Trivia: Cardiac Pharmacology Exam! Quiz

25 Questions | Total Attempts: 195

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Trivia: Cardiac Pharmacology Exam! Quiz

What do you know about cardiac pharmacology? Does your heart miss a beat at the notion of taking this quiz? Luckily, this quiz can help you if you are studying for an exam. Cardiovascular agents are medications that are employed to treat medical conditions associated with heart or circulatory systems. Cardiovascular disease is the prominent cause of death in the United States. This awesome quiz will explain to you about cardiac pharmacology.


Questions and Answers
  • 1. 
    What is pace maker activity?
    • A. 

      Spontaneous, intrinsic rhythm generated by the AV node cells

    • B. 

      Spontaneous, intrinsic rhythm generated by the SA node cells

    • C. 

      The making of paces

    • D. 

      Conduction of charge from the atria to the ventricles

    • E. 

      Spontaneous firing of the purkinje system

  • 2. 
    What is the difference between conduction in SA and AV nodes, compared to normal muscle and nerve conduction?
  • 3. 
    What does the presence of calcium channels, rather than sodium channels, in the SA and AV nodes mean?
    • A. 

      If you drink a glass of milk, you'll get tacchycardias

    • B. 

      Calcium channels, due to their fast conduction, decrease the action potential and time for repolarisation

    • C. 

      Calcium channels, due to their slow conduction, prolong the action potential and time for repolarisation

    • D. 

      Calcium channels decrease arrhythmias

    • E. 

      Increased conduction capacity

  • 4. 
    Which types of Ca2+ channels are present in the heart?
    • A. 

      Voltage dependent plasma membrane

    • B. 

      Intracellular

    • C. 

      Extracellular

    • D. 

      Neurotransmitter-mediated

    • E. 

      Pressure dependent

  • 5. 
    Which are the main voltage-dependent calcium channels in the heart, and what do they do?
    • A. 

      L-type channels, which form part of the his-purkinje system and increase transmission rate of electrical signals

    • B. 

      B-type channels, which are important in transmission of electrical conduction and stimulation of the valves of the heart

    • C. 

      J-type channels, which are important in working myocardium and specialised conducting regions of the heart

    • D. 

      L-type channels, which are important in working myocardium and specialised conducting regions of the heart

    • E. 

      B-type channels, which increase cardiac contraction and spread equally through the two sides of the heart

  • 6. 
    At what membrane potential voltage does rapid depolarisation of the myocardium occur?
  • 7. 
    How long do sodium channels remain depolarised?
    • A. 

      No more than a few milliseconds

    • B. 

      No more than a few seconds

    • C. 

      No more than two microseconds

    • D. 

      No more than a minute

    • E. 

      No more than necessary

  • 8. 
    What follows rapid depolarisation
  • 9. 
    What causes the plateau in cardiac action potentials?
    • A. 

      Sodium channels open, prolonging depolarisation and causing a plateau

    • B. 

      Calcium channels open, triggered by sodium ion depolarisation, and the slow influx maintains the plateau

    • C. 

      Outward potassium conduction is blocked, maintaining the depolarisation

    • D. 

      Potassium channels open, increasing the rate of depolarisation and prolonging cardiac contraction

    • E. 

      Sodium channels close, increasing the rate of depolarisation.

  • 10. 
    What triggers repolarisation?
    • A. 

      Closure of calcium channels

    • B. 

      Closure of sodium channels

    • C. 

      Re-opening of potassium channels and efflux of ions

    • D. 

      Closure of potassium channels

    • E. 

      Opening of sodium channels and influx of sodium

  • 11. 
    What is stage 0 as represented in B?
  • 12. 
    What is stage I as represented in B above, and what causes it?
  • 13. 
    What is II in the image B above, and what causes it?
  • 14. 
    What is number III in section B above, and what causes it?
  • 15. 
    What is indicated by IV in section B above, and what causes it?
  • 16. 
    What can disrupt the order of sinus rhythm?
    • A. 

      Anatomic heart disease

    • B. 

      Myocardial infarction

    • C. 

      Drugs

    • D. 

      Circulating hormones

    • E. 

      Age

  • 17. 
    Which phenomena underlie dysrhythmias?
    • A. 

      Re-entry

    • B. 

      Electrolyte imbalance

    • C. 

      Delayed after-depolarisation

    • D. 

