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DVM 2 - 2 > Nervous 2 > Flashcards

Nervous 2 Flashcards

1
Q

What is the purpose of pain and what is the goal in treating pain

A 
Purpose 
1) to warm against damage
2) to learn something is harmful
3) to protect 
Goal - to avoid pain developing into chronic pain
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2
Q

What are the 3 stages of nociceptive pathway and when do you feel pain

A

1) 1st afferent neurons
- transudction and transmission from periphery to dorsal horn
2) projection neurons - project from the dorsal horn to medulla, pons, midbrain, thalamus and hypothalamus - where modulation occurs
3) supraspinal neurons - project from spinal neurons to sub cortical and cortical areas where pain is perceived - PAIN - thalamus to the cortex

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3
Q

1st stage of the nociceptive pathway what is the stimuli, two types of fibres and the 4 types of nociceptiors and how localised

A

stimuli - mechanical, thermal and chemical
nerves fibres - myelinated Aδ (faster due to myelination) and Unmyelinated C fibres (slower)
1) Mechanical: Aδ fibres
2) Thermal: Aδ fibres
1st reaction - localised
3) Polymodal: C fibres mechanical, chemical and thermal
4) Silent: C fibres; activated by inflammation; chemical and mechanical
○ Don’t do anything until inflammation -> worse pain if present
2nd reaction - more generalised

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4
Q

1st stage of nociceptive pathway what are the 3 types of transduction channels and what is the main neuron involved and neurotransmitters involved

A

Transduction channels
1) Transient Receptor Potential ion channel (TRP)
2) Acid-sensing ion channel (ASIC)
3) Serotonin receptors
• Afferent neurons are bipolar - One neuron in stage 1 -> up to the dorsal horn
- The body is in the DRG (Dorsal Root Ganglia)
- One end is free ending in the periphery
- The other finishes in the dorsal horn
- Corelease of
○ Aminoacids (glutamate, aspartate) - important in acute pain

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5
Q

How does Allodynia occur

A

AlphaBeta nerve fibre (green) are involved in normal touch sensation
if large trauma occurs can get cross over of these fibres to pain fibres leading to pain at normal touch

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6
Q

2nd stage of nociceptive pathway where does it go, along what tracts and the important neurotransmitter involved

A

dorsal horn to thalamus or different area of the brain
• Spinothalamic tract (STT) -> spine to thalamus
- Major ascending pathway
- Crosses midline and communicates with different nuclei in the Thalamus
- Glutamate (neurotransmitter in Thalamus)
• But also Spinohypothalamic (SHT), Spinoreticular (SRT), Spinomesencephalic (SMT)

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7
Q

3rd stage of nociceptive pathway what nuclei, what neurons and what areas of the cortex

A 
Thalamic Nuclei
• 3rd order neurons
• Different area of the cortex
- Sensory-discriminative aspects of pain
- Motivational-affective aspects of pain
- Sensory and motor integration - reaction to the pain
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8
Q

The Gate theory of pain what does it involve and the 2 pathways

A

Nociception
- C fibre activation blocks inhibitory neurons -> pain
Antinociception
- touch fibres of alph beta activate inhibitory neurons - help relieve pain

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9
Q

What are the 2 main dorsal horn transmitters that activate the inhibitory neuron

A

1) Serotonin (5-HT) – Raphe Magnus
- Serotoninergic pathway; serotonin in the dorsal horn
- Selective serotonin reuptake inhibitor (SSRI) - drug used
2) Norepinephrine – Locus Ceruleus
Noradrenergic pathway; norepinephrine in the dorsal horn

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10
Q

What are the 2 types of sensitisation in the pain pathway and what does each result in

A

1) Peripheral sensitisation - enhanced perception of pain (hyperalgesia)
2) central sensitisation - chronic pain

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11
Q

what is the mechanism behind peripheral sensitisation and its function

A

Direct consequence of
- tissue trauma and inflammation
○ Inflammatory mediators from damaged cells (H+, K+, PG), plasma (bradykinin), platelets (serotonin), mast cells (histamine) and macrophages (cytokines)
○ Consequences:
Inflammatory response produces a “sensitising soup” of chemical mediators (reduction of activation threshold)
Function - IMPORTANT
- Secondary to inflammation
- Enhance perception of pain -> hyperalgesia (more painful than usual)
- Promote healing -> need to rest
- Protect against future damage

