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Cardiology SB > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

what activates adenylyl cyclase

A

coupling through Gs protein

Sympathetic

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2
Q

what does coupling through Gi cause

A
  • decreases activity of of adenylate cyclase and reduces [cAMP]
  • opens potassium channels to cause hyperpolarization of SA node
    parasympathetic
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3
Q

what is the inward current/funny current

A

current activated by hyper polarisation and cAMP

carried by sodium

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4
Q

what does blockage of the HCN channel cause

A

decrease in the slope of the pacemaker potential and reduces HR

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5
Q

what do hormones that increase cAMP also do

A

increase HR

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6
Q

how does sympathetic stimulation increase contractility

A

increases phase 2 cardiac AP
enhanced Ca++ entry
increases sensitivity of contractile protein to Ca++

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7
Q

how does sympathetic stimulation decrease duration of systole

A

increased uptake of Ca2+ into the SR

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8
Q

how does parasympathetic stimulation decrease contractility

A

decrease phase 2 cardiac AP

decreased Ca++ entry

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9
Q

how does parasympathetic stimulation decrease conduction in AV node

A

decreased activity of voltage-dependent Ca2+ channels and hyperpolarization via opening of K+ channels

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10
Q

what is located in the t-tuble membrane

A

voltage-gated L-type Ca channels (DHP receptors)

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11
Q

what does calcium activate and what occurs

A

the myofilaments and contraction occurs

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12
Q

how is Ca removed from the cytoplasm

A

SERCA

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13
Q

when is isoprenaline used

A

as a treatment for bradycardia

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14
Q

what does isoprenaline cause

A

bigger calcium ‘transients’

bigger and faster twitches

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15
Q

what is the function of voltage gated calcium channel

A

trigger’ calcium plateau phase of action potential

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16
Q

how is voltage gated calcium channels gated

A

phosphorylated by protein kinase A
increases trigger calcium
increases Ca induced Ca release

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17
Q

what is the function of ryanodine receptors and how is it regulated

A

Ca-induced Ca release from SR

Regulated by protein kinase A

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18
Q

what is the function of troponin

A

regulates actin/myosin interaction using calcium

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19
Q

what phosphorylates troponin and how does the affect it

A

protein kinase A

reduces its affinity for Ca - accelerates relaxation

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20
Q

how do hormones increases FOC

A

increase cAMP and activate PKA

increase Ca influx and release

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21
Q

how do hormones shorten the contractile cycle

A

increase cAMP and activate PKA

increase Ca reuptake

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22
Q

what are the effects of beta-adrenoceptor agonist

A

↑ Force, rate, CO, O2 consumption

↓ cardiac efficiency

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23
Q

what are side effects of beta-adrenoceptor agonist

A

arrhythmias

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24
Q

when is adrenaline used

A

cardiac arrest

anaphylactic shock

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25
Q

drug selective for beta1-adrenoceptors and when is it used

A

Dobutamine

acute heart failure

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26
Q

what is a non-selective beta blocker

A

propranolol

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27
Q

what are beta-adrenoceptor antagonist

A

beta-blockers

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28
Q

what are selective beta 1 blockers

A

atenolol

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29
Q

what does Digoxin do

A

increases contractility of the heart by blocking the SARCOLEMMA Na/K ATPase

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30
Q

what happens in the presence of digoxin

A

Na+/K+ATPase blocked

↑storage of Ca2+ in SR

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31
Q

what is the effect of digoxin on action potentials

A

shortens AP and refractory period in myocytes - useful in HF coupled with AF

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32
Q

side effects of digoxin

A

heart block

dysrhytmias

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33
Q

what are examples of inotropes

A

digoxin, levosimendan

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34
Q

what channels does calcium enter through

A

L-type Ca2+ channel

GPCR coupled to Gq/11

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35
Q

what is the steps to contraction

A 
1 - Ca2+ enters the cell
2 - binds with Calmodulin
3 - Ca-CaM binds with MLCK
4 - active MLCK causes myosin-LC to phosphorylate
5 - contraction
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36
Q

what is the steps to relaxation

A

1 - cGMP binds with Myosin-LC-phosphatase
2 - myosin-LC-phosphatase becomes active
3 - dephosphorylates myosin-LC
4 - relaxation

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37
Q

what are side effects of organic nitrates

A

headaches
hypotension
collapse

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38
Q

which organic nitrate is resistant to first-pass metabolism

A

isosorbide mononitrate

39
Q

what is the receptor for endothelin-1

A

ETa receptor

40
Q

renin inhibitor

A

aliskiren

41
Q

what do ACEi cause

A 
venous dilatation (↓preload) arteriolar dilatation (↓afterload and ↓TPR) 
decreasing BP and cardiac load
42
Q

ACEi increases contractility - true or false

A

false

has no affect on contractility

43
Q

when does ACEi especially cause hypotension

A

in combination with diuretics

44
Q

when should ARB and ACEi not be used

A

Pregnancy

Bilateral renal artery stenosis

45
Q

what do beta 1 blockers do

A

decrease myocardial oxygen requirement

decreases duration of diastole

46
Q

how do beta blockers help restore normal BP

A

reduce CO

reduce renin release

47
Q

what do calcium antagonist interact with and where are they

A

L-type calcium channels

in the heart and smooth

48
Q

what are the three main types of calcium antagonist

A

amlodipine, verapamil, diltiazem

49
Q

what is an immediate selective calcium antagonist

A

diltiazem

50
Q

when are calcium channel blockers used

A

Hypertension
Angina
Dysrhythmias

51
Q

alpha blockers

A

prazosin

doxazosin

52
Q

what is the pathway of platelet reactions following endothelial damage

A 
1 - endothelial damage
2 - adhesion, activation and aggregation of platelets
3 - secretion and synthesis of mediators
4 - further aggregation of platelets
5 - fibrin clot
53
Q

what are the mediators excreted by platelets

A

ADP
TXA2
5-HT

54
Q

what factors cause further aggregation of platelets

A

Thrombin (IIa)

Fibrinogen

55
Q

what is the pathway of blood coagulation following endothelial damage

A

1 - endothelial damage
2 - VIIa, XIIa, XIa cause conversion of X to Xa
3 - Xa causes conversion of Prothrombin (II) to Thrombin (II)
4 - Thrombin causes conversion of fibrinogen to fibrin
5 - fibrin clot

56
Q

what are the clotting factors

A

Prothrombin (II), VII, IX and X

57
Q

what are the serine proteases

A

Thrombin (IIa), VIIa, IXa and Xa

58
Q

what are the stages of conversion by Vit K reductase

A

1 - vitamin K oxidised form - epoxide
2 - vitamin K - quinone
3 - vitamin K reduced form - hydroquinone

59
Q

what does warfarin do

A

competes with vit K for binding to vit K reducatse preventing conversion of epoxide to hydroquinone

60
Q

what factors does warfarin render inactive

A

II, VII, IX and X

61
Q

what is an inhibitor of coagulation

A

Antithrombin III

62
Q

what does Heparin do

A

bind to ATIII increasing its affinity for Xa and IIa to increase rate of inactivation

63
Q

Heparin must bind to both AT III and IIa to inhibit IIa - true or falee

A

true

64
Q

Heparin needs to bind to AT III and Xa to inhibit Xa - true of false

A

false

only needs to bind to ATIII

65
Q

what does LMWH inhibit

A

factor Xa

still works as Xa upstream

66
Q

side effects of heparin and LMWH

A

haemorrhage
osteoporosis
hypoaldosteronism

67
Q

orally active inhibitors

A

dabigatran etexilate - inhibitts thrombin

rivaroxaban - inhibits Xa

68
Q

what is the mechanism of action of aspirin

A

irreversibly blocks COX preventing TXA2 synthesis and production of prostaglandin I2

69
Q

what is the mechanism of clopidogrel

A

Links to P2Y12 receptor

70
Q

when is tirofiban given

A

IV to prevent MI in patients with unstable angina

71
Q

what causes plasminogen to convert to plasmin

A

endogenous tissue plasminogen activator

72
Q

what is the role of plasmin

A

converts fibrin to fibrin fragments

leading to clot lysis

73
Q

what are Alteplase and duteplase

A

recombinant tissue plasminogen activator (rt-PA)

74
Q

how can the risk of haemorrhage from fibrinolytic be controlled

A

tranexamin acid

inhibits plasminogen activation

75
Q

what should a CCB never be given in

A

Heart Failure

76
Q

what is given to treat valvular AF

A

warfarin

77
Q

why should organic nitrates not be stored in a clear bottle

A

as they are photosensitive and are rendered useless

78
Q

what are side effects of statins

A

muscle aches

79
Q

side effects of nicorandil

A

mouth ulcers

80
Q

what is a potassium sparing diuretic

A

Triamterene
Spironolactone
Eplerenone

81
Q

side effects of digoxin

A 
elderly patients with renal impairment can get toxicity
Digoxin Toxicity
Nausea, vomiting
Yellow vision
Bradycardia, Heart Block
Ventricular Arrhythmias
82
Q

what does spironolactone block

A

aldosterone

83
Q

what are anti anginal drugs

A

Beta Blockers
Calcium Antagonists
Nitrates
Nicorandil

84
Q

what are diuretic side effects

A

hypokalaemia (tired + arrhytmias)
hyperglycaemia (diabetes)
increase uric acid (gout)
impotence

85
Q

when are cardioselective beta blockers used

A

angina, hypertension, heart failure

86
Q

when is nonselective beta blockers used

A

thyrotoxicosis/hyperthyroidism

87
Q

what are the two types of CCB

A

Dihydropyridines - Amlodipine

Rate limiting calcium antagonist - verapamil, diltiazem

88
Q

what do alpha blockers do and when are they used

A

Block α adrenoceptors to cause vasodilatation

Hypertension, prostatic hypertrophy

89
Q

side effects of alpha blocker

A

postural hypotension

90
Q

what are SE of anti platelet agents

A

Haemorrhage
Peptic ulcer
Aspirin sensitivity in Asthma

91
Q

when are fibrinolytic drugs not to be used

A 
recent haemorrhage
trauma
bleeding tendencies
severe diabetic retinopathy
peptic ulcer
92
Q

what is used to treat Supraventricular Arrhythmias in acute phase

A

Adenosine

93
Q

what is used to treat Ventricular/Supraventricular Arrhythmias

A

Amiodarone
Beta Blockers
Flecainide

94
Q

what are the side effects of anti-arrhythmic drugs

A

phototoxicity
pulmonary fibrosis
thyroid abnormalities (hypo or hyper)

Cardiology SB (15 decks)

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