Nervous 3 Flashcards
(102 cards)
1
Q
What re the 2 main functions of the ear and the parts of the ear that undergo these
A
hearing
○ auditory system: external ear, middle ear and cochlear part of inner ear
balance
○ vestibular system: vestibular part of inner ear
2
Q
external ear what part of the ear, what consists of and how separated from middle ear
A
- visible part of ear
- consists of pinna (auricle) and external acoustic meatus
- separated from middle ear by tympanic membrane
3
Q
Pinna what also called, what part of the ear, what 4 things made of
A
auricle in external ear • funnel-shaped structure protruding from surface of head • auricular cartilage • auricular muscles (CNVII) • skin • blood vessels
4
Q
external acoustic meatus what is it, what part of the ear, what made of and the shape
A
- canal running from narrow part of auricular cartilage to tympanic membrane in external ear
• cartilaginous (auricular and annular cartilages) and osseous parts of wall
• lined with skin containing sebaceous and ceruminous glands
• fine hairs may be present
• curved in dog (vertical and horizontal portions)
5
Q
tympanic membrane what conissts of and what is on the lateral and medial surface
A
• thin, complete membrane
• consists of fibrous tissue:
○ firmly attached to osseous tympanic ring (temporal bone)
○ covered laterally by epidermis and medially by mucosa
6
Q
what are the 3 features of the middle ear
A
1) tympanic (middle ear) cavity
2) auditory ossicles
7
Q
Tympanic cavity what filled with, how connected to nasopharynx and inner ear, function
A
- air-filled cavity in temporal bone
- separated from external acoustic meatus by tympanic membrane
- connected to nasopharynx by auditory tube
- connected to inner ear by vestibular and cochlear windows
- contains auditory ossicles located dorsally
- changes air vibrations (sound waves) into mechanical movement through auditory ossicles
- expanded ventrally within tympanic bulla
8
Q
Auditory ossicles what are the 3 ossicles, where placed, how moved and function
A
malleus, incus and stapes:
○ Malleus: - ‘handle’ embedded in medial aspect of tympanic membrane
§ visible through tympanic membrane when viewed with otoscope
○ Incus: - sits between malleus and stapes
○ Stapes: - base sits in vestibular window
• attached to wall of tympanic cavity by ligaments
• can be moved by contraction of m. tensor tympani (attached to malleus) and m. stapedius (attached to stapes)
○ dampens transmission (protective device)
• movement transmitted from tympanic membrane to vestibular window causes movement of fluid in inner ear
9
Q
inner ear what consist of and within
A
Bony labyrinth - vestible, semicicular canals, cochlea
Membranous labyrinth - utricle and saccule, semicircular ducts, cochlear duct - contains endolymph and surrounded by perilymph
10
Q
vestibular system where in the ear, function and how works
A
• organ responsible for sensing body position
• static and kinetic sensations perceived by hair cells in specialized sensory regions:
○ 40-80 cilia and one kinocilium on apical surface of hair cells
○ movement of cilia towards or away from kinocilium results in depolarization or hyperpolarization of hair cell, and excitation or inhibition of firing of neuron at base of hair cell
11
Q
Utricle and saccule what are they where found in the ear and main function
A
inner ear Utricle and saccule • two membranous enlargements • utricle - at base of semicircular canals • saccule: § ventral to utricle § connected to endolymphatic duct (probably involved in absorption of endolymph) • sense static position through maculae:
12
Q
how does utricle and saccule sense static position through maculae
A
- monitor position of head with respect to gravity
- kinocilium and cilia of hair cells project into otolithic membrane (gelatinous matrix containing calcium carbonate/protein crystals, i.e.otoliths)
- pull of gravity on otolithic membrane causes shearing force on cilia
- macula in saccule oriented in vertical plane
- macula in utricle oriented in horizontal plane
13
Q
semicircular ducts where in the ear, how many found, what contain
A
three in each ear located at right angles to each other - inner ear
• each duct contains enlargement at one end - ampulla:
○ contains sensory region (crista)
• sense dynamic position due to movement of endolymph
• hair cells located on crista, a ridge of cells projecting from wall of ampulla
• cilia of hair cells project into gelatinous material - cupula:
○ cupula readily deflected by movement of endolymph created by rotation or deceleration of head
14
Q
cochlear part of inner ear what is it, ducts and what communicate with
A
- Cochlea: - region of temporal bone housing cochlear duct
- spiral canal of cochlea winds around an osseous pyramid (modiolus)
- cochlear duct adherent to walls of spiral canal, subdividing perilymphatic space into two longitudinal canals:
- scala vestibuli (dorsal)
- scala tympani (ventral)
- scala vestibuli communicates with perilymphatic space of vestibule
- scala tympani ends at cochlear window
- scala tympani and scala vestibuli communicate with each other at blind apical end of spiral canal
15
Q
Basilar membrane where in the ear, what part of, function and how occurs
A
inner ear
