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cardioresp drugs > ischemic heart disease > Flashcards

ischemic heart disease Flashcards

1
Q

cardioselective BB

A

Atenolol, Metoprolol, Nebivolol

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2
Q

non cardioselective BB

A

Carvedilol, Propranolol

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3
Q

cardioselective receptor

A

β1

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4
Q

Bisoprolol target

A

Beta adrenoceptors

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5
Q

Bisoprolol moa

A

Inhibits binding of normal ligand noradrenaline released from sympathetic adrenergic neurones. This inhibits activation of adenylyl cyclase enzymes leading to reduced cyclic AMP. This in turn leads to reduced intracellular calcium levels.

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6
Q

Bisoprolol common side effects

A

Dizziness; Headache, fatigue, cold hands, impotence

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7
Q

Bisoprolol important side effects

A 
Hypotension 
Bronchoconstriction
Bradycardia and heart block 
Hypoglycaemia 
Peripheral vasoconstriction
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8
Q

Bisoprolol and Peripheral vasoconstriction issue

A

intermittent claudication and Raynaud’s phenomenon

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9
Q

Calcium channel blockers

A

Amlodipine
Diltiazem
Verapamil

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10
Q

amlodipine drug class

A

Dihydropyridine calcium channel blockers

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11
Q

amlodipine target

A

L-type calcium channels

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12
Q

amlodipine moa

A

Inhibit influx of calcium ions into vascular smooth muscle cells through L-type calcium channels

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13
Q

amlodipine affect overall

A

ecreased arterial smooth muscle contratility leading to vasodilatation

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14
Q

amlodipine common side effects

A

Flushing; Headache; Tachycardia; Peripheral oedema

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15
Q

amlodipine bad side effects

A

Heart failure in patients with poor left ventricular function

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16
Q

diltiazem target

A

L-type calcium channels

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17
Q

diltiazem drug class

A

Rate-limiting calcium channel blocker

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18
Q

diltiazem action

A

Inhibit influx of calcium ions into cardiomyocytes through L-type calcium channels

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19
Q

diltiazem common side effects

A 
Headache 
Flushing 
Tachycardia 
Peripheral oedema 
Constipation
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20
Q

diltiazem bad side effect

A

Sino-atrial and AV block

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21
Q

verapamil drug class

A

Class IV anti-arrhythmia agent CCB

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22
Q

verapamil inhibits

A

voltage-dependent calcium channels

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23
Q

GTN target

A

Nitrate membrane receptor

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24
Q

GTN moa

A

Inhibits the entry of calcium ions into the cell leading to reduced intracellular calcium levels

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25
Q

GTN effect

A

Vascular smooth muscle relaxation and vasodilatation

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26
Q

bad thing about long term GTN

A

tolerance

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27
Q

what are nitrites metabolised to

A

NO

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28
Q

what does NO do

A

stimulates guanylate cyclase enzymes to increase production of the second messenger cyclic GMP

29
Q

name a potassium channel opener

A

Nicorandil

30
Q

nicorandil drug class

A

Potassium channel activator

31
Q

nicorandil two moas

A

Potassium channel activator

Nitrate like effect

32
Q

how does nicorandil work as a k+ channel activator

A

Opens ATP-dependent potassium channels, causing K+ to leave the cell. This results in hyperpolarisation of the cell membrane, closure of voltage-gated Ca2+ channels and a reduction in intracellular calcium.

33
Q

nicorandil nitrate moa

A

Stimulates guanylate cyclase enzymes to increase production of the second messenger cyclic GMP (cGMP). This inhibits the entry of calcium ions into the cell leading to reduced intracellular calcium levels.

34
Q

Anti-platelet agents

A 
Aspirin
Clopidogrel
Ticagrelor
Dipyridamole
Tirofiban
35
Q

aspirin target

A

COX

36
Q

aspirin moa

A

Impairs synthesis of thromboxane A2 and prostacyclin = platelets cant aggregate

37
Q

aspirin bad side effect

A

GI irritation, ulceration and bleeding

Bronchospasm

38
Q

what can be co prescribed with aspirin to avoid GI upset

A

PPI

39
Q

dipyridamole drug class

A

antiplatelet

40
Q

dipyridamole 3 moas

A
  1. Inhibitor of platelet phosphodiesterase
  2. Blocks adenosine uptake into RBCs,
  3. Potentiation of PGI2 anti-aggregatory activity and enhancement of PGI2 biosynthesis
41
Q

dipyridamole bad adverse effects

A

Haemorrhage;
Hypotension;
Worsening symptoms of coronary artery disease

42
Q

what happens if adenosine cant get into RBCs

A

increases plasma adenosine levels which has a vasodilatory and anti-platelet effect

43
Q

what happens if platelet phosphodiesterase is inhibited

A

cyclic AMP concentration is increased and platelet activity reduced

44
Q

Isosorbide dinitrate is used to treat what

A

angina

45
Q

what is Isosorbide dinitrate converted to

A

NO

46
Q

Isosorbide dinitrate moa

A

converted to NO which activates the enzyme guanylate cyclase stimulates synthesis of cGMP which activates a series of protein kinase-dependent phosphorylations in the smooth muscle cells, eventually resulting in the dephosphorylation of the myosin light chain of the smooth muscle fiber. The subsequent release of calcium ions results in the relaxation of the smooth muscle cells and vasodilation.

47
Q

ivabradine aim

A

lower heart rate

48
Q

what is guanylate cyclase

A

atrial natriuretic peptide receptor A

49
Q

what does ivabradine inhibits

A

if channels

50
Q

ivabradine moa

A

disrupts If ion current flow, which prolongs diastolic depolarization, lowering heart rate

51
Q

Ranolazine inhibits

A

peak and late sodium channels

delayed rectifier potassium currents

52
Q

clopidogrel class

A

P2Y12 antagonist

53
Q

clopidogrel blocks

A

P2Y12 receptor

54
Q

clopidogrel blocks the binding of what to P2Y12 receptor

A

ADP

55
Q

clopidogrel reduces activation of what receptor

A

GPIIb/IIIa receptor

56
Q

clopidogrel overall aim

A

reduction in fibrinogen binding and thrombus formation

57
Q

what is ADP

A

platelet agonist

platelet activation

58
Q

ticagrelor blocks what receptors

A

adenosine diphosphate (ADP) receptors

59
Q

whats good about ticagrelor compared with the others

A

dosent need liver activion

60
Q

Tirofiban binds to

A

GP IIb/IIIa receptor

61
Q

Tirofiban antogonises

A

fibrinogen

62
Q

what is GP IIb/IIIa receptor

A

the major platelet surface receptor involved in platelet aggregation

63
Q

Alteplase drug class

A

Tissue plasminogen activator.

64
Q

Alteplase binds to

A

fibrin rich clots via the fibronectin finger-like domain and the Kringle 2 domain

65
Q

Alteplase moa

A

protease domain then cleaves the Arg/Val bond in plasminogen to form plasmin

66
Q

what does plasmin do

A

degrades the fibrin matrix of the thrombus

67
Q

Tenecteplase class

A

Tissue plasminogen activator

68
Q

Tenecteplase binds to

A

fibrin rich clots via the fibronectin finger-like domain and the Kringle 2 domain

69
Q

Tenecteplase moa

A

protease domain then cleaves the Arg/Val bond in plasminogen to form plasmin

cardioresp drugs (13 decks)

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