rrd 10 Flashcards

neurological system

1
Q

cerebral blood flow is normally maintained at a rate that matches ___________, ensuring a constant supply of _______.

A
  • metabolic needs of brain
  • oxygen and glucose and waste removal
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2
Q

maintenance of effective cerebral blood flow is dependent on keeping what 2 forces in balance?

A
  • cerebral perfusion pressure (CPP)
  • intracranial pressure (ICP)
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3
Q

cerebral perfusion pressure (CPP)

A

pressure required to get oxygenated blood into the brain to perfuse the cells of the brain

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4
Q

if CPP is too low or high, the result is?

A
  1. ineffective perfusion
  2. ischemia to brain
  3. cellular hypoxia
  4. cell injury and death
  5. loss of cell membrane integrity
  6. water + other cell contents released
  7. cerebral edema + increased ICP
  8. further loss of effective perfusion
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5
Q

if CPP is either too high OR too low, it can lead to?

A
  • cerebral edema
  • increased ICP
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6
Q

intracranial pressure (ICP)

A

totality of pressures in the brain
- atrial & venous pressures (blood) + CSF pressure + Brain (tissue)

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7
Q

bc cranium is a bony structure, _________ in pressure in the brain can be tolerated.

A

very little increase

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8
Q

some degree of pathologic alteration in brain fxn (decreased LOC, impaired sensorimotor fxn, etc.) can be expected from?

A

small amt of increased ICP

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9
Q

the main culprit in causing increased ICP (IICP) and loss of balance btw ICP and CPP is?

A

cerebral edema

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10
Q

example of situation causing cerebral edema

A
  1. ischemia from blockage (plaque or stricture) of an artery in brain or going into brain (carotid)
  2. cells hypoxic
  3. swell, increased vascular permeability
  4. edema
  5. increased ICP
  6. decreased CPP
  7. brain ischemia
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11
Q

what can cause CPP to go out of balance?

A
  • HTN (high)
  • hypotension (low)
  • blockage of arterial flow into brain (low)
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12
Q

what can cause ICP to go out of balance?

A
  • head injury
  • brain tumor
  • brain attack/stroke
  • infections, acid/base imbalance, hypoxemia from resp disorders, meningitis can lead to inflammation of brain tissue
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13
Q

brain attack

A

process of any interruption of the normal blood supply to a part of the brain or entire brain, resulting in damaged brain tissue

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14
Q

other names for brain attacks

A
  • strokes
  • CVAs (cerebrovascular accidents)
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15
Q

most common underlying etiologies of brain attack (BA) are?

A
  • atherosclerosis of cerebral arteries and/or of incoming arteries (carotid+ vertebral)
  • HTN
  • others: brain aneurysms, heart probs that lead to low CO -> decreased blood to brain
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16
Q

risk factors of BA

A
  • preexisting hx of atherosclerosis and/or HTN
  • older age
  • fam hist
  • diabetes
  • lifestyle choices (smoking, high fat diets)
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17
Q

categories of BA are based on? what are they?

A
  • underlying mechanism
  • ischemic cause vs hemorrhagic cause
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18
Q

S/S ____ depend on whether a stroke is ischemic or hemorrhagic. TX ____ depends on knowing which kind is occurring, which is determined by ___.

A
  • does not
  • does
  • CAT scan or MRI of brain
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19
Q

no matter what mechanism the BA falls under, ultimately the actual negative effects of a stroke are still?

A
  • cerebral edema
  • IICP
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20
Q

ischemic brain attack cause is usually the ________ of arteries supplying brain (_______ arteries) or ______ arteries themselves.