part of cochlear duct adjacent to scala tympani
• transduces sound into nerve impulses
• contains hair cells with tips of cilia embedded in gelatinous tectorial membrane (cochlear hair cells have no kinocilia)
• base of hair cells in contact with nerve endings leading to neurons in spiral ganglion (in modiolus)
16
Q
what are the 9 steps in the hearing process
A
vibration of tympanic membrane ⇓ vibration of auditory ossicles ⇓ vibration of stapes against vestibular window ⇓ waves in perilymph of scala vestibuli ⇓ waves in endolymph of cochlear duct ⇓ vibration of basilar membrane ⇓ distortion of hair cell cilia resting against tectorial membrane ⇓ depolarization of hair cells ⇓ impulse in cochlear nerve
17
Q
List the 3 main nerves involved with the ear
A
1) vestibulocochlear nerve
2) facial nerve
3) trigeminal nerve
18
Q
vestibulocochlear nerve what are the 3 ways its involved in the ear
A
- nerve endings in maculae of utricle and saccule, and in ampullae of semicircular ducts have cell bodies in vestibular ganglion in vestibular branch of CNVIII
- nerve endings in basilar membrane of cochlear duct have cell bodies in spiral ganglion in cochlear branch of CNVIII
- vestibular and cochlear branches unite and travel to brainstem through internal acoustic meatus of temporal bone
19
Q
Facial nerve what are the 3 ways it is involved with the ear
A
- enters internal acoustic meatus with CNVIII then travels in facial canal in temporal bone adjacent to inner ear
- gives off a small branch within temporal bone to m. stapedius
- emerges from skull caudal to external acoustic meatus
20
Q
Trigeminal nerve how is it involved with the ear
A
branch of mandibular division supplies m. tensor tympani
21
Q
Within the vestibular system what are the 2 main areas of receptors and receptors within
A
Crista ampullaris
- Movement of endolymph causes deflection of cilia – increase or decrease in firing of CNVIII
1. Ampulla – dilation within the semicircular duct
2. Cupula – gelationous material
3. Neuroepithelium
Macula (one each in utricculus and saccule)
•Neuroepithelium covered by otolithic membrane
22
Q
Within the vestibular system what are the 2 main areas, their function and how achieve
A
- Tell you which way is up and which way your head is moving
1. Cristae ampullaris
• Paired functionally
• Respond to acceleration/changes head position
• Tonic firing from CNVIII each side
2. Maculae
• One oriented vertically one horizontal
• Respond to gravity
• Movement of otoliths relative to hair cells generates firing in CN VIII
23
Q
Function of Semicircular ducts and canals and how it achieves this, what results
A
- Remember 3 ducts on each side (left and right ear), each in different plane either x,y or z therefore no matter the direction you move your head always movement of fluid in at least one semicircular canal
- Head turning generates increased activity in CNVIII on side of turn + decreased activity on opposite side (cristae ampullaris)
- Vestibular nuclei compare input from both sides to determine direction of turn
Example:
1. turn of head to R gives ↑↑ input from R CNVIII and ↓↓ input from L CNVIII
2. Vestibular nuclei (within brainstem) compare R and L CN VIII activity and decide R>L - therefore must be turning our head to the right side
3. This results in increased output from R vestibular nuclei - Efferents from vestibular nuclei result in:
1. Change in eye position (nystagmus) towards side of head turn (fast phase)
2. Increase in ipsilateral extensor tone etc on side of head turn (otherwise body may collapse on that side)
24
Q
Efferents from CNVIII where project to and the 3 areas that are then projected to
A
- Majority project to vestibular nuclei within the brainstem
- Small number project direct to cerebellum
From vestibular nuclei - spinal cord
- brainstem
- cerebellum
25
What occurs with the vestibular nuclei projecting to the spinal cord
Lateral and medial vestibulospinal tract
• Interneurons within ventral horn GM (grey matter)
• Facilitatory to ipsilateral extensors + contralateral flexors
• Inhibitory to ipsilateral flexors + contralateral extensors
26
What occurs with the vestibular nuclei projecting to the brainstem and cerebellum
Brainstem
• Through medial longitudinal fasciculus - nuclei CN III, IV, VI for eyeball movement control
○ Good to look at clinically for issues with midbrain
• Projections to vomiting centre in reticular formation - motion sickness
• Poorly defined projections to thalamus for cerebral awareness
Cerebellum
• Via caudal cerebellar peduncle to flocculonodular lobe + fastigial nucleus
• Coordination movements of eyeballs, head, neck, limbs with rest of body
27
What are the 3 main places that leads to dysfunction in the vestibular system and what disease corresponds
1) CNVIII/receptors (peripheral vestibular disease)
2) Vestibular nuclei (central vestibular disease)
3) Cerebellum (paradoxical vestibular disease)
28
What occurs with peripheral and central vestibular disease and what clinical signs
Peripheral vestibular disease: - very common
- Dysfunction of one side leads to loss of tonic firing CN VIII
- Vestibular nuclei interpret as a head tilt to opposite side (loss of input from the other side - R>L if left is gone)
