Brainscape's Knowledge GenomeTM

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


See full index

HD 2 > Neuropath > Flashcards

Neuropath Flashcards

0
Q

“watershed areas” of brain

A

areas of brain w/ little direct blood supply, but with potential collateral supply close by
(border areas btwn major supplying arteries).
–> could recruit collaterals if slow occlusive process, but 1st to become ischemic w/ acute occlusion.

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

Causes of cerebrovascular events (3)

A

(cerebrovascular event = stroke)

  1. Local vascular occlusion –> ischemia
  2. systemic hypoperfusion w/ O2 (hypoxemia)
  3. hemorrhage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Relative importance of vessels in cerebral circulation

A
  1. major (proximal) arteries = most important & most likely to get atherosclerosis.
  2. distal arteries/capillaries = less likely to be occluded; may spasm.
  3. venous circulation = least devastating w/ cerebrovascular events.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

most common causes of arterial cerebral infarction

A 
#1 & 2: embolism and thrombosis. 
Also: arterial dissection, HTN vasculopathy, arterial spasm/compression, decreased perfusion (systemically) --> watershed areas.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Atherosclerosis & cerebral infarction

A
  • mostly in proximal arteries (internal carotids, MCA, vertebral aa, basilar a., etc.)
    –> cause large areas of pale/non-hemorrhagic ischemia
    (pale bc no reperfusion).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

disease states causing cerebral thrombosis

A
    • bc get hypercoagulable! **
      1. Vasculitis (polyarteritis nodosa, etc.)
      • vasculopathy (SLE)
      • granulomatous –> infectious, primary CNS…
        1. blood abnormalities (sickle cell, thrombocytopenia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Characteristics of Embolic cerebrovascular infarction

A

–> hemorrhage, esp. petechial hemorrhage from damaged vessels (leak when reperfused)
Sources: heart or vasculature, small if not from atherosclerosis

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

transient ischemic attack(s) (“TIA”)

A

= small, temporary CNS artery occlusions, Sx last < 1 hr.

  • -> may be symptomatic if affect important area, or asymptomatic.
    • indicate increased risk of full stroke in (near) future!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

arterial dissection & stroke

A
  • Usually in younger ppl (NOT normal age demographic for stroke).
    = false lumen forming in vessel wall –> blood redirects & compresses actual lumen => lose normal perfusion.
    ** esp. in trauma or chiropractic patients **
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

lacunar infarctions

A

small infarction (< 1.5 cm) caused by hypertension;
= abrupt change from large diameter vessel to small diameter vessel exacerbated by high P ==> low perfusion.
** may be asymptomatic OR symptomatic.
– Binswager Disease (dementia) = severe complication!

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

Pathology of Binswanger Disease

A

= dementia caused by Lacunar stroke.
HTN –> changes in vasculature (promotes hyaline membranes in vessel walls)
–> rarefraction of white matter –> dementia.

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

causes of mechanical occlusion – causing stroke/cerebral ischemia
(2)

A
  1. vasospasm (usually after subarachnoid hemorrhage)

2. uncal herniation (from increased ICP)

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

Types of watershed infarcts

A
  1. ACA-MCA boundary zone –> serious consequences!

2. SCA - PICA boundary –> typically asymptomatic.

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

Areas of selective susceptibility to ischemia

A
  1. Globus Pallidus (esp. w/ CO poisoning)
  2. hippocampus CA1
  3. Purkinje cells of cerebellum – usually die even despite person’s survival of stroke –> lasting symptoms.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

consequences of global cerebral ischemia

A

(usually after severe hypotension or cardiac arrest)

– massive necrosis = poor/no survival (ie: not unless on ventilator) bc continue to infarct brain after initial damage.

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

Pathological changes from cerebral infarction

A
  1. Early stage (1-2 days): neuron death (eosinophilia and nucleus shrinks) + neutrophil infiltration
  2. Subacute stage (1-2 weeks): liquefactive necrosis, BBB breaks down, macrophage infiltration (to remove necrotic debris)
    • astrocytosis & cavitation
  3. long term/resolution: Disappearance of brain tissue (NO fibrosis), degeneration of proximal/distal components of the neural tract.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

characteristics of venous cerebral infarction

A

Causes: hypercoagulable states (pregnancy, etc.) –> thrombosis;
= VERY hemorrhagic, w/ deeper damage than arterial.

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

most common cause of subarachnoid hemorrhage

A

= ruptured saccular aneurysm

- --> diffuse, very bloody hemorrhage (difficult to localize) * *risk clot pressure causing secondary intracerebral hemorrhage! (dissection into parenchyma)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Common causes of intracerebral hemorrhage

A
  • vascular malformations, hypertension
  • tumors, trauma
  • blood abnormalities (–> multifocal hemorrhage)
  • mycotic aneurysms, amyloid angiopathies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

most common sites for cerebral saccular aneurysms

A

1: Internal Cerebral a.

  1. MCA, AVA
  2. Basilar a.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Hypertensive Intracerebral hemorrhage

A

in very poorly controlled HTN, affects lenticulostriate arteries;
= caused by fibrinoid necrosis/degeneration of vessels.
–> often catastrophic damage, esp. to basal ganglia.
(difficult to surgically treat, may result in lasting paralysis if survive)

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

pathophysiology of arteriovascular malformations –> stroke.

A

make arteriovenous shunt(s) –> vessel walls thicken & rupture w/ high pressure.

  • usually fatal if rupture!
    • can also cause seizures (more likely to survive)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Amyoid angiopathy

A

amyloid build up in cerebral vessels –> can cause hemorrhage;

  • may have amyloid pathology w/Out symptoms yet!
    • this hemorrhage not AS fatal as AV malformations.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

pathological mech for stroke from mycotic aneurysm

A

infection weakens vessel wall –> aneurysm + more weakening –> rupture = hemorrhage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

T1 weighted MRI

A

(normal) water is dark, white matter is bright, and cortex is intermediate.

25
Q

T2 weighted MRI

A

(~ negative image of T1)

water is bright, white matter intermediate, and cortex DARK

26
Q

FLAIR MRI

A

“Fluid Attenuated Inversion Recovery”
=> like T2, except only FREE water is bright; CSF is dark.
*most sensitive to pathology in brain parenchyma.

27
Q

Pachymeninges

A

the dura mater

28
Q

leptomeninges

A

the arachnoid and pia maters, + subarachnoid space.

29
Q

intrathecal

A

anything within the subarachnoid space

30
Q

Subdural vs. epidural

A 
SUBdural = the potential space between the dura mater and the arachnoid mater. 
EPIdural = the potential space btwn the dura mater and the skull.
31
Q

striatum

A

refers to all parts of the basal ganglia

  1. putamen
  2. caudate
  3. pallidum/globus pallidus
32
Q

diencephalon

A

refers to both the thalamus and hypothalamus

33
Q

bulbar

A

related to the brainstem, esp. the medulla.

34
Q

Simple atrophy

A

neuronal degeneration associated with systemic illnesses;

- perikaryon “dwindle”
- axons die back
ie: ALS

35
Q

Trans-synaptic degeneration

A

cell damage along neural tract due to loss of trophic factors

  • anterograde: target cells degrade bc afferents damaged/lost
  • retrograde: afferents degrade bc target cells damaged/lost
36
Q

inclusion bodies

A

abnormal accumulations of cytoskeletal proteins.

  • Lewy bodies (parkinson’s)
  • Neurofibrillary tangles (Alzheimers, neurodegen.)
  • lipofuscin pigment (normal sign of aging - NOT pathological)
37
Q

central chromatolysis

A

reaction of perikaryon to severe axon damage – attempt to regrow axon.

  • nucleus pushed to side of cell
  • cytoplasm more eosinophilic/nissl bodies dissipated
  • most often in motor neurons w/ few collaterals
38
Q

Wallerian degeneration

A

after axon severance or cell body death
(axon disconnected from rest of neuron)
- degeneration of axon (axon AND myelin sheath) distal to injury
- chromatolysis of perikaryon
* slower process in CNS
** different from “Dying back” (internal process)

39
Q

Axonal spheroids

A

focal dilatation of axon bc organelle accumulation;
= 1-2 days after axon injury/ischemia or certain neurodegenerative diseases. *helpful in forensics.
- dystrophic terminals: failed transport from terminal back to soma
- “torpedo:” purkinje axon rxns (bulge toward soma)

40
Q

Astrocytosis (aka: gliosis)

A

common CNS rxn to injury, w/ hypertrophy & hyperplasia;

  • may be chronic, metabolic or non-pathologic
  • -> form cellular scars = “gemistocytes.”
  • isomorphic (keep normal shape & structure)
41
Q

Microglia

A

bone marrow-derived cells in CNS,
F(x): phagocytosis, antigen presentation, inflammation
(active inflamm cells AND recruit cytokines)
+ source of macrophages in CNS

42
Q

Possible causes of increased ICP (intracranial pressure)

A
  • increased tissue (tumors)
  • increased blood (hemorrhage, venous congestion)
  • increased water (cerebral edema)
43
Q

2 mechanisms of cerebral edema

A

1: Vasogenic. water leaks out of vessels bc increased permeability (tumors, infarcts) –> EXTRAcellular edema, use T-2 MRI.

2: Cytotoxic. transient cellular ion-ATP pump failure
- -> INTRAcellular edema, use diffusion-weighted MRI.

44
Q

Types of brain herniation (4)

A

(due to swelling)

  1. Subfalcine/cingulate
  2. Uncal/transtentorial
  3. Tonsillar (through foramen magnum)
  4. Extracranial (if part of skull removed)
45
Q

3 types of hydrocephalus

A
  1. non-communicating - obstruction in ventricular system
  2. communicating - subarachnoid obstruction –> reduced CSF reabsorption
  3. atrophic dilatation (“ex vacuo”) - ventricular enlargement due to loss of surrounding brain tissue.
46
Q

Alzheimer’s Disease

A

Neurodegenerative –> dementia (#1 cause).
* increased risk if: ApoE or presenilin mut., Down syndrome
Gross atrophy + B amyloid and neurofibrillary tangles (tau),
- esp. in temporal lobe (use Bielchowski stain).

47
Q

Frontotemporal Dementia

A

= loss of exec. function & memory.

  • Chrom. 17 mut (tau, progranulin)
  • Asymmetrical atrophy w/ Pick bodies & TDP-43 accumulation
48
Q

Spongiform Encephalopathy (Creutzfeldt-Jacob disease)

A

= Prion disease (PrPc proteins); sporadic, familial or acquired.
Sx: progressive dementia, myoclonus
Path: neuron loss & reactive gliosis, use GFAP stain.

49
Q

Lewy Body Dementia

A

2nd most common neurodegen. cause of dementia;
w/ parkinson’s Sxs and dementia
Path: Lewy bodies diffusely, esp. in cortex

50
Q

Tuberus Sclerosis

A

Hamartoma nodules on cortex + atypical neurons & astrocytes;

  • skin: Shagreen patches, cafe au lait spots
  • cogn: mental retardation, seizures
  • astrocytic neoplasms
51
Q

Central Pontine Myelinosis (CPM)

A

pontine demyelination w/ NO inflammation
- only phagocytic macrophage infiltration
* often fatal! + tetraparesis & locked-in syndrome
Causes:
- Too rapid hyponatremia correction
- complication of CO poisoning (after initial recovery)

52
Q

Leukodystrophies

A

= genetic or metabolic structural problems w/ neurons (usually peripheral)
sparing of subcortical arcuate fibers!

53
Q

Metachromatic Leukodystrophy

A

Aut. Recessive, Arysulfatase deficiency

=> accumulation of metachomatic material in peripheral neurons

54
Q

Krabbe’s Disease (a leukodystrophy)

A

aut recessive, galactocerebroside-B-galactosidase deficiency;
=> white matter degen w/ globoid cells (multinuc. macrophages)
*affects peripheral nerves.

55
Q

Adrenoleukodystrophy (ALD)

A

X-linked rec., peroxisome defect -> very long chain FAs build up
=> white matter degen esp in occipital/parietal lobes
+ adrenal cortical atrophy
(“Lorenzo’s Oil” disease)

56
Q

Alexander’s Disease

A

a structural leukodystrophy,
= GFAP protein mutation
==> MANY rosenthal fibers

57
Q

Pelizaeus-Merzbacher Leukodystrophy

A

PLP protein mutation –> defective CNS myelin

58
Q

Guillan-Barre Syndrome
(aka: AIDP…
Acute Inflammatory Demyelinating Polyradiculoneuropathy)

A

Sx: Ascending symmetrical motor weakness, +/- ANS Sxs
may get fatal arrhythmias
= Inflammatory & monophasic, macrophages attack myelin.
- axons intact, remyelinate
- affects peripheral nerves & nerve roots

59
Q

Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)

A

chronic, relasing form of guillan-barre.
-> segmental demyelination w/ some remyelination
=> “onion bulb” concentric rings of Schwann cells

HD 2 (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions