Neurology class 1 Flashcards
1
Q
brain contribution to body weight
A
2%
2
Q
organ that receives 15% cardiac output
A
the brain
3
Q
organ that consumes 20% of the body’s oxygen
A
the brain
4
Q
what the brain requires but cannot store
A
oxygen, nutrition (glucose), does not contain centrioles for tissue recovery
5
Q
how long the brain can survive without oxygen
A
10 seconds
6
Q
brain cell death in what amount of time
A
4-6 minutes
7
Q
neuroplasticity
A
ability of the CNS to compensate for an activity or action that has been lost
8
Q
norepinephrine, epinephrine, glutamate, dopamine, substance P, Ach
A
excitatory neurotransmitters
9
Q
GABA, serotonin
A
inhibitory neurotransmitters
10
Q
what determines consciousness
A
depends on cerebral cortex function and RAS
11
Q
RAS
A
dictates wakefulness and activates higher centers of cerebral cortex
12
Q
low RAS activity
A
low awareness or wakefulness
13
Q
pathology of low RAS due to decreased perfusion
A
decreased perfusion–> altered metabolic state–> altered consciousness
14
Q
pathology of low RAS due to decreased oxygenation
A
decreased oxygenation–> decreased function of brainstem respiratory center–> decreased sensitivity to increased CO2–> irregular respirations
15
Q
key sign of increased CO2
A
agitation
16
Q
GCS
A
out of 15- eye opening, verbal response, motor response
17
Q
eye opening for GCS
A
out of 4
4. spontaneously
3. to speech
2. to pain
1. no response
18
Q
verbal response for GCS
A
out of 5
5. oriented to person, place, time
4. confused
3. inappropriate words
2. inappropriate sounds
1. no response
19
Q
motor response for GCS
A
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
20
Q
pathology of brain injury
A
CVA (stroke), infection, tumor, trauma
21
Q
sequelae of brain injury
A
ischemia (low 02 in tissues), cerebral edema, metabolic acidosis, increased ICP
22
Q
no motor response or brainstem reflexes, apnea
A
brain death
23
Q
gray and white matter damage, maintenance of brainstem reflexes, no awareness of self or surroundings
A
vegetative state
24
Q
dolls eye reflex
A
if normal, when patient rolled onto their side, the eyes will go in opposite direction
25
deficient delivery of oxygen to the tissues
- will cause agitation, decreased LOC, seizures
hypoxia
26
lack of 02 within a tissue
- focal or global
ischemia
27
no nutrient/02 delivery--> depletion of resources--> brain injury
- will cause cerebral edema and electrolyte imbalances
global ischemia (no CO)
28
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
29
heightened focal damage to lowered-flow regions
watershed infarcts
30
injury related to belated reperfusion caused by inflammatory mediators/toxic byproducts/catecholamines/nitric oxide
reperfusion injury
31
blood flow to brain every minute
0.9ml or 3 cups
32
pressure gradient between internal carotid artery and subarachnoid veins and this pressure is required to perfuse oxygen to the brain
- minimum is 45
CPP
33
CPP calculation
MAP-ICP
- 70-5 to 15= normal is 55-65
34
cranial cavity components
brain tissue- 80%
blood- 10%
CSF- 10%
35
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
36
ICP
0-15
37
increase in ICP will cause
obstruction of fluid flow and injures brain cells
38
S&S of increased ICP
cushing's triad
39
cushing's triad
hypertension, bradycardia, irregular respirations
40
cerebral edema causes risk of
increased ICP
41
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
42
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
43
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)
44
'angina' of the brain
- momentary lapse of perfusion
- transient episodes
TIA (transient ischemic attacks)
45
CVA deficits
MCA is most commonly affected artery which deals with the upper limbs and face
- cerebral edema and increased ICP
46
CVA symptoms
occur on opposite side of the brain
47
TIA treatment
anticoagulants, antiplatelets
48
anticoagulants and antiplatelets for TIA treatment
apixaban;dabigatran, ASA (baby aspirin) (81mg)
49
apixaban;dabigatran
anticoagulants
50
ASA (81mg) "baby aspirin"
antiplatelet
51
ischemic CVA treatment
thrombolytics less than 3 hours since onset, thrombectomy less than 24 hours since onset
52
associated ischemic CVA treatment
carotid endarterectomy or angioplasty
- abciximab (antiplatelet)
53
dysarthia
weak muscle control (slurred speech)
54
aphasia
impairment of language and speaking
- includes speaking (expressive aphasia) and comprehension (receptive aphasia)
55
apraxia
moving muscles needed in correct order
- deals with posterior partial cortex
56
agnosia
inability to recognize and identify objects or people
57
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
58
1st S&S of hemorrhagic stroke
headache, vomiting, sudden onset, high BP,
59
ER treatment of hemorrhagic stroke
reverse anticoagulation, osmotic diuretic, hypertonic NS (3% NaCl)
60
osmotic diuretic for hemorrhagic stroke
mannitol
61
hypertonic NS for hemorrhagic stroke
3% NaCl
62
congenital defect in structural formation of cerebral vessels
- bundle of arteries and veins lacking capillary network and normal wall structure
AVM (arteriovenous malformation)
63
AVM pathophysiology
high pressure arterial flow rapidly enters venous vessels due to lack of capillaries and the vessels are thinner than expected--> rupture (hemorrhage)
64
AVM S&S
steals blood flow from surrounding areas leading to..
- ischemia --> slow onset neuro deficits, headaches, seizures
65
AVM treatment
gamma knife radiation, embolization, surgical excision
66
a bulge in a vessel wall
aneurysm
67
caused by an aneurysm rupture in the circle of willis in the cerebral area
subarachnoid hemorrhage
68
aneurysm
cerebral, aortic, abdominal, thoracic
69
risk factors for an aneurysm
atherosclerosis, htn, malformed vessels (congenitally thin tunica intima or media)
70
aneurysm S&S
will relate to area or location
71
clipping, coiling, flow diversion
treatment of unruptured aneurysm
72
aortic aneurysm
age is major factor due to elastin not being synthesized
- bruits are a sign
73
aortic aneurysm treatment
stent to support artery
fluids- LR, NS
surgery
blood products
74
ongoing bleeding within the cerebral lobes due to ruptured aneurysm, ruptured AVM, hemorrhagic CVA, or head injury
- associated with comorbidities
intracerebral hemorrhage
75
bleed located between dura and skull that is commonly caused by a skull fracture
epidural hematoma
76
bleed located between dura and subdural space often caused by venous tearing
- most common hematoma
subdural hematoma
77
acute hematoma
sudden onset with high morbidity and mortality due to high ICP
78
subacute hematoma
slow onset with high morbidity and mortality due to high ICP
79
chronic hematoma
very slow onset and occurs due to brain atrophy causing shrinking and tearing of the veins
80
hematoma sequelae
increased ICP--> coma--> necrosis
81
hematoma treatment
decrease ICP and evacuate bleed through osmotic diuretic (mannitol) and antihypertensives
82
encephalitis
infection that affects brain parenchyma
- neurons and glial cells
83
myelitis
infection that affects spinal cord
84
encephalomyelitis
infection affecting the brain and spinal cord
85
inflammation of pia mater, arachnoid, and subarachnoid (CSF) space and is spread throughout the brain due to infected CSF
meningitis
86
2 main types of meningitis
bacterial (purulent) and viral (lymphocytic)
87
streptococcus pneumoniae, haemophilus influenzae, neisseria meningitidis, listeria monocytogenes, group B streptococcus
common pathogens of meningitis
88
meningitis highest mortality pathogen
strep.pneumoniae
- 34%
89
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
90
brudzinski sign
S&S of meningitis
- flexion of neck, hip, and knee
91
petechial rash
sign of sepsis in meningitis
92
meningitis treatment
- either 3rd gen cephalosporins, penicillins, vancomycin
- and glucocorticosteroids (dexamethasone)
93
neoplasms (abnormal cellular proliferation) which metastasize
brain tumor
94
primary tumors
originate in the CNS and cause 2% of all cancer deaths
95
metastatic tumors
originate in other tissues
- 40% of brain tumors have metastatic origin
96
S&S of brain tumors
focal disturbances, global CNS effects in increased volume causes a sequelae
97
tumor treatment
surgery, radiation, chemotherapy with use of alkylating agents
98
alkylating agents
cause DNA damage
- temozolomide
99
temozolomide
alkylating agent
- side effects include quick replicating eukaryotic cells leading to hair loss, GI upset, bone marrow suppression, and low blood cell counts
100
treatment overview of brain injuries
treat the cause of event
treat the high ICP/cerebral edema
101
spontaneous, abnormal synchronous electrical discharges from neurons in the cerebral cortex
seizures
102
idiopathic seizures
genetic origin with no known acquired cause, otherwise known as epilepsy
- treat with long term anti-epileptic medications
103
symptomatic seizures
due to brain injury resulting in altered action potential/neurotransmitter balance/ electrolyte balance
- treat with short term antiepileptic medications
104
focal seizures
deal with a specific group of neurons in one hemisphere
105
generalized seizures
deal with both hemispheres involved
- absence seizures and tonic seizures
106
seizure treatment
benzodiazepines, barbiturates, anticonvulsants
107
benzodiazepines
CNS depressant drug category
- chloride channel agonist
- will cause respiratory depression, drug interactions and are addictive
108
Clonazepam (Rivotril), Diazepam (Valium) (highly used; IV), Lorazepam (Ativan) (SL)
benzodiazepines
109
receptor antagonist Flumazenil (Romazicon)
benzodiazepine OD treatment
110
Flunitrazepam (rohypnol)
'roofie'
- onset in 15 min
- lasts 4-6 hours
111
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
112
Phenobarbital (Phenobarb), Pentobarbital, Secobarbital
barbiturates
113
activated charcoal; sodium bicarbonate
barbiturate OD treatment
114
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
115
Phenytoin (dilantin) (narrow TI), Carbamazepine (tegretol), Valproic acid (Valproate)
anticonvulsants
116
barbiturates and benzodiasepines
used in assisted death
