Brainscape's Knowledge GenomeTM

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


See full index

Pathology > Cns1 > Flashcards

Cns1 Flashcards

1
Q

Neuron

A

• Cell body
– Nucleus
– Cytoplasm

• Axon

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

Cortical Architecture

A

• Sixlayersparalleltosurface
– I. Molecular: glia, few small neurons
– II. External granular: small neurons with short axons
– III. Outer pyramidal: medium and large neurons
– IV. Inner granular: small stellate neurons
– V. Inner pyramidal: medium neurons, Beta cells
– VI. Polymorphic layer

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

Patterns of Injury in the Nervous System: Neuronal Injury

A

• Within 12 hrs. of an irreversible hypoxic- ischemic injury:

– Acute neuronal injury becomes evident – H&E staining
• Shrinkage of the cell body
• Pyknosis of nucleus
• Disappearance of the nucleolus
• Loss of Nissl substance
• Intense eosinophilia of cytoplasm
• Axonal swelling and disruption of axonal transport

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

Normal Cells
• Neurons

A

– Topographically organized
• Nuclei, ganglia, columns
– Functional domains have been assigned to many anatomic regions

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

Morphologic Patterns of Neuronal Injury

A
  • Coagulation necrosis
    – Hypoxic-ischemic injury
  • Apoptosis
    – Normal development
    – Some hypoxic-ischemic injury
    – Certain toxic agents
    – ? Aging and some neurodegenerative diseases
  • Chromatolysis
  • Cytoplasmic inclusions
    – Infections
    – Neurodegenerative disorders
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Morphologic Patterns of Neuronal Injury

A
  • Axonal injury
    – Leads to cell body enlargement
    – Peripheral displacement of the nucleus
    – Enlargement of the nucleolus
    – Peripheral displacement of the Nissl substance
  • Acute injuries often result in a loss of the blood-brain barrier
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Astrocytes in Injury and Repair

Principal cell responsible for repair and scar formation in the CNS

A

– Gliosis

Astrocytes undergo both hypertrophy and hyperplasia
– Fibroblasts play a limited role in repair following brain injury
– In long-standing gliosis:
• Astrocytic cytoplasm shrinks
• Cellularprocessesbecometightlyinterwoven
• Rosenthal fibers(thick,elongated,eosinophilicprotein aggregates in chronic gliosis and some low-grade gliomas

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

Oligodendrocytes

A

• Most common cells in white matter
• Smaller than astrocytes
• Production and maintenance of CNS myelin

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

Ependyma

A
  • Lines ventricular walls and central canal of spinal cord

* May be the target of infectious agents – CMV

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

Microglial Cells

A

• Derived from the bone marrow
• Function as the resident phagocytic cell of the CNS
• When activated by injury, infection, or trauma – Proliferate
– Take on the appearance of activated macrophages in areas of demyelination, organizing infarct, or hemorrhage

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

Features Unique to the Brain

A

• Function is localized within the nervous system
– It is inherently vulnerable to small focal lesions
– A given type of lesion produces different clinical symptoms when occurring in different parts of the CNS
– Different pathologic lesions can produce similar clinical symptoms when occurring in the same area of the brain

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

Features Unique to the Brain

A

• The brain has a number of unique anatomic features which offer protection against one form of pathologic insult while rendering it more vulnerable to another

– Blood-brain barrier
– Skull
– CSF (shock absorp)
– Selective vulnerability of some areas/neurons

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

Features Unique to the Brain

A

• Similar symptoms or clinical findings can be produced by different pathologic mechanisms
– Example:
• Papilledema
– Hydrocephalus
– Meningitis
– Tumor
– Abscess
– Other

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

Features Unique to the Brain

A

• Certain diseases are unique to neuropathology

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

Increased Intracranial Pressure

A

Cerebral Edema
Herniation
Hydrocephalus

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

Increased Intracranial Pressure

A

• Increase in mean CSF pressure above 200 mm H2O with patient recumbent

• Associated conditions:
– Mass effect:
• Diffuse: generalized edema
• Focal: localized edema, tumor, abscess, hemorrhage

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

Cerebral Edema

A

• Technically brain parenchyma edema
• May be caused by a number of diseases
• Major categories:
– Vasogenic edema
– Cytotoxic edema

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

Vasogenic Edema

A
  • Disruption of normal blood-brain barrier
  • Fluid escapes into the intercellular space
    – Brain has few lymphatics
    – Poor resorption of excess intercellular fluid
  • May be localized or generalized
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Cytotoxic Edema

A

• Increased intracellular fluid
• Secondary to cellular injury
• In conditions associated with generalized edema, one frequently finds elements of both cytotoxic and vasogenic edema

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

Edema: Morphology

A

• Soft parenchyma
• Herniation may be a complication • In generalized edema:
– Gyri are flattened
– Sulci are narrowed
– Ventricular cavities compressed

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

Hydrocephalus

A

• Increased CSF causing enlargement of the ventricles
• Two types:
– Communicating: blockage outside the ventricular system
– Noncommunicating: blockage anywhere along the ventricular system

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

Hydrocephalus

A

• caused by decreased resorption of CSF
• Rarely caused by increased production
• Hydrocephalus ex vacuo: brain atrophy with compensatory expansion of ventricular system

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

Herniation: Types

A
  • Subfalcine
    – Cingulate gyrus under the falx cerebri
  • Transtentorial
    – Displacement of the uncus over the free edge of the opening of the tentorium
  • Tonsillar
    – Displacement of the cerebellar tonsils into the foramen magnum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Malformations

Neural Tube Defects

A

• Anencephaly: absence of the brain and calvarium
• Encephalocele: diverticulum of CNS tissue through a defect in the cranium
• Myelomeningocele: extension of CNS tissue through a defect in the vertebral column
• Meningocele: only meningeal extrusion

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

Neural Tube Defects

A

• Spina bifida: may be asymptomatic bony defect or severe malformation

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

Forebrain Abnormalities

A

• Polymicrogyria: small, unusually numerous gyri
• Megalencephaly & microencephaly: abnormally large or small volumes of brain
• Lissencephaly: absence of gyri
• Holoproprosencephaly: incomplete separation of cerebral hemisheres
• Agenesis of the corpus callosum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Neurons

A

Topographically organized
- nuclei, ganglia, columns

Functional domains have been assigned to many anatomic regions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Posterior Fossa Abnormalities

A
  • Arnold-Chiari malformation: small posterior fossa, malformed cerebellum with extension of the fermis through the foramen magnum, hydrocephalus, lumbar meningomyelocele
  • Dandy-Walker malformation: enlarged posterior fossa, absent or rudimentary cerebellar vermis, midline ependymal cyst
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Perinatal Brain Injury

A
  • Cerebral palsy: any nonprogressive neurologic motor deficit attributable to injury in the prenatal or perinatal period
  • Intraparenchymal hemorrhage: premature infants
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Trauma

A

• Anatomic location of the lesion and the brain’s limited capacity for repair have great significance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Blows to Head

A

• Penetrating
• Blunt
• Open
• Closed
• Repetitive episodes of trauma can lead to later development of neurodegenerative disorders
– Alzheimer disease
– Chronic traumatic encephalopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Skull Fractures

A
  • Displaced skull fracture
    – A fracture in which bone is displaced into the cranial cavity by a distance greater then the thickness of the bone
  • Diastatic
    – When the kinetic energy that causes a fracture is dissipated at a fused suture.
    – The fracture crosses sutures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Traumatic Parenchymal Injuries

Concussion

Contusion

A
  • Concussion: clinical syndrome of alteration in consciousness. Usually includes sudden onset of transient neurologic dysfunction with complete recovery
  • Contusion: caused by rapid displacement, disruption of vascular channels, and subsequent hemorrhage, injury, and edema
    – Coup lesion: injury underlying the point of contact
    – Contracoup lesion: injury opposite the point of contact
34
Q

Traumatic Parenchymal Injuries

A

• Laceration: penetration of an object with tearing of tissue
• Diffuse axonal injury: axonal swelling in white matter. Result of angular deceleration or acceleration

35
Q

Traumatic Vascular Injury

• Epidural Hematoma

A

– Blood between dura & periostium of the skull
– Caused by laceration of the middle meningeal artery
– Patients may be lucid for hours between the moment of trauma & the development of neurologic symptoms
– Neurosurgical emergency

36
Q

Traumatic Vascular Injury

• Subdural hematoma

A

– Blood between the dura mater and the arachnoid layer of the leptomeninges
– Tearing of bridging veins
– Most common over the lateral aspects of the cerebral hemispheres
– Most often become clinically manifest within the first 48 hrs after injury

37
Q

Subdural Hematoma

Acute-
Chronic-

A
  • Acute:
    – Clear history of trauma

* Chronic:
– Less frequently associated with well defined history of trauma
– May be associated with brain atrophy

38
Q

Traumatic Vascular Injury: Morphology

A
  • Acute
    – Freshly clotted blood
    – Underlying brain parenchyma compressed
  • Chronic
    – Granulation tissue contracts
    – Rebleeding may be a problem
39
Q

Sequelae of Brain Trauma

A
  • Post-traumatic dementia
    • Post-traumatic hydrocephalus

* Epilepsy
• Psychiatric disorders
• Infectious disease

40
Q

Hypoxia, Ischemia, and Infarction

Vascular Disease

A
  • Brain normally receives
    – 15% of cardiac output
    – ~20% of O2 consumed by the body
    – Requires a constant supply of glucose
  • Interruption of normal blood flow may produce irreversible injury (parenchymal)
41
Q

Vascular disease

• Autoregulation

A

– The brain is exquisitely sensitive to changes in blood flow
– It is capable of regulating blood flow over a wide range of perfusion pressures

42
Q

Hypoxia: Categories

Functional hypoxia
Ischemia
Permanent

A

• Functional hypoxia
– Low inspired PO2
– Impaired oxygen-carrying capacity of blood (anemia, hemog)
– Inhibition of oxygen use by tissue

• Ischemia
– Transient
• Interruption o fbloodflow
– Permanent
• Cessation of bloodflow

43
Q

Principle Types of Acute Ischemic Injury

A

• Globalcerebralischemia(ischemic/hypoxic encephalopathy)
– Results in generalized reduction in cerebral perfusion (shock)

  • Focalcerebralischemia
    – Reduction or cessation of blood flow to a localized area of the brain (clot)
  • Hemorrhage
    – Within the brain parenchyma or subarachnoid space
44
Q

Global Cerebral Ischemia

A

• Outcome of severe hypotensive episode
• Autoregulatory mechanisms unable to compensate
– Systolic pressures fall below 50 mm/Hg
• Outcome varies with severity and duration of insult

45
Q

Hypoxia / Ischemia

A

• Hypoxia: decrease in oxygen available to the tissues
• Ischemia: decreased tissue perfusion

46
Q

Sensitivity of CNS Cells to Hypoxic/Ischemic

A

• Neurons>glial cells
• Pyramidal cells of the hippocampus
• Purkinje cells of the cerebellum
• Areas of the brain located at the junction of arterial territories (arterial border zones)
– Wedge shaped infarcts

47
Q

Morphology

• Immediately after event: may appear normal

A
  • In those surviving: softened, edematous
  • Early changes: 12 – 24 hrs.
    – Acute neuronal cells change (red neurons)
    – Similar changes in astrocytes and oligodendroglia
48
Q

Morphology

• Subacute changes: 24 hrs. to 2 wks. – Necrosis of tissue
– Influx of macrophages
– Vascular proliferation
– Reactive gliosis

A

• Repair
– After 2 weeks
– Removal of necrotic tissue and gliosis – Loss of normal CNS structure

49
Q

Morphology
•Neurons most susceptible to irreversible injury:
– Pyramidal cells of Sommer’s sector of the hippocampus, Purkinje cells of the cerebellum, and pyramidal neurons in the neocortex

A
  • Laminar necrosis of the neocortex

* Watershed Infarcts:
– Wedge-shaped lesions in areas between major arterial distribution (border zone)

50
Q

Hypoxic/Ischemic Injury: Clinical Features

• May occur in the following circumstances:
– Anything which results in a global decrease in the amount of oxygenated blood available to the brain