A
  • narrowing or blockage
  • carotid or vertebral
  • intracranial
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21
Q

ischemic brain attack is usually related to ____ and other processes that damage arterial walls, resulting in same process as ____ formation in coronary arteries

A
  • atherosclerosis
  • plaque
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22
Q

patho of ischemic brain attack

A
  1. diminished perfusion to brain tissue
  2. cellular ischemia
  3. infarction (cell death)
  4. inflammatory process
  5. swelling, cerebral edema
  6. increased ICP
  7. further decrease in perfusion
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23
Q

thrombotic stroke

A

occurs from a clot or plaque that blocks off the artery in which is has developed and causes ischemia distally

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24
Q

embolic stroke

A

when fragments that break from an arterial thrombus travel downstream until they get stuck in a smaller artery and cause ischemia to brain distally

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25
Q

arterial fibrillation leading to thrombotic/embolic event

A
  1. afib
  2. disorganized motion of LA allows some incoming blood to pool & promotes stasis
  3. small clots develop in atria
  4. break off
  5. travel to brain via carotids
  6. lodge in cerebral artery
  7. ischemia/infarct to distal tissue
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26
Q

atherosclerosis of carotids causing thrombotic/embolic events

A
  1. carotids common place for thrombi to develop
  2. small clots can break off from these
  3. travel downstream
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27
Q

___ emboli can cause thrombotic/embolic events, usually ______, during _____.

A
  • air
  • iatrogenic
  • surgury
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28
Q

clots around ____ or ___ valve prosthesis or _____ from around affected valve can cause thrombotic/embolic event.

A
  • mitral or aortic
  • vegetation
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29
Q

_____ artery plaque can develop in the _____; if breaks, free, can lodge in _____ arteries to cause thrombotic/embolic events.

A
  • intracranial
  • circle of Willis
  • smaller
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30
Q

transient ischemic attack (TIA) can happen in either thrombotic or embolic situation and cause same S/S as a fully-evolved stroke, but?

A

does not damage brain tissue bc is transient (i.e. temporary - resolves itself quickly)

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31
Q

S/S from TIA only last _____ and have ______ neurologic deficit (TIAs last between _______).

A
  • < 24 hrs
  • no lasting
  • 10 mins to < 24 hrs
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32
Q

TIAs are often a warning of?

A

more serious, fully-evolved stroke can occur at later date

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33
Q

hemorrhagic stroke is usually caused by?

A

effects of blood that leaks out directly onto brain tissue

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34
Q

in most areas of the brain, there is normally ____ blood directly on brain tissue. it is carried in _____ and when arrives at ____, O2 + nutrients diffuse into tissue cells & CO2 + other wastes diffuse out of cells.

A
  • NO
  • arteries and veins
  • capillary beds
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35
Q

what happens when an intracerebral aneurysm begins to leak blood onto brain tissue?

A
  1. blood irritates the tissue
  2. inflammatory process
  3. swelling, cerebral edema
  4. increased ICP
  5. cellular ischemia, injury, and/or infarction of the surrounding area
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36
Q

causes of hemorrhagic brain attack

A
  • pressure of HTN
  • weakened arterial walls from atherosclerosis
  • aneurysms
  • congenital vascular malformations
  • bleeding into a tumor
  • coagulation disorders
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37
Q

S/S of BA depend on?

A
  • where the brain attack occurs
  • which blood vessel is affected
  • what part of the brain does the vessel supply blood to
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38
Q

three general areas of brain tissue are?

A
  • brainstem
  • cerebellum
  • R/L hemisphere of the cerebrum
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39
Q

major cerebral blood supply is

A
  • vertebral artery merges w/ basilar artery -> supplies blood to brainstem + cerebellum
  • R/L internal carotid artery forms R/L middle cerebral artery (MCA) -> supplies blood to R/L hemisphere of cerebrum
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40
Q

how to assess patient for S/S of various kinds of BA

A
  1. assess pt’s autonomic status (include LOC (level of consciousness and mental status)
  2. assess sensorimotor system
    (a) assess sensorimotor above the sholders
    (b) assess sensorimotor below the shoulders
  3. assess reflexes
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41
Q

autonomic status includes?

A

involuntarily controlled neuro fxnz

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42
Q

normal VS (_______) are often one indicator that areas in the brain that control respiration (_____) are working normally, that is having _______.

A
  • BP, HR, RR, temp
  • brainstem
  • no cerebral edema and IICP
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43
Q

levels of consciousness (LOC)

A

the brain’s ability to respond appropriately to the environment

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44
Q

changes in LOC are often the first sign of?

A

neurologic event or a worsening of an existing neurologic illness

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45
Q

expected LOC includes?

A
  • being alert/easily arousable to alertness if asleep
  • being orientated X 4 (self, time, place, events)
  • following commands appropriately
  • having norm speech (speech centers in brain ok)
  • conversing appropriately (cognition, mental status ok)
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46
Q

abnormal LOC findings often means that?

A

there has been an event that led to increased cerebral edema and IICP in certain areas of the brain

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47
Q

abnormal of LOC includes?

A
  • not being alert: from being lethargic to inability to awaken the patient at all (coma)
  • not orientated to some or all of self, time, place, events
  • doesn’t follow commands
  • speech might be garbled or no speech at all
  • verbal responses/conversational efforts show inappropriate or dysfxn mental status (confusion or behavior like withdrawal/aggression)
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48
Q

sensorimotor

A

movement and sensation are intricately related

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49
Q

expected sensorimotor findings upon assessment include

A
  • norm sensation, muscle tone, movement that is also…
  • symmetric, the same bilaterally (same on both R/L sides of body)
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50
Q

the ___ cranial nerves (CNs) branch out from the brainstem (______) and rule ______ status ____ the shoulders.

A
  • 12
  • midbrain, pons, medulla
  • sensorimotor
  • above
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51
Q

lesion

A
  • gen term for problem
  • tumor, ischemia, localized increase in cerebral edema and pressure, bleeding, etc.
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52
Q

focal

A

one area of the brain is affected

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53
Q

CN VII

A
  • facial nerve
  • controls facial movement and expression
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54
Q

if there is a focal lesion caused by BA, tumor, or bleeding in RIGHT hemisphere, expect to have _______ findings, with the defect manifesting ______ on the ________ side.

A
  • asymmetric
  • unilaterally
  • opposite/contralateral
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55
Q

what happens when there is a focal cerebral edema around the right CN VII?

A
  • CN VII allows a smile
  • facial drooping on left side of the mouth
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56
Q

ipsilateral

A

same side

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57
Q

CN II

A
  • optic nerve
  • responsible for transmitting visual images to the brain
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58
Q

what happens if there is a focal cerebral edema around the right CN II?

A
  • visual defects in the two left halves of BOTH eyes
  • homonymous hemianopia
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59
Q

CNII (optic) and CNIII (oculomotor) control the _________. when norm fxn is present on both nerves, _____ pupils should respond equally to ______. both pupils should constrict to _________.

A
  • pupillary light reflex
  • both
  • light
  • to the same size
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60
Q

bilateral loss of the pupillary light response

A
  • both pupils are either fixed and dilated OR fixed and pinpoint
  • indicates a lesion in the brain stem
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61
Q

certain parts of the sensorimotor apparatus that connects brain to spine to muscles in torso, arms, legs (below shoulder) are called?

A

corticospinal and spinothalamic tracts

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62
Q

corticospinal tracts

A
  • descending (motor) tracts
  • aka pyramidal tracts
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63
Q

there are bundles of long ____ that originate in the _____ of certain areas of the _____ cortex on either side of the brain.

A
  • axons
  • cell bodies
  • motor
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64
Q

axons in certain areas of the motor cortex cross over, or ________, from their point of origin in the _______ to the opposite side of the body at the _________, giving them their _____ look.

A
  • decussate
  • cerebral cortex
  • junction btw spinal cord + brain stem
  • pyramid
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65
Q

the pyramidal tracts carry impulses that produce ________ from brain via spinal cord to various _______ to _______ between nerves and muscles.

A
  • voluntary movements of purpose + skill
  • peripheral spinal nerves
  • neuromuscular junctions
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66
Q

spinothalamic tracts

A

ascending sensory tracts

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67
Q

spinothalamic tracts carry sensations of? from where to where for processing?

A
  • pain, temp, crude + light touch
  • body to brain (thalamus)
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68
Q

T/F the spinothalamic tracts do not cross over from one side of the body to the other side of the brain.

A

FALSE: they do similar to corticospinal tracts, just in a different area

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69
Q

if there is a focal lesion related to corticospinal or spinothalamic tracts in the brain, expect to see?

A

asymmetric sensorimotor changes

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70
Q

the pathologic changes of focal lesion related to corticospinal/spinothalamic tracts will usually be?

A

unilateral, on the contralateral side of the body because of decussation

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71
Q

a pt with a tumor on the right side of the brain would have decreased strength + sensation of arms + legs on what side of the body?

A

contralateral/opposite side

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72
Q

normal peripheral reflexes include?

A
  • expected degree of response
  • equal bilaterally (symmetric)
  • reflects good connections in reflex arc of spine
  • norm interpretation in the brain
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73
Q

norm central reflexes include?

A

appropriate cough, swallow, gag, etc.

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74
Q

examples of diminished/absent reflexes due to brain lesion

A
  • deep tendon reflexes become hyporeactive
  • gag, swallowing coughing reflexes would fail to protect adequately
75
Q

what does a positive Babinski reflex look like?

A
  • plantar reflex
  • stroking plantar surface of foot makes big toe flex (upgoing toe)
  • norm until after 2 yrs old, sign of neurologic dysfxn after
  • unilateral or bilateral (if diffuse or focal)
76
Q

diffuse

A

all over, all parts of the brain and brain stem

77
Q

example of pt with brain/brain stem stroke

A
  1. patient stops breathing/heart stops beating OR complete occlusion of vertebral-basilar artery
  2. decreased blood flow to brain or brain stem
  3. diffuse brain/brain stem hypoxia
  4. cellular edema
  5. IICP
78
Q

autonomic, LOC, & mental status manifestations seen as a result of brain/brain stem abnormalities

A
  • diminished LOC
  • HR & BP changes due to pressure on medulla (brainstem)
  • breathing pattern changes
79
Q

most often w/ brain stem problems, patient is?

A

comatose or in near-coma state

80
Q

breathing pattern changes due to brain/brain stem stroke

A
  • apnea ( absence of breathing)
  • Cheyne-Strokes (seen in comatose pts who are not on ventilator)
81
Q

sensation, muscle tone, movement, strength would be weaker _____ and often ______ due to brain/brain stem abnormalities

A
  • bilaterally
  • symmetrically
82
Q

example of motor responses seen with comatose pts due to brain/brain stem abnormalities

A
  • bizarre, abnormal
  • decerebrate + decorticate posturing bc cerebral edema effect on brain stem nuclei
83
Q

other sensorimotor manifestations seen as result of bran/ brain stem

A
  • HR probs when CN X (vagus) affected
  • mixed degree of cranial nerve abnormalities
84
Q

reflex manifestations seen as result of brain/brain stem

A
  • protective reflexes (sneeze, cough, gag, swallow) diminished or lost
  • reflexes weaker, usually symmetrical, and sometimes bilateral (+) Babinski’s
85
Q

cerebellar BA

A
  • vertebral - basilar artery occlusion/near-occlusion
  • probs w/ coordination + balance common
  • vertigo, nystagmus (rapid eye move)
  • N & V
  • loss of coordination
  • fall down
86
Q

general patho cerebral hemispheric brain attack

A
  1. lack of blood flow or bleeding of L/R middle cerebral artery (or its branches)
  2. swelling + edema from hypoxia to R/L hemisphere
  3. S/S of three possible deficits
87
Q

what are the three S/S deficits from a cerebral hemispheric BA?

A
  • sensorimotor deficits bc of lesion, pressure on CNs in/near affected area in that hemisphere
  • sensorimotor deficits bc of lesion, pressure on corticospinal tracts in/near affected area in that hemisphere
    AND/OR
  • deficits based on what special fxns are controlled by that hemisphere
88
Q

sensorimotor assessment above the shoulder

A
  • assessing for CN fxn (lesion in a CN and/or in cerebral brain tissue around it?)
  • left side of face = right side in sensation, tone, movement, strength?
  • pupils = and reactive to light?
  • NO, may be focal prob w/ CN
89
Q

sensorimotor assessment below shoulder?

A
  • assessing for certain parts of sensorimotor apparatus (corticospinal + spinothalamic tracts) > lesion in one of them and/or in cerebral brain tissue around it?
  • left side = right side in sensation, tone, movement, strength?
  • NO, may be focal lesion and/or edema where a corticospinal tract passes thru that cerebral hemisphere
90
Q

assessing deficits that are special/specific to left hemisphere

A
  • controls speech + ability to do math, organize, reason, and analyze
  • left hemisphere CVA = dysphasia or aphasia (inability to comprehend, integrate, or express language)
  • impaired abilities
91
Q

assessing deficits that are special/specific to right hemisphere

A
  • controls spatiality, seat of insight (insight to their disease), creativity, face rec, musical ability, etc.
  • RH lesion = left sided neglect: tendency to completely ignore environment on the left side (EX: pt ignore anything of left side of plate of food or nurse to their left)
92
Q

can or can you not tell from clinical presentation whether a stroke is ischemic or hemorrhagic?

A

can not

93
Q

S/S depends on the what for ischemia or hemorrhage BA?

A

on the site(s)

94
Q

hemorrhagic strokes cause same symptoms as before plus?

A
  • intense headaches, “worse headache” ever experienced
  • neck pain
  • light intolerance
  • N & V
95
Q

what is the mortality rate of hemorrhagic stokes compared to others?

A

higher

96
Q

dx of BA is made through?

A
  • history of incident
  • presenting S/S
  • CAT scan
  • MRI
97
Q

public is encouraged to use BE-FAST scale, which is?

A
  • Balance: watch for sudden loss of balance
  • Eyes: check for vision loss
  • Face: look for uneven smile
  • Arms: check if one arm weak
  • Speech: listen for slurred speech
  • Time: if yes, immediately call 911 or go to nearest hospital ER. brain cells r dying!
98
Q

often in an ER, a ____ scale is used for quicker diagnosis

A

severity

99
Q

most important immediate intervention of BA is?

A

prevent further increase in ICP (tru for any brain patho)

100
Q

prevention of further increase in ICP includes

A
  • O1
  • BP management (part of managing CPP)
  • monitoring and control of cerebral edema of HOB up at least 30dg, diuretics, sometimes ICP monitor
101
Q

___ of stroke is important in deciding further interventions.

A

type (ischemic vs hemorrhagic)

102
Q

may need ____ intervention for certain types of hemorrhagic strokes

A

surgical

103
Q

ischemic stroke interventions

A
  • correct underlying problem such as afib with drugs, etc.
  • thrombolytic drugs (clot-busters) but must be w/in 3-4.5 hrs of start of incident
  • institution of anticoag therapy: first Heparin, then send home on Coumadin
104
Q

later interventions will prob include…?

A

rehabilitation and depend on site of stoke (speech therapy, swallowing rehab, teach basic activities of daily living, etc.)

105
Q

types of Alzheimer’s disease

A
  • familial Alzheimer’s (FAD)
  • non-heredity (aka Sporadic)
106
Q

exact cause of Alzheimer’s disease is ______. it is thought to be due to? what is the end result?

A
  • unknown
  • genetic mutation that improperly encodes a norm protein - amyloid
  • end result: accumulation of abnorm amyloid in brain -> abnorm amyloid forms plaque -like material (senile plaques)
107
Q

neurofibrillary tangle

A

microtubules of neurons in the brain become distorted + twisted

108
Q

the amyloid plaques and neurofibrillary tangle combine to?

A

disrupt norm nerve impulses in the brain

109
Q

clinical manifestations of Alzheimer’s

A
  • dementia
  • posterior frontal lobe involved: motor changes like rigidity, postural + gait changes
110
Q

dementia

A

a type of forgetfulness that is diff from norm absentmindedness; emotional upset, behavioral changes

111
Q

in the brain, there is an area that contains cell bodies that form part of the ________ system, aka __________; the nerve tracts from these cell bodies travel _____ outside the pyramidal tracts.

A
  • basal ganglia
  • extrapyramidal tracts (EPS)
  • downward
112
Q

EPS is partly responsible for regulating _____ movements and normal ____ and ____ related equilibrium

A
  • fine motor
  • posture
  • gait
113
Q

normal basal ganglia fxn is based on what neurotransmitters?

A
  • dopamine
  • acetylcholine
114
Q

the ultimate result of norm motor signaling from basal ganglion cell body down the axon of the neuron leading to muscles is?

A

blend of dopamine and acetylcholine effects

115
Q

the effects of acetylcholine (ie. ______ effects) are ______ and the effects of dopamine are _____.

A
  • cholinergic
  • excitatory
  • inhibitory
116
Q

excitatory effects

A

more bombardment upon acetylcholine receptors that initiate movement

117
Q

inhibitory effects

A

subduing effects of acetylcholine receptors so movement is controlled

118
Q

Parkinson’s disease

A

basal ganglia dysfxn caused by unknown source, but suspected to be a genetic, viral, or environmental toxin-induced depletion in dopamine

119
Q

a decrease in dopamine tips the scales of balance towards _____, ______ activity - ____ actually more acetylcholine, but more ______.

A
  • cholinergic
  • excitatory
  • not
  • effect
120
Q

the result of the increased cholinergic effect gives S/S related to?

A
  • hypertonia (rigidity)
  • dyskinesia (movement disorder)
121
Q

any dysfxn of the EPS results in?

A

parkinsonianisms

122
Q

hypertonia manifestations include

A
  • overall rigidity, often noticed in face (mask-like face)
  • cog-wheel rigidity of forearm
  • dysarthria (difficulty forming words)
  • dysphagia (difficulty swallowing)
123
Q

dyskinesia manifested as

A
  • invol facial + trunk movements (Parkinson’s tremor: alternating movements btw thumb + forefinger, pill rolling)
  • inability to make appropriate posture adjustment when tipping or falling = walking called basal ganglion gait, Parkinsonian gait
124
Q

Parkinsonian gait

A

stooped, shuffling posture; decreased arm swing

125
Q

tx Parkinson’s

A

meds w/ dopamine (L-dopa) and anticholinergic meds (benadryl)

126
Q

multiple sclerosis

A
  • relatively common autoimmune disorder
  • onset btw 20 - 50
  • male: female ratio is 1:2
127
Q

multiple sclerosis patho overview

A
  1. pervious viral insult occurred in genetically susceptible person
  2. stimulates abnorm immune response in CNS
  3. person’s own T-cells attack myelin protein in brain neurons
128
Q

myelin

A
  • gives white matter its color
  • fxn is to increase speed of nerve impulse transmission
129
Q

inflammation + injury from T-cell attack _____ the myelin in multifocal areas. this process is known as ____ and the areas are called _____.

A
  • degenerates
  • demyelination
  • demyelinating lesions/plaques
130
Q

depending on degree of demyelination + inflammation, nerve conduction in pt w/ multiple sclerosis is ______ -> over 20 yr period or so, there is often ____________ (_______) of _______ (supporting tissue in brain) and ________ of axons.

A
  • sporadically blocked or altered
  • scarring and hardening
  • sclerosis
  • neuroglia
  • deterioration
131
Q

sclerosis of neuroglia and deterioration of axons in pts w/ multiple sclerosis causes _____ bc?

A
  • progressive loss of fxning
  • axons demyelinated -> transmit nerve impluses 10x slower than norm, myelinated ones
132
Q

S/S of multiple sclerosis is generally? bc?

A
  • variable
  • individualistic
  • asymmetrical
  • plaques are unevenly distributed in brain
  • ca be symmetric, but more uncommon
133
Q

multiple sclerosis S/S

A
  • paresthesia
  • weakness of certain muscles asymmetrically
  • cerebellum affected = vertigo, incoordination, ataxia (staggering gait)
  • depending on lesions: dysarthria (hard to speak bc jaw muscle weak), double vision, bladder control probs
134
Q

migraines

A

severe episodic headaches that occur in typical pattern for each person

135
Q

common elements with migraines

A
  • prodrome
  • headache itself
  • postdrome
136
Q

prodrome of migraine

A
  • S/S b4 headache, may include an aura
  • perception of strange light, an unpleasant smell or confusing thoughts
137
Q

migraine headache

A
  • often unilateral
  • accompanied by N, V, photophobia (light hurts eyes), phonophobia (soun hurts ears)
138
Q

postdrome of migraine

A

washed out, tired, weak

139
Q

exact cause of patho of migraine unknown, but thought to develop when individuals w/ genetic predisposition experience _________. _____ causes an _____ in the production of NT chems that activate the _______ response, resulting in?

A
  • a specific trigger event
  • trigger
  • alteration
  • inflammatory
  • vasodilation, increased cap permeability, pulsating one-sided throbbing headache
140
Q

individualistic triggers for migraines

A
  • chems found in red wine, chocolate, certain cheeses
  • stressful event, a smell, a sound
141
Q

tx migraines

A
  • trigger avoidance
  • NSAIDS help inflamm part that adds to pain
  • abortive drugs (Immitrex) - pts use @ start of migraine/@ first sign of prodrome
142
Q

seizures (convulsions)

A

sudden, explosive, disorderly charge of neurons

143
Q

seizures can be due to?

A
  • congenital seizure disorder (epilepsy)
  • acute prob in brain (head injury or stroke)
144
Q

general seizures (grand mal seizures)

A
  • precipitated by brain irritation due to cerebral edema
  • S/S: pt always unconscious, movement tonic-clonic (alternating rigidity + contraction of muscles)
145
Q

partial seizures

A

begin locally and can have varied level of unconsciousness

146
Q

a synonym for convulsions is ____, and the state of a pt following the end of a seizure is sometimes known as ____.

A
  • ictus
  • post-ictal
147
Q

post-seizure (post-ictal) condition

A
  • pt dazed, confused, sometimes combative
  • brain’s circuits still not back to norm
148
Q

tx seizures

A
  • self-limiting
    and/or
  • stop with meds
  • status epilepticus: unremitting, not-responsive to medications
149
Q

meningitis patho

A
  1. organisms spread via sneezing, coughing, sharing utensils
  2. microbe enters higher vascular nasopharyngeal area + crosses into blood
  3. blood system takes it to meninges via blood-vessel- rich choroid plexus
  4. inflamm process begins
  5. increased vascular permeability and edema
150
Q

most common two organisms that cause meningitis

A

viral and bacterial

151
Q

viral meningitis

A
  • aseptic meningitis (almost never causes sepsis)
  • same spread + entery as bacteria but much milder S/S and clin course
152
Q

bacterial meningitis is more?

A

virulent and dangerous

153
Q

S/S viral meningitis related to edema of meninges surrounding brain due to IICP

A
  • photophobia (pain in eyes when exposed to light)
  • headache, irritability
  • N,V
154
Q

S/S viral meningitis related to edema of meninges surrounding spinal cord

A
  • neck stifness
  • (+) Brudzinski’s and Kernig’s signs: maneuvers that show any kind of meningeal irritation
  • fever
155
Q

S/S bacterial meningitis of edema of meninges surrounding brain due to increased ICP

A
  • photophobia
  • headache
  • irritability
  • restlessness
  • decreased LOC
  • N, V
156
Q

S/S bacterial meningitis of eedema of meninges surrounding spinal cord

A
  • meningeal irritation
  • neck stiffness (muchal rigidity)
  • (+) Brudzinski’s and/or Kernig’s signs
  • fever
  • leukocytosis
  • sometimes petechiae and purpura in meningococcal meningitis
157
Q

why does pt have S/S of petechiae and purpura in meningococcal meningitis?

A
  • bacterial breakdown inflaming vasculature just under skin (med emergency)
158
Q

dz meningitis

A

S/S for bacterial meningitis, but gold standard is lumbar puncture/spinal tap

159
Q

lumbar puncture/spinal tap – specimen of CSF obtained and sent to lab for analysis, which shows what if pt has bacterial meningitis?

A
  • high WBC count
  • higher-than-nrom protein count bc presence of bacteria + protein exudates (from inflamed meningeal blood vessels + increased vascular permeability)
  • lower glucose bc bacteria eating glucose
  • blood
160
Q

main category of PNS disorder is?

A

neuromuscular junction disorders

161
Q

neuromuscular junction (NMJ)

A

synapse btw neuron and effector muscle

162
Q

events @ NMJ that result in muscle movement

A
  1. release of adequate amts of ACh from neuron
  2. ACh binding to receptors of effector muscle cell
  3. body’s checks + balance: cholinesterase released @ synapse to break down any extra ACh that isn’t used @ receptor site
163
Q

abnormalities of PNS

A
  • decrease in ACh production and/or recrption
  • increase in cholinesterase that can cause muscle weakness
164
Q

myasthenia gravis

A
  • chronic autoimmune disease sometimes associated w/ thymic tumor or other changes in thymus
  • antibx produced by boyd’s immune system block, alter, or destroy ACh receptors
165
Q

one of the main signs of Myasthenia gravis is?

A

progressive muscle weakness w/ motor activity

166
Q

why is there progressive muscle weakness w/ motor activity in Myasthenia gravis?

A
  • each repeating nerve impulse, the amt of ACh released usually declines
  • autoantibodies destroy sm receptors, so even norm reduction in ACh quickly results inability to complete nerve transmiss to muscle cells
167
Q

T/F: even norm people have a decline in amt of ACh released

A
  • TRUE
  • norm peeps have lots of receptors to pick up every last drop of ACh
168
Q

hallmark of myasthenia gravis

A

muscle weakness that increases during periods of activity and improves after periods of rest

169
Q

weakness seen in myasthenia gravis includes?

A
  • muscles that control eye + eyelid movements
  • facial expression
  • chewing
  • talking
  • swallowing
  • neck + limb movements
170
Q

if myasthenia gravis affects breathing, its called?

A

myasthenia crisis

171
Q

tx myasthenia gravis

A
  • anti-cholinesterase drugs
  • steroids
  • sometimes thymectomy
172
Q

mydriasis

A
  • pupillary dilation
  • usually occurs equally in both pupils upon exposure to less light
  • less light, more dilation
173
Q

mydriasis results from?

A

sympathetic nervous system releasing norepinephrine + stimulating alpha-1 adrenergic receptors on iris

174
Q

miosis

A
  • pupillary constriction
  • usually occurs equally in both pupils upon exposure to light
175
Q

miosis results from?

A

parasympathetic fibers w/in cranial nerve III (oculomotor nerve) releasing ACh, which act on receptors on iris

176
Q

damage from ischemia and/or bleeding in brain and/or IICP may cause? (related to meiosis)

A

compression of CNIII -> loss/diminish ability of pupil to constrict -> abnormally dilated and will not respond to light (or sluggish response)

177
Q

unequal pupil size looks like? and is a sign of?

A
  • one fixed (not responding to light) and dilated and one pupil constricted
  • sign of neurologic disorder like increased ICP or intracranial hemorrhage (bleeding in brain)
178
Q

diplopia

A
  • double vision
  • caused by weak ocular muscle
  • neuromuscular disease
  • cerebral hemisphere disease
  • thyroid disease
179
Q

nystagmus

A

rhythmic, involuntary, unilateral or bilateral movement of the eyes

180
Q

nystagmus can have ____ or ___ movement

A
  • horizontal
  • vertical
181
Q

nystagmus can be _____ or can be sign of _____ or _____ dysfxn - associated with ___ problems.

A
  • congenital
  • cerebellum
  • inner ear
  • vertigo and balance
182
Q

papilledema

A
  • edema + inflammation of optic nerve where it enters retina
  • can’t be seen by naked eye; assess via ophthalmoscope
183
Q

papilledema is caused by?

A

blockage of venous return from retina mainly bc of IICP