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ESA 2: Cardiovascular > Cardiovascular: Session 4 > Flashcards

Cardiovascular: Session 4 Flashcards

1
Q

What range does the resting membrane potential lie in?(ventricle)

A

-90 to -85 mv

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2
Q

Why isn’t the membrane potential equal to the Ek of potassium which dominate the resting membrane potential?

A

The membrane is slightly permeable to other ions.

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3
Q

How long does the action potential of a cardiac muscle cell last?

A

280 ms

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4
Q

What is the sequence for a ventricular action potential occur?

A
  • Opening of the voltage gated Na+ channels and influx of sodium ions
  • Transient K+ ions channels open and potassium ion efflux occurs
  • Opening of voltage gated calcium channels
  • Calcium channels inactivate and Voltage gated K+ channels open.
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5
Q

What is the consequence of an action potential firing too slowly?

A

Bradycardia

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6
Q

What is the consequence of action potential firing too quickly?

A

Tachycardia

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7
Q

What is it called when an action potential fails to fire?

A

Asystole

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8
Q

What is it called when electrical activity in the heart becomes random?

A

Fibrillation

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9
Q

What is the resting membrane potential for sino-atrial node?

A

It in fact has no proper resting membrane potential. They spontaneously activate.

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10
Q

Which ions are HCN channels permeable to?

A

K+ and Na+ ions.

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11
Q

What is the effect of hyperpolarisation on the HCN channels?

A

The more negative the membrane potential, the more of the HCN channels activate.

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12
Q

What is the initial slow depolarisation called?

A

Pacemaker potential

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13
Q

What is the upstroke due to in a Sino-atrial node action potential?

A

The opening of voltage gated calcium channels and influx of calcium ions

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14
Q

What is the down stroke due to in a Sino atrial node action potential?

A

Potassium channel opening and efflux of potassium ions

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15
Q

What is the function of the HCN channels in the Sino atrial node?

A

This allows the influx of Na+ ions which depolarises the cells.

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16
Q

What is the function of the SA node?

A

It acts as the pacemaker for the heart by setting the rhythm of the heart beat as it is the fastest to depolarise.

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17
Q

What is the normal range that plasma K+ concentration lies in?

A

3.5-5.5 mmol/L

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18
Q

What is hyperkalaemia and what are the effects (consider the graph) ?

A

When plasma K+ concentration is too high so greater than 5.5 mmol/L. The membrane potential depolarises a bit and this can activate some of the voltage gated Na+ channels so upstroke is slowed.

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19
Q

What are the risk of hyperkalaemia?

A
  • The heart can stop

- May initially get an increase in excitability due to the membrane being depolarised slightly

20
Q

What are treatment of Hyperkalaemia?

A
  • Calcium Gluconate

- Insulin + Glucose

21
Q

What is hypokalaemia and what are the effects?

A

When plasma K+ concentration is too low so less than 3.5 mmol/L. The action potential lengthens as a result and the repolarisation is delayed.

22
Q

What are the risks of Hypokalaemia?

A

The longer action potential can lead to early after depolarisations so oscillations in the membrane potential. This can cause ventricular fibrillation.

23
Q

Where in vascular smooth muscle located?

A

Tunica media of arteries, arterioles and veins.

24
Q

What do kinases do?

