multi d final Flashcards
TIA (transient ischemic attack)
less than 24 hours
strong indicator of pending CVA (15% in 90 days)
how to manage TIA
observation
treatment of risk factors
anticoagulation
carotid endarterectomy
CVA
4th leading cause of death in US
sudden onset of neuro deficits within 24 hours
risk factors of CVA
older age
african american or hispanic
male
HTN
CAD
hyperlipidemia
elevated LDL levels
hyper-coagulable state
DMII
obesity
tobacco use
alcohol abuse
sedentary lifestyle
prevalence of strokes
12% of deaths globally
lifetime stroke risk is 25% for those >25 years of age
hemorrhagic stroke
blood leaks into brain tissue
ischemic stroke
clot stops blood supply to an area of brain
present with predetermined syndromes
can predict what vasculature will be affected
ICH (intracerebral hemorrhage)
10-15% of all strokes
from rupture of cerebral vessels
result of high BP
primary symptoms of ICH
spontaneous rupture of small vessels damaged by chronic hypertension
secondary symptoms of ICH
bleeding of cerebrovascular abnormalities, tumors, or impaired coagulation
ICH outcomes
associated with higher risk of fatality
damages brain cells
may increase pressure on brain or spasms in vessels
death prevalence in ICH
nearly half of all pts with primary ICH die within the first month after the acute event
lacunar stroke
25% of ischemic strokes
creates deep cavities in brain tissue
occlusion of vessels from the circle of willis
middle cerebral artery infarction presentation
contralateral hemiparesis
facial paralysis
sensory loss in face and UE
general info about MCAI
90% of all strokes
largest of the brain’s arteries
supplies most of outer frontal, parietal and temporal lobes
MCA syndrome
presents with neglect and poor motivation
MCA syndrome - Gerstmann syndrome
L/R disorientation
acalculia
agraphia
finger agnosia
anterior cerebral artery infarction
involves medial cerebral cortex
compromises motor and sensory of LE
ACAI left sided lesions
transcortical motor aphasia
ACAI right sided lesions
confusional state and motor hemineglect
superficial posterior cerebral artery infarction
visual and somatosensory deficits
larger PCAI
hemisensory loss
hemiparesis due to involvement of thalamus
where does the PCA supply?
occipital lobe
inferior temporal lobe
thalamus
vertebrobasilar infarction (VBI) presentation
ataxia
vertigo
headache
vomiting
oropharyngeal dysfunction
visual-field deficits
abnormal oculomotor findings
VBI - mid basilar artery
locked in syndrome
ipsilateral CN7 palsy
decreases level of consciousness
hemiparesis and hemitaxia
oculomotor deficits
arm posturing
VBI - intracranial vertebral artery
wallenburg syndrome
dizziness
diploplia
VBI - distal basilar artery
comatose state
defective vertical gaze
hemiparesis and hemitaxia
diplolia
speech difficulties
altered mental state
small, poorly reactive pupils
weakness
ataxia
VBI - origin of extracranial vertebral artery
dizziness
blurred vision
ataxia
vomiting
cerebellar infarction
loss of coordination
ataxia
nausea
vomiting
headache
dysarthria
vertigo
BEFAST stroke signs
balance
eyes
face
arms
speech
time
beyond BEFAST
numbness
sudden confusion
trouble seeing
trouble walking
severe headache
ischemic CVA management
cerebral hypo-perfusion
BP control
treatment of risk factors
prognosis of ICVA
85% of all stroke types
13-23% mortality in 30 days
tissue plasminogen activator
strongly recommended within 4-5 hours of stroke symptoms
NOT for hemmoragic stroke
what scan is the earlier indicator for stroke?
MRI
prognosis of hemorrhagic CVA
poor compared it ICVA
30 day mortality rate - 35-50%
PT’s role in strokes
history
vitals are important
other tests and measures
dx, prog, POC
EDUCATION of pt and family
national institutes of health stroke scale (NIHSS)
valid for size and severity
0 = no deficits
42 = worst deficits
must be trained
NIHSS outcomes
very severe - >25
severe - 15-24
mild to moderate - 5-14
mild 1-5
correlation of NIHSS score to discharge disposition
<5: 80% discharged to home
6-13: typically require ARF
>14: frequently require LT skilled care
describe damage to cerebellum
motor dysfunction
postural control
equilibrium
coordination
common deficits of cerebellar damage
dysdiadochokinesia
slurred speech
ataxia
unsteady gait
nystagmus
conditions responsible for cerebellar damage
CVA
head trauma
alcoholism
tumors
toxins
MS
anything that causes oxygen deprivation
UE coordination tests
RAM tests for dysdiadochokinesia
finger opposition
finger to nose
finger to clinician finger and back to nose
LE coordination tests
heel to shin
toe to clinician finger
RAM
balance observations
level of assistance required
# times balance lost
ability to maintain midline
duration of stance
use of support
direction of deviation of movement
presence of postural controls strategies
how does normal cognition help balance?
paying attention to surroundings
making correct decisions about situations
remembering dangerous situations
skin layers
epidermis
dermis
subcutaneous
integ function
temp regulation
protection
sensation
excretion
immunity
blood reservoir
vitamin D synthesis
cardiovascular conditions that affect integ
vascular insufficiency
lymphedema
pulmonary conditions that affect integ
pulmonary edema
CF
msk conditions that affect integ
osteomyelitis
open fracture
neuromuscular conditions that affect integ
SCI
CVA
MS
loss of sensation
endocrine conditions that affect integ
diabetes
liver disease
general observation of integ
color
condition
temp
scars
hair loss
lesions
common disorders of integ
dermatitis
trauma
infection
skin cancer
ulcers
burns
most common type of skin cancer
basal cell carcinoma
deadliest skin cancer
melanoma
ABCDE rule
asymmetry
borders
color variants
diameter
elevation
benign lesions
< 6 mm
uniform color
distinct borders
symmetric
seldom bleed or ulcerate
soft to firm
slow rate of growth or change
malignant lesions
> 6 mm
multiple shades
irregular, blurred borders
asymmetric
often bleed or ulcerate
firm to hard
variable rate of growth
burns
thermal
electrical
chemical
superficial burns
epidermis only
no blisters
red
painful
superficial partial thickness burns
epi and superficial dermis
blisters
red
painful
deep partial thickness burns
majority of dermis
hair follicles/sweat glands intact
full thickness burns
subcutaneous fat layer
minimal pain
susceptible infection
increased depth = decreasing pain
subdermal burns
muscle, bone, adipose tissue
insensate
arterial insufficiency wounds
intermittent claudication
pain with activity
decreased temp and pedal pulses
venous insufficiency wounds
localized limb pain
pedal pulses present
increase skin temp
edema
peripheral neuropathy
nerve damage
diminished sensation
cannot sense trauma
neuropathic ulcers
PVD, peripheral neuropathy, infection
painless
absent pedal pulses if atherosclerosis
deep wound bed at pressure points
loss of sensation
decubitus (pressure ulcers)
tissue ischemia
stage 1 wound
intact, reddened skin that does not blanch
stage 2 wound
shallow open ulcer with red/pink wound bed, denoting partial-thickness loss of dermis, without slough. Can present as open or ruptured blister
stage 3 wound
subcutaneous fat may be visible but no bone, muscle or tendon exposed. May include tunneling or undermining
stage 4 wound
muscle/tendon/bone exposure. Tunneling/undermining, eschar/slough over at least part of wound bed
what to include in assessment for wounds
ROM
sensation
strength
functional mobility
NM coordination
balance
equipment used
PT intervention in wound care
wound treatment/protection
strength/ROM/mobility training