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12
Q

what is the mechanism of central sensitization and what does this result in

A

•Indirect consequence of
- Tissue trauma and Inflammation
• Constant activation of peripheral receptor
- Glutamate, aspartate and substance P are released
○ Constant activation of AMPA and neurokinin receptors on dorsal horn
• Constant activation of AMPA -> chemicals spill over onto other receptors
- Lead to activation of NMDA receptors
-> Increase excitability of dorsal horn projection neurons -> can continue even without pain stimulus
○ Leads to a cascade
• Expansion of receptive fields - amplify the pain
• Increased response to both nociceptive (hyperalgesia) and non-nociceptive (allodynia) stimuli
LEADS TO CHRONIC PAIN

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13
Q

what are the 5 classes of CNS drugs

A
  1. Analgesics
  2. Sedatives
  3. Anxiolytics
  4. Antidepressants
  5. Muscle relaxants
  6. Anaesthetics- general and local
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14
Q

what is the veterinary pain scales

A

0 no pain
1 depressed and anxious
2 increased respiration, reluctant to eat
3 increased respiration and heart rate, won’t eat, very anxious
4 vocalising

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15
Q

List the 4 ways nociceptor afferents can be modulated

A
  • Inhibited by inhibitory neurons in the dorsal horn of the spinal cord
  • Inhibited by descending inhibitory pathways from medulla and midbrain
  • Inhibited by noradrenergic pathways (pons)
  • “wound up” by persistent nociceptor stimulation
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16
Q

List 4 chemical mediators that modulate pain

A
  1. Endogenous opioids
  2. 5 hydoxytryptamine (5HT)
  3. Noradrenaline
  4. Adenosine
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17
Q

Descending inhibitory pathways of pain pathway, where initiated and main neurotransmitters

A 
• Initiated in:
- Mid brain/ pons
- lower pons/medulla
• Major inhibitory neurotransmitters:
- Endogenous opioids:
○ beta endorphins, enkephalins, dynorphin
- Noradrenaline
- Gamma amino butyric acid (GABA)
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18
Q

how does inhibition occur in the spinal cord

A

Multiple receptors and neurotransmitters that lead to:
1. Decreased Ca influx presynaptically therefore reduced transmitter release
2. Increased Cl or K influx postsynaptically therefore hyperpolarisation
○ Preventing the binding of the neurotransmitter

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19
Q

What are the 2 main ways opiods inihibit pain

A
  1. On ascending pathways:
    - By presynaptic inhibition of transmitter release (decreased intracellular Ca)
    By post synaptic membrane hyperpolarisation (increased intracellular Cl)
  2. On descending pathways
    In the CNS, opioids stimulate increased excitation of inhibitory neurons
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20
Q

What are the 3 types of opioid receptors and where are they found,

A

1) μ
- widely distributed, CNS, spinal cord and periphery
- Analgesia μ1 and side effects μ2
2) k
- Spinal cord analgesia -> prevent signal through dorsal horn into spinal gate
- Fewer side effects
3) δ
- peripheral analgesia

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21
Q

List 7 actions of opoids in the CNS

A

CNS

  • Analgesia - best
  • Euphoria - in some patience
  • Excitement - banned in horse racing - stimulant
  • Respiratory depression - can lead to death
  • Cough suppression
  • Nausea and vomiting
  • Pupillary constriction
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22
Q

What are the 4 main types of actions of opioids

A

1) CNS
2) GI tract
3) Histamine release
4) Tolerance and Dependence

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23
Q

What is the main GI tract and histamine release action of opioids

A

Gi tract - reduced motility - need to give constipation drugs
Histamine release - urticaria, bronchoconstriction

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24
Q

What are the 4 classifications of opioids

A

1) pure agonist
2) partial agnoist
3) mixed agnoist/antagnosit
4) antagnoist

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25
Q

List 3 important opioids and what classification

A

1) Morphine - pure agonist
- standard by which other drugs are measured
2) Buprenorphine - partial agonist - less likely to overdose - less respiratory depression
3) butorphanol - agnoist/antagnoist

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26
Q

What are the 4 classes of analgesics

A

1) opioid
2) local anaesthetics
3) alpha-2 agonist
4) NSAIDs - reduction in prostaglandin levels (neurotransmitter)

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27
Q

List the 5 classes of sedatives

A
  1. opioid analgesics
  2. α2 adrenergic agonists
  3. Phenothiazine derivatives
  4. Benzodiazepines
  5. Butyrophenones
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28
Q

