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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
What is the mechanism of Class IV anti-dysrhythmic drugs? Give an example
Calcium channel blocker Verapamil
26
Briefly describe the phases of a cardiac membrane potential
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
27
What phase of cardiac potential are B-agonist most relevant ? Elucidate your reasons why.
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
28
Class I and II anti-dysrhythmic drugs block what phase?
Phase 0 prevent the influx of Na+ via Na+ channels
29
Class IV anti-dysrhythmic drugs block what phase?
Phase 2 (plateau) block ca2+ ion channels
30
Class III and Ia anti-dysrhythmic drugs block what phase?
Phase 3 Repolarisation phase
31
What is the function of anti-dysrhythmic drugs?
to restore normal rhythm and conduction
32
How is cardiac output (L/min) calculated
SV (stroke volume- ml) X heart rate (beats per minute)
33
Heart rate is controlled by the __________ nervous system
autonomic
34
What is the stroke volume?
volume of blood ejected from the ventricle with each heartbeat
35
What are the categories of the factors that affect stroke volume
Intrinsic myocardial contractility Extrinsic circulatory factors
36
List some factors that affect the heart rate
Autonomic innervation hormones fitness levels age
37
List some factors affecting stroke volume
heart size fitness levels gender contractility duration of contraction Preload (EDV) Afterload (resistance)
38
The intrinsic contractility of cardiomyocytes is dependent on ...
Ca2+ ions and ATP availability Ca2+ entry across the plasma membrane Ca2+ release from stores (sacroplasmic reticulum?)
39
What are the extrinsic circulatory factors that affect myocardial contraction?
- elasticity and contractile state of arteries and veins - volume and viscosity of the blood - these together determine the cardiac load (preload and after load)
40
What is preload?
This is the initial stretching of the cardiac myocytes (muscle cells) prior to contraction. It is related to ventricular filling
41
What is afterload?
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
42
What is heart failure?
this is where the cardiac output is not suffcient to meet the demands of the body
43
Heart failure is often a result of ...
conditions which reduce the efficacy of the heart (damaged or increased workload)
44
Consequences of heart failure are often observed during exercise, but as the disease progresses it is also observed at ______.
rest
45
Heart failure is divided into ...
Systolic dysfunction Diastolic dysfunction
46
Systolic dysfunction results from ...
a loss of intrinsic contractility by alterations in signal transduction mechanisms
47
Diastolic dysfunction results from
less compliant ventricles (become stiffer) which impairs ventricular relaxation/filling and causes less ejection of blood
48
What is an important consequence of heart failure?
Oedema
49
How does heart failure cause oedema?
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
50
Drugs that treat heart failure improve cardiac function by ...
reducing blood volume reduce clinical symptoms e.g. oedema, shortness of breath
51
The heart is poorly perfused compared to its oxygen consumption and metabolic need. True or false
True
52
What can lead to an increase in coronary blood flow?
Increased cardiac activity Increased oxygen consumption
53
Coronary blood flow is controlled by ...
Auto-regulation of perfusion pressure (60-200mmHg) Vasodilation by mediators (adenosine, nitric oxide) Autonomic innervation is less important in coronary blood flow
54
When coronary blood flow is reduced, what can this lead to?
Angina
55
Coronary blood flow can be reduced by ...
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)
56
Vasospasms, fixed stenosis and a thrombus in coronary arteries can lead to...
Angina (chest pain)
57
Increased heart rate, contractility, afterload and preload leads to ...
Increased oxygen consumption
58
Increased oxygen consumption and decreased coronary blood flow can lead to...
Angina (chest pain)
59
Angina is caused by...
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
60
What is ischaemia
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
61
What are the types of angina recognised clincally?
Stable angina Unstable angina Variant angina
62
What is stable angina?
chest pain on exertion (exercise) produced by increased demand on the heart
63
What causes stable angina?
fixed narrowing of blood vessels by atheroma coronary vessels ???
64
Angina is referred to as unstable when ...
pain is experienced even at rest
65
What causes unstable angina
thrombi from ruptured plaques form leading to decreased blood flow This is without complete occlusion
66
Variant angina is uncommon. What does it result from?
coronary artery spasm
67
Drugs that increase blood flow in the heart have what effect?
increased oxygen supply
68
Drugs that decrease oxygen demand in the heart lead to ...
a decrease in myocardial oxygen consumption
69
What are the effects of sympathetic innervation on the heart (via B adrenoceptors)?
