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SRNA3AdvancedPatho2 > General Neuropathology > Flashcards

General Neuropathology Flashcards

1
Q

Involuntary actions

A

maintain homeostasis

Regulated by ANS

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2
Q

Voluntary actions

A

Reflex activities

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3
Q

Meninges: Dura Mater

A

Outer layer

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4
Q

Meninges: Arachnoid

A

Middle layer

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5
Q

Subarachnoid space

A

Contains cerebrospinal fluid (CSF)

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6
Q

Meninges: Pia mater

A

Adheres to surface of brain

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7
Q

Meninges other parts

A

Subdural space

Arachnoid

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8
Q

Protection of the Brain

A

BBB

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9
Q

Blood-brain barrier Role (LCL)

A

Limits passage
Controls balance of electrolytes, glucose, and proteins in brain
Lipid-soluble substances pass easily

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10
Q

BBB and neonates

A

Poorly developed in neonates

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11
Q

Blood-CSF barrier

A

At the choroid plexus for CSF

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12
Q

Each hemisphere is divided into four major lobes.

A

Frontal
parietal
temporal
occipital

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13
Q

Longitudinal fissure

A

separates two hemispheres

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14
Q

Cortex

A

“Gray matter” – nerve cell bodies

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15
Q

Corpus callosum

A

“White matter” – myelinated nerve bundles (tracts)

Connect the hemispheres

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16
Q

Right and left hemispheres similar in

A

structure, not necessarily in function

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17
Q

Dominant hemisphere

A

Side of brain that controls language

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18
Q

Dominant hemisphere- in most people

A

Left hemisphere

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19
Q

Broca area

A

Motor speech

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20
Q

Wernicke area

A

comprehends language

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21
Q

Functional Areas – Diencephalon

A

Central portion of the brain

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22
Q

Functional Areas – Diencephalon contains what?

A

Contains the thalamus and hypothalamus

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23
Q

Functional Area - Diencephalon - Thalamus role

A

Relay station for incoming sensory impulses

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24
Q

Hypothalamus
Key role
What does it control?

A

Key role in maintaining homeostasis of the body
Controls autonomic nervous system and much of the
endocrine system

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25
Q

Hypothalamus regulates (BRESS F)

A 
Body temperature, 
Regulation of sleep cycles
Emotional responses
Sex drive
Stress response, 
Fluid and food intake,
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26
Q

Functional Areas – Brainstem 3 parts

A

Midbrain
Pons
Medulla oblongata
RAS

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27
Q

Functional Areas – Brainstem- Midbrain

A

Visual activities

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28
Q

Functional Areas – Brainstem- Pons (HS)

A

Helps regulate respiration

Several nuclei of cranial nerves

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29
Q

Functional Areas – Brainstem- Medulla oblongata (CCN)

A

Control center for respiratory and cardiovascular
function
Coordination of cough reflex, swallowing, vomiting
Nuclei for several cranial nerves

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30
Q

RAS (Reticular-Activating System)/Reticular formation

A

Network of nuclei and neurons throughout brainstem

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31
Q

RAS and connection

A

Connected to many parts of the brain

Determines the degree of awareness of the cerebral cortex

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32
Q

*Anesthetic drugs and RAS

A

inhibit RAS causing reversible loss of consciousness

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33
Q

Cerebellum Role

A

Coordination of movements

Maintenance of posture & equilibrium

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34
Q

Cerebellum receives input from

A

Receives input from proprioceptors in muscles &
joints
Input from visual and vestibular pathways

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35
Q

Cranial Nerves: How many pairs and where does it originates?

A

12 Pairs

Originate from various parts of the brain

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36
Q

Cranial nerve numbered how?

A

Numbered from ventral to dorsal

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37
Q

Cranial nerves may contain

A

–Motor only
–Sensory only
–Both (mixed)

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38
Q

Spinal Cord is protected by

A

Protected by vertebral column, meninges, CSF

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39
Q

Spinal Cord continuous with

A

Continuous with medulla

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40
Q

Where does the SC end?

A

Ends at lower border of L1-L2

Conus medullaris, cauda Equina

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41
Q

White and gray matter

A

Core

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42
Q

Posterior horns

A

Interneurons (association neurons)

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43
Q

Anterior horns

A

Cell bodies of motor neurons

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44
Q

Spinal nerves named by

A

Named by location in the vertebral column where

they emerge

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45
Q

Nerve Roots Ventral anterior root

A

Motor (efferent) fibers (VME)

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46
Q

Dorsal (posterior) root

A

Sensory (afferent) fibers (DSA)

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47
Q

What are reflexes?

A

Automatic, rapid, involuntary responses to a

stimulus

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48
Q

Sensory stimulus, what is it?

A

From receptor – conducted along afferent fiber

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49
Q

What is a Synapse?

A

In the spinal cord or for cranial reflexes in the brain

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50
Q

Efferent impulse serve to

A

to elicit the response

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51
Q

Connecting and interneurons

A

Transmit sensory information to the brain

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52
Q

Neurotransmitters; ACh

A

Excitatory @ NMJ

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53
Q

ACH found in

A

In ANS and brain

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54
Q

Neurotransmitters Epi & Norepi ? Found where?

A

Excitatory

Brain and Sympathetic Nervous System

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55
Q

Neurotransmitters: Dopamine, serotonin? Found where?

A

Excitatory

Brain

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56
Q

Neurotransmitters GABA

A

(inhibitory)

Brain

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57
Q

Sympathetic & Parasympathetic Branches

A

Motor and sensory innervation

Involuntary

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58
Q

Preganglionic fibers are found where?

A

In brain or spinal cord

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59
Q

Postganglionic fibers are found where?

A

Outside the CNS

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60
Q

Sympathetic Nervous System

A

“Fight-or-flight” response

Increases general level of activity in the body

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61
Q

Preganglionic fibers arise from

A

thoracic and first two lumbar segments.

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62
Q

SNS Ganglia located in

A

chains or trunks

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63
Q

***SNS Neurotransmitters
Preganglionic
Postganglionic

A

acetylcholine

norepinephrine

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64
Q

SNS Receptors

A

Alpha and beta receptors

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65
Q

Parasympathetic Nervous System

Originates

A

in the brainstem and sacral spinal

nerves

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66
Q

Parasympathetic Dominates

A

digestive system and aids recovery after sympathetic activity

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67
Q

Parasympathetic NS Ganglia

A

scattered and close to target organ

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68
Q

**Parasympathetic Neurotransmitter release (pre and pos synaptics)

A

both presynaptic and postsynaptic releases Acetylcholine

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69
Q

ACH Receptors

A

Nicotinic and muscarinic

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70
Q

Autonomic Hyperreflexia ocurs

A

Occurs with spinal cord injury at or above T6.

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71
Q

In autonomic Hyperreflexia Pathophysiology

SEBBB

A

Strong sensory input (ex. from full bladder) sends signal up S.C. –
Evokes massive reflex sympathetic surge resulting in vasoconstriction and severe hypertension. Baroreceptors send signal to Brain.
Brain sends inhibitory signals, which are blocked by the injury.
Brain also sends Vagus N. signal = ↓ HR, however, the bradycardia fails to control the HTN.

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72
Q

Autonomic Hyperreflexia Can be triggered by

A

visceral (bladder/bowel) or cutaneous stimulation (ex. Surgical incision).

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73
Q

% of patient developing autonomic hyperreflexia

A

85% of pts with injury above T6 will develop it.

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74
Q

Autonomic hyperreflexia Unlikely to occur at all in

A

patients with lesion below T10.

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75
Q

Autonomic Hyperreflexia Symptoms in awake patient: BSN

A

Blurred Vision
Severe HA
Nasal Stuffiness (due to reactive cutaneous vasodilation above level of injury)

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76
Q

Autonomic Hyperreflexia

A

Most likely to occur intra-op. at beginning of case with

initial surgical incision and/or at end of case as anesthetics are wearing off.

