Test 4: lab eyes and brain Flashcards

1
Q

Tissue from a 5-month-old calf with acute onset of blindness, mental dullness, and head-pressing
Description:

Morphologic diagnosis:

A

Polioencephalomalacia- grey matter

The cerebral cortex (occipital and parietal lobes) is diffusely soft, tan, and thin (about 1-3 mm thick), with loss of the underlying deep cortical tissue (at the junction of the grey and white matter).

Cerebrum (occipital and parietal lobes): severe regional (laminar) cortical necrosis and loss (Alternatively: severe regional polioencephalomalacia)

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2
Q

What are potential causes for this condition?

A

Thiamine deficiency, ingestion of thiaminases (certain plants including Bracken fern), overgrowth of thiaminase- producing ruminal microbes (such as Bacillus thiaminolyticus, etc.), high sulfur intake, water deprivation.

The pathogenesis of PEM associated with decreased thiamine is not completely understood; however, phosphorylated thiamine is a cofactor for a few enzymes involved in oxidative phosphorylation and the hexose monophosphate shunt, so depletion of thiamine likely ultimately causes damage by ATP depletion and free radical injury.

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3
Q

Tissues are both from young dogs.
Description of the brains:

Morphologic diagnosis:

A

There is severe bilateral enlargement of the lateral ventricles with severe diffuse thinning of the cerebral cortex.

Severe lateral ventricular hydrocephalus

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4
Q

What are the possible mechanisms leading to this lesion?

A
  1. Excessive production/oversecretion of cerebrospinal fluid (CSF)
  2. Obstruction of CSF flow
    * Critical sites for obstruction:
    * Intraventricular: interventricular foramina between the lateral and third ventricles, mesencephalic aqueduct, lateral foramina of the fourth ventricle
    * Extraventricular: subarachnoid space (as arachnoid villi mediate CSF transfer into the dural venous sinuses)
    * Congenital or acquired causes of obstruction:
    * Congenital: stenosis of the mesencephalic aqueduct at a critical time during fetal development
    * Acquired: neoplasia, inflammation, scar (astrocytic sclerosis)
  3. Impaired reabsorption of CSF
  4. Loss of parenchyma (hydrocephalus ex-vacuo)
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5
Q

This is a congenital lesion in this cat. A normal cat brain has been presented for reference.
Description and diagnosis:

A

The cerebellum is severely diffusely small with relatively normal proportions.

Cerebellar hypoplasia.

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6
Q

cause of cerebellar hypoplasia

A

In utero infection with Feline Panleukopenia Virus (feline parvovirus).

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7
Q

Based on the part of the brain that is affected, what clinical signs would you expect this cat to have?

If this cat was instead born normal and developed progressively worse clinical signs, what would be your diagnosis?

A

Cats with cerebellar hypoplasia have deficits in fine motor control and coordination. They have a very wobbly gait, poor balance, and intention tremors.

Cerebellar abiotrophy, which can be genetic or idiopathic.

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8
Q

horse

Description:
Morphologic diagnosis:

A

A wedge-shaped region of the cerebral cortex is soft and discolored dark red to black (peripherally) to pale tan (centrally).

Severe locally extensive unilateral acute to subacute infarct of the cerebral cortex.

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9
Q

What is the term for necrosis of CNS tissue?

A

Malacia. “Polio-” and “leuko-” denote gray or white matter, and “encephalo-” or “myelo-” denote brain or spinal cord tissue, respectively.

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10
Q

Possible causes of this lesion:

A

There are many causes of vascular compromise, including local disease leading to vascular thrombosis (inflammation or neoplasia with damage to local blood vessels) or thromboembolic disease or DIC.

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11
Q

Section of vertebral column from a medium-sized dog. The dog jumped off the bed, howled, and was
paraplegic with pain in the thoracolumbar area.
Description:

A

One of the intervertebral discs is herniated, displacing firm, pale tan, fragmented intervertebral disc material into the spinal canal.

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12
Q

What is the difference between a Hansen Type I vs Type II lesion?

A

Hanson type I involves extrusion of the nucleus pulposus into the spinal canal and Hansen type II refers to a protrusion of the disc still covered by the annulus fibrosis. Both compress the spinal cord, although Hansen Type I lesions are typically more acute and severe.

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13
Q

Which breeds are predisposed to Hansen Type I vs Type II lesions?

A

Chondrodystrophic dog breeds (e.g., dachshunds, basset hounds) are predisposed to Hansen Type I lesions, whereas non-chondrodystrophic breeds are more likely to develop Hansen Type II lesions as an age-related degenerative change.

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14
Q

Sections of brain from a male white-tailed deer.
Description:
Morphologic diagnosis:

A

The leptomeninges are regionally severely expanded by abundant soft, pale tan to gray, purulent material.

Severe regionally extensive acute suppurative meningitis

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15
Q

male white-tailed deer.
By what routes can infectious agents get into the brain?

For this male deer, how might the infection have gotten to this location?

A

Hematogenous, local extension, direct penetration, or retrograde axonal transport.

Suppurative meningoencephalitis and/or intracranial abscesses are an important cause of death in wild and domestic deer, causing 8-10% of all deaths. This is especially common in male deer around breeding season due to antler sparring causing injury as well as rubbing and shedding of antlers allowing entry of bacteria.

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16
Q

Tissue from a 6-year-old female spayed boxer dog. The owner complained of a recent onset of circling to the right and altered (dull)
mentation. Terminally, the patient became non-responsive, and developed respiratory arrest leading to death.
Description of the lesions:

A

A 2 cm diameter irregularly round, mottled dark red, black and tan, soft and gelatinous mass focally effaces and expands the right frontal lobe (and right olfactory bulb) of the cerebrum.
There is caudal displacement (herniation) of the middle cerebellar vermis resulting in slight compression of the medulla.

