Pathology Flashcards

1
Q

Name the species, name and cause of this condition

A

Poliocencephalomalacia (cerebrocortical necrosis) of ruminants.
Thiamin deficiency.

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2
Q

What is shown in the image?

A

Transverse sections of the brain of a 5-year-old golden retriever showing a dilated left lateral ventricle caused by a choroid plexus papilloma obstructing the left interventricular foramen.

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3
Q

Name the most likely disease seen in this subgross image of a feline brain.

A

FIP induced ependimitis

Gross transverse section of the cerebrum and thalamus from the kitten in Fig. 4.31. The cerebrospinal fluid (CSF) has become gelatinous as a result of formalin fixation of the high protein content of the CSF. The ependymal lining of the lateral ventricles is grossly thickened.

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4
Q

What is shown in this subgross transverse section of a kitten brain, what is your top DD?

A

FIP

A perivascular cuff of inflammation surrounds the thickened ependymal lining of the ventricles and extend into the adjacent parenchyma. Just ventral to the dorsal portion of the lateral ventricle is a small granuloma (H&E stain).

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5
Q

What is your top DD in this image of a lamb brain (3 week old)

A

bacterial suppurative meningoencephalitis

(suppurative inflammation obstructing the mesencephalic aqueduct)

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6
Q

What is shown in the image, 4 MO beagle

A

congenital obstructive hydrocephalus

The dorsal half of the cerebrum has been removed to expose the markedly dilated lateral ventricles and the thinned, stretched-out body of the fornix.

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7
Q

What is a digestion chamber?

A

Digestion chamber is a term used for a myelin ellipsoid containing axonal granules.
In Wallerian degeneration the axon degenerates through a process of swelling and subsequent granulation that takes about 3 to 4 days. The myelin degenerates simultaneously with the axons. A close interaction exists between the axon and its myelin, and myelin cannot be maintained if the axon degenerates. This is a secondary demyelination. In this process of wallerian degeneration, this secondary demyelination includes the formation of swellings along the internodes, called ellipsoids, and the fragmentation of myelin into droplets.

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8
Q

What is a Büngner band?

A

After the digestion chamber the Schwann cells that are now reduced to their nuclei and cytoplasmic organelles rapidly proliferate to form a column of cells known as a Büngner band. The adjacent endoneurial cells also proliferate. These columns of Schwann cells provide pathways for regenerating axons to follow to the target that was denervated. They also provide growth factors that induce the outgrowth of axonal buds from the proximal portion of the neuron where the axon is still intact.

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9
Q

How fast do axonal buds grow?

A

1-4 mm/day

With this knowledge, how long it will take for some evidence of regeneration to occur in a patient with a nerve injury can be estimated by measuring the distance from the site of the lesion to the middle of the denervated muscles. Using the slowest rate (1 mm/day), the distance in millimeters is approximately the same as the number of days to reinnervate the muscle.

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10
Q

What are neuromas?

A

If an impediment such as hemorrhage or fibrosis prevents the axonal buds from reaching the nearest bands of Schwann cells, the axonal buds will continue to grow in a haphazard manner and form an observable swelling known as a neuroma. These neuromas may be a source of considerable discomfort. They are often a sequel to the neurectomies that are performed in the distal extremities of the horse to eliminate a source of discomfort, such as a degeneration of the distal sesamoid bone, referred to as navicular disease. The resultant neuroma may then be an additional source of irritation and pain for the patient.

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11
Q

Morphologic diagnosis? What is the main DD?

A

degeneration of the ventral spinal rootlets (black arrows)

Transverse section through the lumbar intumescence of the dog . There is degeneration of the ventral spinal rootlets (arrows) as evidenced by a lack of myelin staining. Note the normal staining of the myelin in the dorsal spinal rootlets (arrowhead) (×2 magnification; Luxol fast blue with cresyl violet counterstain).

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12
Q

What would be your firs DD?
Young retriever dog with slowly progressive PNS signs and elevated muscle enzyme activity.

A

Dystrophinnopathy

Muscle biopsy showing extensive muscle cell necrosis with macrophages, mineralization, and rows of activated satellite cells indicative of regeneration in a young male golden retriever with dystrophinopathy. Hematoxylin and eosin stain.

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13
Q

Most likely DD?
12 YO beagle with monoparesis of the R thoracic limb

A

PNST

Dorsal view of the cervical intumescence with the associated spinal cord roots and spinal nerves (C5 to T2). Image shows a malignant nerve sheath neoplasm of the right C7 dorsal and ventral roots and the spinal nerve.

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14
Q

Most likely DD?

4-­year-­old thoroughbred gelding with bilateral thoracic limb lameness

A

Transverse section of the cervical intumescence of the horse. The discoloration of the spinal cord gray matter is due to a hemorrhagic myelitis caused by Sarcocystis neurona.

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15
Q

Most likely diagnosis?

Dog with an acute onset of paraplegia, no trauma was noted.

A

Hemorrhagic necrosis of the SCS L6-Cd

Most likely FCE

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16
Q

Most likely diagnosis?

Dog with an acute onset of paraplegia, no trauma was noted.

A

Microscopic view of the L7 spinal cord showing diffuse hemorrhagic and ischemic necrosis.

FCE

17
Q

Most likely diagnosis?

8 YO warmblood gelding with rectal impaction and penis prolapse

A

Polyneuritis equi

Dorsal view of the cauda equina of an 8-­year-­old warmblood gelding with polyneuritis equi after the adhered extradural spinal nerves were torn apart at autopsy.

18
Q

Most likely diagnosis?

5 YO cat found paraplegic with loss of deep pain sensation. No fracture was evident on radiography.

A

Ischemic/traumatic poliomyelomalacia

lumbar and sacral spinal cord segments showing poliomyelomalacia of the lumbosacrocaudal spinal cord segments, related to presumptive abdominal injury by compression by being crushed by the tire of a vehicle, referred to as traumatic poliomyelomalacia. This image is the L5 spinal cord segment approximately 5 to 7 days after the injury.

19
Q

Most likely diagnosis?

2-­year-­old thoroughbred, flaccid paraplegia after cryptorchid surgery.

A

2-­year-­old thoroughbred, showing the bilateral symmetric discolouration of gray matter by a poliomyelomalacia associated with recumbency for cryptorchid surgery.

20
Q

Most likely diagnosis and ethiology?

3 MO pig with sudden onset of LMN tetraparalysis.

A

Poliomyelomalacia in pigs due to excessive selen in diet

(less likely if fed with 6-­aminonicotinamide)

The toxic effect of the excessive selenium causes a bilateral symmetric degeneration of the center of the ventral gray columns, primarily in the cervical and lumbosacral intumescences and in a few brainstem GSE nuclei. Neuronal cell bodies are spared on the borders of the lesion, which consists of an abundance of macrophages and has numerous small blood vessels coursing through it

21
Q

Most likely disease process and ethiology?

Caudal surface of a transverse section of the pons of a 4-year-old standardbred gelding unable to close the mouth.

A

The bilateral symmetric discolorations reflect a chronic astrocytosis that has replaced all the neuronal cell bodies in the nuclei of the motor component of the trigeminal nerves. Areas of active nonsuppurative inflammation and necrosis in the pons and medulla were presumed to be caused by infection by Sarcocystis neurona organisms.