Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Study Notes - Cardiology > *Pharmacology 1 (lecture 1) > Flashcards

*Pharmacology 1 (lecture 1) Flashcards

1
Q

What causes phase 4 of the action potential in nodal tissue of the heart?

A

Increased Na+ influx

Decreased K+ efflux

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What causes phase 0 of the action potential in nodal tissue of the heart?

A

Increased Ca2+ influx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What causes phase 3 of the action potential in nodal tissue?

A

Increased K+ efflux

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What transmits Na and K movement during phase 4?

What switches this on? (nodal tissue)

A

The funny current - Hyperpolarisation-activated and cyclic nucleotide gated channels (HCN channels)
Hyperpolarisaiton (Very negative)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What causes stage 3 of the action potential in nodal tissue?

A

Repolarisation caused by K+ efflux (delated rectifier potassium channel)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What causes phase 0 of the action potential in cardiac myocytes?

A

Fast Na+ influx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What causes phase 1 of the action potential in cardiac myocytes?

A

Transient K+ efflux

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What causes phase 2 of the action potential in cardiac myocytes?

A

Ca2+ influx, also a small bit of Na+ influx and NCX1 operating in reverse direction (Normally brings 3 Na in and expels 1 Ca but now brings 1 Ca in and pumps 3 Na out)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What causes phase 3 of the action potential in cardiac myocytes?

A

K+ efflux

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the difference between noradrenaline and adrenaline?

A

Noradrenaline is a post-ganglionic neurotransmitter where as adrenaline is a hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

In terms of the sympathetic system on the heart, what receptor is stimulated and where are these located?

A

B1 adrenoceptor
Nodal cells
Myocardial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What protein does B1 adrenoceptors use and what enzyme is activated?

A

Gs proteins

adenylyl cyclase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does adenylyl cyclase do? (B1 adrenoceptor)

A

Converts ATP to cAMP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What does activation of B1 adrenoceptors cause? (8)

A 
Increased heart rate
Increased contractility
Increased conduction velocity in AV node
Increased automaticity
Decreased duration of systole
Decrease in cardiac efficiency
Increased activity of the Na+/K+/ATPase
Increased mass of cardiac muscle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What causes an increased heart rate due to sympathetic stimulation? (2)

A

Mediated by the SA node and due to an increase in the slope of phase 4 depolarisation (caused by enhanced If and Ica) and reduction in the threshold for AP initiation caused by enhanced Ica

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What causes the positive inotropic effect due to sympathetic stimulation?

A

Increase in phase 2 of the cardiac action potential in atrial ad ventricular mycoses and enhanced Ca2+ influx and sensitisation of contractile proteins to Ca2+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What cause an increased conduction velocity in the heart?

A

Enhancement of If and Ica

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Why is increased activity of the Na+/K+ATPase important in sympathetic stimulation of the heart?

A

For depolarisation and restoration of function following generalised myocardial depolarisaiton

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What happens to the stroke volume due to sympathetic stimulation?

A

It increases along with contractility (Frank-starling curve)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What receptor does the parasympathetic system controlling the heart stimulate?
G protein?
What effect does this have on what enzyme?
What other effect does it have?

A

M2 muscarinic cholinoceptors mainly in nodal cells
Through Gi
Decreases activity of adenylyl cyclase
Opens potassium channels (GIRK) to cause hyper-polarisation of SA node (mediated by Gi B gamma subunits)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What effects does parasympathetic stimulation have on the heart? (3)

A

Decreased heart rate
Decreased contractility
Decreased conduction in AV node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What 3 factors cause the decreased heart rate due to parasympathetic stimulation?

A

Decreased slope of pacemaker potential due to a reduction in the funny current
Opening of GIRK = hyper polarisation
Increase in threshold for AP due to reduced ICa2+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Where does decreased contractility due to para. stimulation effect?

A

Atria only

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What causes decrease contractility due to para. stimulation?

A

Decrease in phase 2 of action potential and decrease in Ca2+ entry

25
Q

How can parasympathetic stimulation predispose to arrhythmias?

A

Predisposes to arrhythmias in the artier as AP duration is reduced ad correspondingly the refractory period (predisposes to re-enterant arrhythmias)

26
Q

What can vagal manoeuvres be attempted to treat?

A

Atrial tachycardia - increases parasympathetic output therefore suppressing impulse conduction through the AV node

27
Q

2 typesof vagal manouvres and what they do?

A

Valsalva manoeuvre - activate aortic baroreceptors by breathing techniques
Massage of bifurcation of the carotid artery to stimulate baroreceptors in the carotid sinus

28
Q

What activates HCN channels (the funny current)?

A

Hyperpolarisaiton

cAMP

29
Q

How does Ivabradine work?

What is it used to treat?

A

It is a selective blocker of HCN channels meaning it slows heart rate by decreasing the slope of the pacemaker potential
Angina - by slowing the heart, O2 consumption is reduced

30
Q

how many different types of HCN channels are there?

what is the most common type in the heart?

A

4

HCN4

31
Q

What is the process by which cardiac smooth muscle contracts?

A

During Phase 2 of ventricular AP, opening of voltage-activated Ca2+ channels occurs
This causes Ca2+ influx that causes Ca2+ induced Ca2+ release from the sacroplasmic reitculum
This causes cross bridges between actin and myosin due to Ca2+ binding to troponin

32
Q

What is the process by which cardiac smooth muscle relaxes?

A

Repolarisation in phase 3 to phase 4 causes voltage activated Ca2+ channels to close
Ca2+ influx ceases and ca2+ efflux occurs by NCX1
Ca2+ dissociates from troponin = cross bridges break

33
Q

How does B1-adrenoceptor activation modulate cardiac contractility`/

A

It activates adenylyl cyclase which converts ATP to cAMP
cAMP activates PKA which phosphorylates the voltage phosphorylate the voltage activated Ca2+ channels causing them to be open for longer, it also increases the sensitivity of the cotnractile proteins making them more sensitive to Ca2+
It also phosphorylates the phospholamban on tCa2+ATPase meaning that it pumps Ca2+ back into the sarcoplasmic reticulum quicker meaning the heart relaxes quicker
(activation of M2 blocks these effects)

34
Q

What are examples of B-adrenoceptor agonists for the heart? (3)

A

Dobutamine
Adrenaline
Noradrenaline

35
Q

What effect do B-adrenoceptor agonists have on the heart?

A

They increase its force, rate and cardiac output (+ O2 consumption)

36
Q

What are 2 disadvantages of B-adrenoceptor agonists?

A

They decrease cardiac efficiency

They can cause arrhythmias

37
Q

Clinical uses of adrenaline (B-adrenoceptor) on the heart?

A

Used during cardiac arrest and anaphylactic shock to redistribute blood to the heart and for its positive inotropic and chronotropic effect

38
Q

Use of dobutamine (B-adrenoceptor) on the heart?

A

on acute but potentially reversible heart failure e.g. following cardiac surgery or septic shock

39
Q

What is an example of a non-selective b-adrenoceptor?

A

Propranolol

40
Q

What is an example of a selective B1-adrenoceptor?

A

Atenolol, bisoprolol, metoprolol

41
Q

What does the effect o B-adrenoceptor blockade depend upon?

A

The degree to which the sympathetic nervous system is activated

42
Q

What effect do B-adrenoceptors have?

A

Little or no effect at rest but during exercise rate, force and CO are greatly depressed

43
Q

Clinical uses of B-adrenoceptors?

A

Treatment of arrhythmias related to excessive sympathetic activity (MI, heart failure)
AF and SVT (b-blockers delay conduction through the AV node)
Angina
Compensated heart failure
Hypertension (no longer first line unless co-morbidities are present)

44
Q

What is a B-adrenoceptor that has additional alpha 1 antagonist activity that is used to treat heart failure?

A

Carvedilol

45
Q

Adverse effects of B-blockers?

A 
Bronchospasm
Aggravation of cardiac failure 
Bradycardia
Hypoglycaemia (release of glucose from the liver is controlled by B2-adrenoceptors)
Fatigue
Cold peripheries
46
Q

Example of a non-selective muscarinic ACh receptor antagonist?
What does this do?

A

Atropine
Increases the HR in normal subjects (no effect on BP as resistance vessels lack a parasympathetic innervation, no effect upon response to exercise)

47
Q

Clinical use of atropine?

A

First line in management of severe, or symptomatic bradycardia, particularly following MI

48
Q

What is the origin of digoxin?

A

Foxglove components

49
Q

What effect does digoxin have on the heart?

A

Increases contractility of the heart
Slows SA node discharge
Slows AV node conduction

50
Q

What is digoxin used to treat?

A

IV in acute heart failure and oral in chronic heart failure when optimal use of other drugs fails to control symptoms (particularly indicated if AF is also present)
AF

51
Q

How does dioxin work?

A

It blocks the Na+K+ATPase therefore increasing the intracellular concentration of Ca2+ which binds to the sarcoplasmic reticulum causing increased contractility
It also increases vagal activity causing a slowing of the SA node discharge and AV node conduction increasing refractory time

52
Q

What ion change is particularly dangerous with digoxin?

A

Hypokalaemia

53
Q

Unwanted effects of digoxin?

A 
Excessive depression of AV node conduction = heart block
Can cause arrhythmias
Nausea/ vomiting
Diarrhoea
Disturbances in colour vision
54
Q

What is a calcium-sensitiser drug?

A

Levosimendan (calcium-sensitisers)

55
Q

How does levosimendan work?

A

It binds to troponin C in cardiac muscle sensitising it to the action of Ca2+
Additionally opens ATP channels in vascular smooth muscle causing vasodilation (reduces afterload and therefore cardiac work)

56
Q

What is levosimendan used to treat?

A

Acute decompensated heart failure (IV)

57
Q

Aside from digoxin and levosimendan, what is another 2 examples of inotropic drugs?

A

Amrinone and milirinone (inodilators)

58
Q

How does amrinone and milirinone work?

A

Inhibit phosphodiesterase (PDE) in cardiac and smotth muscle cells and hence increases [cAMP]i - increases myocardial contractility, decreases peripheral resistance but worsens survival (perhaps due to incidence of arrhythmias)

59
Q

What is amrinone and milirinone used to treat?

A

Acute heart failure (IV)

Study Notes - Cardiology (25 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions