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HHD 2 > Drugs in Cardiovascular disease > Flashcards

Drugs in Cardiovascular disease Flashcards

1
Q

What are the main functions of the CVS?

A

Transport
Protection
Regulation

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2
Q

The cardiovascular system is responsible for the transport of…

A

Oxygen
Nutrients
Hormones
Waste products

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3
Q

How does the CVS contribute towards protection of the body?

A

Contain:
Leukocytes
Antibodies
Complement proteins
Clotting factors

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4
Q

The CVS is responsible for the regulation of …

A

Temperature
pH
Hydration (water content)

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5
Q

List cardiovascular diseases that affect the heart

A

Arrhythmias
Angina
Acute or chronic heart failure
Congenital heart disease
Aortic valve/mitral valve disease

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6
Q

List cardiovascular diseases that affect the blood vessels

A

Hypertension
Hyperlipidaemia
Thrombosis
Atherosclerosis/ Atheroma

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7
Q

In what ways can drugs have an effect on the heart?

A

They can affect:
-rate and rhythm
-myocardial contraction
-metabolism and blood flow

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8
Q

The conduction of the electrical impulse through the heart corresponds to an ECG trace. True or false

A

True

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9
Q

Briefly state the route of the cardiac action potential

A

SA node —> Atrium —> AV node —> Purkinje fibres —> ventricle

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10
Q

What is an arrhythmia/Dysrhythmia?

A

An irregular heartbeat

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11
Q

How are arrhythmias/dysrhythmias clincally classified?

A
  • the site of abnormality- atrial, junctional or ventricular
    -whether the rate is increased (tachycardia) or decreased (bradycardia)
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12
Q

Give examples of tachyarrhythmias

A
  • atrial fibrillation
  • supraventricular tachcardia (SVT)
  • ventricular tachycardia
  • ventricular fibrillation
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13
Q

Give examples of bradyarrythmias

A

SA node dysfunction
AV block

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14
Q

What are the 4 basic phenomena that underlie disturbances of cardiac rhythm?

A
  • delayed after depolarisation
  • re-entry (circus movement)
  • ectopic pacemaker activity
  • Heart block
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15
Q

Delayed after- depolarisation is caused by …

A

an inward current associated with an increase in calcium ion influx

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16
Q

What is delayed after depolarisation?

A

They are transient depolarisations in the diastolic phase following an action potential which has been linked to arrhythmogenesis in cardiac diseases

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17
Q

What is re-entry (circus movement)

A

occurs when parts of the myocardium are depolarised as a result of disease
occurs when a propagating impulse fails to die out after normal activation of the heart and persists to re-excite the heart after expiration of the refractory period

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18
Q

Ectopic pacemaker activity occurs as a result of…

A

increased sympathetic activity in non-nodal tissue (e.g. during disease)

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19
Q

Heart block is often a result of …

A

fibrosis/ischaemic damage to the conducting system

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20
Q

What is the mechanism of Class Ia antidysrhythmic drugs? Give an example

A

Sodium channel blocker (intermediate dissociation)
Disopyramide

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21
Q

What is the mechanism of Class Ib anti-dysrhythmic drugs? Give an example

A

Sodium channel blocker (fast dissociation)
Lidocaine

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22
Q

What is the mechanism of Class Ic anti-dysrhythmic drugs? Give an example

A

Sodium channel blocker (slow dissociation)
Flecainide

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23
Q

What is the mechanism of Class II anti-dysrhythmic drugs? Give an example

A

Beta blocker
Propanolol

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24
Q

What is the mechanism of Class III anti-dysrhythmic drugs? Give an example

A

Potassium channel blocked
Amiodarone

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25
Q

What is the mechanism of Class IV anti-dysrhythmic drugs? Give an example

A

Calcium channel blocker
Verapamil

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26
Q

Briefly describe the phases of a cardiac membrane potential

A

Phase 4: Na+, Ca2+ channels are closed, open K+ rectifier channels keep the membrane potential stable at -90mV

Phase 0: Rapid influx of Na+ through open fast Na+ channels

Phase 1: transient K+ channels opening and efflux of K+ to help membrane potential return to 0

Phase 2: influx of Ca2+ through L type channels which is electrically balanced by K+ efflux through delayed rectifier K+ channels

Phase 3: calcium channels close but delayed rectifier K+ channels remain open and the membrane potential returns to -90mV

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27
Q

What phase of cardiac potential are B-agonist most relevant ? Elucidate your reasons why.

A

Phase 4
Pacemaker potential
result in increased cardiac stimulation

Phase 2 (Plateau)
Beta agonists bind to betaadrenoceptors which are coupled to Gproteins which lead to cAMP dependent activation of pKA.
pKA phosphorylates L- type calcium channels which leads to an increased influx of calcium ions

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28
Q

Class I and II anti-dysrhythmic drugs block what phase?

A

Phase 0
prevent the influx of Na+ via Na+ channels

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29
Q

Class IV anti-dysrhythmic drugs block what phase?

A

Phase 2 (plateau)
block ca2+ ion channels

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30
Q

Class III and Ia anti-dysrhythmic drugs block what phase?

A

Phase 3
Repolarisation phase

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31
Q

What is the function of anti-dysrhythmic drugs?

A

to restore normal rhythm and conduction

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32
Q

How is cardiac output (L/min) calculated

A

SV (stroke volume- ml) X heart rate (beats per minute)

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33
Q

Heart rate is controlled by the __________ nervous system

A

autonomic

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34
Q

What is the stroke volume?

A

volume of blood ejected from the ventricle with each heartbeat

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35
Q

What are the categories of the factors that affect stroke volume

A

Intrinsic myocardial contractility
Extrinsic circulatory factors

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36
Q

List some factors that affect the heart rate

A

Autonomic innervation
hormones
fitness levels
age

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37
Q

List some factors affecting stroke volume

A

heart size
fitness levels
gender
contractility
duration of contraction
Preload (EDV)
Afterload (resistance)

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38
Q

The intrinsic contractility of cardiomyocytes is dependent on …

A

Ca2+ ions and ATP availability
Ca2+ entry across the plasma membrane
Ca2+ release from stores (sacroplasmic reticulum?)

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39
Q

What are the extrinsic circulatory factors that affect myocardial contraction?

A
  • elasticity and contractile state of arteries and veins
  • volume and viscosity of the blood
  • these together determine the cardiac load (preload and after load)
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40
Q

What is preload?

A

This is the initial stretching of the cardiac myocytes (muscle cells) prior to contraction. It is related to ventricular filling

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41
Q

What is afterload?

A

force or load the heart must pump against to eject blood to the lungs or the body. Afterload goes down when aortic pressure and systemic vascular resistance decreases through vasodilation

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42
Q

What is heart failure?

A

this is where the cardiac output is not suffcient to meet the demands of the body

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43
Q

Heart failure is often a result of …

A

conditions which reduce the efficacy of the heart (damaged or increased workload)

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44
Q

Consequences of heart failure are often observed during exercise, but as the disease progresses it is also observed at ______.

A

rest

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45
Q

Heart failure is divided into …

A

Systolic dysfunction
Diastolic dysfunction

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46
Q

Systolic dysfunction results from …

A

a loss of intrinsic contractility by alterations in signal transduction mechanisms

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47
Q

Diastolic dysfunction results from

A

less compliant ventricles (become stiffer) which impairs ventricular relaxation/filling and causes less ejection of blood

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48
Q

What is an important consequence of heart failure?

A

Oedema

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49
Q

How does heart failure cause oedema?

A

less renal retention of sodium and water, this increases blood volume and venous pressure
Results in oedema of peripheral tissues (swelling of legs) and lungs (breathlessness)- promotion of fluid extravasation

sodium and water reabsorption is promoted in the kidneys during heart failure

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50
Q

Drugs that treat heart failure improve cardiac function by …

A

reducing blood volume
reduce clinical symptoms e.g. oedema, shortness of breath

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51
Q

The heart is poorly perfused compared to its oxygen consumption and metabolic need. True or false

A

True

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52
Q

What can lead to an increase in coronary blood flow?

A

Increased cardiac activity
Increased oxygen consumption

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53
Q

Coronary blood flow is controlled by …

A

Auto-regulation of perfusion pressure (60-200mmHg)
Vasodilation by mediators (adenosine, nitric oxide)
Autonomic innervation is less important in coronary blood flow

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54
Q

When coronary blood flow is reduced, what can this lead to?

A

Angina

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55
Q

Coronary blood flow can be reduced by …

A

Transient constriction of the coronary arteries (vasospasm)
Chronic narrowing of a coronary artery (i.e fixed stenosis) caused by atherosclerosis
Formation of a blood clot within the vessel lumen (i.e. coronary thrombosis)

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56
Q

Vasospasms, fixed stenosis and a thrombus in coronary arteries can lead to…

A

Angina (chest pain)

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57
Q

Increased heart rate, contractility, afterload and preload leads to …

A

Increased oxygen consumption

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58
Q

Increased oxygen consumption and decreased coronary blood flow can lead to…

A

Angina (chest pain)

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59
Q

Angina is caused by…

A

insufficient oxygen supply to the myocardium which leads to pain distributed in the chest, arm (left) and back

Decreased coronary blood flow
Increased oxygen consumption

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60
Q

What is ischaemia

A

This is when there is insufficient blood flow to provide adequate oxygenation
Blood flow and thus oxygen is restricted or reduced in a certain part of the body

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61
Q

What are the types of angina recognised clincally?

A

Stable angina
Unstable angina
Variant angina

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62
Q

What is stable angina?

A

chest pain on exertion (exercise) produced by increased demand on the heart

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63
Q

What causes stable angina?

A

fixed narrowing of blood vessels by atheroma
coronary vessels ???

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64
Q

Angina is referred to as unstable when …

A

pain is experienced even at rest

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65
Q

What causes unstable angina

A

thrombi from ruptured plaques form leading to decreased blood flow
This is without complete occlusion

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66
Q

Variant angina is uncommon. What does it result from?

A

coronary artery spasm

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67
Q

Drugs that increase blood flow in the heart have what effect?

A

increased oxygen supply

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68
Q

Drugs that decrease oxygen demand in the heart lead to …

A

a decrease in myocardial oxygen consumption

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69
Q

What are the effects of sympathetic innervation on the heart (via B adrenoceptors)?

A
  • increased heart rate
  • increased force of contraction
  • increases automaticity- spontaneous activity of pacemaker cells
  • reduces cardiac efficiency- O2 consumption in relation to cardiac work
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70
Q

An increase in heart rate demonstrates a positive _________ effect.

A

chronotropic

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71
Q

An increase in contractility/force of contraction demonstrates a positive ________ effect.

A

inotropic effect

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72
Q

What is the effect of parasympathetic innervation on the heart (via muscarinic M2 receptors- smooth muscle and heart)

A
  • Decrease heart rate
  • decrease force of contraction- in the atria only
  • reduces automaticity- spontaneous activity of pacemaker cells
  • inhibits atrio-ventricular conduction
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73
Q

Inhibition of AV conduction is also referred to as…

A

negative dromotropy

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74
Q

A decrease in heart rate demonstrates a negative _________ effect

A

chronotropic

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75
Q

What are drugs that affect the myocardial cells directly?

A

Autonomic neurotransmitters and related drugs (B blockers)
Anti-dysrhythmic drugs (calcium channel blockers)
Cardiac glycosides (digoxin- inhibits Na+/K+ ATPase)

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76
Q

What is the mechanism of action of digoxin?

A

Inhibits Na+/K+ ATPases in cardiac myocytes
Increases intracellular Na+
This in turn increases intracellular Ca2+ ions
This increases cardiac contractility

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77
Q

Give examples of drugs that affect cardiac function indirectly (effect is elsewhere in vascular system)

A

Nitrates
Diuretics
ACEIs

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78
Q

Nitrates are used to treat…

A

Angina

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79
Q

Diuretics and ACEIs are used to treat…

A

heart failure

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80
Q

Calcium antagonists are a category of drugs that affect cardiac function in what ways?

A

both directly and indirectly

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81
Q

What is the mechanism of action of ACEIs

A

Prevent production of Angiotensin II
Angiotensin II raises blood pressure

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82
Q

In what ways is angiotensin II able to raise blood pressure?

A

Vasoconstriction
Increased aldosterone synthesis
Sympathetic nervous stimulation

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83
Q

B1 adrenoceptor subtypes have a ________ effect. Give examples of tissues they can be expressed in

A

stimulatory effect
Heart, juxtaglomerular apparatus (kidney)

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84
Q

B2 adrenoceptor subtypes have a _______ effect. Give examples of tissues they are expressed in.

A

relaxation effect
bronchial, vascular, uterine smooth muscle

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85
Q

B3 adrenoceptors are often found in __________ tissue

A

Adipose
For lipolysis

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86
Q

What is the mechanism of action of B-blockers

A

competitively bind to B-adrenergic GPCRs
block sympathetic effects of adrenaline and noradrenaline

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87
Q

What are the cardiac effects of Beta- blockers ?

A
  • decreased contractility (negative inotropy)
  • decrease relaxation rate (nageive lusitropy)
  • decreased heart rate (negative chronotropy)
  • decreased conduction velocity ((negative dromotrophy)
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88
Q

What are the vascular effects of beta- blockers?

A

smooth muscle contraction (mild vasoconstriction)

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89
Q

What are the therapeutic indications for beta- blockers?

A

Angina
Heart failure
Arrhythmia
Hypertension
Open angle glaucoma, hyperthyroidism, anxiety, tremor

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90
Q

Why are beta blockers indicated for angina?

A

Reduces heart rate, contractility, arterial pressure, workload and oxygen demand of the heart
This improves O2 supply/demand ration which can relieve anginal pain

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91
Q

Why are beta blockers indicated for heart failure?

A

blockade of excessive, chronic sympathetic input to the heart (poorly understood)

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92
Q

Why are beta blockers indicated for arrhythmias?

A

decreased sinus (heart rate) and conduction velocity and inhibit aberrant pacemaker activity.
increase action potential duration and effective refractory period (in non pacemaker cells).
effective in blocking re-entry arrhythmias

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93
Q

Why are beta blockers indicated for HTN?

A
  • reduce cardiac output
  • inhibit renin release by kidneys- enhanced renal loss of sodium and water and further diminishes arterial pressure
  • decrease in blood pressure
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94
Q

List some B1/B2 non selective betablockers (B adrenoceptor antagonists)

A

Carvedilol
Labetalol
Nadolol
Pindolol
Propanolol
Sotalol
Timolol

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95
Q

What B1/B2 non-selective Beta blockers are indicated for therapeutic use against hypertension and angina?

A

Carvedilol
Labetalol
Nadolol
Pindolol
Propanolol
Sotalol
Timolol

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96
Q

What B1/B2 non-selective beta blockers are indicated for therapeutic use against arrhythmias?

A

Nadolol
Propanolol
Sotalol

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97
Q

What B1/B2 non-selective beta blockers are indicated for therapeutic use as prophylaxis after MI?

A

Propanolol
Timolol

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98
Q

What B1/B2 non-selective beta blocker is indicated for therapeutic use as an adjunctive therapy in heart failure

A

Carvedilol

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99
Q

What are some other therapeutic uses of nadolol?

A

Migraine prophylaxis
Thyrotoxicosis

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100
Q

What are some other therapeutic uses of propanolol?

A

Migraine prophylaxis
Thyrotoxicosis
Anxiety (palpitation, sweating and tremor)
Pheochromocytoma

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101
Q

What are some other therapeutic uses of timolol?

A

Open- angle glaucoma
Migraine prophylaxis

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102
Q

Give examples of B1 cardio-selective beta- blockers

A

Acebutolol
Atenolol
Betaxolol
Bisoprolol
Esmolol
Metoprolol
Nebivolol

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103
Q

Give examples of B1 cardio-selective beta- blockers indicated for hypertension

A

Acebutolol
Atenolol
Bisoprolol
Esmolol
Metoprolol
Nebivolol

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104
Q

Give examples of B1 cardio-selective beta- blockers indicated for angina

A

Acebutolol
Atenolol
Bisoprolol
Metoprolol

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105
Q

Give examples of B1 cardio-selective beta- blockers indicated for arrhythmias

A

Acebutolol
Atenolol
Esmolol
Metoprolol

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106
Q

Give examples of B1 cardio-selective beta- blockers indicated for use as early intervention within 12 hours of MI

A

Atenolol
Metoprolol

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107
Q

Give examples of B1 cardio-selective beta- blockers indicated for use as adjuncts in heart failure

A

Acebutolol
Bisprolol
Nebivolol

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108
Q

What are other therapeutic uses of atenolol?

A

Migraine prophylaxis

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109
Q

What are other therapeutic uses of betaxolol?

A

Open- angle glaucoma

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110
Q

What are other therapeutic uses of metoprolol?

A

Migraine prophylaxis
Hyperthryroidism (adjunct)
In surgery

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111
Q

List some common/ very common side effects of beta blockers

A

Abdominal discomfort
Bradycardia
Bronchospasm
Confusion
Constipation
Depression
Diarrhoea
Dizziness
Dry eye
Dyspnoea- shortness of breath
Erectile dysfunction
Fatigue
Headache
Heart failure
Nausea
Parasthesia
Peripheral coldness
Peripheral vascular disease
Rash
Sleep disorders
Syncope
Visual impariment
Vomiting

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112
Q

Give some uncommon side effects of beta-blockers

A

Atrioventricular block

113
Q

Give some rare/very rare side effects of beta blockers

A

Hallucination
Psoriasis exarcebated

114
Q

What are contraindications of Beta blocker use?

A

Asthma(main)
COPD(main)
Cardiogenic shock
Hypotension
Marked bradycardia
Metabolic acidosis
AV block
Severe peripheral arterial disease
Uncontrolled heart failure
Diabetes (symptoms of hypoglycaemia may be masked)

115
Q

According the the BNF, what type of drugs should be avoided in patients with asthma, bronchospasm and COPD when treating CVD?

A

Beta-blockers (including cardio selective B1 blockers)
However if there is no alternative a cardio selective B-blocker is given to patients with caution and under specialist supervision.

116
Q

What is the function of calcium channel blockers?

A

Inhibit calcium influx in voltage activated, L type calcium channels

117
Q

Calcium channel blockers are a heterogenic group of drugs. Why are they described to be heterogenic?

A

this is because they have different binding sites on the calcium channel pores
they also have different selectivity for L-type calcium channels in vasculature and myocardium

118
Q

An increase in intracellular calcium ion concentration leads to…

A
  • increased contractility- inotropy
  • increased heart rate- chronotropy
  • increased conduction velocity- dromotropy

(lead to vasoconstriction of vasculature)

119
Q

Class IV anti-dysrhythmic drugs are calcium ion channel blockers. They are classified into 3 groups which differ in ______ and _______.

A

structure
selectivity

120
Q

What are the 3 classes of class IV anti-dysrhythmic drugs?

A

Dihydropyridines
Non- dihydropyridines
Benzothiazapine

121
Q

Briefly state some characteristics of dihydropyridines

A
  • smooth muscle selective
  • primarily used in hypertension (CVD of vasculature)
  • end in “pine” e.g. nifedipine
122
Q

Non- dihydropyridines are used to treat what kinds of CVD?

A

Angina
Arthythmias
(CVD of the heart)

123
Q

Non- dihydropyridines are ________ specific

124
Q

Non-dihydropyridines are phenylalkylamines. Give an example of a phenylalkylamine

125
Q

Diltiazem is an example of a _________ Ca2+ channel blocker

A

Benzothiazapine

126
Q

List some characteristics of benzothiazapines

A
  • intermediate selectivity (both cardio-depressant and vasodilatory effects)
  • reduced atrial pressure without compensatory cardiac stimulation caused by dihydropyridines
127
Q

Verapamil has a _______ effect on systemic and coronary vasodilation.

A

Moderate effect

128
Q

Describe, briefly, the effect that verapamil has on myocardial contractility.

A

moderate reduction in myocardial contractility

129
Q

What is the effect of verapamil and diltiazem on heart rate?

A

Causes a minimal reduction in heart rate

130
Q

What is the effect of Verapamil on atrioventricular conduction (dromotropy)?

A

causes a strong reduction in AV conduction

131
Q

What are the clinical uses of verapamil?

A

Angina
Hypertension
Arrhythmias

132
Q

Diltiazem has a _____ effect of systemic vasodilation whilst it has a _____ effect on coronary vasodilation.

A

Mild effect
Moderate effect

133
Q

What is the effect of diltiazem on myocardial contractility?

A

causes a mild reduction on myocardial contractility

134
Q

What is the effect of diltiazem on AV conduction?

A

moderate reduction

135
Q

What are the therapeutic uses of diltiazem?

A

Angina
Hypertension

136
Q

Describe the effect of nifedipine, amlodipine and felodipine on systemic and coronary vasodilation

A

Strong effect

137
Q

Describe the effect of nifedipine, amlodipine and felodipine on myocardial contractility.

138
Q

Describe the effect of nifedipine, amlodipine and felodipine on AV conduction.

139
Q

What is the effect of nifedipine on heart rate?

A

causes a mild increase

140
Q

What is the effect of amlodpine and felodipine on heart rate?

A

causes a minimal increase

141
Q

What are the clinical uses of amlodipine and felodipine?

A

Angina prophylaxis
Hypertension

142
Q

What are the clincal uses of nifedipine

A

Angina prophylaxis
Hypertension
Raynauds syndrome

143
Q

What are the therapeutic indications of calcium channel blocker use

A

Angina due to coronary vasospasm
Arrhythmia
Hypertension
Raynauds syndrome

144
Q

List some reasons why calcium channel blockers are indicated for use in Angina

A
  • anti angina effects through both vasodilator and cadio-depressant actions
  • reduce arterial pressure which reduces ventricular afterload (wall stress) thereby decreasing oxygen demain
  • cardio-selective CCBs (verapamil, diltiazem) decrease heart rate and contractility, decreasing oxygen demand
  • dilate coronary arteries reversing coronary vasospasm, increasing oxygen supply to the myocardium
145
Q

Why are CCBs indicated for arrhythmia?

A
  • decrease the firing rate of aberrant pacemaker sites
  • decrease the conduction velocity through AV node and prolong repolarisation (block re-entry mechanisms)
146
Q

Why are CCBs indicated for hypertension?

A

cause relaxation of the vascular smooth muscle (vasodilation) which lowers arterial blood pressure

147
Q

Why are CCBs indicated for raynauds syndrome?

A

Raynauds syndrome is caused by a reduction in blood supply to extremeties as a result of vasoconstriction
Treatment with nifedipine produces vasodilation of blood vessels (smooth muscle selective)

148
Q

What are the side effects of dihydropyridines

A

Headache
Flushing
Reflex tachycardia
Peripheral oedema (vasodilation)
Gingival hyperplasia

149
Q

What are the side effects of dihydropyridines?

A

Bradycardia
Block of AV conduction
low ejection fraction
constipation
gingival hyperplasia with verapamil

150
Q

What are the contraindications for dihydropyridine use?

A

Cardiogenic shock
decompensated heart failure
severe aortic stenosis (narrowing)
obstructive cardiomyopathy

151
Q

What are the contraindications for non-dihydropyridine?

A

Severe bradycardia
disorder of conduction
sick sinus syndrome
congestive heart failure
cardiogenic shock

152
Q

What preventative measures can be implemented for CCB induced hyperplasia?

A

Hygiene therapy

153
Q

If symptoms of CCB induced hyperplasia persist, what should you do?

A

Liasise with overseeing GP

154
Q

You should never stop medication without first consulting GP. True or false.

155
Q

What are cardiac glycosides (digoxin)?

A

these are compounds that are derived from the foxglove plant (digitalis purpurea)

156
Q

Cardiac glycosides are a a potent inhibitor of …

A

Na+/K+ ATPase

157
Q

What is the mechanism of action of cardiac glycosides?

A

The mechanism is poorly understood, but it causes an increase in intracellular Ca2+ which increases contractility of the heart

158
Q

What are the cardiac actions of cardiac glycosides?

A

-cardiac slowing and reduced rate of conduction through AV node
increased force of contraction (positive inotropic effect)

159
Q

What are the therapeutic uses of cardiac glycosides such as digoxin?

A

arrhythmias (to slow ventricular rate in rapid atrial fibrillation)
heart failure

160
Q

What are the side effects of cardiac glycosides?

A
  • muscle Na+/K+ ATPase acts as a large binding reservoir; narrow therapeutic index (before it becomes toxic)
    Arrhythmias
    Cerebral impairment
    Diarrhoea
    Eosinophilia
    Nausea
    Skin reactions
    Vision disorders
161
Q

What types of drugs affect myocardial cells directly?

A

Autonomic transmitters and related drugs (beta-blockers)
Antidysrhythmic drugs (Ca2+channel blockers- class IV)
cardiac glycosides (digoxin)

162
Q

What types of drugs affect cardiac function indirectly (elsewhere in the vascular system)?

A

Nitrates (Angina)
Diuretics (heart failure)- help rid body of salt and water; helps reduce blood pressure
ACEI (heart failure)- prevents Angiotensin II from forming and thus prevents vasoconstriction and increase of blood pressure

163
Q

What drugs affect cardia function directly and indirectly?

A

Calcium antagonists

164
Q

What is systemic hypertension?

A

Sustained elevated blood pressure above 140/90 mmHg

165
Q

Hypertension is a major risk factor for what other diseases?

A

Atherosclerosis
Thrombosis
Stroke
Aneurysms
Renal failure

166
Q

What are the classes of hypertension?

A

Primary (essential) hypertension
Secondary hypertension

167
Q

What is the cause of primary (essential) hypertension?

A

No known cause

168
Q

What is secondary hypertension?

A

There is usually an identifiable cause

169
Q

Primary hypertension constitutes ____% of hypertension whilst secondary hypertension constitutes ___%.

170
Q

In most cases, essential hypertension is characterised by…

A

increased vascular resistance, cardiac output remains normal
thickening of resistant vessel walls
vasoconstriction

171
Q

What are the characteristics of secondary hypertension ?

A

Increased cardiac output
Increased systemic vascular resistance

172
Q

Give instances that can lead to increased cardiac output

A
  • Hypervolemia:
    renal artery stenosis
    renal disease
    hyperaldosteronism
    hypersecretion of ADH
    Aortic coarctation
    pregnancy (preeclampsia)
  • Stress:
    Sympathetic innervation
  • Pheochromocytoma
    increased catecholamines
173
Q

Give instances that lead to an increase in vascular resistance

A

Stress: sympathetic innervation
Atherosclerosis
Renal artery disease (increased angiotensin II)
Pheochromocytoma (increased catecholamines)
Thyroid dysfunction
Diabetes
Cerebral ischaemia

174
Q

What determines the state of vascular tone?

A

Vasodilator and vasoconstrictor influences acting on arteries and veins

175
Q

An increase in vascular (smooth muscle) intracellular calcium leads to…

A

vasoconstriction

176
Q

A decrease in vascular (smooth muscle) intracellular calcium lead to …

A

Vasodilation

177
Q

What is the effect noradrenaline on vascular smooth muscles?

A

release of calcium from sacroplasmic reticulum (store)
Increase in intracellular calcium
vasoconstriction

178
Q

What is the effect of NO and PGI2 produced by vascular endothelial cells on smooth muscle cells

A

Vasodilation

179
Q

What are the two types of nitrates (vasodilator)?

A

Release NO following enzymatic process (organic nitrates, glyceryl trinitrate GTN)
Releases NO spontaneously (sodium nitroprusside)

180
Q

What are the effects of nitrates on systemic vasculature ?

A

Vasodilation (venous dilation> arterial dilation)
decrease in venous pressure
decrease in arterial pressure (small effect)

181
Q

What are the cardiac effects of nitrates?

A

decreased preload and afterload (decreases wall stress)
decreased oxygen demand (good for angina)

182
Q

What are the coronary effects of nitrates?

A

prevents/reverses vasospasms
vasodilation (primarily epicardial vessels- vessels that supply epicardium)
increase subendocardial perfusion
increased oxygen delivery

183
Q

Briefly describe how organic nitrates produce NO

A

Organic nitrates —>RNO2 (Nitrogen dioxide) —> S-nitrosothiol —-> NO

184
Q

What is the effect of cGMP on smooth muscle cells?

A

Relaxation
Vasodilation

185
Q

What is function of NO in smooth muscle?

A

Activation of guanylyl cyclase

186
Q

What is the function of guanylyl cyclase?

A

conversion of GTP to cGMP

187
Q

Give examples of short acting nitrates

A

Sodium Nitroprusside
Glyceryl trinitrate (GTN)

188
Q

What are the therapeutic uses of sodium nitroprusside?

A

Hypertensive emergencies
Acute and chronic heart failure
controlled hypotension in anasthesia during surgery (IV)

189
Q

What are the therapeutic uses of GTN

A

Treatment and prophylaxis of angina
congestive heart failure

190
Q

Sublingual GTN exists in what forms?

A

Tablets or aerosol sprays

191
Q

What are the uses of IV infusions of GTN?

A

control of hypertension, myocardial ischaemia during and after cardiac surgery

192
Q

Give examples of long acting nitrates

A

Isosorbide mononitrate
Isosorbide dinitrate

193
Q

What are the therapeutic uses of isosorbide mononitrate?

A

Angina prophylaxis
Adjunct for heart failure

194
Q

What are the therapeutic uses of isosorbide dinitrate?

A

Angina prophylaxis
Left ventricular failure

195
Q

In both isosorbide mononitrate and dinitrate, tolerance develops, leading to …

A

Reduced therapeutic effects

196
Q

How long are transdermal patches of isosorbide mononitrate and dinitrate left off?

A

8-12 hours overnight

197
Q

Modified release tablets of isosorbide mononitrate and dinitrate are delivered in ____ doses

198
Q

What are the therapeutic indications for nitrates

A

Angina
Heart failure (acute and chronic)
Hypertensive emergencies

199
Q

Why are nitrates indicated for use in angina?

A

increases coronary blood flow by reversing and inhibiting coronary vasospasm (variant angina)
reduces preload by producing venous dilation which decreases myocardial oxygen demand (stable and unstable angina)
reduces systemic vascular resistance and arterial pressure (dose dependant) which leads to a decrease in myocardial oxygen demand and a decrease in anginal pain

200
Q

Why are nitrates indicated for use in acute and chronic heart failure?

A

Reduces afterload in failing ventricle by arterial dilation by increasing stroke volume and ejection fraction
Venous dilation reduces venous pressure which oedema

201
Q

Why are nitrates indicated for hypertensive emergencies

A
  • not used to treat chronic primary or secondary hypertension-
    sodium nitroprusside and GTN are used to lower blood pressure in acute hypertensive emergenies
    -pheochromocytoma, renal artery stenosis, aortic dissection, during surgery to control arterial pressure
202
Q

What are the side effects of nitrates?

A

headache (caused by cerebral vasodilation)
cutaneous flushing
postural hypotension
reflex tachycardia
nausea and vomiting
thiocyanate toxicity (with prolonged sodium nitroprusside use)

203
Q

What are the contraindications for nitrates use?

A

cGMP dependent phosphodiesterase inhibitors (sildenafil- viagra)
- this inhibits cGMP degradation, combined with nitrates, this greatly potentiates cGMP levels
- this leads to hypotension and impaired coronary perfusion
Dry mouth can also reduce the effectiveness of sublingual GTN tablets

204
Q

Renin is released from the kidneys in response to …

A
  • decreased perfusion pressure
  • decreased glomerular filtration
  • increased sympathetic nerve activity
  • increased beta agonists (binding to B-adrenoceptors)
205
Q

How is renin release modulated?

A

it is modulated by natriuretic peptides that are released by the heart- counter regulatory system

206
Q

What is the mechanism of action of renin?

A

Acts on circulating susstrate, angiotensinogen which undergoes proteolotic cleavage into angiotensin I
ACE enzyme in the vascular endotheliym breaks down angiotensin I into angiotensin II

207
Q

Angiotensin II binds to AT1 receptors which results in…

A

Vasoconstriction- increasing systemic vascular resistance and arterial pressure
stimulates Na+ reabsorption at renal tubules which increases Na+ and fluid retention (to increase blood pressure)
releases aldosterone (adrenal cortex) which acts on the kidneys to increase Na+ and fluid retention
releases antidiuretic hormone, ADH (posterior pituitary gland) which increases fluid retention by the kidneys
releases noradrenaline from sympathetic nerves enhancing systemic function
stimulates thirst centres within the brain
stimulated cardiac hypertrophy and vascular hypertrophy

208
Q

What are the effects of ATII on the AT1 subtype receptors

A

Vascular growth- hyperplasia and hypertrophy
Vasoconstriction- direct or via increased NA release from sympathetic nerves
salt retention: aldosterone release, tubular Na+ reabsorption

209
Q

Give examples of ACEI (ACE inhibitors)

A

Captopril
Enalapril (prodrug)
Lisinopril

210
Q

ACEI are indicated for …

A

Primary hypertension (increased peripheral vascular resistance; no effect on cardiac output)
Renal hypertension caused by renal artery stenosis leading to renin release

211
Q

ACEIs decrease the production of ATII which causes

A

arterial and venous dilation; reduction in vascular effects
natriuresis and diuresis which leads to a decrease in blood volume and cardiac output and a decrease in arterial pressure

212
Q

What is natriuresis?

A

excretion of sodium ions in the urine

213
Q

What is diuresis?

A

increased urine production

214
Q

Why are ACEIs indicated for use in heart failure and post-myocardial infarction?

A

decrease afterload, increase stroke volume and ejection fracture
decrease preload, decrease pulmonary and systemic congestion and oedema
decrease sympathetic activation which can cause damage to the heart
improved oxygen supply/demand ratio (less demand through less preload and afterload)
prevents harmful cardial remodelling (during heart failure and post-MI)

215
Q

What are the side effects of ACEI?

A

headache
dizziness
fatigue
nausea
dry cough (10% of patients), bradykinin induced
hypotension especially in heart failure patients
angioedema (life- threatening airway swelling in 0.1-0.2% of patients, more common in afro-carribeans)
hyperkalemia (high plasma K+ levels due to aldosterone)

216
Q

What are the contraindications of ACEIs?

A

pregnancy (teratogenic- structural or functional change to the foetus)
bilateral renal stenosis (patients may experience renal failure with ACEIs)
- less of a problem with unilateral renal artery stenosis (unaffected kidney can maintain sufficient filtration)

217
Q

What are angiotensin receptor blockers (ARBs)

A

non peptide orally active AT1 antagonists

218
Q

Give examples of ARBs

A

Sartans
Losartan
Candesartan
Valsartan
Irbesartan

219
Q

What group of drugs share the same therapeutic properties and indications as ARBs?

220
Q

What are the indications for ARBs?

A

Hypertension
Heart failure

221
Q

What ARB is approved for MIs ?

222
Q

ARBs have similar side effects and contraindications as ACEIs except that there is no …

A

bradykinin induced coughing

223
Q

What is the function of Diuretics?

A

They increase the urine output by kidneys (promote diuresis)

224
Q

What is the mechanism of action of diuretics

A

They diminish reabsorption of Na at different renal tubular elementswhich also prevents water reabsorption; increasing sodium and water loss

225
Q

Diuretic drugs include…

A
  • loop diuretics
  • thiazides
    -K+ sparing diuretics
226
Q

What is the order of potency for diuretic drugs?

A

Loop diuretics>Thiazides >K+ sparing diuretics

227
Q

What is the MOA of Loop Diuretics?

A

Inhibit Na+/K+/Cl- cotransporter in thick ascending loop of Henle

228
Q

What is the MOA of thiazides?

A

Inhibits Na+/Cl- co-transporters in distal convoluted tubule

229
Q

What is the MOA of K+ sparing diuretics

A

Aldosterone receptor antagonist in the collecting duct
Inhibit Luminal Na+ channels in the collecting duct

230
Q

What is the function of aldosterone?

A

helps to regulate bodys blood pressure by managing the levels of sodium and potassium in the body

231
Q

What are the indications for diuretics?

A

Hypertension
Heart failure and oedema

232
Q

What are the effects of diuretics in hypertensive patients?

A

Decreased blood volume
Decreased cardiac output
Decreased systemic vascular resistance (long term therapy)
leads to a decrease in blood pressure

233
Q

Diuretics are used to effectively treat what kind of hypertension?

A

Primary hypertension
90-95% with primary are effectively treated with diuretics

234
Q

What adjunctive therapy (or behaviour) is particularly effective when coupled with diuretics?

A

Reduced sodium intake

235
Q

What type of diuretics are most commonly used in hypertension?

236
Q

What drugs can be used to prevent hypokalemia?

A

K+ sparing diuretics (aldosterone receptor antagonists) with thiazide treatment

237
Q

What is hypokalemia?

A

Low level plasma K+

238
Q

What diuretics can produce hypokalemia?

A

Loop diuretics
Thiazides

239
Q

What are the effects of diuretic use in patients with heart failure and oedema?

A

Renin-angiotensin-aldosterone system are activated in heart failure (increase blood pressure)–> this leads to an increase in Na2+ and H2O retention; this therefore leads to an increase in blood volume and this venous pressure. This can cause an increase in pulmonary andsystemic oedema.

Diuretic use in heart failure is to decrease pulmonary/or systemic oedema

240
Q

Give examples of Loop Diuretics

A

Bumetanide
Furosemide
Torsemide

241
Q

What are the side effects of Loop diuretics?

A

Dehydration
Dizziness
Electrolyte imbalance
GI disorder
Headache
Hypotension
Metabolic alkalosis
Nausea
Skin reactions

242
Q

Give some examples of thiazide diuretics

A

Bendroflumethiazide
Hydrochlorothiazide
Chlortalidone
Indapamide
Metolazone

243
Q

What are the side effects of thiazides?

