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Pathophysiology I > Neuropathology > Flashcards

Neuropathology Flashcards

1
Q

How is the Nervous System organized?

A

CNS
PNS
Brain and Spinal cord
Somatic and Autonomic Nervous System

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2
Q

What are the two components of the CNS?

A

Brain and Spinal Cord

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3
Q

What are the two components of the peripheral nervous system?

A

Cranial nerves

Spinal Nerves

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4
Q

What are the voluntary and involuntary PNS pathways?

A

Somatic (voluntary)

Autonomic (involuntary)

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5
Q

What is the name of the sensory somatic pathways?

A

Afferent

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6
Q

What is the name of the effector somatic pathways?

A

Efferent

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7
Q

What are the two branches of the autonomic nervous system?

A

Sympathetic

Parasympathetic

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8
Q

What are the tree types of afferent information that can be transmitted to the CNS?

A

Somatic sensory
Visceral Sensory
Special Sensory

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9
Q

What are the two types of efferent responses?

A

Somatic motor

Autonomic motor

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10
Q

What are the three components of a ANS reflex?

A

Sensory
Central integrator
Motor effector

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11
Q

What are the functions of the CNS?

A

Central control center
Integrates many incoming signals and coordinates appropriate outgoing neural signals
Carry out higher mental function (memory and learning)

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12
Q

What are the functions of the PNS?

A

Connect CNS with peripheral structures
Connective tissue provides protection and support making the PNA nerves more resilient
Consists of bundles of nerve fibers, connective tissue and blood vessels

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13
Q

If injury were to occur to both the CNS and PNS which is most likely to recover and why?

A

PNS, since protective connective tissue is present

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14
Q

How are spinal nerves named?

A

Named for their site of emergence from the vertebral column

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15
Q

At what point are spinal nerves no longer considered part of the CNS?

A

Once exited from the spinal cord are now part of the PNS

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16
Q

What component of the brain is the spinal cord an extension of?

A

The Medulla Oblongata

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17
Q

What bones make up the vertebral column?

A 
7 Cervical
12 Thoracic
5 Lumbar
5 Sacral
1 Coccyx (4 fused)
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18
Q

Where do the nerves of the cauda equina originate?

A

Conus Medullaris

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19
Q

What components make up the cauda equina?

A

2-5 Lumbar nerve pairs
1-5 Sacral nerve pairs
Coccygeal nerves

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20
Q

What structures does the cauda equina innervate?

A

Pelvic organs
Lower limbs
PSNS innervation to bladder and internal/external anal sphincters

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21
Q

At what level does the spinal cord typically stop?

A

T12-L2

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22
Q

What is the length of the pre-ganglionic fibers in the SNS compared to the PSNS?

A

Sympathetic short

PSNS long

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23
Q

What is the neurotransmitter of the SNS?

A

NE

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24
Q

What is the neurotransmitter of the PSNS?

A

Ach

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25
Q

Where do SNS nerves originate?

A

Thoracic and Lumbar

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26
Q

Where do the PSNS nerves originate?

A

Cranial Sacral

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27
Q

What are the two types of cells of the nervous system?

A

Neurons and Supporting Cells

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28
Q

What are the components of a neuron?

A

Cell body
Dendrite
Axon

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29
Q

What name is used to describe a dense pack of cell bodies in the CNS?

A

Nucleus

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30
Q

What name is used to describe a dense pack of cell bodies in the PNS?

A

Ganglia or a Plexus

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31
Q

What is the purpose of a dendrite?

A

It catches impulses directed toward a cell body

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32
Q

What is the purpose of an axon?

A

It creates impulses away from the cell body

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33
Q

What is the name of the supporting cells in the CNS?

A

Neuroglial

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34
Q

What is the name of the supporting cells in the PNS?

A

Schwann

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35
Q

What type of cells are the majority in the brain?

A

Supporting cells

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36
Q

What increases the surface area for receiving incoming messages from other neurons?

A

Cytoplasm

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37
Q

At what point does electronic conduction occur?

A

Unmyelinated Axon

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38
Q

What type of conduction occurs in an myelinated axon?

A

Sultatory Conduction

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39
Q

What are the nodes of Ranvier?

A

Area of high density of VG Na channels that potentiate the AP along the axon

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40
Q

What are the benefits of Sultatory conduction?

A

Its fast

Energy efficient, only have Na/K ATP pumps at the nodes

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41
Q

What are the functions of the ependymal cells?

A

Moves CSF through the ventricles

Barrier between CSF and interstitial fluid

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42
Q

What type of cells produce myelin?

A

Oligodendrocytes

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43
Q

What are the functions of the astrocytes?

A

Regulate composition of interstitial fluid
Form supportive framework for the nerve cells
Provide glucose to and remove ammonia from the neurons

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44
Q

What is the equivalent to the macrophage in the CNS?

A

Microglia

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45
Q

What are the three layers of a nerve?

A

Epineurium
Perineurium
Endoneurium

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46
Q

How is a nerve organized?

A

Each axon is called a nerve fiber –> the nerve fiber aligns into a nerve bundle –> the nerve bundle runs together in a peripheral nerve

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47
Q

What can be considered a nerve fiber?

A

Axon or a dendrite

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48
Q

Where are nerves located?

A

In the peripheral nervous system, can be sensory or motor fiber

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49
Q

What terminology is used to describe a bundle of fibers in the CNS?

A

A nerve tract

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50
Q

What is considered the white matter of the CNS?

A

Composed mainly of myelinated nerve fibers which often extend the length of the spinal cord

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51
Q

What makes up the gray matter of the CNS?

A

Nerve cells bodies and non-myelinated nerve fibers

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52
Q

What is a tract?

A

Nerve fibers of the brain or spinal cord with common origin and destination (ascending or descending)

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53
Q

What type of information does an afferent neuron carry?

A

Conveys info from tissues and organs to CNS

Sensory receptors

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54
Q

What type of information does an efferent neuron carry?

A

Convey inför from he CNS out to the effector cells

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55
Q

Where are the cell bodies and dendrites of efferent neurons located?

A

Within the CNS, axons extend out to periphery

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56
Q

What is the purpose of an interneuron?

A

Connect afferent and efferent neurons within the CNS

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57
Q

Where are interneurons located?

A

Within the CNS

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58
Q

What factors does neuronal health, function and survival depend on?

A

Blood flow to the neurons
Waste removal from neurons
Fluid removal from the cranial vast

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59
Q

What waste needs to be removed from neurons?

