Trivia: Cardiac Pharmacology Exam! Quiz

25 Questions | Total Attempts: 133

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Trivia: Cardiac Pharmacology Exam! Quiz

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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