A

Constipation
Electrolyte imbalance
Postural hypotension
Headache

244
Q

What are the contraindications for loop diuretics?

A

Renal failure due to nephrotoxic or hepatotoxic drugs
Hypokalemia
Hyponatraemia
Caution: exarcebate diabetes

245
Q

What are the contraindications of diuretic thiazedes?

A

Addisonsn disease
Hypercalacemia
Hyponatraemia
Hyperuricaemia (uric acid and gout)
Caution: exacterbate diabetes

246
Q

What are the types of K+ sparing diuretics?

A

Aldosterone antagonists
Na+ channel inhibitors

247
Q

Give examples of Aldosterone agonist K+ sparing diuretics

A

Spinolactone
Eplerenone

248
Q

Give examples of Na+ channel inhibitors K+ sparing diuretics

A

Triamterene
Amiloride

249
Q

What are the side effects of K+ sparing diuretics?

A

Diarrhoea
Hyperkalemia
Nausea
Vomiting
Check BNF

250
Q

Whar are the contraindications of K+ sparing diuretics

A

Addisons disease
Anuria
Hyperkalaemia
Caution: exarcebate diabetes

251
Q

What is a caution to patients taking any type of diuretics?

A

exarcebate diabetes

252
Q

What is atherosclerosis ?

A

It is a focal disease of large and medium sized arteries

253
Q

What is the pathophysiology of atherosclerosis? (briefly)

A

athermatous plaques occurs over time
Plaque ruptures and leads to platelet activation and thrombosis

254
Q

Athetosclerosis is the most common cause of death (MI and Stroke). True or false

255
Q

What are the earliest structurally apparent lesions in atherosclerosis

A

Fatty Streaks

256
Q

When do symptoms of atherosclerosis begin to occur?

A

When the blood flow through the vessel is not sufficient to meet the demand of the downstream tissues

257
Q

What else plays a key role in the pathophysiology of atherosclerosis?

A

Chronic inflammation to injury

258
Q

What are the modifiable risk factors for atherosclerosis?

A

Dyslipidaemia- unhealthy levels of certain kinds of lipids; high LDL
Hypertension
Diabetes mellitus
Smoking
Obesity
Physical activity

259
Q

Lipids consist of …

A

cholesterol and triglycerides

260
Q

Lipids are transported in plasma as 4 classes of lipoproteins. Name them.

A

Chylomicroms
VLDLs
LDLs
HDL

261
Q

What is the function of chylomicrons

A

transport cholesterol and triglycerides from GI tract to tissues

262
Q

Triglycerides split into _____ and _______ which are then taken up by what tissue?

A

Gylcerol and fatty acids

Muscle and adipose tissue

263
Q

What happens to chylomicron remnants?

A

They are taken up by the liver and converted into VLDLs

264
Q

What is the function of VLDLs ?

A

They transport cholesterol and newly synthesised triglycerides to tissues.

265
Q

Lipoprotein particles become smaller LDLs. True or false

266
Q

LDLs have a large ______ component. LDL is taken up by the ______ via specific LDL receptors.

A

Large cholesterol component

Taken up by the liver

267
Q

What are the physiological and pathological functions of LDL?

A

Provide a source of cholesterol for steroids

Also involved in atherogenesis

268
Q

What is the function of HDL?

A

Absorbs cholesterol (from cell breakdown) and transfers to VLDLs and LDLs

269
Q

Briefly describe the balance of LDL and HDL cholesterol in ischaemic heart disease

A

Higher LDL cholesterol and lower HDL cholesterol present (usually from cell breakdown)

270
Q

What is the rate limiting enzyme in cholesterol production?

A

HMG CoA reductase

271
Q

What is the first step in cholesterol synthesis and what enzyme catalyses this reaction?

A

HMG-CoA converteed to mevalonic acid

Catalysed by HMG CoA reductase

272
Q

What is the MOA of statins

A

Inhibits the activ site of HMG CoA reductase enzyme (prevents production of mevalonic acid)

273
Q

What kinds of statins are simvastatin and pravastatin

A

Specific reversible competitive inhibitors of HMG CoA reductase

274
Q

Atorvastatin and Rosuvastatin are ________ inhibitors of HMG CoA reductase

A

Long lasting inhibitors

275
Q

What is the effect of statins?

A

decrease hepatic cholesterol — > increase LDL receptor synthesis —-> LDL clearance from plasma to hepatocytes increases —> a decrease in triglycerides and an increase in plasma HDL concentration

276
Q

What are the other reported effects of statins?

A

improved endothelia function
decreased vascular inflammation
decreased platelet aggregation
Plaque stabilisation

277
Q

What are the therapeutic indications for statins

A

Primary prevention of arterial disease in high risk patients with elevated serum cholsterol
Secondary prevention of I and stroke in patients with symptomatic atherosclerotic disease
Familial hypercholesteraemia; genetic disorder causing high levels of LDL cholesterol in the blood

278
Q

What are the generally well tolerated side effects of statins?

A

Asthenia (weakness)
constipation
diarrhoea
dizziness
flatulence
GI discomfort
headache
muscle pain
nausea
sleep disorders
thrombocytopenia (low platelet levels)

279
Q

What are the contraindications of statins?

A

should be avoided in pregnancy and those trying to conceive

congenital anomalies; decreased synthesis of cholesterol possibly affects foetal development

HHD 2 (37 decks)

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