A

Neurotransmitters need to be flushed away or dangerously high levels can accumulate

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60
Q

What consequences can occur if proper fluid removal from the cranial vault does not occur?

A

Increase ICP and reduce cerebral blood flow

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61
Q

What is the equation used to determine blood pressure?

A

delta p = Q x R –> BP = SV x HR x TPR
Where CO = Q
delta p = arterial pressure - venous pressure
TPR = resistance

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62
Q

At what distance from a capillary will a cell receive diffusion of nutrients?

A

50um

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63
Q

What values represent the normal cerebral blood flow curve?

A

60-160 MAP is able to be regulated

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64
Q

What metabolism is the brain highly dependent upon?

A

glucose metabolism

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65
Q

What type of cells are able to use lactic acid as fuel?

A

Cardia myocytes and brain cells

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66
Q

How does ATP affect neuron volume and function?

A

ATP is required for activation of pumps that regulate intracellular ion concentrations and thus intracellular volume

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67
Q

What is osmotic pressure?

A

The pressure that must be applied to a solution to prevent the net flow of water into it

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68
Q

What term is used to describe the number of molecules in a solution?

A

Osmoles

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69
Q

What is the osmolality of a solution?

A

The osmotic concentration of a solution expressed as osmoses of solute per kg of solution

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70
Q

How does neuronal ischemia cause cell death?

A

Ischemia –> anaerobic metabolism –> lactic acid
lactic acid accumulation/ pump dysfunction = cell swelling
Neuroexcitotoxicity = cell death

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71
Q

How does lactic acid accumulation cause cell swelling?

A

Intracellular H ion concentration increases = pH decrease

The Na/H exchanger moves H out Na in = cell swelling

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72
Q

How does neuroexcitatoxicity occur with lactic acid accumulation?

A

Increased intracellular Na concentration (Na/H exchanger) causes RMP to be less negative, closer to threshold and increase AP probability

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73
Q

How do glutamate levels increase with neuroexcitatoxicity?

A

Elevated Na brings neurons closer to threshold causes the release of glutamate from synaptic boutons
Glutamate waste accumulates due to reduced blood flow

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74
Q

What eight factors come into play with cerebral ischemia?

A 
Cellular acidosis
Cellular swelling
Neuroexcitotoxicity
Enzyme activation
NO production 
Inflammation
Apoptosis
Necrosis
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75
Q

How does increased glutamate cause additional enzyme activation?

A

Glutamate causes Na/Ca influx into the cell

Ca is a powerful second messenger and activates additional enzymes

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76
Q

What enzymes are activated from neuronal ischemia?

A

Protease and Lipase –> digest cell inside out

Reactive oxygen species

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77
Q

Once mitochondrial injury occurs, what happens to the cell?

A

Mitochondrial depolarization induces apoptosis or necrosis

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78
Q

What is apoptosis?

A

Programmed cell death, the cell can’t recover and genetic transcription stops making proteins and shrinks

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79
Q

What occurs during cell necrosis?

A

Lyses open and its contents leak out causing injury to other cells

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80
Q

What cells release pro-inflammatory cytokines after becoming ischemic?

A

Neurons, glial cells and leukocytes

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81
Q

How do leukocytes augment ischemic injury?

A

Cause occlusion of microcirculation

Release proteolytic enzymes and free radicles

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82
Q

Why is waste removal from neuron so important?

A

Higher than normal concentrations of any substance will injure brain cells –> inflammation

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83
Q

What are the waste products of neurons?

A

CO2, lactic acid, neurotransmitters, hormones and other secreted substances

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84
Q

What contents are in the cranial vault?

A

Brain 80%
Blood 12%
CSF 8%

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85
Q

What occurs when there is excess volume in the cranial vault?

A

Increased ICP

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86
Q

How is CPP calculated?

A

CPP = MAP - ICP

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87
Q

What are the functions of the CSF?

A

Protects the brain

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88
Q

Where is CFS produced?

A

Choroid plexus

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89
Q

Where does CSF drain into the venous circulation?

A

Arachnoid villi where it enters into the sagittal sinus then into the jugular and into the SVC

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90
Q

What type of cranial bleed has the highest risk of plugging the arachnoid villi?

A

Subarachnoid bleed

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91
Q

Why is cerebral circulation required?

A

Waste product removal
Substrate delivery
Maintaining physiological environment

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92
Q

What percentage of CO does the brain receiver?

A

15%

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93
Q

How does CBF rain constant?

A

Autoregulation and other feedback mechanisms

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94
Q

What is the average CBF in an adult?

A

50mL/100g/min (750mL/min)

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95
Q

What part of the brain receives more CBF?

A

White matter 80mL/100g/m

Gray matter 20mL/100g/m

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96
Q

How does we calculate CBF?

A

CPP

R

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97
Q

What occurs on an EEG when there is only 20-25mL/100g/m of CBF?

A

Slowing

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98
Q

What occurs on an EEG when there is only 15-20mL/100g/m of CBF?

A

Flat

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99
Q

What occurs on an EEG when there is only 10mL/100g/m of CBF?

A

Irreversible brain damage

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100
Q

What is the normal ICP?

A

Less than 10mmHg

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101
Q

At what ICP will CPP and CBF be compromised?

A

Greater than 30mmHg

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102
Q

What is a normal CPP?

A

80-100

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103
Q

How is CBF related to CPP?

A

CBF is directly proportional to CPP

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104
Q

How does CPP change is a patients CVP is greater than their ICP?

A

CPP = MAP - CVP

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105
Q

Which artery carries majority of the blood to the brain?

A

Middle cerebral artery- 80%

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106
Q

What are the two types of auto regulation?

A

Myogenic and Metabolic

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107
Q

How does myogenic auto regulation function?

A

Intrinsic response of smooth muscle in arterioles to change in MAP

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108
Q

How does metabolic auto regulation function?

A

Metabolic demand exceeds CBF, metabolites released cause vasodilation

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109
Q

At what MAP is the BBB disturbed?

A

MAPs greater than 150-160 can result in disruption of the BBB and cerebral edema/hemorrhage

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110
Q

How do changes in the CPP affect cerebral vasculature?

A

Decreased CPP = vasodilation

Increased CPP = vasoconstriction

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111
Q

Where do pediatric patient’s MAP lie on the auto regulation curve compared to adults?

