Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
120 Cards in this Set
- Front
- Back
|
what does a normal neuron look like?
|
Prominent Nucleolus
Cytoplasmic Basophilia due to RNA |
|
|
What happens when said neuron goes ischemic?
|
Basophilia is lost-->red/pink eosinophilic
|
|
|
How long does it take for oxygen or glucose deprivation to cause an Acute Neuronal Injury?
|
More than 5-7 minutes
|
|
|
How long does this deprivation take to show up on H&E stain?
|
6-12 hours after IRREVERSIBLE event
(so this isn't a good test cause its slow) |
|
|
Sensitivity Spectrum of Cells to Injury (most to least)
|
Neurons
Axons Myelin Oligodendroglial Cells Astrocytes Microglial Cells Capillary Endothelial Cells |
|
|
Of the Neurons, who is most susceptible?
|
1. CA1 sector of Hippocampus
Also Cerebral CTX layers III and V Also Purkinje Layer ofCerebellar CTX |
|
|
So when damaged what do the cells do?
|
Most of them are destroyed, but some of them proliferate
|
|
|
Who proliferates upon damage?
|
Capillaries
Microglials (to eat destruction) Astrocytes |
|
|
Define Central Chomatolysis?
|
Potentially Reversible change in neurons due to axonal damage/disease.
|
|
|
Appearance of Central Chromatolysis?
|
Neuron appears Rounded and Swollen
Cytoplasmic RNA clumps at periphery Nucleus heads to periphery |
|
|
where are astrocytes and oligodendrocytes normally located?
|
in white matter
|
|
|
who do they normally appear?
|
Astrocytes have larger nuclei
Oligodendrocytes have fried egg appearance |
|
|
What happens to Astrocytes upon CNS injury?
|
They proliferate w/in 1 week (reactive gliosis)
|
|
|
What role do fibroblasts play in repair in the CNS?
|
NONE
|
|
|
What is a gemistocyte?
|
a Reactive Astrocyte
|
|
|
What can be seen in chronic reactive gliosis?
|
Rosenthal Fibers
Corpora Amylacea |
|
|
In the early stages of activation, what do microglial cells look like?
|
rod cells
|
|
|
with infarcts and demyelination, what happens to microglial cells?
|
They become lipid laden macrophages (glitter cells)
|
|
|
What the difference between ischemia and hypoxia?
|
Hypoxia means decreased O2
Ischemia means decreased perfusion = decreased velocity and volume of blood = decreased O2 AND decreased removal of toxic metabolites |
|
|
How fast do Ischemia, Hypoxia, and Hypoglycemia take to cause irreversible damage?
|
Ischemia: 6-10 minutes
Hypoxia: 10-25 minutes Hypoglycemia: 30-60 minutes |
|
|
Two main types of Cerebral Edema?
|
Vasogenic Edema
Cytotoxic Edema |
|
|
Vasogenic Edema vs Cytotoxic Edema
Location |
Vasogenic: Extracellular
Cytotoxic: Intracellular |
|
|
Causes of Vasogenic Edema
|
Disruption of BBB
Resorption Impaired |
|
|
Causes of Cytotoxic Edema
|
Abnormal Ion Transport
|
|
|
Examples of Vasogenic Edema
|
Around Masses
Ischemia (local or generalized) |
|
|
Examples of Cytotoxic Edema?
|
Ischemia (local or generalized
|
|
|
Three Types of Herniation
|
Uncal (trans-tentorial)
Tonsillar Sub-Falcine |
|
|
What herniates in each of the types?
|
Uncal: Mesial Temporal
Tonsillar: Cerebellar Tonsil Sub-Falcine: Cingulate Gyrus |
|
|
What part of brain or nerve gets compressed in each type of herniation?
|
Uncal: 3rd nerve w/ parasymp. fibers
Tonsillar: BS Sub Falcine: Adjacent structures |
|
|
Effects of compressed brain/nerve for each type?
|
Uncal: EOM dysfunction, pupil dilation
Tonsillar: Resp Arrest |
|
|
Which vessels get compressed with each type?
|
Uncal: Penetrating branches of Basilar A
Sub-Falcine: Branches of ACA |
|
|
Effect of compressed vessel with each type?
|
Uncal: Duret Hemorrhage in midline midbrain, pons
Ischemia to visual CTX Sub-Falcine: Ischemia to parts of motor/sensory CTX |
|
|
Different presentation of Hydrocephalus in adults and infants?
|
Adults: inc ICP
Infants: inc head circumference |
|
|
Causes of Hydrocephalus
|
Decreased Resorption (majority)
Increased Production (rare) Hydrocephalus ex-vacuo |
|
|
Different Causes of Decreased CSF Resorption
|
Non-Communicating=obstruction in ventricles
Communicating = obstruction of arachnoid granulations |
|
|
Examples of Non-communicating Decreased CSF resorption?
