NAS Flashcards
Manifestations of lower motor neurone damage
Flaccid muscle weakness
Hypotonia/atonia
Hyporeflexia/areflexia
Denervation muscle atrophy (muscle wasting)
Fasciculations
What do nerves supply?
Skeletal muscle
Smooth muscle
Glands
Caused of degeneration of nerves
Acquired through injury
Genetics of the body
Natural processes of aging
Which nerves regenerate?
Peripheral have the capacity to regenerate and Reinnervate
Central nervous system does not (capacity is there already)
Dysfunction of nerves
Environment damaged or interfered
Severity depends on nature of insult
Structured of neurone
Epineurium
Perineurium
Endoneurieum
Myelin sheath
Axon
(Getting more deep as you go down)
Fascicle
A collection of axons
Seddon’s classifications of nerve injuries
Neuropraxia
Axonotomesis
Neurotmesis
Neuropraxia
Most minimal
Damaged to peripheral aspects
Temporary loss of function
Most probably at level of myelin sheath
Restoration would be complete upon recovery (ie blood supply back to limbs)
Axonotomesis
Damage to axon
Connective tissue tubes remain intact but myelin and axon damaged -> means recovery can attract a new axon to restore function
Result of a severe crush injury to peripheral nerve
Neurotmesis
Fractioning of nerve/completely transected
Most severe
Axon and connective tissue all flanged
No recovery of function occurs
Nerve injury is divided into two parts called..
Proximal segment
Distal segment
Proximal segment will survive?
Yes as closer to cell body and will recurve support
Distal segment will survive?
No
Often cut off
Loses potential repairs
Loss of nutritional support
Becomes vulnerable to phagocytosis by glia, some tissues may be preserved to form hollow tubes
Sends signals of death
wallerian degeneration
3 classes of glial
Myelin forming -> oligodendrocytes, Schwann cells
Astrocytes (create a good environment)
Microglia (immune)
What happens to the axons after injury? minutes
Produce ?injury potentials from proximal
Axons will start leaking intracellular fluid
?neuroma
Sealing and swelling
Synaptic transmission stops
How do microglia react to damaged neurones?
Change from surveillance cells to phagocytes
What happens to synapses after injury?
hours after AstroGlia remove terminals and move away
So lose input and output
Synaptic terminal degenerates accumulation of neurofilaments/vesicles
Chromatolysis
Proximal segments undergoes a few days after injury
Cell body becomes very active -> produce proteins for repair
Swells with new products
Nucleus moves to peripheral
Nerve seals and forms neuroma
Change in colour of cell body
Minutes after injury…
Synaptic transmission cut off
Cut end swells
Denervation
Loss of nerve supply
Re-innervation
Re growth of nerve to re supply
Biochemical structure of muscle
Determined by chemicals released by neurone
Ie will change type of neurone that is connected is different
Acute phases of denervated muscle
Paralysis immediately
Areflexic
Fasciculate
Atonic
If not reinnervated then fasciculations will subside
Disuse atrophy
Loss of muscle due to no use
Chronic phase of denervated muscle
Fasciculation subside -> lose bulk due to lack of innervation
Will die
Muscle replaced with connective tissue including fat
State of fibrosis
Rhabdomyolysis
Life threatening disorder
Breakdown of skeletal muscle
Release of intracellular contents into circulation
Leads to acute renal failure
Possible death
Causes:
Crush syndrome
Vehicular accidents
Injected substances of abuse into muscle
Over exercise
Certain forms of pathologies that can damage muscles
Reflex definition
Stereotyped (predictable)
Involuntary
Rapid
In both somatic and autonomic
Autonomic system
Smooth muscles or glands
Somatic system
Skeletal muscle
Testing reflexes in clinical
Pupillary reflex
Deep tendon reflex
Function of reflexes
Protection (limb withdrawal)
Postural control (eg walking)
Homeostasis (Bp)
Neural components of a reflex arc…
Sensory receptor
Afferent neurones
Somatic: directly though integration or to efferent
Efferent
Effector
Interneurones
-> relay neurones
Take information from various inputs
Found in CNS - spinal cord, brain stem nuclei, and enteric
Part of integration
Can influence integration?
Can modulate by other inputs
Eg your brain can over come something hot etc
Efferent neurones
Bring about response
Inner age effectors
Effectors
Glands/muscle
Appropriate response
Myotatic
Simple stretch reflex
Posture
Adjust degrees of contraction in skeletal muscle
Sensory receptors: proprioreceptors
Proprioreceptors types
Muscle spindle
Golgi tendon organ
Muscle spindle reflex
Found in skeletal muscles
Monosynaptic, no interneurone (Direct afferent efferent connection)
Increased stretch ie lifting weight
Increase sensory/Motor activity -> increase ach
Why is muscle spindle reflex useful?
Why?
Increase contraction so prevent damage
Why is it important that the muscle spindle sensor neurone branches?
Relaxes paired muscle
The branch will then go to interneurone where inhibits motor
Golgi tendon organ
Reverse myotatic reflex
Increase contraction
Increase sensory activity
Interneurone is inhibitory
So will block efferent activity
Muscle activity decrease
What does GTO help?
Prevent damage due to over work
Stops the ripping of muscle
Fine control of muscle tension
Crossed extensor reflex
Pain
Sensory neurone increased activity and branches
Communication with brain -> ouch
Effects motor neurones from many interneurones
Effect:
-lift foot with pair of muscle (contract and relax)
-transfer weight back onto other foot
Connections through spinal cord to other side of body
Electrical excitability
Are able to momentarily discharge the standing electrical potential between the intra and extra compartments
How all living cells establish a resting membrane potential
Selectively concentrating various combinations of species of charge carrying particles within the intracellular compartment
Results in conc differences
Energy differences then give rise to an electrical potential
Use of a cells membrane
Defines the cells boundaries
Encloses the organelles
Enables the cell to create an internal environment that promotes normal functions
Creates an internal environment that is different from outside
A phospholipid is made from…
Phosphate
Glycerol
Fatty acid
What are charge carrying molecules?
Organelle
Proteins
Anions and cations
What is the resting potential of nerve cells?
-65 to -70mv
Relatively negative inside cell
What happens to the resting membrane potential at death?
Discharge permanently
What are excitable tissues?
Nerve
Muscle
And some gland
How to create an intracellular compartment?
Selectively permeable membrane
Some particles can cross (assisted maybe)
Some can’t
Transport ATPases
Presence of ion channels
Non-selective ion channels
What factors effect the movement of a particle across the membrane?
Size
Electrical charge
Whether it’s recognised by transport systems
What are ion channels?
Protein in the membrane
Trans-membrane spanning proteins
Water filled central pore
Facilitate passive movement
Some are selective/some not
Most common ion channel types
Voltage gated
Ligand gates
Mechanically gated
Non-gated
Leak
What are ion pumps?
In cell membrane
maintain rmp
Don’t set up RMP
Some Known as ion-exchange pumps
Without max 10mv difference in RMP so not crucial
What is discharge?
No unequal distribution
No RMP
0mv
Concentration gradients of:
Na+
K+
Cl-
Ca2+
Inside
Low Na+ 15mM
High K+ 150mM
Low Cl- 9mM
Low Ca2+ 10^-7mM
Outside
High Na+
Low K+
High Cl-
High Ca2+
What is a graded depolarisation?
The level that the membrane is depolarised is linked to the strength of the stimulation
Threshold level…
Is the level of membrane potential at which graded depolarisations become an action potential
It’s different in different tissue types
Factors that determine the movement during an action potential
The concentration differences at RMP
depolarisation
When the AP is generated
At rest, what is the movement of ions?
K+ under a conc gradient of them moving outside, however the negative charge prevent diffusion
Na+ large conc outside cell, want to diffuse in
Nernst equation used for?
Calculate the membrane potential at equilibrium for each of ions
Nernst equation is
Eion = RT/zF ln ([outside]/[inside])
R is gas Constant
T is temp in kelvin
Z is valency of ion
F is faradays number
What is the Goldman Hodgkin Katz equation?
Modification of Nernst equation
Takes into account relative permeability of ions
As ion channels can change permeability
How is RMP maintained?
Slow leak of Na+ ions into cell and K+ ions out of the cell
Sodium potassium ATPase maintains ionic conc grad over time
Why is the RMP close to the Ek?
As the membrane is more permeable to potassium
Why is there little cl- movement?
As RMP is very close to E Cl-
Depolarisation steps in AP
Na+ enters cell
Membrane depolarises
To threshold
Na+ channels open (vg)
K+ channels open (vg)
Peak
Inactivates Na+ channels
More vg K+
K+ efflux
Repolarises