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PATHO/PHARM II > Conditions Effecting the Nervous System and PharmacotherapyPart Two: Select Conditions > Flashcards

Conditions Effecting the Nervous System and PharmacotherapyPart Two: Select Conditions Flashcards

Exam 3

1
Q

Traumatic Brain Injury TBI Patho: What is it usually caused by?

A

Usually caused by a sudden violent blow or jolt to the head (closed injury) or a penetrating (open injury) head wound that disrupts the normal brain function.

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2
Q

Traumatic Brain Injury TBI Patho: What do TBIs do to the brain?

A

The injury can bruise the brain,

damage to axon & nerve fibers, and

cause hemorrhaging.

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3
Q

Traumatic Brain Injury: How does it vary?

A

Varies from mild to severe

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4
Q

Traumatic Brain Injury: Who are person’s at high risk?

A

Persons at highest risk:

males, children 0–4 years old, adolescents 15–19 years old, adults 65 years of age or older, certain military personnel, and individuals with history of substance abuse

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5
Q

Traumatic Brain Injury:

What is Secondary brain injury?

A

Secondary brain injury: indirect result of primary injury, strokes, trauma.

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6
Q

Traumatic Brain Injury:

What are contributing factors of Secondary brain injury?

A

Contributing factors include:

hypotension,

hypoxia,

anemia,

hyper/hypocapnia,

cerebral inflammation,

cerebral edema,

IICP,

decreased cerebral perfusion,

cerebral ischemia,

herniation

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7
Q

TBI Complications: What changes?

A

Changes in thinking, sensation, language, or emotions

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8
Q

TBI Complications: How do seizures occur?

A

Seizures – can occur early or up to 2-5 yrs or longer

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9
Q

TBI Complications: How does Alzheimer’s occur?

A

Alzheimer’s disease – repeated brain injury, diffuse axonal injury provides the potential for tau and amyloid to develop

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10
Q

TBI Complications: How does Parkinson’s disease occur?

A

Parkinson’s disease – deposits of proteins clumps build up axons & neurons

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11
Q

TBI Complications: other complications include?

A

Memory decline
Depression
IICP
Death

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12
Q

Types of Traumatic Brain Injuriesinclude:

A

Closed head injury

Open head injury

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13
Q

Types of Traumatic Brain Injuries:

What are the types of Closed Head Injury?

A

Concussion

Contusion

Coup/Contrecoup

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14
Q

Types of Traumatic Brain Injuries:

What is a Closed Head Injury?

A

Skull is not fractured, but blood vessels rupture, and brain is injured

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15
Q

Types of Traumatic Brain Injuries:

What are causes of Closed Head Injury?

A

Causes: head strikes hard surface (e.g. falls, MVA) or object strikes head (e.g. baseball)

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16
Q

Types of Traumatic Brain Injuries:

What occurs in closed head injury?

A

Brain lesion occurring in precise location

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17
Q

Types of Traumatic Brain Injuries:
What is a Concussion:

A

momentary interruption of brain function, mild TBI

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18
Q

Types of Traumatic Brain Injuries:

How many Concussions vary? What does it depend on?

A

Maybe mild (LOC < 30 min or none), mod (LOC 30 min – 6 hrs), severe (LOC >6hrs)

Depends on loss of consciousness

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19
Q

Types of Traumatic Brain Injuries:

What are symptoms of concussions?

A

Sx: h/a, n/v, diff concentrating, sleeping–> permanent deficits in brain function

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20
Q

Types of Traumatic Brain Injuries:

What kind of damage occurs with concussions?

A

Brainstem damage

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21
Q

Types of Traumatic Brain Injuries:

Contusion (brain bruising): What is it?

A

Compression of skull

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22
Q

Types of Traumatic Brain Injuries:

What occurs with Contusion (brain bruising)?

A

Blood leaking from injured vessel. Immediate loss of consciousness < 5min

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23
Q

Types of Traumatic Brain Injuries:

What kind of damage occurs with Contusion (brain bruising)?

A

Edema, hemorrhage, infarction, necrosis to contused areas

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24
Q

Types of Traumatic Brain Injuries:

Closed head injury: Coup/Contrecoup

What is a coup injury?

A

Coup injury: injury at site of impact

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25
Q

Types of Traumatic Brain Injuries:

Closed head injury: Coup/Contrecoup

What is a contrecoup injury? What occurs with it?

A

Contrecoup: injury to the opposite side of the brain from the actual impact.

Axonal sheering

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26
Q

Types of Traumatic Brain Injuries:

Closed head injury: Coup/Contrecoup

Contrecoup injury: What is the damage due to?

A

Damage due to the brain bouncing off the opposite side of the skull.

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27
Q

Types of Traumatic Brain Injuries:

Closed head injury: Coup/Contrecoup

Contrecoup injury: When are these injuries commonly seen?

A

Seen commonly in acceleration and deceleration injuries.

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28
Q

Types of Traumatic Brain Injuries:

Open head injury: What is it?

A

Skull is fractured and bone or other projectiles enter the brain tissue

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29
Q

Types of Traumatic Brain Injuries:

TDX & Approach to Management cont.

How is Diagnosis made?

A

Diagnosis:

history, physical examination (including using the Glasgow Coma scale), head computed tomography (CT), head magnetic resonance imaging (MRI), and ICP monitoring

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30
Q

Types of Traumatic Brain Injuries:

TDX & Approach to Management cont.

What treatment is done?

A

Treatment: rest, analgesics (specifically acetaminophen [Tylenol]), cold compresses, osmotic diuretics (e.g., mannitol), antiseizure agents, sedatives, surgery, rehabilitation (e.g., physical, speech, and occupational therapy)

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31
Q

Increased Intracranial Pressure (IICP):

Patho of IICP: What is IICP? What is it caused by?

A

Increased intracranial content caused by tumor, cerebral edema, excess CSF, hemorrhage.

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32
Q

Increased Intracranial Pressure (IICP):

Patho of IICP: What happens in nonexpendable compartments?

A

Brain, blood, & CSF in nonexpendable compartment

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33
Q

Increased Intracranial Pressure (IICP):

Compensatory mechanisms: When there is an increase in intracranial contents what happens?

What is another compensatory mech?

A

An increase in intracranial contents –> equal reduction of volume of other contents (blood, CSF) to maintain cerebral perfusion

Cerebral Autoregulation:

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34
Q

Increased Intracranial Pressure (IICP):

Compensatory mechanisms:

What occurs with Cerebral Autoregulation:

A

Compensatory alteration in the diameter of intracranial blood vessels

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35
Q

Increased Intracranial Pressure (IICP):

Compensatory mechanisms:

What occurs with Cerebral Autoregulation: What is it designed to do?

A

Designed to maintain a constant blood flow during changes in cerebral perfusion pressure

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36
Q

Patho of IICP:

What is IICP caused by?

A

Caused by disruption of blood brain barrier & loss of autoregulation by brain injury

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37
Q

Patho of IICP:

What does IICP cause?

A

Causes fluid shifts into brain –> cerebral edema

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38
Q

Patho of IICP: What happens to brain tissue? Why?

A

Increased pressure compresses brain tissue

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39
Q

Patho of IICP: What occurs with arteries?

A

Hypoxia, retained CO2 & acidosis dilate cerebral arteries

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40
Q

Four Stages of ICP:

Stage 1 of ICH

A

Compensatory mechanisms (vasoconstriction) to decrease ICP

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41
Q

Four Stages of ICP:

Stage 2 of ICH: What is it?

A

Cont’d expansion of intracranial contents

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42
Q

Four Stages of ICP:

Stage 2 of ICH: What occurs? Why?

A

Systemic arterial vasoconstriction occurs to elevate SBP to overcome IICP & maintain perfusion

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43
Q

Four Stages of ICP:

Stage 2 of ICH: What are signs and symptoms?

A

Subtle transient s/sx: confusion, restlessness, drowsiness

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44
Q

Four Stages of ICP:

Stage 2 of ICH: What is the most sensitive indicator?

A

LOC most sensitive indicator

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45
Q

Four Stages of ICP:

Stage 3 of ICH: What is it?

A

ICP = arterial pressure

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46
Q

Four Stages of ICP:

Stage 3 of ICH: What happens to brain tissue?

A

Brain tissue hypoxia, hypercapnia, condition deteriorates

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47
Q

Four Stages of ICP:

Stage 3 of ICH: What are signs and symptoms?

A

S/sx: decreasing LOC, abnormal breathing, widened pulse pressure, bradycardia, small sluggish pupils

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48
Q

Four Stages of ICP:

Stage 3 of ICH: What happens to compensation mechanism?

A

Compensation mechanism become exhausted

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49
Q

Four Stages of ICP:

Stage 3 of ICH: What is lost? What does that lead to?

A

Autoreg is lost –> intracranial vessels vasodilate

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50
Q

Four Stages of ICP:

Stage 3 of ICH: What happens to brain volume and ICP?

A

Brain volume increases, ICP rises

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51
Q

Four Stages of ICP:

Stage 4 of ICH (herniates)
What happens to brain tissue?

A

Brain tissue herniates to compartment of less pressure

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52
Q

Four Stages of ICP:

Stage 4 of ICH (herniates)
What happens to blood supply? What does that lead to?

A

Blood supply compromised –> ischemia, hypoxia in herniated tissues

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53
Q

What is a feared complication of increased ICP?

A

Herniation

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54
Q

What does Herniation refer to?

A

Refers to displacement of brain tissue

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55
Q

Herniations: Where can they occur?

A

Herniations can occur both above and below the tentorial membrane.

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56
Q

What are the two major groups of herniations:

A
  1. Supratentorial:
  2. Infratentorial:
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57
Q

What are the types of supratentorial herniations?

A
  1. uncal (transtentorial);
  2. central;
  3. cingulate;
  4. transcalvarial (external herniation through opening in skull).
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58
Q

What are the types of Infratentorial herniations?

A

upward herniation of cerebellum;

cerebellar tonsillar move down through foramen magnum.

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59
Q

Manifestations of IICP: What changes occur?

A

Changes in LOC

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60
Q

Manifestations of IICP:

A

Pupillary reactions

Cushing’s Reflex (Cushing’s Triad)

CV: late ICP sx

Other signs:

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61
Q

Manifestations of IICP: How are changes in LOC?

A

Decreased LOC from pressure on the brainstem & cerebral cortex

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62
Q

Manifestations of IICP: Pupillary reactions- what do they indicate?

A

Indicates presence & level of brainstem dysfunction

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63
Q

Manifestations of IICP: Pupillary reactions- Pinpoint pupils & midpoint reflect tell what?

A

Pinpoint pupils & midpoint reflect brainstem compression

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64
Q

Manifestations of IICP: Pupillary reactions- Dilated, fixed reflect what?

A

Dilated, fixed reflect compression of CN 3

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65
Q

Manifestations of IICP: Pupillary reactions- Dilated, Unilateral, fixed tell what?

A

Unilateral, fixed – compression of 1 CN 3

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66
Q

Manifestations of IICP: Cushing’s Reflex (Cushings’ Triad)

A

Respirations:

Bradycardia:

Htn:

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67
Q

Manifestations of IICP: Cushing’s Reflex (Cushings’ Triad): How are respirations?

A

Respirations: Resp shallower, irreg from brainstem compression

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68
Q

Manifestations of IICP: Cushing’s Reflex (Cushings’ Triad): How is bradycardia?

A

baroreceptor response

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69
Q

Manifestations of IICP: Cushing’s Reflex (Cushings’ Triad): How is htn?

A

Htn: ICP rises, the body increases BP to ensure adequate blood flow to the brain.

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70
Q

Manifestations of IICP: What does CV indicate?

A

CV: late ICP sx

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71
Q

Manifestations of IICP: What are CV symptoms?

A

↑ SBP, widening pulse pressure, bradycardia

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72
Q

Manifestations of IICP: What are other symptoms?

A

Hypothalamus: high fevers
Vomiting (projectile, results from pressure on medulla)
Decreased reflexes
Posturing

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73
Q

Posturing: What are the two types?

A

Decorticate: bring arms to the core

Decerebrate: Extended arms

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74
Q

Posturing: Decorticate- WHat is it?

A

bring arms to the core

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75
Q

Posturing: Decerebrate: - WHat is it?

A

Decerebrate: Extended arms

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76
Q

Posturing: Decorticate- What happens to upper extremities?

A

Flexion of arms, wrists, and fingers with adduction in the upper exts

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77
Q

Posturing: Decorticate- What happens to lower extremities?

A

External, internal rotation, and plantar flexion of feet

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78
Q

Posturing: Decorticate: bring arms to the core

Where are lesions

A

Lesions in hemispheres or inferomedial part of each cerebral hemisphere of the brain

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79
Q

Posturing: Decorticate: What is prognosis?

A

Better prognosis

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80
Q

Posturing: Decerebrate- What happens to extremities?

A

All four extremities in rigid extension with hyperpronation of the forearms and plantar extension of the feet

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81
Q

Posturing: Decerebrate- What is the effect on the brain?

A

Midbrain or upper pons damage

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82
Q

IICP: Approach to Management cont.

A

Respiratory support

CSF drainage

ICP monitoring

Drug Therapy:

Positioning

Temperature control

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83
Q

IICP: Approach to Management cont.

What is Respiratory support?

A

Mechanically ventilated

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84
Q

IICP: Approach to Management cont.

Why is CSF drainage?

A

Ventricular drainage to ↓ CSF volume & pressure

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85
Q

IICP: Approach to Management cont.

What is drug therapy?

A

Mannitol – reduce cerebral edema, produce rapid diuresis

Anticonvulsants – prevent seizures

Antacids/PPIs – prevent stress ulcers

Dexamethasone – to ↓permeability of
cerebral capillaries, ↓ cerebral edema.
Keeps capillaries from leaking plasma into brain tissue to minimize edema

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86
Q

IICP: Approach to Management cont.

What is drug therapy: Mannitol

A

Mannitol – reduce cerebral edema, produce rapid diuresis

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87
Q

IICP: Approach to Management cont.

What is drug therapy: Anticonvulsants –

A

Anticonvulsants – prevent seizures

88
Q

IICP: Approach to Management cont.

What is drug therapy: Antacids/PPIs

A

Antacids/PPIs – prevent stress ulcers

89
Q

IICP: Approach to Management cont.

What is drug therapy: Dexamethasone –

A

Dexamethasone – to ↓permeability of
cerebral capillaries, ↓ cerebral edema.

Keeps capillaries from leaking plasma into brain tissue to minimize edema

90
Q

Hematomas: Patho

A

A collection of blood in the tissue that develops from ruptured blood vessels.

91
Q

Hematomas: Patho- How fast do they develop?

A

Hematomas can develop immediately or slowly because of a TBI or surgery.

92
Q

How are hematomas named?

A

Hematomas are named according to their placement in relation to the meninges, the three continuous membranes covering the brain and spinal cord.

93
Q

Epidural hematoma: What are causes of it?

A

Causes: severe blow to head, MVA, falls

94
Q

Epidural hematoma: Where does bleeding occur?

A

Bleeding between the dura and skull

95
Q

Epidural hematoma: What is it usually caused by? (Specific injury not like blow to head)

A

Usually caused by an arterial tear to the middle meningeal artery in temporal area

96
Q

Epidural hematoma: Accounts for what percent of head injuries?

A

Accounts for 1-2% of major head injuries. Venous bleed – slower – lucid for a few minutes  days

97
Q

Epidural hematoma: What occurs at injury?

A

Loss Of Consciousness at injury

98
Q

Epidural hematoma: What occurs that would be considered a medical emergency?

A

Expands quickly….. Medical emergency requiring surgical evacuation

99
Q

Epidural hematoma: What develops hours after injury?

A

Marked neurologic dysfunction that usually develops within a few hours of injury.

100
Q

Epidural hematoma: How do symptoms start?

A

Decreasing responsiveness, followed by a short period of alertness if it’s a venous bleed….slower, moving to unconsciousness as hematoma expands

101
Q

Epidural hematoma: As hematoma accumulates, what symptoms occur?

A

As hematoma accumulates sx: increasing h/a, vomiting, drowsiness, seizures

102
Q

Subdural hematomas : How common?
What are causes of this?

A

Is more common

Cause: venous tear, trauma, anticoag tx, chronic alcohol

103
Q

Subdural hematomas : Three types

A

Acute:

Sub acute:

Chronic:

104
Q

Subdural hematomas :

Acute: Where does it develop, how fast, when are symptoms?

A

Acute: Develop rapidly, located top of skull, sx occur within 24 hours.

105
Q

Subdural hematomas :

SubAcute: How long to develop? What develops?

A

IICP occurs over approximately 48hrs  2 weeks

106
Q

Subdural hematomas:

Chronic: How long and who does it develop in? How does it develop?

A

Chronic: Weeks –> months.

Occurs in older adults - brain atrophy - more space for hematoma to develop.

107
Q

Subdural hematomas: WHat does it lead to?

A

Acts like expanding mass –> IICP –> brain herniation

108
Q

Subdural hematomas: What are symptoms?

A

Sx: chronic h/a, drowsiness, restless, agitation, slow cognition, confusion –> loss of consciousness, resp pattern changes, pupil dilation, visual changes

109
Q

Subdural hematomas: How fast does it progress?

A

Progresses rapidly and has a high mortality.

110
Q

Subdural hematoma: What else occurs with it?

A

80% have headaches, tenderness on palpation over hematoma

Dementia with rigidity

111
Q

Subdural hematoma: What may it require?

A

May require clot evacuation or breakdown on its onw

112
Q

Types of Hematomas:

Intracerebral hematoma: What does it result from?

A

Result from bleeding in the brain tissue itself – 2-3% of cases

113
Q

Types of Hematomas:

Intracerebral hematoma: What are causes?

A

Cause: trauma, spontaneous due to AVM, htn-small vessel disease, hemorrhagic stroke

114
Q

Types of Hematomas:

Intracerebral hematoma: What does it act like? What does it lead to?

A

Acts as expanding mass –> increasing ICP, compresses brain tissue

115
Q

Types of Hematomas:

Intracerebral hematoma: When do Delayed intracerebral hematomas occur?

A

Delayed intracerebral hematomas may occur 3-10d after head injury

116
Q

Types of Hematomas: symptoms?

Intracerebral hematoma

A

Sx: decreasing LOC, contralateral hemiplegia.

117
Q

Types of Hematomas:

Intracerebral hematoma- delayed
symptoms?

A

Delayed intracerebral hematoma will present like hypertensive brain hemorrhage (sudden decreased LOC, pupillary dilation, breathing pattern changes, Babinski reflex, contralateral hemiplegia)

118
Q

Intracerebral hematoma: What is treatment?

A

Tx: reduce ICP, allow hematoma to reabsorb

119
Q

Subarachnoid hemorrhage: What is it a type of?

A

Type of hemorrhagic stroke

120
Q

Subarachnoid hemorrhage: Where is the bleed?

A

Bleed between arachnoid mater and the pia mater from injured vessel

121
Q

Subarachnoid hemorrhage: What is the primary cause?

What are other causes?

A

htn

Other causes: tumors, coag disorders, trauma, cocaine, AVM, head injury, family hx, ruptured aneurysm

122
Q

Subarachnoid hemorrhage: Where is there traumatic bleeding?

A

Traumatic bleeding from the base of the brain

123
Q

Subarachnoid hemorrhage: What occurs with bleeding?

A

Blood oozes from leaking vessel into subarachnoid space & coats nerve roots, impairs CSF reabsorption & obstructs passages

124
Q

Subarachnoid hemorrhage: What does ruptured vessel cause?

A

Ruptured vessel causes sudden throbbing explosive headache

125
Q

Subarachnoid hemorrhage: What are symptoms?

A

Other sx: n/v, visual disturbances, motor deficits, loss of consc

126
Q

Subarachnoid hemorrhage: What are symptoms? *Major symptoms?

A

Meningeal irritation/inflammation: nuchal rigidity, photophobia, blurred vision, irritability, restlessness & low-grade fever

127
Q

Subarachnoid hemorrhage: What are symptoms? *Kernig and Brudzinki?

A

(+) Kernig sign & (+) Brudzinki sign

128
Q

Subarachnoid hemorrhage: What are complications?

A

Complications: die soon after rupture or rebleed

129
Q

Kernig’s sign

A

When the patient is lying with the thigh flexed on the abdomen, the leg cannot be completely extended

130
Q

Brudzinkski’s sign

A

When patient’s neck is flexed flexion of the knees and hips is produced, when the lower extremity of one side is passively flexed, a similar movement is seen in the opposite extremity

131
Q

Effects of Hematomas:

Regardless of the type of hematoma, the effects are very similar:

What does bleeding lead to?

A

Bleeding leads to localized pressure on nearby tissue and increases ICP.

132
Q

Effects of Hematomas:

Regardless of the type of hematoma, the effects are very similar:

What happens to hematomas?

A

The hematoma becomes encapsulated by fibroblasts, blood begins to clot and forms a more solid mass. Blood cells begin to hemolyze.

133
Q

Effects of Hematomas:

Regardless of the type of hematoma, the effects are very similar:

Why is more fluid pulled into the tissue?

A

Hemolysis creates osmotic pressure, which pulls more fluid into the tissue.

134
Q

Effects of Hematomas:

Regardless of the type of hematoma, the effects are very similar:

How is size and pressure of the mass?

A

Size and pressure of the mass increases leading to a further increase in intracranial pressure.

135
Q

Effects of Hematomas:

Regardless of the type of hematoma, the effects are very similar:

What does increased pressure lead to?

A

Increased pressure may cause the brain to herniate (move out of its current position).

136
Q

Effects of Hematomas:

Regardless of the type of hematoma, the effects are very similar:

What occurs that leads to additional ischemia and increased damage?

A

Vasospasm (cerebral vasoconstriction) may also occur leading to additional ischemia and increased damage.

137
Q

Spinal Cord Injuries:

What are causes of it?

A

Causes: MVAs, trauma, males (16-30), falls, violence, sports injuries, and weakening vertebral structures (e.g. RA or osteoporosis)

138
Q

Spinal Cord Injuries:

What do they result from?

A

Result from direct & secondary injury to the spinal cord or indirectly from damage to surrounding bones, tissues, or blood vessels, myelin from stretching or lacerations

139
Q

Spinal Cord Injuries:

What is a primary injury?

A

Primary injury - initial mechanical disruption of nerve cells,

140
Q

Spinal Cord Injuries:

What is a secondary injury? (When does it occur?)

A

Secondary injury (within a few min after injury –> weeks)

141
Q

Spinal Cord Injuries:

What occurs with secondary injury?

A

Hemorrhages, inflammation, cord edema
Vasospasm, occlusions, ischemia - Hypoxia
Stimulation by excitatory NTs (e.g. glutamate), intracellular calcium overload, oxidative damage, cell death
Spared neurons become damaged
Cystic cavities containing fluid, connective tissue & leukocytes form a barrier that prevents regeneration
C1-C4 cord swelling life-threatening

142
Q

Clinical Manifestations of Spinal cord injuries:

A

Spinal shock: temporary loss of spinal cord function below lesion

Neurogenic shock: vasogenic shock

Autonomic Hyperreflexia

143
Q

Clinical Manifestations of Spinal cord injuries: Spinal shock?

A

temporary loss of spinal cord function below lesion

144
Q

Clinical Manifestations of Spinal cord injuries: Neurogenic shock?

A

vasogenic shock

145
Q

Clinical Manifestations of Spinal cord injuries: Spinal shock- When does it develop?

A

Develops immediately after injury from loss of discharges from brain/stem & impulse inhibition

146
Q

Clinical Manifestations of Spinal cord injuries: Spinal shock- What ceases? For how long?

A

Normal activity of spinal cord cells at & below level of injury ceases temporarily

147
Q

Clinical Manifestations of Spinal cord injuries: Spinal shock- What is lost completely?

A

Complete loss of reflex function

148
Q

Clinical Manifestations of Spinal cord injuries: Spinal shock- Complete loss of reflex function

A

flaccid paralysis, absence of sensation, loss of bowel & bladder control, transient hypotension, bradycardia, poor circulation, loss of thermal control b/c SNS damage – hypothalamus can’t minimize heat loss through vasoconstriction – pt assumes air temp (poikilothermia)

149
Q

Clinical Manifestations of Spinal cord injuries: Spinal shock- How long does it last?

A

Lasts from 2 to 3 days –> months

150
Q

Clinical Manifestations of Spinal cord injuries: Spinal shock- What are signs of improvement?

A

reflex return, spasticity, hyperreflexia, reflex emptying of bladder (can control urine), tingling sensation to legs

151
Q

Clinical Manifestations of Spinal cord injuries: Neurogenic shock: What can it occur with?

A

Occurs with cervical or upper thoracic cord injury above T6

Can occur with spinal shock

152
Q

Clinical Manifestations of Spinal cord injuries: Neurogenic shock: What is it a disruption of?

A

Disruption of autonomic pathways

153
Q

Clinical Manifestations of Spinal cord injuries: Neurogenic shock: What is there an absence of?

A

Absence of sympathetic activity & unopposed parasympathetic tone controlled by vagus nerve

154
Q

Clinical Manifestations of Spinal cord injuries: Neurogenic shock: what are symptoms?

A

Sx: vasodilation, hypotension, bradycardia, failure to regulate body temp

155
Q

Clinical Manifestations of Spinal cord injuries: Autonomic Hyperreflexia? What are example?

A

When a noxious stimulus occurs below the level of the spinal cord injury, it triggers reflex sympathetic activity.

(ex; Bladder distension from blocked catheter or urinary retentions, fecal impaction)

156
Q

Clinical Manifestations of Spinal cord injuries: Autonomic Hyperreflexia- How does bp increase?

A

Diffuse vasoconstriction, increase in BP

157
Q

Clinical Manifestations of Spinal cord injuries: Autonomic Hyperreflexia- How does parasympathetic response travel? What does that lead to?

A

Normally, the body compensates by activating the parasympathetic system, causing vasodilation and correcting BP.

However, the parasympathetic response cannot travel below the lesion site.

As a result, continued vasoconstriction leads to dangerously high blood pressure. (life threatening)

158
Q

Clinical Manifestations of Spinal cord injuries: Autonomic Hyperreflexia- What are symptoms?

A

Sx: throbbing h/a, blurred vision, sweating, pilorection

159
Q

Clinical Manifestations of Spinal cord injuries: Autonomic Hyperreflexia- What are pns response from the medulla?

A

Parasymp response from medulla: facial flushing & nasal congestion (vasodilation), bradycardia from vagal stimulation

160
Q

Spinal Cord Injuries:
Immediate Management:

What is done to spine? What is given for swelling?

A

Immobilization of the spine

Corticosteroid agents to reduce swelling

Spinal traction to reduce the fracture and immobilize the spine

161
Q

Spinal Cord Injuries:
Immediate Management:
What does surgery or removal of fluid do?

A

Surgical repair of vertebral fractures or surgical removal of the fluid compressing the spinal cord (decompression laminectomy)

162
Q

Spinal Cord Injuries:
Immediate Management:
What should be managed?

A

Respiratory management

163
Q

Spinal Cord Injuries:
Immediate Management:
What should be given for hypotension?

A

Vasopressor drugs if hypotensive

164
Q

Patho of TIA

A

A temporary episode of cerebral ischemia that results in neurologic deficits

165
Q

Spinal Cord Injuries:
Long Term Management:

A

Physical, occupational, and speech therapy
Mobility assistive devices
Long-term respiratory management
Meticulous skin care
Bowel and bladder training or management
Stool softeners
Antispasmodic agents to treat muscle spasms
Pain management
Nutritional support
Prompt treatment of infections

166
Q

Patho of TIA: How long does it last?

A

Last less than an hour, typically deficits resolve within 24 hours

167
Q

Patho of TIA: Why are they called mini strokes?

A

Also called ministrokes because these neurologic deficits mimic a cerebral vascular accident (CVA) or stroke. May occur singly or in a series

168
Q

Patho of TIA: What are they a warning signs of?

A

Warning sign that a CVA may be impending; however, not all CVAs are preceded by a TIA

169
Q

Patho of TIA: What can occur with TIA? WHy?

A

Ischemia can occur because of a cerebral artery occlusion (e.g., thrombus, embolus, or plaque), cerebral artery narrowing (e.g., atherosclerosis or spasms), or cerebral artery injury (e.g., inflammation or hypertension).

170
Q

Patho of TIA: What are clinical manifestations?

A

Clinical manifestations: weakness, numbness, sudden confusion, loss of balance, sudden severe h/a, remains conscious, visual disturbances, or numbness and paresthesia in the face, may occur

171
Q

Patho of TIA: What are complications?

A

Complications: permanent brain damage, injury from falls, and CVA.

172
Q

TIA: DX & Approach to Management

What is Diagnosis:

A

history, physical examination (including a neurologic assessment and blood pressure), head CT, head CTA, head MRI, head MRA, carotid ultrasound, serum clotting studies, blood chemistry, complete blood count, erythrocyte sedimentation rate test, and serum lipids test

173
Q

TIA: DX & Approach to Management

What is Treatment?

A

manage any underlying conditions, antiplatelet aggregation agents, anticoagulants, angioplasty, carotid endarterectomy, smoking cessation, minimizing dietary cholesterol/fat, anti-hyperlipidemics, increasing dietary fruits and vegetables, exercising regularly, limiting alcohol consumption, and eliminating illicit drug use

174
Q

Cerebral Vascular Accident CVA:

AKA?

A

Also known as a stroke or brain attack.

175
Q

Cerebral Vascular Accident CVA:

What is it?

A

An interruption of cerebral blood supply from thrombus formation, an embolus, or hypoperfusion due ↓’d blood volume or heart failure

176
Q

Cerebral Vascular Accident CVA:

What are causes?

A

Causes: total vessel occlusion (e.g., thrombus, embolus, or plaque) or cerebral vessel rupture (e.g., cerebral aneurysm, arteriovenous malformation, or hypertension)

177
Q

Cerebral Vascular Accident CVA:

What are complications?

A

Complications: neurologic deficits and death

178
Q

CVA:

Who is it most common in?

A

Most common in African Americans and those living in the Southeast region

179
Q

Cerebral Vascular Accident CVA:

What are modifiable risks factors?

A

Modifiable Risk factors: afib, physical inactivity, obesity, uncontrolled htn, smoking, hypercholesterolemia, DM, atherosclerosis, oral contraceptive usage, excessive alcohol consumption, and illicit drug use

180
Q

CVA: Stroke Types

A

Thrombotic

Embolic

Lacunar

Hemorrhagic

181
Q

CVA: Stroke Types

Thrombotic? What forms? How is onset?

A

Thrombus forms in arteries supplying brain/intracranial vessels

Gradual occlusion of arteries—slow onset – 20-30 yrs

182
Q

CVA: Stroke Types

Thrombotic?

A

Smooth stenotic area degenerates –> macrophages (foam cells), ulcerated –> platelets & fibrin adhere to damaged wall –> clot forms

183
Q

CVA: Stroke Types
Thrombotic:
What increases risk of Thrombotic?

A

Risk ↑: conditions causing increased coagulation or inadequate cerebral perfusion

Dehydration, hypotension, or prolonged vasoconstriction from malignant htn

184
Q

CVA: Stroke Types

Embolic: What happens?

A

Fragments break off from thrombus formed in heart, aorta, carotid artery

Embolus plugs vessel entirely or shatters into fragments becoming part of blood flow

185
Q

CVA: Stroke Types

Embolic: What are sources of it?

A

Sources: fat, air, tumor, bacterial clumps, foreign bodies

186
Q

CVA: Stroke Types

Embolic: What does it involve (What brain parts)?

A

Involves small brain vessels, obstructs bifurcation/narrowing

187
Q

CVA: Stroke Types

Embolic: What are risk factors?

A

Risk factors: afib, lt vent aneurysm, thrombus, recent MI, cardiac defects

188
Q

CVA: Stroke Types

Lacunar: What is it?

A

Small vessel disease, occlusion of single deep perforating artery that supplies small penetrating vessels causing ischemic lesions deep in brain

189
Q

CVA: Stroke Types

Lacunar: What does small area of infarction lead to?

A

Small area of infarction –> motor or sensory deficits

Pure motor & sensory deficits

190
Q

CVA: Stroke Types

Lacunar: What is it associated with?

A

Associated with untreated high BP

191
Q

CVA: Stroke Types

Hemorrhagic stroke: Why does it occur?

A

hemorrhagic stroke from bleeding into the subarachnoid space

192
Q

Patho of cerebral infarction:

What is it?

A

Cerebral anoxia lasting longer than 10 minutes causes cerebral infarction with irreversible changes.

193
Q

Patho of cerebral infarction:

Penumbra:

A

Penumbra - Core surrounded by a rim of borderline hypoxic tissue, which is not severe enough to cause structural damage – still viable!

194
Q

Patho of cerebral infarction:

What is needed to treat?

A

Prompt perfusion of by thrombolytic agents (TPA) promotes perfusion & may prevent necrosis & loss of neuro function

195
Q

Patho of cerebral infarction:

“Time is Brain” means?

A

“Time is Brain” Save the penumbra

196
Q

Patho of cerebral infarction:

What happens to the affected area hours later? (6-12hrs and 48-72 hours later)

A

Affected area becomes pale & softens 6-12 hrs post occlusion

Necrosis, swelling around the insult & mushy disintegration appear 48-72 hrs after

197
Q

Patho of cerebral infarction:

What infiltrates necrotic tissue?

A

Macrophages & phagocytes infiltrate necrotic tissue

198
Q

Patho of cerebral infarction:

When does necrosis resolve?

A

Necrosis resolves by 2nd wk, leaving glial scarring

199
Q

Slide 40

A
200
Q

Clinical Manifestations of CVA: Nervous System Dysfunction- include?

A

Cognitive Changes

Motor Changes

Sensory Changes

Cranial Nerve Dysfunction

201
Q

Clinical Manifestations of CVA: Nervous System Dysfunction:

Cognitive changes: What are they?

A

Level of consciousness

Impaired memory, judgment or problem-solving, and decision-making abilities

Proprioceptive (awareness of body position)

Aphasia (speaking)

Difficulty read, writing, recognizing things, performing simple tasks

202
Q

Clinical Manifestations of CVA: Nervous System Dysfunction:

Motor Changes

A

Hemiplegia/Hemiparesis

Ataxia/Hypotonia or hypertonia

Flaccid paralysis

Incontinence of bowel and bladder

Apraxia (movement/coordination)
Swallowing

203
Q

Clinical Manifestations of CVA: Nervous System Dysfunction:

Sensory Changes that occur?

A

Unaware of existence of paralyzed side

Amaurosis fugax (blindness in one eye)

Hemianopsia (blindness in half of the visual field)

Agnosia (problems perceiving familiar sensory info)

204
Q

Clinical Manifestations of CVA: Nervous System Dysfunction:

Cranial Nerve Dysfunction

A

Dysphagia (trouble swallowing)

Facial paralysis

Absent gag reflex

Impaired tongue movement

Nystagmus (involuntary movements of the eye)

Pupil constriction or dilation

Ptosis (eye lid dropping)

205
Q

Clinical Manifestations of Cerebrovascular Accident: Aphasia

What are the types of aphasia?

A

Expressive (Motor)

Receptive (Sensory)

Global

206
Q

Clinical Manifestations of Cerebrovascular Accident: Aphasia

Expressive: What is the site of damage?

A

Broca’s area

Left frontal lobe

207
Q

Clinical Manifestations of Cerebrovascular Accident: Aphasia

Expressive: Broca’s area site of damage?

A

Cannot speak or write fluently or appropriately.

208
Q

Clinical Manifestations of Cerebrovascular Accident: Aphasia

Expressive: Left frontal lobe

A

Patient is aware of deficit and may become frustrated or angry.

Patient understands what is said but cannot communicate verbally.

209
Q

Clinical Manifestations of Cerebrovascular Accident: Aphasia

Receptive (Sensory): Sites of damage

A

Werincke’s area

Left temporal lobe, prefrontal

210
Q

Clinical Manifestations of Cerebrovascular Accident: Aphasia

Receptive (Sensory): Werincke’s area

A

Unable to understand written or spoken language.

211
Q

Clinical Manifestations of Cerebrovascular Accident: Aphasia

Receptive (Sensory): Left temporal lobe, prefrontal

A

Patient may be able to talk, but language is often meaningless.

Neologisms (made up words) are common parts of speech.

212
Q

Clinical Manifestations of Cerebrovascular Accident: Aphasia

Global: Site of damage

A

Broca’s and Wernicke’s areas and connecting fibers

213
Q

Clinical Manifestations of Cerebrovascular Accident: Aphasia

Global: Broca’s and Wernicke’s areas and connecting fibers effects?

A

Patient cannot express self or comprehend others’ language. Reading and writing ability are equally affected.

214
Q

Evaluation & Treatment

What is eval?

A

History, physical examination (including a neurologic assessment), head computed tomography, head magnetic resonance imaging, carotid ultrasound, cerebral arteriogram, serum clotting studies, blood chemistry, and complete blood count

215
Q

What is treatment for CVA?

A

Intravenous thrombolysis:

Neurovascular interventions

Antiplatelets, anticoagulants and antihyperlipidemic long term

Anticonvulsants

Antihypertensives

Dexamethasone/Corticosteroids

216
Q

What is treatment for CVA:

Intravenous thrombolysis:

A

Intravenous thrombolysis: tissue-type plasminogen activator (tPA) is given within 3-4.5 hr onset of sx for ischemic strokes

217
Q

What is treatment for CVA:

Antihypertensives

A
  • modest BP reduction, target blood pressure of 160/90 mm Hg

PATHO/PHARM II (27 decks)

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