Brainscape's Knowledge GenomeTM

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


See full index

Systemic Pathology > Neuro > Flashcards

Neuro Flashcards

1
Q

What is the function of oligodendrocytes?

A

Form myelin that wraps around axons (same function as Schwann cells in PNS)

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

What is the function of astrocytes?

A

Star shaped cells whose processes form blood brain barrier

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

What is the function of microglia?

A

Phagocytic cells, fixed macrophages of CNS

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

What is central chromatolysis?

A

Degenerative change, dispersal of Nissl substance

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

What is neuronophagia?

A

Microglia gather around necrotic neuron and phagocytose it to remove the debris

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

What are the histological characteristics of axonal degeneration?

A

Empty, dilated

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

What is a spheroid?

A

Focal axonal swellings filled with degenerate organelles

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

What kind of necrosis is typically seen in the CNS, and what are the characteristics of this type of necrosis?

A

Liquifactive necrosis

Empty looking brain

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

What is astrocytosis?

A

Increase in size and number of astrocytes in response to injury

Repair of CNS after injury (not very good at their job though)

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

What are gemistocytic astrocytes?

A

Plump, reactive astrocytes with eosinophilic cytoplasm

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

What is the appearance of Alzheimer’s type II astrocytes, and what disease process are these cells typically seen in?

A

Enlarged, vesicular nuclei

Classic of hepatic encephalopathy (lots of ammonia)

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

What is hydrocephalus?

A

Excess fluid in the brain

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

What are the different types of hydrocephalus?

A

Internal: fluid in ventricles (most common in veterinary medicine: in mesocephalic aquaduct)
External: fluid in arachnoid space
Communicating: fluid in both

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

In which breeds of dog is hydrocephalus most common?

A

Brachycephalic breeds and some toys breeds (chihuahuas)

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

Microencephaly

A

Abnormally small brain, seen in BVD in cattle and Border Disease in sheep

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

Hydranencephaly

A

Near complete or complete absence of cerebral hemispheres, leaving fluid filled sacs formed by meninges lined by CSF

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

Porencephaly

A

Cystic cavitation of brain (less severe manifestation of hydranencephaly)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Lissencephaly

A

Brain lacks normal gyri and sulci

Not normal for any domestic animals, but normal for some exotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Anencephaly

A

Absence of brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Prosencephalic hypoplasia

A

Absence of cerebral hemispheres with preservation of some portion of brain stem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Cranium bifidum/spina bifida

A

Defect through which brain/spinal cord and meninges can protrude; almost always on dorsal midline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the most common brain malformation seen with BVD infection?

A

Cerebellar hypoplasia

23
Q

What is the underlying cause of storage diseases?

A

Accumulation of substance in cells

24
Q

What happens to cells which accumulate substrate in lysosomal storage diseases?

A

Loss of function, distended cells, don’t normally die

25
Q

How are storage disease inherited, and when do they typically present with neurologic signs?

A

Autosomal recessive; present early in life, progressive, die

26
Q

How are storage diseases named (in general, you do not need to know specific names)?

A

Named according to substance that doesn’t degrade

27
Q

Which cells in the CNS are most sensitive to ischemia?

A

Neurons and oligodendroglia most susceptible (gray matter)

28
Q

What are the causes of polioencephalomalacia? Where are the lesions located?

A

Thiamine deficiency, high sulfur intake (which inactivates thiamine), some cases of water deprivation

Necrosis of gray matter of brain

29
Q

What is the cause of leukoencephalomalacia? Where are the lesions located?

A

Eating moldy corn for longer than 1 month

Necrosis of white matter of brain

30
Q

What is the cause of indirect salt poisoning?

A

Ingestion of high salt diet WITH restricted water intake for several days

Think pigs

31
Q

What are the ways in which bacterial infections get to the CNS?

A
  1. Most are secondary to septicemia
  2. Septic emboli from endocarditis
  3. Abscesses from hematogenous spread or direct invastion – usually through cribiform plate or middle ear
32
Q

In what species do we most often seen listeriosis?

A

Sheep (and other ruminants)

33
Q

What is the causative agent of listeriosis?

A

Listeria monocytogenes

Outbreaks associated with heavy feeding of silage

34
Q

What are the characteristic lesions of listeriosis, and where are the lesions typically located?

A

No gross lesions, but microabscesses histologically

Lesions located in brainstem

35
Q

What is the pathogenesis of the listeriosis encephalitis?

A

Bacteria invade oral mucosa and then spreads up branches of trigeminal nerve

36
Q

What is the causative agent of thrombotic meningoencephalitis? Which species does it affect?

A

Histophilus somni

Affects cattle (and sheep)

37
Q

What is the pathogenesis of development of CNS lesions for thrombotic meningoencephalitis, and what are the lesions?

A

Septicemia causes vasculitis with hemorrhage, necrosis, and thrombosis

Lesions include hemorrhage, vasculitis, thrombosis, infarction, neutrophilic meningoencephalitis

38
Q

What are the general histologic features of viral infections?

A
  1. Non-supperative meningoencephalitis
  2. Perivascular cuffing
  3. Gliosis
  4. +/- viral inclusions
  5. +/- neuronal necrosis
39
Q

What are the principal reservoirs for rabies in the US?

A

skunks, foxes, racoons, bats

40
Q

What tissues is the rabies virus tropic for?

A

CNS and salivary gland

41
Q

What is the pathogenesis of rabies viral infection from inoculation to spread to the CNS?

A

Virus inoculated into wound –> replicates in muscles cells –> spreads to sensory paravertebral ganglia –> travels along peripheral nerves to CNS

42
Q

What are the lesions for rabies?

A

Non-supperative encephalomyelitis, ganglioneuritis, and parotid adenitis

Negri bodies in hippocampus of carnivores
Negri bodies in Purkinje cells of herbivores

43
Q

What is the cause of pseudorabies? What species are affected by this disease? What are the clinical signs?

A

Caused by suid herpesvirus 1

Can affect ALL common domestic species

Clinical signs in pigs: NO pruritis, mild fever, prostrate, convulsions, SMEDI in sows

Clinical signs in non pigs: INTENSE pruritis, high fever, neurologic signs, ALWAYS fatal

44
Q

What are the clinical signs of caprine arthritis-encephalitis virus and visna-maedi virus?

A

CAE: hind limb ataxia, paresis, paralysis, death in GOATS
VM: hind limb ataxia, paralysis, death due to starvation in SHEEP

In both: pneumonia, arthritis, mastitis

45
Q

In what age animals is neurologic disease typically observed with CAE and VM?

A

CAE: young kids 2-4 months of age
VM: sheep > 2 years of age

46
Q

What are the lesions of CAE and VM?

A

CAE: non-supperative leukoencephalomyelitis, demyelination
VM: non-supperative meningoencephalitis most severely affecting white matter, demyelination

47
Q

What species are typically affected by fungal infections with Cryptococcus neoformans?

A

Cats (but also dogs and horses)

Immunocompromised animals

48
Q

How do Cryptococcus neoformans infections get into the brain?

A

Starts as nasal or sinus infection –> directly enters brain through cribiform plate

May spread hematogenously from pulmonary lesions

49
Q

What are the histologic lesions of Cryptococcus neoformans?

A

Mucopolysaccharide capsule, non-staining

50
Q

What is the cause of equine protozoal myelitis? Why are organisms not seen in most cases?

A

Cause is Sarcocystis neurona

Not seen because animal has been treated prior to euthanasia

51
Q

What is the cause of transmissible spongiform encephalopathies (TSEs)?

A

Cause by prions, abnormal isoforms of a normal cellular protein called prion protein

52
Q

How do animals typically acquire TSEs?

A

Transmitted horizontally through consumption of infected feed material

53
Q

What are the lesions of TSEs?

A

Intracytoplasmic neuronal vacuolation, astrocytosis

54
Q

What are the histologic lesions of FIP?

A

Loss of ependymal cells
Reactive astrocytes
Periventricularitis

Systemic Pathology (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions