Brainscape's Knowledge GenomeTM

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


See full index

Patho 2 > The CNS > Flashcards

The CNS Flashcards

1
Q

types of cells of the NS

A
  • the neuron

- neuroglia

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

types of neurglial cells

A
  • astrocytes
  • oligodendrocytes
  • ependymal cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

neuron

A
  • brains immune cells

- protect against injury and disease

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

astrocytes

A
  • metabolic buffer, detoxifies
  • modulate how neurons communicate
  • surround blood vessels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

oligodendrocytes

A
  • produce myelin

- myelin wraps around axons as insulation

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

ependymal cells

A
  • lines spinal cord and ventricles of brain

- produces CSF

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

where does sensory information go to in the brain

A
  • medulla, pons, mesencephalon
  • cerebellum
  • thalamus
  • cerebral cortex
  • SC at all levels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are effectors

A
  • muscles or glands

- anatomical features that do the function the brain tells them to do

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

major levels of CNS function

A
  • SC
  • lower brain or subcortical level
  • higher brain or cortical level
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

spinal cord level of CNS function

A
  • upper levels send signals to SC

- SC performs functions necessary

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

lower brain function

A
  • subconscious activity
  • controlled by:
  • medulla
  • pons
  • mesencephalon
  • hypothalamus
  • thalamus
  • cerebellum
  • basal ganglia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

higher brain function

A
  • done by cerebral cortex
  • essential for thought processes
  • cannot function by itself
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

cerebral cortex function

A
  • thinking
  • learning
  • remembering
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

thalamus function

A
  • interprets sensory messages like pain, temp, pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

hypothalamus function

A
  • controls homeostatic functions

- i.e. temp, respiration, HR

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

cerebellum function

A
  • muscle tone
  • posture
  • balance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

brain stem function

A
  • HR and breathing

- plays role in consciousness

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

blood brain barrier

A
  • selectively inhibits substances that reach the brain or CSF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

components of the BBB

A
  • capillaries
  • astrocyte foot
  • efflux transporters
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

role of capillaries in BBB

A
  • have continuous tight junctions

- limit passage of most substances

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

astrocyte foot in BBB

A
  • surrounds BV
  • allows small and lipophilic molecules
  • contributes to brain swelling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

efflux transporters

A
  • proteins

- help expel foreign substances that pass through capillaries

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

where does wallerian degeneration occur

A

in the distal axon of a severed axon

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

characteristics of wallerian degeneration

A
  • swelling in distal axon
  • neurofilament hypertrophy
  • myelin sheath disintegrates
  • axon degenerates and disappears
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what happens at the proximal end of an injured axon?

A
  • similar to wallerian degeneration but only to the next node of ranvier
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what happens to the cell body of an injured nerve

A
  • swells

- undergoes apoptosis

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

what happens 7-14 days after nerve injury

A
  • new terminal sprouts project form proximal segment

- increase incidence of scar formation

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

astrocyte reaction to injury

A
  • causes cellular swelling

- due to hypoxia, hypoglycemia, or toxic injuries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

oligodendrocyte reaction to injury

A
  • results in demyelinating disorders
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

where is CSF produced

A

choroid plexus of each ventricle

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

CSF function

A
  • shock absorber for brain
  • deliver nutrients and remove waste from brain
  • regulate ICP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

hydrocephalus

A
  • increase in CSF within ventricles

- due to reduce flow or decreased resorption of CSF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what is the result of hydrocephalus in infancy?

A

enlargement of head due to unfused cranial sutures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what is the result of hydrocephalus after infancy?

A

expansion of ventricles and increased ICP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

cerebral autoregulation

A
  • BF maintained at constant levels

- range of 60- 150 mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

when is cerebral autoregulation lost?

A

at 180 mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what is the result of lost cerebral autoregulation?

A
  • cerebral vasodiation

- cerebral edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what are the types of cerebral edema?

A
  • vasogenic

- cytotoxic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

vasogenic edema

A
  • irreversible increase in extracellular fluid

- caused by BBB disruption and increased vascular permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

cytotoxic edema

A
  • reversible
  • increase in fluid secondary to neuronal, glial, or endothelial damage
  • caused by hypoxia or ischemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

intracranial components

A
  • cerebral parenchyma
  • CSF
  • Blood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

ICP

A
  • pressure inside cranial cavity
  • normally <15 mmHg
  • pathologic HTN > 20 mmHg
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

intracranial compliance

A
  • displacement of CSF into thecal sac

- decrease in volume of cerebral venous blood via venoconstriction and extracranial drainage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what happens if ICP increase?

A

blood supply to brain decreases and results in cerebral ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

herniation

A
  • displacement of brain tissue past dural folds or through openings in skull
  • due to increased ICP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

when do you often see herniation?

A
  • cerebral edema
  • increased CSF volume
  • mass lesions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what is the most common type of herniation

A
  • tonsillar herniation
  • causes brainstem to compress
  • compromises vital respiratory and cardiac centers in medulla
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

causes of hypoxia

A
  • low partial pressure of oxygen
  • impaired o2 carrying capacity
  • toxins
  • ischemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

broad classifications of ischemia

A
  • global

- focal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

global cerebral ischemia

A
  • happens when BP is less than 50 mmHg
  • usually due to cardiac arrest
  • outcome depends on duration
  • severe global ischemia -> brain dead pt
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

focal cerebral ischemia

A
  • cerebral artery occlusion leading to focal ischemia then infarction
  • causes are embolic infarction or thrombotic occlusions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

clinical deficits due to ischemia depend on

A
  • duration of ischemia

- magnitude and rapidity of reduction of flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

cerebrovascular disease classifications

A
  • intrinsic issue of vessels
  • process might originate elsewhere
  • result of inadequate cerebral BF
  • rupture of vessles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

cerebrovascular disease classifications that can cause TIA or ischemic stroke

A
  • when issue is intrinsic
  • when process originates elsewhere
  • when there is inadequate BF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

cerebrovascular disease classifications that can cause hemorrhagic strokes

A
  • when vessels rupture
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

TIA

A
  • transient neurologic dysfunction due to ischemia

- no acute infarction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

ischemic stroke

A
  • infarction due to ischemia

- causes permanent damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

mechanisms of TIA

A
  • large artery TIA due to atherosclerosis
  • embolic TIA
  • lacunar/ small artery due HTN
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

what is the penumbra

A
  • area surrounding infarcted brain tissue that have the potential to recover
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

mechanism of ischemic cell injury

A
  • inhibition of protein synthesis
  • glucose utilization increases
  • anaerobic glycolysis and tissue acidosis
  • neuronal electrical failure
  • membrane failure
  • cell death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

what happens if the brain structural integrity is lost

A
  • breakdown of BBB
  • cerebral edema
  • hemorrhage into brain parenchyma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

what is matrix metalloprotease (MMP)

A

protease that mediates loss of brain structural integrity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

causes of intracranial hemorrhage

A
  • HTN
  • structural lesions
  • tumors
64
Q

types of intracranial hemorrhage

A
  • intracerebral hemorrhage

- subarachnoid hemorrhage

65
Q

causes of intracerebral hemorrahge

A
  • HTN
  • trauma
  • vascular malformations
66
Q

cause of subarachnoid hemorrhage

A

rupture of aneurysms

67
Q

primary brain damage

A
  • parenchymal blood accumulates
  • tissue is disruputed
  • mechanical damage due to mass effect
  • increased ICP
  • damaged BBB -> edema
68
Q

secondary brain damage

A
  • thrombin activation
  • lysis of RBC -> release of Hb which is converted to heme and iron
  • inflammatory reaction
69
Q

what is another name for spina bifida

A

myelomeningocele

70
Q

neural tube defect

A
  • portion of neural tube doesnt close or reopens after closure
  • can occur in brain, spine, spinal column
  • present at birth
71
Q

myelomeningocele

A
  • cleft in vertebral column
  • defect in skin so meningnes and SC exposed
  • usually results in damage to SC and nerves
  • can cause physical and intellectual disabilities
72
Q

risk factor for myelomeningoceles

A

folate deficiency during first weeks of gestation

73
Q

neurologic abnormalities of myelomeningoeceles

A
  • SC problems -> issues with trunk, legs, bladder, bowel
  • brain stem probelms -> chiari malformation
  • hydrocephalus due to chairi II malformation
74
Q

chairi malformation

A

structural defect when cerebellum pushes through foramen magnum

75
Q

chairi II malformation

A
  • brainstem and cerebellum pushed through foramen magnum
76
Q

cerebral palsy

A
  • permanent non-progressive motor dysfunction

- affects muscle tone, posture, and movement

77
Q

cause of cerebral palsy

A
  • most due to prenatal factors
  • sometimes due to peri and postnatal factors
  • prematurity/ low birth weight*
78
Q

low birth weight and CP associations

A
  • periventricular leukomalacla (PVL)
  • intraventricular hemorrhage
  • bronchopulmonary dysplasia
79
Q

pathogenesis of CP

A
  • necrosis of periventricular white matter
80
Q

what is PVL

A
  • necrosis of white matter near vetricles
  • often occurs in premature infants
  • due to decreased oxygen/ blood flow and damage to glial cells
81
Q

diffuse brain injury (DBI)

A
  • most common type of TBI
  • due to impact, acceleration, and deceleration forces
  • develops due to tissue seharing at interface of gray and white matter
82
Q

what is the most severe form of DBI

A

diffuse traumatic axonal injury (DAI)

83
Q

pathophys of diffuse axonal injury (DAI)

A
  • axonal swelling
  • release of excitatory neurotransmitters
  • generation of free radicals causes secondary injury
84
Q

types of focal brain injury

A
  • brain contusion
  • intraparenchymal brain hemorrhage
  • subdural hematoma
  • epidural hematoma
85
Q

brain contusion

A
  • bruising of brain tissue
  • blunt trauma between brain and skull
  • can be in location of impact (coup) on opposite side of brain (countercoup)
86
Q

intraparenchymal brain hemorrhage

A
  • develops from tears in brain tissue and/or vasculature
87
Q

subdural hematoma

A
  • dura is still intact
  • bridging blood vessels cross subdural space
  • cerebral cortical hemorrhage caused by direct brain trauma
88
Q

epidural hematoma

A
  • after blunt trauma

- may be result from disruption of middle meningeal artery and vein

89
Q

TBI

A
  • heterogenous disease

- rated based on glasgow coma scale

90
Q

pathophys of primary brain injury

A
  • shearing mechanisms leads to DAI
  • focal cerebral contusions
  • extra axial hematomas
91
Q

pathophys of secondary TBI

A
  • neurotransmitter mediated excitotoxity
  • electrolyte imbalances
  • mitochondrial dysfunction
  • inflammatory responses
  • apoptosis
  • secondary ischemia
92
Q

concussion

A
  • acute mild TBI

- based on glasgow scale rating measured 30 min after injury

93
Q

pathophys of concussion

A
  • result of direct external contact forces
  • can also be from brain being slapped against intracranial surfaces
  • may result in neurological changes
  • acute clinical sx related to function
94
Q

traumatic vascular injury

A
  • near universal feature of severe TBI

- direct trauma or disruption of vessel wall

95
Q

pathophys of traumatic vascular injury

A
  • injured cerebral microvasculature -> microthrombi and neuronal death
  • BBB disruption, edema, focal ischemia
  • in elderly stretched bridging veins -> subdural hematoma
96
Q

chronic traumatic encephalopathy (CTE)

A
  • dementing illness that develops after repeated head trauma

- leads to build up of tau proteins in superficial cortical layers

97
Q

etiology of CTE

A
  • repreated concussions cause cumulative neuropsych deficits
  • parkinsonism
  • speech and gain abnormalities
98
Q

how can infections cause damage to CNS?

A
  • directly injuring glia or neurons
  • indirectly through microbial toxins
  • inflammatory response
  • immune-mediated mechanisms
99
Q

how can microbes access the CNS?

A
  • hematogenous spread- most common
  • direct implantation
  • local extension
  • peripheral nerves
100
Q

meningitis

A
  • inflammation of leptomeningies in subarachnoid space

- mainly due streptococcus pneumoniae or neisseria meningitidis

101
Q

how is meningitis classified

A
  • acute pyogenic
  • aseptic
  • chronic
102
Q

what is the difference between meningitis and meningoencephalitis?

A
  • meningitis- only meninges are infected

- meningoencephalitis- meninges AND brain parenchyma infected

103
Q

pathogenesis of meningitis

A
  • cytokines produced
  • increased BBB permeability
  • altered cerebral BF
  • increased ROS
  • all lead to neuronal damage and increased ICP/ edema
104
Q

bacterial meningitis

A
  • infection of arachnoid mater and CSF in subarachnoid space and ventricles
105
Q

triad of bacterial meningitis

A
  • pathogen penetration
  • NF-kB activation
  • leukocyte transmigration at BBB
106
Q

what is the role if NF-kB

A
  • transcription factor
  • activated when bacteria invade BBB
  • causes cascade of events in meningitis infection
107
Q

viral meningitis

A
  • most common type of meningitis
  • less severe- self limiting
  • fever, no neurologic dysfunction
108
Q

main cause of viral meningitis

A
  • enteroviruses
109
Q

clinical features of meningitis

A
  • fever
  • HA
  • stiff neck
  • altered mental status
  • N/V
  • sx are the same for viral and bacterial
110
Q

early onset dementia (EOD)

A
  • significant acquired cognitive impairment
  • interferes with independence in daily activities
  • affects learning, memory, language
  • onset: 18-65 y/o
111
Q

causes of EOD

A
  • Alzheimers disease
  • parkinsons disease
  • prion disease
  • MS
112
Q

what is the most common cause of dementia in older adults

A

Alzheimer disease

113
Q

neuropathologic changes seen in AD

A
  • neuritic plaques
  • extracellular deposits of amyloid beta peptides
  • neurofibrillary degeneration by tau proteins
114
Q

how are neuropathologic changes ranked in AD?

A
  • amyloid beta plaque distribution score
  • tau protein distribution stage
  • neuritic plaque density score
115
Q

what are the two types of AD

A
  • early onset= familial
  • sporadic, occurs in people over 65 y/o
  • 95% of cases are sporadic
116
Q

pathogenesis of early onset AD

A
  • APP mutation
  • PSEN1 mutation (most common)
  • PSEN2 mutation
  • also due to role of inflammation
  • basis of cognitive impairment due to presence of plaques and tangles
117
Q

what are the three enzymes that normally cleave amyloid precursor proteins?

A
  • alpha secretase
  • beta secretase
  • gamma secretase
118
Q

result of APP mutation

A
  • increased activity of beta secretase

- results in amyloid beta protein accumulation

119
Q

result of PSEN1 or 2 mutations

A
  • increased activity of gamma secretase

- results in accumulation of amyloid beta proteins

120
Q

why do tau proteins aggregate in AD

A

they become hyperphosphorylated

121
Q

what is the gene mutation associated with sporadic AD

A
  • ApoE

- inhibits clearance of amyloid beta proteins

122
Q

what are the cardinal clinical sx of AD

A
  • memory impairment
  • executive function and judgement/ problem solving issues
  • behavioral and psychological sx
123
Q

parkinson disease

A
  • progressive neurodegenerative disease
  • due to basal ganglia death leading to less DA production
  • multifactorial disease
124
Q

basal ganglia circuits in parkinson disease

A
  • basal ganglia produce DA
  • have increased inhibition of thalamus
  • also have reduced excitatory input to the motor cortex
125
Q

compensatory mechanisms in PD

A
  • increased synthesis of DA in surviving neurons
  • proliferation of DA receptors
  • gap junctions allow rapid communication between neurons
126
Q

three stages of compensation during presymptomatic period of PD

A
  • early period where compensation can mask disease
  • increased basal ganglia activity
  • increased intensity in motor cortex
127
Q

clinical features of PD

A
  • resting tremor
  • bradykinesia
  • rigidity
  • postural instability
128
Q

amyotropic lateral sclerosis (ALS)

