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103 Theme 3 - Cardiovascular System > Drug treatments for cardiovascular disease 3 & 4 - ischaemic heart disease > Flashcards

Drug treatments for cardiovascular disease 3 & 4 - ischaemic heart disease Flashcards

1
Q

Complete the diagram on the imbalance in demand and supply is ischaemic heart disease

A
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2
Q

What compound is important in regulation of coronary blood flow?

A

Endothelium-derived relaxing factor (nitric oxide)

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3
Q

How does NO causes relaxation of coronary blood vessels?

A
  1. Sheer stress - the sheer stress caused by the flow of fluid against the walls of the BV (resistance) increases
  2. Causes influx of Ca2+ into endothelial cells
  3. Ca2+ acts as co-factor for nitric oxide synthase
  4. Converts arginine to NO
  5. NO is permeable to cell membranes - can pass from endothelium (where its made) to smooth muscle cells
  6. NO causes GPT -> Cyclic GMP
  7. Cyclic GMP increase causes relaxation
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4
Q

What systems regulate end diastolic volume (preload)?

A

Sympathetic system

RAAS, (contractility of venules, Na+ and H2O retention)

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5
Q

How does cGTN cause vasodilation of coronary vessels?

A

cGMP stimulates the enzyme that dephosphorylates myosin light chain

Leads to relaxation of smooth muscle

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6
Q

Complete the diagram on GTN spray action.

A
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7
Q

What is heart rate regulated by?

A

Sympathetic system/ Ca2+

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8
Q

What is contractility regulated by?

A

Sympathetic system/Ca2+

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9
Q

What is total peripheral resistance regulated by?

A

Sympathetic system, RAAS

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10
Q

What 4 factors affect regulation of cardiac workload?

A
  • End Diastolic Volume (preload)
  • Heart Rate
  • Contractility
  • Total peripheral resistance
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11
Q

What is the definition of stable angina?

A

A predictable pattern of pain during exercise that is relieved by rest

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12
Q

What 2 things are drug treatments for stable angina designed to do?

A

Drug treatment designed to decrease work done by the heart and/or increase blood supply and treat risk factors.

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13
Q

Complete the diagram on the actions of nitrates

A
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14
Q

What are the side effects of nitrates?

A
  • Postural hypotension
  • Headache
  • Dizziness
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15
Q

What does GTN spray stand for?

A

E.g. Glyceryl trinitrate (GTN)

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16
Q

How do nitrates cause reflex tachycardia?

A

Due to activation of sympathetic nervous system.

Baroreceptors detect decrease in BP so release noradrenaline to increase HR to increase BP

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17
Q

How is reflex tachycardia treated?

A

If treatment causes reflex tachycardia, then should look to block effects of sympathetic nervous system using a beta blocker, such as bisoprolol.

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18
Q

What do beta blockers do?

A

Decrease frequency and force of contraction which decreases cardiac output.

Beta blockers also inhibit renin release from kidney and so inhibit RAAS.

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19
Q

What are the side effects of beta blockers?

A
  • Bronchoconstriction
  • Fatigue
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20
Q

Which patients are beta blockers contraindicated in?

A

Contraindicated in patients with peripheral vascular disease - Raynaud’s disease

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21
Q

Name an example of a beta blocker

A

Bisoprolol

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22
Q

What are the 3 types of calcium channel antagonists and what is the difference between them?

A

Phenyalkylamines/Benzothiazepines cause decrease in frequency and force of contraction

Dihydropyridines cause increased dilation of arterioles

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23
Q

What do calcium channel blockers do?

A

Decrease cardiac workload

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24
Q

What drug is used when beta blockers are contraindicated?

A

In asthmatics or other groups where beta blockers are contraindicated then cardiac selective calcium channel blockers can be used, such as verapamil and diltiazem.

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25
Q

Mixtures of what 2 drugs can cause severe bradycardia and even heart block?

A

Mixtures of cardiac selective calcium channel blockers and beta blockers

26
Q

How do calcium channel blockers decrease the frequency and force of contraction?

A

CCBs can reduce heart beat by blocking L-type channels in the SA and AV-nodes. This will slow the rate of depolarisation and therefore reduce the rate of action potential generation. They also decrease the force of contraction of the ventricles by reducing calcium entry through L-type channels.

27
Q

What does ivabradine do?

A

Blocks the pacemaker current (Ih/f) in the nodal tissue of the heart.

28
Q

What are the side effects of ivabradine?

A

Luminous phenomena (Ih) in retina

Blurred vision

Dizziness

29
Q

Name a long acting nitrate

A

Isosorbide mononitrate

30
Q

What do long acting nitrates do?

A

Decrease preload

31
Q

What does nicorandil do?

A
32
Q

What is the result of blockade of Ih/f?

A

Blockade of Ih/f will decrease cardiac rate.

Ivabradine will reduce Na+ entry through If channels and so slow the rate of depolarisation of the SA node cells and reduce firing frequency and therefore heart rate. It will not directly alter the force of contraction of the heart

33
Q

What current becomes longer in pathological situations?

A

Late sodium current

Late INa

34
Q

How does an extended late sodium channel cause angina?

A
  1. When heart muscle cells damaged, late sodium channel becomes over expressed
  2. Lots of Na+ enters cell in action potential followed by some calcium ions but because of the increased Na+ in cell the sodium-calcium pump doesn’t work (works with the concentration gradient pumping sodium in cell and calcium out of cell)
  3. Less Na+ enters cell through pump so less Ca2+ leaves
  4. Increased Ca2+ increases contraction
  5. Can cause angina
35
Q

What does ranolazine do?

A

Blocks late sodium current

36
Q

What are the 2 types of mechanisms of drugs to reduce cholesterol?

A

Drugs designed to either inhibit uptake from GI tract or reduce production in liver.

37
Q

What is the frontline treatment to reduce hypercholesterolaemia 2o Prevention

A

STATINS

38
Q

What is the suffix for statins and name 2 examples

A

________statin

e.g. simvastatin, atorvastatin

39
Q

How do statins decrease cholesterol?

A

Statins decrease the production of cholesterol in the liver by inhibiting the HMG CoA enzyme. This stimulates the liver cells to express LDL receptors and allows the liver cells to scavenge LDL cholesterol from the plasma. This reduces plasma LDL cholesterol levels.

40
Q

Complete the diagram on the action of statins

A
41
Q

What are the 2 other types of secondary prevention

A
  • Aspirin - antiplatelet agents (aspirin/clopidpgrel)
  • ACE inhibitors (e.g. ramipril) and ARBs (losartan)
42
Q

Why are ACE inhibitors and ARBs used as secondary prevention?

A

Decrease the workload on the heart

43
Q

What are the 3 acute coronary syndromes?

A

Unstable angina, NSTEMI and STEMI

44
Q

What is the treatment for acute coronary syndromes?

A

As for stable angina + antiplatelet

45
Q

What antiplatelets are used for acute coronary syndromes?

A

Aspirin; aspirin + clopidogrel (prasugrel, ticagrelor)

46
Q

How does platelet action work?

A

Platelet activation occurs when the endothelial cells become damaged. This releases ADP which acts on P2Y12 receptors to stimulate the platelet to express GPIIb/IIIa receptors. Fibrinogen binds to these receptors to cross link different platelets. Activation of COX also helps platelet activation through the production of Thromboxane A2.

47
Q

What is the mechanism of action for aspirin?

A

Aspirin inhibits COX irreversibly

48
Q

What is the mechanism of action for clopidogrel and prasugrel?

A

Clopidogrel and Prasugrel are ADP antagonists and block P2Y12 receptors.

49
Q

Which ant-platelet drug has to be activared by CYP450 enzyme?

A

Clopidogrel

50
Q

What are the symptoms of an MI?

A
  • Pain
  • Sweating, tachycardia, cold clammy skin
51
Q

What is the treatment for an MI?

A

Pain Relief

  • Diamorphine m-opioid receptors
  • Decreases pain, anxiety, sympathetic drive, vasodilates

Oxygen

Aspirin/GTN

Clot busting drugs - Tenecteplase

52
Q

How does tenecteplase work?

A

Tissue plasminogen activator

Fibrin is a major component of thrombus

53
Q

What do beta blockers do?

A

Decrease cardiac workload, prevents arrhythmias

54
Q

Name a short and long acting beta blocker and where would each be used?

A

E.g. metoprolol-short acting (hospital)/bisoprolol-longer acting (community).

55
Q

What do ACE inhibitors do?

Name an example

A

Decrease cardiac workload, prevents remodelling development of heart failure E.g. Ramipril.

56
Q

What do anticoagulants do for an MI?

A

In case of long term bed rest, prevents thrombus formation

57
Q

Name some anti-coagulants used for an MI

A

E.g. warfarin/apixaban, rivaroxaban/dabigatran/LMWH (e.g.tinzaparin)

58
Q

How is heart failure treated?

A

Digoxin

59
Q

How does digoxin treat heart failure?

A

Digoxin binds to the Na+/K+ ATPase and inhibits its action. This will increase levels of Na+ ions inside the heart muscle cells. This increase will in turn inhibit the Na+/Ca2+ exchanger which will lead to a build up of Ca2+ inside the muscle cell and a stronger contraction

60
Q

How are dysrhythmias treated?

A

Amiodarone

61
Q

How does amiodarone treat dysrhythmias?

A

It is a K+ channel blocker that increases the refractory period of ventricular myocytes and can terminate arrhythmias

103 Theme 3 - Cardiovascular System (19 decks)

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