A

They are involved in phosphorylation

25
What do phosphatases do?
They reverse the action of kinases. They de-phosphorylate.
26
What is the process of the contraction mechanism of vascular smooth muscle?
- Depolarisation open the Voltage gated calcium channels. - Influx of the calcium ions - Calcium ions are also released from sarcoplasmic reticulum when noradrenaline binds to alpha 1 receptors initiating secondary messengers IP3 and DAG through the cleavage of PIP2 by Phospholipase C. - Calcium ions bind to calmodulin which activates MLCK. - MLCK phosphorylates the myosin light chain to permit interaction with actin - Relaxation occurs when the Ca2+ levels decline and myosin light chain phosphatase dephosphorylates the myosin light chain
27
How can calcium levels be decreased in cells?
- Sodium-calcium exchanger - SERCA - PMCA
28
Why must myosin light chain be phosphorylated?
This allows binding to facilitate actin-myosin interaction..
29
What is the effect of phosphorylation of MLCK by PKA?
This inhibits the action of MLCK and therefore inhibits phosphorylation of the myosin light chain. This inhibits contraction.
30
What are the physiological functions of the Autonomic nervous system?
Regulates heart rate, body temperature, exocrine secretion, smooth muscle, rate and force of contraction., peripheral resistance, and amount of venoconstriction
31
Under what conditions are the divisions of the ANS more active?
- Sympathetic is more active under increased stress. (fight or flight) - Parasympathetic is more dominant under basal conditions (Rest and digest) - They both work together to maintain balance
32
The autonomic nervous system cannot initiate electrical activity? true/false
True. The autonomic nervous system controls the speed and force of contraction. A denervated heart would beat at a faster rate.
33
Where does the parasympathetic innervation of the heart originate from and where does it synapse at the heart?
- Originate from the Vagus nerve (10th cranial nerve) | - Synapse with post-ganglionic cells at the SA node and AV node
34
What do the post-ganglionic cells of the parasympathetic system release at the heart, what receptors are stimulated and the effect of this?
- Release of acetyl choline - Acts on M2 receptors - This decreases the heart rate - Decrease AV node conduction velocity
35
Where do the post-ganglionic fibres of the sympathetic input into the heart originate from and where do they innervate?
- The sympathetic trunk | - Innervation of SA node, AV node and myocardium
36
What is released from the post ganglionic fibres at the heart from sympathetic innervation, what does it act on and what is the effect?
- Noradrenaline is released - Acts mainly on the B1 adreno-receptors - Increases heart rate (+ve chonotropic effect) and increase force of contraction (+ve ionotropic effect)
37
What is the sympathetic effect of the ANS on pacemaker potential?
- Mediated by B1 receptors (G-protein coupled receptors) - Increases cAMP - Speeds up pacemaker potential
38
What is the parasympathetic effect of the ANS on. pacemaker potential?
- Mediated by the M2 receptors (G-protein coupled receptors) | - Increase in K+ conductance and decrease cAMP
39
How does Noradrenaline increase force of contraction?
- Noradrenaline acting on B1 receptors in myocardium causes an increase in cAMP so activates PKA - Increased phosphorylation of C2+ channels - Increased Ca2+ entry during the plateau of the action potential. - Increased uptake of Ca2+ in sarcoplasmic reticulum - Increased sensitivity of contractile machinery to Ca2+ - All lead to increased force of contraction
40
What GPCR are on most of the vessels? What do some vessels have as well?
Alpha 1 receptors adrenoreceptors. Some of the vessels have B2 receptors as well such as coronary and skeletal muscle vasculature.
41
How does vasomotor tone allow vasodilation to occur?
- Decreased sympathetic output allows for vasodilation | - Converse is true and Increased sympathetic output allows for vasoconstriction
42
What does noradrenaline released at the blood vessels at on?
-A1 adrenoreceptors
43
At physiological level what adrenoreceptor does circulating adrenaline have higher affinity with and what does it also activate at higher concentrations?
- B2 adrenoreceptor | - At higher concentrations can also activate the A1 adrenoreceptor
44
What is the effect of activating the B2 adrenoreceptor at the blood vessels?
- Increase cAMP - Activation of PKA so phosphorylation of the MLCK - Inhibition of MLCK - Opens potassium channels - Relaxation of smooth muscle - Vasodilation
45
What is the effect of A1 adrenoreceptors?
- Stimulates the IP3 production - Increase in Ca2+ from intracellular stores and via influx of extracellular Ca2+ - Contraction of smooth muscle - Vasoconstriction
46
What is the role of local metabolites?
They are more important for ensuring adequate perfusion of skeletal and coronary muscle than activation of B2 receptors. e.g. Adenosine, K+, H+, increase in PCO2
47
What are the drugs that act on the ANS?
- Sympathomimetics - alpha adrenoreceptor agonists - beta adrenoreceptor agonists -Adrenoreceptor Antagonists - Cholinergics - muscurinic agonists and antagonists

ESA 2: Cardiovascular (11 decks)

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