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CVS > Lecture 10 > Flashcards

Lecture 10 Flashcards

1
Q

What does the ANS (involuntary) regulate/exert control over?

A

-heart rate, BP, body temp (homeostatic functions)
-co-ordinating the body’s response to exercise and stress
Exerts control over:
-smooth muscle
-exocrine secretion
-rate and force of the contraction of the heart

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2
Q

What are the 2/3 divisions of the ANS + how are they divided into these categories?

A

Parasympathetic (cranial/sacral origin)
Sympathetic (thoracic/lumbar origin)
Based on anatomical grounds only rather than type of neurotransmitter
(some include the enteric nervous system-surround GI tract-parasympathetic + sympathetic fibres)

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3
Q

Where are the preganglionic cell bodies?

A

CNS

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4
Q

Difference in length of preganglionic/post ganglionic neurones in sympathetic/parasympathetic neurones:

A

Sympathetic

  • pre:short (synapse in ganglion)
  • post:long (innervate target tissue)

Parasympathetic

  • pre:long
  • post:short (close to/within target tissue)
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5
Q

Can a tissue be innervated by parasympathetic + sympathetic nerves?

A

Yes.
They often have opposite effects to work together to maintain balance.
(Parasympathetic NS is more dominant under basal conditions, whereas sympathetic activity is increased under stress)

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6
Q

Can sympathetic drive be independently regulated?

A

Yes. Sympathetic activity to heart can be increased without increasing the activity of the GI tract

(Fight/flight is more generalised activation of sympathetic nervous system)

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7
Q

What does the ANS do/not do in the CVS?

A

Controls:

  • HR
  • force of contraction of the heart
  • peripheral resistance of blood vessels

Does not:

  • initiate electrical activity in the heart
  • denervated heart still beats, at a faster rate, as at rest it is normally under influence of vagus nerve (parasympathetic input)
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8
Q

What is the structure of parasympathetic nerves to the heart?

A
  • preganglionic fibres from 10th cranial nerve: Vagus nerve
  • synapse with postganglionic cells on epicardial surface/ within walls at AV/SA node (not much innervation of myocardium itself- targets nodes: meaning it can change HR but NOT force of contraction)
  • postganglionic cells release ACh
  • acts on M2 receptors (G-protein coupled)
  • decreases HR, decreases AV node conduction velocity
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9
Q

What do the postganglionic sympathetic fibres innervate?

A

-from postganglionic fibres from sympathetic trunk
-innervate SA/AV node AND myocardium
Release noradrenaline
Acts on B1 adrenoreceptors (B2/3 adrenoceptors are present in the heart also)
-increasing force of contraction (positive inotropic effect-due to innervation of the myocardium)
-increasing heart rate

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10
Q

How does ANS effect pacemaker potential (slow depolarisation to threshold)?

A
  • sympathetic activity will steepen pacemaker potential (quicker to reach threshold-AP fire faster): NA on beta 1 receptors- G protein, Gs, increase cAMP, HCN channels open allowing Na+ influx= reach TV
  • parasympathetic activity will lengthen pacemaker potential (longer to reach threshold): ACh on M2 receptors- G protein, Gi, decreases cAMP + beta/gamma unit increases potassium conductance
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11
Q

How does NA increased force of contraction of heart?

A

-acts on B1 receptors in myocardium and nodes: (Gs coupled) causing an increase in cAMP-> activates PKA
-phosphorylation of Ca2+ channels (L type), increases Ca2+ entry during plateau phase
-increased uptake of Ca2+ in ER
= increased force of contraction

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12
Q

What is the more common innervation of vessels?

A

-sympathetic innervation (except specialised tissue e.g. erectile tissue which have parasympathetic)

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13
Q

What type of receptor is present in vascular smooth muscle?

A

Alpha 1 adrenoceptors

Coronary and skeletal muscle vasculature also have some B2 adrenoceptors

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14
Q

How you how control the diameter of vessels by sympathetic innervation?

A

-normal vasomotor tone (some sympathetic output (NA) acting on alpha 1 receptors)
(Basal tone allows constriction and dilation)
-relaxation: decrease sympathetic outflow, alllowing vasodilation
-constriction: increase sympathetic output: allowing vasoconstriction

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15
Q

Which blood vessels have B2 adrenoceptors as well as A1, and what is the effect of NA/adrenaline on these?