- increased heart rate - increased force of contraction - increases automaticity- spontaneous activity of pacemaker cells - reduces cardiac efficiency- O2 consumption in relation to cardiac work
70
An increase in heart rate demonstrates a positive _________ effect.
chronotropic
71
An increase in contractility/force of contraction demonstrates a positive ________ effect.
inotropic effect
72
What is the effect of parasympathetic innervation on the heart (via muscarinic M2 receptors- smooth muscle and heart)
- Decrease heart rate - decrease force of contraction- in the atria only - reduces automaticity- spontaneous activity of pacemaker cells - inhibits atrio-ventricular conduction
73
Inhibition of AV conduction is also referred to as...
negative dromotropy
74
A decrease in heart rate demonstrates a negative _________ effect
chronotropic
75
What are drugs that affect the myocardial cells directly?
Autonomic neurotransmitters and related drugs (B blockers) Anti-dysrhythmic drugs (calcium channel blockers) Cardiac glycosides (digoxin- inhibits Na+/K+ ATPase)
76
What is the mechanism of action of digoxin?
Inhibits Na+/K+ ATPases in cardiac myocytes Increases intracellular Na+ This in turn increases intracellular Ca2+ ions This increases cardiac contractility
77
Give examples of drugs that affect cardiac function indirectly (effect is elsewhere in vascular system)
Nitrates Diuretics ACEIs
78
Nitrates are used to treat...
Angina
79
Diuretics and ACEIs are used to treat...
heart failure
80
Calcium antagonists are a category of drugs that affect cardiac function in what ways?
both directly and indirectly
81
What is the mechanism of action of ACEIs
Prevent production of Angiotensin II Angiotensin II raises blood pressure
82
In what ways is angiotensin II able to raise blood pressure?
Vasoconstriction Increased aldosterone synthesis Sympathetic nervous stimulation
83
B1 adrenoceptor subtypes have a ________ effect. Give examples of tissues they can be expressed in
stimulatory effect Heart, juxtaglomerular apparatus (kidney)
84
B2 adrenoceptor subtypes have a _______ effect. Give examples of tissues they are expressed in.
relaxation effect bronchial, vascular, uterine smooth muscle
85
B3 adrenoceptors are often found in __________ tissue
Adipose For lipolysis
86
What is the mechanism of action of B-blockers
competitively bind to B-adrenergic GPCRs block sympathetic effects of adrenaline and noradrenaline
87
What are the cardiac effects of Beta- blockers ?
- decreased contractility (negative inotropy) - decrease relaxation rate (nageive lusitropy) - decreased heart rate (negative chronotropy) - decreased conduction velocity ((negative dromotrophy)
88
What are the vascular effects of beta- blockers?
smooth muscle contraction (mild vasoconstriction)
89
What are the therapeutic indications for beta- blockers?
Angina Heart failure Arrhythmia Hypertension Open angle glaucoma, hyperthyroidism, anxiety, tremor
90
Why are beta blockers indicated for angina?
Reduces heart rate, contractility, arterial pressure, workload and oxygen demand of the heart This improves O2 supply/demand ration which can relieve anginal pain
91
Why are beta blockers indicated for heart failure?
blockade of excessive, chronic sympathetic input to the heart (poorly understood)
92
Why are beta blockers indicated for arrhythmias?
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
93
Why are beta blockers indicated for HTN?
- reduce cardiac output - inhibit renin release by kidneys- enhanced renal loss of sodium and water and further diminishes arterial pressure - decrease in blood pressure
94
List some B1/B2 non selective betablockers (B adrenoceptor antagonists)
Carvedilol Labetalol Nadolol Pindolol Propanolol Sotalol Timolol
95
What B1/B2 non-selective Beta blockers are indicated for therapeutic use against hypertension and angina?
Carvedilol Labetalol Nadolol Pindolol Propanolol Sotalol Timolol
96
What B1/B2 non-selective beta blockers are indicated for therapeutic use against arrhythmias?
