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Flashcards in Pathology Deck (29):
1

what are the 2 questions you should try to answer?

1- where is the lesion

2- what is (are) the lesions
(vascular, tumor, traumatic)

2

what is a lesion?

refers to a zone of localized dysfunction w/in the NS

anatomic- structural damage

physiologic- dysfunction in absence of structural lesions

3

symptoms=

subjective sensations resulting from the disorder

"I have a headache"

4

signs=

objective abnormalities detected on exam

"hyperactive reflexes"

5

syndrome=

a constellation of signs and symptoms associated with each other and suggest a common origin

6

neurologic manifestations may be ___ or ___

negative- loss of function

position- result from inappropriate excitation (seizure)

7

diagnosis depends on:

history**
observation of behavior **
time course
neuroexam
neuro imaging techniques

8

neuro exam:

history

cognitive function
-level of consciousness (confusion, alertness, etc)

gait
requires coordination of sensory, cerebellar, visual and vestibular functions

cranial nerves

motor system
weakness, endurance, side, fine finger movements, reflexes

sensory system
distribution

imaging
CT, MRI, xrays, PET, SPECT, etc

EMG

(PNS- check myotome and dermatome)
(CNS- cranial nerve testing- motor and sensory- some sort of provocative action)

9

what are the different diseases of the motor unit?

neurogenic diseases

myopathies

muscular dystrophies

myotonic disorders

disease of the synapse

10

neurogenic diseases tend to be more:

distal (glove- stocking distribution (hands/feet))

11

what are the 2 types of neurogenic diseases?

1- motor neuron
2-peripheral neuropathies

12

what are s/s of neurogenic diseases?

muscular spontaneous firing
-fasciculation
-fibrillations

13

neurogenic in the PNS

neuropathies

14

myopathies=

diseases of muscle

weakness is primary problem

tends to be proximal

15

muscular dystrophies=

myopathies with special characteristics
-heredity
-progressive weakness and wasting

**first thing to go that causes death is respiratory system

16

myotonic disorders:

abnormality of muscle fiber membrane

leads to marked delay in relaxation= increase stiffness

17

what is myasthenia gravis?

a disease of the synapse

"ALS"

autoimmune disorder-antibodies attack ACh receptors (Ach receptors on post-synaptic side disappear and there is no where for ACh to bind)

slow progressive course

weakness is patchy and does not confirm to the distribution of any single nerve

fluctuating weakness and decrease endurance are the major complaints

any age and more common in females

die from respiratory failure- too weak to breath (diaphragm)

18

classification of myasthenia gravis:

class I: eye muscle weakness

class II: eye muscle weakness; mild ms weakness
IIa: limb /axial muscles
IIb: bulbar/resp muscles

Class III: eye ms weakness; moderate ms weakness
IIIa: limb/axial ms
IIIb: bulbar/resp ms

Class IV: eye ms weakness; severe ms weakness
IVa: limb/axial ms
IVb: bulbar/resp ms

Class V: intubation needed to maintain airway

19

peripheral nerve injury:

chromatolysis= dissolution of neuron cell bodies

wallerian degeneration =
-1 day=neurofilaments break up; axons get shorter
-10 days= myelin sheaths breaks into lipid droplets around axon
-month= myelin gets denatured chemically
-3 months= macrophages invade degenerating myelin and phagocytose debris

20

nerve regeneration:

the single nerve fiber will "sprout" to form a regenerating unit. at the tip of each sprout is a growth cone with multiple filopodia. these filopodia will adhere to the basal lamina of the Schwann cell. the Schwanna cells are intimately associated with the regenerating fibers.

as the regenerating unit matures, the individual sprouts become myelinated. regeneration occurs along the basal lamina of the Schwann cells

21

CNS and PNS go through same process_____ degeneration

wallerian degeneration

22

axotomy in the PNS

not only affects injured neuron but also its synaptic partners and neighboring cells

the axon distal to the cut will degenerate and so will the myelin surrounding it. The Schwann cells will stay intact. axon degenerates and breaks down into little pieces; neurolemma sheaths stay intact; from cut to synapse the axon is gone. phagocytes clean out neurolemma sheath so its a clean tube.

proximally, the axon will also regenerate/retract one or 2 internodes and regenerates.
cell body starts producing lots of protein

23

transneuronal degeneration=

atrophy of certain neurons after interruption of afferent axons or death of other neurons to which they send their efferent output.

anterograde- "dying forward"
retrograde- "dying backward"

24

transneuronal atrophy

CNS neurons have a trophic effect upon each other

25

apoptosis=

a mechanism of orderly, genetically programmed cell death

26

synaptic stripping=

when synaptic terminals withdraw from the neurons and are replaced by the processes of glial cells

27

peripheral regeneration:

Good

chemotropic factors secreted by schwann cells attract axons
-schwann cells give off facilitory factors that help peripheral nerve regeneration

failure to contract a schwann cell causes a neuroma and cell death

adhesive molecules within the distal stump promote axon growth along cell membranes

inhibitory molecules in the perineurium prevent the regenerating axons from going astray

has neurolemma sheath

surgery-3 weeks

28

the more proximal the injury the higher the change the nerve will:

die
a lot of length of nerve needs to be regenerated

29

central regeneration:

poor

glial scare

growth inhibition by oligodentroglia
-neurite growth inhibitors (in myelin)

generally don't have the trophic factors required for successful regeneration
-no neurolemma sheath