○ Subsequent increase in extensor tone and extraocular signals on side opposite lesion lead to clinical signs
§ Head tilt/circling towards side that is damaged and eyes to the opposite side
- SAME THING WITH CENTRAL VESTIBULAR DISEASE
29
What occurs with paradoxical vestibular disease and what clinical signs and how know this is occurring
- Normally cerebellar nuclei suppress vestibular nucleus function
- Cerebellar lesions (ipsilateral) - ↓inhibition of one side vestibular nuclei (i.e. disinhibition)
- Comparison of vestibular nuclei activity – ipsilateral side ‘appears’ more active suggesting head is being turned to the side of the lesion
- Vestibular signs appear suggesting vestibular lesion contralateral to side of lesion
○ Get head tilt towards side that is normal and eyes to the side that is damaged
- To know this is occurring get cerebellum signs on the side opposite to the head tilt (neuro exam is opposite to the head tilt)
30
What are the 4 main clinical signs of vestibular disease
1) Head tilt (towards side of lesion)
2) Nystagmus (fast phase of eye away from side of lesion)
3) Circling/rolling/falling to side of lesion
4) Nausea/vomiting
Paradoxical is opposite
31
Cerebellum what is its function and what side of the body does it control
- Coordinate fine motor control
○ Doesn't initiate anything - from what we know at the moment
- Right side of cerebellum controls ride side of the body
32
What are the 2 main areas of pathways that come from the cerebellum and list some pathways within
From the spinal cord
- Spinocerebellar tracts
○ Dorsal spinocerebellar
○ Ventral spinocerebellar
○ Spinocuneocerebellar
○ Cranial spinocerebellar
- Transmit unconscious proprioception - Ipsilateral
2. From the motor centres for feedback
1. Pyramidal system (cerebral cortex)
○ Via pontine nuclei
○ Contralateral control
2. Extrapyramidal system - more important in dogs and cats
○ Indirect (via olivary nucleus; contralateral)
○ Direct (from tectum and vestibular nuclei)
○ From hindbrain motor centres
33
What and how pathways feed into the cerebellar cortex and what leads to
Level of foramen magnum
- Dorsal, and cranial spinocerebellar tract and Spinocuneocerebellar tract come up ipsilateral to cerebellar cortex, ventral spinocerebellar is contralateral (crosses twice)
Brainstem
- Other motor pathways have to feed in via brainstem nuclei (pyramidal and extra-pyramidal pathways)
- From contralateral brainstem goes to cerebellar cortex except vestibular nuclei (ipsilateral)
SAME TIME SEND INFORMATION TO THE CEREBELLUM
- Compared with proprioception information from the spinal cord
- To fine tune the action
Eventually sending signals to skeletal muscle
34
Feedback circuits or pathways leaving the cerebellum what are the 2 main neurons and their functin
Neuron 1: Purkinje neuron cerebellum
○ Has projections and collects information from all the pathways
Neuron 2: Cerebellar nuclei; projections to:
1. Thalamus (Pyramidal and extrapyramidal feedback)
2. Midbrain motor centres (extrapyramidal feedback)
3. Hindbrain motor centres (extrapyramidal feedback)
○ To readjust the motor programs that go back down into the spinal cord
• There are NO descending spinal pathways efferent from the cerebellum – the cerebellum cannot initiate movement
35
What are the 3 main regions of the cerebellum and what input/output involved
1) vestibular areas - vestibular input
2) proprioceptive areas - spinocerebellar input
2) feedback areas - from pyramidial and extrapyramidial system feedback
36
what are the 3 cerebellar functions
1) coordination and regulation of movement - combination of proprioceptive input + copy of information from motor centres of pyramidal/extrapyramidal systems
1. pre-control projections from motor centres (commands issued) compared with feedback pathways
2. Movement regulation – comparison of spinocerebellar input with intended action; feedback pathways alter motor command centre output subsequently
2) Control of Posture
- Similar functioning to coordination/regulation steps
- Addition of special senses (vision, balance)
- Major action over postural muscles (hypaxials/epaxials)
3) Other functions
- Mood/emotion;
37
What are the 3 areas of dysfunction in the cerebellum and the clinical signs associated
1) Vestibulocerebellum
- Vestibular signs: positional nystagmus, truncal sway, paradoxical vestibular syndrome
2) Spinocerebellum
- Exaggerated postural testing, increase in motor tone (extensors)
3) Pontocerebelum
Intereference with feedback: dysmetria (hypermetria), intention tremors
38
Conscious and subconscious proprioception where project to and function
Conscious proprioception
- Projects to the contralateral cerebral cortex
- Start off the movement
Subconscious proprioception pathways
- Project to the ipsilateral cerebellar cortex directly so only 2 neuron system
- Ensure the movement is smooth and coordinated by using patterns stored within the brain
39
where does conscious proprioception travel and what does defect result in
Conscious proprioception primarily travels in the dorsal funiculus = dorsal column which becomes the medial lemniscus in the brainstem
- fasciculus gracilis from caudal to the forelimbs (ie hindlimbs etc)
- fasciculus cuneatus from the forelimbs and neck.
DEFECTS - foot in normal position but abnormal weight bearing -> abnormal posture of the limb
40
where does subconscious proprioception travel ad what does dysfunction result in
Subconscious proprioception primarily travels in the lateral funiculus
- dorsal and ventral spinocerebellar tracts (still in lateral funiculus) from the caudal body
- cranial spinocerebellar tract from the forelimbs and neck
DEFECTS - abnormal positions of the limb -> such as standing on themselves (may lead to tripping)
41
What are the 5 effects from light entering the eye
1. Vision
2. Control over pupil size
3. Input into movement of pupils
4. Input into turning the head and neck
5. Arousal to the cerebral cortex
42
How many neurons involved in the vision pathway and the pathway itself
3 neuron pathway
1) Retina - neuron 1
2) Optic nerve - neuron 2
3) Optic chiasm
4) Optic tract
5) Lateral geniculate nucleus (thalamus) - neuron 3
6) Optic radiation
7) Occipital (visual) cortex
- now can see
43
Optic chiasm what occurs here that is important and how is it species specific
Axons decussate at optic chiasm
How much of the axons that cross at the optic chiasm changes
• Species specific - predator and prey different vision and visual field overlapping
○ 50% in primates
○ 65% cats
○ 75% dogs
○ 80-90% sheep/cows/horses
44
what is the menance response and what is important about it
- Move something towards eye quickly and watch the eye blink
• Learned: - THEREFORE NOT A REFLEX
- 14-16 wks in dogs
- 6mnths humans
45
what is the 12 steps in the menance response and what pathway does it include
1) Retina - neuron 1
2) Optic nerve - neuron 2
3) Optic chiasm
4) Optic tract
5) Lateral geniculate nucleus (thalamus) - neuron 3
6) Optic radiation
7) Occipital (visual) cortex
Visual pathway
8) Parietal (motor) cortex
9) Ipsilateral cerebellar
10) Ipsilateral motor nucleus of facial nerve in the medulla oblongata
11) Facial nerve
12) Orbicularis oculi (eyelid constrictor) muscle
46
What are the 9 steps in the pupillary light reflex
1) Retina
2) Optic nerve
3) Optic chiasm
4) Optic tract
5) Pretectal nucleus (instead of lateral geniculate like in visual)
○ Cross over in midbrain so if one eye stimulated - Both react
6) Parasympathetic nucleus of oculomotor nerve
7) Ciliary ganglion
8) Ciliary nerves
9) Iris constrictor muscle
47
What are the 4 areas that the pretectal nucleus/rostral colliculus projects to and the result
1) Eyeball movement
- Projections from rostral colliculus to CN III, IV, VI nuclei
- Keeps objects in centre of field of view
2) Pupil constriction
- From rostral colliculus to pretectal area – CN III (parasympathetic nucleus)
3) Control over turning of head and neck
- From rostral colliculus to tectospinal pathway - reflex movement to move head to where sound came from
4) Arousal
- From rostral colliculus projections into reticular activating formation
- General arousal stimuli to cerebral cortex
48
Dysfunction of the pupillary light reflex what occurs if optic nerve or retina lost in one eye or optic tract defect
1. Optic nerve or retina lost in one eye
- If shine in the contralateral eye - still get reflex in both due to midbrain cross
- If shine in the ipsilateral eye no pupillary light reflex
2. Optic tract defect
- Pupillary light reflex in both
49
Hearing how many neurons involved and the pathway
1) Neuron 1
- receives input from neuroepithelial cells in spiral organ inner ear
- Synapses in cochlear nucleus
2) Neuron 2
- Cochlear nuclei – axons decussate forming trapezoid body, then – lateral lemniscus then synapse on…
3) Neuron 3
- Medial geniculate nucleus (contralateral) - tells the brain what information is coming in
50
Taste how many neurons and the pathway
1) Neuron 1
- Ganglion CN VII/IX (rostral 2/3, caudal 1/3 tastebuds); axons – CN VII, IX
2) Neuron 2
- Nucleus of solitary tract
3) Neuron 3
- Ventral thalamic nuclei
51
Smell how many neurons and the pathway
1) Neuron 1
- Olfactory neuroepithelial cell; axon – central process – passes through cribiform plate and synapses in olfactory bulb
2) Neuron 2
- Olfactory bulb; axon – olfactory peduncle, divides into medial and lateral olfactory tracts – lateral olfactory tract axons – olfactory tubercle
3) Neuron 3
- Olfactory tubercle; axons project to pyriform lobe
- No relay in thalamus
52
What are the 9 clinical signs in forebrain disease
1) Blindness (with intact pupillary light reflexes - no menace response)
2) Proprioceptive deficits (contralateral) - generally normal gait
3) Circling
4) Compulsive walking
5) Head pressing, stuck in a corner
6) Changes in behaviour
7) Changes in sensitivity to stimuli
8) Hemineglect/hemiinattention
9) Seizures and epilepsy
53
The limbic system, what is the function and how areas of the brain does it involve
§ Emotion, memory, behaviour, personality
§ Rage syndrome in cocker spaniels – episodic dyscontrol; limbic epilepsy?
