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Pathophysiology > Exam #5- Neurology Pathophysiology > Flashcards

Exam #5- Neurology Pathophysiology Flashcards

1
Q

temperature regulation

A

varies in response to location, activity, environment, circadian rhythm, and gender

regulation is mediated by hypothalamus

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2
Q

thermoreceptors

A

peripheral=skin

central=hypothalamus

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3
Q

heat protection

A

chemical reactions of metabolism, skeletal mucle contractions (shivering), chemical thermogenesis

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4
Q

temperature conservation

A

vasoconstriction, voluntary mechanisms

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5
Q

temperature loss

A

radiation, conduction, convection, vasodilation, decreased muscle tone, sweat evaporation, increased ventilation

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6
Q

when does fever happen?

A

when there is a release of pyrogens from leukocytes/other cells in immune response (endogenous pyrogens) and bacteria (exogenous pyrogens)

both are s/s of disease and normal response to disease

hypothalamic thermostat is now reset to a high level

when fever breaks set point goes back to normal

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7
Q

benefits of fever

A

kills microorganisms, fever helps infectious processes (decreases iron, zinc, copper that are needed for bacteria to replicate), promotoes lysosomal breakdown and apoptosis of cells, increases lymphocytic transformation and phagocyte motility, augments antiviral inferferon production and phagocytosis

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8
Q

older pts and fever

A

decreased or no fever in response to infection

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9
Q

kids and fever

A

get higher temps than adults for minor infections and can have febrile seizures

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10
Q

hyperthermia

A

NOT mediated by pyrogens

there is no resetting of the hypothalamic set points

at 41 C nerve damage produces convulsions

at 43 C you die

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11
Q

heat cramps

A

severe spasmodic cramps in ABD and extremities

following prolonged sweating and sodium loss

happens to those not used to heat/strenuous activity in warm climates

s/s are fever, fast HR, HTN with cramps

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12
Q

heat exhaustion

A

prolonged high temperature

s/s are dizziness, weakness, nausea, confusion, syncope

stop working, lie down, rest

stopping activity decreases muscle work with decreases heat production

lying down redistributes vascular volume

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13
Q

heatstroke

A

lethal d/t overstressed thermoregulatory center

brain, heart, and thermoregulatory centers don’t work with temps>40.5 C

s/s are cerebral edema, degeneration of CNS, swollen dendrites, renal tubular necrosis, death unless treated

cooling too quickly causes vasoconstriction and limits cooling

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14
Q

what is the major sleep center?

A

hypothalamus

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15
Q

phases of sleep

A

rapid eye movement (REM) and non rapid eye movement (NREM)

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16
Q

REM phase of sleep

A

vivid dreaming

90 minute

1-2 hours after falling asleep

eyes flutter

breathing is irregular

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17
Q

NREM phase of sleep

A

slow wave

most of the time is NREM

stages evaluated by EEG

restorative and reparative

growth occurs here

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18
Q

three stages of NREM sleep cycle

A

N1- right after you fall asleep (phase is only about 10 minutes)- light sleep

N2- lasts 30-60 minutes, muscles relax, slow waves

N3- deep sleeps, lasts 20-40 minutes, hard to wake up

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19
Q

dyssomnias

A

intrinsic and extrinsic sleep disorders and circadian rhythm sleep disorders

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20
Q

parasomnias

A

arousal and sleep wake transition disorders and REM sleep disorders

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21
Q

OSAS

A

trouble breathing while you sleep related to upper airway obstruction and is related to decreased O2 and increased CO2

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22
Q

risk factors for OSAS

A

obesity, male, age

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23
Q

s/s of OSAS

A

snoring, gasping, apnea 10-30 seconds, fragmented sleep, daytime sleepiness

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24
Q

pathophysiology of OSAS

A

obstruction d/t soft palate or base of tongue collapsing against pharyngeal walls d/t decreased muscle tone during REM sleep

negative introthoracic pressure wakes up pt

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25
Q

systemic illnesses associated with OSAS

A

HTN, pulmonary HTN, HF, nocturnal cardiac dysrhythmias, MI, CVA

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26
Q

people spend most time in what phase of sleep?

A

NREM

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27
Q

age-related macular degeneration (AMD)

A

drusen (retinal) waste products build up in deep retinal layers

wet AMD is the worst, dry is most common

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28
Q

wet AMD

A

too many abnormal vessels leads to leak and bleed which leads to retinal detachment

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29
Q

dry AMD

A

loss of retinal pigment epithelium photoreceptors with overall atrophy of cells

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30
Q

glaucoma

A

intraocular pressure>normal pressure

build up of aqeous humor fluid

trabecular meshwork

damage to the optic nerve

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31
Q

scotoma

A

a defect of the central field of vision

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32
Q

conductive hearing loss

A

impaired sound from outer to inner ear

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33
Q

sensorineural hearing loss

A

impaired organ of corti or its central connections

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34
Q

presbycusis hearing loss

A

a type of sensorineural hearing loss

age related hearing loss (high frequencies)

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35
Q

mixed hearing loss

A

conductive and sensorineural

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36
Q

functional hearing loss

A

no reason but could be emotional/psychological factors

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37
Q

vertigo

A

spinning feeling that occurs from inflammation of ear’s SEMICIRCULAR CANALS

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38
Q

arousal

A

state of being AWAKE

mediated by RAS

breathing patterns, oculomotor responses, and pupil changes=change in arousal

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39
Q

awareness

A

cognitive functions that embody awareness of self, environment, and mood

CONTENT of thought

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40
Q

coma

A

no verbal response to external environment or any stimuli

noxious stimuli (deep pain, suctioning produces movement)

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41
Q

light coma

A

purposeful movement with stimulation

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42
Q

deep coma

A

no response to any stimulus

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43
Q

brain death

A

brain will not recover and can’t maintain body’s homeostasis

state laws: entire brain, brainstem, and cerebellum stop functioning

brain autolyzes (self-digests)

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44
Q

cerebral death

A

cerebral hemispheres die but not brainstem or cerebellum

braintstem may maintain normal respiration and cardiac fucntions, temp control, and GI function

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45
Q

pathophysiology of seizures

A

sudden, impermanent alteration of brain function caused by explosive, disorderly discharge of cerebral neurons

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46
Q

generalized seizure

A

neurons bilaterally

ex: absent, myoclonic, clonic, tonic-clonic, atonic

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47
Q

partial (focal) seizure

A

neurons unilaterally

begins in specific region of cortex

ex: simple, complex

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48
Q

secondary generalization seizure

A

partial becomes generalized

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49
Q

status epilepticus

A

emergency

seizure lasts longer than 5 minutes, 2nd seizure occurs before LOC is regained from 1st, or 1 seizure lasts longer than 30 minutes

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50
Q

aura

A

partial seizure (weird sensation) leads to generalized seizure

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51
Q

prodromal seizure

A

early s/s like malaise, HA, depression

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52
Q

tonic seizure

A

contraction

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53
Q

clonic seizure

A

relaxation

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54
Q

post ictal seizure

A

period immediately following end of seizure

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55
Q

broca aphasia

A

can understand, but can’t communicate

expressive dysphagia

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56
Q

wernicke problem

A

can’t understand (verbal/reading)

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57
Q

delirium

A

acute

onset abrupt

ANS is overactive

common in ICU’s, post surgeries, withdrawal (ETOH, narcs)

58
Q

dementia

A

progressive

onset gradual

progressive nerve cell degeneration and brain atrophy

age is greatest risk factor

59
Q

a major difference between delirium and dementia is what?

A

related to degeneration of nerve cells

60
Q

pathophysiology of alzheimers

A

exact cause unknown, but thought to be mutation for encoding amyloid precursor protein, alteration in apoliporotein E, or loss of NT stimulation of choline actyltransferase

early onset is AUTOSOMAL DOMINANT

61
Q

s/s of alzheimers

A

neurofibrillary tangles, senile plaques, amyloid deposits (limit blood flow), forgetfulness, emotional upset, disoriented, confused, lack of concentration, decline in abstraction, problem solving, judgement

62
Q

diagnosis of alzheimers

A

when you rule out other causes

definitive on postmortem exam

63
Q

herniation

A

brain tissue is pushed from one compartment to another

from infection, hemorrhage, tumor, ischemia, infarct, hypoxia

64
Q

vasogenic cerebral edema

A

disruption of BBB

caused by increased permeability of capillary endothelium of brain after injury to vasculature

65
Q

cytotoxic cerebral edema

A

metabolic

BBB is not disrupted

toxic factors impact brain

failure of active transport system

cells swell d/t loss of K+ and gain of Na+ (then H2O follows Na+)

66
Q

interstitial cerebral edema

A

caused by trans-ependymal movement of CSF from ventricles into extracellular spaces of brain tissues

67
Q

hydrocephalus

A

caused by interference in CSF flow

too much fluid within cranial vault, subarachnoid space, or both

68
Q

decreased reabsorption with hydrocephalus

A

ex: blockage of arachnoid vili from SAH or infection

69
Q

increased fluid production with hydrocephalus

A

ex: choroid plexus tumor

70
Q

obstruction within ventricular system with hydrocephalus

A

tumor or congenital malformation

71
Q

communicating (extra-ventricular) hydrocephalus

A

from impaired absorption

normal pressure hdyrocephalus

72
Q

non-communicating hydrocephalus

A

blockage occurs along narrow pathways that connect ventricular system

most common narrowing of aqueduct of sylvius “aqueductal stenosis” between 3rd and 4th

73
Q

acute hydrocephalus

A

develops in several hours

rapidly increases ICP and deterioration

74
Q

obstructive sources of hydrocephalus are classified as what?

A

non-communicating hydrocephalus

75
Q

paresis

A

weakness

76
Q

paralysis

A

loss of motor function

77
Q

upper motor neuron syndromes

A

spastic paresis or paralysis

associated with HYPERREFLEXIA

SPINAL SHOCK- complete paralysis, loss of reflexes, below lesion

78
Q

lower motor neuron syndromes

A

dysfunction impairs voluntary and involuntary movement

flaccid paresis or flaccid paralysis- muscle has reduced or absent tone

associated with HYPOREFLEXIA or AREFLEXIA

79
Q

what is an example of a lower motor neuron disease?

A

drop foot

80
Q

huntington disease

A

autosomal dominant hereditary degenerative disorder

short arm chromosome 4

enlargement of the frontal horns of the lateral ventricles

81
Q

s/s of huntington disease

A

abnormal movement (CHOREA) and progressive dementia

82
Q

parkinson disease

A

severe breakdown of basal ganglia involving the dopaminergic nirgostriatal pathway (dopamine secreting)

loss of dopaminergic pigmented neurons in substantia nirga pars compacta with dopaminergic deficiency in putemen portion of striatum DECREASES activity of DIRECT motor pathway (normally FACILITATES movements) and INCREASES activity of INDIRECT motor loop (normally INHIBITS movement)

83
Q

s/s of parkinson’s disease

A

parkinsonian tremor, rigidity, bradykinesia (slowed movement), abnormal posture, cognitive-affective s/s, tremor at rest, cogwheel rigidity, hypoakinesia, stooped posture, not sleeping, fatigue, pain, autonomic dysfunction, depression, dementia with or without psychosis

84
Q

decorticate posturing

A

flexed upper extremities and close to body

brainstem is NOT inhibited by motor function of cerebral cortex

85
Q

decerebrate posturing

A

angel wings

severe brain and brainstem injury

86
Q

central sensitization

A

nonpainful stimuli creates a pain response

87
Q

contusion

A

brain bruise

coup-contrecoup

88
Q

laceration

A

brain tissue tear

89
Q

extradural (epidural) hematoma

A

blood ABOVE dura mater

90
Q

subdural hematoma

A

blood between dura and arachnoid

91
Q

intracerebral hematoma

A

bleeding IN the brain

92
Q

open brain injury

A

head trauma

skull fracture with exposed cranial vault

93
Q

diffuse brain injury

A

d/t head rotation (primary) or shaking

brain undergoes shearing stress which leads to axonal damage (concussion leads to severe DAI)

O2 free radials r/t secondary injury

categories are mild concusion, classical consussion, mild/mod/severe DAI

94
Q

three grades of mild concussion

A

I. confusion, disorientation, momentary amnesia

II. momentary confusion and retrograde amnesia

III. confusion with retrograde and anterograde amnesia with loss of consciousness

no loss of consciousness with grade I and II

95
Q

grade IV concussion

A

cerebral systems are disconnected from brain stem and RAS

physiologic and neuro dysfunction without bad anatomic disruption

loss of consciousness<6 hours

post concussive syndrome

96
Q

post concussive syndrome

A

HA, cognitive impairments, psych and somatic complaints, cranial nerve S/S

happens with a grade IV concussion

97
Q

diffuse axonal injury (DAI)

A

form of TBI

98
Q

mild DAI

A

coma 6-24 hours

residual impairments

decerebrate/decorticate posturing

99
Q

moderate DAI

A

coma >24 hours

widespread impairment through cerebral cortex and diencephalon

ACTUAL TEARING of some AXONS in both hemispheres

recovery is incomplete

decerebrate and decorticate posturing

100
Q

severe DAI

A

many axons are messed up extending to diecephalon and brainstem

high mortality

101
Q

pathophysiology of spinal cord trauma

A

occurs from vertebral injuries

simple fx, compressed fx, communited fx and dislocation

102
Q

complete spinal cord transection

A

loss of motor function

muscles are flaccid

lost reflexes

lost pain, temp, touch, proprioception, respiratory impairment

103
Q

s/s of spinal cord trauma

A

paraplegia- paralysis of LE

quadriplegia- paralysis of all extremities

104
Q

spinal shock

A

a result of spinal cord trauma

loss of motor, sensory, reflex, and autonomic functions below cut across area

105
Q

partial spinal cord transection

A

asymmetric flaccid motor paralysis/reflex loss, some senses

106
Q

brown-sequard syndrome

A

ipsilateral paralysis/loss of touch

contralateral loss of pain and temp

107
Q

central cord syndrome

A

motor deficits>UE than LE

108
Q

anterior cord syndrome

A

loss of motor, pain, temp

intact=touch, pressure, position, vibration

109
Q

posterior cord syndrome

A

impaired light touch and proprioception

110
Q

cauda equina syndrome

A

LE motor deficits, sensorimotor dysfunction

B/B and sexual dysfunction

111
Q

autonomic hyperreflexia (dysreflexia)

A

massive/uncompensated heart response to stimulation of SNS

sudden/dangerous increase in BP (life threatening)

112
Q

s/s of autonomic hyperreflexia

A

HTN, bradycardia, pounding HA, blurred vision, piloerection

113
Q

thrombotic stroke

A

arteries supplying brain occluded from thrombi d/t atherosclerosis and inflammatory disease

damaged artery walls

114
Q

embolic stroke

A

fragment breaks off a thrombus that’s formed outside of the brain d/t a-fib

115
Q

hemorrhagic stroke

A

d/t HTN, ruptured aneurysm, AV malformations, cavernous angioma or from TBI

116
Q

lacunar stroke

A

really tiny infarct in tiny vessels d/t lipohyalinosis, subintimal lipid-loading foam cells, or fibrinoid materials that thicken the arterial walls

r/t smoking, HTN, DM

117
Q

a patient is diagnosed with a fib and then has a CVA

A

embolic stroke

118
Q

TIA

A

BRIEF episode of neuro dysfunction d/t focal disturbance/brain/retinal ischemia

s/s last<1 hour

thrombus particles lead to INTERMITTENT blockage

119
Q

subarachnoid hemorrhage (SAH)

A

blood escape from defective/injured vasculature into subarachnoid space

120
Q

s/s of subarachnoid hemorrhage

A

VASOSPASM- d/t blood breakdown

free radicals disrupt blood vessel layers and release inflammatory factors

delayed cerebral ischemia

thunderclap HA, N/V, loss of LOC, neuro problems d/t increased ICP

KERNIG/BRUDZINSKI sign: when the patient is lying with the thigh flexed on the abdomen, the leg cannot be completely extended. when the 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

121
Q

intracranial aneurysm

A

d/t defect in vascular wall

s/s is acute SAH, intracerebral hemorrhage, or a combination

122
Q

migraine

A

genetic and environment

phases (premonitory, aura, HA)

unilateral throbbing, worse with movement, N/V, photophobia

123
Q

cluster headaches

A

trigeminal activation

unilateral TRIGEMINAL distribution of severe pain with ipsilateral autonomic s/s (tearing on affected side, ptosis of same eye, stuffy nose)

124
Q

tension type headache

A

central and peripheral mechanism

feeling of a tight band/pressure around head with gradual onset

125
Q

bacterial meningitis

A

infection of pia mater and arachnoid of fluid or subarachnoid space

bacteria makes pus

vessels are hyperemic and netrophils move to subarachnoid space

inflammatory reaction leads to exudation

126
Q

aseptic meningitis

A

viral, non-purulent, lymphocytic

limited to meninges

127
Q

fungal meningitis

A

chronic, less common

128
Q

meningitis s/s

A

depends on type

can be throbbing HA, neck stiffness, rigidity, decreased responsiveness, kernig and brudzinski

129
Q

encephalitis

A

acute febrile illness (viral) with nervous system affected

130
Q

s/s of encephalitis

A

fever, delirium, confusion, seizures, involuntary movement, increased ICP

131
Q

MS

A

acquired autoimmune

it’s a progressive, inflammatory, DEMYELINATION disorder of CNS

scarring, plaque formation, and loss of axons

132
Q

mixed MS

A

optic signs

brainstem signs (diplopia, vertigo, nystagmus, dysarthria)

133
Q

spinal MS

A

spinal tracts and dorsal column involved

weakness, numbness, or both

spastic ataxia

bladder/bowel s/s

134
Q

cerebellar MS

A

motor ataxia, hypotonia, asthenia

135
Q

pathophysiology of ALS

A

upper and lower motor neurons of cerebral cortex, brainstem, and spinal cord affected

DEGENERATION of NON-MOTOR NEURONS in cortices and spinal cord

136
Q

s/s of ALS

A

disease

progressive weakness

respiratory failure and death

137
Q

myasthenia gravis pathophysiology

A

acquired chronic autoimmune disease resulting from defect in nerve impulse transmission at NMJ

IgG antibody is produced against acetylcholine receptors

138
Q

s/s of myasthenia gravis

A

weakness/fatigue of muscles of eyes and throat

diplopia and trouble chewing, talking, or swallowing

c/o fatigue after exercise and history of recurring URI’s

139
Q

myasthenia crisis

A

severe muscle weakness

quadriparesis/quadriplegia, respiratory problems with SOB, extreme problems with swallowing

140
Q

cholinergic crisis

A

can be d/t drug overdose

looks like myasthenic crisis BUT it happens 30-60 minutes after taking anticholinesterase med

141
Q

s/s of cholinergic crisis

A

diarrhea, cramping, fasciculation, decreased HR, pupil constriction, increased salivation, increased sweating

142
Q

myasthenia gravis is the result of what?

A

autoimmune destruction of acetylcholine receptors

Pathophysiology (5 decks)

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