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Year One - Science For Medicine > Autonomic Physiology > Flashcards

Autonomic Physiology Flashcards

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1
Q

What two main neurones make up the PNS?

A

Afferent

Efferent

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2
Q

What are afferent neurones?

A

Known as sensory neurones

Involved in sending electrical signals from sensory receptors to interneurones

In charge of detecting changes within the environment

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3
Q

What are efferent neurones?

A

Known as motor neurones

Involved in sending electrical signals from interneurones to effector cells

Involved in carrying out a response within muscles or glands

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4
Q

What are the subdivisions of efferent neurones?

A

Somatic

Autonomic

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5
Q

Can afferent neurones be subdivided into different sections?

A

No

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6
Q

What are the role of somatic neurones?

A

Control voluntary actions

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7
Q

What are autonomic neurones?

A

Control involuntary action

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8
Q

What are the three divisions of autonomic neurones?

A

Sympathetic

Parasympathetic

Enteric

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9
Q

What structure do the efferent neurones exit the spinal cord through?

A

Ventral horn

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10
Q

What is the anatomical difference between autonomic and somatic nerves?

A

Somatic - extend all the way from their cell body to synapse directly onto their skeletal muscle target receptor

Autonomic - extend from the cell body to around the midpoint of the neurone pathway and synapse onto a second neurone. This second neurone will extend its axon all the way to the target receptor. In between the first and second neurone there is a cell body, known as an autonomic ganglion. The neurone before the ganglion is referred to the pre-ganglionic nerve and the neurone after is referred to as the post-ganglionic nerve.

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11
Q

Do the pre-ganglionic and post-ganglionic fibres in the autonomic system have a myelin sheath?

A

Pre - small amount

Post - no

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12
Q

What are the pharmacological differences between the autonomic and somatic NS?

A

Somatic - junctions in between neurones are specialised. This means that the neurotransmitters released from the presynaptic axon terminal are specific to the receptors on the postsynaptic membrane. The receptors on the postsynaptic membrane are ionotropic, which means that they are connected to ion channels are generate fast EPSPs and IPSPs. In fact, they will all generate fast EPSPs, as the neurotransmitter will always cause a response that depolarises the cell past the threshold. This means that they will always generate an action potential.

Autonomic - junctions between neurones are less specialised, as there is not one presynaptic terminal but multiple varicosities along the axon of the presynaptic neurone. These varicosities can release two different neurotransmitters and all the receptors on the postsynaptic neurone can respond to them. The receptors on the postsynaptic membrane are metabotropic, which means that they are connected to G-proteins and activate slow EPSPs and IPSPs. These neurones can generate both as the neurotransmitter can either hyperpolarise or depolarise the cell.

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13
Q

What process releases neurotransmitters from the axon terminal in both the somatic and autonomic NS?

A

Calcium dependent exocytosis

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14
Q

What is the role of the sympathetic NS?

A

Involved in flight or flight

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15
Q

What is the role of parasympathetic NS?

A

Involved in rest or digest

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16
Q

What are the sympathetic responses?

A 
Airways Dilate
Heart Rate Increases
Heart Beats Stronger
Blood Diverts To Muscle 
Gut Motility Decreases
Enzyme Secretion In Gut Inhibited 
Stored Energy Released
Pupils Dilate 
Eyes Focus Far Away
Hair Stands On End 
Mouth Gets Dry
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17
Q

What are the parasympathetic responses?

A 
Airways Constrict
Heart Rate Decreases 
Heart Beats Weaker
Blood Diverts To Gut
Gut Motility Increases 
Enzyme Secretion In Gut Stimulated
Stored Energy Remains Stored
Pupils Constrict 
Eyes Focus Close Up
Hair Lies Flat
Mouth Starts Drooling
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18
Q

What are the differences between the autonomic and somatic NS?

A

Anatomical

Function

Pharmacology

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19
Q

What are the differences between the sympathetic and parasympathetic NS?

A

Spinal cord regions

Ganglion

Neurotransmitters

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20
Q

What are the differences between the sympathetic and parasympathetic NS in terms of the spinal cord regions?

A

Sympathetic - cell bodies are found in the thoracic and lumbar regions. Explains why they are referred to as thoracic lumbar neurones

Parasympathetic - cell bodies are found in in the cranial and sacral regions. Explains why they are referred to as cranial sacral neurones

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21
Q

What are the differences between the sympathetic and parasympathetic NS in terms of the ganglion?

A

Sympathetic - two types; paravertebral ganglia and prevertebtral ganglia.

The paravertebral ganglia are close to the spinal cord and they converge to form the sympathetic trunk. This means that the paravertebral ganglia are found in the sympathetic trunk. The prevertebral ganglia are ganglia that are not found in the sympathetic trunk. In this case, the preganglionic fibres will go straight through the sympathetic trunk and synapse onto a postganglionic neuron further on in the pathway. This means that prevertebral are further away from the spinal cord than the paravertebral ganglia. Generally, preganglionic fibres are short and postganglionic fibres are long.

Convergence and divergence also occurs. Convergence is when several preganglionic fibres synapse onto one postganglionic fibre. Divergence is where one preganglionic fibre synapses onto several postganglionic fibres.

Parasympathetic - only has one type of ganglia. They all lie close to, or within, the target receptor cell. This means that they will have a long preganglionic fibre and a short postganglionic fibre.

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22
Q

What is the problem with convergence and divergence?

A

It is difficult for the body to just activate one set of fibres and therefore one response. Instead it will activate them all and carry out all the responses. This concept is known as mass activation.

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23
Q

What two neurotransmitters are involved in the autonomic NS?

A

Acetylcholine

Noradrenaline

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24
Q

What receptors does acetylcholine act on?

A

Cholinergic receptors.

