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CHEM358 Pharmacology > cardiovascular pharmacology I > Flashcards

cardiovascular pharmacology I Flashcards

1
Q

sinus rhythm (normal heart rhythm) is generated by ??? which arise from the SA node

A

pacemaker impulses

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2
Q

Cardiac cells possess electrical excitability due to ??? which allow the movement of Na+, K+ and Ca2+ across the plasma membrane

A

voltage-sensitive plasma membrane channels

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3
Q

L-type channels are voltage dependant ??? which play important roles in controlling cardiac rate and rhythm

A

voltage-dependent Ca2+ channels

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4
Q

Cardiac cells also possess intracellular Ca2+ channels (ryanodine receptors and inositol trisphosphate-activated Ca2+ channels) important in myocardial ???

A

contraction

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5
Q

dysrhythmia is caused by four basic phenomena:
* Delayed after-depolarisation
* Re-entry
* Ectopic pacemaker activity
* ???

A
  • Heart block
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6
Q

Delayed After-depolarization:
Most commonly due to abnormally raised INTRACELLULAR or EXTRACELLULAR (?) [Ca2+] causing an increase in inward currents and abnormal train of action potentials

A

intracellular

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7
Q

Delayed after-depolarisation:
Caused less often by hypokalaemia (low extracellular K+) or rarely hypercalcaemia (high extracellular
Ca2+), as a result of drugs targeting ??? in other tissues or other factors

A

ion channels

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8
Q

??? Describes a situation in which the impulse re- excites regions of cardiac muscle causing continuous circulation of action potentials.

A

Re-entry

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9
Q

Re-entry results from ??? or anatomical anomalies. Underlies many types of dysrhythmia

A

myocardial damage

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10
Q

Ectopic pacemaker activity is the result of an excitable group of cells that causes a ??? outside the SA node. This serves as a safety feature but can also cause tachyarrhythmias

A

premature heartbeat

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11
Q

TRUE or FALSE: Ectopic pacemaker activity serves as a safety feature

A

TRUE

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12
Q

Ectopic pacemaker activity is often associated with increased ??? activity

A

sympathetic

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13
Q

Heart block is the result of fibrosis or ischemic damage to the conducting system, often the ??? node. Often treated by implanting an artificial pacemaker

A

atrioventricular (AV)

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14
Q

Cardiac output is the product of heart rate and mean left ventricular stroke (blood volume ejected per heartbeat) and is controlled by the ??? system

A

Autonomic Nervous system

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15
Q

Stroke volume is controlled by intrinsic factors (e.g. intracellular Ca2+ and ATP) and extrinsic circulatory factors (e.g. state of arteries and veins, volume and ??? of blood)

A

viscosity of blood

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16
Q

myocardial contractility depends on intracellular calcium concentrations from ??? and ???

A

intracellular storage
calcium entry across cell membrane

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17
Q

ventricular function is influence by ??? (cardiac filling pressure) and ??? (peripheral pressure)

A

preload,
afterload

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18
Q

True or False: the heart is very well perfused and as such is not at greater risk of ischemic damage

A

FALSE: It is relatively poorly perfused (small blood supply compared to O2 consumption) and thus at greater risk of ischemic damage

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19
Q

Most drugs that effect cardiac heart metabolism, do so by influencing ???

A

Coronary blood flow

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20
Q

What physiological factors effect coronary blood flow?

A
  • physical factors (narrowing of valves, stenosis)
  • Vascular contol of metabolites (adenosine causes vasodialtion)
  • Neural + humoral control (autonomic innervation)
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21
Q

Physical Factors Affecting Coronary Blood Flow:
(1) shortening diastole, when heart rate ???
(2) increased ventricular end-diastolic pressure;
(3) reduced diastolic arterial pressure

A

When heart rate increases;

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22
Q

which receptor is stimulated by noradrenaline or epinephrine?

A

Adrenoceptors are stimulated by norepinephrine or epinephrine

23
Q

Cholinergic receptors (muscarinic acetylcholine receptors) are stimulated by ???

A

acetylcholine

24
Q

the resting heart is affected by which nervouss systems and what do they do?

A
  1. sympathetic NS: mediated mainly via b1 adrenoceptors to increase cyclic AMP formation and Ca2+ channel activity, increasing action potentials
  2. parasympathetic NS: mediated mainly via muscarinic M2 acetylcholine receptors to reduce cyclic AMP formation and increase K+ channel activity, causing hyperpolarisation
25
Q

SA node: SNS causes heart rate to INCREASE or DECREASE? PNS does the opposite

A

increase

26
Q

Atrial muscle: SNS causes force of contraction to INCREASE or DECREASE? PNS does opposite

A

INCREASE

27
Q

AV node: SNS causes automacity to INCREASE or DECREASE? PNS causes opposite effect as well as conduction velocity to decrease

A

INCREASE

28
Q

main effects on the heart by sympathetic NS is:
* ??? force of: contraction, heart rate, automaticity (ectopic heart beats – skipped or extra beats; not often a cause of concern)
* Restoration of heart function following cardiac depolarisation
* Reduced cardiac efficiency (increased O2 consumption relative to cardiac work)
* Cardiac hypertrophy (due to stimulation of myocardial a and b adrenoceptors)

A

Increased

29
Q

Main effect os PNS on heart are:
* Cardiac slowing
* Decreased ???
* Inhibition of atrioventricular (AV) node conduction

A

automaticity

30
Q

Atrial natriuretic peptide (ANP) is released from ??? (cells of the upper heart chambers) in response to ??? (atria stretching) or intravenous saline infusion

A

atrial cells,
volume overload

31
Q

B-natriuretic peptide (BNP) is released from ??? cells to oppose ventricular fibrosis and is increased in HF, with pro-BNP used to aid diagnosis of this disease

A

ventricular muscle

32
Q

C-natriuretic peptide (CNP) is released from endothelium impacting both heart function and ??? development

A

bone

33
Q

TRUE or FALSE: Cardiac natriuretic peptides bind natriuretic peptide receptors to mediate their function

A

TRUE

34
Q

ANP and BNP are inactivated by neutral endopeptidase (neprilysin), with the inhibitor ??? used with the angiotensin type I receptor receptor antagonist valsartan in treating chronic heart failure

A

sacubitril

35
Q

effects of natriuretic peptides:
* Increase renal Na+ and ??? excretion
* Relax vascular smooth muscle
* Increase vascular permeability
* Inhibit the release or actions of vasoconstrictor or salt-retaining hormones such as aldosterone, angiotensin II, endothelin and antidiuretic hormone

A

water excretion

36
Q

Angina occurs when ??? to the myocardium is insufficient for its needs,
resulting in pain to chest, arm and neck

A

O2 supply

37
Q

Myocardial infarction occurs when a coronary artery is blocked by a thrombus (atherosclerotic plaque), resulting in death due to mechanical failure or dysrhythmia. what happens to heart tissue to cause this?

A

Ischaemia of myocardium

38
Q

Angioplasty is used to open ??? as soon as possible when atherosclerois threatens to cause/ already is causing ischaemia of myocardium

A

occluded artery

39
Q

pharmacological therapies for stable type Angina include ??? Statins (to reduce atherosclerosis) Aspirin or other antiplatelet drugs (to prevent thrombosis)

A

organic nitrates, b-adrenoceptor antagonists, Ca2+ antagonists

40
Q

pharmacological therapies for unstable type Angina include: ??? (to reduce pain) Aspirin, clopidogrel or other antiplatelet drugs (to prevent
thrombosis)

A

Organic nitrates

41
Q

pharmacological therapies for variant type Angina include vasodialters such as ??? and Ca2+ antagonists

A

organic nitrates

42
Q

Thrombolytic, antiplatelet drugs (aspirin, clopidogrel), antithrombotic (heparin), are used to open blocked ??? and prevent reocclusion

A

artery

43
Q

TRUE or FALSE: O2 is used in myocardial infarctions to relieve ???

A

arterial hypoxia

44
Q

organic nitrates promote vasodilation and ???

A

reduce pain

45
Q

opioids prevent pain and reduce excessive ??? activity

A

sympathetic

46
Q

b-Adrenoceptor antagonists reduce myocardial O2 consumption and demand by lowering the heart rate, blood pressure, myocardial ???

A

contractility

47
Q

Angiotensin converting enzyme inhibitors (ACEIs) and angiotensin type I receptor antagonists (ARBs)
are used to treat heart attack to reduce cardiac work and improve cardiac ???

A

efficiency

48
Q

drugs that affect ??? directly:
- Autonomic transmitters & related drugs
- Antidysrhythmic drugs / physical means
- Cardiac glycosides & other ionotropic drugs
- Other drugs (e.g. doxorubicin) and hormones (e.g. thyroxine, glucagon)

A

myocardial cells

49
Q

drugs that affect vasculature/cardiac function indirectly:
- ??? (e.g. nitrates)
- Heart failure drugs (e.g. diuretics, angiotensin converting enzyme inhibitors)

A

Anti-anginal drugs

50
Q

drugs that effect calcium antagonists Affect myocardial cells directly
as well as cardiac function indirectly by relaxing ??? (i.e. verapamil)

A

smooth muscle

51
Q

Drugs that Increase Myocardial Contraction:
Cardiac glycosides: ??? is clinically most important. Net effect results in increased intracellular Ca2+ during each action potential

A

Digoxin

52
Q

what drug that increases myocardial contraction causes a block of atrioventricular conduction and increased ectopic pacemaker activity (rhythm)

A

digoxin

53
Q

Collateral arteries interconnect epicardial coronary arteries and provide an alternative source of
??? to the myocardium in cases of occlusive coronary artery disease

A

blood supply

CHEM358 Pharmacology (11 decks)

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