A
  • progressive neurodegenerative disease
  • leads to muscle weakness, disability, death
  • 90-95% sporadic
129
Q

risk factors for ALS

A
  • age
  • family history
  • smoking*
  • environmental toxin exposure
  • military servce
130
Q

possible etiology of ALS

A
  • largely unknown
  • abnormalities in RNA metabolism
  • excitotoxicity
  • viral infections- polio and enterovirus
  • inflammatory responses
131
Q

pathology of ALS

A
  • intracellular inclusions in degenerating neurons and glia
  • motor neuron degeneration and death with gliosis
  • SC becomes atrophic
  • affected muscles show denervation atrophy
132
Q

hallmark sx of ALS

A
  • combo of upper and lower motor neuron signs and sx
  • weakness
  • slowness
  • hyperreflexia
  • spasticity
  • atrophy
  • fasciculations
133
Q

multiple sclerosis

A
  • autoimmune inflammation due to auto-reactive lymphocytes (T cells)
134
Q

major pathologic mechanisms of MS

A
  • inflammation
  • demyelination
  • axonal degeneration
135
Q

pathogenesis of MS

A
  • immune mediated
  • microglia form complex with activated T cells -> destruction of myelin and oligodendrocytes
  • see lesions or plaques in brain
136
Q

classifications of MS

A
  • clinically isolated syndromes
  • relapsing- remitting
  • secondary progressive
  • primary progressive
137
Q

clinicaly isolated syndromes of MS

A
  • first attack of a disease
  • shows characteristics of inflammatory demyelination
  • doesn’t fulfill MS dx criteria
138
Q

relapsing- remitting MS

A
  • clearly defined relapse with full recovery

- sequeelae and residual deficit upon recovery

139
Q

secondary progressive MS

A
  • initial RR disease that gradually worsens
140
Q

primary progressive MS

A
  • progressive accumulation of disability

- from disease onset with occasional plateaus, temporary minor improvements, or acute relapses

141
Q

types of glial cell tumors

A
  • astrocytoma
  • oligodendrogliomas
  • ependymomas
  • mixed gliomas
142
Q

classifications of primary brain tumors

A
  • Grade I
  • Grade II
  • Grade III or IV- malignatn or high grade gliomas
143
Q

generalized sx of brain tumors

A
  • HA
  • seizures
  • N/V
  • depressed level of consciousness
  • neurocognitive dysfunction
144
Q

focal sx of brain tumors

A
  • seizures
  • weakness
  • sensory loss
  • aphagia
  • visual spatial dysfunction
145
Q

glioma

A
  • primary brain tumor
  • histological features of glial cells
  • diffuse gliomas are most common
  • generally affect cerebral hemispheres of adults
146
Q

classifications of diffuse gliomas

A
  • histologic characteristics

- molecular characteristics like IDH mutant astrocytomas

147
Q

astrocytoma formation

A
  • inactivation of p53 tumor suppressor gene
  • point mutations in IDH 1
  • mutations in chromatin regulator gene
148
Q

why are IDH mutations associated with astrocytomas

A
  • leads to accumulation of 2-HG
  • causes global changes in DNA and histone methylation
  • impairment of cellular differentiation
  • tumorigenesis
149
Q

glioblastoma multiforme (GBM)

A

most malingnat form of astrocytoma

150
Q

transition from low-grade to malignant glioma associated with

A
  • cell cycle checkpoint inactivation
  • tumor suppressor gene inactivation
  • angiogenesis
151
Q

pathophys of GBM

A
  • complex
  • multiple genetic mutations
  • upregulation of vascular endothelial GF (VEGF)
152
Q

result of VEGF

A
  • increases vascular permeability
  • increases endothelial gaps
  • increases fenestrations
  • allows for rapid growth of tumor
153
Q

meningioma

A
  • mainly benign tumor of adults
  • arise from meninges
  • main risk factor is radiation therapy to head and neck
154
Q

what is the most common cytogenic cause of meningiomas

A

abnormal chromosome 22 mutations

155
Q

clinical features of meningioma

A
  • usually slow growing tumors
  • HA and weakness in arm or leg are most common sx
  • express progesterone receptors so may grow more rapidly during pregnancy
156
Q

primary sites of origin of metastatic brain tumors

A
  • lung
  • breast
  • skin (melanoma)
  • kidney
  • GI tract
  • most common brain tumor in adults
157
Q

clinical features of metastatic brain tumors

A
  • HA that has changing pattern, worsens with change in position
  • seizures

Patho 2 (15 decks)

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