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25
What are the two main cholinergic receptors?
Nicotinic Muscarnic
26
What are nicotinic receptors?
Ionotropic, which means that they are bound to an ion channel These ionotropic channels are specific and are only activated by nicotine
27
What are muscarinic receptors?
Metabotropic, which means that they are bound to G-protiens These ionotropic channels are specific and are only activated by muscarine There are three types of muscarinic receptor, depending on what G-protein that they are coupled to - M1, M2, M3
28
What receptors do noradrenaline and adrenaline act on?
Adrenergic receptors
29
What are the two main adrenergic receptors?
Alpha Beta
30
What are alpha adrenergic receptors?
Metabotropic, which means that they are coupled to a G-protien Many sub-types - alpha one, two and three Drugs not very selective to each subtype, normally activates them all
31
What are beta adrenergic receptors?
Metabotropic, which means that they are coupled to a G-protien Many sub-types - alpha one, two and three Drugs not very selective to each subtype, normally activates them all
32
What are the differences between the sympathetic and parasympathetic NS in terms of the neurotransmitters?
Sympathetic - preganglionic fibres release Ach which act on nicotinic receptors. The postganglionic fibres release NA which acts on alpha OR beta adrenergic receptors. However, there are some preganglionic fibres in the thoracic regions that extend all the way to the adrenal gland. Therefore, the adrenal gland is the postganglionic cell. However, adrenal glands don't have an axon. Instead they release hormones in the blood called adrenaline, which still binds to alpha OR beta adrenergic receptors and cause the same response. Parasympathetic - preganglionic fibres release acetylcholine, which act on nicotinic receptors. The postganglionic fibres release acetylcholine, however these neurotransmitters act on muscarinic receptors.
33
What are the two complications of the sympathetic NS?
Some innervate sweat glands. When they do this Ach is the neurotransmitter released, however they usually release NA Some postganglionic neurones release non-adernergic non-cholinergic (NANC) transmitters. They instead release peptides or nitric oxide.
34
What happens to the eye when the sympathetic NS is activated?
It causes the pupil to dilate, by contracting the radial muscle of the iris. To carry out this response, NA or A is released from the postganglionic neuron and binds to alpha1 receptors. It causes the eyes to focus far away, by relaxing ciliary muscle, which surround the lens. To carry out this response, noradrenaline or adrenaline is released from the postganglionic neuron and binds to beta2 receptors.
35
What happens to the eye when the parasympathetic NS is activated?
It causes the pupil to constrict, by contracting sphincter muscle. To carry out this response, Ach is released from the postganglionic neuron and binds to muscarinic receptors. It can cause the eyes to focus close up, by contracting ciliary muscle, which surrounds the lens. To carry out this response, Ach is released from the postganglionic neuron and binds to muscarinic receptors.
36
What happens to the heart when the sympathetic NS is activated?
It causes the heart rate to increase. To carry out this response, NA or A is released from the postganglionic neuron and binds to beta1 receptors on pacemaker cells. It increases the contraction strength of the heart. To carry out this response, NA or A is released from the postganglionic neuron and binds to beta1 receptors on myocytes.
37
What happens to the heart when the parasympathetic NS is activated?
It causes the heart rate to decrease. To carry out this response, Ach is released from the postganglionic neuron and binds to muscarinic receptors on pacemaker cells. The parasympathetic nervous system has little effect on the strength of contraction, as there is little effect when Ach binds to myocytes.
38
What happens to the lungs when the sympathetic NS is activated?
It causes smooth muscle to relax and the airways to become dilated and allow more air into the airways. To carry out this response, NA or A is released from postganglionic neurons and bind to beta2 receptors on smooth muscle of airways.
39
What happens to the lungs when the parasympathetic NS is activated?
It causes smooth muscle to contract and constricts airways and allow less air into the airways. To carry out this response, Ach is released from postganglionic neurons and bind to muscarinic receptors on smooth muscle of airways.
40
What happens to the blood vessels when the sympathetic NS is activated?
It causes smooth muscle to contract and blood flow to decrease. To carry out this response, NA or A is released from postganglionic neurones and bind to alpha1 receptors on smooth muscle of vessels. It causes smooth muscle to relax and blood flow to increase. To carry out this response, NA or A is released from postganglionic neurones and bind to beta2 receptors on smooth muscle of vessels.
41
What happens to the blood vessels when the parasympathetic NS is activated?
Most of your blood vessels are not innervated by parasympathetic nerves, so they have no effect on the receptors on smooth muscle of vessels.
42
How do the effects that the sympathetic NS have on blood vessels display the important of 'tone' in single innervation?
We want decrease blood flow to the gut, so we have lots of alpha1 receptors present on the gut. We want increase blood flow to the skeletal and cardiac muscle, so we have lots of beta2 receptors present on these muscle tissues. This means that the response that occurs depends on what receptors each tissue expresses.
43
What happens to the gut when the sympathetic NS is activated?
It causes a decrease in gut motility. To carry out this response, NA or A is released from postganglionic neurones and bind to alpha or beta receptors on smooth muscle of gut. It inhibits the secretion of enzyme. To carry out this response, NA or A is released from postganglionic neurones and bind to alpha receptors in the pancreas.
44
What happens to the gut when the parasympathetic NS is activated?
It causes an increase in gut motility. To carry out this response, Ach is released from postganglionic neurones and binds to muscarinic receptors on smooth muscle of gut. It causes an increase in the secretion of enzymes. To carry out this response, Ach is released from postganglionic neurones and binds to muscarinic receptors in the pancreas.
45
What happens to the energy stores when the sympathetic NS is activated?
It stimulates glycogenolysis and gluconeogenesis. To carry out this response, NA or A is released from postganglionic neurones and bind to alpha/beta receptors on liver cells, hepatocytes. It increases lipolysis. To carry out this response, NA or A is released from postganglionic neurones and bind to alpha/beta receptors on fat cells, lipocytes.
46
What happens to the energy stores when the parasympathetic NS is activated?
The parasympathetic nervous system will have no effect on energy stores, as Ach won’t cause an effect when binding onto receptors on liver or fat cells
47
What happens to the salivary glands when the sympathetic NS is activated?
It stimulates thick secretions that is rich in enzymes. To carry out this response, NA or A is released from postganglionic neurones and bind to beta receptors.
48
What happens to the salivary glands when the parasympathetic NS is activated?
It stimulates watery secretions. To carry out this response, Ach is released from postganglionic neurones and binds to muscarinic receptors.
49
What happens to the bladder when the sympathetic NS is activated?
It causes smooth muscle in the bladder wall to relax and thus reduce pressure. To carry out this response, NA or A is released from postganglionic neurones and binds to beta2 receptors on the smooth muscle of the bladder wall. It causes smooth muscle of the sphincter to contract and to stop urination. To carry out this response, NA or A is released from postganglionic neurones and binds to alpha1 receptors.
50
What happens to the bladder when the parasympathetic NS is activated?
It causes smooth muscle in the bladder wall to contract and increase pressure. To carry out this response, acetylcholine is released and binds to muscarinic receptors. It causes smooth muscle in the sphincter to relax and allow urination. To carry out this response, acetylcholine is released from postganglionic neurones and bind to muscarinic receptors.
51
What happens to the reproductive tract when the sympathetic NS is activated?
It causes smooth muscle to contract and causes ejaculation. To carry out this response, NA or A is released from postganglionic neurons and binds to alpha1 receptors on smooth muscle of the urethra.
52
What happens to the reproductive tract when the parasympathetic NS is activated?
It causes smooth muscle to relax and causes erection. To carry out this response, acetylcholine is released from the postganglionic neurones and binds to muscarinic receptors on sphincter smooth muscle.
53
What are the two mechanisms that control the responses of the sympathetic and parasympathetic system?
Autonomic reflexes Central control from the hypothalamus
54
What receptors will always be activated when we are relaxing muscle?
Beta 2
55
What receptors will always be activated when we release Ach
Muscarinic
56
What is dual innervation?
When both the parasympathetic and sympathetic system act on the same organ.
57
What is dual innervation with antagonistic effects?
Where one NS does the opposite of the other NS
58
What is dual innervation with complementary effects?
Where one NS does not do the complete opposite of the other NS
59
What is single innervation?
When only the sympathetic system affects the organ and not the parasympathetic system.
60
What controls single innervation?
Single innervation is controlled by varying tone which means that we don’t start a new process we just alter an ongoing one (diming effects).
61
What neurotransmitter is always released in the NJM?
Ach
62
What receptor does Ach always act on in the NJM?
Nicotinic
63
How is Ach removed from the synaptic cleft in NJM?
Enzyme degradation via acetylcholinesterase Acetyl and choline are then taken back up by the presynaptic neurone and recycled into new Ach
64
What are the five ways that we can inhibit NJM synapses?
Inhibit choline transporter. This prevents acetylcholine from being packaged into vesicles. Example - hemicholinium Block voltage gated calcium channels. This prevents calcium from flowing into the cell and stimulating calcium dependent exocytosis. Block vesicle fusion. This prevents the neurotransmitters from being released into the synaptic cleft. Example - botulin toxins Use non-depolarising nicotinic receptor blockers. This means that acetylcholine cannot activate the postsynaptic nicotinic receptors due to a competitive antagonist. Example - d-tubocurraine Use depolarising nicotinic receptor blockers. This means that an agonist will activate the ion channel and keep it activated to cause a brief muscle twitching and then paralysis as the voltage gated channels stay in their refractory state. Example - succinylcholine
65
What are the two ways that we can stimulate the NJM?
Prolong the action potential. We do this by letting more calcium into the axon terminal, which therefore triggers more acetylcholine release. We can also do this by blocking potassium voltage gated channels, as they are involved in stopping the action potential. Block acetylcholinesterase, which is the enzyme that breaks down acetylcholine. This means that we have more acetylcholine in the synaptic cleft which can continuously activate transmission. Example - eserine
66
What are the three clinical applications of the NJM?
We can inhibit NJM transmission in order to paralyse patients for surgical procedures, electroconvulsive (ECT) therapy or to control spasms in tetanus. To do this, we usually use non-depolarising or depolarising blockers due to the speed of the action. We can inhibit NJM transmission in order to treat muscle spasms and for cosmetic procedures. To do this, we usually use botulinum toxin. We can improve NJM transmission in order to treat myasthenia syndrome, to reverse the action of non-depolarising blockers and to counter botulinum poisoning. To do this we use acetylcholinesterase
67
What are the six ways that we can inhibit the ANS (between preganglionic and postganglionic fibres)?
Inhibit choline transporter. This prevents acetylcholine from being packaged into vesicles. Example - hemicholinium Block voltage gated calcium channels. This prevents calcium from flowing into the cell and stimulating calcium dependent exocytosis. Block vesicle fusion. This prevents the neurotransmitters from being released into the synaptic cleft. Example - botulin toxins Block the acetylcholine activated channel using hexamethonium. The reason why this is different from the NJM is because there are two slightly different variations of the nicotinic receptors present in the ANS and the NJM. This means that hexamethonium can only block the acetylcholine activate channels in the ANS and not the NMJ. Example - hexamethaneum Use non-depolarising nicotinic receptor blockers. This means that acetylcholine cannot activate the postsynaptic nicotinic receptors due to a competitive antagonist. Example - d-tubocurraine Use depolarising nicotinic receptor blockers. This means that an agonist will activate the ion channel and keep it activated to cause a brief muscle twitching and then paralysis as the voltage gated channels stay in their refractory state. Example - succinylcholine
68
What is the way that we can stimulate the ANS (between preganglionic and postganglionic fibres)?
Activate more nicotinic receptors by releasing more nicotine molecules into the synaptic cleft, as these molecules activate them. The reason why we can’t do this at the NJM, is because there is not much nicotine present near the terminal of the efferent neuron. However, there is a lot of nicotine present at the ganglia.
69
Why are there no clinical applications of the ANS?
The ANS is less specific due to the fact that any modulations would affect both sympathetic and parasympathetic ganglionic transmission. This means that the effects would be too widespread so there is no clinical applications.
70
What is the way that we can inhibit the parasympathetic NS (between postganglionic fibre and target receptor)?
Use muscarinic receptor antagonists, which will bind competitively to G-protein coupled receptors and block the acetylcholine neurotransmitter from binding. This means that acetylcholine won’t be able to produce an effect. Example - atropine
71
What is the way that we can stimulate the parasympathetic NS (between postganglionic fibre and target receptor)?
Use muscarinic receptor agonists, which will bind to G-protein coupled receptors and stimulate the same response as acetylcholine. Example - pilocarpine
72
What are the five ways that we can inhibit the sympathetic NS (between postganglionic fibre and target receptor)?
Block the enzymes that produce noradrenaline. These are several enzymes that are involved in producing noradrenaline, and if one of them is blocked by carbidopa it stops the whole pathway from occurring. This means less noradrenaline is packaged into vesicles and released. Block the transporter that fills the vesicles with NA. This prevents NA from being packaged into the vesicles. Example - reserpine Introduce a ‘false’ transmitter. These are taken up by neurones are synthesised into methyl-noradrenaline which is packaged into vesicles and released but cannot activate the adrenergic receptors. Activate inhibitory presynaptic autoreceptors. Remember that autoreceptors are receptors that fed back and inhibit release. Drugs can target these autoreceptors, which means that when they bind to them, they inhibit voltage-gated calcium channels. This prevents calcium ions from flowing into the cell and causing calcium dependent exocytosis. Block alpha or beta postsynaptic receptors.
73
What three ways that we can can stimulate the sympathetic NS (between postganglionic fibre and target receptor)?
Stimulate NA and adrenaline release. Amphetamine is taken up by a carrier protein into the axon terminal, where it is packaged into the vesicles. This displaces some of the NA and adrenaline in the vesicles which can then leaks out through the same carrier protein working in reverse. Inhibit NA or adrenaline uptake into neurones or glia. We do this by inhibiting the uptake carrier protein, which leaves more NA and adrenaline in the synaptic cleft to activate the postsynaptic receptors. Activate postsynaptic receptors. We do this by releasing more alpha and beta molecules into the synaptic cleft, which can then bind to the alpha and beta receptors and activate them.
74
What are alpha1 antagonists used for?
Decongestants Dilate the pupil
75
What are alpha2 antagonists used for?
Hypertension
76
What are beta1 antagonists used for?
Asthma
77
What are beta2 antagonists used for?
Hypertension, angina, cardiac arrythmias. glaucoma

Year One - Science For Medicine (16 decks)

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