|
tumor
abscess |
|
|
Examples of communicating decreased resorption of CSF
|
Meningitis
Subarachnoid Hemorrhage |
|
|
Example of cause of Increased Production of CSF?
|
Choroid Plexus Papilloma
|
|
|
Reason for Hydrocephalus Ex-vacuo?
|
Cerebral Atrophy (like in Alzheimer's)
|
|
|
what is the most prevalent neurological disorder with morbidity and mortality in the US?
|
Cerebral Vascular Disease (STROKE)
|
|
|
Where does Stroke fall on the top ten causes for death in US?
|
THIRD
|
|
|
Two main types of stroke?
|
Ischemic 80%
Hemorrhagic 20% |
|
|
Main type of Ischemic Stroke?
|
Focal Ischemic
|
|
|
Types of Focal Ischemic Strokes
|
Thrombotic
Embolic Lacunar |
|
|
Other bad type of Ischemic Stroke
|
Hypoxic-ischemic encephalopathy (global)
|
|
|
Two main types of Hemorrhagic Stroke?
|
Intracerebral
Subarachnoid |
|
|
Mechanism of Injury in ischemic stroke?
|
not clear
maybe glutamate excitotoxicity |
|
|
What age are Ischemic strokes most common?
|
7th decade
|
|
|
Gender prevalence of Ischemic strokes?
|
Men
|
|
|
Major Risk Factors for Ischemic Strokes?
|
HTN
DM Smoking |
|
|
Most common sites of Ischemic Strokes?
|
MCA branches
|
|
|
Main causes of Ischemic Strokes?
|
Thrombotic (atherosclerosis)
Embolic |
|
|
Transient Ischemic Attacks
Definition |
Episode of neurologic dysfunction do to focal brain ischemia where all sx's resolve w/in 24 hours (usually w/in 30 minutes)
|
|
|
How many TIA victims experience a big stroke w/in 3 months?
|
10-15%
|
|
|
Thrombotic vs Cardio-embolic
Frequency? |
both are 15-30% of ischemic strokes
|
|
|
Thrombotic vs Cardio-embolic
source of clot |
T: atherosclerosis (intra or extra cranial)
E: Heart (MI's, fibrillation) |
|
|
Thrombotic vs Cardio-embolic
Affected Areas? |
T: major arterial areas
E: Mainly MCA branches |
|
|
Thrombotic vs Cardio-embolic
Which is usually hemorrhagic? |
Embolic
|
|
|
Thrombotic vs Cardio-embolic
Time of Day? |
T: while asleep or early morning
E: during day, with activity |
|
|
Thrombotic vs Cardio-embolic
Rx |
T: Anti-platelet drugs, endarterectomy (extracranial)
E: anti-coagulants |
|
|
Lacunar Infarct
prevalence? |
15-30% of ischemic strokes
|
|
|
Lacunar Infarct
Risk factors |
HTN
Diabetes |
|
|
Lacunar Infarct
Affects which parts of brain? |
Basal Ganglia
Deep White matter BS |
|
|
Lacunar Infarct
Specific Clinical Syndromes |
Internal Capsule/Base of Pons: pure motor hemiparesis or ataxic hemiparesis
Thalamus: pure sensory stroke |
|
|
Other causes of Cerebral Infarct?
|
Cryptogenic
Arterial Dissection Others |
|
|
What does cryptogenic imply?
|
Undetermined cause
|
|
|
Who typically experiences Arterial Dissections?
|
20% of strokes in young adults < 30yrs
|
|
|
Risk Factors for formation of infarct?
|
Presence of Arterial Anastomoses
Rate of Occlusion (t vs e) Systemic Perfusion Pressure |
|
|
Predictors of the severity of neuro deficits w/ infarcts?
|
Location
Size of infarct Severity of Edema Brain Herniation |
|
|
Gross findings of Infarcts over time (<6hr, 24hr, 48-72hrs, 7-10days, 3-4wks)
|
<6hr = nada
24hr = nada 48-72hrs = pale, soft swollen, blurred gray-white junction 7-10days = gelatinous, friable 3-4wks = cystic cavity |
|
|
Microscopic Findings over same time
|
<6hr = nada
24 hours = pink neurons, edema, neutrophils 48-72 hrs = macrophages, granulation tissue 7-10 days = Astroctyic Gliosis 3-4 wks = cystic cavity w/ macrophages and surrounding gliosis |
|
|
What can cause Venous Infarction?
|
Infections (fungal infection in sinuses)
Hypercoaguable States (severe dehydration) |
|
|
Microscopic Zones at 7 days post-infarct
|
Subpial Sparing
Central Pan-necrosis Peripheral Cap Prolif (repair) |
|
|
when is the greatest risk of death from a stroke?
|
1st month
|
|
|
Usually cause of death?
|
Medical > Neuro
bed sores, aspiration pneumonia |
|
|
High Risk Factors for death
|
old
Cardiovascular disease Severe Neuro Deficits |
|
|
Risk of Recurrent Stroke
|
First Month After (3-10%)
Thrombotic Infarct (lowest for lacunar) |
|
|
How many people return to independent living?
|
2/3
|
|
|
How long does it take them?
|
3-6 months
|
|
|
Causes of Global Hypoxia-Ischemia
|
Shock
Cardiac Arrhythmias Marked rise in ICP cuts off blood flow |
|
|
Predictors of tissue injury w/ GHI?
|
Old age is bad
Hypothermia is good |
|
|
GHI deficits?
|
transient to death
|
|
|
What are the differences in gross finding after GHI?
|
48-72hrs
Watershed Infarcts Laminar Cortical Necrosis Cerebellar Necrosis (purkinje) Diffuse Cerebral Edema 3-4 weeks Cystic Gliotic CTX (laminar and watershed areas) |
|
|
What are watershed areas?
|
border zones (e.g. area between ACA and MCA supplies
|
|
|
Where is the laminar CTX area?
|
Layers 3 and 5
|
|
|
What are the microscopic differences after GHI?
|
24 hrs
damage seen in zones with highest susceptibility (CA1 of hippo) 48-72hrs Less Mac's 3-4 weeks Laminar Cortical Necrosis |
|
|
2 more things you can see after GHI?
|
Dusky Discoloration
Cerebellar fragmenting |
|
|
3 susceptible sights where we see GHI Damage?
|
Hippocampus CA1 (sommer)
Cerebellar Purkinje Neurons Cerebral Cortical Pyramidal Neurons (laminar) |
|
|
What is the major cause of Primary Intra-parenchymal Hemorrhage?
|
HTN (>50%)
|
|
|
Other causes of IPH?
|
Amyloid Angiopathy
Arterio-Venous Malformation |
|
|
Peak age of HTN IPH?
|
60
|
|
|
Onset of HTN IPH?
|
Abrupt, 30-90 minutes
|
|
|
Presentation of HTN IPH
|
rapid increase in ICP
Rapid Loss of Consciousness BS Compression: deep coma, irregular breathing, decerebration/decortication, dilated pupils |
|
|
5 main sites of HTN IPH?
|
Basal Ganglia (putamen**)
Thalamus Pons Cerebral White Matter Cerebellum |
|
|
Effects of HTN IPH?
|
ACUTE
mass effect scant necrosis CHRONIC cystic gliotic cavity Only scant parenchymal loss |
|
|
Two types of vessels to rupture in HTN IPH?
|
Large Arteries
Arterioles |
|
|
Cause of Large Artery HTN IPH?
|
accelerated atherosclerosis
|
|
|
causes of Arteriole HTN IPH?
|
Hyaline Atherosclerosis (most common)
Fibrinoid Necrosis Charcoat-Bouchard micro-aneurysm |
|
|
How many pts survive acute IPH?
|
30-50%
|
|
|
of those, how many had slight or no disability
|
42%
|
|
|
Poor Prognostic Factors for IPH
|
Old (>80)
Decreased level of consciousness at presentation Large Hematoma (>30ml) Infratentorial location Intraventricular Extension |
|
|
For Amyloid Angiopathy IPH, what are the hemorrhage patterns?
|
Lobar and Superficial
|
|
|
How do these patterns influence mortality?
|
most people survive
|
|
|
How does amyloid show up under microscope?
|
pink on H&E
Green on Congo Red |
|
|
Causes of Subarachnoid Hemorrhages/
|
Trauma**
**Rupture of saccular aneurysm Vascular Malformation Tumors |
|
|
Prevalence of Saccular aneurysms?
|
1% of general population
|
|
|
how many actually rupture?
|
<1%
|
|
|
where do most saccular aneurysms form?
|
anterior circulation
|
|
|
Causes of Saccular Aneurysms?
|
Mostly Sporadic
Maybe congenital weakness of wall and/or acquired degeneration of muscle in wall (htn smoking) |
|
|
Three conditions with increased risk of saccular aneurysms
|
Polycystic renal disease
Coarctation of aorta NF1 |
|
|
how many people with saccular aneurysms have multiple
|
20%
|
|
|
Two big presenting sx's of subarachnoid hemorrhage?
|
loss of consciousness (50%)
worst headache of life (50%) |
|
|
What does the CSF look like?
|
RBC's
no neutrophils normal glucose |
|
|
Mortality in 1st rupture?
|
25-50%
|
|
|
Delayed Deficits and their mortality?
|
Vasospasm - 30% w/in 2wks
Re-rupture - 30% w/in 2 wks Hydrocephalus |
|
|
normal site of rupture
|
fundus of aneurysm
|
|
|
What is an arterio-venous malformation?
|
cluster of developmentally abnormal vessels that directly connect a to v
|
|
|
Common sites for AVM?
|
anywhere
most common though in posterior cerebral hemisphere (posterior branches of MCA) |
|
|
when do AVM's bleed?
|
10-30 yrs of age
|
|
|
Sx's of AVM Bleed
|
HA
Seizures (30%) Rupture (50%) |
