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Nurs 216B > Neurology class 1 > Flashcards

Neurology class 1 Flashcards

1
Q

brain contribution to body weight

A

2%

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2
Q

organ that receives 15% cardiac output

A

the brain

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3
Q

organ that consumes 20% of the body’s oxygen

A

the brain

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4
Q

what the brain requires but cannot store

A

oxygen, nutrition (glucose), does not contain centrioles for tissue recovery

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5
Q

how long the brain can survive without oxygen

A

10 seconds

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6
Q

brain cell death in what amount of time

A

4-6 minutes

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7
Q

neuroplasticity

A

ability of the CNS to compensate for an activity or action that has been lost

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8
Q

norepinephrine, epinephrine, glutamate, dopamine, substance P, Ach

A

excitatory neurotransmitters

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9
Q

GABA, serotonin

A

inhibitory neurotransmitters

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10
Q

what determines consciousness

A

depends on cerebral cortex function and RAS

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11
Q

RAS

A

dictates wakefulness and activates higher centers of cerebral cortex

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12
Q

low RAS activity

A

low awareness or wakefulness

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13
Q

pathology of low RAS due to decreased perfusion

A

decreased perfusion–> altered metabolic state–> altered consciousness

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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

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15
Q

key sign of increased CO2

A

agitation

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16
Q

GCS

A

out of 15- eye opening, verbal response, motor response

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17
Q

eye opening for GCS

A

out of 4
4. spontaneously
3. to speech
2. to pain
1. no response

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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

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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

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20
Q

pathology of brain injury

A

CVA (stroke), infection, tumor, trauma

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21
Q

sequelae of brain injury

A

ischemia (low 02 in tissues), cerebral edema, metabolic acidosis, increased ICP

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22
Q

no motor response or brainstem reflexes, apnea

A

brain death

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23
Q

gray and white matter damage, maintenance of brainstem reflexes, no awareness of self or surroundings

A

vegetative state

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24
Q

dolls eye reflex

A

if normal, when patient rolled onto their side, the eyes will go in opposite direction

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25
Q

deficient delivery of oxygen to the tissues
- will cause agitation, decreased LOC, seizures

A

hypoxia

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26
Q

lack of 02 within a tissue
- focal or global

A

ischemia

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27
Q

no nutrient/02 delivery–> depletion of resources–> brain injury
- will cause cerebral edema and electrolyte imbalances

A

global ischemia (no CO)

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28
Q

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

A

electrolyte imbalance sequelae

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29
Q

heightened focal damage to lowered-flow regions

A

watershed infarcts

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30
Q

injury related to belated reperfusion caused by inflammatory mediators/toxic byproducts/catecholamines/nitric oxide

A

reperfusion injury

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31
Q

blood flow to brain every minute

A

0.9ml or 3 cups

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32
Q

pressure gradient between internal carotid artery and subarachnoid veins and this pressure is required to perfuse oxygen to the brain
- minimum is 45

A

CPP

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33
Q

CPP calculation

A

MAP-ICP
- 70-5 to 15= normal is 55-65

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34
Q

cranial cavity components

A

brain tissue- 80%
blood- 10%
CSF- 10%

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35
Q

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

A

Monro-kellie hypothesis

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36
Q

ICP

A

0-15

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37
Q

increase in ICP will cause

A

obstruction of fluid flow and injures brain cells

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38
Q

S&S of increased ICP

A

cushing’s triad

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39
Q

cushing’s triad

A

hypertension, bradycardia, irregular respirations

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40
Q

cerebral edema causes risk of

A

increased ICP

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41
Q

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

A

vasogenic cerebral edema

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42
Q

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

A

cytotoxic cerebral edema

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43
Q

are 80% of all strokes
- hypoxia–> ischemia–> injury to affected areas
- risk factors include: htn, dyslipidemia, stenosis, diabetes, atrial fib due to embolus

A

ischemic stroke (CVA) (thrombus/embolus)

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44
Q

‘angina’ of the brain
- momentary lapse of perfusion
- transient episodes

A

TIA (transient ischemic attacks)

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45
Q

CVA deficits

A

MCA is most commonly affected artery which deals with the upper limbs and face
- cerebral edema and increased ICP

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46
Q

CVA symptoms

A

occur on opposite side of the brain

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47
Q

TIA treatment

A

anticoagulants, antiplatelets

48
Q

anticoagulants and antiplatelets for TIA treatment

A

apixaban;dabigatran, ASA (baby aspirin) (81mg)

49
Q

apixaban;dabigatran

A

anticoagulants

50
Q

ASA (81mg) “baby aspirin”

A

antiplatelet

51
Q

ischemic CVA treatment

A

thrombolytics less than 3 hours since onset, thrombectomy less than 24 hours since onset

52
Q

associated ischemic CVA treatment

A

carotid endarterectomy or angioplasty
- abciximab (antiplatelet)

53
Q

dysarthia

A

weak muscle control (slurred speech)

54
Q

aphasia

A

impairment of language and speaking
- includes speaking (expressive aphasia) and comprehension (receptive aphasia)

55
Q

apraxia

A

moving muscles needed in correct order
- deals with posterior partial cortex

56
Q

agnosia

A

inability to recognize and identify objects or people

57
Q

tell tale sign is if pool of blood on CT
- less common stroke
- risk factors include: htn, arterial deficits (arteriovenous malformation, aneurysm), bleeding disorders

A

hemorrhagic stroke

58
Q

1st S&S of hemorrhagic stroke

A

headache, vomiting, sudden onset, high BP,

59
Q

ER treatment of hemorrhagic stroke

A

reverse anticoagulation, osmotic diuretic, hypertonic NS (3% NaCl)

60
Q

osmotic diuretic for hemorrhagic stroke

A

mannitol

61
Q

hypertonic NS for hemorrhagic stroke

A

3% NaCl

62
Q

congenital defect in structural formation of cerebral vessels
- bundle of arteries and veins lacking capillary network and normal wall structure

A

AVM (arteriovenous malformation)

63
Q

AVM pathophysiology

A

high pressure arterial flow rapidly enters venous vessels due to lack of capillaries and the vessels are thinner than expected–> rupture (hemorrhage)

64
Q

AVM S&S

A

steals blood flow from surrounding areas leading to..
- ischemia –> slow onset neuro deficits, headaches, seizures

65
Q

AVM treatment

A

gamma knife radiation, embolization, surgical excision

66
Q

a bulge in a vessel wall

A

aneurysm

67
Q

caused by an aneurysm rupture in the circle of willis in the cerebral area

A

subarachnoid hemorrhage

68
Q

aneurysm

A

cerebral, aortic, abdominal, thoracic

69
Q

risk factors for an aneurysm

A

atherosclerosis, htn, malformed vessels (congenitally thin tunica intima or media)

70
Q

aneurysm S&S

A

will relate to area or location

71
Q

clipping, coiling, flow diversion

A

treatment of unruptured aneurysm

72
Q

aortic aneurysm

A

age is major factor due to elastin not being synthesized
- bruits are a sign

73
Q

aortic aneurysm treatment

A

stent to support artery
fluids- LR, NS
surgery
blood products

74
Q

ongoing bleeding within the cerebral lobes due to ruptured aneurysm, ruptured AVM, hemorrhagic CVA, or head injury
- associated with comorbidities

A

intracerebral hemorrhage

75
Q

bleed located between dura and skull that is commonly caused by a skull fracture

A

epidural hematoma

76
Q

bleed located between dura and subdural space often caused by venous tearing
- most common hematoma

A

subdural hematoma

77
Q

acute hematoma

A

sudden onset with high morbidity and mortality due to high ICP

78
Q

subacute hematoma

A

slow onset with high morbidity and mortality due to high ICP

79
Q

chronic hematoma

A

very slow onset and occurs due to brain atrophy causing shrinking and tearing of the veins

80
Q

hematoma sequelae

A

increased ICP–> coma–> necrosis

81
Q

hematoma treatment

A

decrease ICP and evacuate bleed through osmotic diuretic (mannitol) and antihypertensives

82
Q

encephalitis

A

infection that affects brain parenchyma
- neurons and glial cells

83
Q

myelitis

A

infection that affects spinal cord

84
Q

encephalomyelitis

A

infection affecting the brain and spinal cord

85
Q

inflammation of pia mater, arachnoid, and subarachnoid (CSF) space and is spread throughout the brain due to infected CSF

A

meningitis

86
Q

2 main types of meningitis

A

bacterial (purulent) and viral (lymphocytic)

87
Q

streptococcus pneumoniae, haemophilus influenzae, neisseria meningitidis, listeria monocytogenes, group B streptococcus

A

common pathogens of meningitis

88
Q

meningitis highest mortality pathogen

A

strep.pneumoniae
- 34%

89
Q

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)

A

meningitis pathology sequelae

90
Q

brudzinski sign

A

S&S of meningitis
- flexion of neck, hip, and knee

91
Q

petechial rash

A

sign of sepsis in meningitis

92
Q

meningitis treatment

A
  • either 3rd gen cephalosporins, penicillins, vancomycin
  • and glucocorticosteroids (dexamethasone)
93
Q

neoplasms (abnormal cellular proliferation) which metastasize

A

brain tumor

94
Q

primary tumors

A

originate in the CNS and cause 2% of all cancer deaths

95
Q

metastatic tumors

A

originate in other tissues
- 40% of brain tumors have metastatic origin

96
Q

S&S of brain tumors

A

focal disturbances, global CNS effects in increased volume causes a sequelae

97
Q

tumor treatment

A

surgery, radiation, chemotherapy with use of alkylating agents

98
Q

alkylating agents

A

cause DNA damage
- temozolomide

99
Q

temozolomide

A

alkylating agent
- side effects include quick replicating eukaryotic cells leading to hair loss, GI upset, bone marrow suppression, and low blood cell counts

100
Q

treatment overview of brain injuries

A

treat the cause of event
treat the high ICP/cerebral edema

101
Q

spontaneous, abnormal synchronous electrical discharges from neurons in the cerebral cortex

A

seizures

102
Q

idiopathic seizures

A

genetic origin with no known acquired cause, otherwise known as epilepsy
- treat with long term anti-epileptic medications

103
Q

symptomatic seizures

A

due to brain injury resulting in altered action potential/neurotransmitter balance/ electrolyte balance
- treat with short term antiepileptic medications

104
Q

focal seizures

A

deal with a specific group of neurons in one hemisphere

105
Q

generalized seizures

A

deal with both hemispheres involved
- absence seizures and tonic seizures

106
Q

seizure treatment

A

benzodiazepines, barbiturates, anticonvulsants

107
Q

benzodiazepines

A

CNS depressant drug category
- chloride channel agonist
- will cause respiratory depression, drug interactions and are addictive

108
Q

Clonazepam (Rivotril), Diazepam (Valium) (highly used; IV), Lorazepam (Ativan) (SL)

A

benzodiazepines

109
Q

receptor antagonist Flumazenil (Romazicon)

A

benzodiazepine OD treatment

110
Q

Flunitrazepam (rohypnol)

A

‘roofie’
- onset in 15 min
- lasts 4-6 hours

111
Q

barbiturates

A

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
Q

Phenobarbital (Phenobarb), Pentobarbital, Secobarbital

A

barbiturates

113
Q

activated charcoal; sodium bicarbonate

A

barbiturate OD treatment

114
Q

Anticonvulsants

A

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
Q

Phenytoin (dilantin) (narrow TI), Carbamazepine (tegretol), Valproic acid (Valproate)

A

anticonvulsants

116
Q

barbiturates and benzodiasepines

A

used in assisted death

Nurs 216B (19 decks)

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