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Intro to Med > Physiology and pharmacology of the sympathetic nervous system > Flashcards

Physiology and pharmacology of the sympathetic nervous system Flashcards

1
Q

What does the sympathetic nervous system prepare the body for and what is it present during?

A

-Sympathetic nervous system prepares the body for ‘fear, fight and flight.’
-Present during anxiety, stress response, hypovolemia

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2
Q

What are some of the effects of the sympathetic nervous system?

A

-Increased
-Heart rate
-Contractility
-Constriction of blood vessels
-Increase blood pressure
-Air into the lungs
-Fuel in muscles
-Sweating
-Decreased
-Non essential function like GI tract activity

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3
Q

Where is the signal sent from in the sympathetic nervous system?

A

-Signal is sent from the hypothalamus in fight, flight or fear

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4
Q

Steps in signal transmission in sympathetic nervous system?

A

-Signal is sent from the hypothalamus in fight, flight or fear
-This sends a signal down the excitatory bulbospinal fibres to the T1 to L2/L3 levels of spinal cord
-Inter- medio- Lateral(IML)
-The preganglionic fibres(short) originate from the T1 to L2/L3 levels of spinal cord(thoracolumbar region) and transmit signals to the ganglia where Acetylcholine is secreted to stimulate the post ganglionic fibres(Long)
-The post ganglionic fibres will secrete Noradrenaline at their target sites

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5
Q

What else is stimulated from the signal from the T1 to L2/L3 level of spinal cord and what does this secrete? What does it stimulate?

A

-Signals from the T1 to L2/l3 levels of spinal cord stimulate the adrenal medulla, secreting Adrenaline and Noradrenaline.
Stimulates alpha 1, alpha 2, beta 1 and beta 2 receptors

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6
Q

What receptors does noradrenaline and adrenaline act on in the heart and what effect does this have? What are these effects called?

A

-NA and adrenaline act on beta 1-adrenoceptors in Sino-atrial (SA) node:
-this increases generation of electrical activity which produces an increase in heart rate
-This is known as the Chronotropic effect
-NA and adrenaline act on beta 1-adrenoceptors in muscle cells
-This increases force of contraction of atria and ventricles as well as stroke volume
-this is known as the inotropic effect

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7
Q

What does sympathetic nerve stimulation in the heart do?

A

-Sympathetic nerve stimulation increases cardiac output(CO) and blood flow to tissues and organs
-CO or blood flow (vol/min) = SV(vol/beat) x Heart rate(beats/min)

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8
Q

What receptor does noradrenaline and adrenaline act on in blood vessels? What effects does this have?

A

-NA and adrenaline act on alpha-1-adrenoceptors on arterioles
-This causes vasoconstriction resulting in an increase in blood vessel resistance (TPR)
-NA and adrenaline act on alpha-1-adrenoceptors on veins
-This causes venoconstriction resulting in an increased return of blood to the heart, increasing cardiac output

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9
Q

What does sympathetic nervous innervation in blood vessels do?

A

-Sympathetic nervous system increases blood pressure as
-BP=Cardiac output x TPR(total peripheral resistance)

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10
Q

What receptor does noradrenaline act on in the kidney and what effect does this have?

A

-Noradrenaline acts at beta-1-adrenoceptors to release renin
-Renin is released from granular cells in the kidney which causes production of angiotensin II
-Angiotensin II increases blood pressure

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11
Q

Why are beta blockers successful in decreasing BP in terms of kidneys?

A

-One of the reasons why beta-1 blockers are successful at decreasing BP is because they prevent Renin release hence prevent angiotensin II production

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12
Q

What receptor does the Sympathetic nervous system stimulate in liver and skeletal muscles and what does this cause?

A

Stimulation of alpha/beta adrenoceptors causes:
-Breakdown of glycogen into glucose (glycogenesis)
-Promotes glucose synthesis (glucogenesis)

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13
Q

What receptor does the sympathetic nervous system stimulate in the pancreas and what does this cause?

A

Stimulation of alpha/beta adrenoceptors
-Decreases insulin response, which normally stores glucose
-This increases glucagon, therefore increased glycogen stores into free glucose

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14
Q

What receptor does the Sympathetic nervous system stimulate in adipose tissue and what does this cause?

A

-Stimulation of beta3-adrenoceptors
-Increase lipolysis which converts triglycerides into free acid and glycerol
-Both fatty acids and glycerol increase ATP levels

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15
Q

What receptor does the Sympathetic nervous system stimulate in the eye and what does this cause?

A

-Stimulation of alpha1-adrenoceptors on dilator pupillae (radial muscle of iris) cause dilation of the pupil

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16
Q

What receptor does the Sympathetic nervous system stimulate in sweat glands and what does this cause?

A

-Release of Ach acting at Mus receptors (not NA, exception) induces sweating
-Temperature control during fear flight fight

17
Q

What are the steps involved in the stimulation of receptors in the adrenergic synapse and the negative feedback?

A

-Noradrenaline is synthesised in the post ganglionic sympathetic nerve and stored in vesicles
-These vesicles fuse with the pre-synaptic terminal, releasing the noradrenaline to bind to alpha/beta adrenoceptors on the post synaptic membrane of the heart, blood vessels etc.:
-These will lead on to biological responses such as increased cardiac contraction, vasoconstriction, bronchodilation
-The released noradrenaline and circulating adrenaline may bind to alpha2 receptors on presynaptic terminal(Post ganglionic sympathetic nerve):
-This stimulates a negative feedback mechanism to the diffusion of vesicles with the pre synaptic terminal, to reduce concentration of noradrenaline and adrenaline in synapse
-Noradrenaline and adrenaline may also be actively be taken back into the pre synaptic terminal by an uptake transporter :
-This will then result in either breakdown by monoamine oxidase(MAO) or recycled back into vesicles

18
Q

How is dopamine synthesised?

A
  1. Tyrosine becomes DOPA by tyrosine hydroxylase, which is present in the cytoplasm
    a. This is a rate limiting step
  2. Dopa is then converted into dopamine by DOPA decarboxylase
    a. Pathway up to here found in dopamine nerve
19
Q

How is noradrenaline synthesised?

A
  1. Tyrosine becomes DOPA by tyrosine hydroxylase, which is present in the cytoplasm
    a. This is a rate limiting step
  2. Dopa is then converted into dopamine by DOPA decarboxylase
    a. Pathway up to here found in dopamine nerve
  3. Dopamine then becomes noradrenaline by dopamine dehydroxlase
    a. Pathway up to here found in sympathetic nerves
20
Q

How is adrenlaine synthesised?

A
  1. Tyrosine becomes DOPA by tyrosine hydroxylase, which is present in the cytoplasm
    a. This is a rate limiting step
  2. Dopa is then converted into dopamine by DOPA decarboxylase
    a. Pathway up to here found in dopamine nerve
  3. Dopamine then becomes noradrenaline by dopamine dehydroxlase
    a. Pathway up to here found in sympathetic nerves
  4. Noradrenaline then becomes adrenaline due to phenylethanolamine-N-methyl transferase(PNMT)
    a. This is found in the adrenal medulla, which is the main site for adrenaline release
21
Q

What may facilitate release in adrenergic transmission and what does this do?

A

-Amphetamine/ephedrine reverse the uptake transporters, causing release of NA into cleft.
-This increases sympathetic actions

22
Q

What is ephedrine, and what is it involved in?

A

-Ephedrine (decongestant in cold symptom relief medication) is involved in vasoconstriction of nasal blood vessels

23
Q

What drugs may facilitate inhibition of release in adrenergic transmission? and what emergencies can these drugs be used in?

A

-Guanethidine competes with noradrenaline for inclusion into vesicle, reducing NA release
-Clonidine stimulates presynaptic alpha 2 receptors and this reduces NA release
-These 2 drugs may be used in hypertensive emergencies to reduce sympathetic activity at BP

24
Q

What steps cause adrenergic transmission to terminate?

A

-NA is terminated by re-uptake unchanged into pre-synaptic terminal
-Noradrenaline is then
1. Recycled back into vesicles
2. Metabolised by monoamine oxidase (MAO) in neurones or catechol-O-methyltransferase(COMT) in non neuronal sites (e.g. adrenal medulla)

25
Q

What drug inhibits uptake of noradrenaline and adrenaline?

A

Cocaine inhibits uptake

26
Q

Pathway for alpha 1 receptors

A

Gq

27
Q

Pathway for alpha 2 receptors

A

Gi

28
Q

Pathway for beta 1,2 and 3 receptors

A

Gs

29
Q

Adrenergic receptor agonists drugs and receptors it acts on

A

VIEW NOTES

30
Q

Adrenergic receptor antagonists drugs and receptors it acts on

A

VIEW NOTES

Intro to Med (46 decks)

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