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932 Pathophysiology > Neuropathophysiology > Flashcards

Neuropathophysiology Flashcards

1
Q

Describe the difference between the CNS & the PNS

A

The CNS are any neurons that are located in the brain and spinal cord (and do not exit) and the PNS are any neurons that are located in the periphery and outside of the CNS

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2
Q

Describe the organization of the Nervous system

A

The CNS is composed of the brain and spinal cord
The PNS is composed of the cranial nerves and spinal nerves it is further broken down into the somatic nervous system and the autonomic nervous system. The autonomic nervous system can further be broken down into the SNS, PSNS, and enteric systems

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3
Q

The SNS outflow leaves through the

A

thoracolumbar spinal cord region

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4
Q

PSNS outflow is via the

A

craniosacral region

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5
Q

Describe the reflex arc.

A

Sensory neurons in the periphery bring signal into spinal cord
interneurons provide a place for modulation from the brain
efferent neurons cause a response to the sensory neurons

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6
Q

Describe the meaning of cauda equina.

A

The spinal cord stops growing at ~T12-L1/L2 and this is known as the conus medullaris. The spinal cord axons however continue to grow and this is known as the cauda equina. This is where a spinal would be placed. An epidural could be placed anywhere

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7
Q

Describe the pathways of the autonomic nervous system.

A

PSNS: pre–> Ach onto nAChr–> post–> Ach onto muscarinic
SNS: pre–>Ach onto nAcher–> post–> norepi onto adrenergic
Adrenal medulla: pre–> Ach onto nAchr–>epi and norepi released into blood to act on adrenergic receptors

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8
Q

The composition of a nerve is important in understanding that

A

a lot of information can go in one nerve (receive sensory information and send out motor information)
Cranial nerves can innervate skeletal muscle and autonomic nervous system

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9
Q

The role of interneurons is to

A

provide an opportunity for modulation by the brain

Interneurons lie entirely within the CNS

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10
Q

Describe the generation of an action potential

A

The cell is at resting membrane potential
Action potential is generated and VGNa+ channels open and sodium comes into the cell
The second door of the VGNa+ channels close (putting them in an inactivated state) and the VGK+ channels open and K+ leaves the cell
As the cell begins to repolarize the VGNa+ channels move into the ready state

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11
Q

Describe the role of myelin.

A

Myelin allows for saltatory conduction and allows for quicker propagation of an action potential

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12
Q

Neuronal health and survival is dependent upon

A

blood delivering O2 and fuel and waste removal

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13
Q

Describe autoregulation in the brain.

A

Autoregulation in the brain is composed of the myogenic response (response to pressure) and the metabolic response (O2 lack theory)
Cerebral blood flow can be maintained over a wide range of MAP due to autoregulation in the brain

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14
Q

Osmotic pressure is

A

the pressure that opposes movement of water across the membrane

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15
Q

List the cellular processes activated by ischemia:

A
  1. Cellular acidosis
  2. Cellular swelling (cytotoxic edema)
  3. Neuroexcitotoxicity
  4. Enzymatic activation
  5. Nitric oxide production
  6. Inflammation
  7. Apoptosis
  8. Necrosis
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16
Q

Describe cellular acidosis.

A

Anaerobic metabolism leads to cell swelling because of lactic acid accumulation, increased intracellular H+, Na+/H+ exchanger protein moves H+ out of the cell in exchange for Na+ into the cell
Cell swells due to increased Na+
RMP becomes less negative, increasing AP probability

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17
Q

Describe cellular swelling (cytotoxic edema).

A

Reduced function of Na+/K+ ATP pump leads to swelling due to increased concentration of Na+ inside the cell

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18
Q

Describe neurotoxicity.

A

Brain glutamate levels rise because elevated intracellular Na+ brings neurons closer to threshold causing release of glutamate

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19
Q

Describe enzymatic activation.

A

Results from elevated brain glutamate levels because excessive glutamate causes Na+/Ca2+ influx into cell
causes neuron membrane damage and mitochondrial injury resulting in cell death

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20
Q

Describe the composition of the cranial vault.

A 
Fixed space
brain: 80%
blood: 12%
CSF: 8%
Little reserve and no stretch
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21
Q

Cerebral perfusion pressure is equal to

A

MAP-ICP

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22
Q

Describe CSF in the cranial vault.

A

CSF is made in the choroid plexus. It circulates around the brain and drains via the arachnoid villi. If the arachnoid villi become blocked and CSF is unable to drain, there could be an increase in ICP which compromises CBF

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23
Q

Characteristics of cerebral blood flow

A

Brain receives 15% of cardiac output
little reserve of nutrients and O2; constant supply of blood is required
CBF remains constant due to autoregulation and other feedback mechanisms (not limitless though)

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24
Q

Cerebral blood flow averages

A

50 mL/100 g/min.

grey matter averages more than white matter

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25
Q

Cerebral blood flow is equal to

A

CPP/R

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26
Q

Normal ICP is

A

<10 mmHg

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27
Q

Normal Cerebral perfusion pressure is

A

80-100 mmHg

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28
Q

The middle cerebral artery is important because

A

it carries 80% of the blood to the brain

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29
Q

Cerebral autoregulation is composed of the

A

metabolic: Co2 and metabolites (increased metabolic rate)
and the
myogenic: VSMC stretch (increased CPP

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30
Q

An increase in CPP will result in

A

vasoconstriction

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31
Q

A decrease in CPP will result in

A

vasodilation

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32
Q

CBF remains constant between MAPs of

A

60 to 160 mmHg

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33
Q

As the pressure increases, the amount of

A

vasoconstriction has to go up to keep blood flow constant

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34
Q

In chronic hypertension, the cerebral autoregulation curve is

A

shifted to the right

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35
Q

When the metabolic demand exceeds cerebral blood flow, we get

A

release of metabolites that cause vasodilation

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36
Q

When you have uncoupling of autoregulation,

A

you have an even narrower range where smooth muscle can adjust

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37
Q

Cerebral blood flow can be regulated via

A

Temperature- hyperthermia increases CBF & CMR
Blood viscosity- decreased hct decreases viscosity and can increase CBF
Anesthetics- increased CBF and decrease CMR

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38
Q

The average CMRO2 is

A

3 to 3.8 mL 02/ 100 grams/ minute

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39
Q

The movement of substances through the blood-brain barrier is governed by

A

Size
charge
lipid solubility
protein binding

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40
Q

What can get past the blood brain barrier?

A

O2, CO2, H2O, lipid soluble, anesthetics

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41
Q

What cannot get past the blood brain barrier?

A

H+, HCO3-, other small ions, proteins, mannitol

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42
Q

Mannitol can be used to

A

draw water out of the brain

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43
Q

The blood brain barrier can be disrupted by:

A

severe hypertension, cerebral ischemia, infection, marked hypercapnea, hypoxia, tumor, trauma, stroke, seizure activity

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44
Q

What is the adult production of CSF/day?

A

500 mL/day

the total volume of cranial and spinal CSF is 150 mL

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45
Q

The function of the CSF:

A

Protect CNS from trauma

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46
Q

CSF is found in:

A

ventricles of the brain
cisterns surrounding the brain
subarachnoid space of the brain and spinal cord

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47
Q

CSF is produced by:

A

predominantly choroid plexuses of the lateral ventricles

secreted by the ependymal cells of the choroid plexus

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48
Q

Central venous pressure is a

A

back pressure that hinders cerebral fluid drainage

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49
Q

Once compensation is exhausted within the cranial vault, the

A

ICP will increase dramatically

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50
Q

The brainstem is important because

A

within the brainstem we have the medulla (NTS, VMC, and DRG), pons, and the cerebellum

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51
Q

Discriminating touch pathway

A

crosses high
afferent to medulla
tracts travel via dorsal column

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52
Q

Pain, temperature pathway

A

cross low
afferent to spinal cord
travel via lateral column

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53
Q

Conduction velocity of pain is related to

A

the type of fiber and diameter of the neuron

type C fibers are the aching pain fibers

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54
Q

Persistent pain is composed of

A

nociceptive pain & neuropathic pain

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55
Q

Neuropathic pain results from

A

direct injury to the nerves

often have burning or electrical sensation

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56
Q

Nociceptive pain results from

A

the direct activation f nociceptors in the skin or soft tissue in response to tissue injury and arise from inflammation

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57
Q

With the pain pathways and CNS ascending tracts,

A

we don’t distinguish between the lateral spinothalamic (fast pain) and the anterior spinothalamic (slow pain)
we just want to block all of the pathways

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58
Q

Enkephalins are

A

part of the brain’s endogenous opioids and are released at the brain stem and spinal cord

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59
Q

Endorphins are

A

part of the brain’s endogenous opioids and are released at the hypothalamus and pituitary gland

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60
Q

Referred pain occurs when

A

we have two sensory inputs that synapse at the same interneuron and the brain is unable to distinguish the particular area
occurs more frequently in men>women

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61
Q

Describe the ischemia pathway in the brain.

A

ischemia leads to low oxygen leading to low ATP leading to cell acidosis and ion pump failure
leads to chemical injury & neuroexcitotoxic injury

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62
Q

A neuroexcitotoxic injury causes

A

increased RMP and Action potentials–> increased glutamate–> increased calcium—> increased enzymes, ROS–> cell death

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63
Q

A chemical injury causes

A

damage to endothelial cells–> BBB disruption–> increase in ISF protein, increase in proinflammatory mediators–>inflammation–> cell death

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64
Q

eNOS is

A

an isoform of nitric oxide that is beneficial in ischemia because it causes arteriolar vasodilation, anti-inflammatory, and anti-thrombotic

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65
Q

iNOS and nNOS are formed from

A

ischemia and they combine with free radicals to damage cellular proteins, membranes, and DNA

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66
Q

Inflammation causes:

A

edema, clotting, and release of chemicals that are injurious or degradative

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67
Q

Cell derived chemical mediators such as

A

histamine, serotonin, and kinin cause disruption of the BBB because they increase the leakiness of the capillaries

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68
Q

Types of cerebral edema include:

A

cytotoxic, vasogenic, hydrostatic, osmotic, and interstitial

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69
Q

Cytotoxic edema result from

A

ischemia induced neuronal ion influx–> cell swelling

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70
Q

Vasogenic edema results from

A

ischemia–> damages endothelial cells–> BBB breakdown

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71
Q

Compare global ischemia to focal ischemia

A

global–> due to hypoperfusion

focal–> due to thrombus or embolus; discreet area

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72
Q

Types of stroke include

A

ischemic: thrombotic, embolic
hemorrhage: aneurysm rupture, AVM, intracerebral bleed, SAH

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73
Q

Global hypoperfusion results from

A

reduced CPP due to decreased MAP (shock) and/or increased ICP (CVA, trauma, infection, tumor)

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74
Q

Hemorrhagic intracerebral bleeds are associated with

A

hypertension, anticoagulation therapy or other coagulopathy, drug and alcohol abuse, neoplasia (tumors), amyloid angiopathy, infection

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75
Q

Aneurysm rupture can occur from

A

trauma, inflammation, atherosclerosis, or congenital

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76
Q

Aneurysm rupture typically occurs at

A

age 35-60

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77
Q

Aneurysms are typically (symptoms)

A

asymptomatic until rupture

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78
Q

Individuals are more susceptible to formation of aneurysm if they have

A

structural abnormalities, genetics, atherosclerosis, HTN, coarctation of aorta, or connective tissue disorder

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79
Q

The circle of willis (significance)

A

allows for collateral blood flow; if one area is blocked, blood can go all the way around and still perfuse other areas

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80
Q

With aneurysm rupture (pathophysiology of rupture)

A 
there will be large increase in ICP
decrease in CPP
spread of blood--> inflammation
cerebral vasoconstriction 
decrease in CBF (which may help stop further bleeding)
loss of cerebrovascular autoregulation
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81
Q

Aneurysm rupture presents as

A

sudden onset of severe headache
nausea, vomiting, neck stiffness, photophobia
possible loss of consciousness
hypertensive and may have EKG abnormalities

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82
Q

Major sources of morbidity and mortality as it relates to aneurysm rupture include

A

Neurologic (ischemia from vasospasm and elevated ICP)
cardiopulmonary (arrhythmias, myocardial injury, pulmonary edema)
electrolyte abnormalities (hypomagnesemia, kalemia, natremia)

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83
Q

Many aneurysms occur at the

A

middle cerebral artery

devastating because it supplies a massive amount of brain tissue

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84
Q

An arteriovenous malformation is

A

vascular mass where blood flows directly from arteries to veins (no capillaries or neural innervation)
feeder vessels become dilated and shunt blood into malformation at the expense of surrounding tissue (steal)

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85
Q

An AVM manifests as

A

headache, cerebral hemorrhage, seizure, increased ICP or neurologic signs secondary to cerebral ischemia (steal effect)

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86
Q

An AVM is a result of

A

a congenital lesion

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87
Q

Anesthetic implications with AVM

A

can be very bloody surgery
deliberate hypotension may be used to decrease blood loss
avoid rise in CVP

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88
Q

An ischemic stroke is primarily the result of

A

thrombotic and embolic

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89
Q

The third leading cause of death in the United States is due to

A

ischemic stroke

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90
Q

An ischemic stroke is

A

an interrupted cerebral perfusion

creates vicious cycles of cell hypoxia, edema, and metabolic derangements

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91
Q

An embolic stroke is where

A

fragments from outside the brain break off and circulate and become lodged in intracranial vessels
can be thrombi, fat, air, tumor

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92
Q

There is a relationship between people who have cerebral artery disease and

A

CAD

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93
Q

A thrombotic stroke is the result of

A

thrombi formed in carotid or cerebral vessels

associated with atherosclerosis, hypercoagulation, sickle cell disease, and polycythemia vera

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94
Q

Conditions that favor a thrombus include

A

hypercoagulation and decreased perfusion

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95
Q

Risk factors for ischemic stroke include

A

increasing age, underlying atherosclerotic disease, history of prior transient ischemic attacks, associated with cardiovascular disease (a-fib, valve prosthesis, carotid disease, valve or carotid surgery, bacterial endocarditis)

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96
Q

For patients at risk of stroke, it is important to control

A

diabetes, HTN, and coagulation therapy

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97
Q

For patients who have already had a stroke, they may have

A

impaired cerebral autoregulation

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98
Q

Venous air embolism is the

A

entrainment of air or delivered gas into the venous or arterial vasculature

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99
Q

Takeaway for venous air embolism:

A

air into vein only occurs if PB> Pvenous (i.e. when the heart is lower then the brain and doing surgery above the heart), vein gets stuck open

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100
Q

The biggest concern with the venous air embolism is the

A

large volume of gas which can circulate to the lungs and lead to pulmonary embolism causing impaired gas exchange or for patients with a patent foramen ovale who could have a right to left shunt (causing MI & stroke)

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101
Q

The appropriate positioning for a patient with a PFO who has a VAE would be

A

on the left side

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102
Q

Clinical manifestations of VAE include

A

cardiovascular: chest pain, bradyarrhythmias, tachyarrhythmias, increased filling pressure, ST segment changes
pulmonary: dyspnea, tachypnea, gasp reflex, hypoxemia, hypercarbia
Neurological: decreased CO leading to cerebral hypo-perfusion

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103
Q

VAE is detected via

A

abrupt decline in end-tidal carbon dioxide

may also see unexplained hypotension

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104
Q

Subarachnoid hemorrhage risk factors include

A

hypertension, diabetes, CAD

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105
Q

When a bleed that is intra-axial enters the subarachnoid space

A

it is now considered extra-axial and becomes a SAH

106
Q

The meningeal layers include

A

the Pia mater
the arachnoid
the dura mater

107
Q

Subarachnoid hemorrhages can originate

A

inside or outside the brain (intra or extra axial)

108
Q

SAH key points:

A

If the villi become blocked, ICP will increase resulting in signs and symptoms

  • can see a catecholamine surge d/t increased ICP and bleeding- pressure and inflammation on the brain
  • brain inflammation can move systemically and can lead to increased adrenal release of catecholamines/ norepi release
  • Second stroke due to cerebral vasospasm due to RBC+iron–> quenches NO–> NO can’t act on VSMC
109
Q

The catecholamine surge results in

A

hypertension, dysrhythmias, and cardiac damage

110
Q

An anesthetized brain is less

A

vulnerable to ischemic injury because anesthesia increases CBF and decreases CMR

111
Q

For those who have suffered an ischemic brain event, it is important to

A

avoid hypotension
can allow for modest increases in BP
avoid hypocapnia as this reduces blood flow to the ischemic brain

112
Q

Factors that affect (can be influenced by the CRNA) cerebral blood flow include

A

PaO2- decreased PaO2 leads to cerebral vasodilation
PaCO2- increased PaCO2 leads to cerebral vasodilation
H+-increased metabolites leads to cerebral vasodilation
Cell activity: increased activity leads to cerebral vasodilation
Temp is proportional to CBF
Viscosity is inversely proportional to CBF
MAP- autoregulation

113
Q

Recovering from a CVA can take

A

4-6 weeks before autoregulation and CO2 sensitivity is re-established because it is an inflammatory mess

114
Q

Hyperglycemia is associated with

A

an exacerbation of ischemic cerebral injury because it decreases tissue pH and further compromises the ischemic injury

115
Q

The spinal cord is supplied with blood via

A

Ventral spinal blood supply: 2 posterior & 1 anterior

Segmental spinal blood supply (horizontal): provides additional blood supply to some but not all spinal cord levels

116
Q

The adamkiewicz artery is

A

a major segmental supply of blood to the spinal cord
clamping the spinal cord at T9 will reduced blood supply to the spinal cord because that is above the level of Adamkiewicz

117
Q

The Artery of Adamkiewicz is also known as

A

a radicular artery

118
Q

Concerns with aortic cross clamping:

A

surgical procedures involve the thoracoabdominal aorta–> high 30 day mortality at 8% to 35%
hemodynamic changes can cause myocardial ischemia or heart failure

119
Q

Hemodynamic changes related to cross clamping includes

A

increased blood pressure due to increased preload: veins distal to clamp empty and see myogenic constriction–> decreased capacitance–> blood shifts to heart/arterial side, increases preload resulting in increased BP
Increased SVR: cross clamp causes increased SVR secondary to increased catecholamines and ANGII release (decreased blood supply to the kidneys activates the RAAS)

120
Q

With aortic unclamping, we may see

A

decreased blood pressure (decreased preload) b/c the veins re-open increasing the vascular capacitance and blood volume shifts to venous side
decreased SVR because metabolites accumulate distal to the clamp and result in reactive hyperemia and cause massive vasodilation
Clamp needs to gradually be released

121
Q

Carotid artery disease is

A

atherosclerosis in the carotid artery

plaque in the artery wall–> arterial narrowing–> increased resistance–> decreased blood flow

122
Q

Carotid artery disease is a risk for

A

ischemic stroke
difficult to manage because if they’re being treated for coronary plaque then they’re a stroke risk and if they’re being treated for their carotid plaque then they’re an MI risk

123
Q

The medical management of the patient with carotid artery disease includes:

A

control of hypertension, hypercholesterolemia, and diabetes, smoking cessation, increased physical activity, and anti-platelet therapy

124
Q

For patients undergoing a carotid endarterectomy,

A

regional anesthesia is preferred

probably have had a stroke previously so want to recognize implications of this

125
Q

Patients undergoing carotid endarterectomy for carotid artery disease have significantly increased risk of

A

MI because venous stasis on same side as clamp, stress on heart to provide collateral enough blood flow, and surgery is pro-inflammatory

126
Q

With carotid endarterectomy, positioning during surgery is important because

A

part of the surgery is one of the carotids is clamped

extreme head rotation can compress the artery and decreases CBF

127
Q

Encephalopathy signs and symptoms include

A

motor cortex–> cerebral palsy
occipital lobe–> blindness
cerebral cortex–> cognitive impairment

128
Q

Encephalopathy is

A

when the function of the brain is affected by some agent or condition

129
Q

Brain insult/injury can be a result of (pathophysiology of encephalopathy)

A

chromosomal abnormalities, infection, trauma, radiation, exposure to toxic substances
fetal injury- due to maternal toxemia, DM, malnutrition
Perinatal injury- due to anoxia, trauma, infection
Postnatal injury- infection, metabolic disturbance, trauma, toxins, vascular disease
infectious- access CNS via brain or intraneuronal route

130
Q

The epidural space is the

A

space between the vertebral column and the dura mater (there is only a ‘potential’ epidural space in the head between the skull and the dura mater)

131
Q

The subdural space is the

A

space between the dura mater and the arachnoid mater

132
Q

The subarachnoid space is the space

A

between the arachnoid mater and the pia mater

133
Q

Causes of traumatic brain injury include

A

head strikes an object or vice-versa
deceleration events
trauma causes neural and glial injury, vascular injury

134
Q

Types of traumatic brain injury include

A

extradural hematoma- can lead to herniation
subdural hematoma- can lead to herniation
intracerebral bleed

135
Q

The best predictor of TBI outcome is

A

the glascow coma scale

50% of patients who present with GCS of 8 or less will die

136
Q

Signs and symptoms of TBI include

A

altered consciousness, coma, seizures, vomiting, irritability, acute temporary cognitive decline

137
Q

TBIs and children

A

children are especially susceptible to TBI
children have lower BP reserve
BUT have greater intracranial compliance

138
Q

Causes of TBI include

A

fall, car accident, explosion

higher incidence among males

139
Q

When treating a TBI, fluid resuscitation

A

should not contain glucose because it facilitates anaerobic metabolism and inflammation

140
Q

Treatment of adult/pediatric TBI is directed at

A

preventing secondary brain injury from systemic hypotension, hypoxia, hypocapnia, and hyperglycemia

141
Q

Patients who have had a TBI are at higher risk for

A

seizure

excitotoxicity due to glutamate release can lead to eptileptogenic focus

142
Q

Types of seizure disorders include

A

generalized seizures
partial (focal) seizures
status epilepticus

143
Q

A seizure is

A

action potentials gone awry from neurons that are hyper-excitable leading to release of glutamate

144
Q

A seizure causes an increase in

A

cerebral oxygen demand and ATP demand

145
Q

A seizure stops when

A

neurons are refractory or acidosis–> hyperpolarization

146
Q

The time period immediately following a seizure is known as

A

postictal state and involves disorientation, confusion, fatigue, and headache

147
Q

A prodroma is

A

the early manifestations of a seizure: malaise, headache hours to days before onset of seizure

148
Q

An aura is

A

a peculiar sensation preceding onset of generalized seizure

149
Q

The epileptogenic focus is

A

a group of neurons–> sudden changes in normal membrane potential makes them extremely hyperexcitable

150
Q

With a seizure, we may see an increase in

A

O2 demand and ATP demand
Cerebral blood flow increase due to autoregulatory metabolic effect
length seizures however can lead to hypoxia, decreased pH, lactic acid and brain tissue injury

151
Q

Status epilepticus is

A

a prolonged partial or generalized seizure without recovery between attacks or one seizure of >5 min duration
may or may not include convulsions

152
Q

Risk factors for seizure include

A 
genetic-idiopathic
genetic predisposition for disorder associated with seizures- hypoparathyroid or hypocalcemia
tumor, trauma, infection, or fever
SAH, stroke damage
metabolic origin- fever, uremia, hypoxemia, hyperglycemia, hyponatremia
drugs or alcohol overdose or withdrawal
fatigue or stress
excessive sensory stimuli
153
Q

Additional risk factors for seizure include

A

hyperthermia (increased brain glutamate release)
hypoxia, hypoglycemia/hyperglycemia- brain metabolism altered leading to decreased GABA neurotransmission and increased glutamate neurotransmission
Hyponatremia- neuron swelling due to extracellular hypoosmolarity leading to cerebral edema
sleep disorders- OSA, insomnia, restless leg syndrome
precipitating anesthesia- some anesthetics lower the AP threshold

154
Q

Status epilepticus is a medical emergency because:

A

increased O2, ATP, and glucose use
need to check for clear airway, administer O@
consider using antiepileptic drugs

155
Q

Elevated ICP is defined as

A

intracranial pressure >20 mmHg

156
Q

Raised ICP is directly associated with

A

poor outcomes (the higher the ICP, the poorer the outcome)

157
Q

Increased ICP can occur due to

A

brain edema
increased cerebral blood volume (reduced venous outflow or increased CBF)
Increased intracranial CSF volume
Intra and extra-axial mass lesions

158
Q

The types of brain edema include

A

cytotoxic, vasogenic, hydrostatic, osmotic, and interstitial

159
Q

Cytotoxic edema is

A

ischemia induced neuronal ion influx–> cell swelling

160
Q

Vasogenic edema is

A

ischemia–> damages endothelial cells–> BBB breakdown in 2-3 days–> BBB breach–> plasma protein moves into cerebral ISF–> edema

