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Cardiovascular > Pharmacology 2 + 3 > Flashcards

Pharmacology 2 + 3 Flashcards

1
Q

How is vascular smooth muscle tone regulated?

A

Balancing the processes of contraction and relaxation

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2
Q

How is contraction of vascular smooth muscle caused? (6)

A
  • Begins either with hormone activation of GPCR coupled to Gq11 or depolarisation activating Ca+ channels
  • Both trigger release of calcium from SR
  • Ca++ binds to calmodulin to form Ca-calmodulin
  • Ca-calmodulin activates myosin light chain kinase
  • ATP phosphorylates myosin cross bridge to bind actin
  • Contraction
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3
Q

How is relaxation of vascular smooth muscle caused? (3)

A
  • Myosin light chain phosphatase activated by phophokinase G which is activated by cGMP
  • Dephosphorylates myosin light chain kinase
  • Relaxation
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4
Q

What is the role of endothelium in vascular smooth muscle tone regarding NO and exogenous organic nitrates? (5 + 1 extra thing)

A
  • Vasodilating substances increase Ca++ in endothelial cell
  • Combines with calmodulin and activates endothelial nitric oxide synthase
  • ENOS catalyses conversion of L-arginine to NO and citrulline
  • NO enters vascular smooth muscle cells and activates guanylyl cyclase which converts GTP to cGMP
  • cGMP activates PKG which causes relaxation
  • NO also activates K+ channels causing hyperpolarisation and thus relaxation
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5
Q

How else is NO delivered to vascular smooth muscle cells?

A

Organic nitrates (e.g. GTN) donate NO to smooth muscle, activating guanylyl cyclase and so on…

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6
Q

What is the function of organic nitrates?

A

Relax all types of smooth muscle via their metabolism to nitric oxide

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7
Q

What are the clinical effects of organic nitrates? (3)

A
  • Venorelaxation - decreased CVP (preload) reduces SV, but CO maintained by HR so no change in arterial pressure
  • Arteriolar dilatation – decreases arterial pressure reducing afterload, reduces pulse wave reflection from arterial branches
  • Increased coronary blood flow in normal individuals (in angina, no increase but blood is redirected towards ischaemic zone)
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8
Q

Why are organic nitrates beneficial in treating angina? (3)

A

Decreased myocardial oxygen requirement due to:-

  • decreased preload
  • decreased afterload
  • improved perfusion of ishaemic zone
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9
Q

How do organic nitrate increase blood flow to ischaemic zone in angina?

A

Dilate collateral vessels below blocked artery

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10
Q

What are clinical uses of organic nitrates? (2)

A

Stable angina and acute coronary syndrome

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11
Q

What are examples of organic nitrates used clinically? (3)

A
  • Glyceryltrinitrate (GTN)
  • Isosorbide mononitrate (ISMN)
  • Isosorbide dinitrate
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12
Q

What are the clinical features of GTN? (3)

A
  • Short-acting (30 min)
  • Administered sublingually or as spray (for rapid effect before exertion in stable angina) or IV with aspirin in acute coronary syndrome (not given orally cause undergoes extensive first pass metabolism)
  • More sustained effect if delivered by transdermal patch
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13
Q

What are the clinical features of isosorbide mononitrate?

A
  • longer-acting than GTN (t1/2 4 hours) as resistant to first past metabolism (note: DInitrate is NOT)
  • Orally for prophylaxis of angina
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14
Q

What are unwanted effects of organic nitrates? (4)

A
  • Repeated usage can result in diminished effect (tolerance)
  • Postural hypotension
  • Headaches
  • Formation of methaemoglobin
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15
Q

What is the role of endothelium in vascular smooth muscle tone with regards to Endothelin? (4 + extra info)

A
  • Enchanced gene expression from vasoconstrive agents (e.g. adrenaline, angiotensin II, ADH)
  • Results in production of endothelin-1
  • Activates ETa receptor on vascular smooth muscle cell which activates signalling pathways including Gq/11
  • Contraction

(Vasodilators like NO, NPs and sheer stress reduce gene expression and so reduced contraction of smooth muscle)

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16
Q

What agents are used in the treatment of pulmonary hypertension?

A

Antagonists of ETa receptor e.g. bosentan and ambrisentan

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17
Q

What triggers renin release from the kidneys? (3)

A
  • Increased renal sympathetic nerve activity
  • Decreased renal perfusion pressure
  • Decreased glomerular filtration
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18
Q

What is angiotensin converting enzyme? What does it do? (2)

A
  • Membrane-bound enzyme on surface on endothelial cells
  • Converts inactive angiotensin 1 to active angiotensin II (vasoconstrictor)
  • Inactivates bradykinin (vasodilator)
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19
Q

What is an example of an ACE inhibitor?

A

Lisinopril (if drug name ends in “opril” it is an ACE inhibitor

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20
Q

What do ACE inhibitors do?

A

Block conversion of angiotensin I to angiotensin II

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21
Q

What do AT1 receptor antagonists do? Example?

A

Block the agonist action of angiotensin II at AT1 receptors in a competitive manner e.g. Losartan ends in “sartan”

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22
Q

How does RAAS lead to contraction of vascular smooth muscle and thus increased MABP? (2)

A
  • Activation of smooth muscle AT1 receptors by angiotensin II
  • Increased release of noradrenaline from sympathetic nerve fibres
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23
Q

What are the effects of angiotensin converting enzyme inhibitors? (ACEI) (5)

A
  • Cause venous dilatation (decrease preload)
  • Arteriolar dilatation (decrease afterload and TPR) decreasing arterial blood pressure and cardiac load
  • Has no effect on cardiac contractility (CO increases as a result of decreased SVR)
  • Can cause small fall in MABP
  • Reduce direct growth action of angiotensin II to heart and vasculature
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24
Q

Where do ACE inhibitors have the greatest effect?

A

In angiotensin-sensitive vascular beds (brain, heart, kidney – important because may help maintain perfusion of critical organs)

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25
Q

When does the fall in MABP caused by ACE-I have the greatest effect?

A

In hypertensive patients (especially if renin secretion is enhanced e.g. as a consequence of diuretic therapy)

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26
Q

What are the adverse effects of ACE-Inhibitors? (2)

A
  • Hypotension (especially in patients treated with diuretics)
  • Dry cough
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27
Q

What are angiotensin receptor blockers (ARBs)?

A

Have properties similar to ACEIs in clinical practice (but ARBs do not inhibit the metabolism of bradykinin)

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28
Q

When are angiotensin receptor blockers useful?

A

In patients who find dry cough produced by ACEIs intolerable

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29
Q

When are ACEIs and ARBS contraindicated? (2)

A
  • In pregnancy (foetal toxicity)

* Bilateral renal artery stenosis

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30
Q

What are clinical uses of ACE inhibitors and AT1 receptor antagonists? (3)

A
  • Hypertension (reduced SVR and MABP, decreased vessel hypertrophy)
  • Cardiac failure (decrease SVR improving perfusion, increase excretion of Na+ and H2O, regression of left ventricular hypertrophy)
  • Following myocardial infarction
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31
Q

What are adrenoceptors?

A

G-protein-coupled receptors (GPCRs) activated by sympathetic transmitter noradrenaline (norepinephrine) and the hormone adrenaline (epinephrine)

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32
Q

What are the structurally and pharmacologically distinct subtypes of adrenoceptor?

A
  • a1 (constrict blood vessels)
  • a2
  • B1 (increase cardiac rate, force and decrease AV node delay)
  • B2 (relax blood vessels)
  • B3
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33
Q

What are clinical uses of B-adrenoceptor antagonists? (3)

A
  • Treatment of angina pectoris (but not variant angina)
  • Treatment of hypertension (not first line treatment)
  • Treatment of compensated heart failure
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34
Q

How are B1-selective B-blockers effective in treating angina pectoris? (3)

A
  • Decrease myocardial O2 requirement (decrease HR, SV, cardiac work and so O2)
  • Counter sympathetic activity associated with ischaemic pain
  • Increase amount of time spend in diastole (decreased HR) improving perfusion of left ventricle
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35
Q

How does increasing the amount of time spent in diastole improve the perfusion of the left ventricle?

A

Aortic pressure must exceed ventricular pressure for blood to flow through coronary circulation (so most blood delivered to heart in diastole)

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36
Q

Why are B-blockers used to treat hypertension? (3)

A
  • reduce cardiac output (MABP = CO x TPR)
  • reduce renin release from kidney
  • CNS action that reduces sympathetic activity
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37
Q

What is the problem with B-blockers reducing cardiac output? How is this overcome?

A
  • CO returns to normal over time

* MABP remains suppressed by ‘resetting’ of TPR to a lower level

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38
Q

How are B-blockers used to treat compensated heart failure?

A

In combination with other drugs to suppress adverse effects caused by inappropriate activation of sympathetic system and RAAS

(start low, go slow)

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39
Q

What are calcium antagonists?

A

Prevent opening of L-type channels in excitable tissues in response to depolarisation and so limit intracellular concentrations of Ca++

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40
Q

What is a feature of clinically useful calcium antagonists?

A

Interact preferentially, or solely, with L-type calcium channels found: 1) in the heart; 2) in smooth muscle and 3) other locations

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41
Q

What do L-type channels mediate? (2)

A
  • Upstroke of AP in SA and AV nodes (Ca++ antagonists reduce rate of AP and conduction through AVN)
  • Phase 2 of ventricular AP (Ca++ antagonists reduce force of contraction through blocking Ca++ entry)
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42
Q

What causes contraction in vascular smooth muscle cells?

A

L-type Ca++ channels allow Ca++ entry into cell that is blocked by Ca++ antagonists

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43
Q

Explain the process of contraction in vascular smooth muscle cells (3)

A
  • Noradrenaline activates a1 adrenoceptor, which opens Na+ channels (receptor operated channel)
  • Na+ channels cause depolarisation
  • Depolarisation opens L-type Ca++ channels which causes CICR from SR and contraction
44
Q

What are the 3 main types of calcium antagonist?

A
  • Verapamil (relatively selective for cardiac L-type Ca++ channels)
  • Amlodipine (dihydropyridine compound - relatively selective for smooth muscle L-type channels)
  • Diltiazem (intermediate selectivity)
45
Q

What is amlodipine?

A

Dihydropyridine compound that its as Ca++ antagonist

46
Q

What are clinical uses of calcium antagonists?

A
  • Hypertension
  • Angina
  • Dysrhythmias/arrythmias
47
Q

Why are calcium antagonists used to treat hypertension?

A

Reduce Ca++ entry into vascular smooth muscle cells causing arteriolar dilation which reduces TPR and MABP (little effect on veins)

48
Q

What calcium antagonists are preferred for treatment of hypertension?

A

Those with selectivity for smooth muscle L-type channels (e.g. amlodipine) to minimise unwanted effects on cardiac muscle e.g. in patients with both hypertension and heart failure/heart block

49
Q

Why are Ca+ antagonists useful for patients suffering from both angina and hypertension? (2)

A
  • Cause coronary vasodilation which helps angina

* Cause vasodilation in other vessels reducing blood pressure

50
Q

What are adverse effects of calcium antagonists?

A
  • Hypotension
  • Dizziness
  • Flushing
  • Ankle oedema
51
Q

How are calcium antagonists used to treat angina?

A

Used as prophylactic treatment in combination with GTN (particularly if B-blockers are contraindicated eg. in asthma)

52
Q

Why are calcium blockers effective in treatment of angina? (2)

A
  • Cause peripheral arteriolar dilatation - decreasing afterload and myocardial oxygen requirement (preload not really changed)
  • Coronary vasodilatation – especially useful in patents with variant angina
53
Q

What specific calcium antagonists are used in the treatment of angina?

A
  • Amlodipine (has little effect on the heart and is long-acting)
  • Diltiazem and verapamil - negative inotropic effects but baroreceptor reflex counters this once activated in response to vasodilation and increased sympathetic activity
54
Q

How do calcium antagonists treat dysrythmias?

A

Ventricular rate in rapid atrial fibrillation reduced by suppression of conduction through the AV node

55
Q

What calcium blocker is used to treat dysrhythmias?

A

Verapamil

56
Q

What are potassium channel openers?

A

Open ATP-modulated K+ channels in vascular smooth muscle

57
Q

How do K+ channel openers open channels? What do they cause? What tissues do they act upon?

A
  • Antagonise intracellular ATP (ATP closes K+ channels)
  • Cause hyperpolarisation which switches off L-type Ca++ channels
  • Act potently and primarily on ARTERIAL smooth muscle
58
Q

What are example of potassium channel openers? (2)

A
  • Minoxidil - drug of last resort for hypertension

* Nicorandil - drug used in angina, also has nitric oxide donor activity

59
Q

What are the side effects of minoxidil? How are these overcome?

A
  • Reflex tachycardia (prevented by B-blocker)

* Salt + water retention (alienated by diuretic)

60
Q

What is the function of a1 adrenoceptor antagonists? What is their effect?

A
  • Cause vasodilation by blocking a1 adrenoceptors

* Reduced sympathetic transmission results in decreased MABP

61
Q

What are examples of a1 adrenoceptor antagonists? (2) What are they?

A
  • Prazosin
  • Doxazosin
  • Both competitive antagonists of a1 adrenoceptors
62
Q

What are a1 adrenoceptor antagonists used to treat? (2)

A
  • Provide symptomatic relief in benign prostatic hyperplasia
  • Particularly indicated for hypertensive patients with this condition
63
Q

What is an adverse effect of a1-adrenoceptor antagonists?

A

Postural hypotension

64
Q

What are anti-arrythmmic drugs?

A

Inhibit specific ion channels to suppress abnormal electrical activity of the heart

65
Q

How are anti-arrhythmic drugs classified? What classes are there?

A
  • Vaughn Williams classification - classified pharmacologically based on their effects on cardiac AP
  • Classes I, II, III and IV, with class I subdivided into subclasses Ia, Ib and Ic
66
Q

Are anti-arrythmic drugs selective blockers of ion channels?

A

Many antiarrhythmic agents are not entirely selective blockers of Na+, K+, or Ca2+ channels and may block more than one channel type (e.g. amiodarone)

67
Q

What anti-arhythmic drugs do not fit the Vaughn Williams classification? (2)

A
  • Adenosine

* Digoxin

68
Q

What cardiac action potential is class I anti-arhythmic drugs associated with? Class II? III? IV?

A
  • Class I - atrial and ventricular myocyte AP (phase 1)
  • Class II - Nodal tissue AP (phase 2)
  • Class III - Nodal tissue (phase 3), atrial and ventricular myocyte (phase 3)
  • Class IV - nodal tissue (phase 2), atrial and ventricular myocyte (phase 2)
69
Q

What is the target of class Ia anti-arhythmic drugs? Example? Action?

A
  • Voltage-activated Na+ channel
  • Disopyramide
  • Associate with and dissociate from Na+ channels at a moderate rate - slow rate of AP rising and prolong refractory period
70
Q

What is the target of class Ib anti-arhythmic drugs? Example? Action?

A
  • Voltage-activated Na+ channel
  • Lignocaine
  • Associate with and dissociate from Na+ channels at a rapid rate - prevent premature beats
71
Q

What is the target of class Ic anti-arhythmic drugs? Example? Action?

A
  • Voltage-activated Na+ channel
  • Flecainide
  • Associate with and dissociate from Na+ channels at a slow rate - suppress conduction
72
Q

What do class I anti-arrhythmic drugs block?

A

Voltage activated Na+ channels

73
Q

What is the target of class II anti-arhythmic drugs? Example? Action?

A
  • B-adrenoceptor (as antagonists)
  • Metoprolol
  • Decrease rate of depolarization in SA and AV nodes
74
Q

What is the target of class III anti-arhythmic drugs? Example? Action?