Nadolol Propanolol Sotalol
97
What B1/B2 non-selective beta blockers are indicated for therapeutic use as prophylaxis after MI?
Propanolol Timolol
98
What B1/B2 non-selective beta blocker is indicated for therapeutic use as an adjunctive therapy in heart failure
Carvedilol
99
What are some other therapeutic uses of nadolol?
Migraine prophylaxis Thyrotoxicosis
100
What are some other therapeutic uses of propanolol?
Migraine prophylaxis Thyrotoxicosis Anxiety (palpitation, sweating and tremor) Pheochromocytoma
101
What are some other therapeutic uses of timolol?
Open- angle glaucoma Migraine prophylaxis
102
Give examples of B1 cardio-selective beta- blockers
Acebutolol Atenolol Betaxolol Bisoprolol Esmolol Metoprolol Nebivolol
103
Give examples of B1 cardio-selective beta- blockers indicated for hypertension
Acebutolol Atenolol Bisoprolol Esmolol Metoprolol Nebivolol
104
Give examples of B1 cardio-selective beta- blockers indicated for angina
Acebutolol Atenolol Bisoprolol Metoprolol
105
Give examples of B1 cardio-selective beta- blockers indicated for arrhythmias
Acebutolol Atenolol Esmolol Metoprolol
106
Give examples of B1 cardio-selective beta- blockers indicated for use as early intervention within 12 hours of MI
Atenolol Metoprolol
107
Give examples of B1 cardio-selective beta- blockers indicated for use as adjuncts in heart failure
Acebutolol Bisprolol Nebivolol
108
What are other therapeutic uses of atenolol?
Migraine prophylaxis
109
What are other therapeutic uses of betaxolol?
Open- angle glaucoma
110
What are other therapeutic uses of metoprolol?
Migraine prophylaxis Hyperthryroidism (adjunct) In surgery
111
List some common/ very common side effects of beta blockers
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
112
Give some uncommon side effects of beta-blockers
Atrioventricular block
113
Give some rare/very rare side effects of beta blockers
Hallucination Psoriasis exarcebated
114
What are contraindications of Beta blocker use?
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
According the the BNF, what type of drugs should be avoided in patients with asthma, bronchospasm and COPD when treating CVD?
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
What is the function of calcium channel blockers?
Inhibit calcium influx in voltage activated, L type calcium channels
117
Calcium channel blockers are a heterogenic group of drugs. Why are they described to be heterogenic?
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
An increase in intracellular calcium ion concentration leads to...
- increased contractility- inotropy - increased heart rate- chronotropy - increased conduction velocity- dromotropy (lead to vasoconstriction of vasculature)
119
Class IV anti-dysrhythmic drugs are calcium ion channel blockers. They are classified into 3 groups which differ in ______ and _______.
structure selectivity
120
What are the 3 classes of class IV anti-dysrhythmic drugs?
Dihydropyridines Non- dihydropyridines Benzothiazapine
121
Briefly state some characteristics of dihydropyridines
- smooth muscle selective - primarily used in hypertension (CVD of vasculature) - end in "pine" e.g. nifedipine
122
Non- dihydropyridines are used to treat what kinds of CVD?
Angina Arthythmias (CVD of the heart)
123
Non- dihydropyridines are ________ specific
cardiac
124
Non-dihydropyridines are phenylalkylamines. Give an example of a phenylalkylamine
Verapamil
125
Diltiazem is an example of a _________ Ca2+ channel blocker
Benzothiazapine
126
List some characteristics of benzothiazapines
- intermediate selectivity (both cardio-depressant and vasodilatory effects) - reduced atrial pressure without compensatory cardiac stimulation caused by dihydropyridines
127
Verapamil has a _______ effect on systemic and coronary vasodilation.
Moderate effect
128
Describe, briefly, the effect that verapamil has on myocardial contractility.
moderate reduction in myocardial contractility
129
What is the effect of verapamil and diltiazem on heart rate?
Causes a minimal reduction in heart rate
130
What is the effect of Verapamil on atrioventricular conduction (dromotropy)?
causes a strong reduction in AV conduction
131
What are the clinical uses of verapamil?
