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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
Q

What do phosphatases do?

A

They reverse the action of kinases. They de-phosphorylate.

26
Q

What is the process of the contraction mechanism of vascular smooth muscle?

A
  • 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
Q

How can calcium levels be decreased in cells?

A
  • Sodium-calcium exchanger
  • SERCA
  • PMCA
28
Q

Why must myosin light chain be phosphorylated?

A

This allows binding to facilitate actin-myosin interaction..

29
Q

What is the effect of phosphorylation of MLCK by PKA?

A

This inhibits the action of MLCK and therefore inhibits phosphorylation of the myosin light chain. This inhibits contraction.

30
Q

What are the physiological functions of the Autonomic nervous system?

A

Regulates heart rate, body temperature, exocrine secretion, smooth muscle, rate and force of contraction., peripheral resistance, and amount of venoconstriction

31
Q

Under what conditions are the divisions of the ANS more active?

A
  • 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
Q

The autonomic nervous system cannot initiate electrical activity? true/false

A

True. The autonomic nervous system controls the speed and force of contraction. A denervated heart would beat at a faster rate.

33
Q

Where does the parasympathetic innervation of the heart originate from and where does it synapse at the heart?

A
  • Originate from the Vagus nerve (10th cranial nerve)

- Synapse with post-ganglionic cells at the SA node and AV node

34
Q

What do the post-ganglionic cells of the parasympathetic system release at the heart, what receptors are stimulated and the effect of this?

A
  • Release of acetyl choline
  • Acts on M2 receptors
  • This decreases the heart rate
  • Decrease AV node conduction velocity
35
Q

Where do the post-ganglionic fibres of the sympathetic input into the heart originate from and where do they innervate?

A
  • The sympathetic trunk

- Innervation of SA node, AV node and myocardium

36
Q

What is released from the post ganglionic fibres at the heart from sympathetic innervation, what does it act on and what is the effect?

A
  • 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
Q

What is the sympathetic effect of the ANS on pacemaker potential?

A
  • Mediated by B1 receptors (G-protein coupled receptors)
  • Increases cAMP
  • Speeds up pacemaker potential
38
Q

What is the parasympathetic effect of the ANS on. pacemaker potential?

A
  • Mediated by the M2 receptors (G-protein coupled receptors)

- Increase in K+ conductance and decrease cAMP

39
Q

How does Noradrenaline increase force of contraction?

A
  • 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
Q

What GPCR are on most of the vessels? What do some vessels have as well?

A

Alpha 1 receptors adrenoreceptors. Some of the vessels have B2 receptors as well such as coronary and skeletal muscle vasculature.

41
Q

How does vasomotor tone allow vasodilation to occur?

A
  • Decreased sympathetic output allows for vasodilation

- Converse is true and Increased sympathetic output allows for vasoconstriction

42
Q

What does noradrenaline released at the blood vessels at on?

A

-A1 adrenoreceptors

43
Q

At physiological level what adrenoreceptor does circulating adrenaline have higher affinity with and what does it also activate at higher concentrations?

A
  • B2 adrenoreceptor

- At higher concentrations can also activate the A1 adrenoreceptor

44
Q

What is the effect of activating the B2 adrenoreceptor at the blood vessels?

A
  • Increase cAMP
  • Activation of PKA so phosphorylation of the MLCK
  • Inhibition of MLCK
  • Opens potassium channels
  • Relaxation of smooth muscle
  • Vasodilation
45
Q

What is the effect of A1 adrenoreceptors?

A
  • Stimulates the IP3 production
  • Increase in Ca2+ from intracellular stores and via influx of extracellular Ca2+
  • Contraction of smooth muscle
  • Vasoconstriction
46
Q

What is the role of local metabolites?

A

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
Q

What are the drugs that act on the ANS?

A
  • Sympathomimetics
    • alpha adrenoreceptor agonists
    • beta adrenoreceptor agonists

-Adrenoreceptor Antagonists

  • Cholinergics
    • muscurinic agonists and antagonists

ESA 2: Cardiovascular (11 decks)

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