Where are the alpha 2 receptors

A

In CNS
• In brainstem locus coeruleus (modulator of wakefulness) sedation
• In brainstem, cardiovascular regulating centre
• In dorsal horn of spinal cord analgesia
• In thalamus analgesia
• In sympathetic neurones analgesia
In periphery
• In autonomic ganglia
• In blood vessels -> pre and post-synaptic location of blood vessels

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29
Q

What does the activation of alpha 2 receptors lead to pre and postsynaptically

A 
Presynaptically
- inhibition of noradrenaline release
○ Large amount of NA leads to NA binding to pre-synaptic membrane 
§ Inhibiting release 
Postsynaptically
- contraction of vascular smooth muscle
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30
Q

What are the 4 main CNS effects of α2 adrenergic agonists and when important

A

1) sedation - dose dependent
2) analgesia - shorter than sedation
3) emesis (vomiting) - important in cats
4) muscle relaxation - greater in cows than horses - important if want to access legs or underside

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31
Q

What are the 4 main cardiovascular effects of α2 adrenergic agonists

A

1) Blood pressure
- Initial increase (phase 1)
- Then decrease to normal or below (phase 2)
2) Bradycardia - profound decrease in heart rate
3) Decreased cardiac output
- Increased afterload
- Coronary artery vasoconstriction -> reduce nutrient delivery to heart muscle
4) Muddy mucus membranes -> poor perfusion

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32
Q

What occurs with phase 1 of α2 adrenergic agonists blood pressure affect

A
  • drug binding to postsynaptic receptors on peripheral vascular smooth muscle
    –> contraction -> hypertension (increase blood pressure)
    THAT CAUSES
    –> reflex bradycardia (feedback)
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33
Q

What occurs with phase 2 of α2 adrenergic agonists blood pressure affect

A
  • Drug binding to presynaptic receptors in CNS
    –> decreased sympathetic drive -> cannot respond to stimulus - fight or flight
    –> normal/hypotension (reflex bradycardia)
    –> profound bradycardia -> leads to decrease heart rate and blood pressure
    § Problem with surgery
  • Coronary and small peripheral arteries larger ratio of post synaptic α2:α1 receptors
    –> preferentially leading to muddy mucous membranes and reduced coronary perfusion
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34
Q

List the 4 metabolic effects of alpha 2 receptor agonist

A

1) Hyperglycaemia
- due to inhibition of insulin release
2) Inhibition of lipolysis
3) Impairment of temperature regulation
4) Kidneys diuresis
- due to inhibition of renin release

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35
Q

List the 9 cautions and contraindications of alpha 2 receptor agonists

A

1) • Heart disease
2) • Hypotension or shock
3) • Renal or hepatic impairment
4) • Final trimester of pregnancy
5) • Epilepsy
6) • ANY DEBILITATED ANIMAL!
7) • Beware sleeping dogs!
8) • Additive effect with other CNS drugs
9) Cattle particularly sensitive

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36
Q

Phenothiazine derivatives what are the 2 main receptors they work on and its effects

A

Earliest of sedatives used in vet practice
Blockade of dopamine receptors
- Decreased motor activity, catalepsy
- Block emesis (CTZ)
• Peripheral alpha adrenoceptor blockade
- Effect on blood pressure -> increase beta adrenoceptor response -> dilation of blood vessels
○ This occurs when increase sympathetic drive (stressed) - DON’T GIVE IN THIS SITUATION
• Inhibition of adenosine uptake into neurones
• (Also antimuscarinic and antihistaminic)
• NO ANALGESIA

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37
Q

What is the main example of a phenothiazine derivative what used as, list 4 warnings and 2 other side effects

A

Acepromazine
• Extensively used as premed
Warnings:
• Shock
• Colic
• Seizure threshold - lower threshold - higher risk
• Potentiation of anaesthetic effect -> additive effect
Hypotension:
- alpha blockade–> vasodilation
- exacerbated by high circulating catecholamines (eg stress)
Decreased PCV
- Splenic vasodilation–>sequestration of RBC in spleen

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38
Q

Benzodiazepines what are the 6 main actions on the CNS

A
  • Hypnotic
  • Sedative
  • Anxiolytic
  • Anticonvulsant
  • Skeletal muscle relaxant
  • Amnesic -> humans forget unpleasant procedures
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39
Q

