cAMP levels
Stimulation of adnylate cyclase, which catayses the conversion of ATP to cAMP
51
What are pharmacological properties of aprotinin
Anti-fibrinolytic agent inhibits serine proteases including; plasmin, kallikren side effects: renal dysfunction, graft patency HMMERSMITH regime BART-study killed it
52
What are pharmacological properties of ARB
ARB are similar to ACE but do not break down bradykinin TGF--can be used in those with family history of TAAA/Marfan
53
What is difference between abicimab and Intergrellin and Aggra stat
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
What are difference among calcium channel blockers
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
How do ACE and ARB effect afterload
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
How does spironalctone work for heart failure
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
What is role for nitrates in systolic heart failure
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
What is role for BNP therapy in heart failure
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
List exams of each of the VW class of antiarrythmics
Class I ---Na+ channel (procainamide) Class II---metoprolog Class III *most accurate to say prolong action potential duration * Soltalol* Class IV--verapamil
60
What does Sotalol do and what is risk
Nonselective beta-blocker that also has K chalennl-blocking activity risk of Torsade de Pointe
61
What is quick action of Digoxin
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
How does Adenosine work
Decreases AV node conductivity and breaks AV nodal reentrant tachycardia
63
How does Epi work
alpha and beta1 effects but little beta2 | both an inotrope and a vasopressor
64
What is Levosimendan
Calcium sensitizer | used to treat decompensated heart failure
65
How does Acetazolamide function
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
What is mechanism of action in HCTZ
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
How does Spironolactone (Aldactone) function
competitive antagonist of aldosterone Late distal tuble Decreases the electrogenic Na+ entry into cells (which is the driving
68
What is mechanism of Mannitol
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
List common herbs and the potential effects
``` Ginger---potentiate ASA and warfarin Ginkgo-- potentiate ASA and warfarin Eichancea--decrease effect of steroids Garlic----potentiate warfarin Ginseng--decrease effects of warfarin ```
70
What is methylene blue? What is dose?
.
71
What is penicillin G
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
What is Prostaglandin E1
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
What are the pharmacological properties of aspirin
Class: cyclo-oxygenase inhibitor ASA inhibits platelet cyclo-oxygenase reducing the production of thromboxane A2 and effecting platelet adhesiveness

From Flashcardlet big (79 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions