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CVS-Alaa > Excitation-contraction Coupling > Flashcards

Excitation-contraction Coupling Flashcards

1
Q

Which nerve parasympatheticaly innervates the heart?
where on the heart does it innervate?
What effect does it have on heart?

A
  • VAGUS 10th Cranial nerve
  • synapses with SA and AV node
  • post ganglionic cells release Ach
  • acts on M2 receptors

DECREASE Heart Rate
DECREASE AV node conduction velocity

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2
Q

describe how the resting membrane potential of cardiac cells is
generated

A
  • K+ PERMEBAILITY SETS THE RMP*
  • cardiac myocytes r more permeable to K
  • K+ ions leave the cell down their concentration gradient
  • this makes the inside negative
  • as charge builds up an electrical gradient is made.
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3
Q

draw the changes in membrane potential and describe the ionic currents underlying the cell AP of

(i) ventricular cells
(ii) pacemaker cells

A

P

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4
Q

describe the processes of excitation - contraction coupling in ventricular myocardial cells.

A

P

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5
Q

describe the factors influencing the changes in intracellular free Ca + concentration of ventricular cells during the AP

A

O

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6
Q

explain the effects of hyper and hypokalaemia on the heart

A

hyper > Increased extracellular K levels result in depolarization of the membrane potentials of cells, due to the increase in the Ek. This depolarization opens some voltage-gated sodium channels, but also INACTIVATES them at the same time.&raquo_space;SLOWER DEPOLARISATION UPSTROKE

Hypo > delays repolarization
LENGTHENS AP

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7
Q

describe the membrane potential changes in pacemaker cells associated with increases and decreases in heart rate.

A

P

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8
Q

detail the neurotransmitters and receptors involved in the

autonomic nervous system

A

O

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9
Q

explain the cellular mechanisms by which the autonomic nervous system controls

1) heart rate
2) force of contraction in the normal heart

A

O

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10
Q

describe the mechanisms which control contraction of vascular smooth muscle cells

A

O

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11
Q

explain the role of the ANS in controlling peripheral resistance

A

P

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12
Q

what r pacemaker cells?

A

specialised cells that generate an electrical event at regular intervals.
the AP

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13
Q

distinguish btw AP in Pacemaker cells & ventricular myocardial cells

A

,

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14
Q

what structure conducts excitation through the ventricular myocardiam?

A

purkunjee fibers

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15
Q

why is the cardiac AP much longer?

A

bc of the ‘plateu phase’ caused mainly by calcium

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16
Q

describe how RMP is made

A
  • K+ PERMEBAILITY SETS THE RMP*
  • cardiac myocytes r more permeable to K
  • K+ ions leave the cell down their concentration gradient
  • this makes the inside negative
  • as charge builds up an electrical gradient is made.
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17
Q

what channel is responsible for the upstroke of the AP in pacemaker cells?

A

L-type Ca channels!

*

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18
Q

*AT AN EQAULAIBREM OF AN ION, THE CONCENTRATION GRADIENT AND ELECTRICAL GRADIENT R THE SAME

A

reminder

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19
Q

describe what happens during platue phase

A

voltage-gated ca+ channels (L-type)&raquo_space;ca+ influx
FEW K channels&raquo_space; efflux

this balances the potential

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20
Q

what is the pacemaker potential?

A

refers to a LONG SLOW depolarization to threshold, its due to a ‘funny current’ which r made by channels called HCN

In SA and AV node

21
Q

what is meant by the “funny current?” what channels r responsible for it

A

during pacemaker potential, it spontaneously depolarises from its most negative value (-60mv) due to HCN channels (open due to hyper polarisation). this initial depolarisation is known as the funny current

22
Q

draw the SA node action potential, what shape does the graph give?

A
  • LONG depolarisation to threshold via HCN
  • upstroke via L-type voltage gated ca channels
  • downstroke opening of voltage-K channels
23
Q

what is a special feature about the SA node AP

A

they don’t ever sit at rest, they spontaneously depolarise, they don’t need neighbouring cells to activate them (3ala kayf umhum)

24
Q

what channels make the funny current?

A

HCN channels, influx of Na+ channels (SLOW sodium channels)

25
Q

special features of voltage channels

A

they activate as well as inactivates

26
Q

what is the difference btw the Na channels in pacemaker & and ventricular myocyte

A

Na+ channels in the pacemaker r HCN slow Na channels that make the funny current

Na+ channels in the ventricles r voltage-gated & r responsible for the upstroke depolarisation.

27
Q

what do HCN channels stand for? what do they do

A

Hyperpolarisation-activated Cylcic Nucleotide-gated channels.

allow INFLUX of Na channels which depolarises cell to threshold

28
Q

why is the AV node delayed?

A

to allow atria to finish contraction

29
Q

which has a higher conducting velocity, purkunjee or SA/AV node? why?

A

purkunjee, bc their cells r wider > less resistence, less cells involved and less membranes to cross, has FAST na channels which help in fast conduction.
BUT its depolarisation is slow than SA

30
Q

if AP failed to occur we have________

A

asystole

31
Q

what is normal K value in the blood|?

A

3.5-5.5 mmol/L

32
Q

values for hyperkalameia, hypokalmeia

A

hypokalmeia&raquo_space;»less than 3.5

hyperkalameia»»more than 5.5

33
Q

why r cardiac myoctyes so sensitive to changes in K+ levels?

A

bc their RMP is very close to the K equilibrium potential (Ek).
so any change in Ek, will effect the RMP

and they’ve got a lot of Potassium channels!

34
Q

risks of hyperkalemia and treatment and why

A
  • asystole > heart can stop> bc ur slowing conduction down (wayid ur inactivating na channels)
  • increase in excitability

TREATMENT

  • Ca gluconate> makes heart less excitable
  • Insulin & glucose> insulin promotes K to move into cells
  • b2 agonist > pushes K inside
35
Q

stages of hyperkalmeia

A

mild > 5.5-5.9 mmol/L
moderate> 6.0-6.4 mmol/L
Severe> 6.5 & more

36
Q

a patient wants to undergo an open heart surgery, what do we give him to temporarily stop the heart from pumping?

A

cardioplegic solution :

-high K solution used to bring the heart to asystole or heart paralysis.

37
Q

why in hypokalemia, is it dangerous that the AP in longer?

A

u leave it more prone to arrhythmias forming

leads to oscillations in MP > leading to ventricular fibrillation> Less CO

38
Q

excitation-contraction coupling & different receptors involved

A
  • depolarisation opens L-type Ca channels

- this ca will stimulate CICR channels (RyR) in the SR (theres a close link btw these 2 channels

39
Q

receptor involved in exitation-contraction

A

CICR
RyR
L-type volatage Ca channels

40
Q

describe regulation of cardiac myocyte contraction

hint: start with troponin

A

ca binds to troponin C
conformation change moves tropomyosin away from actin’s binding site
‘site exposed’
myosin head can now bind to actin

41
Q

during excitation contraction coupling, where did most of the calcium come from? how r these calciums taken back to normal levels again

A

SR STORES!!

pumped back in via SERCA

42
Q

which artery has the thickest smooth muscle wall?

A

arterioles

43
Q

excitation contraction coupling in vascular SMC and its regulation

A

2 ways :
via VGCC
via Gq recepters. (via a-adrenorecepter)

Ca+ comes in, binds with calmodulin, activates MLCK (myosin high chain kinase) which will phosphorylate the myosin light chain to allow interaction with actin.

DAG> PKC> MLCP> will dephosphorylate the myosin light chain leaving it inactive.

look at lecture for detailed pathways

44
Q

**Troponin C doesn’t have a role in SMC, what r ca bound to then?

A

CaM&raquo_space; calmodulin

45
Q

The cardiac action potential is very long, so over most of the heart a single action potential will produce a sustained contraction of the cell lasting about__________ms

A

200-300ms

46
Q
  • If action potentials fire too slowly →
  • If action potentials fail →
  • If action potentials fire too quickly →
  • If electrical activity becomes random →
A

bradycardia
asystole
Tachycardia
fibrillation

47
Q

what happens to all the calciums when its time for the cardiac myocytes to relax?

A

ca must return back to its resting levels

  • most pumped back in SR via (SERCA)
  • some exit across cell membrane via Ca Atpase & na/ca exchanger
48
Q

in which layer is most smooth muscle found?

tunica intima
media
adventita

A

Tunica media

CVS-Alaa (21 decks)

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