CARDIOVASCULAR THERAPEUTICS ICT SET at University Of Portsmouth | Flashcards & Summaries

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Lernmaterialien für CARDIOVASCULAR THERAPEUTICS ICT SET an der University of Portsmouth

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TESTE DEIN WISSEN
Class 3 agents: potassium channel blockers
Lösung anzeigen
TESTE DEIN WISSEN
Amiodarone, dronedarone, vernakalant 
Delay phase 3 repolarisation( inhibit potassium loss) + extend phase 2 in non-nodal cells
Increase action potential duration + refractory period 
Reduce possibility of re-entry circuits 
Lösung ausblenden
TESTE DEIN WISSEN
Increased diameter of vessels results in:
Lösung anzeigen
TESTE DEIN WISSEN
Decreased vascular resistance.

RAAS raises TPR and CO
Lösung ausblenden
TESTE DEIN WISSEN
B1–adrenoceptor antagonists (beta 1 blockers) in heart failure, MOA and examples: 
Lösung anzeigen
TESTE DEIN WISSEN
carvedilol, bisoprolol, metoprolol

MOA
- protection against excessive sympathetic stimulation

use with caution since may worsen heart failure
Lösung ausblenden
TESTE DEIN WISSEN
what causes rise in Total peripheral resistance (TPR) to raise afterload, leading to and increase in BP causing tissue perfusion pressure?

Lösung anzeigen
TESTE DEIN WISSEN
Rises in TPR may occur due to:
  • Vasoconstriction 
    • in small arteries and arterioles
    • may involve endothelial dysfunction (ET)
    • loss of endothelium-derived vasodilators e.g. nitric oxide (NO), PGI2 and/or increased release of vasoconstrictors e.g. ET-1
  • Arteriosclerosis 
    • arteriolar vessel wall hypertrophy, which is itself a response to hypertension = self-perpetuating mechanism
  • Rarefaction: where there is loss of vessels in tissue
Lösung ausblenden
TESTE DEIN WISSEN
Positive cardiac inotropes; Phosphodiesterase type III (PDE III) inhibitors also known as inodilators e.g. milrinone, enoximone:
Lösung anzeigen
TESTE DEIN WISSEN
  • inhibit enzyme (PDE III) responsible for metabolising cardiac cAMP, thus raising  myocardial cAMP and force of contraction
  • also raise cAMP in blood vessels, leading to vaso- and venodilation 
  • known as inodilators in respect of these multiple cardiac and vascular effects
Lösung ausblenden
TESTE DEIN WISSEN
Class 4 agents : calcium entry blockers
Lösung anzeigen
TESTE DEIN WISSEN
Verapamil, diltiazem
Block cardiac L-type calcium channels
Depress phase 0 (inhibit calcium entry) in nodal cells
Shorten phase 2 (reduced calcium entry) in non-nodal cells
Reduce nodal excitability + firing rate of SAN + conduction rate of AVN
Increased action potential duration + refractory period in nodal cells
Reduce action potential duration + refractory period in non-nodal cells
Lösung ausblenden
TESTE DEIN WISSEN
RAAS inhibition can as well help reduce pathological structural changes in the failing heart:
Lösung anzeigen
TESTE DEIN WISSEN
associated with cardiac remodelling, fibrosis and inflammation.
Lösung ausblenden
TESTE DEIN WISSEN
Blocking RAAS with RAAS inhibitors such as:
  • ramipril, perindopril (ACEIs)
  • candesartan, losartan, valsartan (ARBs)
leads to vasodilation and venodilation, natriuresis and diuresis and thereby reduces
Lösung anzeigen
TESTE DEIN WISSEN
preload and afterload as well as providing relief from oedema
Lösung ausblenden
TESTE DEIN WISSEN
Class 1C agent
Lösung anzeigen
TESTE DEIN WISSEN
Flecainide 
Marked sodium channel blockade 
Associates and dissociated slowly with sodium channel 
Effect normal + damaged myocardium non-selectively 
Lösung ausblenden
TESTE DEIN WISSEN
Class 1B agent
Lösung anzeigen
TESTE DEIN WISSEN
Lidocaine 
Mild sodium channel blockade 
Associates and dissociates rapidly with sodium channel, prefers open and inactivated states for binding 
Targets ischaemic tissue with little effect on normal myocardium 
Lösung ausblenden
TESTE DEIN WISSEN
Class 2 agents : beta-adrenoceptor blockers 
Lösung anzeigen
TESTE DEIN WISSEN
Propranolol( non-selective), atenolol, metoprolol, bisoprolol(beta1-adrenoceptor cardio selective)
Block catecholamine + cAMP-mediated electrical events in : phase 4 of nodal tissue (slope depressed); phase 2 of non-nodal tissue (extended due to delayed onset of phase 3 + reduced calcium entry) 
Increase action potential duration + refractory period 
Oppose pro-arrhythmic actions of catecholamines
Prevent sinus tachycardia, abnormal + triggered automaticity 
Lösung ausblenden
TESTE DEIN WISSEN
Details of Chronic heart failure (HF):
Lösung anzeigen
TESTE DEIN WISSEN
The Left heart failure often leads to the Right heart failure:
Lösung ausblenden
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Q:
Class 3 agents: potassium channel blockers
A:
Amiodarone, dronedarone, vernakalant 
Delay phase 3 repolarisation( inhibit potassium loss) + extend phase 2 in non-nodal cells
Increase action potential duration + refractory period 
Reduce possibility of re-entry circuits 
Q:
Increased diameter of vessels results in:
A:
Decreased vascular resistance.

RAAS raises TPR and CO
Q:
B1–adrenoceptor antagonists (beta 1 blockers) in heart failure, MOA and examples: 
A:
carvedilol, bisoprolol, metoprolol

MOA
- protection against excessive sympathetic stimulation

use with caution since may worsen heart failure
Q:
what causes rise in Total peripheral resistance (TPR) to raise afterload, leading to and increase in BP causing tissue perfusion pressure?

A:
Rises in TPR may occur due to:
  • Vasoconstriction 
    • in small arteries and arterioles
    • may involve endothelial dysfunction (ET)
    • loss of endothelium-derived vasodilators e.g. nitric oxide (NO), PGI2 and/or increased release of vasoconstrictors e.g. ET-1
  • Arteriosclerosis 
    • arteriolar vessel wall hypertrophy, which is itself a response to hypertension = self-perpetuating mechanism
  • Rarefaction: where there is loss of vessels in tissue
Q:
Positive cardiac inotropes; Phosphodiesterase type III (PDE III) inhibitors also known as inodilators e.g. milrinone, enoximone:
A:
  • inhibit enzyme (PDE III) responsible for metabolising cardiac cAMP, thus raising  myocardial cAMP and force of contraction
  • also raise cAMP in blood vessels, leading to vaso- and venodilation 
  • known as inodilators in respect of these multiple cardiac and vascular effects
Mehr Karteikarten anzeigen
Q:
Class 4 agents : calcium entry blockers
A:
Verapamil, diltiazem
Block cardiac L-type calcium channels
Depress phase 0 (inhibit calcium entry) in nodal cells
Shorten phase 2 (reduced calcium entry) in non-nodal cells
Reduce nodal excitability + firing rate of SAN + conduction rate of AVN
Increased action potential duration + refractory period in nodal cells
Reduce action potential duration + refractory period in non-nodal cells
Q:
RAAS inhibition can as well help reduce pathological structural changes in the failing heart:
A:
associated with cardiac remodelling, fibrosis and inflammation.
Q:
Blocking RAAS with RAAS inhibitors such as:
  • ramipril, perindopril (ACEIs)
  • candesartan, losartan, valsartan (ARBs)
leads to vasodilation and venodilation, natriuresis and diuresis and thereby reduces
A:
preload and afterload as well as providing relief from oedema
Q:
Class 1C agent
A:
Flecainide 
Marked sodium channel blockade 
Associates and dissociated slowly with sodium channel 
Effect normal + damaged myocardium non-selectively 
Q:
Class 1B agent
A:
Lidocaine 
Mild sodium channel blockade 
Associates and dissociates rapidly with sodium channel, prefers open and inactivated states for binding 
Targets ischaemic tissue with little effect on normal myocardium 
Q:
Class 2 agents : beta-adrenoceptor blockers 
A:
Propranolol( non-selective), atenolol, metoprolol, bisoprolol(beta1-adrenoceptor cardio selective)
Block catecholamine + cAMP-mediated electrical events in : phase 4 of nodal tissue (slope depressed); phase 2 of non-nodal tissue (extended due to delayed onset of phase 3 + reduced calcium entry) 
Increase action potential duration + refractory period 
Oppose pro-arrhythmic actions of catecholamines
Prevent sinus tachycardia, abnormal + triggered automaticity 
Q:
Details of Chronic heart failure (HF):
A:
The Left heart failure often leads to the Right heart failure:
CARDIOVASCULAR THERAPEUTICS ICT SET

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