A

• Cardiac dysrythmias, shock, increase in intracranial pressure – Factors modifying the parenchymal injury
• Age
• Temperature • Duration

51
Q

Focal Cerebral Ischemia:
Infarction

A

•Cerebralarterialocclusionmayleadtoischemiaor infarction
• Anatomiclocationofthelesiondeterminesthe symptoms
• Caused by in situ thrombosis (atherothrombus) or embolization
– Embolic infarct more common than thrombotic
• Maybehemorrhagicornonhemorrhagic
• Mostcommonformofcerebrovasculardisease

52
Q

Cerebral Infarction: Nonhemorrhagic

A
  • Usually associated with emboli (thrombus less common)
    – Mural cardiac thrombus, MI, valvular disease, atrial fibrillation, atherosclerosis, arteritis,
  • In first 6 hours, no change in macroscopic appearance
  • By 48 hrs., area is swollen, pale, indistinct corticomedullary junction
53
Q

Cerebral Infarction: Nonhemorrhagic

A

• 2 to 3 weeks: there is neutrophilic emigration followed by mononuclear phagocytic cell emigration
• Macrophages containing myelin or red cell breakdown products cam be preset for months to years
• The process of liquefaction proceeds with astrocytic reaction around the edges

54
Q

Cerebral Infarction: Hemorrhagic

A

• Results from reperfusion of ischemic tissue – Collaterals
– After dissolution of emboli
• The evolution parallels that of nonhemorrhagic infarction with the addition of blood extravasation and resorption

55
Q

Infarction: Clinical S&S

A

• Typically sudden
• May be preceded by transient ischemic attacks (TIA’s)
• Neurologic deficits related to:
– Location
– Amount of tissue damage
• Occur most commonly in area supplied by the middle cerebral artery

56
Q

Intracranial Hemorrhage (in brain parenchyma)

• Associated with:

A

– Hypertension and other diseases leading to vascular wall injury
– Structural lesions (arteriovenous and cavernous vascular malformations)
– Tumors

57
Q

Primary Brain Parenchymal Hemorrhage

• Most important predisposing factor: hypertension

A

– Accounts for >50% of clinically significant hemorrhage
– Brain hemorrhage accounts for ~15% of deaths among those with HTN (chronic)
• Hyalin arteriolosclerosis
– Weaker walls
– Chracot-Bouchard microaneurysms

58
Q

Intraparenchymal Hemorrhage (Nontraumatic)

A

• Hypertensive hemorrhages most often involve the putamen, thalamus, pons, and cerebellar hemispheres
• Clinical outcome depends on the size and location of the lesion

59
Q

Intraparenchymal Hemorrhage (Nontraumatic)
• Cerebral Amyloid Angiopathy (CAA)

A

– A condition in which amyloidogenic peptides (typically the same ones found in Altzheimer disease, deposit in the walls of medium and small-caliber meningeal and cortical vessels
– Can result in weakening of the vascular wall
– Is a relationship between a polymorphism in the gene that encodes apolipoprotein E and the risk of disease

60
Q

Vascular Malformations
• Classified into four types:

A

– Arteriovenous (AVM)
– Cavernous
– Capillary telangiectasias
– Venous angiomas

61
Q

AVM

A

• Most common type of vascular malformation
• M>F (2:1)
• Frequently between the ages of 10 to 30 years
• Clinical
– Siezures, intracerebral hemorrage or subarachnoid hemorrhage

62
Q

Intraparenchymal Hemorrhage: Clinical S&S

A
  • Abrupt onset
  • Evidence of increased intracranial pressure
    – Headache, vomiting, rapid loss of consciousness
    – Nuchal rigidity infrequent
  • Localizing signs may be present
    – Hemiparesis, slurred speech
63
Q

Clinical S&S

A

• Progression may lead to herniation and brain stem compression
• Large and medium
-sized cerebral clots
– Grave prognosis
• Location as well as size are important in considering prognosis

