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Patho Exam 1 > CNS -1 > Flashcards

CNS -1 Flashcards

0
Q

Explain the process following initial injury/stimulus/growth that leads to the clinical manifestations. -sorry didnt know how else to ask this : )

A

Initial insult –> 1) invasion –> focal deficits & cerebral edema

               - -> 2) compression ---> cerebral edema ---> increase ICP
               - -> 3) Increased ICP --> leads to clinical manifestations
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1
Q

What 2 mechanisms can cause brain cell death?

A

1) Anaerobic metabolism (ATP driven ie NaKpump)

2) Deterioration of ion gradients

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2
Q

What are some clinical manifestations of Increase ICP?

A 
Decrease cognitive function --> behavioral changes
HA, vomitting, seizures 
papilledema
unsteady gait 
loss of sphincter control
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3
Q

A direct insult of the initial insult is what type of brain injury?

A

Primary

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4
Q

Progressive damage resulting from body’s physio response to initial insult is what type of brain injury?

A

Secondary

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5
Q

What is the critical factor in determining neuronal cell fate after injury?

A

degree of ATP depletion = decrease cellular function

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6
Q

What is a contributing factor to the primary insult or part of the secondary response?

A

decrease blood flow = decreased 02 at cellular level & cant wash out metabolites

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7
Q

Under anaerobic metabolism, what is the importance of mitochondrial dysfunction?

A

Normally under 02 –> Oxidative phosphorylation occurs in mitochondria highly efficient in forming ATP. w/o 02 –> anaerobic glycolysis

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8
Q

Due to mitochondrial dysfunction the anaerobic glycotic pathway is initiated and therefore ____________ is converted to _____________.

A

pyruvate —> lactate

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9
Q

In the anaerobic metabolism pathway what affects neuronal integrity, the cell membrane?

A

H ions —> acidosis

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10
Q

How does inadequate ATP, which maintains ion gradients, lead to cell injury and death?

A

Anoxic depolarization (K leaves, Na Cl Ca enter) w/o functional ATP pump.. tries to equilibrate …H20 follows solute cell swells = death

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11
Q

What excitatory neurotransmitter binds to NMDA receptors?

A

Glutamate

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12
Q

Where does Glutamate act and what ion influx causes depolarization?

A

Post synaptically. NMDA ligand gated Ca Channel, Ca influx depolarizes

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13
Q

Normal glutamate is cleared/reuptake by ATP pump, when ATP is depleted what can occur?

A

failure to remove excessive glutamate (excitotoxin)

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14
Q

Excess glutamate can stimulate nearby neurons to then uptake large amounts of what ions ? and what is the result?

A

Calcium ions overload injury cytotoxic edema and swelling

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15
Q

NMDA receptor activation stimulates production of what? in turn excess of this can increase production of what?

A

Nitric Oxide–> reactive Nitrogen species, free radicals damage cell components

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16
Q

How does reperfusion cause cell death?

A

02 re-enters = produce reactive products behave as free radicals (hydroxyl radicals, superoxide, peroxide)

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17
Q

How does reperfusion (secondary injury) cause injury to the cell membrane therefore not allowing it to act as a barrier?

A

lipid peroxidation formation of arachidonic acid= more 02 free radicals and mediators of inflammation

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18
Q

What contributes to ability to maintain perfusion, supply of 02 and nutrients, to both sides and remove wastes?

A

Auto regulation (myogenic reflex)

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19
Q

Metabolic vasodilation is influenced by what 3 factors?

A

pH, C02, 02 in arterial blood. stimulus to bring in blood flow and wash out metabolites

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20
Q

Interference with vessel dilation leads to ?

A

ischemia

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21
Q

Impaired vasoconstriction causes what 2 things to occur?

A

hyperperfusion and edema formation as to not deplete the other side

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22
Q

As ICP increases volume increases and compliance _________?

A

decreases

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23
Q

The cranium is composted of what 3 elements that are effected by ICP? and what is a normal ICP

A

brain tissue CSF blood

ICP 0-15

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24
Q

What are some causes of increase ICP related to increase blood volume?

A

high C02 & acidosis -vasogenic (vessels) metabolite vasodilation to increase flow
increase RAP
dural sinus thrombis

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25
Q

Causes of increased ICP related to CSF?

A

obstruction and nonobstructive hydrocephalus

excess CSF production

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26
Q

Causes of increased ICP related to brain tissue?

A 
tumor masses lesions 
hemorrhage 
infection 
edema
ischemia and necrosis
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27
Q

Clinical manifestation of increased ICP?

A

HA vomiting altered LOC

blurry vision edema of optic disk (papilledema)

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28
Q

Motor clinical manifestations of increase ICP?

A

as ICP increase LOC decreases… impaired pupil response to light
altered resp patterns unresponsive to stimuli
unable to move verbalize or open eyes

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29
Q

Order of clinical manifestation with increase ICP?

A

LOC -> sensory -> motor

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30
Q

Management for herniation?

