Patho 1 Flashcards
Nervous system
- what is functional unit
- what type is most common
- neuron
- multipolar
Ratio of neurons to glial cells
1:10 neuron:glia
Where are bipolar neurons mostly found?
specialized sensory organs (eye, ear, etc.)
Describe alpha motor neuron
- multipolar
- branching collaterals that form motor end plate
- collateral branches to other parts of nervous system: modulation
Neurons to areas with fine motor movement vs. less fine movement
- gross muscle w/o fine movement: one neuron will branch to supply 100s of muscle cells. No fine control
- extraoccular muscles have a one to one relationship between muscle cells and motor nerve for very fine control
Two cells that myelinate and where they are found
- Oligodendrocyte (CNS)
2. Schwann cells (PNS)
Describe myelin
concentric rings of the Schwann cell/oligodendrocyte’s plasma membrane
How much myelination do un-myelinated cells have?
a single layer
Number of axons wrapped by oligodendrocyte vs. Schwann cell
- 1 oligodendrocyte can wrap multiple axons
- 1 schwann cell per axon
Neural transmission
- nodes of Ranvier
- type of transmission
- nodes of ranvier: spaces between myelin
- action potential jumps from node to node, speeds up signal
- called saltatory conduction
- faster bc don’t have to change na/k flux the entire length of the axon, just at nodes
Synapses
- describe
- contact between neurons
- contain neurotransmitters released by axon terminal
Synapses
- elements
- presynaptic membrane
- postsynaptic membrane (contain receptors)
- synaptic cleft (very narrow)
Types of neural connection
- Axosomatic
- Axodendritic
- Axospinous to spine of dendrite
- Axoaxonic - usually inhibitory to modulate the action of the post synaptic axon
Difference between damage to peripheral vs. central nerve?
- Schwann cells in periphery can grow back
- Oligodendrocytes not only don’t grow back, they have an inhibitor for neural regrowth, why SC injury so bad…
How does a peripheral nerve repair?
- If cut a peripheral nerve, can reattach cut nerve to Schwann cell (tube).
- The cut axon will grow sprouts (like roots) and if one finds its way into the Schwann cell, it will regrow!
- 1 mm/day to reinnervate the downstream target
What is synaptic strength
- can create and remove synapses hourly
- the more synapses on a neuron, the more likely it will fire
what is quantal release of neurotransmitter?
Describes how much nt is released at one time
- if lots of nt is released, more likely to have downstream action
- if just a little nt is released, might just have a jump in voltage but not a true action potential
What is the general relationship between neurons and neural output?
What is the one exception?
- Most neurons do not have a one to one relationship, usually lots of input.
- One exception is neuromuscular junction with alpha motor neurons. If alpha fires, muscle will contract
Synaptic plasticity
- can create new synapses all the time
- occurs most in growing neuro system (children)
Memory theory
- part of synaptic plasticity
- if repeat something over and over, make new synapses to remember that information
What is long term potentiation?
- explanation for how neurons learn
- first, an action potential from one neuron will cause an action potential on a second neuron the first has a synapse on
- if the first neuron fires in a rapid burst, the second will still fire but the interaction at the synapse is different that the first situation
- The second neuron will “memorize” the first neuron’s impulse
- memory: excite neurons to the point the biochemistry is changed between the two neurons
Synaptic density
- two types
- spatial summation: lots of neurons fire at the same time on one neuron to cause 2nd neuron to fire
- temporal summation: one neuron releases nt over and over (rapid firing) which causes the 2nd neuron to fire
- Dr. McNeill explained temporal slightly different…
Axonal release of nt
- contain vesicles with Ach and other neuromodulators
- axon “knows” what to release, won’t release them all at once, depending on what is released has different downstream effects.
neuromodulators
substance P somatostatins bradykinins etc. peptide hormones
Transport of vesicles to axon terminal
- vesicles are made int eh cell body and transported to axon terminal
- sometimes have to travel a long distance! From SC to toe for instance
- attach to axon membrane via docking proteins (SNARES)
List the 5 types of glia
- astroctyes
- axon sheath cells (oligodendrocytes and Schwann cells)
- Microglia
- Ependyma
- Satellite cells
Astrocytes
- stromal cells between neurons
- protoplasmic, fibrous
- most numerous
function:
- support, form scaffolding the neurons exist in
- nutrient function for neurons
Microglia
- derived from monocytes
- scavengers that clean up “garbage” in the nervous system
- garbage from normal metabolism or injury
Ependyma cells
- line ventricles and central canal
- ciliated, beat to keep CSF moving
Satellite cells
- in DRG
- support cells
4 reasons the nervous system is vulnerable to injury
- metabolically active, requires constant O2
- Blood-brain barrier
- Glucose is only real fuel used in metabolism, no anaerobic metab products
- Large number and variety of receptors means targeted by many viral and chemical insults
Why does blood-brain barrier create vulnerability in the nervous system?
- when bad stuff gets past the barrier, it’s hard to get it back out
- otherwise it’s a good barrier to keep stuff out :)
What % CO to the brain?
25%
Timing of O2 deprivation and results in brain
- few seconds interruption is bad
- 30 seconds - unconscious
- 6 minutes - brain dead
Class example of viral attach on the nervous system
- HIV
- can have viral load of 0 in the periphery but every neuron in the CNS has HIV DNA in it
What factors contribute to neurotic symptoms in neuro disorders
- size of lesion: bigger usually cause more symptoms all else equal
- location: small lesion in wrong place can be worse than big lesion in less bad spot
- Momentum of lesion: faster worse
Two examples of different speed neuro disorders
- Stage 1 astrocytoma: grows very slowly
- Stage 4 glioblastoma: have months to live, very aggressive tumor
What causes symptoms in neuro disorder
Destruction of neuronal cell bodies or axons in a pathway
what is the principle nt in the brain?
glutamate
Two ways neurons can be damaged
- directly
- via stress due to dumping of excitatory nt (glutamate for ex)
Explain the collateral damage due to glutamate release after stroke
- glutamate excites nearby neurons to death
- extends the lesion through hyper-excitability
what is recommended therapy post stroke to reduce collateral damage
- don’t reduce bp
- want blood flow to wash out glutamate and keep area perfused
What are two nonspecific CNS reactions to injury
- cerebral edema
2. increased intracranial pressure
cerebral edema
- can be local or generalized
- brain swelling
two ways to avoid cerebral edema
- DM with high blood sugar. Reduce bs slowly (no more than 100 mg/dL/hour)
- alcoholic passed out, don’t give glucose without also given 150 IM shot of thiamine or thiamine deficiency can cause edema (Wernicke Korsakoff syndrome)
Increased intracranial pressure
- NL pressure
- what measurement is considered increased
- NL: 10-25 cm
- CSF opening > 25 cm is high
- happens when CSF volume exceeds physical capacity for expansion
causes of intracranial pressure
- tumor
- abscess
- edema
- blood
etc
Clinical presentation of increased intracranial pressure
- intermittent HA
- nuchal regidity
- mental slowness, confusion
- papilledema (will look like step off of arteries and veins)
List the three herniation syndromes
- Falx herniation
- Uncal herniation
- Tonsillar herniation
Falx herniation
- location
- cause
- describe
- what does it cause
- symptoms
- how common
- located under falx cerebri
- caused by pressure OR absences of pressure
- herniation of medial portion of parietal or frontal lobe
- impinge the anterior cerebral artery which can lead to stroke
- weakness in opposite LE
- rarest herniation
Uncal herniation
- location
- cause
- what does it cause/ symptoms
- Medial portion of temporal lobe (uncus)
- pressure from above the tentorium cerebelli pushes down to cause uncal herniation which presses on the side of the midbrain
- supra-tentorial
- pressure on CN III and IV = extraoccular eye movement issues one of first manifestations
- progressive weakening in body on opposite side of herniation dt pressure on midbrain
Tonsillar herniation
- cerebellar tissue (tonsils) is displaced through foramen magnum
- pressure on medulla
- suppresses cardiac and respiratory centers in medulla
- infra-tectorial
Uncus
- how sensitive?
- related to what common neuro issue
- one of the most sensitive areas of the brain, earliest to be affected by hypoxia
- related to seizures, prodrome of seizure in this location is bad smell
Where is CSF produced?
choroid plexus in ventricles
Path of CSF
- Lateral ventricle to third ventricle through cerebral aqueduct to the fourth ventricle the inferior as central canal
- fourth ventricle has 3 openings to allow CSF into subarachnoid space
- CSF reabsorbed into venous circulation by arachnoid granulations in venous sinus
- two lateral foramina of Luschka and one central foramen of Magendie
Hydrocephalus
increase in CSF volume in ventricles, may result in compression of brain tissue
hydrocephalus prior to skull bone sutures closing
head expands
think poor baby with huge head
current common treatment to avoid hydrocephalus
shunts in ventricles
Where is the MC cause of blocked CSF flow?
- cerebral aqueduct (very small canal)
- easily blocked by mesencephalon tumor
- results in expansion of third ventricle and two lateral ventricles
What are sx of hydrocephalus
sx of increased intracranial pressure: - HA - nausea - vomiting etc.
Slowly progressive hydrocephalus
- aka
- CSF pressures
- normal pressure hydrocephalus
- spinal tap opening pressure will be normal BUT pressure in ventricles is not normal
- seen in geriatric population
Slowly progressive hydrocephalus
- clinical manifestation
- progressive dementia
- gait disturbance
- urinary incontinence