Benzodiazepines what is the mechanism of action and the 3 main side effects

A

Mechanism of action
- An allosteric effect on the GABA receptor
1) Binding of B-Z to GABA receptor -> changes the structure and enhances binding of GABA
2) Opens chloride channels
3) Increases GABA’s inhibitory effects
Other pharmacological effects - minimal side effects
Cardiorespiratory- minimal effects
• Skeletal muscle–> relaxation -> surgical point of view

40
Q

Benzodiazepines list 6 main clinical uses

A
  1. Anxiolytic–> behaviour modifiers
  2. Hypnotics
  3. Premedicants -> given before anaesthesia
  4. Anaesthesia induction
  5. Anticonvulsants (status epilepticus)
  6. Appetite stimulation (cats)
41
Q

Butyrophenones mechanism of action

A

Reduced motor activity and catalepsy through central dopamine and noradrenaline blockade

42
Q

what features of the aterial blood supply in the brain render it susceptible to ischaemic injury and where do emboli tend to lodge

A
  • once an arterial branch or arteriole penetrates the brain, it is essentially an end-artery
  • large emboli tend to become trapped in the leptomeningeal vessels
  • small emboli often tend to lodge at or close to the grey-white matter junction
43
Q

What are possible consequences of obstruction of venous drainage

A
  • cerebral veins are abundant and have many anastomoses

○ occlusion of a single vein is therefore usually not of clinical significance

44
Q

List 3 structures that help protect the brain for external trauma

A

1) rounded shape of the skull - favours glancing blows
2) internal bony ridges - such as tentorium osium that help direct lines of applied force
3) cerebrospinal fluid (CSF) - in subarachnoid space and ventricular system help to cushion the brain

45
Q

What are the clinical signs that suggest that a patient has increased intracranial pressure

A

anisocoria (discrepancy in pupillary size), mydriasis (pupillary dilation), non-responsive pupils, dull mentation or altered state of consciousness, rigid paresis, abnormal respiration pattern, bradycardia and coma

46
Q

What can cause a concussion and what factors influence the trauma on the brain

A

primarily from rapid acceleration/deceleration forces

1) a brain in a freely mobile skull is much more susceptible to traumatic injury than is a brain in a stationary supported skull
- free skull moves away from impact, static brain moves towards point of impact
2) young animals - brain virtually fills the cranial vault so that relative displacement of the brain in response to head trauma is usually minimal
3) aged animals - senile brain atrophy may permit greater movement of the brain in response to head trauma so that subdural haemorrhage may follow relatively minor head trauma

47
Q

what are potential consequences of concussion

A

Concussion is usually reversible unless there is repeated head trauma

  • mild concussion may last only seconds to minutes and is unassociated with microscopic lesions
  • severe concussion, there may be microscopic evidence of axonal degeneration and central chromatolysis of neurons
  • repeated episodes of concussion, more widespread neuronal degeneration and loss may occur (including in the cerebral cortex) (chronic traumatic encephalopathy) -> Willerian degeneration
48
Q

what causes a cerebral contusion

A

similar to that of concussion but the applied external force, the displacement of the brain within the skull, and the induced shearing and other forces acting on the brain are all of greater magnitude -> greater blood vessel damage -> haemorrhage

49
Q

what is the difference between a coup contusion and a contrecoup contusion

A
  • a coup contusion = a contusion located at the site of impact
  • a contrecoup contusion = a contusion located on the opposite side from the site of impact - generally worse
50
Q

What is the typical location of traumatic meningeal haemorrhage within the skull and why

A

leptomeninges (arachnoid, subarachnoid space and pia mater) or the brain itself

51
Q

what causes cerebral laceration and the potential consequences

A
  • most often from penetrating injuries but also blunt head trauma
    consequences
    ○ with blunt trauma, contrecoup lacerations typically develop on the surfaces of gyri which have been displaced over bony prominences
    ○ shear forces developing during brain deformation may also cause deep haemorrhage and even shearing of grey from white matter over small areas of the cerebral cortex
52
Q

What are potential consequences of a skull fracture

A

readily detectable because of displacement of bone fragments and associated haemorrhage
some skull fractures, however, may be subtle and only detectable at necropsy by careful dissection of the dura mater from the skull or by radiography
e.g. basisphenoid fractures in horses that rear backwards and strike the occiput -> may lead to sudden onset blindness)

53
Q

List some common causes of localised cerebral oedema

A

focal traumatic lesions (especially sites of laceration and haemorrhage), meningeal or brain tumours, or inflammatory foci (especially abscesses) and may contribute more than the primary lesion to the clinical signs, brain enlargement and ICP increase

54
Q

list some common causes of generalised cerbral oedema

A

head trauma, diffuse meningitis, diffuse viral encephalitis, thiamine deficiency (polioencephalomalacia) in ruminants, clostridial enterotoxaemia, lead poisoning, and salt poisoning

55
Q

what gross features are indicative of cerebral oedema

A

mild - may look grossly swollen, pale, soft and wet, especially the white matter
chronic - the brain may appear firm and dry, with pallor or faint yellow discolouration
caudal cerebellar vermis may herniate through the foramen magnum (the herniated vermis becomes flattened dorsoventrally = “lipping of the cerebellum”

56
Q

What are the 4 main mechanisms responsible for CNS oedema, which is most common, which is associated with disruption of the blood-brain barrier and give some examples

A

1) Vasogenic oedema - increase vascular permeability due to injury to vascular endothelium - MOST COMMON
1. Mulberry heart disease - vit E/selenium
2. annual ryegrass toxicity
2) Hydrostatic oedema - increased hydrostatic pressure within the ventricles of the brain or, less commonly, in the central spinal canal due to obstruction of flow of CS
3) Cytotoxic oedema - increased intracellular fluid
Eg - ammonia toxicity in sudden death syndrome of phalaris toxicity in sheep
4) Osmotic oedema - indirect salt poisoning in pigs

57
Q

what is the cause and pathogenesis of CNS lesions of annual ryegrass toxicity

A

infestation of the seed head of Lolium rigidum (and occasionally other grasses) by a nematode (Anguina agrostis), with infection of the nematode gall by a toxin-producing bacterium (Corynebacterium rathayi)
- the bacterial corynetoxins are glycolipids which inhibit glycosylation -> depletion of basement membrane glycoproteins -> increased vascular permeability -> pulmonary oedema and severe cerebral vasogenic oedema

58
Q

what is the cause and pathogenesis of CNS lesions of mulberry heart disease

A
  • young pigs with vitamin E/selenium deficiency and hence inadequate anti-oxidant capacity
  • reactive oxygen species (free radicals) damage small blood vessels in multiple body systems
    ○ Generally leads to sudden death
59
Q

what is the cause and pathogenesis of CNS lesions of Focal Symmetrical Encephalomalacia (Clostridial Enterotoxaemia) (Pulpy Kidney Disease)

A
  • young unvaccinated sheep
  • absorption of epsilon toxin of Clostridium perfringens type D from the intestines into circulation -> toxin binds to endothelial receptors -> vascular injury in multiple body systems
60
Q

what is the cause and pathogenesis of CNS lesions of Oedema Disease (Enterotoxaemic Colibacillosis)

A
  • young pigs with intestinal colonisation by 0139 and 0141 strains of Escherichia coli producing Shiga-like toxin type IIe (SLT-IIe)
  • toxin absorption from the intestines into the circulation -> toxin binds to endothelial receptors -> vascular injury in multiple body systems
61
Q

What is the pathogenesis of indirect salt poisoning in pigs and what are the characteristic lesions

A

hypernatraemic animals are then allowed free access to water, the blood [Na+] falls rapidly so that the brain becomes relatively hyperosmolar
○ within minutes, the brain will eliminate Na+, K+ and Cl- ions but this is insufficient to negate the osmotic gradient -> entry of water into the brain -> acute cerebral oedema
- the characteristic lesions in affected pigs are acute cerebral oedema, laminar cortical necrosis (neuronal necrosis and malacia within the middle layers of the cerebral cortex, with excitotoxic necrosis of neurons), and eosinophilic infiltration of the leptomeninges and perivascular spaces

62
Q

list 5 conditions that lead to cerebral hypoxia

A

1) vascular obsturction
2) complete cessation of cerebral circulation
3) sustained hypotention
4) hypoxaemia
5) impaired cell utilisation of oxygen