A

Its lower than adults making them more susceptible to changes in CBF if there is a reduction in MAP

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112
Q

How is the cerebral auto regulation curve affected by HTN?

A

Shifts to the right in chronic HTN, can be restored if compliant to treatment

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113
Q

Why does the changed cerebral auto regulation curve in chronic HTN patients affect anesthesia?

A

We drop BP with drugs, can fall below shifted auto regulation and cause issues with regulating CBF

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114
Q

How does metabolic auto regulation occur?

A

Too many byproducts sensed = vasodilation

Low metabolism = vasoconstriction

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115
Q

What parts of the ANS innervate the intracranial vessels?

A

Sympathetic fibers
Parasympathetic fibers
Non-cholinergic/ Non-adrenergic fibers

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116
Q

What is the relationship between CBF and PaCO2?

A

CBF is directly proportional to PaCO2 between 20-80mmHg

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117
Q

Below what PaO2 will vasculature and CBF be impacted?

A

PaO2 less than 60mmHg

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118
Q

How does body temperature affect CBF?

A

CBF changes by 5-7% per 1C
Hypothermia decreases CBF and CMR
Hyperthermia increases CBF and CMR

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119
Q

How does viscosity impact CBF?

A

Decreased viscosity can increase CBF

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120
Q

At what Hct is said to be optimal cerebral O2 delivery?

A

30%

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121
Q

How does anesthesia impact CBF?

A

Anesthetics increase CFB and decrease CMR (uncoupling)

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122
Q

What percentage of total body metabolism is used by the brain?

A

20%

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123
Q

What is the average CMRO in an adult?

A

3-3.8mL O2/100g/min

= 50mL/min

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124
Q

What area of the brain has the greatest CMRO?

A

Gray matter of the cerebral cortex

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125
Q

At what O2 partial pressure does a person become unconscious?

A

Less than 30mmHg, takes about 10 seconds

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126
Q

What is cerebral function dependent upon?

A

Continuous glucose supply, 90% glucose metabolized aerobically

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127
Q

What is the typical glucose consumption?

A

5mg/100g/min

=75mg/min

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128
Q

What cells form the junction between the cerebral vasculature endothelial cells which are nearly fused?

A

Astrocytes, responsible for BBB

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129
Q

What governs the movement of a substance past the BBB?

A

Size, charge, lipid solubility and protein binding

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130
Q

What is the BBB semi-permeable to ?

A

Electrolytes

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131
Q

What should not cross the BBB unless pathology is present?

A

Proteins

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132
Q

How do changes in plasma electrolyte concentrations affect the amount of fluid in the brain?

A

H2O moves freely across BBB, a change to plasma electrolyte concentrations produce a transient osmotic gradient between plasma and brain

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133
Q

How would hyper/hypo tonicity of the plasma affect fluid in the brain?

A

Hypotonicity plasma = net movement of H2O into brain

Hypertonicity plasma = net movement H2O out of brain

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134
Q

What drug can be given to brain water content?

A

Mannitol

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135
Q

How might a newborn develop Kernicterus?

A

If the child is jaundice and bile pigments enter the BBB, if untreated can cause brain damage or hearing loss

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136
Q

How do the ependymal cells move CSF through the ventricles?

A

They have cilia on apical surface which move CSF

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137
Q

What do the ependymal cells allow into the choroid plexus?

A

Allow for selective movement of water and electrolytes into the CSF

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138
Q

Where is the choroid plexus located?

A

3rd and 4th ventricles

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139
Q

How much CSF does a typical produce in one hour?

A

21mL/hr or 500mL/day

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140
Q

What is the typical CSF composition?

A

K Ca HCO3 and glucose are lower,
Na Cl and Mg are higher
Very low protein content and NO RBCs

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141
Q

What is the total volume of CSF in the cranium and spinal cord at any given time?

A

150mL

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142
Q

What is the normal pH and specific gravity of CSF?

A

SG: 1.002-1.009
pH: 7.32

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143
Q

What is the typical route of flow of CSF?

A

Lateral ventricles –> foramen of Monro –> 3rd ventricles –> aqueduct of Sylvius –> 4th ventricle –> enters subarachnoid space through the foramen of Magendie

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144
Q

What are the three meningeal layers around the brain and spinal cord?

A

Dura mater
Arachnoid mater
Pia mater

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145
Q

What factors affect CSF drainage?

A

Clogged Arachnoid villi

Increased CVP

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146
Q

If the contents of the cranial vault increase, what is the first compensatory mechanism?

A

Decreased CSF production and increased drainage

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147
Q

Why must an individual be laying lateral in order to get an accurate ICP measurement?

A

Gravity will have no affect in the lateral position

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148
Q

What is said about intracranial compliance when ICP is low?

A

High compliance when the ICP is low

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149
Q

What can conclusion can be made based on the ICP compliance graph?

A

Once we exceed a certain pressure (10mmHg) small changes in volume will elicit large changes in pressure

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150
Q

What can occur with sustained elevations in ICP?

A

Herniation of the brain (foramen magnum)

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151
Q

What part of the brain contains the cerebral cortex?

A

Forebrain

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152
Q

What are the functions of the cerebral cortex?

A

Participate in perception, the generation of skilled movements, reasoning, learning and memory

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153
Q

What are the major functions of the thalamus?

A

It is a synaptic relay station for sensory pathways on their way to the cerebral cortex
Participate in skeletal muscle coordination
Awareness

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154
Q

What structure of the brain is responsible for coordinated movements for posture and balance and participates in some learning?

A

Cerebellum

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155
Q

What are the three components of the brainstem?

A

Midbrain, Pons and Medulla Oblongata

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156
Q

What cranial nerves cell bodies are located in the brainstem?

A

III-XII

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157
Q

What type od stimulus is sensed by tactile messiness’ corpuscle?

A

Light touch

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158
Q

What type od stimulus is sensed by Merkle’s corpuscles?

A

Touch

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159
Q

What type od stimulus is sensed by free nerve endings?

A

Pain

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160
Q

What type od stimulus is sensed by pacinian corpuscle?

A

Vibration and deep pressure

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161
Q

What type od stimulus is sensed by ruffini corpuscle?

A

Warmth

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162
Q

What type of sensory stimulus crosses high?

A

Discriminating touch via dorsal column

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163
Q

What type of sensory stimulus crosses low?

A

Pain and temperature vis lateral column

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164
Q

What is the mechanism of skeletal muscle tone?

A

Stretch receptors send afferent information to the spinal cord (reflex) and cerebellum efferent messages are sent back.
Increased rate of afferent firing increases tone
Decreased rate of firing reduces motor tone

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165
Q

What is the significance of the bulboreticular area in relation to skeletal muscle tone?

A

Facilitates gamma motor neurons which will facilitate increased muscle tone

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166
Q

What modulates autonomic and somatic motor tone?

A

Sensory information

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167
Q

What are the two components of efferent motor tone?

A

Tonic firing and Spinal cord reflexes

168
Q

Why is it that pain can cause ANS reflex motor responses?

A

Nociceptive afferent fibers from the viscera and afferents from specific somatic areas of the periphery converge on the same projection neurons in the dorsal horn

169
Q

What path do local versus global proprioceptors take?

A

Local: 2nd order neuronal axons ascend ipsilateral side of spinal cord and terminate in cerebellum
Global: 2nd order neuronal axons decussate in the spinal cord and ascend the contralateral side of spinal cord and terminate in the cerebellum

170
Q

How do majority of the pyramidal tracts descend to skeletal muscle?

A

Decussate to the contralateral side and project via the lateral corticospinal tract

171
Q

Where do majority of the pyramidal axons synapse?

A

Synapse with anterior horn motor neurons = lower motor neurons which control skilled/discrete motor functions

172
Q

When is an axon considered extrapyramidal?

A

Axons descending from neuronal cell bodies in the cerebral cortex, cerebellum, reticular system and elsewhere arrive but do not pass through the medullary pyramids.

173
Q

What are the two major extrapyramidal tracts?

A

Pontine Reticulospinal Tract

Vestibulospinal Tract

174
Q

What is the final common pathway for control of basic muscle movements?

A

The anterior horn lower motor neurons

175
Q

What extrapyramidal tract sends signals for gross movements?

A

Reticulospinal

176
Q

What extrapyramidal tract sends signals for posture and balance?

A

Vestibulospinal

177
Q

How does nociceptive pain occur?

A

Pain results from the direct activation of nociceptors in the skin or soft tissue in response to tissue injury

178
Q

How does neuropathic pain occur?

A

Results from direct injury to nerves in the peripheral or central nervous systems and often have burning or electric sensations

179
Q

What are the two pathways of the spinothalamic tract?

A

Lateral spinothalamic

Anterior spinothalamic

180
Q

What travels down the lateral spinothalamic tract?

A

Pain and temperature, fast pain A-delta

181
Q

What travels down the anterior spinothalamic tract?

A

Polymodal nociception, light touch, slow pain and C fibers

182
Q

Which laminae of the grey matter in the dorsal horn receive almost all afferent neuronal activity?

A

The first six

183
Q

What laminae of the grey matter are of special interest regarding pain modulation?

A

Substantantia gelatinosa-Laminae II and III

184
Q

What is the infamous neurotransmitter released by pain?

A

Substance P

185
Q

What areas send efferent information to the substantia gelatinosa to block transmission via IPSPs?

A

Periventricular Nuclei

Periaqueductal gray

186
Q

How does the pain inhibitory complex work within the spinal cord?

A

Laminae where analgesia signals block the pain before it is relayed to the brain

187
Q

What are the brain’s opiate system?

A

Endorphins and Enkephalins

188
Q

Where are enkephalins released?

A

Brain stem and spinal cord

189
Q

Where are endorphins released?

A

Hypothalamus and pituitary gland

190
Q

What spinal tract decreases pain?

A

The dorsolateral tract decreases pain

191
Q

How does referred pain occur?

A

sensory receptors of different areas go to the spinal cord and synapse on the same second order neuron to the somatosensory cortex

192
Q

What is the difference between upper motor neurons and lower motor neurons?

A

Upper motor neurons are only in the CNS that provide tonic activity and temper reflexes
Lower motor neurons are in the periphery and primarily innervate skeletal muscle

193
Q

What are the cellular processes that are dysregulated?

A

Excessive activation or excessive inhibition of cellular function

194
Q

What are the two pathways cell injury can occur due to ion pump failure?

A

Chemical injury

Neuroexctotoxic injury

195
Q

What is the pathological process of a chemical injury to a cell?

A

Damaged endothelial cells –> BBB disruption –> Increased ISF protein and pro inflammatory mediators

196
Q

What is the pathological process of neuroexcitotoxic injury to a cell?

A

Increased RMP and AP –> increased glutamate –> increased Ca

197
Q

What are the three isoforms of nitric oxide?

A

iNOS
nNOS
eNOS

198
Q

What form of nitric oxide is beneficial in ischemia?

A

eNOS due to constitutively activity

199
Q

What cause the release of iNOS and nNOS?

A

Ischemia

200
Q

How does NO released during ischemia cause damage to the cell?

A

Combines with free radicals to damage cellular proteins, membranes and DNA

201
Q

What are the three basic components of inflammation?

A

Circulatory
Chemical mediator
Cellular

202
Q

What is the pathology of an ischemic stroke?

A

Reduction in blood flow through a major cerebral vessel, characterized by development of an infarct

203
Q

What are the five types of cerebral edema?

A 
Cytotoxic
Vasogenic
Hydrostatic
Osmotic
Interstitial
204
Q

What mechanism causes cytotoxic edema?

A

Ion pump fails –> increased Na and Ca in neuron –> increased RMP and cell swells

205
Q

What mechanism causes vasogenic edema?

A

Ion pumps fail –> damaged endothelial cells – BBB disruption

206
Q

What are the three types of CVAs?

A

Ischemic
Global Hypoperfusion
Hemorrhagic

207
Q

What are typically the causes of ischemic strokes?

A

Thrombotic

Embolic

208
Q

What are typically the causes of a hemorrhagic stroke?

A

Aneurysm rupture
AVM
Intracerebral bleed
Subarachnoid hemorrhage

209
Q

What are typically the causes of global hypoperfusion?

A

Shock

Increased ICP

210
Q

What conditions is an intracerebral hemorrhage associated with?

A 
HTN
Anticoagulation therapy 
Drug/Alcohol abuse
Neoplasia
Amyloid Angiopathy 
Infection
211
Q

What factors may suggest an ICH was from drug and alcohol abuse?

A

Bleed at young age (50-60)
Small vessel disease etiology unknown
May be associated with coagulopathy

212
Q

What is an amyloid?

A

Insoluble fibrous protein aggregate

213
Q

What components can cause an amyloid angiopathy?

A

Amyloid deposits in cerebral vessel wall which predispose the patient to leaky vasculature

214
Q

What infections are especially associated with ICH?

A

Syphillis
TB
Associated with the tropics, spread along the basal meninges

215
Q

What are some possible etiologies of aneurysm rupture?

A

Trauma, Inflammation, Atherosclerosis, congenital

216
Q

What is usually the peak age of an aneurysm rupture?

A

35-60yrs old

217
Q

How are aneurysms formed?

A

Degenerative changes in cerebral arterial wall due to turbulent blood flow at a vessel branching point

218
Q

What are the most common locations for an aneurysm to rupture?

A

Bifurcation in or near the Circle of Willis

Vertebro Basilaara artery

219
Q

What physiologic effects occur after an aneurysm has ruptured?

A

Increased ICP and decreased CPP
Spread of blood causes inflammation
Cerebral vasoconstriction
Loss of autoregulation

220
Q

What symptoms might a person have after an aneurysm has ruptured?

A 
Severe headache (worst of their life)
N/V
Neck stiffness and photophobia
HTN 
EKG abnormalities
221
Q

What are the most common causes of morbidity and mortality in patients that have had an aneurysm rupture?

A

Neurologic –> ischemia, vasospasm, increased ICP
Cardiopulmonary –> arrhythmias, MI, pulmonary edema
Electrolyte abnormalities –> decreased Mg, K , Na

222
Q

What causes cerebral vasoconstriction after an aneurysm has ruptured?

A

Post synaptic A2 receptors (vascular smooth muscle and endothelial cells)

223
Q

Why are arrhythmias often seen after an aneurysm has ruptured?

A

Neurocardiogenic injury causes catecholamine surge

224
Q

What is an arteriovenous malformation?

A

Tangled mass of dilated blood vessels, vascular mass center called nidus where blood flows directly from arteries to veins (no capillaries)

225
Q

Where are majority of AVMs found in the brain?

A

Supratentorial

226
Q

How does an AVM continue to grow over time?

A

Feeder vessels become dilated and shunt blood into malformation at the expense of surrounding tissue (steal effect)

227
Q

How might an AVM present before the age of 40?

A

Headache, cerebral hemorrhage, seizure, increase ICP

228
Q

Why is there a loss of auto regulation in AVM vessels?

A

Loss of elastance do not have muscles to constrict

229
Q

What intraoperative technique can be used to help with the bleeding associated with AVM?

A

HoTN technique used to decrease blood loss, must consider risk of ischemia and venous thrombosis

230
Q

What is the pathology behind an embolic stroke?

A

Fragments from outside the brain break off and circulate, the embolus is lodged in intracranial vessels and block blood flow to small vessels

231
Q

What elements are possible causes of emboli formation?

A

Thrombi
Fat
Air
Tumor

232
Q

What comorbidities are associated with a thrombotic stroke?

A

Atherosclerosis
Hypercoagulation
Sickle cell disease
Polycythemia vera

233
Q

What signs may indicate an embolic stroke has occurred in broker’s area?

A

Aphasia Expressive

234
Q

What signs may indicate an embolic stroke has occurred in Werkicke’s area?

A

Aphasia receptive

235
Q

What signs may indicate an embolic stroke has occurred in the motor area?

A

Contralateral upper and lower extremity, face

236
Q

What signs may indicate an embolic stroke has occurred in the somatosensory area?

A

Contralateral upper and lower extremity and face

237
Q

What cardiovascular pathology predisposes a patient to an ischemic stroke?

A

A-fib, valve prosthesis, carotid disease, valvular surgery and bacterial endocarditis

238
Q

What type of surgery has the highest risk for post op stroke?

A

CV surgery

239
Q

How might the provider want to measure blood pressure in a patient with a previous history of a stroke?

A

Central monitoring BP, auto regulation may be impaired from previous stroke

240
Q

What is a venous air embolus?

A

Entrainment of air or exogenously delivered gas from operative field into the venous or arterial vasculature

241
Q

What is thought to be a fatal amount of air given to the patient that may cause a VAE?

A

200-300mL or 3-5mL/kg

242
Q

What two criteria must be present to cause a VAE?

A

Low venous pressure

The vein must remain patent

243
Q

How does a VAE occur?

A

The pressure in a vein is sub atmospheric then air could be suctioned into the vein before it collapses

244
Q

What surgery is VAE mostly associate with?

A

Neurosurgery, veins in the skull may attach to cranium rudder and do not collapse during intracranial surgery

245
Q

How does a VAE cause pulmonary edema?

A

Air in vasculature cause vasoconstriction, edema, leaky capillaries = pulmonary edema

246
Q

What cardiopulmonary effects can lead to arterial hypoxemia?

A

Decreased right heart CO and Pulmonary edema

247
Q

How can air move to the left side of the heart?

A

Inracardiac right to left shunt

Incomplete pulmonary filtering of air emboli

248
Q

What are the cardiovascular effects of a VAE?

A

Chest pain
Brady/tachy arrhythmias
Increased filling pressure
ST Changes

249
Q

What are the pulmonary effects of a VAE?

A

Dyspnea, tachypnea, gasp reflex, hypercarbia and hypoxemia

250
Q

What are the neurological effects of a VAE?

A

Cerebral hypo-perfusion

251
Q

What hemodynamic changes should cause a provider to suspect a VAE?

A

Unexplained HoTN or sudden decrease in end tidal CO2

252
Q

What is the most sensitive monitoring of a VAE?

A

TEE

253
Q

What medical condition is contraindicated with the surgical sitting position?

A

Patent foramen ovale

254
Q

What are risk factors for a subarachnoid hemorrhage?

A

HTN
DM
CAD

255
Q

If a bleed occurs inside the brain what is another name for it?

A

Intra-axial bleed

256
Q

If the bleed originates in the brain but moves to the subarachnoid space what type of bleed is it?

A

Extra axial bleed

257
Q

What is a major complication associated with SAH?

A

Clogging of the arachnoid cilli which causes a decrease in CSF absorption = Increased ICP

258
Q

How might secondary hydrocephalus develop after an injury to the meninges has occurred?

A

Scarred meninges impair reabsorption of CSF

259
Q

How might a SAH develop?

A

Ruptured aneurysm or bleeding from arterial or venous vasculature in arachnoid space

260
Q

What causes HTN, dysrhythmias and cardiac damage after a SAH?

A

Catecholamine surge and Increased ICP

261
Q

How does anesthesia affect CBF?

A

Increases CBF and decreases CMR

262
Q

How do barbiturates affect an ischemic brain?

A

Protect the brain at doses less than required to suppress EEG burst = vasoconstriction

263
Q

How do volatile anesthetics affect an ischemic brain?

A

Delay but do not prevent neuronal cell death

264
Q

How does propofol affect an ischemic brain?

A

Only protective for mild ischemia

265
Q

How does etomidate affect an ischemic brain?

A

Increases the incidence of brain injury

266
Q

How should anesthetic providers treat a patient with a known ischemic brain event?

A

Modest increases in BP
NO HoTN
Do not hyperventilate = vasoconstriction and increase ischemia

267
Q

How long does it take to reestablish auto regulation after a CVA?

A

Autoregulation and CO2 sensitivity re-established at 4-6 weeks

268
Q

How does DM contribute to an exacerbation of ischemic cerebral injury?

A

Hyperglycemia –> more substrate for glycolysis –> greater reduction in tissue pH

269
Q

Where is the epidural space located?

A

Between the dura and the vertebral column

270
Q

What are the causes of a traumatic brain injury?

A

Head strikes an object
Trauma causes neural or glial injury
Vascular injury

271
Q

What are the three types of traumatic brain injury?

A

Extradural hematoma
Subdural hematoma
Intracerebral bleed

272
Q

What is usually the cause of an extradural hematoma?

A

Usually arterial source of bleeding

273
Q

What is usually the cause of a subdural hematoma?

A

Usually torn bridging vein or venous sinus

274
Q

What is usually the cause of an intracerebral bleed?

A

Small vessel trauma, shearing or penetration

275
Q

Why are children especially susceptible to TBIs?

A

Less myelinated tissue, larger head to body size and thinner bones that provide protection

276
Q

Why do children have greater intracranial compliance?

A

Cranial bones have not fused, vaults more expandable

277
Q

What is the goal in treating a TBI?

A

Preventing secondary brain injury from systemic HoTN, hypoxia, hyperglycemia
Optimize CPP without increasing ICP

278
Q

What is the best predictor of a TBI outcome?

A

Glasgow coma scale

279
Q

What type of fluid should we avoid while trying to resuscitate a patient with a TBI?

A

Should not contain dextrose, facilitates anaerobic metabolism and inflammation

280
Q

What are the three types of seizure disorders?

A

Generalized seizures
Partial seizures
Status Epilepticus

281
Q

What is the most common generalized seizure?

A

Grand Mal

282
Q

What are the components that make up a grand mal seizure?

A

Tonic: periods of intense muscle rigidity
Clonic: periods of relaxation
Post ictal amnesia

283
Q

What are the most common characteristics of a seizure?

A

Sudden explosive disorderly discharge of cerebral neurons
Transient alteration in brain function
Increased cerebral O2 demand (60%)
Increased cerebral ATP demand (250%)

284
Q

What is the prodroma period of a seizure?

A

Hours to days before onset of seizure

285
Q

What symptoms are associated with the prodroma period of a seizure?

A

Malaise and headache

286
Q

What is an aura?

A

Peculiar sensation preceding onset of generalized seizure

287
Q

What is the postictal state of a seizure?

A

Time period immediately following seizure activity, disorientation, confusion, fatigue and headache

288
Q

What causes a seizure?

A

Epileptogenic focus (group of neurons) –> sudden changes in normal membrane potential = hyper excitable

289
Q

What are some causes of seizures?

A

Hyperthermia, hypoxia, hypoglycemia, hyponatremia, repeated sensory stimulation and sleep phases

290
Q

What causes the RMP instability?

A

K conductance and Ca channel abnormalities
Deficit in GABA inhibitory system
Enhancement excitatory transmission

291
Q

How can a lengthy seizure lead to a brain tissue injury?

A

Hypoxia from increased O2 demand, decreased pH and lactic acid build up

292
Q

What medical conditions can predispose a patient to a seizure?

A

Digeorge syndrome, hypoparathyroidism and hypocalcemia

293
Q

What metabolic conditions can predispose a patient to a seizure?

A

Fever, uremia, hypoxemia, hyperglycemia and hyperventilation

294
Q

What are primarily the causes of a seizure?

A

Release of excitatory neurotransmitters or a decrease in inhibiting neurotransmitters and change in RMP

295
Q

How does hyperthermia affect seizure threshold?

A

Increased brain glutamate release, induces respiratory alkalosis leasing to an increased pH

296
Q

How can a sleep disorders impact the chance of a seizure?

A

Sleep disorders decrease seizure threshold

297
Q

What anesthetics can precipitate a seizure?

A

Enflurane, Laudanosine (metabolite of NMBA), Methohexital, Ketamine and Normeperidine

298
Q

What anesthetics can be given to increase AP seizure threshold?

A

Benzodiazepines
Barbituates
Volatile agent
Acidosis

299
Q

How can hyperventilation contribute to causing a seizure?

A

H+ leaves the cell –> K goes in making the RMP less negative
Ca binds to proteins and instability of Na occurs

300
Q

How can sensory stimulation alter seizure activity?

A

Interferes with ability to recruit brain structures that transmit paroxysmal activity to other regions

301
Q

What is inter cranial HTN?

A

ICP > 20mmHg

302
Q

How can an elevated ICP occur?

A

Brain edema, increased CB volume, increased intracranial CSF volume and intra, extra axial mass lesions

303
Q

Why can’t cytotoxic edema cause an increase in ICP by itself?

A

Simply a movement of fluid from the brain interstitium into the cell

304
Q

What type of edema will actually cause an increased ICP?

A

Vasogenic, once brain interstitial fluid is reduced fluid will move from the plasma. Loss of tight junctions allows proteins to move and water to follow

305
Q

At what PaCO2 does auto regulation occur?

A

20-80mmHg

306
Q

At what PaO2 does auto regulation occur?

A
307
Q

What is the pathology behind communicating hydrocephalus?

A

Decreased CSF absorption at the arachnoid villi

308
Q

What is the pathology of obstructive hydrocephalus?

A

Obstructing to CSF circulation

309
Q

When does hydrocephalus occur?

A

Excess fluid within the cranial vault or subarachnoid space

When production of CSF volume is not matched by CSF absorption

310
Q

Why shouldn’t the provider give mannitol before the cranium has been opened if a hemorrhagic event has occurred?

A

The increased ICP is essentially back pressure on stopping additional bleeding, give mannitol can restart the bleed

311
Q

What are the three components of cushings triad?

A

HTN
Bradycardia
Irregular respirations

312
Q

What cranial nerve dysfunction is associated with blurred vision?

A

CN II (optic)

313
Q

What cranial nerve dysfunction is associated with inability to adduct the eye?

A

CN III (occulomotor)

314
Q

What cranial nerve dysfunction is associated with inability to abduct the eye?

A

CN IV Trochlear

315
Q

What is the cushing’s reaction?

A

Initiation of CNS ischemic response due to low perfusion to the brain
Results in increased arterial pressure sufficient to move blood into cranial vault

316
Q

What interventions could the anesthetic provider implement in order to treat ICP?

A 
Diuretics
Hyperventilate the patient = vasoconstriction
Hypothermia
Normotensive 
Fluid restriction
317
Q

How can PEEP affect ICP?

A

Increases ICP by generating large intrathoracic pressures which reduces venous return into the right heart
Increased CVP due to back pressure in drainage from CSF from the brain

318
Q

How does acute hydrocephalus usually occur?

A

Result of a head injury

319
Q

What is the pathophysiology of hydrocephalus?

A

Obstructed CSF –> ventricular dilation proximal to block –> increased CSF –> atrophy of cerebral cortex = degeneration of white matter tracts

320
Q

What two drugs are known to increase ICP?

A

Ketamine

Succinylcholine

321
Q

How does a VP shunt function?

A

A catheter is passed into a ventricle of the brain and pump is place to direct flow to the peritoneum

322
Q

What type of ANS dysfunction do people with Parkinson’s disease have?

A

Gastric retention
Inappropriate diaphoresis
Orthostatic HoTN

323
Q

Why do people with Parkinson;s disease have a tremor?

A

Basal ganglia initiate the tremor via a cerebellar circuit

324
Q

What causes bradykinesia to occur in Parkinson;s disease?

A

Basal ganglia send tonic inhibitory impulses to the motor connections in the thalamus (excess GABA and decreased glutamate)

325
Q

How can dopamine help a patient with Parkinson;s disease?

A

Dopamine can release the basal ganglia inhibition, dopamine initiates a motor response

326
Q

What is the cardinal feature of Parkinson’s disease?

A

Impaired initiation of movement

327
Q

What occurs in Parkinson’s disease that causes movements to remain inhibited?

A

Dopamine neurons are destroyed

328
Q

What drugs would exacerbate the symptoms of Parkinson’s disease?

A

Reglan
Phenothiazines
Butyrophenones

329
Q

What is the role of Ach in a normal brain?

A

Ach interneurons modulate dopamine input to the GABA neurons

330
Q

How does Ach affect PD?

A

Excess Ach can exacerbate PD due to inhibition of GABA

331
Q

What is the role of GABA in the CNS?

A

Tempers the release of glutamate from the sub thalamic necleus

332
Q

What is the purpose of the substantia Nigra pars compacta?

A

Group of neurons that release dopamine

333
Q

What type of drugs would be helpful in the treatment of Parkinson’s disease?

A

D1R agonists
D2R agonists
Anticholinergics
NMDA antagonists

334
Q

Why might it be beneficial to give nicotine to a patient with PD?

A

Nicotinic receptors located pre-synaptically on dopamine neurons activate increase release of dopamine

335
Q

What is the pathology of Alzheimer’s disease?

A

Neurofibrillary tangles and plaques

336
Q

How do senile plaques affect the neurons?

A

Remodels the synaptic terminal

337
Q

Where does a lot of the damage occur in AD?

A

Hypo campus where short term memory is converted to long term memory

338
Q

Why do later stages of AD cause impaired motor function?

A

Later stages occur in the cerebral cortex

339
Q

What genetic component contributes to the formation of AD?

A

Functional deficit in apolipoprotein E

340
Q

What type of disturbances are typically seen in AD?

A

Memory, language, personality, motor system and intellect

341
Q

What post op complication are patients with AD at risk for?

A

Emergence delirium

342
Q

What drugs have been associated with emergence delirium?

A

Ketamine, Sevoflurance, Desflurane

343
Q

If an anticholinergic was required for a patient with AD which would you use?

A

Glycopyrolate, it does not cross the BBB

344
Q

What is the initiating event of cerebral palsy?

A

Cerebral hypoxia

345
Q

Damage to what parts of the brain will cause dyskinetic cerebral palsy?

A

Basal ganglia and extrapyramidal tract damage

346
Q

What symptoms are typically seen with dyskinetic cerebral palsy?

A

Fine motor coordination is poor, jerky movements

347
Q

Damage to what part of the brain causes spastic cerebral palsy?

A

Cerebral cortical damage

348
Q

What symptoms are seen with spastic cerebral palsy?

A

Increased muscle tone, exaggerated deep tendon reflexes, contractors, scoliosis

349
Q

What is the pathology of MS?

A

T-cells attack CNS myelin protein resulting in a decrease in number of dendrites and axons in the CNS

350
Q

What symptoms in MS may occur if brain demyelination ensues?

A

Seizures, spasticity, emotional lability, visual loss, dysarthria, dysphagia, congenital dysfunction

351
Q

What symptoms are seen in patient with MS that develop spinal cord lesions?

A

Paresthesia, Limb weakness, bowel and bladder symptoms

352
Q

What symptoms are seen in patients with MS that develop brain stem lesions?

A

ANS dysfunction

Abnormal ventilatory drive

353
Q

What causes a relapse in MS?

A

Caused by focal inflammatory demyelination

354
Q

What causes remission of MS?

A

When inflammation subsides and conduction is restored

355
Q

When does permanent dysfunction of MS occur?

A

When axons are destroyed

356
Q

How might anesthesia impact a patient with MS?

A

May worsen symptoms, especially spinal anesthesia

357
Q

How might hyperthermia affect patients with MS?

A

Slows conduction and if high enough can block conduction in demyelinated fibers

358
Q

What is the pathology of ALS?

A

Progressive, degenerative motor disease involving both upper and lower motor neurons

359
Q

What crania nerves are spared in MS?

A

CN III, IV, and VI

360
Q

Destruction of what neurons causes lower motor neuron symptoms?

A

Destruction of the ventral horn neurons (amyotrophic)

361
Q

Destruction of what neurons causes upper motor neuron symptoms?

A

Scarring of lateral cortic-spinal tracts (lateral sclerosis)

362
Q

What type of symptoms are seen with lower motor neuron demyelination?

A

Flaccid paralysis, muscle weakness, atrophy, hypotonia, permanent paralysis

363
Q

What symptoms are seen with upper motor neuron demyelination?

A

Spastic paresis, stiff tight muscles causing weakness of movement patterns, more likely to be repaired

364
Q

What respiratory impairments are associated with ALS?

A

Progressive respiratory muscle weakness
Aspiration risk
Difficult mechanical ventilation weaning

365
Q

How can anesthesia affect a patient with ALS?

A

Subclinical autonomic dysfunction could lead to exaggerated decreases in CV function

366
Q

What is the pathology in guillain barre syndrome?

A

Inflammatory/immune disorder of the peripheral nerves immune cells/AB attack the schwann cells resulting in destruction of the myelin sheath

367
Q

What is abnormal on a spinal tap in patients with GBS?

A

Elevated CSF proteins

368
Q

What hematologic complication is associated with GBS?

A

Thromboembolic complications

369
Q

Why should patients with GBS be considered for enteral feeding?

A

Bulbar weakness

370
Q

What is the pathology of myasthenia gravis?

A

Antibodies block nAchR at muscle endplate, increase their turnover flattening postsynaptic folds
Antibodies damage postsynaptic membrane complement

371
Q

What is the pathology of Lambert Eaton Myasthenic Syndrome?

A

There is a decreased Ach release causing muscle weakness

372
Q

What disease process is LEM strongly correlated with?

A

60% association with small cell lung cancer

373
Q

What is the pathology of muscular dystrophy?

A

There is a defect in the muscle fibers, absence of dystrophin protein in muscle leads to weakness

374
Q

What population is predisposed to MD?

A

Males, recessive trait in X-chromosome

375
Q

Where does the spinal cord extend?

A

From the base of the skull to L1

376
Q

What does the spinal cord turn into at L1-L2?

A

Conus medullaris

377
Q

What is the branching of nerves from the conus medullaris called?

A

Cauda equina

378
Q

How many segments is the spinal cord divided into?

A

31 segments, each with a pair of ventral (motor) and dorsal (sensory) spinal nerve roots

379
Q

What are the contents of the Grey matter?

A

Nerve cell bodies

380
Q

What are the contents of the white matter?

A

Ascending and descending nerve tracts

381
Q

What are majority of the causes of spinal cord injuries?

A

MVA and Sports in the male population

382
Q

Where do most spinal cord injuries occur?

A

C1-C2
C4-C7
T1-L2
They are the most mobile portions of the vertebral column

383
Q

What causes the secondary spinal cord injury?

A

Cytokine and amino acid release from injured cells leads to inflammation, free radicals formation, cellular edema, and cellular apoptosis

384
Q

How far can spinal cord edema extend past the injury?

A

Two spinal cord levels above or below the injury

385
Q

What is spinal cord shock?

A

Temporary loss or depression of all or most spinal reflex activity below the level of the injury = flaccid paralysis

386
Q

When is spinal cord shock said to be resolved?

A

Determined by the return of somatic and autonomic reflex arcs

387
Q

Why are patients in spinal shock unable to control their body temperature?

A

No sweating paired with cutaneous vasodilation

388
Q

What is upper motor neuron syndrome?

A

Damage to the descending motor pathways gives rise to a set of symptoms

389
Q

What is the pathology of upper motor neuron syndrome?

A

The spinal reflex circuits are suddenly deprived of input from the motor cortex and brainstem

390
Q

What is the importance of C5-T1?

A

Brachial plexus

391
Q

What is the importance of C3-C5?

A

Phrenic nerve

392
Q

What is the importance of C5?

A

External intercostals

393
Q

What is the importance of T1-T5?

A

Cardioaccelerator fibers

394
Q

Where are the SNS fibers located?

A

C7-L1

395
Q

What is the importance of S2-S4?

A

PSNS fibers exit

396
Q

At what level of spinal cord injury would a patient be prone to autonomic hyperreflexia?

A

Above T6

397
Q

What is scoliosis?

A

Lateral rotational curvature of the spine

398
Q

What is the difference between structural and non-structural scoliosis?

A

Structural- is due to rotation of the spine itself

Non-structural rotation due to reasons other than spine such as posture

399
Q

What is the pathophysiology of scoliosis?

A

Muscles, ligaments and soft tissue becomes shortened on the concave side of the curvature

400
Q

What determines the degree of deformity in scoliosis?

A

The compressive forces

401
Q

What does a patient with scoliosis look like?

A

May have rounded shoulders, prominence of one hip and rib prominences

402
Q

What type of scoliosis can compromise alveolar ventilation?

A

Structural scoliosis

403
Q

What word is used to describe a posterior and lateral spinal curvature?

A

Kyphoscoliosis

404
Q

What is ankylosing spondylitis?

A

Chronic inflammatory joint disease

405
Q

What structures does ankylosing spondylitis primarily affect?

A

Vertebral joints

406
Q

How can ankylosing spondylitis affect pulmonary function?

A

Chest movements can become restricted

407
Q

What is thought to cause ankylosing spondylitis?

A

Autoimmune disease that attacks antigens on cartilage

408
Q

What is spina bifida?

A

Congenital disorder characterized by a defect in the closure of the neural tube

409
Q

Where do vertebral laminae remain unfused in spina bifida?

A

Most often at the lumbosacral level

410
Q

What clinical manifestation are typically seen with spina bifida?

A

Lower limb muscle weakness
Gait abnormalities
Bowel and bladder dysfunction

411
Q

What position might impair ventilation in a patient with spina bifida?

A

Prone

412
Q

What nerve pairs are associated with the cauda equina?

A

Lumbar 2-5 nerve pairs
Sacral 1-5 nerve pairs
Coccygeal nerves

413
Q

What branch of the ANS innervates the bladder, internal and external anal sphincters?

A

PSNS

414
Q

How does cauda equina syndrome occur?

A

Compression of nerve roots below L1 caused by spoke fracture or disk herniation

415
Q

What type of spinal anesthetic can trigger cauda equina syndrome?

A

Hyperbaric LA

416
Q

What type of LA would you want to avoid when performing a saddle block?

A

5% Lidocaine

Pathophysiology I (4 decks)

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