A
  • Voltage-activated K+ channels
  • Amiodarone
  • Prolong AP duration increasing refractory period
75
Q

What is the target of class IV anti-arhythmic drugs? Example? Action?

A
  • Voltage-activated Ca2+ channels
  • Verapamil
  • Slows conduction in SA and AV nodes - decrease force of cardiac contraction (negative inotropic effect)
76
Q

What are the 3 states of voltage-activated Na+ channels? How do they shift between these states?

A
  • Resting, open and inactivated
  • Goes from resting state to open state during depolarisation
  • Goes from open state to inactivated state when depolarisation is maintained
  • Goes from inactivated state t resting state during repolarisation
77
Q

What happens to voltage-gated Na+ channels in tachyarrythmias?

A

High frequency firing means more time spent in open and inactivated states

78
Q

What voltage-gated Na+ channels to class I agents bind to? (2)

A
  • Will bind to channels in open state to inactivate them

* Will bind to channels in inactivated state to stabilise them

79
Q

When do class I agents have very little effect? What does use of anti-arhythmic drugs depend on? What is the benefit of this?

A
  • When myocardium is beating at normal frequency
  • Us elf anti-arhythmic drugs depends on frequency
  • Allows them to target areas of myocardium in which frequency is highest without preventing heart from beating at normal frequency
80
Q

When will zones of the heart have a higher firing frequency?

A

When they are ischaemic - zones are slightly depolarised and discharge APs at an abnormally high frequency

81
Q

When do class I agents dissociate from the Na+ channel?

A

When it is in the resting state i.e. during diastole (vascular smooth muscle)

82
Q

What happens to steady-state block if heart rate increases?

A
  • if heart rate increases, less time is available for unblocking (dissociation) and more time available for blocking (association)
  • so steady state block increases (particularly for agents with slow dissociation rates)
83
Q

What happens to the action potential in ischaemic myocardium? What are the effects of this? (2)

A
  • In ischaemic myocardium, myocytes are partially depolarized and the action potential is of longer duration

So…

  • The inactivated state of the Na+ channel is available to Na+ channel blockers for a greater period of time
  • The rate of channel recovery from block is decreased
84
Q

What is an important determining factor in steady-state block of Na+ channels?

A

Dissociation rate of class I agents

85
Q

What does the higher affinity of Na+ channel blockers for the open and inactivated states of the channel allow them to do?

A

Act preferentially on ischaemic tissue and block an arrhythmia at its source

86
Q

Look at diagram (pic)

A

…

87
Q

What are arrhythmias classified according to? (2) Examples? (2)

A
  • Their site of origin e.g. supraventricular (atria, AV node) and ventricular
  • Whether heart rate is increased or decreased (tachycardia/bradycardia)
88
Q

What is the site based classification of anti-arhythmic drugs?

A
  • Atria (rate control of supra ventricular tachycardia (SVT)) - classes Ic, III
  • Ventricles - classes Ia, Ib, II
  • AV node (rhythm control of SVT) - adenosine, digoxin, classes II, IV
  • Atria and ventricles, AV accessory pathways - amiodarone, sotalol, classes Ia and Ic
89
Q

What is the effect of anti-arhythmic drugs on atria? AV node?

A
  • Atria - rate control of SVT

* AV node - rhythm control of SVT

90
Q

What are examples of drugs used in supra ventricular arrhythmias? How are they administered?

A
  • Adenosine (IV bolus)
  • Digoxin (IV or oral)
  • Verapamil (Oral)
91
Q

What is the function of adenosine in the treatment of supra ventricular arrhythmias? What are the effects of this? (3)

A
  • Activates a1-adenosine receptors coupled to Gj/o
  • Opens ACh-sensitive K+ channels (GIRK)
  • Hyperpolarises AV node briefly suppressing impulse conduction
92
Q

What is adenosine used to treat? What is this?

A
  • Paroxysmal supraventricular tachycardia

* Atrial firing rate of 140-250 bpm

93
Q

What is the function of digoxin in the treatment of supra ventricular arrhythmias? What are the effects of this? (1)
What is digoxin used to treat?

