peripheral nervous system Flashcards
are pre ganglionic or post ganglionic neurones always myelinated
pre ganglionic
where is the ganglion in parasympathetic NS
near or embedded in the target organ
what do the preganglionic and postganglionic neurones release in para ?
ACH (acts on nicotinic receptors of postgang, muscarinic receptors on target organ)
where is the ganglion in sympathetic NS
nearer the CNS
what is secreted by the preganglionic neurone in symp?
ACH
what is secreted by the postganglionic neurone in symp?
NA (except in innervating the sweat glands-ach)
where is sympathetic outflow restricted by?
T1-L3
where do axons of the symp enter?
symp chain
where is parasymp outflow restricted to
head and the pelvis
what do all preganglionic neurones release and act on what receptors
ACH, at on nicotinic receptors
what else do post ganglionic neurones release in sympathetic
peptide (neuropeptide Y)
where is neuropeptide Y prominent and what is its action
prominent in blood vessels prolongs constriction by the NA
what is released when ACH is released
VIP (vasoactive intestinal polypeptide). released with ACH in symp and para
what is the action of VIP
increases blood flow through glandular tissue
how do postganglionic neurones terminate in the ANS
not attached as organs variable in size, located near
where is the neurotransmitter release from on postganglionic neurones
from varicosities on branches in the target
what are the cranial nerves carrying parasympathetic fibres
CN 3, 7, 9, 10
parasympathetic outflow divided into
cranial part and sacral spinal cord
where are the paravertebral ganglia found
ganglia of the sympathetic chain
where are the prevertebral ganglia found
in front of the vertebral column
what is the target in the enteric NS
smooth muscle of the wall, embedded between its 2 layers
sensory info comes in via which horn
dorsal horn- POSTERIOR (ventral-motor)
what are the types of axons that all peripheral spinal nerves contain
somatic motor, somatic sensory, visceral motor, visceral sensory
where do somatic motor come from to supply what?
come from lower motor neurones, supply skeletal muscle (myelinated)
where do somatic sensory (primary afferents) come from
from peripheral receptors. cell body in DRG. C fibres and A delta fibres
what are visceral motor and where do they come from
postganglionic sympathetic axons (autonomic), supply organs in the skin
what are visceral sensory and where do they come from
sympathetic afferents, from structures such as vascular beds in the skin
in a nerve fascicle what part do blood vessels run through, function?
epineurium , contain white adipocytes for protection
what does the perineurium act as
barrier to infection, tough and resistant only blood vessels can traverse it
what does the endoneurium contain
collagen and ECF
what direction do orthograde axons go. what motor component is involved
cell body to terminal. kinesin
what direction do retrograde axons go, what motor component is involved
terminal to cell body. dynein
what can lead to nutrition being a factor in peripheral neuropathy
vitamin B deficiency, malabsorption
what remains following a cut/crush in wallerian degeneration
myelin sheath
the completeness of regrowth of the axon depends on what?
how clean the damage is, if adequate blood supply, age
what is neuropathic pain due to
incomplete neuronal regeneration
symptoms of neuropathic pain
tenderness, burning, tingling, electric shock like
what is neuropathic pain caused by
neuroma with new membrane altered Na+ and K+ channels leading to abnormal action potentials. neuroma goes into spinal cord and leads to pain as cant interpret abnormal info
what is the function of schwann cells apart from myelination
secrete glycoprotein (laminin) which is important when a nerve is trying to regenerate as provides a surface area
what must occur in nerve regeneration
angiogenesis (laminin provides surface for this)
unmyelinated axons contain plenty of what and whats this important for
mitochondria. for axonal transport- have to maintain the axon and maintain a synapse
what happens in axonal transport. what are responsible
molecules are sent down the length of the axon (ATP dependent process). neurotubules are responsible.
what protein is important in axonal transport
tau. if overexpressed or destroyed then axonal transport would cease- molecules produced wouldn’t be able to leave and the neurone would die
what are the 3 portions of an anaesthetic
aromatic, ester/amide, amine portion
examples of amide anaesthetics
lignocaine, bupivacaine
examples of ester anaesthetics
cocaine, amethocaine
which type of anaesthetic is more commonly used and why?
amides as esters are less stable in solution, and they can be associated with allergic reactions whereas amides rarely lead to allergic reaction
what are the 4 states of conformation of Na+ channels
resting state; intermediate closed formation; open conformation; inactivated conformation (immediately after AP)
which channels do the local anaesthetics interact with and which channels do they have the highest affinity for
highest affinity for intermediate and inactivated conformation. some affinity for open channel (lowest for resting)
how do the anaesthetics work
prevent channel from opening, bind channel pore if its open, prolong refractory period in the inactive
where do the local anaesthetics target
where there is injury and higher rate of nociceptive firing
which pain fibres have a greater susceptibility for Local anaesthetics?
A delta > c fibres
what part of the LA contributes to lipid solubility and what is the function
aromatic group and hydrocarbon chain length. potency
what is the function of pKa and protein binding in LA
pka (due to the amine) contributes to the speed of onset, protein binding- duration of action
what form does the LA need to be in to cross the membrane, and to bind and have activity on voltage gated Na+ channels
unionised to cross membrane, ionised to bind VGNa+
how do LAs cross membrane and bind VGNa+
they are weak bases and as intracellular is more acidic than extracellular they are in unionised form to cross the membrane and dissociate intracellularly and so can bind the VGNa+
what does a lower pka show
greater proportion of drug ionised at lower ph, so has a more rapid onset of action
why does lignocaine have a faster onset of action than bupivacaine
because lignocaines pka is 7.8 and so more is unionised outside the cell (which is 7.4) and so can cross the lipid membrane faster than bupivacaine (pka 8.1)
why is adrenaline used in conjunction with LA
reduces blood flow, so prolongs effect of LA
which is short acting lignocaine or bupivacaine
lignocaine, (bupivacaine more longer acting)
what is an amide LA and how is used
amethocaine. used topically
where does a large output of SNS go?
adrenal medulla. no ganglia so acts directly on nACHRs on chromaffin cells to release adrenaline
out of nicotinic and muscarinic receptors which are ionotropic(pass ions through)
nicotinic. (muscarinic- metaohtropic- GPCR)
what does an overdose in organophosphates (cholinesterase inhibitors) lead to
SLUDGEM- salivation, lacrimation, urination, defacation, GI upset, emesis, miosis (antidote- atropine)
what can cholinesterase be used in clinically
glaucoma, myasthenia gravis, urinary retention/ileus, alzheimers
examples of cholinesterase inhibitors, which is longer acting
neostigmine, pyrimidostigmine
what are the effects of muscarinic agonists
increased empyting of bladder, GI trqact and salivary tracts. decrease sweating and lacrimation, slow heart decrease BP
useful muscarinic agonists
bethanechol, pilocarpine
effects of muscarinic antagonists
increase HR, blurred vision, decrease GI motility. major CNS effects- delirium, confusion, disorientation, hallucinations
examples of muscarinic antagonists
atropine, tropicamide
what is the term for agonists (NA)
sympathomimetic
what is the term for antagonists (NA)
sympatholytic
where are alpha 1 receptors found (NA)
in arterial and veno contraction, found in vasculature
where are alpha 2 receptors found (NA)
in CNS, platelets, fat cells.decrease sympathetic activity
where are beta 1 receptors found (NA)
in heart. increase HR, contractile force, increase cardiac output
where are beta 2 receptors found (NA)
causes bronchodilation, vasodilation. found in skeletal muscle and liver
where are beta 3 receptors found (NA)
in fat cells
what drugs alter the NA release, uptake or breakdown in SNS
cocaine (reuptake), amphetamines (release), pargyline (anti depressant and anti hypertensive)
what does an antagonist of alpha 1 treat
hypertension
what does antonising alpha 2 lead to
increased sympathetic activity
what can non selective B agonists be used for
bradycardia, heart block. B2 agonist- bronchodilation (salbutamol)
what can non selective B antagonists be used for
hypertension, stage fright (propranolol used). B1 antagonist- atenolol.