Involves A LOT of brain centers - dont need to know
54
What are seizures and epilepsy
Seizures:
- Paroxysmal discharge electrical from group of neurons within the brain that results in transient change in behaviour or neurological status
- Usually synchronous and excessive
- seizure is physical manifestation of neuronal activity
• Epilepsy:
- Recurrent seizures
- Abnormally low seizure threshold
55
What is involved with seizures and how occur
```
All brains have a seizure threshold
• Imbalance between excitatory and inhibitory mechanisms governing neuronal depolarisation:
• Excitatory NTs: aspartate, glutamate
• Inhibitory NTs: GABA, glycine
- likely to be very complex
```
56
Bony orbit what is difference between horses and the dog
- In horse it is complete
| - In other animals such as the dog it is incomplete with the orbital ligament to complete it
57
Auriculopalpebral nerve how to block and why would you block
- Blocked by an injection between the caudal end of the zygomatic arch and the base of the ear
○ This facilitates examination of the eye as it blocks innervation to the orbicularis oris that closes the eye
58
What occurs with peripheral vestibular disease if lesion is on the left
- Right interpret as increase signalling
○ Think it's turning to the right
- Slow phase to the left
- Fast phase flick back to the right
- Flexor stimulation (extensor inhibition) on the left
○ Circles to the left and head tilt on the left
59
Slow and fast phase movement of the eye what normally occurs in turns of moving the head
Slow phase movement of eyes as turning head, phase fast then flicks eyes back towards the field of vision as get to the end of the field of vision
§ Fast phase is to the way you are turning your head, slow phase is the opposite way
§ MOVE TO THE RIGHT NORMALLY -> slow phase to the left and fast phase to the right
60
if Cat repeatedly falls to the left, left head tilt and nystagmus and fast phase to the right where is the lesion?
Lesion is in the LEFT VESTIBULAR APPARATUS
61
What is horners syndrome and the 4 main clinical signs
Disruption of sympathetic innervation of the eye results in:
- Pupillary constriction (miosis)
- Retraction of the eye (enophthalmos)
- Narrowing of the palpebral fissure (ptosis)
- Prolapse of the third eyelid
62
List 4 reasons the eye is a delicate structure
1) External, fully exposed, vessels limited in extent and location
2) The optical function requires that cornea, lends and internal fluids be transparent
3) Closed hollow sphere filled with fluid or gel in which are suspended soft tissues and a hard lens, all in delicate balance.
4) Closely integrated set of tissues of very different densities that each have different, although generally limited, capacities for repair, and no capacity for job sharing
63
List 7 things that result from a blunt trauma glancing blow and why occur
1) Chemosis - oedema swelling of the conjunctiva
2) Haemorrhage within the eye
○ Can get corneal blood staining -> forms hemosiderin
3) Epiphora -> tear production (pain)
4) Blepharospasm -> squinting
5) Loss of epithelial barrier - may permit bacterial or other infectious agents entry
6) Corneal ulceration
7) Corneal oedema - if blow is sufficiently energetic that it disrupts the endothelium
○ Damage to endothelium -> failure of endothelium pump resulting in movement of water into corneal
64
what occurs with active deformation of the globe without rupture and the 2 main results
1. Deformation of the cornea
2. Iris is pushed backwards onto lens
○ Ring of pigment on the lens may be left behind after
Increase intra-ocular pressure
RESULTS
1. pupillary block to aqueous flow
2. contraction causes change in the shape of the eye
65
pupillary block to aqueous flow how occurs and what are the 3 main things it may result in
compression of the iris against the anterior surface of the lens
- Fluid wave into the fragile tissue (root of the iris) 1. -> counter coup injury (on the opposite side of the blunt tumour)
2. May result in tear
3. Haemorrhage (Hyphema - pooling of blood inside the anterior chamber of the eye)
§ small amount readily cleared
large amount obstruction of the angle of the eye, hypoxia of the eye, clot formation within the eye (long time)
66
Changes to the shape of the eye what is the main result and the 4 main results from this
disruption of the lens capsule
1. Traumatic cataract
2. Lens luxation - inclined to fall forward
§ Leads to oxygenation deficits and vascular hyperplasia
□ May lead to Rubeosis iridis (red iris)
- Movement of blood vessels across the eye that are not supported within tissues therefore they easily haemorrhage
3. Photoreceptor damage - partial vision loss
- May repair spontaneously
4. Uveitis with rubeosis and flare (protein loss)
If have green eyes
67
Open eye trauma how occurs
severe enough can cause the globe to rupture
| The uvea will readily herniate through a rupture or a wound - iris prolapse
68
Sharp.penetrating trauma what are the 10 main results
1) epithelialisation - implantation of epithelium from outside to inside - cover surface
2) fibrosis - fibrosis lodged within impedes the function
3) retinal detachment - hypoxic injury
4) infection - endopthalmitis
5) foreign bodies
6) retinal tear
7) hyphaemia
8) corneal oedema
9) cataract - cloudy lens
10) cyclitic membrane
69
what occurs with foreign bodies within the eye and what is interesting about the lens
Foreign bodies
○ Inert materials can cause little to no reaction
○ iron and copper can cause issues -> oedematous reaction caused by toxic effects of these metals
○ Some objects may carry bacteria into the eye
○ Grass seed pushed around the orbit and damaging the tissue due to movements of the eye
Lens
○ The body doesn't recognise the lens material as self so if capsule around lens is broken then inflammatory response
○ Does not heal
70
what tissue is capable to repair and how does it repair
Cornea
- similar to skin wound healing, scaring less than skin
- no endogenous blood vessels to assist
○ Various soluble factors that are required for repair must be delivered by indirect means such as tears, aqueous humour or limbal vessels
○ Inflammatory cells enter a wound after about 12-24 hours -> Entry from the limbus and tear film
71
For erosions (loss of epithelium) what are 4 results
1) remaining epithelium is quick to cover defect - no visible evidence
2) superficial epithelium damage (small sharp foreign bodies) -
3) deep stromal injury or corneal performation - exposure to aqeous humour which may close small wounds
4) mild stromal injury and soem full thickness epithelial injuries
72
What are the 2 main negative outcomes of erosions of the eye and 4 important healing factors
1) scarring
2) hazing
Important healing factors
○ Degree of wound edge apposition
○ Sterility of the wound
○ Host factors are important
○Integrity of the endothelial layer
73
Retina what cells regenerate and which don't, what occurs with tearing of the retina and retinal detachment
- Glia such as muller cells and retinal pigment epithelium can repair
- Photoreceptors and neurons don't regenerate or repair
○Tearing of the retina leads to glial scar but usually inconsequential
○ Retinal detachment can spontaneously reattach or may stay off leading to irreversible blindness
74
Lens how important, what occurs with lens luxation and catarct formation, small penetrating wounds
- More likely to be of importance to vision in animals
- Cataract formation and lens luxation will be irreversible
- Small penetrating wounds may heal via fibrous metaplasia of the lens epithelium
○ Maturation into myofibroblast like cells
Contract, distorting the capsule and further impairing vision
75
What are the 3 important preliminaries in a neurological examination and important things within
```
Signalment:
- Breed – many breed related conditions
- Age
- sex
• History
- Prior disease
- Worming, vaccination hx
- Current medications
- Potential exposure to toxins/ environmental factors
• Current problem:
- Onset
- Progression
- Time course gives important clues as to underlying aetiopathogenesis
```
76
What are the 3 main areas a neurological lesion could be and the things to look for
```
• Is the problem in the brain?
- Mentation
- Cranial nerve tests
- Gait
• Is the problem in the spinal cord?
- Gait
- Proprioception function tests:
○ Which limbs are normal and which are abnormal?
- Reflexes
○ UMN or LMN lesion?
• Is the problem in the peripheral nervous system or musculoskeletal?
- Weakness and exercise tolerance
- LMN signs
```
77
List 4 signs of forebrain syndrome - telencephalon
1) animal usually normal giat
2) seizures
3) altered behaviour or mental state
3) pacing, circling, head pressing
4) postural reactions depressed contralterly
78
List 4 signs of diencephalic syndrome
1) normal gait
2) vision impariment if optic chiasm affected
2) abnormal temperature regulation
3) endocrine abnormalities
4) altered mental status and behvaiour
79
list 3 clinical signs of midbrain syndrome
1) weakness and paralysis of all 4/hemi
2) postural reaction deficits contralterally or ipsilaterally
3) mental depression, stupour and coma if large lesions
80
cerebellar syndrome list 4 clinical signs
1) intention tremors of head and eyes
2) postural reactions present but exagerated
3) menace deficit but normal vision
4) truncal ataxia
81
how to test the olfactory nerve
- Alcohol sniff test - should produce aversion in normal animals
- licking nose
82
How to test the optic and oculomotor nerve
OPTIC
1) menace response test
2) pupillary light response
OCULOMOTOR
1) pupillary light response
2) strabismus - all extraocular muscles except for the dorsal oblique and lateral rectus
Leads to dorsolateral deviation and medial rotation of the dorsal part of the pupil
83
How to test trochlear and Abducens
TROCHLEAR
- Strabismus - dorsal oblique muscle of the eye
○ Leads to lateral rotation of the dorsal pupil
ABDUCENS
- Strabismus - innervates lateral rectus of the eyeball
○ Dysfunction results in medial deviation of the eyeball
84
How to test trigeminal nerve
1. Corneal reflex - should get blink (CNVII - facial as well)
2. Palpebral (medial and lateral) - medial and lateral canthus of the eye should elicit a blink
○ Medial innervated by opthalmic branch of CNV
○ Lateral innervated by mandibular branch
○ Also tests CNVII - facial
3. Pinching the lip - gently pinch the upper and lower lips of the animal and lips should be withdrawn
○ Upper lip -> maxillary branch
○ Lower lip -> mandibular branch
○ Also tests CNVII - facial
85
How to test the Facial nerve
1. Menace response
2. Corneal reflex
3. Palpebral reflex
4. Pinching/stimulation of the lips
5. Facial asymmetry - drooped lip, dropping food, difficulty prehending food
86
How to test the vestivulocochlear and glossopharyngeal nerve
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Vestibulocochlear
1. Oculocephalic reflex (physiological nystagmus) - normally get slow phase away from direction of movement and fast phase towards
○ CN III (oculomotor)
○ CN IV (trochlea)
○ CN VI (abducens)
2. Head tilt, spontaneous nystagmus, leaning/falling/circling towards the side of the lesion
Cranial nerve IX - Glossopharyngeal
- Gag reflex
○ CN IX (glossopharyngeal)
○ CNX (Vagus)
○ CN XII (Hypoglossal)
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87
How to test the vagus, accessory and hypoglossal nerve
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VAGYS
1. gag reflex
2. megoesophagus and laryngeal paralysis
ACCESSORY
- difficult to assess
HYPOGLOSSA
- gag reflex, decreased tongue movement
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88
List the 4 signs with UMN and LMN lesions
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UMN
1) spastic paralysis
2) increased reflexes
3) increased extensor tone
4) may lose sensation
LMN
1) flaccid paralysis
2) reduced extensor tone
3) decreased/absent reflexes
4) often sensation is intact
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89
What is clinical signs occur with cervical (C1-5) syndrome
- UMN signs to thoracic limbs, hindlimbs and bladder
○ Weakness or paralysis in all four limbs (tetraparesis/tetraplegia) or hemiparesis/hemiplegia
○ Normal or increased reflexes and muscle tone in all limbs, extensor rigidity in limbs on the same side as the lesion
- Proprioceptive deficits in limbs on the same side as the lesion or in all limbs
- Respiratory difficulty – phrenic nerve damage (C5)
90
what is the clinical signs that occur with Cervicothoracic (C6-T2) syndrome
- LMN signs in thoracic limb(s)
○ muscle atrophy after 1-2 weeks
○ Loss of motor tone
○ Flaccid paralysis
○ Decreased/absent reflexes
- UMN signs to hindlimb and bladder
○ without muscle atrophy
○ Normal or increased reflexes and muscle tone
- Postural reaction deficits in one thoracic limb, in limbs on the same side, or in all limbs
- Cutaneous trunci reflex depressed or absent (unilaterally or bilaterally)
- Horner's syndrome
91
what are the clinical sgins that occur with thoracolumbar (T3-L3) syndrome
- UMN signs in hindlimb and urinary bladder
○ Increased muscle tone in pelvic limbs
○ Pelvic limb reflexes normal or brisk may see clonus or crossed extensor reflex
○ No muscle atrophy in pelvic limbs
○ Urinary incontinence
○ Hindlimb reflexes increased or normal
- Forelimbs unaffected
- Proprioceptive deficits in pelvic limbs
- Reduced/absent cutaneous trunci reflex behind level of lesion
- Increased local sensitivity (hyperesthesia) at level of lesion
- + Schiff-Sherrington posture (severe lesions) -> high state of extension of the forelimbs - Crossed extensor reflex
92
what are the clinical signs that occur with lumbosacral (L4-S3) syndrome
- LMN sings to the hindlimbs and urinary bladder
○ Weakness/paralysis of pelvic limbs and tail
○ Depressed pelvic limb reflexes and flaccid muscle tone
○ Muscle atrophy in pelvic limbs, and/or hip muscle
○ Urinary incontinence
- Forelimbs unaffected
- proprioceptive and deficits in pelvic limbs
93
what are the 5 main properties of an ideal general anaesthetic
1. Should render the patient unconscious
2. Should also provide:
a. ANALGESIA
b. MUSCLE RELAXATION
c. MINIMAL CARDIORESPIRATORY DEPRESSION
3. Induction and recovery rapid and smooth
4. Depth of anaesthesia easily titrated
5. Non-irritant and non-toxic
94
What are the 4 main signs of depth of anaesthesia
1. Depression of brain function
- Eyeball rotation-nystagmus, pupil dilation/constriction other - MARKERS OF CNS DEPRESSION
2. Cardiovascular depression (HR, BP)
3. Respiratory depression (O2-sat, RR)
4. Muscle relaxation
95
What are the 4 stages of anaesthesia and what stage do you want
Stage 1 - amnesia, euphoria
Stage II - "excitment", delirium, resistance to handling
Stage III - surgicial anaesthesia - unconsciousness, regular respiration, decreasing eye movement
Stage IV - medullary depression, respiratory arrest, cardiac depression and arrest
Need to give the right dose quickly enough to go through stage 1 and 2 quickly and bypass
96
Anaesthetic risk what are the problems with respiratory and cardiovascular
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Respiratory
All anaesthetics increase likelihood of:
- Impaired ventilation
- Depression of respiratory centre
- Obstruction of airways
- Retention of secretions
Cardiovascular
All anaesthetics increase likelihood of:
- Decreased vasomotor centre function
- Peripheral vasodilation
- Cardiac arrythmias - hypotensive
Inadequate response to fall in BP or CO -> baroreflex is blunted
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97
inhalaed anaesthetic what are the two types and what is the important property of the inhaled anaesthetics
- Gas in the tube or liquid that vaporises at room temperature
Solubility
○ Anaesthetic gases and vapours dissolve in blood and tissues
- Solubility in blood and tissues determines speed of induction and recovery
98
Solubility of an anaesthetic agents what expressed as, the two types and why important
- Solubility is expressed as partition coefficient (PC)
○ Partition coefficient: ratio of anaesthetic in two phases
§ Compartments -> on with the gas and other with the blood or oil and how moves between
- Blood/gas PC--> speed of induction and recovery
- Oil/gas PC--> lipid solubility-->potency--> kinetics of distribution and recovery
○ Higher lipid soluble move into fatter parts of the animal -> longer recovery
99
What is the main thing that makes a good inhalation anaesthetic
A good anaesthetic is readily controllable
- -> induction and recovery are rapid
- -> depth of anaesthesia is easily adjusted
100
What are the 2 main facotrs that determine the speed of induction and recovery of anaesthetics
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Properties of anaesthetic
- Blood gas / PC
- Oil/gas PC
• Physiological factors
- Alveolar ventilation rate
- Cardiac output
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101
What occurs with low and high lipid solubility with anaesthetics
- Low blood solubility--> GOOD THING - not being bound by the water in the plasma so readily moves out to the brain where you want it
○ More rapid equilibration between phases
○ More rapid induction
○ More precise control
○ More rapid elimination and recovery
- High lipid solubility--> NOT A GOOD THING
○ They do have to have some lipid solubility to gain access to the brain
○ Gradual accumulation in body fat
○ May produce prolonged hangover with long procedure, particularly in obese patients (larger fat compartment)
102
What are the steps in the pharmacokinetics of inhalaed gas anaesthetics
1) Dose of gas delivered = concentration X flow rate
2) Ventilation into pulmonary capillary
3) All dose goes to the heart
4) Most of the dose goes to the heart (large blood supply)
- Concentration in the brain mirrors the concentration in the blood (sample blood to determine concentration in the brain)
5) Some of the dose goes to the muscle and fat compartments of the body
- Muscle larger blood supply than fat so larger amount
6) Overtime redistribution from brain -> muscle -> fat
7) Overtime get equilibration between all 3 compartments -> takes a long time for the fat compartment