      Ectopic pacemaker activity

    • E. 

      Heart block

  • 18. 
    In ventricular muscle, what is the main cause of delayed after-depolarisation?
    • A. 

      Abnormally raised Na+, which causes an influx of ions and triggers abnormal action potentials, causing VT

    • B. 

      Abnormally raised K+, which causes an influx of ions and triggers abnormal action potentials, causing VT

    • C. 

      Abnormally raised Ca2+, which causes an influx of ions and triggers abnormal action potentials, causing VT

    • D. 

      Abnormally low Na+, which causes an efflux of ion and decreases cardiac reactivity, causing bradycardia

    • E. 

      Abnormally low Ca2+, which causes an efflux of ion and decreases cardiac reactivity, causing bradycardia

  • 19. 
    How does re-entry occur?
    • A. 

      The impulse conducted to the atria doesn't die out in surrounding refractory tissue after contraction, and instead re-excites the myocardium

    • B. 

      The impulse in the sinoatrial node doesn't die out in surrounding refractory tissue after contraction, and instead re-excites the myocardium

    • C. 

      The impulse in the sinoatrial node travels through the ventricles and back up to the node again, triggering a premature impulse and sudden contraction

    • D. 

      The impulse conducted to the ventricles doesn't die out in surrounding refractory tissue after contraction, and instead re-excites the myocardium

    • E. 

      The impulse in the atrioventricular node travels through the ventricles and back up to the node again, triggering a premature impulse and sudden contraction

  • 20. 
    Physiologically, why do other cardiac tissues have the ability to take on pacemaker activities?
    • A. 

      It's a safety mechanism, so if the AV node is damaged, pacemaker activity can continue.

    • B. 

      It's a safety mechanism, so if the SA node is damaged, pacemaker activity can continue.

    • C. 

      It's a safety mechanism, so if the purkinje fibres are damaged, contractile activity can continue.

    • D. 

      It's additional contractility, so if increased volume load occurs, more tissue can contract to cope with the increased demand

    • E. 

      It's additional pacemaking, so if increased volume load occurs, more tissue can contract to cope with the increased demand

  • 21. 
    What is the problem with ectopic pacemakers?
    • A. 

      If they don't fire, can cause bradycardias

    • B. 

      If they're inappropriately firing, can cause bradycardias

    • C. 

      If they don't fire, can cause tacchyarrhythmias

    • D. 

      If they're in the wrong place, can interfere with valvular function

    • E. 

      If they're inappropriately firing, can cause tacchyarrhythmias

  • 22. 
    What triggers heart block, and what is the consequence?
    • A. 

      Fibrous or ischaemic damage to the conducting system (usually SA node)

    • B. 

      Atria and ventricles firing independently of each other, with atria supplied by ectopic pacemakers

    • C. 

      Fibrous or ischaemic damage to the conducting system (usually AV node)

    • D. 

      Atria and ventricles firing independently of each other, with ventricles supplied by ectopic pacemakers

    • E. 

      Dilatation of the chambers obliterates the conducting system, causing heart failure

  • 23. 
    What is the sequence of conduction through the heart?
    • A. 

      SA node - atrium - AV node - purkinje fibres - ventricle

    • B. 

      SA node - purkinje fibres - AV node - atrium - ventricle

    • C. 

      AV node - purkinje fibres - atrium - SA node - ventricle

    • D. 

      Ventricle - AV node - purkinje fibres - atrium - SA node

    • E. 

      Atrium - SA node - purkinje fibres - AV node - ventricle

  • 24. 
    How is delayed after-depolarisation mediated?
    • A. 

      High calcium causes influx of ions into the cell transiently, which increases the normal after-depolarisation waves (can be seen as peaked T waves)

    • B. 

      Can be caused by cardiac glycosides, NA or phosphodiestesterase inhibitors that increase intracellular calcium

    • C. 

      Mediated by high levels of extracellular calcium

    • D. 

      Increased normal after-depolarisation waves trigger a repetitive discharge and contraction that is independent of pacemaker stimulus

    • E. 

      Can occur in the non-pacemaker cells of the heart.

  • 25. 
    What intrinsically influences myocardial contractility and pulse pressure?
    • A. 

      Binding rates of ATP to actin and myosin fibres

    • B. 

      Troponin, to which Ca2+ binds and triggers a conformational change

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