Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

CV System - Alex's Cards (ESA2) > Session 4 Lectures > Flashcards

Session 4 Lectures Flashcards

(69 cards)

Start Studying
1
Q

What sets the resting membrane potential in cardiac myocytes?

A

Potassium permeability

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

What is the intra and extracellular concentration of potassium in a cardiac myocyte?

A

4mmol extracellular

140mmol intracellular

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

Does resting membrane potential reach potassium equilibrium in a cardiac myocyte? (Ek)

A

No not quite
Ek = around -95mv and RMP = -85mv
This is because there is small permeability to other ions at rest

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

What ion generates contraction?

A

Calcium ions

Need for actin and myosin interaction

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

What is another term for the cardiac action potential?

A

The ventricular action potential

These are action potentials generated in non-nodal cells eg purkinje fibres

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

In ventricular action potentials - what stage number is rest and which is the plateau phase?

A

Rest = stage 4
Plateau phase = stage 2

Upstroke (depolarisation) = stage 0
Start of repolarisation = stage 1
Plateau phase = stage 2
Repolarisation = stage 3

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

What happens to VG sodium channels after opening?

When can they re-open?

A

They inactivate

When at negative membrane potential they close again and can be reopened

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

How long does diastole last compared to systole?

A

Diastole is 2/3 of time

Systole is 1/3 of time

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

What are the x and y axis when labelling the ventricular action potential?

A

x axis = Time (ms)

y axis = Membrane potential (Mv)

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

In cardiac action potential what causes upstroke?

A

Opening of VG Na+ channels (fast acting) and influx of Na+

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

What causes the plateau phase?

A

Opening of VG Ca2+ channels (Ca2+ influx) and K+ channels also being open (K+ efflux)
They are balanced so plateau

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

Do cardiac myocytes have more than one type of K+ channel?

A

Yes

Don’t need to know them all yet

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

What is another term for the pacemaker action potential?

A

The SA node action potential

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

What is unusual about the pacemaker cells?

A

They never sit at rest and spontaneously depolarise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the difference between HCN channels and VG Na+ channels?

A

HCN channels = cause gradual depolarisation of pacemaker cells (in SA node)
They are slow opening Na+ channels

VG Na+ channels = generate action potential in cardiac cells (ventricular action potential)
They are fast opening Na+ channels

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

What is the pacemaker potential?

A

Gradual opening of HCN channels (funny current) and gradual influx of Na+

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

What is the membrane potential in the SA node?

What is the resting membrane potential?

A

Membrane potential around -60mV

There is no resting membrane potential - the cells are never at rest

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

What drives the action potential in the SA node?

A

Opening of L type VG calcium channels

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

What membrane potential do VG Na+ channels need to reach before opening/activated?

A

Membrane potentials that are more negative than -50m/v

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

What does HCN channels stand for?

A

Hyperpolarisation-activated, Cyclic Nucleotide-Gated channels

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

Are the cells in the AV node the name as the SA node?

A

Yes they also spontaneously depolarise and have no resting membrane potential
However the SA node depolarises quicker - this is why it sets the rhythm

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

What is bradycardia?

A

When action potentials fire too slowly (decreased heart rate)

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

What is asystole?

A

When action potentials fail to fire - no heart beat

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

What is tachycardia?

A

When action potentials fire too quickly (increased heart rate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What happens if electrical activity becomes random?
You get fibrillation
26
What is the normal range for K+ plasma concentration?
3.5-5.5 mmol
27
What is hypokalaemia?
Low potassium plasma concentration (less than 3.5 mmol)
28
What is hyperkalaemia?
A high K+ plasma concentration | Over 5.5 mmol
29
What is the effect on membrane potential in hyperkalaemia?
The membrane potential becomes less negative - depolarises slightly
30
Why does hyperkalaemia slow the upstroke of the action potential? (2 reasons)
1. Increased extracellular K+ = membrane potential slightly depolarised (less negative) You reduce the driving force for K+ efflux 2. Some of the VG Na+ channels are inactivated which also slows upstroke
31
What K+ plasma concentration is severe hyperkalaemia?
Over 6.5 mmol | Normal = 3.5-5.5mmol
32
What are two possible treatments for hyperkalaemia?
Calcium gluconate - this makes the heart less excitable | Give insulin and glucose - promotes K+ moving into cells
33
Explain why hypokalaemia leads to a lengthened action potential and delays in depolarisation
Hypokalaemia = decreased extracellular K+ levels Means there is an increased concentration gradient K+ slower to move back into the cell and repolarise L-type Ca+ channels also work best at negative membrane potential so remain open for longer
34
What can a longer action potential lead to?
Early after depolarisations | This can lead to oscillations in membrane potential and ventricular fibrillation
35
In a cardiac myocyte, what % of calcium for contraction is received extracellularly?
25% across the plasma membrane | 75% of the calcium comes from the sarcoplasmic reticulum (via CICR - ryanodine receptors)
36
What does Ca2+ bind to in order for contraction to occur?
It binds to troponin C -Troponin complex sits on top of tropomyosin and winds around the actin filament When calcium binds it causes a conformational change - tropomyosin is moved out the way to allow myosin to bind at the binding site on the actin filament
37
What does most the Ca2+ go during relaxation of cardiac myocytes?
Into the sacroplasmic reticulum via SERCA
38
In the vascular system where is the smooth muscle and which vessel has the most?
In the tunica media layer of blood vessels | Arterioles have the most
39
In vascular smooth muscular cells - what 2 ways can Ca2+ levels be increased?
1. Depolarisation of VG Ca2+ channels | 2. Noradrenaline or adrenaline activating alpha 1 q (GPCR) resulting in IP3 acting on IP3R and SR Ca2+ release
40
In vascular smooth muscle cells - what does Ca2+ bind to and what does this do?
It binds to calmodulin Calmodulin activates MLCK (myosin light chain kinase) which phosphorylates the light chain on the myosin head - allowing myosin to bind with actin
41
What enzyme in smooth muscle cells inactivates the acting of myosin on actin (contraction)?
Myosin light chain phosphatase
42
Can myosin light chain kinase be phosphorylated itself? What happens when it is?
Yes it can | When this happens it inhibits its ability to phosphorylate the myosin light chain and inhibits contraction
43
What can phosphorylate myosin light chain kinase to inhibit contraction?
Protein kinase C
44
What is a nicotinic receptor?
A ligand gated ion channels All pre-ganglionic receptors are nicotinic Most post-ganglionic receptors of sympathetic nervous system are nicotinic
45
Give a location where Ach is used as a post-ganglionic neurotransmitter rather than NA (in sympathetic nervous system)
Sweat glands
46
What are the 2 divisions of the autonomic nervous system &a where do their pre-ganglionic roots emerge from?
1. Sympathetic (sacral and cranial) | 2. Parasympathetic (lumbar and thoracic)
47
For sympathetic and parasympathetic nervous system - which receptors affect pupil of eye and what do they do?
Sympathetic = a1 receptor Dilates the pupil Parasympathetic = m3 receptor Constricts the pupil
48
For sympathetic and parasympathetic nervous system - which receptors affect lungs and what do they do?
Sympathetic = b2 receptor Relaxes lungs Parasympathetic = m3 receptor Constracts lungs
49
For sympathetic and parasympathetic nervous system - which receptors affect heart and what do they do?
Sympathetic = b1 Increased rate and force of contraction Parasympathetic = m2 Decreased rate and force of contraction
50
For sympathetic and parasympathetic nervous system - which receptors affect sweat glands and what do they do?
Sympathetic = a1 Localised secretion Parasympathetic = m3 Generalised secretion
51
What happens if you denervate the heart?
It will continue beating - as the pacemaker cells spontaneously depolarise The heart will beat more quickly as it is usually under vagal control (of parasympathetic nervous system)
52
What are the postganglionic receptors of parasympathetic nervous system and what do they do?
M2 receptors | Decreases heart rate and decreases speed of AV node conduction
53
Where are the main sites of parasympathetic innervation in the heart? (postganglionic cells?)
The SA and AV node
54
Where do the preganglionic fibres of parasympathetic nervous system in heart come from?
The 10th cranial nerve - the vagus nerve
55
Where are the majority of sympathetic postganglionic cells in the heart?
In the SA node, AV node or myocardium (muscular tissue of heart)
56
Where the CV control centre located?
Within the medulla oblongata of the brain stem
57
What are baroreceptors? Where are they located?
They measure the arterial blood pressure | In carotid sinus and arch of aorta
58
How does NA increase force of contraction?
NA acts on B1 receptors which cause an increase in cyclic AMP - activating PKA This leads to phosphorylation of Ca2+ channels and increased entry of Ca2+ during plateau phase There is an increased uptake of Ca2+ in SR and increased sensitivity of contractile machinery to Ca2+
59
What receptors do most arteries and veins have - are they innervated by sympathetic or parasympathetic nervous system?
Most have a1 receptors (some also have b2) | Most vessels therefore receive sympathetic innervation
60
What does the vasomotor tone allow?
Vasodilation of vasoconstriction depending on level of sympathetic output
61
Where might you find blood vessels with a1 and b1 receptors?
Liver Skeletal muscle Myocardium
62
At physiological concentration which receptor in vasculature will adrenaline prefer to bind to?
b2 - they are more sensitive to adrenaline than a1 which is in all vessels
63
What neurotransmitter binds to a1 receptors in vasculature?
Noradrenaline At very high concentrations adrenaline will also bind here (but it prefers to bind to b1 receptors at physiological concentration)
64
Activating b1 receptors on smooth muscle vasculature causes what?
Vasodilation B2 = Ga (s) GPCR Causes increases in cAMP - activates PKA which opens potassium channels and inhibits MLCK needed for contraction (so relaxation occurs)
65
Activating a1 receptors on smooth muscle vasculature causes what?
``` Vasodilation A1 = Ga(q) GPCR Stimulates IP3 production Acts on IP3R on SR increase in Ca2+ release from stores = contraction of muscle ```
66
What causes the largest vasoconstriction effect of smooth muscle vasculature?
Increase in local metabolites eg K+, H+ and CO2
67
What type of nerves control input to medulla oblongata?
Afferent nerves
68
What do sympathimimetic drugs do?
Mimic the sympathetic nervous system e.g. alpha or beta adrenoreceptor agonist
69
Give a few examples of alpha and beta adrenoreceptor antagonist drugs
1. Prazosin (for hypertension) - A1 2. Propanolol (slows HR and force of contraction but also acts on bronchial smooth muscle to cause vasoconstriction) - non selective B1/2 3. Atenolol (slows HR and force of contraction) - B1

CV System - Alex's Cards (ESA2) (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions