M2-C2-L61 --> Cytologic Basis Of Neurologic Disease

Front 1

List the Neuronal reaction of injury for General (nonspecific) changes. x6

Back 1

1. Simple Chromatolysis
2. Central (axonal) Chromatolysis
3. Acute neuronal injury
4. Neuronal atrophy and degeneration
5. Pigmentary degeneration
6. Ferrugination

Front 2

Simple Chromatolysis
- Type of change
- Affects what cells
- Description

Back 2

General

Neurons

Swollen
Central nucleus

Front 3

Central (Axonal) Chromatolysis
- Type of change
- Affects what cells
- Description

Back 3

General

Neurons

Swolllen
Eccentric nucleus
Powdered nissl bodies

Front 4

Acute Neuronal Injury
- Type of change
- Affects what cells
- Description

Back 4

General

Neurons

Eosinophilic cytoplasm
Dark Red nucleus (red dead neurons)

Front 5

Neuronal Atrophy and Degeneration
- Type of change
- Affects what cells
- Description

Back 5

General

Neurons

Smaller
Flat
Deformed nucleus

Front 6

Pigmentary Degeneration
- Type of change
- Affects what cells
- Description

Back 6

General

Neurons

Large amounts of lipofuscin

Front 7

Ferrugination
- Type of change
- Affects what cells
- Description

Back 7

General

Neuron

Mineral encrustation of cells and processes

Front 8

Ischemic Necrosis is associated with what type of change?

Back 8

Acute Neuronal Injury

Front 9

List the Neuronal reaction of injury for Semi-specific changes. x4

Back 9

1. Large Irregular neurons
2. Intraneuronal storage
3. Neurofibrillary degeneration
4. Cytoplasmic inclusion bodies

Front 10

Large Irregular Neurons
- Type of change
- Affects what cells
- Description

Back 10

Semi-specific

Neurons

Large and Irregular

Front 11

Tuberous sclerosis is associated with what type of change?

Back 11

Large irregular Neurons

Front 12

Intraneuronal storage
- Type of change
- Affects what cells
- Description

Back 12

Semi-specific

Neurons

Large, bulbous neuron
Abnormally large amounts of normal and abnormal substances
Eccentrically located nucleus

Front 13

Neurofibillary Degeneration (tangles)
- Type of change
- Affects what cells
- Description

Back 13

Semi-specific

Neurons

Paired helical neurofillament protein

Front 14

Alzheimers is associated with what type of change? x2

Back 14

Neurofibillary degeneration (tangles)

Granulovacuolar bodies

Front 15

List all the cytoplasmic inclusion bodies. x5

Back 15

1. Granulovacuolar bodies
2. Lewy bodies
3. Lafora bodies
4. Pick bodies
5. Negri bodies

Front 16

Lewy bodies are associated with what diseases?

Back 16

Parkinson's

Lewy Body Dementia

Front 17

Pick bodies are associated with what diseases?

Back 17

Pick's Disease

Front 18

Lafora bodies are associated with what diseases?

Back 18

Myoclonic epilepsy

Front 19

Negri bodies are associated with what diseases?

Back 19

Rabies

Front 20

List dendrite reactions to injury. x3

Back 20

1. Stellate bodies
2. Arborization Reduction
3. Severely distorted orientation of dendritic tree

Front 21

List axonal reactions to injury. x4

Back 21

1. Injury
2. Wallerian (secondary) degeneration
3. Accumulation of 10 nm filaments
4. Spheroids

Front 22

Describe Axonal injury

Back 22

Irregular swelling

Fragmentation

Front 23

Describe Wallerian (Secondary) degeneration.

Back 23

Distal axon break up

Front 24

Describe Spheroids

Back 24

Rounded or oval, pink

non-nucleated

smooth or granular masses

of axoplasm.

Front 25

In NORMAL brain, what are the functions of astrocytes? x3

Back 25

1. Physical & BCHM support

2. Electrical insulation

3. Estabilshment of Blood Brain Barrier

Front 26

In DAMAGED brain, what are the function of astrocytes?

Back 26

Acts just like fibroblasts of PNS except lays down glial fibers rather than collagen.

Front 27

Describe the general process that occurs when astrocytes are injured.

Back 27

They slowly react (4-5 days)

Astrocytes become enlarged (gemistocytes)

with enlarged nucleus (and nucleolus)

and heavier processes

Increase in number

Revert back to normal sized fibrillary astrocytes

Front 28

Define gliosis. List the two types of gliosis.

Back 28

Proliferation of astrocytes in response to injury.

Isomorphic gliosis
Anisomorphic gliosis

Front 29

Define gemistocytes

Back 29

Hypertrophic astrocytes with

enlarged nucleus

nucleolus

heavy processes

Front 30

Isomorphic gliosis:
- when does it happen
- what happens

Back 30

When specific tracts become damaged

Gliosis conform to pattern of tract

Front 31

Anisomorphic gliosis:
- when does it happen
- what happens

Back 31

When gross tissue damage occurs

Gliosis is random

Front 32

Define clasmatodendrosis

Back 32

Fragmentation and degeneration of the astrocytic processes

Body swells and becomes granular

Front 33

What happens with severe damage leading to astrocyte death?

Back 33

Fibroblasts form granulation tissue

and form collagenous scars

Front 34

Alzheimer type I astrocytes
- describe
- associated with?

Back 34

Pale nucleus
Enlarged nucleus
Round nucleus
Visible cytoplasm

Liver disease

Front 35

Alzheimer type II astrocytes
- describe
- associated with?

Back 35

Pale nucleus
Enlarged nucleus
Rounded nucleus
Invisible cytoplasm

Liver disease

Front 36

Rosenthal fibers
- found in what cell
- found in which part of that cell
- found when
- looks like?

Back 36

Astrocytes

Processes of astrocytes

ProLONGed progressive gliosis

Eosinophilic, eLONGated tapering or globular bodies

Front 37

Corpora Amylacea
- found in what cell
- found in which part of that cell
- found when
- looks like?

Back 37

astrocytes

astrocyte processes

gliosis

spherical basophilic bodies

Front 38

What is the function of oligodendrocytes?

Back 38

Production and maintenance of CNS myelin

Front 39

What do oligodendrocytes look like when injured?

Back 39

Acute swelling with perinuclear halo

"Fried Egg"

Front 40

When injured, describe the general appearance of CNS myelin.

Back 40

Swollen and vacuolated

Becomes short segments of ellipsoids

Front 41

Describe the difference between primary and secondary demyelination.

Back 41

Primary - attack on myelin

Secondary - loss of axon

Front 42

Describe the difference between central and peripheral myelin during injury.

Back 42

Central does not usually regenerate, but peripheral usually does

Front 43

Define ependymal granulation.

Back 43

Injury to ependymal cells leads to

ependymal cell loss

gap fills with ependymal granulation (astrocytes and processes)

Front 44

Injury to ependymal cells in aqueduct of Sylvius results in what?

Back 44

Gliosis of aqueduct

Hydrocephalus

Front 45

What is the origin of microglia?

Back 45

Mesoderm

Front 46

Describe the reaction of microglia to injury.

Back 46

Processes retract

Proliferation

Elongation of nucleus

Mobilization to area of injury

Monocytes join in

Accumulation of cytoplasm in both cells

Becomes macrophages and histiocytes

Scavenge up debris

Front 47

Define satelitosis

Back 47

Increase in perineuronal microglial cells due to injury

Front 48

Define Neuronophagia

Back 48

Phagocytosis of irreversibly injured neurons

Front 49

Rod cells
- what are they?
- when do they occur?

Back 49

Elongated microglial cells

Slow and/or incomplete CNS injury

Front 50

Glial nodules
- AKA
- characteristic of what?

Back 50

Lamellar cells

Viral infection
Protozoal infection
Rickettsial infection

Front 51

Increased intracranial pressure is produced by what type of lesions?

Back 51

Space occupying lesions

Front 52

Increased intracranial pressure has what level of pressure?

Back 52

>200 mm H20

while lying down

Front 53

Symptoms of increased intracranial pressure.

Back 53

HA

N/V

mental slowness

+/- focal signs

+/- papilledema

Front 54

Gross changes in increased intracranial pressure. x2

Back 54

Flattening of gyri

+/- compressed or distorted ventricles

Front 55

List herniations associated with increased intracranial pressure. x3

Back 55

1. Subfalcine

2. Uncal (uncinate transtentorial)

3. Cerebellar tonsillar

Front 56

List the lymphatics of brain.

Back 56

There is none

Front 57

Types of cerebral edema

Back 57

1. Interstitial edema

2. Vasogenic edema

3. Cytotoxic edema

Front 58

Describe subfalcine herniation.

Back 58

Cingulate gyrus herniation

(compresses vessels)

Front 59

Uncal herniation
- structural affects x4
- include symptoms for each

Back 59

Stretched 3rd nerve
- dilated pupil

Compression of contralateral cerebral peduncle
- paralysis

Compression of PCA
- infarct

Downward displacement of midbrain
- Duret hemorrhages
- dilated pupils
- change in respiration
- change in consciousness

Front 60

Cerebellar tonsillar herniation goes into which foramen? Compresses what?

Back 60

Foramen Magnum

Respiratory center

Front 61

Interstitial edema
- seen during?
- how occurs?

Back 61

Non-communicating hydrocephalus

Excess fluid crosses ependymal lining

Front 62

Vasogenic edema
- how occurs?
- structural change? x2
- histology x2

Back 62

Accumulation of edema fluid in EXTRACELLULAR space

Swollen and soft white matter
with gyral flattening

Microvacuolation
Separation of myelin

Front 63

Cytotoxic edema
- how occurs?
- affect on homeostasis?

Back 63

Excess of INTRACELLULAR fluid

Can not maintain

Front 64

CSF
- produced by?
- resorbed by?

Back 64

Choroid plexus

arachnoid villi

Front 65

Describe criteria for non-communicating hydrocephalus.

Back 65

Blockage within the brain

Front 66

Describe criteria for communicating hydrocephalus

Back 66

Blockage within subarachnoid space

Malfunction of arachnoid villi

Front 67

Symptoms of slow and insiduous hydrocephalus seen in adults.

Back 67

Dementia

Incontinence

Gait disturbance

Front 68

Define Hydrocephalus ex vacuo.

Back 68

Compensatory enlargement of the ventricles with an increase in CSF volume

Because of brain loss