63
Q

which parts and cellular components of the brain are most vulnerable to hypoxia

A
  • neurons and oligodendrocytes are most vulnerable to hypoxia
    he most vulnerable neurons are those of the deep cerebral cortical laminae, hippocampus (especially the dentate gyrus), some basal ganglia and the Purkinje cells of the cerebellar cortex
64
Q

excitotoxicity what else besides hypoxia leads to this

A

indirect salt poisoning, lead poisoning, organomercurial poisoning, thiamine deficiency, prolonged convulsive seizures (status epilepticus), and in humans with repetitive cerebral concussion (chronic traumatic encephalopathy)

65
Q

how common are cerebrovascular accidents in humans and non-humans and give some examples of how it occurs

A

○ they occur infrequently in domestic animals, largely because significant atherosclerosis or arteriosclerosis of the internal carotid or cerebral arteries is uncommon in these species

  • common in humans
    1) cerebral trauma
    2) feline cardiomyopathy
    3) vasculitis
66
Q

what gross features are suggestive of CNS infarct and how does it heal if animal survives

A

CNS infarcts tend to undergo liquefactive necrosis and soften (malacia) and swell
- arterial infarcts of grey matter tend to be red (haemorrhagic) in the acute phase whereas those of white matter tend to be pale; this is probably because the grey matter has a denser capillary network than does the white matter
- venous infarcts in both grey and white matter are expected to appear haemorrhagic
in animals that survive a cerebral infarct, repair follows the same sequence as described for traumatic brain injuries

67
Q

What do LMN and UMN do in terms of the bladder and therefore what results from LMN and UMN dysfunction

A

the LMN causes inhibitory signals keeping the external sphincter closed and the UMN inhibits this inhibition causing the sphincter to open

  • If problem with UMN there is less inhibition on the limb reflexes leading to relaxation of the muscle resulting in bladder not opening
  • If LMN due to lesion at S1-S3 results in flaccid bladder and dribbling urine
68
Q

where on the spinal cord is the needle inserted when performing a lumbar myelogram

A

L4-L5 or L6-L7 intervertebral space

As any further back from L7 the spinal cord becomes smaller and therefore more likely to miss the subarachnoid space

69
Q

why is there a reduced liklihood of intervertebral disc protrusion between T1-11

A
  • In this area the vertebrae are stabilised by the ribs so less prone to rotational and lateral forces
70
Q

What is the punniculus response and how occurs

A
  • Is a twitch reflex of the cutaneous trunci muscle
  • Each spinal nerve has sensory innervation of a dermatome (which is a region of skin innervation by a single sensory neuron)
    1) Dermatome region touched or pinched
    2) Sensory afferents move up the spinal cord to C8-T1 (afferents in T1-L2)
    3) Synapse with lateral thoracic nerve
    4) Supplies innervation to the cutaneous trunci muscle
    5) Cutaneous trunci muscle causes the body to twitch
71
Q

What are the two types of vision and the characteristics of each

A

1) Ocular - broad field of view of the eye however doesn’t overlap - blind spot rostral to the nose
2) biocular vision - visual axis is longitudinal to body, facing forward - high amount of cross-over, no blind area to give depth perception

72
Q

What are the 3 tunic layers that create the eyeball, which involves the lens

A
  1. outer fibrous tunic
  2. middle vascular tunic
  3. internal nervous tunic
    • lens for focussing light on receptors
    • partly liquid, partly gelatinous centre
73
Q

What are the 2 parts of the fibrous tunic (outer most layer) of the eye, its function and what made of

A

consists of 1. sclera (posteriorly) and 2. cornea (anteriorly) which meet at limbus
Continuous around the eyeball however limbus where the two areas meet
• dense collagenous tissue
• resists internal pressure

74
Q

Sclera what part of the eye, colour, what continues with and function

A

Fibrous tunic
• opaque - the “white of the eyes”
• penetrated by fibres of optic nerve
• continuous with dura mater of optic nerve
• provides attachment for tendons of extrinsic muscles of eye

75
Q

Cornea what made of, what layers, blood supply and special characteristic

A
  • specialized transparent, dense connective tissue - light can pass through
  • covered by anterior and posterior epithelial layers
  • avascular - nutrition by diffusion from lacrimal fluid (tears) and aqueous fluid of anterior chamber
  • very sensitive due to nerve endings (branches of ophthalmic division of CNV)
76
Q

Vascular tunic what layer, what also known as and what are the 3 things it consists of

A

middle layer
• also known as uvea
• consists of choroid, ciliary body and iris (from posterior to anterior)

77
Q

Choroid what layer of the eye, where found, blood supply, special structure and function

