Brainscape's Knowledge GenomeTM

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


See full index

System Pathology > Nervous System Disorders > Flashcards

Nervous System Disorders Flashcards

1
Q

Pathological responses from CNS features

A 
Protection by bony enclosures
Metabolic requirements
Absence of central lymphatics
Cirrculation of CSF
Distinctive pattern of wound healing?
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Ways that neurons differ from one another

A

function
distribution of connections
Use of neurotransmitters
Metabolic requirements

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

Selective vulnerability

A

A group of functionally related neurons may be damaged as a result of specific injury

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

exposure to limited hypoglycemia and hypoxia

A

Cause greatest damage to portions of teh hippocampus, pyramidal cells of the cortex, purkunje cells of the cerebellum and the basal ganglia

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

hippocampus is affected most extensibly in

A

Alzheimer’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

______ are most susceptible to the effects of mercury

A

cerebellar granular neurons

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

_______ selectively infects and destroys anterior horn cells

A

Poliomyelitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Reactions of neurons to injury

A

Acute neuronal injury (red neurons)
Axonal reaction
atrophy and degeneration of nerve cells in chronic progressive degenerative diseases
Intraneuronal deposits may appear with certain neurodegenerative disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Acute Neuronal Injury

A

Contributing causes include ischemia, overwhelming infections, toxicity, and others that lead to neuronal death
Alterations characterized by loss of Nissl, increased angularity, and nuclear pyknosis appear after 12-24
hours of irreversible injury

Fragmentation occurs

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

Pyknosis

A

Irreversible condensation of chromatin in the nucleus of a cell undergoing necrosis or apoptosis. It is followed by karyorrhexis, or fragmentation of the nucleus.

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

Axonal reaction

A

Reactions in the cell bod that accompany axonal regenration
Associated with synthesis of proteins and sprouting of axons

Causes: Axon trauma, hypoxia, conditions that prevent a cell from maintaining its axon

Perikaryon swells and rounds up and nissl substance disappears from the central portions of the cell body and nucleus moves to the periphery

Wallerian degenration of distal axon

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

Atrophy and degeneration of nerve cells in

chronic progressive degenerative diseases and aging

A

Reduction in size, lipofuscin deposits, neuronal death and necrosis
Progressive loss of neurons results in loss of functionally associated neurons and gliosis (though singular loss does not produce this effect)

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

Transynaptic degenration occurs in

A

Communicating neurons (ex. visual pathways)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Neurofibrillary tangles

A

composed of twisted cytoskeletal filaments (stainable with silver)
Contains ubiquitin which tags abnormal proteins for removal

Alzheimer’s disease, postencephalitic parkinsonism, parkinson’s dementia, boxer’s dementia

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

Lewy bodies

A

pink staining spheroids made largely of ubiquitin typical of idiopathic Parkinson’s (loss of substantia nigra) and lewy body dementia (affects cortex)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Inclusion bodies (virus particles)

A

Appear in infected cells in polio and viral encephelitis

in rabies these structures are known as Negri bodies

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

Lipofuscins

A

(wear and tear pigment)

Accumulate in neurons under the of old age and chronic hypoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Metabolic storage diseases

A

Contribute to accumulated intraneuronal deposits of complex lipids
Degenration of neuronal elements contribute to a cherry red spot in the fovea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Myelin loss only leads to neuronal degeneration if the loss is _____

A

Extensive or prolonged

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

The most sensitive glial elements

A

Oligodendrocites

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

Most resilient glial element

A

Astrocytes

Survive all but the most prolonged and severe hypoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Astrocytes and neuronal injury

A

Participate in repair and produce glial scars (other types of scars are less common in the CNS)
With a penetrating injury the astrocytic scars may cause distortion of the cortex and lead to seizures

Prolonged mild ischemia may cause necrosis of astrocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Microglia and neuronal injury

A

Mesodermal cells functioning as phagocytes of the CNS, numbers may increase in response to injury and infection of components of the CNS

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

Oligodendrocytes

A

Wrap myelin around several neurons
Most vulnerable to injury and swell when stressed

Multiple sclerosis and other disease that affect myelination affect oligodendrocytes
replaced by astrocytic scars

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Increased intracranial pressure can occur due to

A

Space occupying lesions
Swelling and edema
Hydrocephaly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Edema and swelling of the CNS

