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Cardio - mine > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

what affect does (nor)adrenaline have on HR

A

increases

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2
Q

what affect does (nor)adrenaline have on contractility

A

increases

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3
Q

what affect does (nora)adrenaline have on conduction velocity in AV node

A

increases

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4
Q

what affect does (nora)adrenaline have on duration of systole

A

decrease

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5
Q

explain the effect of (nora)adrenaline on HR

A

it increases the slope pacemaker potential (phase 4)

it reduces the threshold for AP initiation

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6
Q

explain the effect of (nora)adrenaline on contractility

A

it increases phase 2 via enhancing Ca2+ influx

increases sensitisation of contractile proteins to Ca2+

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7
Q

explain the effect of (nora)adrenaline on systole duration

A

increases uptake of Ca2+ into SR

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8
Q

what does (nora)adrenaline act upon in heart

A

B1-adrenoceptors in nodal and myocardial cells

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9
Q

what do B1-adrenoceptors do once they are activated by (nora)adrenaline

A

couple to Gs protein which activates adenylyl cyclase to increase [cAMP]

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10
Q

what does B1-adrenoceptors couple with

A

Gs protein

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11
Q

what does Gs protein activate

A

adenylyl cyclase

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12
Q

what does activated adenylyl cause an increase in

A

[cAMP]

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13
Q

what affect does acetylcholine have on HR

A

decreases

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14
Q

what affect does acetylcholine have on contractility

A

decrease

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15
Q

what affect does acetylcholine have on conduction in AV node

A

decrease

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16
Q

explain the effect of acetylcholine on HR

A

increases threshold for AP initiation

decreased slope of pacemaker potential via hyperpolarization caused by opening of GIRK channels

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17
Q

explain the effect of acetylcholine on contractility

A

decrease in phase 2 due to decreased Ca2+ entry

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18
Q

explain the effect of acetylcholine on conduction in AV node

A

decreased activity of voltage activated Ca2+ channels

hyperpolarization via opening K+ channels

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19
Q

what does acetylcholine act upon

A

M2-muscarinic cholinoceptors in nodal cells

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20
Q

what does M2-muscarinic cholinoceptors do once activated by acetylcholine

A

couples to Gi protein which decreases the activity of adenylyl cyclase reducing [cAMP] it also opens GIRK channels causing hyperpolarization of SA node

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21
Q

what do M2-muscarinic cholinoceptors couple to

A

Gi proteins

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22
Q

what do Gi proteins do once activated by M2-muscarinic cholinoceptors

A

decrease activity of adenylyl cyclase

open GIRK channels

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23
Q

what does opening on GIRK channels cause (SA node)

A

hyperpolarization of SA node

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24
Q

what does a decrease in adenylyl cyclase activity result in

A

decrease in [cAMP]

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25
Q

what is ivabradine

A

selective blocker of HCN channels

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26
Q

describe the affect of ivabradine on HR

A

decrease

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27
Q

what is the clinical use of ivabradine

A

treatment of angina (if uncontrolled with beta blockers and Calcium channel blockers)
chronic HF

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28
Q

describe the mechanism of ivabradine

A

blocks HCN channels which decreases the slope of pacemaker potential

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29
Q

what do HCN channels do

A

mediates the “funny current” which modulates the pacemaker potential

30
Q

what is the full name of HCN channels

A

cyclic AMP gated HCN channels

31
Q

explain the process of contraction in cardiac muscle

A

ventricular AP causes L-type Ca2+ to open during phase 2

this causes a Ca2+ influx into the cytoplasm activating RyR2 on the SR causing Ca2+ to flow out of the SR (this process is called CICR)

Ca2+ binds to troponin C and shifts the tropomyosin out of the actin cleft allowing cross-bridge formation

contraction occurs via the sliding filament mechanism

32
Q

explain the process of relaxation in cardiac muscle

A

Ca2+ dissociates from troponin C and leaves the cell in 2 ways:

  1. via NCX1 (Na+/Ca2+ exchanger)
  2. returns to the SR via SERCA (Ca2+ATPase of Ca+)
33
Q

give examples of adrenoceptor agonist

A

adrenaline

dobutamine

34
Q

what effects do adrenoceptor agonist have on the heart (5)

A

increase: force, HR, CO, O2 consumption
decrease: cardiac efficiency

35
Q

what can long term use of adrenoceptor agonist cause

A

arrhythmias

36
Q

what type of adrenoceptor agonist is adrenaline

A

alpha AND beta agonist

37
Q

what are the clinical uses of adrenaline

A 
cardiac rest (IV)
anaphylactic shock (IM)
38
Q

what affect does adrenaline have on HR and force, what is it acting on

A

increases

β1

39
Q

what affect does adrenaline have on blood vessels, what is it acting on

A

constricts the skin, mucosal, and abdomen vessels

α1

40
Q

what affect does adrenaline have on coronary arteries, what is it acting on

A

dilatation

β2

41
Q

what type of adrenoceptor agonist is dobutamine

A

selective beta

42
Q

what are the clinical uses of dobutamine

A

acute heart failure (IV)

43
Q

give examples of β-adrenoceptor antagonists

A

propranolol, atenolol, bisoprolol, metoprolol

44
Q

give examples of SELECTIVE β-adrenoceptor antagonists

A

atenolol, bisoprolol, metoprolol

45
Q

give examples of NON SELECTIVE β-adrenoceptor antagonists

A

propranolol

46
Q

what type of β-adrenoceptor antagonist is propranolol

A

non selective (β1 and β2)

47
Q

what type of β-adrenoceptor antagonist is atenolol

A

selective (β1)

48
Q

what type of β-adrenoceptor antagonist is bisoprolol

A

selective (β1)

49
Q

what type of β-adrenoceptor antagonist is metoprolol

A

selective (β1)

50
Q

what affect do β-adrenoceptors have at rest

A

none

51
Q

what affect do β-adrenoceptors have during exercise or stress (6)

A

decreased: HR, force of contraction, CO , maximal exercise tolerance, coronary vessel diameter, myocardial O2 requirement

52
Q

what are the clinical uses of β-adrenoceptors antagonists (4)

A

angina, hypertension, arthymias (AF, SVT), heart failure

53
Q

what are the adverse effects of β-adrenoceptors antagonists

A

bronchospasms, aggravation of cardiac failure, bradycardia, cold extremities

54
Q

in what condition are β-adrenoceptors contraindicated

A

asthma

55
Q

give an example of muscarinic receptor antagonist

A

atropine

56
Q

what are the clinical uses of atropine

A

bradycardia (1st line)
MI (IV)
anticholinesterase poisoning

57
Q

what are the affect of muscarinic receptor antagonists

A

increased HR

58
Q

give an example of a cardiac glycoside

A

digoxin

59
Q

what are the clinical uses of digoxin

A 
acute HR (IV)
chronic HR (orally)
60
Q

what are the side effects of digoxin

A

heart block/arrhythmias
disturbance of colour vision
vomiting/diarrhoea/nausea

61
Q

what is the direct action of digoxin

A

shortens AP and refractory period

62
Q

what is the indirect action of digoxin

A

increases vagal activity

63
Q

what is the mechanism of digoxin

A

binds to alpha-subunit of Na+/K+ ATPase in competition with K

increases contractility by blocking the sarcolemma ATPase

64
Q

what is the mechanism of levosimendan

A

binds to troponin C and densities it to the action of Ca2+

opens K+ channels

65
Q

what is the affect of levosimendan

A

increases contractility

66
Q

what is the affect of digoxin

A

increases contractility

67
Q

what is the affect of am- and mil-rinone

A

increases contractility

68
Q

what is the mechanism of am- and mil-rinone

A

inhibits phosphodiesterase (PDE) in cardiac and smooth muscle cells = increase [cAMP]

69
Q

what is the clinical use of am- and mil-rinone

A

acute HF (IV)

70
Q

what is the clinical use of levosimendan

A

acute decompensated HF (IV)

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