autonomic nervous system Flashcards

(50 cards)

1
Q

ganglion neurone

A

collection of neuronal bodies found in the voluntary and autonomic branches of the peripheral nervous system (PNS).

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2
Q

Parasympathetic paths

A

Cranial nerve III controls eyes
Vagus nervous system controls glands
sacral s2-s4 controls the bladder and genitals

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3
Q

What acetylcholine affects

A

Somatic- skeletal muscle
Sympathetic-glands, adrenal medulla
Parasympathetic- salivary glands

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4
Q

Types of receptors for acetylcholine

A

Muscuerinic

Nicotonic

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5
Q

Nicotinic acetylcholine receptor

A

Ligand gated channel that has 5 sub units
Has 2 binding spots for Ach
Stimulates adrenaline secretion from adrenal medulla

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6
Q

Muscarinic Ach receptor

A

G protein coupled receptor
Causes release of calcium ions and inhibits
Causes activation of sweat glands

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7
Q

M2 receptor(cardiac)

A

Decreased cAMP
Causes inhibitory affect
Potassium ion increase and calcium ion decrease
Ca2+ decreases heart rate

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8
Q

M1 receptor(neural)

A

Activates phospholipase C increasing IP3 and DAD

Excites CNS and ganglia

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9
Q

M3 receptor

A

Activates phospholipase C and increases IP3 and DAG

Causes smooth muscle contraction and vasodilation

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10
Q

cholinergic transmission

A

Acetylcholine can be taken back to the presynaptic terminal by the transporter choline carrier
Choline can then be catalysed by choline acetyltransferase to form Ach again
This can then be transported back to the vesicle through Ach carrier choline

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11
Q

Drugs on cholinergic transmission

A

Atropine inhibits the effect of acetylcholine by complexing the acetylcholine receptor
Cholinesterase inhibitors function to decrease the breakdown of acetylcholine

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12
Q

depolarizing agents vs nondepolarizing

A

depolarizing muscle relaxants act as ACh receptor agonists, whereas nondepolarizing muscle relaxants function as competitive antagonists

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13
Q

Muscuerinic agonists

A
Acts for parasympathetic system
Decreased heart rate
smooth muscle contraction
Sweating and salvation 
Affects CNS by causing excitation
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14
Q

Nicotine

A

stimulates ganglia and neuromuscular junction and causes a depolarising block
Depolarising block is now desensitised to anymore depolarisation
It can cause many undesirable effects

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15
Q

Ganglion blockers

A

Block muscle contractions therefore blocking skeletal muscle BY BLOCKING OF nicotine receptors
This can be dangerous because the diaphragm needs to be able to contract so therefore we need artificial ventilation to assist breathing

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16
Q

Non depolarising agents

A

Can be long term, short term or intermediate
Eventually all the drugs will need to be metabolised in the liver and released from the kidney
If these organs are impaired then they can remain in the body longer and cause more effects

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17
Q

Acetylcholine in muscle cells

A

Muscle cells cannot be repolarised so when acetylcholine binds to the receptor they cannot cause further depolarisation causing desensitisation
Phase 2 is consistently depolarised and cannot repolarise causing muscle relaxation

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18
Q

Acetylcholinesterase

A

AChe main function is to hydrolyse acetylcholine in the blood
Causes increased skeletal muscle contraction
Has short, medium and irreversible duration

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19
Q

Sympathetic and parasympathetic systems

A

Sympathetic pathway(adrenergic) uses norepinephrine neurotransmitter and parasympathetic uses acetylcholine

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20
Q

Adrenaline

A

Adrenaline can cause vasoconstriction in vascular beds

There is alpha adrenaline receptor neuroadrenaline> adrenaline>isoproternal

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21
Q

adrenoreceptors

A

Two subtypes for alpha adrenoreceptors
Three subtypes for beta adrenoreceptors
All use G proteins

22
Q

A1 adrenoreceptor

A

Activates phospholipase C increasing IP3 and DAG

Constriction of smooth muscle in blood vessel

23
Q

A2 adrenoreceptors

A

mainly expressed in the presynaptic terminal
Reduces cAMP
Inhibition of neurotransmitters
Decreased insulin secretion

24
Q

adrenoreceptor antagonist

A

Non selective can reduce blood pressure

Selective can cause hypertension

25
B1 adrenoreceptors
Mainly expressed in the heart Use in heart failure which is when heart activity is reduced Increases cAMP Increases heart rate and contraction
26
B2 adrenoreceptors
Increases cAMP | Relaxes smooth muscle in bronchi
27
B3 andrenoreceptor
Exercise’s are mediated by B3 receptors Increased cAMP B3 have many clinical usage renin is a Chemical substance produced in the kidney and activated during exercise Can be used to correct irregular heart contraction and chest pain
28
B adrenoreceptor antagonist
Decrease blood pressure and sympathetic output | B adrenoreceptor causes reduction of heart rate and reduces bronchoconstriction
29
Selectivity in drugs
Ideal drug will be selective to a certain subtype beta 1 adrenoreceptor specific to slow heart rate Drugs are selective not specific
30
Adrenergic neurotransmission
Processes in the synapse of somatic nerve terminal Localised effect on vasoconstriction)Noradrenaline CA has 3 neurotransmitters that is secreted at adrenal medulla into the blood and cause a widespread effect
31
CA
Adrenaline, noradrenaline and dopamine secreted as a hormone to cause widespread effect
32
synthesis of CA
Synthesis of CA uses multiple enzymes to catalyse the reaction First enzyme adds an hydroxyl group Next enzyme removes of carboxyl group Next enzyme adds a hydroxyl group on to form noradrenaline PNMT adds another carboxyl group The first enzyme called Tyrosine hydroxlase is red limiting step and is critical for all production of adrenaline
33
Dopamine in CA
Dopamine is transported into the vesicle of nerve terminal by transporter Once in the vesicle it can form noradrenaline due to the presence of DBH enzyme
34
Noradrenaline in CA
Noradrenaline is released via exocytosis calcium is required. Noradrenaline is released onto post synaptic adrenoreceptors Indirectly acting sympathomimetic amine promotes the release of noradrenaline Once noradrenaline is released into the synaptic cleft there can be re uptake and go back into the vesicle again
35
CA stages
``` synthesis storage release interaction of adrenoreceptors on target organ and glands Degradation or re-uptake ```
36
Reuptake of noradrenaline in CA
Uptake occurs in the nerve terminals and is transported into the vesicles via VMAT's
37
Dales principle(outdated)
a given neuron contains and releases only one neurotransmitter and exerts the same functional effects at all of its termination sites.
38
co transmission
Neurotransmission usually uses co transmission We know that released neurotransmitters can also act on presynaptic neurones causing pre synaptic modulation Neurotransmitter release can also vary during development and injury
39
Neuromodulation
It is difficult to differentiate from neurotransmissions and neuromodulation Neuromodulation is usually slower Neuromodulation acts via second messenger system whereas neurotransmission acts via ligand gated ion channels
40
NANC | Non-adrenergic and non cholinergic transmitters
Two types: Ganglionic transmission:serotonin, GABA and dopamine Post ganglionic terminal:Nitric oxide
41
Presynaptic modulation
Usually inhibitory | Co transmitters can affect transmitter release
42
post nerve terminal tissue
Activation of post nerve terminal tisssue cause biological response
43
Homotropic auto inhibition
Pre synaptic auto receptor activation causes inhibition of neurotransmitter release in cholinergic and adrenergic
44
hetrotropic presynaptic inhibition
Noradrenaline inhibits Ach in nerve terminals rELEASE neurotransmitter x can act on another nerve terminal which can inhibit neurotransmitter Y and works in the opposite direction
45
Serotonin
Inhibits noradrenaline release and causes vasodilation and excitatory effect on eccentric neurones
46
Post synaptic medators
Mediators modify excitability Mediator Y can also cause an individual effect by itself But when and X and y act together they cause a strong effect X and Y act on different tissues
47
NPY
NPY enhances the function of noradrenaline by increasing calcium
48
Co transmission of ATP and noradrenaline
Neuroadranaline and ATP are co stored in the vesicle at a ratio of 4:1 NA can also act on presynaptic a2 adrenoreceptor so GI coupled receptor can inhibit adynlayse cyclase inhibiting cAMP reducing calcium channel function reducing calcium
49
ATP
Stored in synaptic vesicle at terminals Allows for fast transmission in autonomic ganglia Co transmitter with noradrenaline causes contraction in bladder
50
Nitric oxide
Nitric oxide is synthesised from L-argine which is an amino acid cGMP increases the vasodilation in the lungs Sildenafil increases NO by inhibiting breakdown of cGMP(Localised effect) Can reduce blood pressure which can cardiovascular reflex response to reduce vascocontrisction