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Cardiology > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What is the funny current?

A

A current mediated by hyperpolarization-activated and cyclic nucleotide gated (HCN) channels that conduct Na+ and K

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2
Q

What constitutes phase 4 in nodal (AV and SA) cells

A

Funny current (inward), increase in transient Calcium channels (outward) and decrease in delayed rectifier potassium channel (inward)

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3
Q

Range of action potential in nodal cells?

A

-60 mV to +10 mV, lasts for 200ms

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4
Q

What happens during the plateau phase of action potential?

A

Plateau is largely a fine balance of inward Ca2+ current that slowly inactivates and outward K+ current that slowly activates

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5
Q

What receptors are activated by adrenaline and noradrenline; neurotransmitters of the sympathetic nervous system?

A

Beta-1 adrenoceptors in nodal and myocardial cells. Coupling through Gs protein activates adenylyl cyclase to increase cAMP

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6
Q

How does sympathetic system affect heart rate?

A

Increase heart rate (positive chronotropic effect) – mediated by SA node and due to (i) an increase in the slope of phase 4 depolarization (‘the pacemaker potential’) caused by enhanced If and ICa, (ii) reduction in the threshold for AP initiation caused by enhanced ICa

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7
Q

How does sympathetic system affect stroke volume?

A

Increase contractility (positive inotropic response) – due to (i) increase in phase 2 of the cardiac action potential in atrial and ventricular myocytes and enhanced Ca2+ influx and (ii) sensitisation of contractile proteins to Ca2+

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8
Q

How does sympathetic system affect AV nodal delay?

A

Increase conduction velocity in AV node (positive dromotropic response) – due to enhancement of If and ICa

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9
Q

How does sympathetic system affect duration of systole?

A

Decrease duration of systole (positive lusitropic action) – due to increased uptake of Ca2+ into the sarcoplasmic reticulum

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10
Q

What receptors are activated by M2 muscarinic cholinoceptors?

A

Acetylcholine (post-ganglionic transmitter) – activates M2 muscarinic cholinoceptors, largely in nodal cells. Coupling through Gi protein: (i) decreases activity of adenylate cyclase and reduces [cAMP]I and (ii) opens potassium channels (GIRK) to cause hyperpolarization of SA node (mediated by Gi βγ subunits)

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11
Q

Ivabradine in Angina

A

Ivabradine is a selective blocker of HCN channels that is used to slow heart rate (HR) in angina (a condition in which coronary artery disease (CAD) reduces the blood supply to cardiac muscle). Slower HR reduces O2 consumption

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12
Q

Muscular contraction

A

Ventricular action potential
Opening of voltage-activated Ca2+ channels (L-type) during phase 2 of action potential
Ca2+ influx into cytoplasm
Ca2+ release from the sarcoplasmic reticulum (Calcium-Induced Calcium Release – CICR). Caused by Ca2+ activating the ryanodine type 2 channel (RyR2)
Ca2+ binds to troponin C and shifts tropomyosin out of the actin cleft
Cross bridge formation between actin and myosin resulting in contraction via the sliding filament mechanism

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13
Q

Muscular relaxation

A

Repolarization in phase 3 to phase 4
Voltage-activated L-type Ca2+ channels close
Ca2+ influx ceases. Ca2+ efflux occurs by the Na+/Ca2+ exchanger 1 (NCX1)
Ca2+ release from the sarcoplasmic reticulum ceases. Active sequestration via Ca2+-ATPase (SERCA) of Ca2+ from the cytoplasm now dominates
Ca2+ dissociates from troponin C
Cross bridges between actin and myosin break resulting in relaxation

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14
Q

Agonists of Beta-Adrenoceptor ligand upon the heart

A

Dobutamine, Adrenaline and Noradrenaline

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15
Q

Pharmacodynamic effects of the agonists of Beta-Adrenoceptor ligand upon the heart

A

Increase force, rate and cardiac output (i.e. HR x SV) and O2 consumption
Decrease cardiac efficiency (O2 consumption increases more than cardiac work)
Can cause disturbances in cardiac rhythm (arrhythmias)

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16
Q

How is Adrenaline generally delivered?

A

Intramuscular unless there’s cardiac arrest along with shock, then intravenously

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17
Q

Effect of Adrenaline on the heart?

A

Alpha and Beta agonist
Positive inotropic and chronotropic actions (β1)
Redistribution of blood flow to the heart (constricts blood vessels in the skin, mucosa and abdomen (α1))
Dilation of coronary arteries (β2)

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18
Q

Which drug causes the least tachycardia among Beta1 agonists?

A

Dobutamine given intravenously
Given for acute, but potentially reversible, heart failure (e.g. following cardiac surgery, or cardiogenic, or septic, shock)

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19
Q

Examples of non-selective beta-adrenoceptors blockers

A

Propranalol

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20
Q

Examples of selective beta-adrenoceptors blockers

A

Atenolol, Bisoprolol, Metoprolol

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21
Q

Examples of non-selective and beta-adrenoceptors and partial agonists

A

Alprenolol

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22
Q

Pharmacodynamic effects of non-selective blockers

A

No effect on HR, SV, CO or MAP at rest

Significantly depressed during exercise or stress

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23
Q

Clinical uses of Beta-adrenoceptor antagonists

A

Treatment of disturbances of cardiac rhythm (arrhythmias) - decrease excessive sympathetic drive and help restore normal sinus rhythm
Treatment angina - First line as an alternative to calcium entry blockers
Treatment of heart failure (compensated) - low-dose β-blockers improve morbidity and mortality, presumably by reducing excessive sympathetic drive (Carvedilol)
Treatment of hypertension (HT) - No longer first-line unless co-morbidities (e.g. angina) are present

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24
Q

When are beta-adrenoceptor antagonists prescribed for hypertension?

A

No longer first-line unless co-morbidities (e.g. angina) are present

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25
Q

What can be used as an alternative to Calcium entry blockers?

A

Beta-Adrenoceptor antagonists

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26
Q

Drug used in treatment of compensated heart failure

A

Carvedilol - By reducing excess sympathetic drive. Also is a additional α1 antagonist activity causing vasodilation

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27
Q

What should not be prescribed for asthmatic patients with cardiac issues?

A

Beta-blockers best avoided in asthmatic subjects

28
Q

Adverse effects of Beta-blockers

A

Bronchospasms
Aggravation of cardiac failure (patients with heart disease may rely on sympathetic drive to maintain an adequate CO) – but low dose beta-blockers are used in compensated heart failure
Bradycardia
Hypoglycaemia (in patients with poorly controlled diabetes – the release of glucose from the liver is controlled by beta2-adrenoceptors).
Fatigue – CO (β1) and skeletal muscle perfusion (β2) in exercise are regulated by adrenoceptors
Cold extremities – loss of beta2-adrenoceptor mediated vasodilatation in cutaneous vessels

29
Q

Effects of Atropine

A

It is a non-selective Muscarinic ACh receptor antagonist
Increase in HR in normal subjects (at all but low doses) – more pronounced effect in highly trained athletes (who have increased vagal tone)
No effect upon arterial BP (resistance vessels lack a parasympathetic innervation)
No effect upon the response to exercise

30
Q

Clinical use of Atropine

A

First line in management of severe, or symptomatic bradycardia, particularly following myocardial infarction (in which vagal tone is elevated). In MI given IV (with caution) in incremental doses
In anticholinesterase poisoning

31
Q

Why is the recommended dose of Atropine 300-600mg

A

Some practitioners recommend no less than 600 micrograms as low-dose atropine may paradoxically transiently slow heart rate

32
Q

Alternative to Atropine?

A

Glycopyrronium

33
Q

Examples of Inotropic drugs

A

Digoxin, Dobutamine

34
Q

How does Digoxin function?

A

Digoxin functions by blocking the Na/K ATPase. This leads to increase storage of Calcium in the Sarcoplasmic Reticulum, causing in increase in Calcium Induced Calcium Release and contraction

35
Q

Clinical use of Digoxin

A

IV in acute heart failure, or orally in chronic heart failure, in patients remaining symptomatic despite optimal use of other drugs (e.g. ACE inhibitors, diuretics)
Heart failure with atrial fibrillation (AF)

36
Q

Side effects of Digoxin

A 
excessive depression of AV node conduction (heart block)
propensity to cause arrhythmias
nausea
vomiting
diarrhoea
disturbances of colour vision
37
Q

How does Levosimendan work?

A

Binds to troponin C in cardiac muscle sensitizing it to the action of Ca2+

38
Q

Effects of Levosimendan

A

Additionally opens KATP channels in vascular smooth muscle causing vasodilation (reduces afterload and cardiac work)
Relatively new agent, used in treatment of acute decompensated heart failure (IV)

39
Q

Last resort Inotrophic drugs

A

Amrinone and Milrinone
Inhibit phosphodiesterase (PDE) in cardiac and smooth muscle cells and hence increase [cAMP]
Increase myocardial contractility, decrease peripheral resistance (haemodynamic indices are improved), but worsen survival – perhaps due to increased incidence of arrhythmias
Use limited to IV administration in acute heart failure

40
Q

General action of anti-arrhythmatic drugs

A

Anti-arrhythmic drugs generally inhibit specific ion channels with the intention of suppressing abnormal electrical activity

