Basic CNS Reactions/Pathology Lecture 7 Flashcards Preview

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Flashcards in Basic CNS Reactions/Pathology Lecture 7 Deck (28)
1

What happens when axons are cut/what is the axonal reaction? 

Proximally = Central Chromatolysis - swelling of cytoplasms and displacement of nissl chrome out of center to periphery (nissl = rough ER and is bluish) due to disruption of neurofilaments/organelles and transport

 

Distally  = Wallerian Degeneration where distal axon degenerates 

2

What is a Louis Body? 

can see easily in substantia nigra pigmented nuerons where see rounded eosinophilic core structure with halo around it

 

proteinacious inclusions of alpha synuclein

3

What is Lipofuschin? 

Prominent non-pathological accumulation that occurs with age

4

What are astrocytes? what is their role in the CNS? what is Gemistocytic? 

Astrocytes are supportive and detoxify and respond to injury

 

like the fibroblasts of the CNS - get injury and get astrocye activation and proliferation where they start using GFAP (instead of collagen) as an intermediate filament for "scarring" in response to disease process 

 

Gemistocytic = cells stuffed with GFAP

5

What are 2 Major Accumulations in AStrocytes? 

Rosenthal Fiber --> proteinacious accumulation of alpha-Be-Crystalline seen in Astrocytoma or Leukodystrophy or Alexander Disease

 

Corpora Amylacea = purple things that are age-related starch accumulations 

6

What happens to astrocytes in Liver Failure Cirrhosis? What is that called? 

Elevated ammonia results!!

Normally, astrocytes detoxify excitatory NT like Glutamate and transfer ammonias between glutamate and glutamine 

With elevated ammonia, astrocytes respond with enlarging their nucleus and forming more heterochromatin and losing their GFAP 

 

Results in Big, watery looking atrocytes 

**Alzheimer's Type 2 Astrocytosis = brain changes with hepatic encephalopathy 

7

What is Alzheimer's Type 2 astrocytosis? 

Brain changes seen with hepatic encephalopathy (NOTHING TO DO WITH ALZHEIMER'S) where you see enlarged nucleus orf astrocytes that are watery-looking and form more heterochromatin and lose their GFAP staining 

8

What are oligodendrocytes? What are some pathologies seen in oligodendrocytes? 

Cells that form myelinin CNS and have limited response to injury 

 

JC-Virus with PML - see Viral inclusions in Oligodendrocyte 

Multiple System Atrophy - see accumulation of Alpha Synuclein!!!! 

 

See picture 

9

What are Ependymal cells? What happens with they get damaged? 

Ependymal cells line ventricles 

 

when get damaged - not too responsive to injury - slough off and don't come back

Leads to proliferation of Sub-Ependymal Glia --> exposure to CSF stimulates proliferation of glial fragments and can see GLANDULAR EPENDYMITIS 

10

What are microglia? What are some changes that happen with them? What happens when stimulated with antigen? 

Brain Macrophages!!!!

get stimulated by antigen and get Rod-Shaped Morphology and migrate towards antigenic stimulus

Then reach stimulus and cluster around it making Microglia Nodule

 

Then proliferate and phagocytose infected neuron - Neuronophagia 

(see picture - example West Nile Virus) 

 

 

11

What are the 3 main types of edema? where are they more prominent? 

1) Cytotoxic Edema = cell death resulting from incompetence of membrane and water and salt go into the neurons and swells them up --> GRAY MATTER

2) Vasogenic Edema = incompetence of BBB, endothelial TJ breakdown and BV breakdown causing serum components to leak into tissues and cause mass effect --> WHITE MATTER more prominent and extracellular water

 

3) Interstitial Edema - Forcing water through ependymal lining into deep white matter in setting of obstructive hydrocephalus 

12

What are the three types of herniation phenomena and what's happening with each? 

Transtentorial - "Uncal" Herniation - Displacement of medial temporal lobe over the free ege of the tentorium --> *Cerebral Peduncle and 3rd cranial nerve there so see Ipsilateral Fixed Pupil Dilation and Contralateral weakness

Cerebellar Tonsillar Herniation - Displacement of Cerebellar tonsils into Foramen Magnum --> Cerebellar tonsils next to medullary cardiorespiratory centers and life threatening!!!

Subfalcine/Cinglate Herniation -- Displacement of Cingulate gyrus under Falx Cerebri --> less life threatening and results in associated weakness in loewr extremities

 

(SEE PICTURE) 

13

Where is CSF made and what's it's flow pathway? Where is it absorbed? 

CSF is made by the choiroid plexus in lateral, 3rd, and 4th ventricles and exits the foramen of Lushke/Megendie to circulate in subarachnoid spaces and is resorbed in the arachnoid granulations in the Parasagital Regions 

14

What's the difference between communicating and non-communicating hydrocephalus? 

Communicating is where the ventricular system is patent and can communicate with subarachnoid space --> Typically arachnoid granulation obstruction

 

Non-Communicating is where the ventricular system is obstructed --> implies obstruction in the ventricular outflow tracts like the brainstem  and can see interstitial edema and water being pushed along the outside surfaces/ependymal surfaces 

15

Describe contusions? What kinds are there? 

Contusion is parenchymal brain injury - like brain bruising

 

Coup Contusion = blow to stationary head making contusion at point of impact

 

Contrecoup Contusion = fall on back of head while rotating making contusion on Opposite point of impact

 

Remote Contusion = reselmbles an old infarct and can see a lot in orbitofrontal area  where blood disrupts tissues and they become necrotic and fall away, can see hemosiderin there, can get post-traumatic epliepsy from these 

16

What happens in diffuse traumatic axonal injury? ?How does that present? 

Shearing forces deep in brain cause by low strain rate injury like MVA

Acutely, swollen axons 

Presentation= prolonged traumatic unconsciousness

 

Example - MVA and instantly comatose at impact but no hemorrhage

17

What is chronic traumatic encephalopathy? What parts of the brain do you see it in? 

Progressive Taupathy occurs as a consequence of repetitive mild TBI and clinically is associated with symptoms of irritability, impulsivity, aggression, depression, short term memory loss, and heightened suicidality 8-10 years after injury 

 

 

Seen in Deep sulci and perivascular areas

Random tau in cortical areas 

18

What is an Epidural hematome? How does it present and what causes it? 

ARTERIEAL BLEEDS 

Due to damaged meningeal artery (often middle meningeal) 

Unilateral 

 

Associated with skull fracture

19

What is a subdural Hematoma? What do you see with a subdural hematoma? How does it heal? 

Rupture of Bridging Veins that drain the cortical surface into sinuses 

can be unilateral or bilateral

often due to Trauma in elderly people and can be very large bc more space available from age-related atrophy

Heals by forming "neomembrane" to wall off the hemorrhage and at risk for repeat bleeds and chronic neurologic dysfunction (see picture) 

 

20

Compare and contrast epidural and subdural hematomas? 

Epidural - often from skull fracture puncturing an ARTERY and mostly unilateral causing Dura to press down into brain

Subdural - often in old people and comes from bridging VEINS rupturing into subdural space and can form neomembranes between dura and brain from arachnoid proliferation 

 

BOTH have mass effect and can be life threatening 

See Picture 

21

What do you see in brain after ischemia? 

Liquefactive Necrosis 

 

Edema and mass effect 

22

What areas are most vulnerable in global ischemia? (ie cardiac arrest) What kind of necrosis do you see? 

Arterioborder zone ischemia - area between vascular teritorries with most remote blood supply 

 

Laminar necrosis - selective damage to cerebral neocortex in global ischemic events (layers 3, 5, 6 more vulnerable) 

 

23

What is the temporal pathology of ischemia? 

Acute - cytotoxic edema, red dead neurons

Subsacute - Foamy macrophages and vascular proliferation

Remote - cavitation 

24

What kind of lesions do you see in HTN cerebrovascular disease? 

Lacunar Infarcts - occur when you KO small penetrating vessels coming off the circule of willis 

*Indicative of Chronic HTN and see Small punched out lakes 

 

 

25

What happens in Subarachnoid hemorrhage? 

is a Ruptured Saccular aneurysm until proven otherwise 

Occur at branch points in circle of willis 

get rupture and massive hemorrhage 

 

Clinical Presentation = HA --> Prostrate --> bleed --> die 

26

What's probably causing intra-parenchymal bleeding in deep areas? 

HTN!!!! 

spontaneous deep intracerebral hematoma from longstanding cerebroascular disease 

associated with HTN 

27

What are you more likely to think if lobar intra-parenchymal hemorrhage? like in a lobe of cortex? 

Older patient with sudden lobar hemorrhage in lobe of cortex --> AMYLOID DEPOSITS IN BV WALL!!!! 

 

Lobar Intracerebral Hematoma!!!! 

spontaneous in otherwise healthy person but in old person think Amyloid Angiopathy 

28

What is Amyloid Angiopathy? 

Stain with Congo-red to see vascular deposits of Amyloid Beta Protein 

more common in elderly 

 

(VS Amyloid Beta Precursor protein used to ID damaged axons in diffuse axonal injury)