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NURS351-Pathophysiology I > Module 11 > Flashcards

Module 11 Flashcards

1
Q

Parenchymal Unit of The Nervous System

A

The Neuron

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2
Q

Afferent means…

A

Sensory

Periphery –> Brain

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3
Q

Efferent means…

A

Motor

Brain –> Periphery

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4
Q

2 Types of Cells for Nervous Tissue

A

Supporting Cells (Microglial, Schwan (PNS), Appendimal, etc)

Neurons

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5
Q

Soma

A

Cell body of the neuron with DNA/RNA for protein synthesis in the cytoplasm

The cytoplasm extends into the dendrite and axon length

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6
Q

Dendrite

A

Conducts information toward the cell body through the synaptic terminal

Communicates with axons and dendrites

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7
Q

Axons

A

Long efferent processes carrying information away from the cell body

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8
Q

Myelin Sheath

A

White Color - Made up of lipids

Surrounds the axons and allows for the sending of nerve impulses

The more heavily myelinated, the faster the velocity of the nerve impulse

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9
Q

Multiple Sclerosis

A

Loss of myelin sheathe in the CNS in patches

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10
Q

Gullain Barre Disease

A

Loss of myelin sheathe in the PNS in patches

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11
Q

Nodes of Ranvier

A

Interruptions of myelin insulation at intervals across the axon allowing for saltatory conduction (Jumps of action potential) which allows rapid neuron impulse travel

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12
Q

Neurons communicate via …

A

Action Potentials (Depolarization, Repolarization, Resting Membrane Potential Set by K, Na and K pump, and Threshold is set by calcium)

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13
Q

Grey Matter

A

Outer layer of brain

Made up of cell bodies (soma)

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14
Q

White Matter

A

Inner layer of brain

Made up of axons (white due to myelin)

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15
Q

How does grey and white matter differ in the spinal cord?

A

It is backward

Instead of grey matter being outside like the brain, it is the inside

Instead of white matter being inside like the brain, it is outside

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16
Q

Divisions of the Nervous System

A

NS –> CNS and Peripheral NS

CNS –> Brain and Spinal Cord

Peripheral NS –> Motor (efferent) Neurons and Sensory (Afferent) Neurons

Motor (Efferent Neurons) –> ANS and Somatic NS

ANS —> SNS and PNS

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17
Q

Covering/Layers Protecting the Brain (Outward to Inward)

A

Bony Skull –> Dura Mater –> Subdural Space –> Arachnoid Membrane –> Subarachnoid Space –> Pia Mater

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18
Q

Subarachnoid Space

A

Where CSF circulates to prevent brain damage / cushion

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19
Q

Choroid Plexus

A

Where CSF is made

Concentrated area of ependymal cells of the CNS with a rich vascular network allowing them to make cerebral spinal fluid

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20
Q

The spinal cord runs from …

A

the Lumbar to Sacral area

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21
Q

What protects the spinal cord

A

Boney Vertebrae

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22
Q

Dorsal Horn

A

Sensory/Afferent Information enters here and some of it will cross over while some of it stays on the same side

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23
Q

Anterior/Ventral Horn

A

Efferent/Motor information will travel through the front of the spinal cord and through here

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24
Q

Cervical Nerve Roots

A

lower segment (of the root)

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25
Q

Lumbar Nerve Roots

A

upper segment (of the root)

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26
Q

How many peripheral nerves are there?

A

8 Cervical

12 Thoracic

5 Lumbar

1 Coccygeal

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27
Q

What parts of the nervous system do motor neurons oversee?

A

ANS (SNS + PNS)

Somatic NS (Voluntary)

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28
Q

Things that Parasympathetic NS Causes

A 
Constricts pupil
Stimulates Salivations
Inhibits Heart
Constricts Bronchi
Stimulates Digestive Activity
Stimulates Gallbladder
Contracts Bladder
Relaxes Rectum

Cholinergic (Muscarinic) Receptors - stim by acetylcholine

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29
Q

Things that the Sympathetic NS Causes

A 
Dilates pupil
Inhibits Salivation
Relaxes Bronchi
Accelerates Heart
Inhibits Digestive Activity
Simulates Glucose Release by the Liver
Secretion of EP and NEP from kidney
Relaxes Bladder 
Contracts Rectum

Adrenergic (Beta) Receptors - stim by EP and NEP

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30
Q

Anterolateral Afferent (Sensory) Tracts

A

Ascending cell bodies/pathways

Unmyelinated or Lightly Myelinated causing slow Conduction

Cell bodies are in the contralateral dorsal horn

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31
Q

Posterior Afferent (Sensory) Tracts

A

Ascending cell bodies/pathways

Large caliber axons and heavily myelinated causing Fast Conduction

Cell bodies are in the ipsilateral dorsal horn

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32
Q

Where are the anterolateral tract cell bodies?

A

Contralateral dorsal horn

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33
Q

Where are the posterior tract cell bodies?

A

Ipsilateral Dorsal Horn

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34
Q

What sort of sensation is the anterolateral tracts responsible for?

A

Pain

Temperature

Crude or Light Touch

Itch

Tickle

Sexual Sensation

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35
Q

What sort of sensation is the posterior tracts responsible for?

A

Position Sense

Discriminative Touch

Vibration Sense

Stereognosis

Graphesthesia

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36
Q

Stereognosis

A

Ability to recognize the form of an object/what it is when holding it

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37
Q

Graphesthesia

A

Can tell what someone wrote with their finger on your back/ back of hand

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38
Q

Efferent (Motor) Tracts

A

Descending pathways allowing for voluntary control of muscle movements

Cell bodies are in the contralateral motor cortex

Fiber crossed in the pyramidal decussation (medulla) and then synapse with ipsilateral interneurons

These tracts influence the activity of lower motor neurons (LMNs) which allow voluntary muscle control, movement, and motor function

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39
Q

Pyramidal Decussation

A

In the medulla oblongata

Axons crossing over and stacking up to form a pyramid shape. Allows crossing over and then ipsilateral synapsing for motor neurons

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40
Q

Frontal Lobe

A

Front

Higher Order thinking

Awareness, Memory, Emotion, Behavior, Skilled Movements

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41
Q

Temporal Lobe

A

lower area close to brainstem

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42
Q

Occipital Lobe

A

Back of the brain

vision and visual recognition

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43
Q

Parietal Lobe

A

upper part of the brain

processing sensory information

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44
Q

What lobe possesses the Motor Cortex?

A

frontal lobe

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45
Q

What lobe possesses Wernickes Area?

A

Temporal lobe

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46
Q

What lobe possesses Brocas Area?

A

frontal lobe

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47
Q

Motor Cortex

A

Area of the frontal lobe anterior to the central sulcus

Controls basic movements

next to central fissure

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48
Q

Cerebellum

A

part of the brainstem

the “bulb” in back of the brain

controls balance and muscle coordination

“Bella” Balance

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49
Q

Right v Left Brain Functions

A

Right: Reasoning, Language, Scientific Skills

Left: Insight, Spatial Awareness, Creativity

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50
Q

Cranial nerves

A

12 nerves connecting the CNS to various parts of the body/head

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51
Q

CN I

A

Olfactory Nerve

Smell

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52
Q

CN II

A

Optic Nerve

Vision

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53
Q

CN III

A

Oculomotor Nerve

Eye movements

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54
Q

CN IV

A

Trochlear Nerve

Eye movements

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55
Q

CN V

A

Trigeminal Nerve

Facial sensation and jaw movements

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56
Q

CN VI

A

Abducens Nerve

Lateral eye movements

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57
Q

CN VII

A

Facial nerve

Facial expression and taste

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58
Q

CN VIII

A

Acoustic (Vestibulocochlear) Nerve

Hearing and Balance

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59
Q

CN IX

A

Glossopharyngeal Nerve

Taste and Throat Sensations

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60
Q

CN X

A

Vagus nerve

Breathing, circulation and digestion

*unique as it runs throughout the whole body

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61
Q

CN XI

A

Spinal Accessory Nerve

Movements of neck and back muscles

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62
Q

CN XII

A

Hypoglossal Nerve

Tongue Movements

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63
Q

Mechanisms of Injury for the Brain

A

Hypoxic and Ischemic Injury

Injury from Excitatory Amino Acids

Increased Volume and Pressure

Brain Herniation

Cerebral Edema

Hydrocephalus

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64
Q

How is the brain a selfish organ?

A

Body is 2% of the body weight, but received > 15% of cardiac output and consumes 20% of the oxygen available to the body

This is important to know since it relates to hypoxic and ischemic injury

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65
Q

Without oxygen, how long will it take before death of brain cells occur?

A

4-6 minutes

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66
Q

The brain cannot do what in regard to oxygen?

A

cannot store oxygen or do anaerobic metabolism

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67
Q

Hypoxia

A

Deprivation of oxygen with maintained bloodflow

So its bloodflow w/ no oxygenation

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68
Q

What does Hypoxia do to the brain?

A

Depressant effect on the brain –> Euphoria, Listlessness, Drowsiness, Impaired Problem Solving ability

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69
Q

Examples of Hypoxic Injury/Situations for the brain?

A

Reduced Atmospheric Pressure from living at high altitude

Carbon Monoxide poisoning

Severe Anemia

Failure to oxygenate blood

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70
Q

Ischemia

A

Reduced or interrupted blood flow (with metabolic toxin byproduct buildup occurring as a result)

Can be focal or global

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71
Q

Hypoxia and Ischemia:

You can have ____ and no ____, but if you have ____ you do have ____

A

You can have hypoxia and no ischemia, but if you have ischemia you do have hypoxia

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72
Q

Focal Ischemia

A

when blood flow is inadequate to meet the metabolic demands of a PART OF THE BRAIN

ex: Stroke

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73
Q

What is Global Ischemia

A

when blood flow is inadequate to meet the metabolic demands of the ENTIRE BRAIN

ex: Cardiac arrest or circulatory shock

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74
Q

Shock

A

massive vasodilation and blood movement to the periphery, taking away from the brain, and leading to global ischemic injury

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75
Q

How fast does global ischemia use up brain resources?

A

Oxygen - used up in 10 seconds

Glucose Stores - exhausted in 2-4 minutes

Cellular ATP Stores - depleted in 4-5 minutes

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76
Q

What occurs, in regard to sodium, calcium, and potassium during global ischemia?

A

Excessive influx of Na and Ca occurs, with efflux of K

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77
Q

What does a large influx of sodium in neuronal cells cause?

A

Neuronal and Interstitial edema

*The sodium has water follow it down its concentration gradient leading to the in between cell edema (interstitial) *

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78
Q

Calcium Cascade

A

Excessive influx of calcium into neuronal cells (Where it does not belong)

Causes release of intracellular and nuclear enzymes causing cell destruction

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79
Q

Watershed Zones

A

Type of global ischemic injury

Concentrated injury occurs in anatomically vulnerable BORDER ZONES BETWEEN OVERLAPPING TEZRRITORIES supplied by major arteries

Since areas overlap, a lot of deficit, damage, and infarction occurs in junctions of two vascular territories

This type occurs due to a blockage of the cerebral vessel

Essentially, these areas of the brain are receiving shared blood supply from multiple arteries, and those arteries get blocked meaning widespread damage occurs between areas sharing the arteries

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80
Q

3 Major Cerebral Arteries

A

Middle

Anterior

Posterior

(MAP)

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81
Q

Laminar Necrosis

A

Type of global ischemic injury

In areas supplies by penetrating (the grey matter) arteries of the cerebral cortex (These are small penetrating arteries)

Necrosis occurs in a laminar way (along a parallel plane or layer) and is most severe in the deeper layers of the cortex

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82
Q

How is laminar necrosis like broccoli?

A

The grey cell bodies are like the florets

The axons are like the stems

A lot of fluid can go in and around the stems/axons during global ischemia (from Na, K, and Ca Influx and Efflux)

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83
Q

What is post-ischemic hypoperfusion?

A

Damage to blood vessels and CHANGES IN BLOOD FLOW as a result of [any] ischemia that prevents the return of adequate tissue perfusion despite reestablishment of circulation

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84
Q

What happens to fluid during post-ischemic hypoperfusion?

A

Inflammatory response launches causing fluid to move from vessels to brain tissue (leading to edema in the brain) and what is left in the capillaries clots and grows sludgy making reperfusion difficult

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85
Q

What mechanisms are involved with post-ischemic hypoperfusion?

A
  1. Desaturation of Venous Blood
  2. Capillary and Venous Clotting
  3. Increased blood viscosity –> Increased flow resistance
  4. Ischemic vasoconstriction
  5. Increased cerebral metabolic rate and increased need for energy producing substrates
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86
Q

How and why does venous blood become desaturated during post-ischemic hypoperfusion?

A

VENOUS (not arterial) blood is drained of all the oxygen left in it due to the brain needing oxygenation for metabolic processes despite the capillaries being clotted with blood

This causes the venous blood to become sludgy and start clotting too

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87
Q

What does the capillary and venous clotting cause in Post-ischemic hypoperfusion?

A

Clotting –> Sludging of blood –> Increased blood viscosity –> Increased resistance to blood flow in the brain

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88
Q

What leads to ischemic vasoconstriction during post-ischemic hypoperfusion?

A

immediate vasomotor paralysis d/t extracellular acidosis

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89
Q

What causes vasomotor paralysis during post-ischemic hypo perfusion?

A

Acidic conditions/extracellular acidosis leads to vasomotor paralysis immediately

This becomes dangerous because they constrict and are constricted permanently which then causes vasospasm (ischemic vasoconstriction)

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90
Q

Why is hypermetabolism a part of post-ischemic hypoperfusion?

A

To try and rescue the brain (compensatory) EP and NEP is released and circulates which causes increased cerebral metabolic rate and increased need for energy producing substrates (hypermetabolism) which just leads to more substrates and waste products in circulation (which makes circulation even more difficult to fix)

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91
Q

Treatment for Global Ischemia

A

Aimed at providing oxygen and lowering metabolic needs during times when cerebral flow is not occurring as it should

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92
Q

Methods of Treatment for Global Ischemia?

A

Decreasing Brain Temperature

Normovolemic Hemodilution to Overcome Sludging during reperfusion

Control of blood glucose 100-200 mg/dL

93
Q

How do they decrease brain temperature to treat global ischemia?

A
  1. A cerebral cooling collar around the common carotids
  2. Whole Body cooling (more used now) where temp is brought down while intubated during it and then carefully warmed after a few days
    * Bringing down the temperature will decrease cerebral metabolic demands
94
Q

How does normovolemic hemodilution treat global ischemia?

A

Normal saline is isotonic and stays in vessels

The purpose is that it overcomes sludging in the capillaries/veins during reperfusion, so fluid and flow starts going once again

95
Q

Why do we control global ischemia patients blood glucose level at 100-200 mg/dL as treatment for global ischemia?

A

Giving glucose higher than the recommended need is important since the metabolic demand in the brain and tissues is high

We want to reduce the metabolic demand with cooling, but we also need to give glucose to help meet demands

96
Q

Excitotoxicity

A

Injurt d/t excitatory amino acids (neurotransmitters)

Overstimulation of receptors for specific AA that act as excitatory neurotransmitters

Overproduction stimulates nervous tissue as a response to injury, and this overabundance leads to increased metabolic injury and nervous tissue damage

97
Q

Main 2 Excitatory Neurotransmitters (AA) that can lead to excitotoxicity?

A

Glutamate

Aspartate

98
Q

Glutamate

A

Principal Excitatory neurotransmitter in the brain involved in normal brain function

Causes calcium cascade and glutamate toxicity w/ neuronal swelling

99
Q

How does Glutamate cause symptoms/excitotoxicity?

A

Injury occurs –> Extracellular glutamine accumulated –> glutamate toxicity –> Initial symptoms (w/in minutes) are neuronal swelling (d/t sodium influx w/ water following) –> Later symptoms (w/in hours) the calcium cascade influence begins

100
Q

How does Glutamate related to the calcium cascade?

A

Its activity is coupled with receptor operated calcium ion channels normally –> Calcium cascade

This causes the enzyme release and tissue/cell destruction

101
Q

Research on excitotoxicity is being directed at…

A

pharmacologic methods to prevent brain damage from excitatory amino acids

102
Q

A person with excitotoxicity can do better recovery if …

A

the there is a focus on prevention of the slower effects of the calcium cascade

103
Q

Normal Intracranial Pressure (ICP)`

A

5-15 mmHg

104
Q

Swelling from Sodium and Calcium Cascade leads to what?

A

Intracranial volume increases followed by increases in intracranial pressure

105
Q

The skull is a confined cavity meaning it is non-expandable, so if volume increases what areas of the brain can make up for the increase be reducing?

A
  1. Blood Volume (10%)
  2. Brain Tissue (80%) (Realistically this cannot change)
  3. CSF (10%)
106
Q

Communicating versus Non-communicating Hydrocephalus

A

Communicating means theres too much CSF produced but theres no obstruction between ventricles

Non-communicating means theres too much fluid and an obstruction is blocking flow between ventricles

107
Q

What things can undergo reciprocal compensation for change in ICP?

A

CSF and BV (Blood volume)

108
Q

What ways does CSF amount increase?

A

Excess production

Decreased absorption

Obstructed Circulation

109
Q

What ways does CSF amount decrease?

A

Translocation to the spinal subarachnoid space

Move some to Basal Cisterna at the bottom of the spinal column

Increased reabsorption

(This decreases volume and pressure)

110
Q

What ways does BV amount increase?

A

Vasodilation of cerebral blood vessels

Obstruction of venous outflow

111
Q

What ways does BV amount decrease?

A

Low pressure venous system has limited volume buffering capacity and blood flow is controlled by autoregulatory mechanisms

Basically, autoreg mechanisms like hyperventilation to decrease PCO2 will cause vasoconstriction to lower BV

112
Q

Monroe-Kellie Hypothesis

A

Reciprocal Compensation

If ICP and Volume increase, CSF and BV need to decrease to compensate

113
Q

What occurs with excessive intracranial pressure?

A
  1. It obstructs cerebral blood flow
  2. Destroys brain cells (infarction of brain tissue)

3 Herniation (displaces brain tissue)

114
Q

What things increase cerebral volume?

A

Brain tumor

Cerebral edema

Bleeding into brain tissue (hematoma)

115
Q

Cerebral Compliance

A

Change in Volume / Change in pressure

116
Q

What does the pressure-volume curve show?

A

once compensatory mechanisms have been exceeded, even small changes in volume result in dramatic increases in pressure (only so much can vasoconstrict or go to spinal areas)

117
Q

Normal Cerebral Perfusion Pressure (CPP)

A

70-100 mmHg

118
Q

CPP Equation

A

MABP - ICP

*Mean Arterial Blood Pressure Minus Intracranial Pressure

119
Q

What occurs if CPP is below 50-70 mmHg

A

Brain Ischemia (trouble with perfusion)

120
Q

What occurs if ICP is greater than or equal to MABP in the CPP equation?

A

Inadequate tissue perfusion

cellular hypoxia

neuronal death

121
Q

Stages of Intracranial Hypertension

A

1 - Compensation
2 - Increased ICP
3 - Decompensation
4 - Herniation or Loss of CPP

122
Q

Intracranial HTN is not stair like steps/stages, they are …

A

a pressure-volume curve

123
Q

Stage 1 Intracranial HTN

A

Compensation:

Increase in volume in an intracranial compartment leads to decrease in one or both (CSF&BV) of the other volumes

ICP pressure remains normal due to compensation

124
Q

Stage 2 Intracranial HTN

A

Increase in ICP:

Brain responds by constricting the cerebral arteries to reduce pressure but results in hypoxia, hypercarbia, and deterioration of brain function

(The constriction causes inadequate tissue perfusion, so there’s a lack of O2 and buildup of CO2 leading to acidosis and deterioration)

!!!!Once O2 drops, reflex vasodilation occurs causing stage 3!!!!

125
Q

Stage 3 Intracranial HTN

A

Decompensation:

Cerebral arteries respond to O2 drop with reflex vasodilation –> Increase in blood volume –> Increase further of ICP

At this point a small change in intracranial volume results in LARGE changes in ICP

126
Q

Stage 4 Intracranial HTN

A

Herniation or Loss of CPP:

Swelling and Pressure increases lead to herniation

When ICP = MABP –> No cerebral perfusion is occurring

127
Q

What are 2 important things to keep in mind when you have ICP patients?

A
  1. Elevate the head of the bed to a maximum of 30 degrees to promote venous passive drainage from gravity (but also has minimal effect on arterial pressure)
  2. Make sure head position is midline to prevent kinking of head veins
128
Q

What is the BEST sign of increased ICP? (Test Question)

A

A decrease in Level of Consciousness is the earliest and most reliable sign of increased ICP

Decreased LOC –> Increased ICP

129
Q

Cushing Reflex

A

A CNS ischemic response triggered by ischemia of the vasomotor center of the brain

130
Q

What things does the Cushing Reflex cause?

A
  1. Increased MABP (to perfuse the brain)
  2. Widening Pulse Pressure (Systolic goes way higher than Diastolic)
  3. Reflex Slowing of the Heart Rate (bradycardia) via efferent vagus nerve system to compensate for an increase in BP and ICP (Reflex Bradycardia)
131
Q

What is the brain trying to do with the Cushing Reflex?

A

It is a “last ditch” effort to maintain cerebral circulation and stay alive, but we hope to catch things before it gets this bad (and we usually do through ICP monitoring- so this is rarely seen)

132
Q

The cushing reflex is an important but _____ indicator of increased ICP

A

LATE

133
Q

Increases in cerebral volume lead to dramatic ____ in pressure once ________ ______ are overwhelmed

A

increases; compensatory mechanisms

134
Q

Cerebral Edema

A

Brain swelling; Increase in tissue volume d/t abnormal fluid accumulation

May or may not increase ICP

135
Q

Way can a cerebral edema may or may not come with an increase in ICP?

A

It depends on whether its just a small edema and if the brains compensatory mechanisms can handle it by moving CSF or BV

136
Q

Types of Cerebral Edema

A

Interstitial

Vasogenic

Cytotoxic

137
Q

Interstitial Edema

A

Interstitium (spaces between cells) swells between axons, involving movement of CSF across the ventricular wall

It is associated with an increase in Sodium and Water content of the peri ventricular white matter, and it passing into it

The sodium and water movement cause ischemia, neuronal interstitial edema, and the calcium cascade

138
Q

What condition causes interstitial edema?

A

Non-communicating hydrocephalus

CSF is pushed through the ventricular walls so its moving into interstitial spaces thus blocking CSF flow, causing more to move into the interstitium

139
Q

Vasogenic Edema

A

Increase in Extracellular fluid (ECF) - Mainly BLOOD- surrounding brain cells

Vessels are affected

Occurs mostly in white matter since its more compliant and offers less resistance to fluid accumulation than grey matter

can make the cerebral hemisphere displace and cause herniation

140
Q

What leads to vasogenic edema?

A

Brain Injury –> Blood brain barrier disrupted –> increased permeability and free diffusion of blood across capillaries that used to not allow most things to cross

141
Q

What are some manifestations of vasogenic edema?

A

Focal Neurological Deficits (part of the brain, so only part of the function is affected)

Disturbances in Consciousness

Severe Intracranial HTN

*all of these things depend on how much ECF is moving

142
Q

What are some conditions leading to vasogenic edeam?

A

Anything that interrupts the blood brain barrier or allows fluid into the interstitial space:

Tumors

Prolonged Ischemia

Hemorrhage

Brain Injury

Infectious processes that impair fxn of the blood brain barrier and allow transfer of water and protein into the interstitial space

143
Q

Cellular Hypoxia

A

Actual swelling of brain cells from not enough O2, too much CO2 for the brain cells, so the brain enters anaerobic metabolism, has decreased ion pump function, and pre-synaptic hypo-polarization

The increased intracellular fluid primarily occurs in gray matter (since that’s where the cell body is), but can also occur in white matter

Slowly progressive process

144
Q

In cytotoxic edema, decreased blood flow leads to cellular hypoxia and then what?

A
  1. Cellular Hypoxia –> Decreased ATP production and E stores –> Decreased ion pump function –> Water entry and cellular swelling from sodium rushing in
  2. Cellular hypoxia –> Anaerobic metabolism –> Increase lactic acid and extracellular acidosis –> water entry and cellular swelling
145
Q

What does pre-synaptic hypo-polarization in cytotoxic edema lead to?

A

Hypo-polarization –> Calcium Cascade from broken gates causing increased intracellular Ca –> NT like Glutamate and Aspartate is then increased in conjunction with the cascade –> There is no reuptake of calcium or NTs leading to low osmotic states, hyperpolarization, Ca channels remaining open, and loss of cellular function

146
Q

The extra Ca and NTs from hypo-polarization in cytotoxic edema can lead to what outcomes?

A
  1. Electrical Hyperactivity (Seizure) until exhaustion –> 2. Electrical silence (Death)
147
Q

Potassium sets…

A

the resting membrane potential

148
Q

The Na-K Pump determines …

A

signals

149
Q

Calcium sets …

A

the threshold

150
Q

What 3 things determine neuronal activity/impulses?

A
  1. K
  2. Na-K pumps
  3. Calcium
151
Q

Cytotoxic edema may be severe enough to cause what?

A

rupturing of cells and production of cerebral infarction with necrosis of brain tissue after

152
Q

What sort of cells can have cytotoxic edema occur in them?

A

Vascular Endothelium

Smooth Muscle Cells

Astrocytes

Oligodendrocytes

Neurons

153
Q

Manifestations of Cytotoxic Edema

A

Major Changes like:

Stupor

Coma

Eventual seizure

Potential brain infarction and necrosis

154
Q

Conditions that can cause cytotoxic edema?

A

Hypo-osmotic states such as water intoxication

Severe ischemia that impairs the Na-K pump

Hypoxia

Acidosis

Brain Trauma

155
Q

Cerebral edema does not necessarily disrupt brain function unless…

A

there is an increase in ICP

156
Q

Ways to treat Cerebral Edema?

A

Localized Edema - Corticosteroids

Stabilize cell membranes and scavenge free radicals

Osmotic Diuretics

157
Q

How are corticosteroids used to treat cerebral edema?

A

They are used on localized edema surrounding brain tumors

But, the use on generalized edema is controversial/does not work well

158
Q

Why are osmotic diuretics a double edged sword for treating cerebral edema?

A

Diuretics like mannitol may be useful in the acute phase of vasogenic and cytotoxic edemas when hypo-osmolarity is present

But, the potent diuretics need balance because you could dierese so much volume that they cannot maintain CPP

159
Q

Consciousness

A

state of awareness of self and the environment and the ability to become oriented to new stimuli

160
Q

The most important manifestation of brain injury is…

A

complications with level of consciousness (LOC)

161
Q

What are the components of consciousness?

A
  1. Arousal and Wakefulness: State of wakefulness, ability to respond to external stimuli, mediated by RAS
  2. Content and Cognition: Moods, awareness of self, awareness of environment, cognitive function, mediated by cerebral cortex in conjunction with RAS
162
Q

What do the components of consciousness reflect?

A

Person
Place
Time

163
Q

Important Levels of consciousness to consider with brain injury?

A 
Confusion
Delirium
Obtundation
Stupor
Coma
164
Q

Confusion

A

Impaired ability to think clearly

Disorientation

Inability to perceive, respond to, or remember current stimuli with customary repetition

165
Q

Delirium

A

Disturbed consciousness with motor restlessness

Transient hallucinations

Disorientation and sometimes delusions

166
Q

Obtundation

A

decreased alertness with psychomotor retardation

167
Q

Stupor

A

not unconscious, but exhibits little or no spontaneous activity

If they were fully conscious, they would push you away or react to you pinching their skin

168
Q

Coma

A

No pinching of the skin response whatsoever, unlike stupor

Unarousable and unresponsive to external stimuli or internal needs

Just because they are in a coma and are unresponsive does not mean they cannot hear you

169
Q

What determines coma / coma level?

A

The glascow coma scale

170
Q

What causes abnormal rigidity?

A

Brain/ Brain Stem Damage

171
Q

Decorticate

A

Abnormal rigidity:

Upper arms held tightly to the sides with elbows, wrists, and fingers flexes

Legs are extended and internally rotated with feet plantar flexed

172
Q

What causes Decorticate position?

A

Destructive lesion of the corticospinal tracts within or very near cerebral hemispheres

173
Q

Decerebrate

A

Abnormal Rigidity

Jaws clenched and neck extended

Arms adducted and stiffly extended at the elbows, with forearms pronated and wrists and fingers flexed

Legs stiffly extended at knees with feet plantar flexed

174
Q

What causes Decerebrate position?

A

Lesion in the diencephalon, midbrain, or pons

Could also be due to severe metabolic disorders like hypoxia or hypoglycemia

175
Q

What is more dangerous: Decorticate or Decerebrate?

A

Decerebrate is more dangerous since it comes from brain stem lesions - a person could survive cortex issues, but not necessarily lower brain ones

176
Q

Flaccidity

A

Abnormal motor response where no motor response is exhibited

If you pick up their arm it will just flop when let go

177
Q

Purposeful Movement

A

Should be present, if not that is abnormal

It localizes to pain –> unconsciously attempts to remove painful stimulus

178
Q

Complete Flexion

A

Should be present, if not that is abnormal

Withdraws or flexes extremity indiscriminately in response to painful stimuli

179
Q

Focal Motor Responses that are Abnormal in Adults

A

Grasp Reflex
Sucking Reflex
Babinski Reflex

180
Q

Grasp Reflex

A

baby should pull fingers around your finger

goes away by 6 mo old

181
Q

Sucking Reflex

A

put something in babies mouth, and they suckle on it

182
Q

Babinski Reflex

A

run nail across foot, under toes and across the side, and the toes should flare out

Should be gone by 2 y/o

183
Q

Consensual Pupillary changes

A

When light is shined in one eye, the other pupil should constrict too and then dilate when light is removed

184
Q

Direct pupillary changes

A

When light is shined in one eye, that pupil should constrict and then dilate when the light is removed

185
Q

Pupillary Change Issues

A
  1. Unequal or react sluggishly
  2. Pinpoint or midpoint fixed
  3. Dilated, fixed
  4. Unilateral, fixed
186
Q

Pupillary responses can be ___ or ___

A

unilateral or bilateral

187
Q

Unequal or Sluggish Reaction of Pupillary changes is caused by …

A

compression

188
Q

Pinpoint or midpoint fixed pupillary changes is caused by …

A

compression of the brainstem

189
Q

Dilated and fixed pupillary changes is caused by …

A

compression of CN III

190
Q

Unilateral and fixed pupillary changes is caused by …

A

compression of one CN III

191
Q

Oculomotor Response means…

A

an intact brainstem

192
Q

What signifies a poor prognosis (brain death) in regard to oculomotor response?

A

No response after > 48 hours

193
Q

2 Oculomotor Response Tests?

A
  1. Oculocephalic Reflex

2. oculovestibular Reflex

194
Q

Oculocephalic reflex

A

The Doll’s Eyes Reflex

Normally - when the head turns side to side the eyes rotate together to the opposite side/stay at one point

Abnormal - eyes rotate together in the same direction as the head

195
Q

Oculovestibular Reflex

A

Cold or Water Caloric Test

Normally - when the ear canal is irrigated with (cold) water the eyes will turn toward the side being stimulated

Abnormal - absence of eye movement upon stimulation

196
Q

Nystagmus

A

Eyes working backward and forward repeatedly, back and forth, and non-voluntarily

197
Q

Important Breathing Patterns for Brain Injury Patients to watch for

A
  1. Cheyne Stokes
  2. Central neurogenic ventilation
  3. Apneustic Ventilation
  4. Cluster Breathing
  5. Ataxic Breathing
198
Q

Cheyne-Stokes Breathing

A

Alternating pattern of deep and shallow breathing with periods of apnea

common with diffuse cortical injury or coma from metabolic causes

199
Q

Central neurogenic ventilation

A

Rapid breathing due to direct stimulation of the respiratory center

A regular hyperpneic pattern occurs (Deep and fast breathing) –> Decrease in PCO2 and Increase in pH (Alkalosis)

200
Q

What kind of breathing might a patient with diabetic ketoacidosis display?

A

Kussmaul breathing

201
Q

Apneustic Ventilation

A

Breathing in and out very slowly and prolonged

Prolonged Inspiratory cycle followed by a 2 to 3 second pause, alternating with a prolonged expiratory cycle

Found in lesions of the lower pons - which usually has conduction fibers for chewing food and manipulating the jaw during speech

202
Q

Cluster Breathing

A

Clusters of breaths alternating with irregular periods of apnea

indicates damage to lower pons or high medulla

203
Q

Ataxic Breathing

A

Chaotic respiratory effort - No pattern at all!

Chaotic

Indicates damage to the medullary respiratory control center

204
Q

Apnea

A

periods of 20 seconds of absolutely no breathing at all

205
Q

What are some vital signs changes that occur with brain injury?

A

Hypo or Hyperthermia

Cushings Triad

206
Q

How does Hypo and Hyperthermia relate to brain injury?

A

Hypothalamic or Pituitary injuries or head trauma can lead to inappropriate thermoregulation

207
Q

How does cushings triad effect vital sign changes in brain injury patients?

A

Increase in Systolic BP and Decrease in diastolic BP (Widening pulse pressure) and decreased HR alongside reflex bradycardia

Occurs with increase pressure on the lower brain stem before brain herniation

208
Q

Glascow Coma Scale

A

scale of 3 elements for coma patients

209
Q

3 important elements of the Glascow Coma Scale

A
  1. E - Eye Opening
  2. M - Motor Response
  3. V - Verbal Response
210
Q

In the glascow coma scale what are the range of results?

A

3 to 15

NEVER 0

(can be +4, +6, +5 - or - +1 +1 +1)

211
Q

What vessels provide arterial blood flow in cerebral circulation?

A

2 Internal Carotids

2 Vertebral Arteries –> Basilar Artery

Circle of Willis

212
Q

What vessels provide venous blood flow in cerebral circulation

A

2 sets of veins without valves (Deep and Superficial Cerebral Vein Systems)

2 Internal Jugular Veins

213
Q

Why do the veins of the cerebral circulatory system have no valves?

A

because the flow depends on gravity and pressure in the venous sinuses to increase ICP

214
Q

Circle of Willis

A

allows for shared blood flow in the brain, and if there is a blockage of bloodflow then this allows offsetting of that issue

215
Q

Deep Cerebral Venous System

A

Veins that drain the inner parts of the brain

216
Q

Superficial Cerebral Venous System

A

Veins that drain the outer parts of the brain

217
Q

A large portion of the brain is fed by what artery, and what can occur if there is infarct for this artery?

A

The Middle Cerebral Artery

It supplies a lot of the brain and major damage can occur if infarct happens

*look at the slide on cerebral arteries

218
Q

Important Cerebral Arteries

A 
Anterior Cerebral Artery
Middle Cerebral Artery
Posterior Cerebral Artery
Anterior Choroid Artery
Basilar Artery
219
Q

How much of cardiac output goes to the brain

A

750 mL/min (1/6 of resting CO)

15% of bloodflow goes to the brain

220
Q

What regulates cerebral blood flow?

A

Autoregulatory or local mechanisms that respond to metabolic needs

Examples of local mechanisms are pH and CO2 that function to trigger vasodilate or constrict to increase or decrease cerebral blood flow

221
Q

What regulates deep cerebral blood flow?

A

Autoregulatory mechanisms

Metabolic Factors

222
Q

What regulates superficial cerebral blood flow?

A

Sympathetic NS - it is responsible for vasospasm as seen in a cerebral aneurysm rupture

223
Q

Aneurysm

A

outpouching of the wall in the brain and potential for things to collect in that area and potentially rupture

224
Q

What sort of metabolic factors influence cerebral blood flow?

A
  1. CO2 Concentration
  2. pH
  3. O2 concentration
225
Q

2x the amount of CO2 concentration means what for cerebral blood flow?

A

2x the cerebral blood flow

Vasodilation occurs (which can increase ICP) to prevent acidosis

226
Q

How does Hydrogen ion concentration (pH) regulate cerebral blood flow?

A

low pH can cause vasodilation in most cases to prevent an acidotic brain –> get more O2 and get rid of CO2

BUT, extracellular acidosis also induces vasomotor paralysis making vessels unconstrictable/dilateable past wherever they were when paralysis occurred

227
Q

How does O2 concentration regulate cerebral blood flow?

A

decrease in oxygen –> increase in blood flow to the brain

228
Q

Metabolic Factors regulating blood flow are all…

A

local factors of affecting brain blood flow

NURS351-Pathophysiology I (11 decks)

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