Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

DeLahunta Book > DeLahunta Chapter 14 - Visual system > Flashcards

DeLahunta Chapter 14 - Visual system Flashcards

1
Q

From which embryological later to the following structures originate?
a) Sclera and uvea
b) Lens and cornea
c) Retina

A

Sclera and uvea – mesoderm
Lens and cornea – ectoderm
Retina – neuroectoderm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What toxin can cause cycloptic malformation in ewes, and at what time point? And in cats?

A

cyclopamin, Veratrum calliifornicum, 14-15d of gestation
gene PAX6

cat: griseofulvin in queen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Name the 10 layers of the retina, from starting from the scleral surface

A

from out to in:

Retinal pigmented epithelium
Photosensitive later
External limiting membrane
External nuclear layer
External plexiform layer
Internal nuclear layer
Internal plexiform layer
Ganglion layer
Nerve fibre layer
Internal limiting membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Through which bone does the optic canal run through?

A

presphenoid bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the percentage of decussation at the optic chiasm in dogs, cats, horses, primates?

A

bird-fish 100%
LA - 80-90%
d - 75%
c - 65%
primates -50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the reported cause for congenital pendular nystagmus in Siamese cats?

A

Increased decussation at the optic chiasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Name the following steps of the menace pathway

A

1) retina
2) optic nerve
3) optich chiasm
4) optict tract
5) LGN
6) optic radiation
7)occipital visual cortex
8) internal capsule associateiion fibers
9) motor cortex
10) internal capsule projection fibers
11) crus cerebri
12) longitudinal fibers of pons
13) pontine nucleus
14) (cross) transverse fibers of pons
15) cerebellar cortex
16) efferent cerebellar pathway
17) facial nucleus
18) facial muscles and orbicularis oculi muscle (blink)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Name the PLR pathaway

A

1) retina
2) optic nerve
3) optich chiasm
4) optict tract
5) bypass LGN
6) Pretectal nucleis
7) decussate to caudal commisure
6) parasymp nucleus of oculomotor
7) oculomotor nerve
8) ciliary ganglion
9) short shiliary nerves
10) ciliary muscle and constrictor pupillae muscle (sphincter)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Name the sympathetic innervation to the eye?

A

1) Hypothalamus
2) ARAS
3) lateral tegtotegmental tract
4) T1-3 SCS of lateral grey horn (preganglionic neurons)
5) nerve roots -spinal nerve until foramen
6) by pass at ramus communicans
7) thoracic sympathetic trunk
8) vagosympatehtic trunk
9) cranial cervical ganglion
10) via bullae or via internal carotid arteries - join ophthalmic nerve
11)exit calvarium - orbital fissure
12) long ciliary nerves
13) dilator puppilae muscle, ciliary muscle, and orbiatlis muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Regarding Horner syndrome, which branches are responsible for ptosis and miosis?

A

T1 – miosis
T2 and T3 – ptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What structures can be found in the middle cranial fossa? Why may internal ophthalmoplegia be the first initial sign?

A

CN III GSE and GVE, IV, VI, V ophthalmic, sympathetic supply to the eye
Sympathetic supply
all of them exiting through ORBITAL FISSURE

The oculomoor is located on the medial surface of CN III so vulnerable to compression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

REGARDING ONUA:
a) What were the most common low field MRI features seen with presumed optic neuritis? (Low-Field Magnetic Resonance Imaging Findings in 18 Dogs With Presumed Optic Neuritis, Moris 2021, frontiers)

b) What percentage of animals with presumed optic neuritis had changes on CSF, and how many animals regained vision following treatment? (Presumed optic neuritis of non-infectious origin in dogs treated with immunosuppressive medication: 28 dogs (2000-2015), Bedos 2020, JSAP)

c) What were the prognostic factors associated with recovery of vision in optic neuritis? What was the recovery rate? (Prognostic Factors for Recovery of Vision in Canine Optic Neuritis of Unknown Etiology: 26 Dogs (2003-2018), Posporis 2019, Frontiers)

A

a) What were the most common low field MRI features seen with presumed optic neuritis? (Low-Field Magnetic Resonance Imaging Findings in 18 Dogs With Presumed Optic Neuritis, Moris 2021, frontiers)
Contrast enhancement of the optic nerve 11/18 and chiasm 6/18, changes in CSF volume around the optic nerves, changes to optic disc, changes to size of the chiasm (all 10/18) and concurrent brain lesions 13/18
b) What percentage of animals with presumed optic neuritis had changes on CSF, and how many animals regained vision following treatment? (Presumed optic neuritis of non-infectious origin in dogs treated with immunosuppressive medication: 28 dogs (2000-2015), Bedos 2020, JSAP)
44% of animals had CSF changes (either pleocytosis or increased TP). 50% of animals recovered vision

c) What were the prognostic factors associated with recovery of vision in optic neuritis? What was the recovery rate? (Prognostic Factors for Recovery of Vision in Canine Optic Neuritis of Unknown Etiology: 26 Dogs (2003-2018), Posporis 2019, Frontiers)
23% had complete recovery, 77% had incomplete or no recovery
Presence of reactive PLR and absence of fundoscopic lesions, younger age, lower CSF TNCC were associated with recovery of vision
Dogs with isolated optic neuritis were significantly younger and had lower TNCC compared with MUA.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Give some differentials for the following clinical signs
- Size of the palpebral fissure
-Protrusion of third eyelid
-Mydriasis
-Miosis

A

Size of the palpebral fissure – oculomotor paralysis, sympathetic paralysis, facial nerve paralysis, hemifacial tetany

Protrusion of third eyelid – sympathetic paralysis, tetanus, facial paralysis, severe depression in cats, hyperplasia of the TLR gland, secondary to enophthalmos, retrobulbar mass

Mydriasis – oculomotor GVE paralysis, iris atrophy, glaucoma, spastic pupil, sympathetic stimulation (pourfour du petit), cerebellar disease drugs

Miosis – sympathetic paralysis, uveitis, acute prosencephalic disease, drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

In which period of gestation is the optic nerve formed?

A

33 d

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

When is the first ERG detectable in kittens?

A

35d

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Which cells from the photosensitive retina are responsibel for the night and day
vision?

A

rods - night
cones - day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What can be the aetiology of blindness with dilated unresponsive pupils in calves (steers)? What is the pathomechanism behind it?

A

The aetiology can be chronic vitamin A deficinecy. Occurs in dry seasons when there is lack of green feed (the source of vitamin A, or in feedlots when cattle receive feed with the same deficinecy. Night blindness results from the loss of rod photoreceptor function because of the inability to produce rhodopsin. However, complete blindness is caused by compression and degeneration of the optic nerves where they course through the optic canals. Stenosis occurs at this location because of a thickening of the dura and a failure of the optic canals to enlarge as the calves grow.

18
Q

Please give an example of 5 breeds in which Globoid cell leukodystrphy was recognised.

A

Westie, cairn terrier, beagle, poodle, basset hound, pomeranian,

19
Q

What is the role of rostral colliculus in the visual stimulation pathway?

A

reflex pathway n=4
1) tectonuclear - to EOM nerves (turing the eyes to th visual stimuli)
2)tectospinal - turning neck muscles
3) tectothalamic - feedback to cortex
4) tectocerebellar - coordination of all previous movements

20
Q

What os the effect of distemper on the visual pathway?

A

Demyelinating lesion in the optic tract without obvious visual deficits

21
Q

In which breed germ cell neoplasm is more common?

A

doberman

22
Q

Which are the malformations caused in kittens by griseofulvin administration of the pregnant queens?

A

1) cyclopia
2) microphthalmia
3) meningoencephalocele

23
Q

Which medication cam cause retinal degeneration in cats

A

enrofloxacin

24
Q

Pathophysiology of thiamine deficiency in ruminants.

A

Diet change into carbohydrates, or sulphur intake via water and feed. When the diet is changed abruptly, especially a change that increases the dietary source of carbohydrates, for example, the addition of grain, the bacterial population in the rumen may change, resulting in an increase in bacteria that produce thiaminase. The increase in this enzyme causes a decrease in the ruminal thiamin available for absorption.

25
Q

Diagnosis of thiamine deficiency

A

Erythrocyte transketolase activity which is thiamine dependent.

26
Q

Which are the typical signs of thiamine deficiency in ruminants?

A

typical for this disorder: an acute onset of depression, mild ataxia, blindness, and occasionally tremors followed by rapid progression to recumbency (nonambulatory tetraparesis) with opisthotonus, abnormal positional nystagmus, semicoma (stupor), extremely miotic pupils with dorsal deviation of the medial aspect of both pupils (dorsomedial strabismus), and occasional seizures.

27
Q

What is equine hypoxic ischemic encephalopathy?

A

Also termed neonatal encephalopathy, where a maladjustment syndrome occurs in neonates. They are normal at birth. From 1 to 14 days postnatally, the foals rapidly develop diffuse neurological signs, including lethargy, inability to nurse, seizures. Lesions histopathologically are consistent with cerebrocortical necrosis.

28
Q

Explain what is happening in salt intoxication and which species is very common?

A

Can be caused by salt intoxication. In dogs is either by rapid correction of hyponatremia or drinking salty ocean water. In pig it happens when they eat garbage with excessive salt content. This causes polioencephalomalacia. Clinical signs are blindness and seizures.

29
Q

What is causing the equine leukoencephalomalacia?

A

It is caused by moldy corn intoxication. Ingestion of mycotoxin Fusarium moniliforme, which produces Fumonisin B1 (trichothecene). This affects the liver and brain. Causes lethargy, blindness, ataxia and dysphagia.

30
Q

What is the cause of hepatic encephalopathy in equine? How can it be diagnosed?

A

It is a severe diffuse necrosis of the liver which occurs after receiving equine plasma or serum products made in horses for infectious diseases. Most common, tetanus antitoxin. Theiler disease or serum hepatitis.

Porto-systemic shunt in foals.

Pyrrolizidine alkaloid hepatopathy.

Colonic overproduction of bacterial ammonia – Morgan foals hyperammonemia-hyperornithonemia-hyperhomocitrullinuria.

Diagnosed by measuring ammonia.

31
Q

Which type of astrocytes can be present in the brain with hepatic encephalopathy?

A

Alzheimer type II astrocytes in the cerebral cortex

32
Q

When vision (mature retina), myelination of optic nerve and PLR function, and detectable ERG occurs in dog?

A

mature retina/vision: 6wo
myelination of optic nerve/functional PLR: 21 d
detectable ERG 35do

33
Q

Which axons cross: medial or lateral retina?

A

medial

34
Q

How the dazzle reflex works?

A

Follows the PLR pathway until oculomotor parasympathetic nucleus and then through rostral collucilu goes to tectonuclear axons –> facial nucleus –> blink eyes

35
Q

which trigeminal branch is responsible for the sensory function of the cornea and which for the eyelids?

A

cornea-ophthalmic

eyelids –> ophthalmic/maxillary

36
Q

How the phototranducion is occuring? What is the uniquness of this sensory stimulus?

A

rods and cons have
-cGMP-gated Na channels (open in dark ,close in light)
-nongated K chanlles
-Na-K pumps

-Photon –> rhodopsin/iodopsin (conversion of light to electrical impulse)-> closure of cGMP gated Na channels –> prevention of Na influx (hYPERPOLARISATION OF RODS - the only sensory stimulus to HYper instead of DEPOLARISE neurons)

if dark - polarization of receptiors

37
Q

Which in utero condition can cause optic nerve hypoplasia in calves?

A

BVD virus

38
Q

Traumatic optic neuropathy of foals-why this happens?

A

very long optic canalas, so then they have TBI they may cause traction when eyeballs are moving but head no

39
Q

Causes of hepatic encephalopathy in horses

A

1) Theiler disease or serum hepatitis
2) PSS in foals
3) pyrolizidine alkaloid hepatopathy from palnts (Senecio…etc)
4) unusual colic with bacterial overproduction
5) inherited hyperammonemia-hyuperortinthenemia-hyperhomocitruliunira in MORGAN

40
Q

What is the clinical hallmark and possible cause of adult cheetah leukoencphalopathy?

A

-poss. food oriented
-central blindness

41
Q

Which lysosomal storage disease cause both CNS and PNS signs?

A

Globoid cell leukodystrophy (mainly)
but also fucosidosis

42
Q

Two extra causes of thiamine deficiency in cattle?

A

1) ingestion of pteridium/bracken plants

2) abrupt change in diet –> increased carbs, bacterial dysbiosis - thiaminase producing bacteria in rumen

DeLahunta Book (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions