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Cardiovascular > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

sympathetic nervous system acts on __ receptors mediated by __ causing ___

A

B1 adrenoceptors
adrenaline and noradrenaline
increase in heart rate and contractility

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2
Q

sympathetic nerves innervate nodal and myocardial cells true/false

A

true

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3
Q

how do beta-adrenoceptors increase heart rate and contractility

A

activate G protein coupled receptors - activates adenylyl cyclase - increases cAMP - increases number of L-type channels - triggers release of calcium from SR

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4
Q

increase in heart rate is known as

A

positive chronotropic effect

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5
Q

increase in heart contractility is known as

A

positive inotropic effect

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6
Q

parasympathetic nervous system acts on __ mediated by __ causing ___

A

M2 muscarinic cholinoceptors
mediated by ACh
decrease in heart rate

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7
Q

parasympathetic nerves innervate nodal and myocardial cells true/false

A

false only on nodal cells - therefore only has effect on heart rate but not contractility

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8
Q

how does parasympathetic nerves decrease heart rate in nodal cells

A

when M2 binds to ACh making G protein - cAMP is reduced and potassium channels open decreasing contraction slope

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9
Q

what are the stages occurring for cardiac muscle contraction to occur

A

Ca L-type channels open during phase 2 - influx of Ca - triggers release of Ca from SR (CICR) - Ca binds to troponin C moving tropomyosin causing contraction

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10
Q

describe calcium induced calcium release

A

increasing the intracellular concentration of calcium causes further increase in its concentration from the sarcoplasmic reticulum

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11
Q

how does relaxation of cardiac muscle occur

A

repolarisation in phase 3 and 4 closes L-type channels. Ca influx stops and Ca dissociates from troponin C causing relaxation of muscle

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12
Q

what is the purpose of vagal manoeuvres

A

suppress conduction through the AVN - therefore decreasing heart rate

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13
Q

what are vagal manoeuvres used for

A

SVTs such as atrial fibrillation and atrial flutter

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14
Q

what is the funny current mediated by

A

HCN channels

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15
Q

which drug selectively blocks the HCN channel

A

ivabradine - decreasing slope on pacemaker potential

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16
Q

which conditions is ivabradine used for

A

angina - lowers oxygen requirements

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17
Q

which two areas can drugs act on to alter heart rate and contractility

A

beta-adrenoceptors

muscarinic receptors

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18
Q

what is the effect of B1 adrenoceptor agonists

A

activated adenylyl cyclase increasing cAMP which increases heart rate

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19
Q

name two examples of B-adrenoceptor agonists and their uses

A

dobutamine - IV for heart failure

adrenaline - cardiac arrest and anaphylaxis

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20
Q

what is the effect of beta-blockers

A

either selectively or non-selectively block beta-adrenoceptor slowing conduction through AVN reducing heart rate/oxygen requirement

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21
Q

name a non-selective beta-blocker and what does it act on

A

propanolol acting on B1 and B2 adrenoceptors

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22
Q

name some selective beta-blockers

A

atenolol, bisoprolol, metoprolol

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23
Q

what are the clinical uses of beta-blockers

A

angina
arrhythmias - esp AF
heart failure - start low and go slow as reduces sympathetic drive
(hypertension if extreme)

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24
Q

what are the side effects of beta-blockers

A 
bradycardia 
can trigger bronchospasm esp in asthmatics 
fatigue
hypoglycaemia 
can aggravate heart failure 
cold extremities
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25
Q

what is the effect of muscarinic ACh receptor antagonists

A

block parasympathetic action therefore increase heart rate

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26
Q

name two drugs that are muscarinic receptor antagonists

A

atropine

digoxin

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27
Q

what is the clinical use of atropine

A

used for extreme bradycardia following an MI

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28
Q

what is the clinical use of digoxin

A

treatment of heart failure as increases contractility

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29
Q

what are the side effects of digoxin

A

can cause heart block
arrhythmias
GI disturbances
disturbance to colour vision

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30
Q

what are the classifications of drugs that have direct effect on vasculature and BP

A

organic nitrates
calcium channel blockers
ACEi and ARBs

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31
Q

how does smooth muscle contraction occur in vasculature

A

Ca through L-type channels activates MLCK causing contraction

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32
Q

how does relaxation occur in smooth muscle vasculature

A

myosin light chain phosphatase activated by protein kinase G causes relaxation of smooth muscle

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33
Q

what is the action of organic nitrates

A

organic nitrates metabolised into nitric oxide causing venorelaxation and arteriolar dilatation causing increased coronary blood flow

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34
Q

name a short acting organic nitrate and its use

A

GTN (glycerintrinitrate) administered sublingually

used for symptomatic relief of angina and acute MI

35
Q

name a long acting organic nitrate and its use

A

isosorbide mononitrate administered orally

used for prophylaxis of angina

36
Q

how can organic nitrates improve symptoms of angina

A

reduces myocardial oxygen requirement decreasing preload and afterload

37
Q

what are some of the side effects of organic nitrates

A

over dilatation of blood vessels causing hypotension, headaches, dizziness and nausea

38
Q

what is the effect of repeated administration of organic nitrates

A

can cause diminished effect - therefore nitrate free period overnight is recommended

39
Q

which calcium channel blocker has an effect on cardiac L-type channels

A

verapamil

40
Q

which calcium channel blocker has an effect on smooth muscle L-type channels

A

amlodipine

41
Q

what is the overall effect of blocking Ca channels

A

reduction in intracellular Ca causing arteriolar dilatation

42
Q

what are Ca channel blockers used for

A

hypertension
angina
arrhythmias

43
Q

what are the side effects of calcium channel blockers

A

excessive vasodilation causing hypotension, dizziness and ANKLE OEDEMA

44
Q

what is haemostasis

A

the stopping of blood flow through a damaged vessel

45
Q

what is thrombosis

A

pathological haemostasis - formation of blood clot

46
Q

thrombin from coagulation cascade is activated from ___ by ___ enzyme

A

prothrombin

prothrombinase

47
Q

describe arterial thrombus

A

white thrombus mainly containing platelets

48
Q

where is an arterial thrombus most likely to detach and travel to

A

heart
arteries
brain - stroke

49
Q

describe venous thrombus

A

red thrombus mainly containing fibrin

50
Q

where is a venous thrombus most likely to detach and travel to

A

lung from lower limbs

51
Q

arterial thrombus is treated with

A

antiplatelets

52
Q

venOus thrombus is treated with

A

anticOagulants

53
Q

what is the mechanism of anticoagulants

A

block different points of the coagulation cascade typically prothrombinase, thrombin and factor Xa

54
Q

name the clinical uses of anticoagulants

A

DVTs and PE
atrial fibrillation prophylaxis
post-op thrombosis

55
Q

name some anticoagulants

A

warfarin
rivaroxaban
epixaban
heparin

56
Q

what type of drug is warfarin classed as

A

vitamin K antagonist

57
Q

what is one of the major side effects of taking anticoagulants

A

increased risk of haemorrhage

58
Q

what factors can lessen the effects of warfarin

A

anything increased risk of thrombosis:

  • pregnancy
  • hypothyroidism
  • vitamin K consumption (green salad vegetables)
59
Q

which factors of the coagulations cascade does warfarin interact with

A

factor II, VII, IX and X

60
Q

heparin and LMWHs are which type of anticoagulants

A

antithrombins

61
Q

what is the mechanism of heparin

A

binds to antithrombin III increasing affinity for clotting factors

62
Q

when is the only time heparin is preferred over LMWHs

A

when the patient has renal failure

63
Q

name some examples of antiplatelets

A

aspirin
clopidogrel
ticagrelor

64
Q

what are some of the side effects of antiplatelets

A

haemorrhage

aspirin also causes GI upset

65
Q

when are fibrinolytic drugs used

A

as thrombolysis to reopen occluded arteries in acute stroke or MI

66
Q

name an example of fibrinolytic drug

A

streptokinase

67
Q

what causes renin to be released from the kidneys

A

drop in blood pressure - body thinks there is not enough fluid and so will retain it

68
Q

what is ACE and its function

A

enzyme converting angiotensin I to angiotensin II

acts as a vasoconstrictor and inactivates bradykinin

69
Q

what is bradykinin

A

vasodilator inactivated by ACE

70
Q

what is the effect of an ACE inhibitor

A

blocking the conversion of angiotensin causes arteriolar dilatation and venous dilatation - overall reduces blood pressure and cardiac load

71
Q

what is an ARB

A

angiotensin receptor blocker - very similar effect however doesn’t activate bradykinin

72
Q

what are the clinical uses of ACEis and ARBs

A

hypertension

heart failure following MI

73
Q

what is a common side effect of an ACEi but not an ARB and why

A

dry cough due to the activation of bradykinin

74
Q

are ACEis and ARBs safe in pregnancy

A

no as the have foetal toxicity

75
Q

name two examples of alpha blockers

A

prazosin and doxazosin

76
Q

what is the effect of alpha blockers

A

through blocking A1 channel throughout the rest of the body - sympathetic vasoconstriction is prevented - prevents blood pressure from getting too high

77
Q

what is the indication for alpha blockers

A

severe hypertension

or patient with benign prostatic hyperplasia and hypertension

78
Q

what is an adverse effect of alpha blockers

A

postural hypotension

79
Q

what is the purpose of diuretics

A

acts on kidneys to increase Na, Cl and water excretion - indirectly relaxing vasculature

80
Q

what are the two types of diuretics

A

thiazide diuretics

loop diuretics

81
Q

give an example of a thiazide diuretic and its main uses

A

bendroflumethiazide

used mainly for hypertension as not as effective for removing fluid

82
Q

give an example of a loop diuretic and its main uses

A

furosemide

has strong diuresis and used for acute pulmonary oedema and chronic heart failure

83
Q

what are the main side effects of diuretics

A

can cause severe hypokalaemia and require K supplements or can lead to gout
also thirst and dizziness

Cardiovascular (8 decks)

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