Exam 5 (no drugs) Flashcards
(145 cards)
Describe the key differences b/w necrosis and apoptosis.
- cause
- mechanism
- effector molecules
1. Cause APOPTOSIS -DNA damage -inflammation -neurodegeneration
NECROSIS
-acute, severe, injury (energy failure, trauma)
- Mechanism
APOPTOSIS
-Mediators activate caspases
NECROSIS
- glutamate induced excitotoxicity
- accumulation of intracellular calcium
- oxidative stress
- Effector molecules
APOPTOSIS
-caspases
NECROSIS
-calcium activated phospholipases, proteases and endonucleases
Characteristics of cytotoxic edema
there are 6
• Minutes to hours
• Swelling of cellular elements
• Ion pumps fail
• Rapid accumulation of sodium within cells
• Water follows the sodium to maintain osmotic
equilibrium
• Leads to glutamate excitotoxicity
Characteristics of vasogenic edema (3)
- Hours to days
- Increase in extracellular fluid volume resulting from increased permeability of brain endothelial cells to macromolecular serum proteins
- Brain herniation
Most dangerous period for cerebral infarct and why?
3-4 days -> maximal edema
-risk for herniation
Describe mechanism of glutamate excitotoxicity
- reuptake pumps responsible for removing glutamate from synaptic cleft
- ischemia/hypoxia depletes ATP which shuts off reuptake pump
- Glutamate can’t be removed from NMDA receptor which leads to non-stop influx of calcium
- calcium activates the proteases that ultimate cause the cell death
Central core vs penumbra in cerebral infarct
CENTRAL CORE
- total ischemia and tissue necrosis
- irreversible
PENUMBRA
- zone of borderline ischemic tissue
- receives collateral circulation
- damage is reversible if blood flow is restored w/in 3-4 hours
Describe central chromatolysis
regenerative response to axonal injury
- cell swells
- dispersion of Nissl substance - RNA
- nuclear displacement
Neuronophagia
- what is it?
- often seen with?
- phagocytosis of damaged neurons by microglia and monocytes
- associated w/ rapid cell death: most often seen w/ viral infections
- microglia surround tissue to form nodule
Neurofibrillary tangles seen in?
Alzheimer’s and old age
Granulovacular bodies
- what/where are they?
- seen in?
- autophagic lysosomal vesicles - cytoskeletal components being degraded
- mainly in hippocampus
- seen in AD but not pathognomonic
Lewy body
- describe
- location
- disease association
- inclusion w/ eosinophilic laminated core and halo
- substantia nigra, locus coeruleus
- Seen in parkinson’s and lewy body dementia
Hirano bodies
- describe
- associated with?
- dense hyaline mass
- eosinophilic
- alzheimer’s
- Creutzfeldt-Jacob
- fx of age w/out obvious underlying neurodegeneration
Negri bodies are pathognomonic for?
what is the stain against?
where are the found?
Rabies
stains ribonuclear viral proteins
purkinje cells, CA-1 hippocampus
Psammoma bodies pathognomonic for?
Meningioma
Verocay bodies pathognomonic for?
what do they look like?
Schwannoma
palisading nuclei - lined up around clear areas
What’s left behind after Wallerian degeneration is complete?
Endoneurial tube - plays part in repair
Dying back (distal axonopathy) is seen with what conditions?
Histo findings?
- most common type of pathologic rxn in generalized polyneuropathies
- often attributed to a metabolic etiology (DIABETES)
HISTO
- myelin fragments
- ellipsoids
- axonal fragments
- macrophages w/ phagocytosed lipid
Diffuse axonal injury/axonal spheroids
- cause
- contents of the spheroids
- disruption of cytoskeleton
- stretching/tearing of axon -> battered baby syndrome
-spheroids contain accumulation of organelles being brought down by cell body
What causes withdrawal of presynaptic neuron terminals?
Blocking NGF from being delivered to the postsynaptic neuron
Axonal regeneration can occur after transection of axon only if?
Integrity of endoneurial tube is maintained
IN THE PNS
Neuropraxia
- cause
- can recovery occur
- Block in conduction
- Recovery takes place without Wallerian degeneration
- Biochemical lesion caused by a concussion or shock-like injury to the nerve fiber
Common examples
• Peroneal paralysis from prolonged cross-legged position
•Radial or Saturday night paralysis caused by compression of the axilla
Axonotmesis
- cause
- can recovery occur
- Involves loss of the relative continuity of the axon and its covering of myelin
- Preservation of the connective framework of the nerve – endoneurial tube
Neurotmesis
- cause
- can recovery occur
- This results from more severe contusion, stretch, or laceration and not only axons, but the investing connective tissues lose their continuity
- Both the endoneurial and perineurial connective tissue layers and the axon are disrupted
- Regenerating axons reach the distal stump but fail to find their preinjury pathwyas
- No functional regeneration
Gliosis (astrocytosis)
- response to?
- what happens?
- prevents?
- what produced?
- over time
- seen in?
- response to injury
- gliotic tissue formation -> walling off of damaged area
- prevents regeneration in CNS b/c axons can’t get through
- GFAB to form the wall
- scar formation due to astrocytic cytoplasm (NOT FIBROBLAST)
seen in
- seizures
- infarcts
- chronic degeneration