161
Q

Hydrostatic edema occurs when

A

cerebral autoregulation is disrupted

162
Q

Osmotic edema is

A

dilution of the blood

163
Q

Interstitial edema is

A

transependymal movement of CSF

164
Q

Increased CSF volume can result from

A

decreased CSF absorption at the arachnoid villi
Obstruction to CSF circulation
Increased production of CSF

165
Q

Decreased CSF absorption at the arachnoid villi can result from

A

SAH & infection

166
Q

Obstruction to CSF circulation can result from

A

obstructive hydrocephalus, neoplasm, traumatic and spontaneous hemorrhage, infection

167
Q

Increased production of CSF can result from

A

meningitis or choroid plexus tumors

168
Q

Cushing’s triad is

A

a bad sign of increased ICP and it includes hypertension, bradycardia, and irregular respirations

169
Q

Symptoms of elevated ICP include

A

headache, nausea/vomiting, paresthesia, somnolence, visual disturbances, auditory disturbances, and mental changes

170
Q

Signs of elevated ICP include

A

hypertension, bradycardia, periodic breathing, seizures, midline shift > 0.5 cm.

171
Q

Escalating signs and symptoms of elevated ICP include

A

headache, N/V, pupillary dilation, blurred vision, inability to adduct and abduct eye
focal neurological deficits, apathy, decreased consciousness, seizures, coma, Cushing’s triad, symptoms of brain herniation

172
Q

The cushing reaction occurs when

A

increased ICP is equal to arterial pressure and blood supply to the brain is extremely diminished initiating the CNS ischemic response

173
Q

When treating a patient with elevated ICP it is important to

A

delay mannitol administration until the cranium is open (AVM, Cerebral aneurysm or hemorrhage) hematoma can expand as brain tissue volume decreases

174
Q

Anesthetic implications with elevated ICP include

A

head tilt 15 to 30 degrees, avoid coughing as this will increase CVP and PEEP

175
Q

Hydrocephalus is

A

excess CSF fluid within the cranial vault

can be within the ventricles, subarachnoid space or both

176
Q

Hydrocephalus has two types including

A

non-communicating (intraventricular) within ventricles and communicating (extraventricular) outside ventricles and into brain interstitium

177
Q

Causes of hydrocephalus include

A

communicating- neoplasm, traumatic and spontaneous hemorrhage, infection
non-communicating- congenital deformity of aqueducts or ventricles

178
Q

Acute hydrocephalus is

A

an emergent event because there is no time for stretch or compensation so a quick rise in pressure occurs

179
Q

Signs and symptoms of hydrocephalus include

A

declining memory and cognitive function, unsteady gait, history of falling, inattentiveness, apathy, indifference

180
Q

Anesthetic implications in regards to hydrocephalus include

A

preventing additional increase in ICP
avoid succinylcholine and ketamine as they increase ICP
hyperventilate patient if ICP symptoms arise

181
Q

A ventriculoperitoneal shunt is

A

used to treat an excess of CSF

allows CSF to be reabsorbed through the lymph system

182
Q

Signs and symptoms of Parkinson’s disease include

A

tremor, rigidity, bradykinesia, postural instability, dementia, depression, and ANS dysfunction

183
Q

Parkinson’s disease is where neurons are

A

present but beginning to fail

184
Q

The concern with bradykinesia in Parkinson’s patients is

A

increased aspiration risk because slow movement of all skeletal muscles

185
Q

The takeaway for Parkinson’s disease includes

A

pathways are extremely complex and never assume giving NT will have local effects
series of excitatory and inhibitory proccesses
give dopamine for these patients
involves the loss of dopamine neurons–> too much GABA activity–> inhibits ability to create motion

186
Q

Patients with Parkinson’s disease are prone to

A

opioid induced rigidity because opioid agonist inhibit dopamine

187
Q

Anesthetic considerations for Parkinson’s patients include:

A

regional anesthesia is preferred because less anesthetics to the brain
PD patients are prone to hypotension b/c DA causes vasodilation
required continued L-dopa therapy so may have to give intraop
predisposed to rigidity with opioids
response to muscle relaxants is normal

188
Q

Takeaways for Alzheimer’s disease include

A
  1. will need POA present but need to still speak to patient
  2. At risk for emergence delirium
  3. Ach disease (too little Ach) in the brain neurons so if giving anticholinergic make sure it does not cross BBB
189
Q

Symptoms of Alzheimer’s disease include

A

memory loss, impaired learning, spatial disorientation, anomia, apraxia, paranoia, delusions and hallucinations

190
Q

Risk factors for Alzheimer’s disease include

A

genetic (30% familial, functional defect in apolipoprotein E), chronic hypertension, head injury, female, chronic TIA

191
Q

For patients with Alzheimer’s Disease, they may be taking

A

acetylcholinesterase inhibitors and thus we may choose to give glyco as this does not cross the BBB

192
Q

Cerebral palsy is

A

a non-progressive syndrome where the neurons do not work from gestational brain damage

193
Q

The initiating event of cerebral palsy is

A

cerebral hypoxia–> low ATP–> pump failure–> cell swelling–> inflammation–> damaged neurons

194
Q

Hypoxia can occur in cerebral palsy due to

A

prenatal hypoxia, birth asphyxia, or low birth weight

195
Q

Clinical manifestations of cerebral palsy include

A

basal ganglia and extrapyramidal tract damage–> dyskinetic cerebral palsy
poor fine motor coordination, jerky movements

cerebral cortical damage–> spastic cerebral palsy
increased muscle tone, exaggerated deep tendon reflexes, contractures, scoliosis

developmental delay, sensory abnormality, seizure risk

196
Q

Anesthetic implications for patients with cerebral palsy include:

A

higher seizure risk, developmental delays may impair patient comprehension
often experience GERD–> aspiration risk
motor issues may lead to prolonged response to muscle relaxants

197
Q

Demyelinating disorders include

A

multiple sclerosis, ALS, and Guillan Barre

198
Q

Disorders of the neuromuscular junction include

A

LEMS & myasthenia gravis

199
Q

Clinical features of multiple sclerosis include

A

fatigue, parasthesias, unsteady gait, muscle weakness, and atrophy, respiratory insufficiency, ANS dysfunction

200
Q

Multiple sclerosis is the

A

chronic degeneration of all CNS neuron types

201
Q

Multiple sclerosis predominantly occurs in

A

females and is an autoimmune disorder

202
Q

Lesions in the spinal cord can cause

A

paresthesia, limb weakness, and bowel and bladder symptoms

203
Q

Lesions in the brain stem can cause

A

autonomic dysfunction & abnormal ventilatory drive

204
Q

Brain demyelination can cause

A

seizures, spasticity, emotional lability, visual loss, dysarthria, dysphagia, and cognitive dysfunction

205
Q

For patients with MS it is important to avoid

A

succinylcholine due to risk for hyperkalemia since they have upregulation of nAchR

206
Q

The MS neuron type summary:

A

Only CNS neurons involved

CNS neurons include: somatic motor, somatic sensory, autonomic, and higher brain neurons, PNS neurons are spared

207
Q

If the patients disease involves ANS, then

A

cardiac arrhythmias and neurogenic bowel and bladder may occur

208
Q

ALS is a

A

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

209
Q

ALS is more common in

A

males> females

usually occurs after the 4th decade with peak occurrence at age 50

210
Q

ALS can be caused by

A

heavy metal exposure
glutamate excitotoxicity
oxidant stress
hereditary component

211
Q

ALS stands for

A

amyotrophic lateral sclerosis

212
Q

Clinical manifestations of ALS include

A

muscle atrophy, fasiculations, difficulty swallowing, dysarthria (articulation), dysphonia (volume)
sensory, autonomic and cognitive functions preserved

213
Q

Anesthetic implications of ALS include:

A

succinylcholine contraindicated due to hyperkalemia risk
non-depolarizing MR will have a prolonged response
aspiration risk and difficulty weaning mechanical vent

214
Q

ALS neuron type summary:

A

only SOMATIC motor neurons are involved (not sensory)
cranial nerve somatic motor activity impaired but eye movement is spared
ANS, sensory, and non-motor CNS neurons are spared

215
Q

Guillain-Barre syndrome is caused from

A

an inflammatory/immune disorder of the peripheral nerve immune cells/ Ab attack the Schwann cells resulting in destruction of the myelin sheath

216
Q

Clinical features of Guillain-Barre include

A

muscle weakness that is progressive (more often legs than arms)
areflexia
cranial nerve and autonomic involvement
respiratory muscle failure
pulmonary aspiration
ANS involvement- sinus tachy bradyarrhythmia, excessive sweating

217
Q

Guillain-Barre neuron type summary:

A

PNS neurons are impaired (both somatic and autonomic)
ANS function is impaired
Somatic motor is impaired
Somatic sensory is impaired
Cranial nerve function is impaired
CNS neurons are spared (cognition preserved)

218
Q

Myasthenia gravis clinical features include

A

muscle weakness- increases with exercise- fatigability
eye, facial, bulbar, and limb muscle weakness
respiratory muscle weakness rare but possible postop complication

219
Q

Myasthenia gravis is a

A

chronic autoimmune neuromuscular disease affecting nicotinic receptors at the endplate and decreasing chance of action potential

220
Q

For patients with myasthenia gravis, _____ should be withheld on the day of surgery

A

acetylcholinesterase inhibitors because they can prolong the action of sux and increase the need for nondepolarizing neuromuscular blocking drugs

221
Q

Muscular blocking drugs and myasthenia gravis:

A

relatively resistant to succinylcholine- may need increased dose
extremely sensitive to nondepolarizing neuromuscular blockers (faster onset and more prolonged block)

222
Q

LEMS disease is known as

A

Lambert-Eaton Myasthenic syndrome

223
Q

LEMS is an

A

autoimmune disease of the neuromuscular junction that acts on presynaptic VGCa2+ channels and prevents release of acetylcholine resulting in muscle weakness

224
Q

Anesthetic implications of LEMS include:

A

paralytic reversal is often ineffective
autonomic disturbances may be present
increased sensitivity to succinylcholine
increased effectiveness of NDMR

225
Q

Muscular dystrophy is

A

a defect of muscle fiber due to the absence of dystrophin protein which leads to weakness

226
Q

Muscular dystrophy is found in

A

males because it is located on the X chromosome

227
Q

The absence of dystrophin in muscular dystrophy

A

causes muscle weakness because it prevents contractile filaments from being connected to extracellular matrix and doing work

228
Q

Anesthesia risks related to muscular dystrophy include

A

acute respiratory depression
rhabdomyolysis
hyperkalemic cardiac arrest
heart failure/ arrhythmia

229
Q

Muscle relaxants used in muscular dystrophy include

A

avoidance of succinylcholine and use of short-acting NDMR

230
Q

Spinal cord injury is caused by

A

MVA, sports, and penetrating injuries

most injuries occur due to acceleration/deceleration, deformation forces

231
Q

About half of the kids with a spinal cord injury have

A

an associated TBI

232
Q

Spinal cord injury is most common in

A

males>females, age 16-30

233
Q

Most spinal cord injuries occurs at

A

C1-C2, C4-C7, and T1-L2 as these are the most mobile portions of vertebral column

234
Q

Describe a primary spinal cord injury

A

spinal cord stretching, tearing, compression of tissue, penetrating injury, vertebral stenosis, tumor, ischemia

235
Q

Describe a secondary spinal cord injury

A

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

236
Q

Spinal cord stunning does not always

A

lead to neurogenic (spinal) shock

237
Q

Management of an acute spinal cord injury includes:

A

immobilization of the injury, check for other injuries, support respiration, hypoxia and hypotension will exacerbate the SCI due to ischemia so need to treat

238
Q

Spinal cord stunning does not always

A

lead to systemic shock

239
Q

Spinal cord shock is the

A

temporary loss or depression of all or almost all neurological activity below the level of the spinal cord lesion
includes somatic sensory and motor neurons, neurons of the ANS and all spinal cord reflex activity

240
Q

The distinguishing features of spinal cord stunning are

A

flaccid paralysis and absent spinal reflexes caudal to the level of the injury

241
Q

Neurogenic shock is characterized by

A

profound hypotension and bradycardia due to lack of SNS tone

242
Q

An injury above ____ leads to _____, whereas an injury below _____ leads to _____

A

T5 leads to neurogenic shock because loss of innervation of the sphlancnic bed causes hypotension
below T5 is spinal cord stunning

243
Q

Concerns with patients with an abnormal vertebral column include

A

ability to be ventilated could be impaired and might be more difficult to intubate

244
Q

Scoliosis is

A

a lateral rotational curvature of the spine due to a structural issue (rotation of the spine itself) or nonstructural issue (pain, posture)

245
Q

Clinical manifestations of scoliosis include

A

spinal curvature, rounded shoulders, prominence of one hip, rib prominence
structural scoliosis compromises alveolar ventilation

246
Q

Scoliosis is associated with

A

increased risk of mitral valve prolapse, increased pulmonary resistance, and pulmonary hypertension

247
Q

Kyphosis is

A

a posterior rotation of the spine

248
Q

Kyphoscoliosis is

A

both a posterior and lateral spine curvature

249
Q

Ankylosing spondylitis is

A

chronic inflammatory joint disease that can affect vertebral joints and lead to joint remodeling

250
Q

Ankylosing spondylitis is caused by

A

genetic predisposition

autoimmune disease attacks antigens on cartilage

251
Q

Clinical manifestations of ankylosing spondylitis include

A

low back pain and stiffness, restricted motion of the spine, reflex muscle spasms, chest movement can be restricted

252
Q

Spina bifida is

A

a congenital disorder characterized by a defect in the closure of the neural tube
not progressive but it will not get better

253
Q

Clinical manifestations of spina bifida include

A

sphincter disturbance at the bowel and bladder

lower limb muscle weakness leads to gait changes and abnormal positioning of the feet

254
Q

Anesthetic considerations of spina bifida include

A

patients are in a prone position and could have injury to eyes, brachial plexus, or impaired ventilation

255
Q

Cauda equina syndrome can occur due to

A

compression of nerve roots below L1 caused by spine fracture or disk herniation

256
Q

Other names for a spinal include

A

spinal, intrathecal, subdural, or subarachnoid

257
Q

When placing a spinal,

A

we want to place below L3 to avoid injury the cell bodies because we are placing the spinal in the subarachnoid space

258
Q

Clinical manifestations of cauda equina syndrome include

A

lower extremity motor deficits, variable sensorimotor dysfunction, variable reflex dysfunction, variable bowel, bladder, and sexual dysfunction

259
Q

Cauda equina syndrome can be triggered by

A

spinal anesthesia that causes pooling of hyperbaric local anesthetics
to reduce risk avoid 5% lidocaine

260
Q

Bleeding can occur in the

A

subdural space
intracerebral space
and subarachnoid space

261
Q

The epidural is injected into the

A

space between the vertebral column and the dural layer

can be inserted at any level

262
Q

If an epidural needle was incorrectly placed in the subarachnoid space, we may see

A

issues with the autonomic sensory such as tingling

dilation of vasculature leading to hypotension

932 Pathophysiology (8 decks)

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