A

vascular tunic - middle layer
• lines sclera from optic nerve almost to limbus
• contains blood vessels in pigmented connective tissue
• provides nutrients for outer layers of retina
• contains avascular tapetum lucidum:
○ area of dorsal choroid
○ Reflective (reflect light at night when low levels of light - back to retina), iridescent - eyes of cats that reflect
○ not present in pigs (or humans)
○ probably assists in nocturnal vision

78
Q

Ciliary body what layer of the eye, what is it, and function

A

vascular tunic - middle layer
thickening of choroid anteriorly in radial ridges (ciliary processes) - towards the lens
• provides anchoring point for zonular fibres, which suspend lens - hold in place
• produces aqueous humour

79
Q

Iris what layer of the eye, what is it, what consists of and function

A

vascular tunic - middle layer
• ring of tissue suspended between cornea and lens
• opening in centre is pupil
• consists of pigmented connective tissue covered with epithelium (pigmented posteriorly) -> amount of pigment determines eye colour
○ Albino animals NO PIGMENT - red
○ connective tissue layer contains smooth muscle sphincter (circular - parasympathetic) and dilator (radial - sympathetic), which regulate pupillary size - pupillary light reflex
• separates anterior from posterior chamber
○ Anterior - iris and cornea
○ Posterior - iris and lens - anterior to the lens

80
Q

internal tunic what made up of, what type of cells it contains, list the neuroepithelial layer from outer to inner

A
  1. retina, 2 lens, 3 aqueous humour and viterous body
    - contains light-sensitive receptor cells (posterior two-thirds of retina)
    • lines vascular tunic from pupillary margin posteriorly to optic nerve
    • thin outer layer (pigmented except over tapetum) and thick inner layer (neuroepithelial)
    • neuroepithelial layer (from outer to inner) - (outer = posterior and inner = anterior)
  2. photoreceptor layer
  3. horizontal cells
  4. bipolar cells
  5. amacrine cells
  6. ganglion cells
81
Q

where would you find photoreceptor and ganglion cells in the eye, function and structure

A

Internal tunic - in the retina
• photoreceptor cells
○ contain light-sensitive receptors in extended membrane of outer segment
○ two types - rods (highly sensitive for night vision) and cones (colour perception)
○ Synapse with bipolar cells, which synapse with ganglion cells
• ganglion cells
○ axons extend across inner surface of retina to optic disc where they meet to form optic nerve, i.e. ganglion cells are cell bodies of CNII

82
Q

where would you find horiztonal and amacrine cells and their function

A

Internal tunic - in the retina
• horizontal cells modify transmission between photoreceptors and bipolar cells
• amacrine cells modify transmission between bipolar cells and ganglion cells (axons form at optic disc to form optic nerve)

83
Q

Lens what layer of the eye, structure, what composed of, blood supply, surrounded by and function

A

• soft, transparent, biconvex structure
• composed of ‘lens fibres’ - epithelial cells running from anterior to posterior poles of lens
○ Are not replaced but new are made
• avascular - nourished by aqueous and vitreous humour
• surrounded by an elastic capsule (basement
• focuses images on retinamembrane)

84
Q

Aqueous humour and viterous body what layer of the eye, where found, what produced by, function

A

Aqueous humour
• fills space between cornea and lens (anterior and posterior chambers) - in front of the lens
• produced by cells of ciliary body
• passes from posterior chamber to anterior chamber
• drains into venous sinuses in sclera at iridocorneal angle
Vitreous body
• occupies space between lens and retina
• gel-like mass consisting of stroma of fine transparent fibres filled with glycosaminoglycans and water

85
Q

Adnexa what is it and the 2 components

A

• structures that protect and move the eye within the orbit

1) Fasciae
2) Periorbita

86
Q

Periorbita what made of, where found, where attach, what contain

A
  • fibrous fascial sheath, which blends with periosteum medially and dorsally
  • inserts in eyelids and surrounds eyeball and extrinsic muscles of eye
  • attached to skull near optic foramen
  • contains smooth muscle which keeps eyeball slightly protruded with normal tone (under sympathetic control) and surrounded by orbital fat (cushions contents of orbit)
87
Q

What are the 3 main groups of extrinsic eyeball muscles and what they do, where insert and originate

A

1) rectus muscles - dorsal, ventral, lateral and medial rectus - movement in that direction
2) oblique muscles - rotate eye about visual axis - ventral and dorsal oblique
3) rectractor bulbi - retracts globe in socket
All but ventral oblique originate near optic foramen
insert on fibrous tunic of the sclera

88
Q

What are the 2 oblique muscles where arise and function

A

• dorsal oblique:
○ travels anteriorly along dorsomedial wall of orbit; then inserts on dorsolateral aspect of fibrous tunic
contraction pulls dorsolateral aspect of eye medially (i.e. medial rotation)
• ventral oblique:
○ arises from ventromedial wall of bony orbit and passes laterally to insert on ventrolateral aspect of eyeball
○ contraction pulls ventrolateral part of eyeball medially (outward rotation)

89
Q

Retractor bulbi what made up, what surrounds, function

A
  • several slips of muscle which insert on posterior aspect of eye
  • surrounds optic nerve
  • retracts globe in socket
90
Q

What is the other name for upper and lower eyelids, where do they meet, when surround and the 4 layers

A 
palpebrae
• meet at medial and lateral angles (canthi)
• surround palpebral fissure
• formed from the following layers:
1) skin 
2) musculofibrous layer 
3) conjunctiva 
4) puncta lacrimalia
91
Q

What makes up the following layers of the eyelid 1. musculofibrous 2. conjunctiva 3. puncta lacrimalia

A
  • musculofibrous layer
    ○ contains orbicularis oculi, fibrous periorbita and smooth muscle
    ○ tarsal glands - open at free edge of lid
    . conjunctiva
  • thin mucous membrane lining posterior surface of eyelids (palpebral conjunctiva) and reflected onto sclera (bulbar conjunctiva)
    . puncta lacrimalia
    ○ minute slits on upper and lower lids adjacent to lacrimal caruncle
    ○ openings to canaliculi leading to nasolacrimal duct (in lateral wall of nasal cavity)
92
Q

Third layer what also called, where found, what covered with, supported by, gland, where normally found and function

A

nictitating membrane’
• between lower lid and eyeball
• covered with conjunctiva on both surfaces
• supported by T-shaped piece of cartilage
• gland of third eyelid surrounds stem of T:
○ secretes towards eyeball from posterior surface
• while eyes open, normally held retracted by smooth muscle (sympathetic control)
• provides additional protection and moisture for eyeball when eye closed or sick animal

93
Q

Lacrimation function how occurs and the 3 layers

A

• lacrimal fluid distributed over anterior aspect of eye by blinking
• required to moisten and nourish cornea and flush away foreign objects
1. outermost lipid layer (from tarsal glands) spreads tear film evenly and prevents evaporation
2. aqueous layer from:
○ lacrimal gland (located on dorsolateral aspect of eye within periorbita; secretes through several fine openings into palpebral sac, i.e. space between palpebral and bulbar conjunctivae)
○ gland of third eyelid
3. inner mucoid layer (from goblet cells in conjunctiva) - binds tears to cornea
• lacrimal fluid drains via lacrimal puncta and canaliculi to nasolacrimal duct

94
Q

Vascular supply of the eye what are the 2 arteries where supply and venous drainage

A

external ophthalmic artery - principal supply to eye
○ branches from maxillary artery then penetrates apex of periorbita
• internal ophthalmic artery - supplies CNII and spreads over retina from optic disc.
• venous drainage via several vorticose veins that emerge through sclera

95
Q

What are the 6 cranial nerves that are involved with eye structures and what they innervate

A 
CNII - perception of light
CNIII - somatic efferent:
○ dorsal, medial and ventral recti
○ ventral oblique
○ levator palpebrae superioris
- visceral efferent:
○ parasympathetic innervation to smooth muscle of iris and ciliary body
CNIV - dorsal oblique
CNV (ophthalmic and maxillary divisions) – sensory to eyeball (especially cornea), eyelids
and conjunctivae
CNVI - lateral rectus, retractor bulbi
CNVII – motor to orbicularis oculi
96
Q

Sympathetic innervation of the eye what is the pathway and what occurs when activated

A

exits cranial thoracic spinal cord and ascends in vagosympathetic trunk to cranial cervical ganglion near tympanic bulla
• postsynaptic neurons travel with CNIII to supply smooth muscle of eye:
○ periorbita (protrudes eyeball)
○ pupillary dilator
○ eyelids (keeps palpebral fissure open)
○ third eyelid (retracts)

DVM 2 - 2 (27 decks)

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