A

Vascular (Vasogenic)
Associated with increased vascular permeability
Most common cause of brain edema

Cellular (cytotoxic)
Increased cell water indicates injury

27
Q

Hydrocephalus

A

Volume of CSF is increased causing the ventricles to dilate
Can be caused by:
If this follows brain atrophy then then CSF does not increase and this condition is known as hydrocephaly ex vacuo

An imbalance of the production and the drainage of CSF

Vascular tears and hemorrhage

Trauma

Infection of the CNS

28
Q

Obstructive (non-communicating) hydrocephalus

A

CSF does not reach the subarachnoid space because it’s path is blocked internally.
results from: congeinital causes, tumors, scarring in the ventricular system, obstruction at the foramina of magdenie or luschka

29
Q

Communicating hydrocephalus

A

CSF enters the subarachnoid space but the circulation or absorption is interrupted
Causes: scars of the arachnoid granulations (following inflammation or hemorrhage) and/or in the meninges. Thrombi, neoplasms, and other obstructions of cerebral (dural) cenous sinuses and associated veins
Severe CHF leads to venous congestion and pooling

30
Q

Sites of narrowing that are vulnerable for obstruction

A

Aqueduct of Silvius
Foramina of Magendie and Luschka
Subarachnoid space between the forebrain and midbrain

31
Q

Manifestation of hydrocephaly

A

Early features of increased intercranial pressure include headache, mental dullness, nausea, and vomiting

Papilledema
Herniation

32
Q

Hydrocephaly herniation

A

Rigid skull and dural reflections force the brain to be squeezed through the openings and around the partitions like putty when it is displaced or undergoes swelling or expansion
Common examples include cingulate (subfalcine), uncal (trans-tentorial), and tonsillar (cerebellar, “coning”) herniation

Tonsillar herniation may lead to compression of the medulla at the foramen magnum and is a common mechanism of death in brain swelling

33
Q

Trauma leading to hydrocephaly

A

Penetrating and crushing injuries: Distortion of cranial vault and vertebral column

Brain trauma with no damage to cranium (Contusion, laceration, concussion, shearing forces from rotation, contrecoup injury {damage to part of the brain opposite the side of impact])

Cord trauma: displacement or distortion of vertebral elements damage cord. Vertebral dislocations.

34
Q

Meningitis

A

Infection of meninges and CSF
Systemic signs of infection in addition to stiff neck, headaches, photophobia, rash and fevers
leads to scarring and obstruction of the CSF

35
Q

Bacterial meningitis

A

Pyogenic
characterized by pus in the meninges
Acute in course with a high risk for death

36
Q

Causes of bacterial meningitis

A

Neissaria (Meningococcus) - most common epidemic form

E Coli., H. Influenza, strep. pneumonia and oppurtunistic infections in the immune compromised

37
Q

CSF findings of bacterial meningitis

A

Increased turbidity, increased polymorphonuclear leukocytes, and bacteria
Elevated protein and reduced glucose

38
Q

Meningococcal septicemia

A

Gives rise to purpurric lesions, high fever, and potentially shock
Consequence of severe infection and skin and organ hemmorhage and mucousal bleeding are common

39
Q

Types of meningitis

A

Bacterial

Acute lymphatic (Vral, "aseptic")
More common with milder clinical effects, increased lymphocytes in CSF, milder inflammation

Chronic
insidious origin
Causes include TB, fungi, and brucellosis

40
Q

Viral encephalitis

A

Most common
general features include an increased number of iniltrates of lymphocytes and macrophages called “inclusion bodies” in infected cells and glial cell reactions

Delayed symptoms is common
Herpes encephalitis, post measeles, congenital malformation (if the mother has rubella), postencephalitic parkinson’s after influenza

41
Q

Selectivity of encephalitis

A

Tropism
May choose a specific are or type of cell
may also be diffuse

42
Q

Viral encephalitis causes

A

Arbor viruses from insect and animal hosts
Chuldhood infectiosn such as measles
Herpes Simplex I and II
Polio, rabies
HIV (60% of AIDS patients have symptoms leading to viral encephalitis)

43
Q

Slow virus diseases

A

Infectiosn characterized by long periods of latency

Subacute Sclerosing Panencephalitis: Associated with infection of measles virus and is fatal in 2-3 years

