Exam #5- Neurology Pathophysiology Flashcards
temperature regulation
varies in response to location, activity, environment, circadian rhythm, and gender
regulation is mediated by hypothalamus
thermoreceptors
peripheral=skin
central=hypothalamus
heat protection
chemical reactions of metabolism, skeletal mucle contractions (shivering), chemical thermogenesis
temperature conservation
vasoconstriction, voluntary mechanisms
temperature loss
radiation, conduction, convection, vasodilation, decreased muscle tone, sweat evaporation, increased ventilation
when does fever happen?
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
benefits of fever
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
older pts and fever
decreased or no fever in response to infection
kids and fever
get higher temps than adults for minor infections and can have febrile seizures
hyperthermia
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
heat cramps
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
heat exhaustion
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
heatstroke
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
what is the major sleep center?
hypothalamus
phases of sleep
rapid eye movement (REM) and non rapid eye movement (NREM)
REM phase of sleep
vivid dreaming
90 minute
1-2 hours after falling asleep
eyes flutter
breathing is irregular
NREM phase of sleep
slow wave
most of the time is NREM
stages evaluated by EEG
restorative and reparative
growth occurs here
three stages of NREM sleep cycle
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
dyssomnias
intrinsic and extrinsic sleep disorders and circadian rhythm sleep disorders
parasomnias
arousal and sleep wake transition disorders and REM sleep disorders
OSAS
trouble breathing while you sleep related to upper airway obstruction and is related to decreased O2 and increased CO2
risk factors for OSAS
obesity, male, age
s/s of OSAS
snoring, gasping, apnea 10-30 seconds, fragmented sleep, daytime sleepiness
pathophysiology of OSAS
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
systemic illnesses associated with OSAS
HTN, pulmonary HTN, HF, nocturnal cardiac dysrhythmias, MI, CVA
people spend most time in what phase of sleep?
NREM
age-related macular degeneration (AMD)
drusen (retinal) waste products build up in deep retinal layers
wet AMD is the worst, dry is most common
wet AMD
too many abnormal vessels leads to leak and bleed which leads to retinal detachment
dry AMD
loss of retinal pigment epithelium photoreceptors with overall atrophy of cells
glaucoma
intraocular pressure>normal pressure
build up of aqeous humor fluid
trabecular meshwork
damage to the optic nerve
scotoma
a defect of the central field of vision
conductive hearing loss
impaired sound from outer to inner ear
sensorineural hearing loss
impaired organ of corti or its central connections
presbycusis hearing loss
a type of sensorineural hearing loss
age related hearing loss (high frequencies)
mixed hearing loss
conductive and sensorineural
functional hearing loss
no reason but could be emotional/psychological factors
vertigo
spinning feeling that occurs from inflammation of ear’s SEMICIRCULAR CANALS
arousal
state of being AWAKE
mediated by RAS
breathing patterns, oculomotor responses, and pupil changes=change in arousal
awareness
cognitive functions that embody awareness of self, environment, and mood
CONTENT of thought
coma
no verbal response to external environment or any stimuli
noxious stimuli (deep pain, suctioning produces movement)
light coma
purposeful movement with stimulation
deep coma
no response to any stimulus
brain death
brain will not recover and can’t maintain body’s homeostasis
state laws: entire brain, brainstem, and cerebellum stop functioning
brain autolyzes (self-digests)
cerebral death
cerebral hemispheres die but not brainstem or cerebellum
braintstem may maintain normal respiration and cardiac fucntions, temp control, and GI function
pathophysiology of seizures
sudden, impermanent alteration of brain function caused by explosive, disorderly discharge of cerebral neurons
generalized seizure
neurons bilaterally
ex: absent, myoclonic, clonic, tonic-clonic, atonic
partial (focal) seizure
neurons unilaterally
begins in specific region of cortex
ex: simple, complex
secondary generalization seizure
partial becomes generalized
status epilepticus
emergency
seizure lasts longer than 5 minutes, 2nd seizure occurs before LOC is regained from 1st, or 1 seizure lasts longer than 30 minutes
aura
partial seizure (weird sensation) leads to generalized seizure
prodromal seizure
early s/s like malaise, HA, depression
tonic seizure
contraction
clonic seizure
relaxation
post ictal seizure
period immediately following end of seizure
broca aphasia
can understand, but can’t communicate
expressive dysphagia
wernicke problem
can’t understand (verbal/reading)
delirium
acute
onset abrupt
ANS is overactive
common in ICU’s, post surgeries, withdrawal (ETOH, narcs)
dementia
progressive
onset gradual
progressive nerve cell degeneration and brain atrophy
age is greatest risk factor
a major difference between delirium and dementia is what?
related to degeneration of nerve cells
pathophysiology of alzheimers
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
s/s of alzheimers
neurofibrillary tangles, senile plaques, amyloid deposits (limit blood flow), forgetfulness, emotional upset, disoriented, confused, lack of concentration, decline in abstraction, problem solving, judgement
diagnosis of alzheimers
when you rule out other causes
definitive on postmortem exam
herniation
brain tissue is pushed from one compartment to another
from infection, hemorrhage, tumor, ischemia, infarct, hypoxia
vasogenic cerebral edema
disruption of BBB
caused by increased permeability of capillary endothelium of brain after injury to vasculature
cytotoxic cerebral edema
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+)
interstitial cerebral edema
caused by trans-ependymal movement of CSF from ventricles into extracellular spaces of brain tissues
hydrocephalus
caused by interference in CSF flow
too much fluid within cranial vault, subarachnoid space, or both
decreased reabsorption with hydrocephalus
ex: blockage of arachnoid vili from SAH or infection
increased fluid production with hydrocephalus
ex: choroid plexus tumor
obstruction within ventricular system with hydrocephalus
tumor or congenital malformation
communicating (extra-ventricular) hydrocephalus
from impaired absorption
normal pressure hdyrocephalus
non-communicating hydrocephalus
blockage occurs along narrow pathways that connect ventricular system
most common narrowing of aqueduct of sylvius “aqueductal stenosis” between 3rd and 4th
acute hydrocephalus
develops in several hours
rapidly increases ICP and deterioration
obstructive sources of hydrocephalus are classified as what?
non-communicating hydrocephalus
paresis
weakness
paralysis
loss of motor function
upper motor neuron syndromes
spastic paresis or paralysis
associated with HYPERREFLEXIA
SPINAL SHOCK- complete paralysis, loss of reflexes, below lesion
lower motor neuron syndromes
dysfunction impairs voluntary and involuntary movement
flaccid paresis or flaccid paralysis- muscle has reduced or absent tone
associated with HYPOREFLEXIA or AREFLEXIA
what is an example of a lower motor neuron disease?
drop foot
huntington disease
autosomal dominant hereditary degenerative disorder
short arm chromosome 4
enlargement of the frontal horns of the lateral ventricles
s/s of huntington disease
abnormal movement (CHOREA) and progressive dementia
parkinson disease
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)
s/s of parkinson’s disease
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
decorticate posturing
flexed upper extremities and close to body
brainstem is NOT inhibited by motor function of cerebral cortex
decerebrate posturing
angel wings
severe brain and brainstem injury
central sensitization
nonpainful stimuli creates a pain response
contusion
brain bruise
coup-contrecoup
laceration
brain tissue tear
extradural (epidural) hematoma
blood ABOVE dura mater
subdural hematoma
blood between dura and arachnoid
intracerebral hematoma
bleeding IN the brain
open brain injury
head trauma
skull fracture with exposed cranial vault
diffuse brain injury
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
three grades of mild concussion
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
grade IV concussion
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
post concussive syndrome
HA, cognitive impairments, psych and somatic complaints, cranial nerve S/S
happens with a grade IV concussion
diffuse axonal injury (DAI)
form of TBI
mild DAI
coma 6-24 hours
residual impairments
decerebrate/decorticate posturing
moderate DAI
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
severe DAI
many axons are messed up extending to diecephalon and brainstem
high mortality
pathophysiology of spinal cord trauma
occurs from vertebral injuries
simple fx, compressed fx, communited fx and dislocation
complete spinal cord transection
loss of motor function
muscles are flaccid
lost reflexes
lost pain, temp, touch, proprioception, respiratory impairment
s/s of spinal cord trauma
paraplegia- paralysis of LE
quadriplegia- paralysis of all extremities
spinal shock
a result of spinal cord trauma
loss of motor, sensory, reflex, and autonomic functions below cut across area
partial spinal cord transection
asymmetric flaccid motor paralysis/reflex loss, some senses
brown-sequard syndrome
ipsilateral paralysis/loss of touch
contralateral loss of pain and temp
central cord syndrome
motor deficits>UE than LE
anterior cord syndrome
loss of motor, pain, temp
intact=touch, pressure, position, vibration
posterior cord syndrome
impaired light touch and proprioception
cauda equina syndrome
LE motor deficits, sensorimotor dysfunction
B/B and sexual dysfunction
autonomic hyperreflexia (dysreflexia)
massive/uncompensated heart response to stimulation of SNS
sudden/dangerous increase in BP (life threatening)
s/s of autonomic hyperreflexia
HTN, bradycardia, pounding HA, blurred vision, piloerection
thrombotic stroke
arteries supplying brain occluded from thrombi d/t atherosclerosis and inflammatory disease
damaged artery walls
embolic stroke
fragment breaks off a thrombus that’s formed outside of the brain d/t a-fib
hemorrhagic stroke
d/t HTN, ruptured aneurysm, AV malformations, cavernous angioma or from TBI
lacunar stroke
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
a patient is diagnosed with a fib and then has a CVA
embolic stroke
TIA
BRIEF episode of neuro dysfunction d/t focal disturbance/brain/retinal ischemia
s/s last<1 hour
thrombus particles lead to INTERMITTENT blockage
subarachnoid hemorrhage (SAH)
blood escape from defective/injured vasculature into subarachnoid space
s/s of subarachnoid hemorrhage
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
intracranial aneurysm
d/t defect in vascular wall
s/s is acute SAH, intracerebral hemorrhage, or a combination
migraine
genetic and environment
phases (premonitory, aura, HA)
unilateral throbbing, worse with movement, N/V, photophobia
cluster headaches
trigeminal activation
unilateral TRIGEMINAL distribution of severe pain with ipsilateral autonomic s/s (tearing on affected side, ptosis of same eye, stuffy nose)
tension type headache
central and peripheral mechanism
feeling of a tight band/pressure around head with gradual onset
bacterial meningitis
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
aseptic meningitis
viral, non-purulent, lymphocytic
limited to meninges
fungal meningitis
chronic, less common
meningitis s/s
depends on type
can be throbbing HA, neck stiffness, rigidity, decreased responsiveness, kernig and brudzinski
encephalitis
acute febrile illness (viral) with nervous system affected
s/s of encephalitis
fever, delirium, confusion, seizures, involuntary movement, increased ICP
MS
acquired autoimmune
it’s a progressive, inflammatory, DEMYELINATION disorder of CNS
scarring, plaque formation, and loss of axons
mixed MS
optic signs
brainstem signs (diplopia, vertigo, nystagmus, dysarthria)
spinal MS
spinal tracts and dorsal column involved
weakness, numbness, or both
spastic ataxia
bladder/bowel s/s
cerebellar MS
motor ataxia, hypotonia, asthenia
pathophysiology of ALS
upper and lower motor neurons of cerebral cortex, brainstem, and spinal cord affected
DEGENERATION of NON-MOTOR NEURONS in cortices and spinal cord
s/s of ALS
disease
progressive weakness
respiratory failure and death
myasthenia gravis pathophysiology
acquired chronic autoimmune disease resulting from defect in nerve impulse transmission at NMJ
IgG antibody is produced against acetylcholine receptors
s/s of myasthenia gravis
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
myasthenia crisis
severe muscle weakness
quadriparesis/quadriplegia, respiratory problems with SOB, extreme problems with swallowing
cholinergic crisis
can be d/t drug overdose
looks like myasthenic crisis BUT it happens 30-60 minutes after taking anticholinesterase med
s/s of cholinergic crisis
diarrhea, cramping, fasciculation, decreased HR, pupil constriction, increased salivation, increased sweating
myasthenia gravis is the result of what?
autoimmune destruction of acetylcholine receptors