A
  • skeletal muscle vessels
  • myocardium vessels
  • liver vessels

-noradrenaline from sympathetic nervous system acts on A1 adrenoceptors to constrict vessel (not all or nothing response- just to regulate BP)
-if you have an increase in circulating adrenaline (fight/flight response), theses act on B2 receptors, adrenaline can also activate A1 receptors at higher concentrations
-B2= dilation
(Predominant effect will be constriction if very high levels of adrenaline, at normal levels they act on B2 receptors for dilation)

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16
Q

How does activating B2 adrenoceptors cause vasodilation?

A

-increased cAMP (Gs coupled)
-increase in PKA
-opens potassium channels, making them less depolarised-more negative, phosphorylation (pKa) inhibits myosin light chain kinase
= relaxation of smooth muscle

17
Q

How does activating A1 adrenoceptors cause vasoconstriction?

A

-stimulate IP3 productions (IP3 receptors on sarcoplasmic reticulum) (Gq)
-increase in Ca2+ from stores/extracellular
= contraction of vascular smooth muscle cells

18
Q

What are some local metabolites that have a vasodilator effect? (More important than nervous stimulation-B2 receptor activation for adequate perfusion)

A

-active tissues produce more metabolites
(Adenosine, K+, H+, CO2)

-vasodilator effect to ensure adequate perfusion

19
Q

What is the overall control of the CVS?

A

Medullary centres: cardiovascular centres
Afferent nerves:
-baroreceptors: pressure receptors in arterial system (in arteriole system)
Activity from these is detected in control centre which influences the activity coming from sympathetic and vagal nerve (parasympathetic)
-atrial receptors (low pressure side)

20
Q

Where are baroreceptors found?

A

-carotid sinus (bulge before the common carotid arteries bifurcate)
-aortic arch
(Increase in blood flow, causes baroreceptors to stretch more= activation to cardiovascular control centres)

21
Q

What is the baroreceptor reflex?

A

Increase in arterial BP
-detected by baroreceptors (stretch)
-afferent pathway to medulla: coordinating centre
-efferent pathways from medulla (decrease sympathetic output/increase parasympathetic output)
-reduce HR and force of contraction + relaxation of vessels
= lower arterial BP

22
Q

Why would a heart beat faster if not innervated?

A

Because it no longer has the parasympathetic input from the ANS which is the major ANS contribution to the heart.

23
Q

What is a negative chronotropic effect?

A

Decreases HR

24
Q

What is a positive inotropic effect?

A

Increase in force of contraction

25
Q

What is the action potential in SA node cells?

A
  • pacemaker potential to threshold (HCN channels)
  • upstroke due to Ca2+ channels opening (not due to Na+ opening as they would be inactivated at that membrane potential)
  • downstroke due to closing of Ca2+ channels and opening of K+ channels
26
Q

What is the pacemaker of the heart?

A

Cells in the SAN
-slow depolarising pacemaker potential
-turning on of slow Na+ conductance (funny current)
-opening of Ca2+ channels
AP firing in the SA node sets the rhythm of the heart

27
Q

What is the action potential in SAN cells?

A
  • slow depolarising pacemaker potential (funny current) via HCN channels
  • opening of fast Ca2+ channels
  • closing of Ca2+ and opening of K+ channels
28
Q

What allows both vasodilation and vasoconstriction to occur?

A

Basal level of tone (vasomotor tone)

29
Q

What happens to baroreceptors if there is persistent high BP? (Not just acute high BP)

A

Baroreceptor reflex re-sets to higher levels with persistent increases in BP

30
Q

What are sympathomimetics?

A

(Alpha/beta adrenoceptor agonists)

  • exogenous adrenaline (restore function of heart after cardiac arrest/anaphylactic shock causes dilation so vasoconstriction occurs: activates alpha 1 receptors overriding B2)
  • Dobutamine (B1 agonist- if in cardiogenic shock)
  • salbutamol (B2 agonist- bronchial smooth muscle: vasodilation)
31
Q

What are adrenoceptor antagonists?

A
  • A1 antagonists (prazosin): anti-hypertensive, inhibits NA action causing vasodilation
  • propranolol (non selective against B1/2 antagonist: slows HR and reduces force of contraction it also acts one B2 bronchial smooth muscle= bronchoconstriction)
  • atenolol (cardioselective: act on B1, less risk of bronchoconstrictive)
32
Q

What are cholinergics?

A

Muscarinic agonists and antagonists

Agonists: pilocarpine (treat glaucoma, activates contraction of pupillae muscle, improving drainage of aqueous humour)

Antagonists: atropine/tropicamide (dilate pupil to examine eye/increases HR/bronchial dilation)

CVS (16 decks)

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