44
Q

Hallmarks of prion diseases of encephalopathies

A

Proteinaceous transmittable agents - NO DNA
Affect nerve tissue in humans and animals

Hallmarks:
Vacuolization (hole formation) of brain tissue and accumulation of prion proteins

45
Q

Prion protein

A

Membrane glycoprotein that becomes changed by misfolding
Acquired through sporadic or inheireted mutations or infected animal tissue, iatrogenic effects (surgery, etc.), exposure to infected humans

46
Q

Creutzfeldt-Jacob disease (encephalopathy)

A

Human-human transmission from breathing and certain medical procedures

47
Q

Scrapie in sheep and mad cow disease

A

Concern for transmission to humans that eat or handle infected meats
Leads to variant CJD

48
Q

Abscesses

A

Focal infection that is usually bacterial
During acute stage local destruction and swelling may cause symptoms
CSF findings are variable
Repair is associated with vascularized collagenous tissue and cortical adhesions may occur

49
Q

Granulomas

A

From tuberculosis
Focal nodular infections consisting of macrophages, giant cells, etc.
Causes local destruction and expansion

50
Q

Pott’s disease

A

Causes a collapse of vertebral bodies that makes a gibbous deformity in the spinal cord

51
Q

Sources of CNS infections

A

Extension from middle ear and sinus infections
Hematogenous disemmination
Direct invasion - trauma, congenital defects, iatrogenic
Extension along peripheral nerves (rabies, encephelitis)

52
Q

Stroke (cerebral vascular accident)

A

Focal loss of neurological function of vascular origin which lasts more than 24 hours
spontaneous in onset due to underlying CV disease
3rd leading cause of death
40-50% of death following the first month
defecits persist in 60%

53
Q

Transient Ischemic Attacks

A

Spontaneous focal reversible neurological disturbance slasting less than 24 hours and results from disruption of blood supply
Most caused by emboli
Risk for stroke is 5% per year

54
Q

Causes of stroke

A

Focal ischemic infarcts

  • thrombi
  • emboli
55
Q

Types of stroke

A

Hemorrhagic - bleeding

Ischemic - obstruction

56
Q

Focal ischemic stroke

A

75-90% of strokes
Atherosclerosis is most common underlying factor (emboli)

inflammatory arthretitis
Arterial spasms
Dissecting aneurysms

3-5 minutes before damage

57
Q

F-A-S-T

A

Face droopin
Assymetrical movement
Slurred speech
Time call 911

TO RECOGNIZE STROKE

58
Q

Ischemic encephalopathy

A

Cause of stroke
Generally caused by ischemia of the entire brain. Hypotension can contribute to this
Effects change from reversible confusion to infarction
May also be limited to watershed regions of the brain and spinal cord

59
Q

Morphology of infarction

A

6-12 hours: discoloration and softening, petechiae may appear in the margin of teh affected area
2-3 Days: Cerebral tissue becomes soft and begins to break up. edema is common and may cause a herniation and exacerbates neurological symptoms but it gets better
Several months: Residual cavity surrounded by astrocytes or a collapsed scar

60
Q

Spontaneous hemorrhage types

A

Intracerebral

subarachnoid

61
Q

Intracerebral hemorrhage

A

peak at 60 years
Rupture of small intraparenchymal arteries

Effects: dissection of nerve tissue, mass effects, and disruption of blood supply
blood may reach the subarachnoid space or ventricles

Arises suddenly and progresses slowly

62
Q

CNS effects of hypertension

A

Accounts for 50% of brain hemorrhage
arteriole sclerosis with occlusion of small lesions known as lacunar infarcts
Rupture of small penetrating arteries may give rise to slit hemorrhages

Multi-infarct dementia: characterized by accumulated effects of repeated brain infarcts due hypertensive arteriosclerotic disease

Exertion may contribute to onset

63
Q

Subarachnoid hemorrhage

A

Rupture of congenital berry aneurysms is most common (other causes include other types of aneurysms, clotting defects, traumatic injury, etc.)

Onset: sudden with signs of meningeal
irritation (e.g. severe headaches)

CSF findings
• 1-24 hours: blood “stained”
• >24 hours: xanthochromia (yellow discoloration of CSF)

System Pathology (1 decks)

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