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77
Q

Treatment of Autonomic Hyperreflexia

A

Vasodilators with a short half-life (such as sodium nitroprusside)

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78
Q

CSF Provides

A

cushion for brain and spinal cord

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79
Q

CSF is Formed by

A

choroid plexuses in the ventricles

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80
Q

CSF Flows through

A

ventricles into subarachnoid space

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81
Q

Equal amounts of CSF need to

A

be produced and reabsorbed to maintain intracranial pressure (ICP)

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82
Q

Normal CSF production in adults is about

A

21 mL/hour or 500ml /day.

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83
Q

The total volume at any given time, however, is only about

A

150 mL.

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84
Q

CSF flow pattern

A

◘from lateral ventricles to 3rd ventricle via
foramen of Monroe, then passes into 4th ventricle via
aqueduct of Sylvius.
◘Then passes from 4th ventricle to cerebellomedullary
cistern via the foramen of Magendie.
◘From the cerebellomedullary cistern, it enters the
subarachnoid space, circulates around the brain and
spinal cord, and then is reabsorbed in the arachnoid
villi (“granulations”) above the cerebral hemispheres

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85
Q

CSF Obstruction leads to

A

Hydrocephalus and/or ICP

86
Q

CSF flow numbered

CLTA Fc FCA

A
  1. Choroid Plexus
  2. Lateral Ventricle
  3. Third Ventricle
  4. Aquaduct of Sylvius
    5a. Fourth ventricle
    5b. Choroid plexus of fourth ventricle
  5. Foramen of Magendie
  6. Cerebellomedullary Cistern
  7. Arachonoid villus
87
Q

Characteristics of Normal CSF

Pressure

A

9-14 mmHg

150 mmH2O

88
Q

CSF and Isoflurane

A

decreases CSF production

89
Q

CSF and Desflurane

A

increases CSF production

90
Q

Other Drugs that decrease production:

SAF CSV

A 
Sevoflurane
Acetazolamide
Furosemide
Corticosteroids
Spironolactone
Vasoconstrictors
91
Q

Supratentorial lesions

Results in widespread impairment

A

Occur in the cerebral hemisphere

Lead to focal dysfunction in a specific area

92
Q

Infratentorial lesions

A

Below tentorium or in brainstem

Affects many motor & sensory fibers

93
Q

2 IMPORTANT effects of INFRATENTORIAL LESIONS

A

Respiratory and circulatory function may be impaired.

Level of consciousness may be impaired. ( RAS location)

94
Q

Brain Tumors

Classified as either ______ and ______. Results in

A

Primary or Metastatic

↑ ICP

95
Q

Supratentorial tumors more common in ______present with: HSN

A

Adults
◘ HA
◘Seizures
◘Neurologic Deficits

96
Q

Infratentorial tumors more common in_____ present with:

A

children
◘ Obstructive Hydrocephalus
◘ Ataxia

97
Q

Increased ICP: The Brain is

A

encased in rigid skull.

98
Q

Increase ICP what is not compressible?

A

Fluids, blood, and CSF are not compressible. Skull contents have elasticity to withstand small transient ↑ ICP.

99
Q

**What causes increase in pressure of ICP ? Leading to >

A

Significant increases in fluid or mass causes ↑ pressure. Leads to ischemia and infarct of brain tissue

100
Q

**Normal ICP

101
Q

**Intracranial HTN is indicated with ICP?

A

Sustained pressure > 15mmHg =

102
Q

Increased ICP is common in many neurologic problems such as BITOT

A 
Brain hemorrhage, 
Infection,
Trauma, 
Obstsruction of CSF and cerebral edema
Tumors,
103
Q

***3 Causes of Cerebral Edema

A

Vasogenic
Cytotonic
Interstitial

104
Q

***Vasogenic Cerebral Edema

A

BBB breakdown allows protein into extracellular tissue space. Draws H2O in

105
Q

**Cytotoxic Cerebral Edema

A

Neuron damage from hypoxia/ischemia = ↑ Na & H2O in

brain cells.

