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Pharmacology and Therapeutics 2 Y2 > Drugs and the Heart > Flashcards

Drugs and the Heart Flashcards

1
Q

what is the main NT driving contraction in the heart

A

Ca2+

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2
Q

What is The major store of calcium within the myocyte

A

sarcoplasmic reticulum

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3
Q

what are the 2 intracellular 2nd messengers of the heart

A

cAMP and Ca2

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4
Q

What causes calcium entry into the myocyte

A

depolarisation

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5
Q

What does calcium enter the cell through

A

dihydropyridine receptors (DHPR)

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6
Q

What are calcium release channels AKA

A

ryanodine receptors (RyR)

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7
Q

Describe how the heart contracts

A

In response to depolarisation, calcium enters the cell through calcium channels in the plasma (dihydropyridine receptors (DHPR))

This calcium then goes on to bind to calcium release channels (ryanodine receptors (RyR)) to stimulate calcium release from the sarcoplasmic reticulum

After stimulating contraction by binding to troponin in the thin filament, the calcium is then removed from the myoplasm by Plasma Membrane Calcium ATPase (PMCA) or Na+-­‐Ca2+ exchangers, both of which are found in the plasma membrane

The calcium can also be taken back up into the sarcoplasmic reticulum by sarco ‐endoplasmic reticulum calcium ATPase (SERCA2a)

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8
Q

2 methods of removing Ca from the myoplasm? what is the main way

A

After stimulating contraction by binding to troponin in the thin filament, the calcium is then removed from the myoplasm by Plasma Membrane Calcium ATPase (PMCA) or Na+-­‐Ca2+ exchangers, both of which are found in the plasma membrane

The calcium can also be taken back up into the sarcoplasmic reticulum by sarco ‐endoplasmic reticulum calcium ATPase (SERCA2a)

The activity of SERCA2a is responsible for the removal of >70% of myoplasmic Ca2+ in humans
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9
Q

How does SERCA2a affect the rate of cardiac muscle relaxation/cardiac contractility

A

As a result, SERCA2a determines both the rate of Ca2+ removal (and consequently the rate of cardiac muscle relaxation) and the size of the Ca2+ store (which affects cardiac contractility in the subsequent beat)

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10
Q

What regulated SERCA2a?

A

PLN (phospholamban)

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11
Q

How does PLN (phospholamban) regulate SERCA2a

A

In its dephosphorylated form, PLN (phospholamban) is an INHIBITOR of SERCA2a

When phosphorylated by PKA, PLN (phospholamban) dissociates from SERCA2a activating the Ca2+ pump

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12
Q

What phosphorylates PLN (phospholamban)

A

PKA

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13
Q

What dephosphorylates PLN (phospholamban)

A

PP1 protein phosphatase

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14
Q

2 proteins involved in removing Ca from the myoplasm?

A

by Plasma Membrane Calcium ATPase (PMCA) or Na+-­‐Ca2+ exchangers

And

phospholamban (PLN)

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15
Q

Which channels do the the sympathetic nervous system use to increase HR

A

If, L type Ca and T type Ca

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16
Q

How is the parasympathetic nervous system through the muscarinic receptor coupled with adenylate cyclase

A

Negatively

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17
Q

Biggest determinant of the myocardial oxygen demand

A

Myocyte contraction

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18
Q

4 determinants of myocardial oxygen demand

A

Heart Rate
Preload
Afterload
Contractility

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19
Q

What effect do BBs have on the heart channels and why

A

Beta blockers reduce the amount of cAMP being produced by it blocking B1 adrenoceptor so you reduce the activation of the If and calcium channels

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20
Q

What channel specifically does Ivabradine target

A

If

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21
Q

What channel specifically does Calcium channel antagonists target

A

Ica

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22
Q

What drug specifically targets Ca channels

A

Calcium channel antagonists

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23
Q

What drug specifically targets If channels

A

Ivabradine

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24
Q

What effect do Ca channel antagonists have on the heart channels and why

A

block the L type calcium channels in the plasma membrane so the reduced influx of external calcium into the cardiac myocyte meaning there is also reduced release of calcium from the SR

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25
Q

2 classes of Calcium Channel Antagonists

A

Rate slowing and non rate slowing

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26
Q

Where are the actions of rate slowing Ca Channel Antagonists

A

Cardiac and smooth muscle

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27
Q

Where are the actions of non-rate slowing Ca Channel Antagonists

A

Smooth muscle actions (more potent)

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28
Q

What do Rate slowing calcium channel blockers do and where (2)

A

will reduce heart rate and cause vasodilation. Have effects on both cardiac and smooth muscle, probably more powerful on cardiac tissue though.

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29
Q

What do non-Rate slowing calcium channel blockers do and where (2)

A

cause REFLEX TACHYCARDIA though profound vasodilation because baroreceptors will detect this and the fall in blood pressure. They have no effect on the heart, only smooth muscle

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30
Q

Example of non-Rate slowing calcium channel blockers

A

Amplodipine

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31
Q

Example of Rate slowing calcium channel blockers (2)

A

Verapamil and Diltiazem

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32
Q

What do Organic Nitrates and Potassium Channel Openers do? What’re they linked to (briefly)

A

ENHANCE MYOCARDIAL OXYGEN SUPPLY. Both linked to hyperpolarisation of tissue.

Both vasodilator.

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33
Q

What is the second messenger of granulate cyclase? what does it do? (think K)

A

GTP –> cGMP

Promotes relaxation coupled with opening of potassium channels. Potassium channels opening causing potassium efflux is associated with hyperpolarisation and this reduces the ability of calcium to enter the cell. This relaxes the tissue, prevents contraction and keeps the tissue in a relaxed state for longer

34
Q

What are substrates for nitric oxide production

A

Organic nitrates

35
Q

What can directly activates Guanylate cyclase

A

NO

36
Q

What are Organic nitrates used

A

Angina when there is is profound atherosclerosis.

You would give the organic nitrate to angina patients before they exercise because it dilates coronary vessels so blood flow is improved.

37
Q

What effect do Potassium channel openers have on what type of muscle

A

promote potassium efflux by keeping potassium channels open for longer

it’ll hyperpolarise the smooth muscle and reduce its ability to contract

38
Q

What type of muscle do Organic Nitrates and Potassium Channel Openers effect

A

vascular smooth muscle

39
Q

What 2 drugs effect vascular smooth muscle to help with angina

A

Organic Nitrates and Potassium Channel Openers

40
Q

How do Organic Nitrates and Potassium Channel Openers help with afterload

A

Vasodilation reduces TPR hence reduces afterload

41
Q

How do Organic Nitrates and Potassium Channel Openers help with preload

A

The drugs also cause venodilation, which reduces venous return to the heart and hence reduces preload and contractility

42
Q

How do Organic Nitrates and Potassium Channel Openers help with contractility

A

The drugs also cause venodilation, which reduces venous return to the heart and hence reduces preload and contractility

43
Q

Organic nitrates not only improve blood supply to the heart and increase oxygen delivery, but they also …..

A

decrease the need for oxygen of the heart by increasing preload and afterload

44
Q

What is angina

A

myocardial ischaemia. The pain is when you can’t match oxygen supply to demand.

45
Q

How are nitrates used for angina

A

used for immediate vasodilation as symptomatic treatment and it is short-acting1

46
Q

MAIN EFFECTS OF NITRATES

A

VASO and VENODILATION

47
Q

How can BB be unhelpful for heart failure

A

They will have some beta 2 blocking effects as well in the vasculature, leading to vascular constriction. This increases the work the heart has to do.

48
Q

to what patient should you not give BB

A

Caution must be taken when giving beta blockers to patients with cardiac failure
or
MUST NEVER GIVE THEM TO ASTHMA / DIABETES PATIENTS.

49
Q

why are BB bad for asthma patients?

A

They also cause bronchoconstriction

50
Q

why are BB bad for diabetes patients?

A

impair your glucose control. Hence why β-blockers are contraindicated for diabetics. They mask any hypoglycaemic episode as your liver can’t respond to the challenge of hypoglycaemia due to blockade of the β-2 receptor on the liver.

51
Q

What are non-rate slowing drugs known as

A

Dihydropyridines

52
Q

What are dihydropyridines

A

non-rate slowing Ca Ch Bl.

53
Q

CCBs that target the heart are going to have similar side effects to ….

A

BBs

54
Q

Side effects of Rate-limiting Ca channel blockers ? (3)

A

radycardia and AV block, as well as constipation by blocking the calcium channels in the smooth muscle of the gut walls.

55
Q

Side effects of non-Rate limiting Ca channel blockers ? (3)

A

ankle oedema (fluid leakage out of capillaries because so much blood is flowing through those regions because of gravity and vasodilation), headache/flushing (due to vasodilation), palpitations (reflex activation of the adrenergic sympathetic system).

56
Q

CCBs that target the heart are going to have similar side effects to ….

A

K channel openers and nitrates

57
Q

Treatments for Supraventricular Arrhythmias

A

(amiodarone and verapamil)

58
Q

Treatments for ventricular Arrhythmias

A

flecainide and lidocaine

59
Q

What is used to classify anti-arrhythmic Drugs, what is this based on?

A

The Vaughan Williams Classification - membrane potential of smooth muscle

60
Q

Which class in the VW classification does adenosine fall into

A

It doesn’t

61
Q

How does adenosine work to fix arrhythmias, what receptor is where

A

Adenosine binds to adenosine receptors in the cardiac muscle (adenosine 1 receptor) and vascular smooth muscle (adenosine 2 receptor)

Adenosine receptors are negatively coupled with adenylate cyclase.

In smooth muscle this means that there is an increase in cAMP meaning which is associated with relaxation in smooth muscle.

In nodal tissue it inhibits AC meaning that there is less cAMP within the nodal tissue and so it impacts on the depolarisation within the AV node
62
Q

why is adenosine safer than verapamil

A

effects of adenosine are short lived (20-30s)

63
Q

What class of drugs in verapamil

A

calcium channel blocker

64
Q

Where does verapamil act, what does it do in each place (2+2, +3)

A

Acts both in nodal tissue to prolong time of depolarisation and restore some kind of normal rhythm, and also acts on ventricular tissue to reduce calcium entry to slow the amount of time between contractions and improve cardiac output.

65
Q

What channel does verapamil target

A

the L‐type calcium channels

66
Q

Selectivity of amiodarone?

A

Not very selective at all

67
Q

What does amiodarone do

A

prolongs repolarisation

68
Q

MOA of amiodarone?

A

potassium channel blockade
By prolonging repolarisation, you’re prolonging the time during which the heart can NOT depolarise, thus restoring normal rhythm

69
Q

What type of anomalous rhythm does amiodarone help with

A

By prolonging repolarisation, you’re trying to reduce re-entry rhythms where the tissue is struggling to repolarise leading to poor cardiac output

70
Q

What is a class I VW drug

A

Sodium channel blockade

71
Q

What is a class II VW drug

A

Beta adrenergic blockade

72
Q

What is a class III VW drug

A

Prolongation of repolarisation

73
Q

What is a class IV VW drug

A

Calcium channel blockade

74
Q

What class is of VW is Calcium channel blockade

A

IV

75
Q

What class is of VW is Prolongation of repolarisation

A

III

76
Q

What class is of VW is Beta adrenergic blockade

A

II

77
Q

What class is of VW is Sodium channel blockade

A

I

78
Q

What class of VW is verapamil

A

II

79
Q

What class of VW is amiodarone

A

III

80
Q

What do Cardiac Glycosides/digoxin do

A

inhibits Na+/K+ pump and blocks the Na/K exchange
If you block the sodium-potassium exchange the sodium builds up inside the cell because you remove the ability to efflux the sodium
Another mechanism of removing sodium is via the Na+/Ca2+ exchanger - this leads to a build-up of calcium within the cell, causing a positive effect on inotropy - more effective contractions

81
Q

What must be taken into account before administering Digoxin and Cardiac Glycosides and why

A

If you’re HYPOKALAEMIC then there is less competition between the potassium and digoxin so the digoxin has a far more powerful effect on this protein and that’s where the toxicity comes from
So when giving digoxin, you need to know the plasma potassium levels to adjust the dose

82
Q

What is the other effect of digoxin (not the binding to the Na/K pump)

A

Vagal stimulation

It stimulates the parasympathetic innervation of the heart so it slows the heart rate via this route as well

Pharmacology and Therapeutics 2 Y2 (24 decks)

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