Neurology class 1 Flashcards
brain contribution to body weight
2%
organ that receives 15% cardiac output
the brain
organ that consumes 20% of the body’s oxygen
the brain
what the brain requires but cannot store
oxygen, nutrition (glucose), does not contain centrioles for tissue recovery
how long the brain can survive without oxygen
10 seconds
brain cell death in what amount of time
4-6 minutes
neuroplasticity
ability of the CNS to compensate for an activity or action that has been lost
norepinephrine, epinephrine, glutamate, dopamine, substance P, Ach
excitatory neurotransmitters
GABA, serotonin
inhibitory neurotransmitters
what determines consciousness
depends on cerebral cortex function and RAS
RAS
dictates wakefulness and activates higher centers of cerebral cortex
low RAS activity
low awareness or wakefulness
pathology of low RAS due to decreased perfusion
decreased perfusion–> altered metabolic state–> altered consciousness
pathology of low RAS due to decreased oxygenation
decreased oxygenation–> decreased function of brainstem respiratory center–> decreased sensitivity to increased CO2–> irregular respirations
key sign of increased CO2
agitation
GCS
out of 15- eye opening, verbal response, motor response
eye opening for GCS
out of 4
4. spontaneously
3. to speech
2. to pain
1. no response
verbal response for GCS
out of 5
5. oriented to person, place, time
4. confused
3. inappropriate words
2. inappropriate sounds
1. no response
motor response for GCS
out of 6
6. obeys command
5. moves to localized pain
4. flexs to withdraw pain
3. abnormal flexion
2. abnormal extension
1. no response
pathology of brain injury
CVA (stroke), infection, tumor, trauma
sequelae of brain injury
ischemia (low 02 in tissues), cerebral edema, metabolic acidosis, increased ICP
no motor response or brainstem reflexes, apnea
brain death
gray and white matter damage, maintenance of brainstem reflexes, no awareness of self or surroundings
vegetative state
dolls eye reflex
if normal, when patient rolled onto their side, the eyes will go in opposite direction
deficient delivery of oxygen to the tissues
- will cause agitation, decreased LOC, seizures
hypoxia
lack of 02 within a tissue
- focal or global
ischemia
no nutrient/02 delivery–> depletion of resources–> brain injury
- will cause cerebral edema and electrolyte imbalances
global ischemia (no CO)
excess intracellular calcium–> calcium cascade–> protein breakdown–> DNA injury–> free radical formation–> mitochondrial injury–> cell death
- all of this causes accumulation or depletion of neurotransmitters
electrolyte imbalance sequelae
heightened focal damage to lowered-flow regions
watershed infarcts
injury related to belated reperfusion caused by inflammatory mediators/toxic byproducts/catecholamines/nitric oxide
reperfusion injury
blood flow to brain every minute
0.9ml or 3 cups
pressure gradient between internal carotid artery and subarachnoid veins and this pressure is required to perfuse oxygen to the brain
- minimum is 45
CPP
CPP calculation
MAP-ICP
- 70-5 to 15= normal is 55-65
cranial cavity components
brain tissue- 80%
blood- 10%
CSF- 10%
brain tissue, blood, and CSF are dependant on each other and a depletion or increase in one will cause displacement of the other
- reduction of venous blood flow/reduction in CSF content
Monro-kellie hypothesis
ICP
0-15
increase in ICP will cause
obstruction of fluid flow and injures brain cells
S&S of increased ICP
cushing’s triad
cushing’s triad
hypertension, bradycardia, irregular respirations
cerebral edema causes risk of
increased ICP
type of cerebral edema
- BBB compromised: head injury, hematoma, hemorrhage, CNS infection
- all of this will cause inflammation leading to increased permeability which leads to high ICP
vasogenic cerebral edema
type of cerebral edema
- increased intracellular fluid shift: electrolyte imbalance, ischemia leading to electrolyte imbalance
- all of this will cause an increased H20 shift into cells which will cause high ICP
cytotoxic cerebral edema
are 80% of all strokes
- hypoxia–> ischemia–> injury to affected areas
- risk factors include: htn, dyslipidemia, stenosis, diabetes, atrial fib due to embolus
ischemic stroke (CVA) (thrombus/embolus)
‘angina’ of the brain
- momentary lapse of perfusion
- transient episodes
TIA (transient ischemic attacks)
CVA deficits
MCA is most commonly affected artery which deals with the upper limbs and face
- cerebral edema and increased ICP
CVA symptoms
occur on opposite side of the brain
TIA treatment
anticoagulants, antiplatelets
anticoagulants and antiplatelets for TIA treatment
apixaban;dabigatran, ASA (baby aspirin) (81mg)
apixaban;dabigatran
anticoagulants
ASA (81mg) “baby aspirin”
antiplatelet
ischemic CVA treatment
thrombolytics less than 3 hours since onset, thrombectomy less than 24 hours since onset
associated ischemic CVA treatment
carotid endarterectomy or angioplasty
- abciximab (antiplatelet)
dysarthia
weak muscle control (slurred speech)
aphasia
impairment of language and speaking
- includes speaking (expressive aphasia) and comprehension (receptive aphasia)
apraxia
moving muscles needed in correct order
- deals with posterior partial cortex
agnosia
inability to recognize and identify objects or people
tell tale sign is if pool of blood on CT
- less common stroke
- risk factors include: htn, arterial deficits (arteriovenous malformation, aneurysm), bleeding disorders
hemorrhagic stroke
1st S&S of hemorrhagic stroke
headache, vomiting, sudden onset, high BP,
ER treatment of hemorrhagic stroke
reverse anticoagulation, osmotic diuretic, hypertonic NS (3% NaCl)
osmotic diuretic for hemorrhagic stroke
mannitol
hypertonic NS for hemorrhagic stroke
3% NaCl
congenital defect in structural formation of cerebral vessels
- bundle of arteries and veins lacking capillary network and normal wall structure
AVM (arteriovenous malformation)
AVM pathophysiology
high pressure arterial flow rapidly enters venous vessels due to lack of capillaries and the vessels are thinner than expected–> rupture (hemorrhage)
AVM S&S
steals blood flow from surrounding areas leading to..
- ischemia –> slow onset neuro deficits, headaches, seizures
AVM treatment
gamma knife radiation, embolization, surgical excision
a bulge in a vessel wall
aneurysm
caused by an aneurysm rupture in the circle of willis in the cerebral area
subarachnoid hemorrhage
aneurysm
cerebral, aortic, abdominal, thoracic
risk factors for an aneurysm
atherosclerosis, htn, malformed vessels (congenitally thin tunica intima or media)
aneurysm S&S
will relate to area or location
clipping, coiling, flow diversion
treatment of unruptured aneurysm
aortic aneurysm
age is major factor due to elastin not being synthesized
- bruits are a sign
aortic aneurysm treatment
stent to support artery
fluids- LR, NS
surgery
blood products
ongoing bleeding within the cerebral lobes due to ruptured aneurysm, ruptured AVM, hemorrhagic CVA, or head injury
- associated with comorbidities
intracerebral hemorrhage
bleed located between dura and skull that is commonly caused by a skull fracture
epidural hematoma
bleed located between dura and subdural space often caused by venous tearing
- most common hematoma
subdural hematoma
acute hematoma
sudden onset with high morbidity and mortality due to high ICP
subacute hematoma
slow onset with high morbidity and mortality due to high ICP
chronic hematoma
very slow onset and occurs due to brain atrophy causing shrinking and tearing of the veins
hematoma sequelae
increased ICP–> coma–> necrosis
hematoma treatment
decrease ICP and evacuate bleed through osmotic diuretic (mannitol) and antihypertensives
encephalitis
infection that affects brain parenchyma
- neurons and glial cells
myelitis
infection that affects spinal cord
encephalomyelitis
infection affecting the brain and spinal cord
inflammation of pia mater, arachnoid, and subarachnoid (CSF) space and is spread throughout the brain due to infected CSF
meningitis
2 main types of meningitis
bacterial (purulent) and viral (lymphocytic)
streptococcus pneumoniae, haemophilus influenzae, neisseria meningitidis, listeria monocytogenes, group B streptococcus
common pathogens of meningitis
meningitis highest mortality pathogen
strep.pneumoniae
- 34%
severe inflammation–> BBB compromised–> inflammation causes capillary leaking, cerebral edema, vascular congestion and cell death–> meningeal thickening–> meningeal adhesions–> vascular congestion and decreased CSF outflow (hydrocephalus)
meningitis pathology sequelae
brudzinski sign
S&S of meningitis
- flexion of neck, hip, and knee
petechial rash
sign of sepsis in meningitis
meningitis treatment
- either 3rd gen cephalosporins, penicillins, vancomycin
- and glucocorticosteroids (dexamethasone)
neoplasms (abnormal cellular proliferation) which metastasize
brain tumor
primary tumors
originate in the CNS and cause 2% of all cancer deaths
metastatic tumors
originate in other tissues
- 40% of brain tumors have metastatic origin
S&S of brain tumors
focal disturbances, global CNS effects in increased volume causes a sequelae
tumor treatment
surgery, radiation, chemotherapy with use of alkylating agents
alkylating agents
cause DNA damage
- temozolomide
temozolomide
alkylating agent
- side effects include quick replicating eukaryotic cells leading to hair loss, GI upset, bone marrow suppression, and low blood cell counts
treatment overview of brain injuries
treat the cause of event
treat the high ICP/cerebral edema
spontaneous, abnormal synchronous electrical discharges from neurons in the cerebral cortex
seizures
idiopathic seizures
genetic origin with no known acquired cause, otherwise known as epilepsy
- treat with long term anti-epileptic medications
symptomatic seizures
due to brain injury resulting in altered action potential/neurotransmitter balance/ electrolyte balance
- treat with short term antiepileptic medications
focal seizures
deal with a specific group of neurons in one hemisphere
generalized seizures
deal with both hemispheres involved
- absence seizures and tonic seizures
seizure treatment
benzodiazepines, barbiturates, anticonvulsants
benzodiazepines
CNS depressant drug category
- chloride channel agonist
- will cause respiratory depression, drug interactions and are addictive
Clonazepam (Rivotril), Diazepam (Valium) (highly used; IV), Lorazepam (Ativan) (SL)
benzodiazepines
receptor antagonist Flumazenil (Romazicon)
benzodiazepine OD treatment
Flunitrazepam (rohypnol)
‘roofie’
- onset in 15 min
- lasts 4-6 hours
barbiturates
CNS depressant; chloride channel agonist
- highly addictive with high degree of tolerance leading to receptor desentization
- side effects include respiratory depression, drug interactions, narrow TI
Phenobarbital (Phenobarb), Pentobarbital, Secobarbital
barbiturates
activated charcoal; sodium bicarbonate
barbiturate OD treatment
Anticonvulsants
alter electrolyte movement and delay action potential and decrease neuronal activity; decrease sodium cellular influx
- side effects include arrhythmias, drug interactions, bleeding due to vitamin K interference and toxicity
Phenytoin (dilantin) (narrow TI), Carbamazepine (tegretol), Valproic acid (Valproate)
anticonvulsants
barbiturates and benzodiasepines
used in assisted death