A
  • Stimulates vagal activity
  • Slows conduction and prolongs refractory period in AV node and bundle of His
  • Atrial fibrillation (AF) – chaotic re-entrant impulse conduction through the atrium
94
Q

What is the function of verapamil in the treatment of supra ventricular arrhythmias? What are the effects of this? (1) What is verapamil?

A
  • blocks L-type voltage-activated Ca2+ channels
  • Slows conduction and prolongs refractory period in AV node and bundle of His
  • Type IV agent
95
Q

What is verapamil used to treat? What is this?

A

Atrial flutter and fibrillation - chaotic re-entrant impulse conduction through the atria that may be conducted via the AV node to the ventricles

96
Q

Why must verapamil be used with caution? (2)

Is verapamil used in acute treatment?

A
  • In high dose may cause heart block
  • Should be used with great caution in combination with other drugs that have a negative ionotropic effect
  • Largely replaced with adenosine in acute treatment but still used for prophylaxis
97
Q

What is an example of a drug used in ventricular arrhythmias? What is this?

A
  • Lignocaine

* Type Ib agent

98
Q

What is the function of lignocaine in the treatment of ventricular arrhythmias? What are the effects of this? (2)
What is lignocaine used in the treatment of?

A
  • rapid block of voltage-activated Na+ channels (blocks inactivated channels with little effect on open channels)
  • Due to rapid unblocking primarily affects Na+ channels in areas of the myocardium that discharge action potentials at high rate (e.g. an ischaemic zone)
  • used (IV) in treatment of ventricular arrhythmias following myocardial infarction
99
Q

What are examples of drugs used in atrial and ventricular arrhythmias?

A
  • Disopyramide
  • Flecainide
  • Propranalol and atenolol
  • Amiodarone and sotolol
100
Q

What is the function of disopyramide and procainamide in the treatment of ventricular arrhythmias? What are the effects of this? (1)
What are disopyramide and procainamide used in the treatment of? (2)

A
  • Moderate rate of block and unblock of voltage-activated Na+ channels (block open channels and so are use-dependent)
  • Moderate rate of dissociation results in insufficient time for unblocking if action potential frequency is high
  • Disopyramide is used (orally) to prevent recurrent ventricular arrhythmias, procainamide (IV) to treat ventricular arrhythmias following myocardial infarction
101
Q

What are disopyramide and procainamide?

A

Type Ia agents

102
Q

What is the function of flecainide in the treatment of ventricular arrhythmias? What are the effects of this? (2)
What is flecainide used in the treatment of? (1)

A
  • slow rate of block and unblock of voltage-activated Na+ channels
  • Strongly depresses conduction in the myocardium and reduces contractility
  • Has negative ionotropic action and may trigger serious ventricular arrhythmias
  • Mainly used for prophylaxis of paroxysmal atrial fibrillation
103
Q

What is flecainide?

A

Type Ic agent

104
Q

What is the function of propranolol and atenolol in the treatment of ventricular arrhythmias? (2)
What are propranolol and atenolol?

A
  • Control SVT by suppressing impulse conduction through the AV node
  • Supress excessive sympathetic drive that may trigger VT
  • Type II agents, B-blockers
105
Q

What is the function of amiodarone and sotolol in the treatment of ventricular arrhythmias? (2)
What are amiodarone and sotolol used in the treatment of? (2)

A
  • slow repolarization of the AP by block of voltage-activated K+ channels and hence increase action potential duration and the effective refractory period
  • Supress re-entry
  • Amiodarone is effective against SVT and VT, as it also has class IA, II and IV actions and blocks β-adrenoceptors
  • Also effective when many other drugs have failed and reduces mortality after MI and congestive heart failure
106
Q

What are amiodarone and sotolol?

Why is long term use of amiodarone compromised? (4)

A
  • Type III agents
  • Has many serious adverse side effects:-
  • pulmonary fibrosis
  • thyroid disorders
  • photosensitivity reactions
  • peripheral neuropathy

Cardiovascular (28 decks)

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