• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/102

Click to flip

102 Cards in this Set

  • Front
  • Back
Increased intracranial pressure
pressure placed on the contents of the cranium
normal intracranial pressure
0-15 mm hg
couses of increased ICP
cerebral edema (most commonn trauma)
tumors
increased blood volume
increased cebral spinal fluid
1st compensation for ICP
displace & reabsorb CSF
s/s of 1st compensation of ICP
subtle drowsiness
slight sluggish pupils
s/s of 2nd compensation of ICP
increasing BP
decreased LOC
pupils don't react (sluggish fixed)
2nd compensation of PCP
constrict blood vessels
worsening s/s of ICP
widening pulse pressure
papilledema
decreased pulse
cheyne-stokes respirations
increased temp due to inflammation
loss of sensory/moter function
headache
vomiting-projectile
unresponsivenss
posturing (Decorticate vs Decerbrate)
hemiplegia
1/2 side weakness
decorticate
curl up towards core
decerbrate
posturing out

Worse
widening pulse pressure
sytolic bp going up & diastolic bp going down
treatment for ICP
treat the cause
maintain ventilation
diuretics (draw water from brain cells)
corticosteroids - to decrease edema
cerbral vascular accident (stroke)
sudden impairments of cerebral activity
usually due to impaired cerebral ciruclation
it's either a plug or leak
impaired ciruculation
can be massive or slight
most common durological disability
CVA/stroke
#3 cause of death
stroke / CVA
FAST
facial
arms
speach
time
2 types of ischemic strokes (plug/clot)
thrombosis
embolism
most common stroke
thrombosis
thrombosis
most common in elderly
associated with ahterosclerosis
narrowing of arterial lumen
atherosclerosis
plaques
risk factors for thrombosis type strokes
atherosclerosis - HTN, High cholestrol, smoking
advancing age
diabetes
FHX
Embolism
often at bifaction (branching)
develops rapidely w/out warning
usuay from thrombi formed in heart
thrombi formed in heart
artrial fibrillation
2nd type of stroke
intracerebral hemorrahge
intracerebral hemorrhage especially common with
HTN and aneurysms

severity depends on age, location, size of hemorrhage
most likely to be fatal
sudden rupture of cerbral artery
compression of brain
increased ICP
usually no warning
patho of CVA
decreased blood flow leads to ischemia
s/s of CVA occur within
one minute of insufficient O2
tissue softens and discolors within
6-12 hours
ncrosis occurs within
48-72 hours
treatment for stroke needs to be within
3 hours for maxium recovery
warnings for stroke are called
transient ischemic attacks
transient ischemic attacks
focal ischemic deficit lasting less than 24 hours (usally minutes)
the pt. feels "silly" becasue they are "all better" when the ambulance arrives
transient ischemic attacks due to
atherosclerosis and emboli that resolve
transient ischemic attacks
WARNING OF IMPENDING STROKE

and are often progressive signs
s/s of transient ischemic attacks
numbness
weakness
aphasia
foggy vision ets
THEY ALL CLEAR UP

symptoms vary based on where in the brain it is
treatment of transient ischemic attacks
locate the lesion/embolism
give ASA daily
decrease BP
seek cause agressively
S/S of CVA
depending on artery effected
CVA on left produced symptoms on the right side of body and vice versa
EXCEPT cranial nerve dysfunctjion (same side)
most effected artery causing CVA
middle cerebral artery
most common s/s ischemic strokes
vision changes
speech chages
headache
sided weakness
balance changes
.......... consciousness OK
most common s/s of hemorrhagic stokes
vision changes
speech changes
headache is worse
sided weakness
balance changes
decreased LOC
N/V
Goals for CVA
normalize BP
minimize infarct
treat ICP
preserve neurological function
rehab and prevention of recurrence
meds for CVA may be
thromolytic/anticoagulants for a clot
possible surgery for a _______ stroke
hemorrhagic stroke
meningitis
infection of the meninges (coverings of the brain)
usually pia matter and arachnoid matter

lower ones that snug up to brain
cause of meningitis
any way organisms can get in:
ottis media
skill fx
sinusitis
denatl infection
immunocompromised
or unknown
patho of meningitis
infection causes inflammatory exudate (pus)
thick CSF as exudate forms
possible obstruction of pus
swollen meninges
increased ICP
eventually infection can spread to brain itself (encephalitis)
s/s of meningitis
worst headache ever
fever
stiff neck (nuccal rigidity)

lethargy
photophobia
decrease in consciousness is rapid
+kernig sign
+brudzinksi sign
cloudy purulent & CSF (exudate)
+ kernig sign
leg will not extend if lying with hip flexed at R angle
+ brudzinski sign
forcible flexion of neck
flexion of hip/knee
treatment of meningitis
ICU
antibiotics
ICP monitoring

HIGH MORTIALITY IF BACTERIA
prevention of meningitis
H. Flu vaccine for kids
meningococal vaccine also available (now routine for teens)
seizure
sudden explosive abnormal electircal impulse in the brain
not a disease but a symptom
may have motor, sensory, autonomic or behavioral symptomes
seizures may be due to
elctrolyte imbalance
drugs
ETOH (alcohol)
fever
trauma
infection
CVA
epilepsy
recurring seizures without a reversible cause
epilepsy due to
birth injury
rapid development of nervous system
structural damage, trauma, tumor, stroke
OR UNKNOWN/IDIOPATHIC
types of seizures
partial seizures
generalized seizures
status epilepticus
partial seizures
only 1/2 brain effected
simple partial seizure
no loss oc consciousness
pt. may have a deja-vu event
queasy stomach
numbness
tingling
sense of fear
can begin with aura & progress to complex partial
compex parital sz
some alteration in consciousness

automatisms are common
last about 60-90 sec
followed by confusion and no recall of episode
can progress to a generalized tonic-clonic seizure
automatisms
lip smacking
rapid eye blicking
etc
s/s of partial seizures
motor symptoms
sensory symptoms
autonomic symptoms
autonomic symptoms of partial
flushing
tachcardia
pupil dilation
sensory symptoms of partial sz
numbness
bad taste
odd smell
flashing lights
motor symptoms of partial sz
often limited to one part of the body
generalized sz
entire brain is involved
usually causes unconsciousness
3 generalized sz
absence (petit mal)
atonic (drop attack)
tonic-clonic (grand mal)
absence sz
most common in kids
impaired responsiveness (stares in space)
no decreased consciousness
last less than 30 seconds
tacher thinks child has lack of focus
atonic sz
sudden loss of all mussle tone
could lead to injury
tonic-clonic sz
starts w/ vague warning (aura)
sudden unconscious jerking of whole body
often yells or bits tongue
no breathing during sz
sleep afterward (brain nds to reboot)
status epileptieus
one sz right after another
usually due to skipping meds
can cause brain damage and/or death from ischemia if goes more than 30-40 minutes
tx for sz
keep pt safe
maintain airway
don't restrain
correct cause if possible
aticonvulsant drugs
surgery or Zap
dementia
focus on alzheimers disease 60-70% of dementia pt
alzheimers
progressive decrease in intellectural function
dure to corical atrophy and loss of neurons
cause of alzheimers
unknown
some genetic mutation
risk factor for alzheimers
age
family history
patho for alzheimers
neurofibrillary tangles form in the brain (fibrous proteins from the neurons are wound together)

senile plaques form in areas of degenearting nerve terminals
increased # of degenerating neve impulses in hippocampus
alzheimers may be due to
loss of neurotramsmitter choline acetyltransferase which helps synthesize acethycholine
an important neurotransmitter
choline acetyltransferase
s/s of alzheimers
gradual onset
starts with forgetfulness
memory loss
lack of insight
forget words
aware they r forgetful at first

progress to
decrease problem solving
impaired language
can't care for self
often leads to wandering

eventually
unable to communicate
incontinence
unable to recognize family
conductive hearing loss
anythng that disrupts passage of sound from outside of body
disrupts air conduction of sound
would not reach CN #8
conductive hearing loss - what can disrupt
ear wax
hole
fluid/pus in the middle ear
ossicles fused together w/age
treatment of conductive hearing loss
correct the cause
surgery can help ostosclerosis
sensorineural hearing loss
CN#8, organ of corti or the auditory pathway to the brain is the problem

birth trauma (rubella)
nerve dead
loud noise - damage organ of Corti
vascular disorders in the brain or vessels of the inner ear
meningitis
DM
drug toxicity
treatment of sensorineural hearing loss
not much - hearing aids don't hlep

imbedded neural hearing aid, surgical attached to brain
otitis media
infection of the middle ear (ossicles r air filled space)
most common in child
otitis media due to
shorter horizontal wide eustachian tube
bottle fed babies are fed lying doing, milk comes to fast and less meternal antibodies
s/s of otitis media
ear ache
fever 101
decreased hearing (fluid there)
tugging on ear

fluid behind the TM (serous)
chronic lasting over 12weeks
dx for otitis media
otoscopic exam
tm looks
red
bulging toward u
dull color
can't see land marks
can't see cone of light
not mobile (yawn)
treatment for otitis media
antibiotics
myringotomy/tmpanostomey tubes
keep child out of water

tubes to drain serous
complications of otitis media

Their uncommon
conductive hearing loss (rupture)
perforated ear drum
meningitis
cataracts
cloudy of lens of eye
congenital - materanal exposure
traumatic - foreigh body, heat tradiation exposure
senile - old fibers become compressed & dehydrated & ineral concentrate in lens
metabolic - drug side effects, diabetes
s/s of cataracts
gradual decrease in visual acuity
need more light
visual blurry
severe pupil appears white
treatment for cataracts
surgery
open angle glaucoma (mystery)
wide open canal schlem
unknown cause
drainage not occluded
pressure is just high
more common than closed angle
starts about age 40
dx for open angle glaucoma
push of air (tonometry)
IOP should be less than 20mm Hg
treatment for open angle glaucoma
antiglaucoma drugs that decrease producion of aqueous humor and increase outflow
constrict pupil
glaucoma
increased intraocular pressure
enough to cause degeneration of the optic nerve
vision loss
normal IOP
12-20 mm Hg
closed angle glaucoma (narrow angle)
inherited narrow anterior chamber of eye from forward placement of iris
leads to decrease outflow through the canal of schlem because lack of space
occurs suddenly due to dilation of the eye (darkenss to lightness) FFF leads to bunching of iris
s/s of closed angle glaucoma
ocular pain
blurred vision
halos around things
red eye
severe headache
treatment for closed angle glaucoma
laser surger