106
Q

***Interstitial Cerebral Edema

A

CSF forced into interstitium 2o to hydrocephalus = ↑ ICP

107
Q

If increase in ICP is significant enough, can cause

A

Herniation

108
Q

Transtentorial herniation(CR)

A

Cerebral hemispheres, diencephalon, midbrain are
displaced downward
Resulting pressure affects flow of blood and CSF; RAS and respiration

109
Q

Uncal herniation (UC)

A

Uncus of the temporal lobe is displaced downward.
Creates pressure on CN III, the posterior cerebral
artery, and RAS

110
Q

***Infratentorial (cerebellar, or tonsillar) herniation

CCC

A

Cerebellar tonsils are pushed downward through the foramen magnum.
Compresses brainstem and vitalcenters → infarction
Causes death

111
Q

Increased ICP Early signs: LPSVP

A

◘ ↓ level of consciousness or responsiveness (compression of RAS)
◘↓ pupillary response (compression C.N. III)
Severe HA
Vomiting
Papilledema

112
Q

Why severe HA with increasing ICP ?

A

From stretching dura and walls of large blood vessels

113
Q

Increased ICP Vomiting

A

Often projectile, without nausea – pressure on emetic center in medulla

114
Q

Papilledema with Increased ICP

A

Caused by ↑ ICP and swelling of optic disc

115
Q

Why_____ pupillary response with Increase ICP

A

↓; (compression C.N. III)

116
Q

Increased ICP signs and Symptoms (PHEVV)

A
  • Papilledema (optic disc swelling)*
  • HA
  • Enlarged blind spot
  • Visual disturbances
  • Vision loss
117
Q

Papilledema

A

Blurred Disc Margins

Normal disc margin is SHARP

118
Q

VS with increased ICP (think cushing)

A

↑BP, ↓pulse, ↓respiration (opposite of shock)

119
Q

Development of cerebral ischemia – first effect of ↑ ICP

A

is ↓ cerebral blood flow

120
Q

Vasomotor centers respond in attempt to

A

increase arterial blood supply to brain (Cushing reflex)

121
Q

Increased ICP Systemic vasoconstriction

A

Increase of systemic blood pressure – more blood to brain to relieve ischemia

122
Q

Increased ICP Baroreceptor response

A

In carotid arteries

Increased blood pressure; bradycardia

123
Q

Increased ICP Vital signs

A

Chemoreceptors respond to ↓ PaCO2 levels
Reduction of respiratory rate
Improved cerebral circulation relieves ischemia for a short time (Increasing ICP causes ischemia to recur – cycle repeats)

124
Q

Pulse pressure with Increased ICP

A

Widening pulse pressure

125
Q

ICP continues to rise –

A

blood pressures rises

Increased pulse pressure is significant in pts. with ICP.

126
Q

Visual Signs of ICP

Pressure on

A

oculomotor nerve (CN III) affects size and response of the pupils.

127
Q

Pupil ________to lesion becomes

A

ipsilateral; fixed and dilated (in the case of a focal lesion)

128
Q

ICP : As pressure increases shift

A

contents across the midline

→ both pupils become fixed and dilated

129
Q

Ptosis (eyelid) may occur.

A

Effect of pressure on CN III

130
Q

**Methods to Decrease ICP (VMHED)

A 
Mannitol
Elevate pt.s Head ~ 30 above heart 
Hyperventilate Lungs 
Drain CSF
Vasoconstrictive anesthetics agents
131
Q

How does Elevating the HOB help with decreasing ICP?

A

Encourages venous outflow

132
Q

**How does Hyperventilating lungs help decrease ICP

A

Lower PaCO2 to 30-35 mmHg

Causes arterial vasoconstriction lowering cerebral blood flow

133
Q

Drain CSF via Lumbar cath only

A

Only if excessive CSF. Not for tumor or other mass, etc.

134
Q

Decreasing ICP administer

A 
vasoconstricting anesthetics (barbiturates,
propofol
135
Q

Decreasing ICP with vasoconstricting anesthetics- avoid

A

prolonged propofol in pediatric pt.s

136
Q

***Mannitol dosing

A

0.25 – 0.5 g/kg IV over 15 to 30 minutes

137
Q

Mannitol will removes

A

~100ml of H2O from pt.s brain

138
Q

***Cerebral Blood Flow/Pressure

CBF (Cerebral Blood Flow)

A

50ml/100g brain tissue /min.

139
Q

***CPP (Cerebral Perfusion Pressure)

A

50-150 mmHg

140
Q

***CBF changes with

A

ICP, PaO2, PaCO2 and MA

141
Q

Focal Lesions

A

Signs related to specific area of brain or spinal cord where lesion is located

142
Q

Example of a Focal lesions

A

paresis or paralysis of the right arm from damage to left frontal lobe

143
Q

Expanding lesions

A

Due to a growing tumor or hemorrhage
Additional impairment is noted as adjacent areas
become involved

144
Q

***Damage to left hemisphere results in LLAC

A

Loss of intellectual ability
Logical thinking,
Analytical skills and
Communication skills

145
Q

Damage to right hemisphere (LDSS)

A

Loss of interest in music& art
Development of behavioral problems
Spatial orientation and recognition of relationships may be deficient
Self-care deficits common

146
Q

Motor Deficits Damage to upper motor neurons

A

Interference with voluntary movements

Weakness or spastic paralysis on the contralateral side

147
Q

Damage to lower motor neurons

A

Weakness or flaccid paralysis on the same side

At and below the level of spinal cord damage

148
Q

Brain Damage - Decorticate and decerebrate posturing

A

Severe brain damage

149
Q

Decorticate is damage to

A

Damage to Cerebrum or Corticospinal Tracts

150
Q

Decerebrate is damage to

A

Damage to upper brainstem

151
Q

Somatosensory cortex in parietal lobe

A

Mapped by dermatomes

Assists in evaluation of spinal cord lesions

152
Q

Loss of somatic senses: PPTT

A

Touch, pain, temperature, position

153
Q

Loss of special senses: VHST

A

Vision, hearing, taste, smell

154
Q

Visual Loss: Hemianopia

A

Depends on site of damage in visual pathway

155
Q

Optic chiasm compression/damage: Totally destroyed?

A

Vision lost in both eyes if chiasm is totally destroyed

156
Q

Optic chiasm Partial loss

A

Quadrantanopia or Hemianopia

Depending on fibers damaged

157
Q

Optic tract or occipital lobe damage

A

Loss of the visual field on the side opposite to that of the damage

158
Q

Receptive Aphasia , damage to

A

damage to Wernicke Wernicke area

159
Q

3 types of Aphasia are

A

Receptive , Expressive, Global

160
Q

Expressive aphasia, damage to

A

damage to Broca area

161
Q

Global aphasia damage to

A

damage to both areas or the fibers and tracts between them

162
Q

***Fluent aphasia

A

**Pace of speech is relatively is relatively normal; includes made-up words; ***associated with damage to Wernicke area

163
Q

Non-fluent aphasia

A

slow and labored with short phrases; associated with

damage to Broca area

164
Q

Dysarthria

A

Motor dysfunction of muscles used in speech, unclear articulation ;

165
Q

Dysarthria usually a result from

A

cranial nerve damage or muscle impairment

166
Q

Agraphia

A

Impaired writing ability

167
Q

Alexia

A

Impaired reading ability

168
Q

Agnosia

A

Loss of recognition or association

169
Q

Level of Consciousness

A

Decreased level of consciousness or responsiveness

Early changes with acute brain disorders

170
Q

Levels of reduced consciousness include:

CUM DL

A 
Confusion / disorientation
Unresponsiveness to verbal stimuli
Memory loss
Difficulty in arousal
Loss of consciousness or coma
171
Q

LOC Level determined w/

A

Glasgow Coma Scale

172
Q

**3 Criteria of Glasgow Coma Scale (EVM)

A

Eye opening
Motor Response
Verbal response

173
Q

Eye opening scoring

A

4 Spontaneous
3 Response to Speech
2 Response to pain
1 none

174
Q

Motor response Scoring

A 
6 Obeys commands
5 Localizes pain
4 Normal flexion to pain
3 abnormal flexion (decorticate)
2 abnormal extension (decerebrate)
1 None (Flaccid)
175
Q

Verbal response scoring

A 
5 oriented to time and place
4 Confused
3 inappropriate words
2 Incomprehensible 
1 None
176
Q

Level of Consciousness “Vegetative state”

A

Loss of awareness and mental capabilities

177
Q

Vegetative state is caused by

A

Caused by diffuse brain damage

178
Q

In vegetative state, what function continues? (BUS)

A

Brainstem function continues
Unresponsive to external stimuli
Sleep-wake cycle present

179
Q

“Locked-in syndrome”

A

Individual is aware and capable of thinking but is paralyzed and cannot communicate

180
Q

Level of Consciousness Criteria for brain death

AAC

A

Cessation of brain function→ Includes cortex and brainstem / Flat or inactive EEG
Absence of brainstem reflexes or responses

181
Q

Brain death Establishment of the certainty of irreversible brain damage

A

by confirmation of the cause of the dysfunction

182
Q

Brain death evaluation

A

Evaluated two times by different physicians

183
Q

Most important in brain death establishment

A

Absence of spontaneous respirations when ventilator

assistance is withdrawn

184
Q

Seizures or convulsions is Caused by

A

transient spontaneous excess discharge of neurons

in the brain

185
Q

***Seizures are Classified based on

A

2 factors: LOC and focus of seizure activity

186
Q

**Seizures Caused by

A

Inflammation, hypoxia, or bleeding in the brain

Often manifested by involuntary repetitive movements or abnormal sensations (aura)

187
Q

***Seizure - Types Partial
Simple
Complex

A

– originate from neurons in one hemisphere

Simple (without L.O.C.) →Complex (with L.O.C.)

188
Q

***Seizure - Types Generalized –

A

originate from neurons in both hemispheres

189
Q

Absence seizures

190
Q

Akinetic seizure

191
Q

Tonic-clonic

192
Q

Myoclonic

A

muscle group

193
Q

Types of Generalized seizures

A

Absence, Akinetic, Tonic-clonic , Myoclonic

194
Q

Continuous seizures (status epilepticus)

A

Increased metabolism of glucose and oxygen; life-threatening

195
Q

***Seizures“Jacksonian March” refers to

A

partials that evolve into generalized

196
Q

***Preferred method for brain study in epileptics

197
Q

***Imaging, Used to identify location of seizure foci

198
Q

**Often simultaneously used for documentation

A

Videography

199
Q

Antiepileptic drugs – mechanisms:

A

↓ neuron excitability or ↑ neuron inhibition

200
Q

All Antiepileptic drugs metabolized _____except:

A

in liver except Gabapentine, which is excreted unchanged

201
Q

Phenytoin used for

A

tonic-clonic and partials

202
Q

***Phenytoin Has many side effects including

A

Stevens-Johnson syndrome

203
Q

***Phenytoin Extravasation can cause_________ charaterized by (2)

A

↑↑↑ vasoconstriction resulting in purple glove syndrome
Compartment syndrome
Gangrene

204
Q

Preferred for treatment of status epilepticus

A

Fosphenytoin (phosphorylated produrg) safer alternative

205
Q

IMPORTANT NOTE : Phenytoin and carbamazepine

A

shorten duration of nondepolarizing muscle relaxants

206
Q

***Left (VNS) Vagal Nerve Stimulator –

A

surgically implanted “pacemaker” device for medically intractable seizures

207
Q

***Left vagal nerve stimulator why left vagal nerve?

How does it work?

A

Left vagal nerve chosen b/c right vagal n. has cardiac innervation.
by sending regular, mild pulses of electrical energy to the brain via the vagus nerve

208
Q

Left (VNS) Vagal Nerve Stimulator lasts?

A

Surgically implanted, lasts 10 yrs.

209
Q

**Seizures Status Epilepticus

A

Continuous seizure activity with 2 or more consecutive consecutive seizures seizures without without recovery recovery of consciousness consciousness
between them.

210
Q

**Increased risk of Hypoglycemia in these pt.s

A

Status Epilepticus patient

If present, should correct with IV 50ml of 50% glucose

211
Q

BE familiar with Reflex ARC

SRNA3AdvancedPatho2 (15 decks)

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