A 
imagining (CT or MRI)
surgical or medical
measure ICP and CPP
removal lesions or CSF
Tx: cerebral oxygentaiton
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31
Q

What is the minimal CPP needed to ensure adequate blood flow to prevent ischemia?

A

CPP of at least 60

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32
Q

What is the most sensitive indicator of altered brain function?

A

change in LOC

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33
Q

The state of alertness and attentiveness is dependent on what activity what system?

A

RAS: reticular activating system

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34
Q

Changes in pupils size, shape and reactivity is an early indicator of what?

A

ICP and possible herniation

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35
Q

Which maneuver, when assessing oculovestivubular reflex, entails rotating head side to side? what is the normal response?

A

Doll’s eyes normally turn to opposite direction of head rotation

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36
Q

Which maneuver to inject cold water into ear? what is normal response?

A

Cold calorics- tonic deviation of both sides toward side irrigated

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37
Q

Absence of blink during assessment of corneal reflex indicates what?

A

severely impaired brain function

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38
Q

How does hypothermia relate to management of increase ICP?

A

reduces brain’s metabolism saving 02 decrease work load

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39
Q

What are some factors that can increase brain metabolism thus increasing ICP?

A 
fever
seizures
agitation
pain 
all should be avoided
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40
Q

What are the three types of primary TBI?

A

focal- primary
polar- opposite (acceleration and deceleration)
diffuse- global injury

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41
Q

What are the three intracranial hematomas (secondary TBI)?

A

epidural subdural subarachnoid

42
Q

Which type of primary TBI is localized to site of impact?

A

focal (coup)

43
Q

Which type of primary TBI is d/t acceleration and deceleration movement of the brain within the skull?

A

Polar injury (coup contracoup) resulting in usually double injury (usually opposite focal injury)

44
Q

Which type of primary TBI is caused by movement of the brain within the skull resulting in widespread axonal injury?

A

diffuse injury

45
Q

What is the criteria for a concussion?

A

mild TBI alteration in LOC <30min but NO evidence of damage on CT
HA N&V dizziness fatigue blurred vision etc

46
Q

Which will show injury on CT or MRI… concussion or contusion?

A

Contusion reveals damage necrosis laceration bruising

47
Q

What is a localized collection of blood in the cranium called?

A

intracranial hematoma–> disruption of vasculature can lead to hemorrhage

48
Q

Which type of hematoma generally involves arterial injury?

A

Epidural hematoma

49
Q

Epidural hematoma has a rapid onset, why is that?

A

arterial injury high pressure

50
Q

Which type of hematoma has a minor primary injury characterized with lucid intervals of disturbed then normal levels of cognition with a final rapid deterioration?

A

epidural

51
Q

Which 2 hematomas generally involve rupture of bridging veins?

A

subdural and subarachnoid

52
Q

A chronic subdural hematoma is prone to what?

A

re-bleeding

53
Q

Subdural hematoma has a slower onset d/t involvement with veins when might you see symptoms in an acute situation?

A

within 24 hours

54
Q

Which hemorrhage is commonly associated with rupture of cerebral aneurysms or AVM (arterial in origin)?

A

Subarachnoid

55
Q

What are important treatments in patients with TBI to reduce brain swelling and decrease ICP?

A

maintain normal body temp or mild hypotherm
normal PaC02
normal glucose
and intravascular volume

56
Q

What is a sudden onset of neurologic dysfunction d/t vascular disease resulting in an area of brain infarction? which is the most common?

A

Stroke- ischemic

57
Q

Ischemic strokes result from sudden occlusion of cerebral artery secondary to thrombus or emboli. Which of the two are associated with atherosclerosis and coaguloaphies?

A

Thrombotic

58
Q

Which type of ischemic stroke is associated with cardiac dysfunction or dysrhythmias (afib)

A

Embolic strokes

59
Q

What are some clinical manifestations of ischemic strokes?

A

contralateral hemiplegia
hemisensory loss
contralateral visual field blindness

60
Q

What is the penumbra?

A

peripheral to the insult, it’s reversible ischemia

salvaging penumbra is aim of early thrombotic therapy

61
Q

What type of ischemic stroke has completely resolved neurologic deficits?

A

TIA symptoms last minutes as long as 24 hours

62
Q

What is an important warning sign of thrombotic disease and carries a significant risk for subsequent stroke?

A

TIA

63
Q

What is the treatment for a TIA?

A

ASA, CEA, or angioplasty if 70% occluded

64
Q

What type of stroke usually occurs secondary to severe, chronic hypertension?

A

Hemorrhagic

65
Q

Where does a hemorrhagic stroke occure?

A

in the midbrain (basal ganglia or thalamus)

66
Q

Which type of stroke has a higher degree of secondary injury and associated morbidity and mortality ?

A

hemorrhagic

67
Q

The treatment for hemorrhagic stroke is aimed at minimizing infarct size and preserving neurologic function, what are some of these treatments?

A

thrombolytics, anticoagulant, antiplatelet, endarterectomy, angioplasty, stents, BP managment (keep mildly HTN at first)

68
Q

Initial motor deficits occurs as ________ or _________; recovery of motor function occurs with onset of ____________.
Does this occur ipsilateral or contralateral on side brain stroke occurred

A

flaccidity
paralysis
spasticity
-contralateral

69
Q

Loss of visual field on the paralyzed side also contributes to?

A

neglect of movement

70
Q

what is it called when the same side of the retina in each is is blinded?

A

homonyzmous hemianopsia

contralateral field blindness

71
Q

Aphasia occurs with brain damage to which cerebral hemiphere?

A

dominant

72
Q

Which aphasia is associated with motor/expressive and consists of poor articulation and sparse vocabulary?

A

Broca

73
Q

Which aphasia is associated with sensory, acoustic, receptive, and characterized by impaired auditory comprehension and speech that is fluent but doesn’t make sense ?

A

Wernicke

74
Q

What are the most common causes of Subarachnoid hemorrhage?

A

AVM and cerebral aneurysms

75
Q

What is characterized as ballooning and dilation of a segment of the vessel?

A

Cerebral aneurysm

76
Q

In Marfans an congenital defect in which layer of the artery becomes weakened causing an eventual burst= hemorrhage?

A

Medial layer (normally has autoregulation to dilate or constrict with changes in pressure) but defected

77
Q

Where are most cerebral aneurysms found?

A

Circle of Willis- saccular/berry aneurysms

areas of bifurcation

78
Q

What are the 3 components of meningismus?

A

1) photophobia
2) N&V
3) stiff neck

79
Q

What does a sudden severe HA with meningismus indicate?

A

cerebral aneurysm rupture

80
Q

what is the treatment for cerebral aneursym?

A

arterial clipping
embo
manage vasospasm by keeping blood volume and blood pressure normal to high and Ca Channel blockers

81
Q

What is the failure of capillary system to develop called?

A

AVM

82
Q

Arterial blood shunted to venous system in the case of AVM, how does this result in rupture and hemorrhage?

A

Vessels englarge=high vasc pressure

83
Q

How might AVM clinically manifest? treatment?

A

seizure and neuro dysfunct.
surgical removal, gamma knife/sterotactic radio surgery
irradiation or glue embo

84
Q

What might dilated vessels on imagining reveal?

A

AVM

85
Q

Which two of the three CNS infections we discussed in class are bacterial infections and which is viral?

A

Bacterial- meningitis and cerebral abscess

encephalitis viral

86
Q

Risk factors for CNS infections?

A

immunocompromised
debilitation
poor nutrition (AA needed for immunoglobulins)
radiation, steroid therapy, contact with vectors

87
Q

Meningitis is most commonly associated with what bacteria?

A

streptococcus pneumoniae

88
Q

Which CNS infection is described as hematogenous dissemination of bacteria ?

A

Meningitis

89
Q

Where does the bacteria colonize in meningitis?

A

nasopharynx, enter blood stream, and enter subarch space and CSF

90
Q

The pathogenesis of meningitis starts with bacterial toxins how does this lead to neuronal necrosis?

A

Bacterial toxins-> neuronal apoptosis-> BBB damange-> vasc permeability-> edema = increase ICP=decrease CPP–> hypoxia->
neuronal necrosis

91
Q

In meningitis there is an accumulation of neutrophils which release their contents to destroy bacteria, what is this called?

A

degranulation- destroys bacteria but also damages normal tissue (brain nerves blood vessels)

92
Q

The degranulation of neutrophils leads to vasculitis and clotting causing cerebral infarcts, accumulation of inflammatory exudate care result in what?

A

obstructive hydrocephalus

93
Q

Diagnose meningitis by lumbar puncture which will show what?

A

bacterial and increase neutrophils in CSF.
Protein elevated
glucose low d/t high cellular use/function

94
Q

Meningitis is treated with IV antibiotics and prevention includes vaccinations for what?

A

Hib and N.meningitis

95
Q

What CNS infection is characterized by inflammation of brain cause by a virus?

A

Encephalitis

96
Q

In encephalitis the virus attacks what membrane ?

A

arachnoid membrane and CSF

97
Q

A patient is bitten by an insect, he is likely to have what CNS infection?

A

Encephalitis

98
Q

Treatment for encephalitis is supportive with control of symptoms, this includes?

A

antripyretics, antivirals, steroids, antiseizure, fluid resuscitation

99
Q

Which CNS infection is characterized by a newly formed cavity filled with pus (pyogenic) ?

A

Brain Abscess

100
Q

Treatment for brain abscess includes?

A

drainage or excision of abscess and IV antibiotics

101
Q

What makes up the infected core in a brain abscess ?

A

neutrophils and tissue debris

102
Q

What surrounds the granulation tissue in a brain abscess? and what occurs there?

A

perifocal edema- proliferation of astrocytes

103
Q

Long term chronic phase of a brain abscess would have what two characeristics?

A

liquefied core and fibrous fliosis- inflamm response - scar tissue

Patho Exam 1 (3 decks)

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