64
Q

Laboratory Studies

• CT scan
– Provides for rapid diagnosis on intracerebral hemorrhage

A
  • MRI
    – Useful in demonstrating brainstem hemorrhages and residual hemorrhages
  • Lumbar puncture
    – Not advised, may precipitate herniation
65
Q

Treatment
• If coma is present
– Maintenance of adequate ventilation
– Monitor ICP
– Selective acute use of controlled hyperventilation

A
  • Supratentorial hemorrhage
    – Surgical evacuation does not improve outcome
  • Cerebellar Hemorrhages
    – Surgical evacuation is a generally accepted Tx.
66
Q

Spinal Cord

A

Infarction

Trauma

67
Q

Spinal Cord Infarction
• Pathogenesis

A

– Occurs most commonly in the territory of the anterior spinal artery
• Supplies the anterior 2/3 of the cord
• Is supplied by only a limited number of feeding
vessels
• Well supplied in the cervical region, so tends to occur caudally

68
Q

Spinal Cord Infarction
• Causes

A

– Trauma
– Dissecting aortic aneurysm

– Aortography
– Polyarteritis nodosa
– Hypotensive crisis

69
Q

Spinal Cord Infarction
• Typical clinical presentation

A

– Acute onset of flaccid, areflexic paraparesis
– As the spinal shock wears off
—evolves into a spastic paraparesis
• Brisk tendon reflexes and extensor plantar responses
• Dissociated sensory impairment
– Pain and temperature lost
– Vibration and proprioception spared

70
Q

Spinal Cord Trauma

• Normally protected within the bony vertebral canal
– Vulnerable to trauma from its skeletal encasement

A

• Most injuries that damage the cord are associated with displacement of the vertebral colum

71
Q

Spinal Cord Trauma

A

• Level of cord injury determines the extent of neurologic manifestations

72
Q

Spinocerebellar Degenerations

A

Spinocerebellar Ataxia

Friedreich Ataxia

73
Q

Spinocerebellar Ataxias

A

• A group of genetically distinct diseases
• Characterized by signs and symptoms referable to the cerebellum, brainstem, spinal cord, and peripheral nerves
• Other brain regions may be affected in different subtypes

74
Q

Spinocerebellar Ataxias: Molecular Genetics

A

• At least 29 distinct entities
• Autosomal dominant
• Three distinct types of mutations
– Polyglutaminde diseases linked to expansion of a CAG repeat
– Expansion of non-coding region repeats – Other types of mutations

75
Q

Friedreich Ataxia

• A distinctive spinocerebellar degeneration
• Autosomal recessive
• Progressive:

A

– Begins in the first decade of life with gait ataxia
– Followed by hand clumsiness and dysarthria
– Depressed or absent deep tendon reflexes
– Proprioception and vibratory sense are impaired
– Some loss of light touch, pain and temperature sensation

76
Q

Friedreich Ataxia
• Other clinical findings:

A

– Pes cavus and kyphoscoliosis
– High incidence of cardiac arrhythmias and CHF
– Wheelchair bound within 5 years of onset
– Cause of death: pulmonary infection and cardiac disease

77
Q

Friedreich Ataxia: Pathophysiology

A
  • Expansion of GAA trinucleotide repeat in the first intron of a gene on chromosome 9q13
  • Encodes a protein called frataxin
    – Affected individuals have very low levels of this protein
78
Q

Friedreich Ataxia: Pathophysiology

• Frataxin normally localizes to the inner mitochondrial membrane:

A

– May have a role in regulating iron levels
– Iron is essential for many of the complexes in oxidative phosphorylation
– Mutations in frataxin cause mitochodrial dysfunction

79
Q

Friedreich Ataxia: Morphology

• Spinal Cord:

A

– Loss of axons and gliosis in the posterior columns, the distal portions of the corticospinal tracts, and the spinocerebellar tracts

– Degeneration of neurons in the spinal cord, brainstem, cerebellum, and the Betz cells of the motor cortex

80
Q

Friedreich Ataxia: Morphology

• Large dorsal root ganglion neurons are also decreased in number, with secondary degeneration of their axons

A

• Heart
– Enlarged
– Multifocal destruction of myofibers with inflammation and fibrosis

Pathology (15 decks)

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