17
Q

What are some differentials for primary and for metastatic neoplasia in the brain? Do you think this is a primary or metastatic neoplasm?

A

Primary neoplasms include glial tumors (astrocytoma, oligodendroglioma, ependymoma), choroid plexus tumors, meningiomas, and lymphoma.

Common neoplasms metastatic to the brain include hemangiosarcoma, lymphoma, malignant melanoma, or mammary carcinoma.

This large, solitary nodule is a primary neoplasm to this location (specifically, this is an oligodendroglioma).

18
Q

How can a focal intracranial mass, regardless of specific location within the cranial cavity, lead to sudden death?

A

A focal lesion (e.g., neoplasm, inflammation, hemorrhage, etc.) occupies space, along with any associated edema and hemorrhage. This results in an increase in volume of the brain (and/or material within the cranial cavity). Due to the limited volume of the cranial cavity, this results in increased intracranial pressure, and subsequent caudal herniation of brain (cerebellum) through foramen magnum. This results in compression of cardiovascular and respiratory centers in medulla, causing coma and/or death.

19
Q

These samples are the same lesion but in two different cats. The clinical history is similar in both cases, with subtle behavioral changes preceding onset of ataxia and seizures.
Description:

Diagnosis:

A

The masses are firm, pale tan, irregularly round, and arising from the meninges. The adjacent cerebral cortex is severely compressed.

Meningioma

20
Q

Are these clinical signs specific for this type of meningioma

A

No. Because of the localized nature of nervous system functions, the same pathologic process present in different locations often presents with different clinical signs. Therefore, a meningioma causing compression of the cerebral cortex may cause seizures, while a meningioma compressing the optic nerve may cause blindness, and a meningioma in the medulla and cerebellum will cause vestibular signs. Conversely, different diseases affecting the same area of the CNS will result in the same clinical signs.

21
Q

What factors do you think determine the clinical signs caused by neoplasms in the CNS?

A
  1. Location within the brain/cranial cavity
  2. Size of the neoplasm
  3. Rate of growth of the neoplasm
  4. Severity of secondary vascular lesions (edema and hemorrhage)
22
Q

There are three sections of brain taken through the level of the lateral ventricles.
Description:
Differential diagnoses for a tumor in this location:

A

here is a large, pale tan, soft, papillary mass filling the left lateral ventricle and compressing the caudate nucleus.

Choroid plexus tumor (papilloma or carcinoma) or ependymoma. This is a choroid plexus papilloma

23
Q

Besides the direct damage to the adjacent brain tissue, what secondary effect might this have on the brain based on the intraventricular location?

A

This is a choroid plexus papilloma.

Obstruction of CSF flow through the ventricles may lead to secondary hydrocephalus.

24
Q

Description:

A

The brain contains multifocal 2 mm – 12 mm firm, irregularly round black masses.

25
Q

Do you think this is a primary neoplasm or metastatic neoplasm?

Based on gross appearance, what are possible diagnoses?

A

The random distribution of many small masses throughout the brain is more consistent with a metastatic process rather than a primary one.

The dark color is most consistent with a malignant melanoma (which this case is). Another possibility would be a hemangiosarcoma, which can often be very dark red-black.

26
Q

More examples of primary neoplasia within the brain:

A

Glioblastoma multiforme (confirmed on histopathology for this case)

27
Q

Larynx of a young male Thoroughbred horse who had abnormal inspiratory sounds when exercising.
Morphologic diagnosis:

A

Severe diffuse atrophy of the left cricoarytenoideus dorsalis muscle

28
Q

What are the histologic features of neurogenic muscle atrophy?

How do the above features differ from disuse atrophy?

A

As motor neurons innervate myofibers in groups (“motor units”) of fibers intermingled with other motor units. There will be decreased diameter (atrophy) of myofibers in a “mosaic” pattern.

Decreased muscle use leads to equal atrophy of all myofibers in the muscle.

29
Q

Eye from a 9-year-old, female spayed, mixed breed dog. Description:

Possible diagnoses for the mass:

A

The anterior uvea is severely expanded and effaced by a well-demarcated, soft to firm, pale tan mass.

The non-pigmented mass is an iridociliary tumor (more specifically, an iridociliary adenoma), although lymphoma is a valid differential diagnosis from gross appearance alone.

30
Q

Regardless of the exact diagnosis, what are some potential sequelae to intraocular neoplasia?

A

Intraocular neoplasia at this location can cause uveitis, hyphema, pre-iridal fibrovascular membranes, or glaucoma, among other ocular changes.

31
Q

Eyes from two different dogs.
Descriptions:

A

Within one eye, the iris is regionally expanded by a 5 mm diameter, irregularly round, firm, dark brown to black mass. The other eye contains a similar but much larger mass that has obliterated most intraocular soft tissues, encases the lens, and has focally penetrated the sclera with extension over the scleral surface.

32
Q

What is the usual behavior of melanocytic tumors in the eye of dogs?

How do the behavior and presentation of intraocular melanocytic tumors differ between cats and dogs?

A

Prognosis is based on histologic criteria, but the majority are benign.

The majority of intraocular melanocytic tumors in dogs are benign, solitary masses within the iris or, less commonly, the choroid. In cats, melanocytic tumors in the eye are usually diffuse rather than a solitary mass, and there is greater risk for distant metastasis than in dogs.