Angina Hypertension Arrhythmias
132
Diltiazem has a _____ effect of systemic vasodilation whilst it has a _____ effect on coronary vasodilation.
Mild effect Moderate effect
133
What is the effect of diltiazem on myocardial contractility?
causes a mild reduction on myocardial contractility
134
What is the effect of diltiazem on AV conduction?
moderate reduction
135
What are the therapeutic uses of diltiazem?
Angina Hypertension
136
Describe the effect of nifedipine, amlodipine and felodipine on systemic and coronary vasodilation
Strong effect
137
Describe the effect of nifedipine, amlodipine and felodipine on myocardial contractility.
No effect
138
Describe the effect of nifedipine, amlodipine and felodipine on AV conduction.
No effect
139
What is the effect of nifedipine on heart rate?
causes a mild increase
140
What is the effect of amlodpine and felodipine on heart rate?
causes a minimal increase
141
What are the clinical uses of amlodipine and felodipine?
Angina prophylaxis Hypertension
142
What are the clincal uses of nifedipine
Angina prophylaxis Hypertension Raynauds syndrome
143
What are the therapeutic indications of calcium channel blocker use
Angina due to coronary vasospasm Arrhythmia Hypertension Raynauds syndrome
144
List some reasons why calcium channel blockers are indicated for use in Angina
- 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
Why are CCBs indicated for arrhythmia?
- decrease the firing rate of aberrant pacemaker sites - decrease the conduction velocity through AV node and prolong repolarisation (block re-entry mechanisms)
146
Why are CCBs indicated for hypertension?
cause relaxation of the vascular smooth muscle (vasodilation) which lowers arterial blood pressure
147
Why are CCBs indicated for raynauds syndrome?
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
What are the side effects of dihydropyridines
Headache Flushing Reflex tachycardia Peripheral oedema (vasodilation) Gingival hyperplasia
149
What are the side effects of dihydropyridines?
Bradycardia Block of AV conduction low ejection fraction constipation gingival hyperplasia with verapamil
150
What are the contraindications for dihydropyridine use?
Cardiogenic shock decompensated heart failure severe aortic stenosis (narrowing) obstructive cardiomyopathy
151
What are the contraindications for non-dihydropyridine?
Severe bradycardia disorder of conduction sick sinus syndrome congestive heart failure cardiogenic shock
152
What preventative measures can be implemented for CCB induced hyperplasia?
Hygiene therapy
153
If symptoms of CCB induced hyperplasia persist, what should you do?
Liasise with overseeing GP
154
You should never stop medication without first consulting GP. True or false.
True
155
What are cardiac glycosides (digoxin)?
these are compounds that are derived from the foxglove plant (digitalis purpurea)
156
Cardiac glycosides are a a potent inhibitor of ...
Na+/K+ ATPase
157
What is the mechanism of action of cardiac glycosides?
The mechanism is poorly understood, but it causes an increase in intracellular Ca2+ which increases contractility of the heart
158
What are the cardiac actions of cardiac glycosides?
-cardiac slowing and reduced rate of conduction through AV node increased force of contraction (positive inotropic effect)
159
What are the therapeutic uses of cardiac glycosides such as digoxin?
arrhythmias (to slow ventricular rate in rapid atrial fibrillation) heart failure
160
What are the side effects of cardiac glycosides?
- 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
What types of drugs affect myocardial cells directly?
Autonomic transmitters and related drugs (beta-blockers) Antidysrhythmic drugs (Ca2+channel blockers- class IV) cardiac glycosides (digoxin)
162
What types of drugs affect cardiac function indirectly (elsewhere in the vascular system)?
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
What drugs affect cardia function directly and indirectly?
Calcium antagonists
164
What is systemic hypertension?
Sustained elevated blood pressure above 140/90 mmHg
165
Hypertension is a major risk factor for what other diseases?
Atherosclerosis Thrombosis Stroke Aneurysms Renal failure
166
What are the classes of hypertension?
Primary (essential) hypertension Secondary hypertension
167
What is the cause of primary (essential) hypertension?
No known cause
168
What is secondary hypertension?
There is usually an identifiable cause
169
Primary hypertension constitutes ____% of hypertension whilst secondary hypertension constitutes ___%.
95% 5%
170
In most cases, essential hypertension is characterised by...
increased vascular resistance, cardiac output remains normal thickening of resistant vessel walls vasoconstriction
171
What are the characteristics of secondary hypertension ?
Increased cardiac output Increased systemic vascular resistance
172
Give instances that can lead to increased cardiac output
- Hypervolemia: renal artery stenosis renal disease hyperaldosteronism hypersecretion of ADH Aortic coarctation pregnancy (preeclampsia) - Stress: Sympathetic innervation - Pheochromocytoma increased catecholamines
173
Give instances that lead to an increase in vascular resistance
Stress: sympathetic innervation Atherosclerosis Renal artery disease (increased angiotensin II) Pheochromocytoma (increased catecholamines) Thyroid dysfunction Diabetes Cerebral ischaemia
174
What determines the state of vascular tone?
Vasodilator and vasoconstrictor influences acting on arteries and veins
175
An increase in vascular (smooth muscle) intracellular calcium leads to...
vasoconstriction
176
A decrease in vascular (smooth muscle) intracellular calcium lead to ...
Vasodilation
177
What is the effect noradrenaline on vascular smooth muscles?
release of calcium from sacroplasmic reticulum (store) Increase in intracellular calcium vasoconstriction
178
What is the effect of NO and PGI2 produced by vascular endothelial cells on smooth muscle cells
Vasodilation
179
What are the two types of nitrates (vasodilator)?
Release NO following enzymatic process (organic nitrates, glyceryl trinitrate GTN) Releases NO spontaneously (sodium nitroprusside)
180
What are the effects of nitrates on systemic vasculature ?
Vasodilation (venous dilation> arterial dilation) decrease in venous pressure decrease in arterial pressure (small effect)
181
What are the cardiac effects of nitrates?
decreased preload and afterload (decreases wall stress) decreased oxygen demand (good for angina)
182
What are the coronary effects of nitrates?
prevents/reverses vasospasms vasodilation (primarily epicardial vessels- vessels that supply epicardium) increase subendocardial perfusion increased oxygen delivery
183
Briefly describe how organic nitrates produce NO
Organic nitrates --->RNO2 (Nitrogen dioxide) ---> S-nitrosothiol ----> NO
184
What is the effect of cGMP on smooth muscle cells?
Relaxation Vasodilation
185
What is function of NO in smooth muscle?
Activation of guanylyl cyclase
186
What is the function of guanylyl cyclase?
conversion of GTP to cGMP
187
Give examples of short acting nitrates
Sodium Nitroprusside Glyceryl trinitrate (GTN)
188
What are the therapeutic uses of sodium nitroprusside?
Hypertensive emergencies Acute and chronic heart failure controlled hypotension in anasthesia during surgery (IV)
189
What are the therapeutic uses of GTN
Treatment and prophylaxis of angina congestive heart failure
190
Sublingual GTN exists in what forms?
Tablets or aerosol sprays
191
What are the uses of IV infusions of GTN?
control of hypertension, myocardial ischaemia during and after cardiac surgery
192
Give examples of long acting nitrates
Isosorbide mononitrate Isosorbide dinitrate
193
What are the therapeutic uses of isosorbide mononitrate?
Angina prophylaxis Adjunct for heart failure
194
What are the therapeutic uses of isosorbide dinitrate?
Angina prophylaxis Left ventricular failure
195
In both isosorbide mononitrate and dinitrate, tolerance develops, leading to ...
Reduced therapeutic effects
196
How long are transdermal patches of isosorbide mononitrate and dinitrate left off?
8-12 hours overnight
197
Modified release tablets of isosorbide mononitrate and dinitrate are delivered in ____ doses
set
198
What are the therapeutic indications for nitrates
Angina Heart failure (acute and chronic) Hypertensive emergencies
199
Why are nitrates indicated for use in angina?
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
Why are nitrates indicated for use in acute and chronic heart failure?
Reduces afterload in failing ventricle by arterial dilation by increasing stroke volume and ejection fraction Venous dilation reduces venous pressure which oedema
201
Why are nitrates indicated for hypertensive emergencies
- 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
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What are the side effects of nitrates?
headache (caused by cerebral vasodilation) cutaneous flushing postural hypotension reflex tachycardia nausea and vomiting thiocyanate toxicity (with prolonged sodium nitroprusside use)
203
What are the contraindications for nitrates use?
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
Renin is released from the kidneys in response to ...
- decreased perfusion pressure - decreased glomerular filtration - increased sympathetic nerve activity - increased beta agonists (binding to B-adrenoceptors)
205
How is renin release modulated?
it is modulated by natriuretic peptides that are released by the heart- counter regulatory system
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What is the mechanism of action of renin?
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
Angiotensin II binds to AT1 receptors which results in...
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
What are the effects of ATII on the AT1 subtype receptors
Vascular growth- hyperplasia and hypertrophy Vasoconstriction- direct or via increased NA release from sympathetic nerves salt retention: aldosterone release, tubular Na+ reabsorption
209
Give examples of ACEI (ACE inhibitors)
Captopril Enalapril (prodrug) Lisinopril
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ACEI are indicated for ...
Primary hypertension (increased peripheral vascular resistance; no effect on cardiac output) Renal hypertension caused by renal artery stenosis leading to renin release
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ACEIs decrease the production of ATII which causes
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
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What is natriuresis?
excretion of sodium ions in the urine
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What is diuresis?
increased urine production
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Why are ACEIs indicated for use in heart failure and post-myocardial infarction?
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
What are the side effects of ACEI?
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)
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What are the contraindications of ACEIs?
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)
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What are angiotensin receptor blockers (ARBs)
non peptide orally active AT1 antagonists
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Give examples of ARBs
Sartans Losartan Candesartan Valsartan Irbesartan
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What group of drugs share the same therapeutic properties and indications as ARBs?
ACEI
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What are the indications for ARBs?
Hypertension Heart failure
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What ARB is approved for MIs ?
Valsartan
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ARBs have similar side effects and contraindications as ACEIs except that there is no ...
bradykinin induced coughing
223
What is the function of Diuretics?
They increase the urine output by kidneys (promote diuresis)
224
What is the mechanism of action of diuretics
They diminish reabsorption of Na at different renal tubular elementswhich also prevents water reabsorption; increasing sodium and water loss
225
Diuretic drugs include...
- loop diuretics - thiazides -K+ sparing diuretics
226
What is the order of potency for diuretic drugs?
Loop diuretics>Thiazides >K+ sparing diuretics
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What is the MOA of Loop Diuretics?
Inhibit Na+/K+/Cl- cotransporter in thick ascending loop of Henle
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What is the MOA of thiazides?
Inhibits Na+/Cl- co-transporters in distal convoluted tubule
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What is the MOA of K+ sparing diuretics
Aldosterone receptor antagonist in the collecting duct Inhibit Luminal Na+ channels in the collecting duct
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What is the function of aldosterone?
helps to regulate bodys blood pressure by managing the levels of sodium and potassium in the body
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What are the indications for diuretics?
Hypertension Heart failure and oedema
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What are the effects of diuretics in hypertensive patients?
Decreased blood volume Decreased cardiac output Decreased systemic vascular resistance (long term therapy) leads to a decrease in blood pressure
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Diuretics are used to effectively treat what kind of hypertension?
Primary hypertension 90-95% with primary are effectively treated with diuretics
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What adjunctive therapy (or behaviour) is particularly effective when coupled with diuretics?
Reduced sodium intake
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What type of diuretics are most commonly used in hypertension?
Thiazides
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What drugs can be used to prevent hypokalemia?
K+ sparing diuretics (aldosterone receptor antagonists) with thiazide treatment
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What is hypokalemia?
Low level plasma K+
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What diuretics can produce hypokalemia?
Loop diuretics Thiazides
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What are the effects of diuretic use in patients with heart failure and oedema?
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
Give examples of Loop Diuretics
Bumetanide Furosemide Torsemide
241
What are the side effects of Loop diuretics?
Dehydration Dizziness Electrolyte imbalance GI disorder Headache Hypotension Metabolic alkalosis Nausea Skin reactions
242
Give some examples of thiazide diuretics
Bendroflumethiazide Hydrochlorothiazide Chlortalidone Indapamide Metolazone
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What are the side effects of thiazides?
Constipation Electrolyte imbalance Postural hypotension Headache
244
What are the contraindications for loop diuretics?
Renal failure due to nephrotoxic or hepatotoxic drugs Hypokalemia Hyponatraemia Caution: exarcebate diabetes
245
What are the contraindications of diuretic thiazedes?
Addisonsn disease Hypercalacemia Hyponatraemia Hyperuricaemia (uric acid and gout) Caution: exacterbate diabetes
246
What are the types of K+ sparing diuretics?
Aldosterone antagonists Na+ channel inhibitors
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Give examples of Aldosterone agonist K+ sparing diuretics
Spinolactone Eplerenone
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Give examples of Na+ channel inhibitors K+ sparing diuretics
Triamterene Amiloride
249
What are the side effects of K+ sparing diuretics?
Diarrhoea Hyperkalemia Nausea Vomiting Check BNF
250
Whar are the contraindications of K+ sparing diuretics
Addisons disease Anuria Hyperkalaemia Caution: exarcebate diabetes
251
What is a caution to patients taking any type of diuretics?
exarcebate diabetes
252
What is atherosclerosis ?
It is a focal disease of large and medium sized arteries
253
What is the pathophysiology of atherosclerosis? (briefly)
athermatous plaques occurs over time Plaque ruptures and leads to platelet activation and thrombosis
254
Athetosclerosis is the most common cause of death (MI and Stroke). True or false
True
255
What are the earliest structurally apparent lesions in atherosclerosis
Fatty Streaks
256
When do symptoms of atherosclerosis begin to occur?
When the blood flow through the vessel is not sufficient to meet the demand of the downstream tissues
257
What else plays a key role in the pathophysiology of atherosclerosis?
Chronic inflammation to injury
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What are the modifiable risk factors for atherosclerosis?
Dyslipidaemia- unhealthy levels of certain kinds of lipids; high LDL Hypertension Diabetes mellitus Smoking Obesity Physical activity
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Lipids consist of ...
cholesterol and triglycerides
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Lipids are transported in plasma as 4 classes of lipoproteins. Name them.
Chylomicroms VLDLs LDLs HDL
261
What is the function of chylomicrons
transport cholesterol and triglycerides from GI tract to tissues
262
Triglycerides split into _____ and _______ which are then taken up by what tissue?
Gylcerol and fatty acids Muscle and adipose tissue
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What happens to chylomicron remnants?
They are taken up by the liver and converted into VLDLs
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What is the function of VLDLs ?
They transport cholesterol and newly synthesised triglycerides to tissues.
265
Lipoprotein particles become smaller LDLs. True or false
True
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LDLs have a large ______ component. LDL is taken up by the ______ via specific LDL receptors.
Large cholesterol component Taken up by the liver
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What are the physiological and pathological functions of LDL?
Provide a source of cholesterol for steroids Also involved in atherogenesis
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What is the function of HDL?
Absorbs cholesterol (from cell breakdown) and transfers to VLDLs and LDLs
269
Briefly describe the balance of LDL and HDL cholesterol in ischaemic heart disease
Higher LDL cholesterol and lower HDL cholesterol present (usually from cell breakdown)
270
What is the rate limiting enzyme in cholesterol production?
HMG CoA reductase
271
What is the first step in cholesterol synthesis and what enzyme catalyses this reaction?
HMG-CoA converteed to mevalonic acid Catalysed by HMG CoA reductase
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What is the MOA of statins
Inhibits the activ site of HMG CoA reductase enzyme (prevents production of mevalonic acid)
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What kinds of statins are simvastatin and pravastatin
Specific reversible competitive inhibitors of HMG CoA reductase
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Atorvastatin and Rosuvastatin are ________ inhibitors of HMG CoA reductase
Long lasting inhibitors
275
What is the effect of statins?
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
What are the other reported effects of statins?
improved endothelia function decreased vascular inflammation decreased platelet aggregation Plaque stabilisation
277
What are the therapeutic indications for statins
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
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What are the generally well tolerated side effects of statins?
Asthenia (weakness) constipation diarrhoea dizziness flatulence GI discomfort headache muscle pain nausea sleep disorders thrombocytopenia (low platelet levels)
279
What are the contraindications of statins?
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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