41
Q

What is the Vaughn William classification

A

Anti-arrhythmic drugs are classified pharmacologically based upon their effects upon the cardiac action potential. Classified as Class I (Ia, Ib, Ic), II, III, IV. Some drugs do not fit in to the Vaughn Williams classification (e.g. adenosine, digoxin)

42
Q

What do Class I drugs target

A

Voltage activated Na channels

43
Q

What do Class II drugs target

A

Beta-adrenoceptor antagonist

44
Q

What do Class III drugs target

A

Voltage activated K channels

45
Q

What do Class IV drugs target

A

Voltage activated Ca channels

46
Q

Action of Class Ia drugs

A

Associate with and dissociate from Na+ channels at a moderate rate. Slow rate of rise of AP and prolong refractory period; Disopyramide

47
Q

Action of Class Ib drugs

A

Associate with and dissociate from Na+ channels at a rapid rate. Prevent premature beats, Lignocaine

48
Q

Action of Class Ic drugs

A

Associate with and dissociate from Na+ channels at a slow rate. Depress conduction; Flecainide

49
Q

Action of Class II drugs

A

Decrease rate of depolarization in SA and AV nodes; Metoprolol

50
Q

Action of Class III drugs

A

Prolong AP duration increasing refractory period; Amiodarone

51
Q

Action of Class IV drugs

A

Slow conduction in SA and AV nodes. Decrease force of cardiac contraction; Verapamil

52
Q

What state do Class I drugs preferentially bind to

A

Collectively the higher affinity of Na+ channel blockers for the open and inactivated states of the channel allows them to act preferentially on ischaemic tissue and block an arrhythmogenic focus at it source

53
Q

What happens to Class I drugs when heart rate increases

A

If heart rate increases, less time is available for unblocking (dissociation) and more time available for blocking (association). Steady state block increases, particularly for agents with slow dissociation rates

54
Q

What is paroxysmal supraventricular tachycardia?

A

Atrial firing of 14-250 beats per minute

55
Q

Types of Lipoprotein

A

HDL particles (apoA1 and apoA2)
LDL particles (apoB-100)
Very-low density lipoprotein (VLDL) - apoB-100
Chylomicrons (apoB-48)

56
Q

Where are apoB100 containing lipoproteins assembled

A

Liver - Hepatocytes

57
Q

Where are apoB48 containing lipoproteins assembled

A

Intestines - Enterocytes

58
Q

Main targets of triglyceride delivery by vLDL and Chylomicrons

A

Adipose and muscle tissue

59
Q

How are Chylomicron and vLDL particles activated

A

Chylomicrons and VLDL particles must be activated by the transfer of apoCII from HDL particles

60
Q

Function of apoCII

A

ApoCII facilitates binding of chylomicrons and VLDL particles to LPL; Lipoprotein lipase – lipolytic enzyme associated with the endothelium of capillaries in adipose and muscle tissue

61
Q

What are Chylomicron and vLDL remnants

A

Particles depleted of triglycerides (but still containing cholesteryl esters) are termed chylomicron and VLDL remnants

62
Q

Clearance of apoB-containing lipoproteins

A

Lipoprotein lipase causes chylomicrons and VLDL particles to become relatively enriched in cholesterol due to triglyceride metabolism
Chylomicrons and VLDL dissociate from LPL
ApoCII is transferred to HDL particles in exchange for apoE which is a high affinity ligand for receptor mediated clearance. Particles are now remnants
Remnants return to the liver and are further metabolised by hepatic lipase
All apoB48-containing remnants and 50% of apo100 containing-remnants are cleared by receptor-mediated endocytosis into hepatocytes
Remaining apoB100-containing remnants loose further triglyceride through hepatic lipase, become smaller and enriched in cholesteryl ester and via intermediate density lipoproteins (IDL) become LDL particles lacking apoE and retaining solely apoB100

63
Q

What is the rate limiting enzyme in de novo synthesis of cholesterol?

A

HMG-CoA reductase

64
Q

What is reverse cholesterol transport?

A

Mature HDL accepts excess cholesterol from the plasma membrane of cells (e.g. macrophages) and delivers cholesterol to the liver, known as reverse cholesterol transport

65
Q

How is cholesterol transferred from HDL to LDL

A

In the plasma of hepatocytes, cholesterol ester transfer protein (CETP) mediates transfer of cholesteryl esters from HDL to VLDL and LDL, indirectly returning cholesterol to the liver

66
Q

What drug is more effective than Aspirin in vascular patients on lipid-lowering drugs?

A

Clopidogrel

Cardiology (11 decks)

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