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patho-pharm > week 2: CNS > Flashcards

week 2: CNS Flashcards

1
Q

most common cause of TBI
(traumatic brain injury) and how are they measured

A

MVC and falls
- measured by glasgow coma scale

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2
Q

glasgow coma scale-mild

A

GCS 13-15

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3
Q

glasgow coma scale- moderate

A

GCS 9-12

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4
Q

glasgow coma scale-severe

A

GCS 3-8

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5
Q

blunt(closed) TBI examples

A

-concussion
- epidural
- subdural
- subarachnoid
- intracerebral hemorrhage

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6
Q

penetrating (open) tbi

A

-missiles
- fractures

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7
Q

characteristics of mild concussion…LOC, GCS, amnesia, diagnostic imaging, symptoms?

A
  • no LOC or LOC of less than 30 mins
  • GCS 13-15
  • mild retrograde amnesia-less than 24 hours
  • no need for diagnostic imaging
  • headache, attention deficit, dizziness
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8
Q

characteristics of moderate concussion…LOC, amnesia, GCS, symptoms, injury to brain…

A

-LOC more than 30 mins
- amnesia 24 hours or more
- GCS 9-12
- basal skull injury…none to brain stem
- confusion, permanent deficits, vision
-transitory decerebration or decortication with unconsciousness

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9
Q

what does decerebration mean

A

abnormal body posture that involves the arms and legs being held straight out, the toes being pointed downward, and the head and neck being arched backward

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10
Q

what does decortication mean

A

they don’t wake up or respond, even with repeated efforts to rouse them

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11
Q

characteristics of severe concussion…LOC, GCS, amnesia, symptoms, what does it increase, associated with what type of injury, what happens to coordination?

A

-LOC can last more than 24 hours
- GCS 8 or less
- brain stem injury
- autonomic dysfunction
- increased icp
- badly compromised coordination

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12
Q

what demonstrates that there is a brainstem injury-severe concussion

A

pupillary reaction, cardiac and respiratory symptoms

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13
Q

what is increased ICP-severe concussion

A

-increased pressure in skull
- increased intracranial pressure

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14
Q

what does DAI stand for

A

diffuse axonal injury

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15
Q

what are DAI’s associated with

A

physical, cognitive, psychologic/behavioural and social consequences

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16
Q

what are examples of physical consequences -DAI

A

spastic paralysis, peripheral nerve injury, dysphagia, dysarthria, hearing and vision, taste and smell

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17
Q

what are examples of cognitive consequences -DAI

A

disorientation, confusion, dysphasia, poor judgement

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18
Q

what are examples of behavioural consequences -DAI

A

agitation, blunted affect, impulsiveness, social withdrawl, depression

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19
Q

symptoms of post concussive syndrome-DAI

A

headache, nervousness or anxiety, irritability, insomnia, depression, inability to concentrate, fatigability

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20
Q

for DAI’s what increased with the severity of the injury

A

decerebrate or decorticate posturing

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21
Q

how are DAI’s diagnosed

A

CT scan or MRI

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22
Q

what is the treatment for DAI

A

control seizures, fluid management

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23
Q

decorticate-where in the brain does the injury occur and abnormal what…destructive lesion of

A

higher level…upper midbrain and above (corticospinal tracts near cerebral hemisphere and basal ganglion)
- abnormal flexion

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24
Q

decerebrate…where in the brain does the injury occur and abnormal what…destructive lesion of

A

lower level…lower midbrain and below (midbrain or cephalic pons)
-abnormal extension

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25
Q

epidural hematomas- what percent of major head injuries and what ages normally

A

1-2%
20-40 y/o

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26
Q

epidural hematomas- source of bleeding, what do 90% of ppl also have, where is the most common site

A
  • artery
  • 90% have a skull fracture
  • temporal fossa
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27
Q

epidural hematomas- symptoms

A

loss of consciousness -> period of lucidity…includes headache, vomiting, drowsiness, seizure, hemiparesis, if temporal lobe herniation begins-ipsilateral pupillary dilation

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28
Q

epidural hematomas- how do you diagnose, prognosis good if, a medical emergency requires you to

A
  • CT scan or MRI
  • prognosis good if intervention before bilateral dilation of pupils
  • evacuate the hematoma (surgery)
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29
Q

subdural hematomas- how many % of TBIs, what do they act as and it evolves to what

A

10-20%
-acts as expanding masses -> ICP-> compresses the bleeding vessels

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30
Q

subdural hematomas- acute and subacute timeline

A

acute: within 48 hours
subacute: over 48 hours- 2 weeks

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31
Q

research subarachnoid hemorrhage

A
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32
Q

for raised ICP

A

-head up
- hyperventilation
- hypertonic saline
- medications
- craniotomy

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33
Q

what medications decrease ICP

A

-mannitol (more blood flow to tissues)
- loop diuretics (reduces sodium reabsorption)
- corticosteroids (anti-inflammatory)
- barbiturates (sedative-hyponotic med)
- anti-seizure drugs

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34
Q

research intracerebral hemorrhage

A
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35
Q

TBI can be due to

A

coup (brain hits front of skull)
contrecoup (brain hits back of skull)

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36
Q

what does SCI mean

A

spinal cord trauma

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37
Q

spinal cord trauma- 40% of due to, about 80% of injuries are what gender, what is the most common sport that causes this

A

-MVC
- men
- diving

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38
Q

spinal cord trauma- how do elderly get this

A

minor falls due to other pathology (ex. osteoporosis)

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39
Q

SCI-pathology: what type of injuries and why

A

vertebral injuries d/t acceleration
deceleration, or deformation injuries

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40
Q

SCI- pathology: how do they injure tissues

A

through compression, exerting tension or traction, or shearing tissues through hyperextension, hyperflexion, vertical rotation of the spine

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41
Q

SCI-pathology: classifications

A

simple fracture, compressed fracture, comminuted fracture (burst or shattered) or dislocation

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42
Q

SCI- pathology: occurs mostly at

A

C1-2, C4-7, T1-L2

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43
Q

SCI- what happens to motor, sensory, reflex, and autonomic functions…

A

all the functions cease below level of transected area, may cease with concussive, contused, compressed or ischemic areas

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44
Q

SCI- what type of paralysis, what occurs slowly

A

-paraplegia, quadriplegia
- return of spinal neuron excitability occurs slowly

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45
Q

hyperreflexia-when does it occur, why does it occur

A
  • syndrome occurs any time after spinal shock ceases
  • massive uncompensated cardiovascular response to stimulation of SNS (sympathetic nervous system)
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46
Q

hyperreflexia- symptoms

A

hypertension, pounding headache, blurred vision, sweating above level of lesion, nasal congestion, nausea, bradycardia

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47
Q

hyperreflexia- most common causes

A

distended bladder or rectum

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48
Q

SCI- diagnoses

A

Dx. made by physical, radiologic and myelographic exam

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49
Q

SCI- treatment (tx)

A
  • immobilize spine (surgical decompression and stabilization are possible)
    -corticosteroids to decrease secondary injury
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50
Q

brain tumours- 2 types

A

primary: intracerebral, extracerebral
metastatic

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51
Q

brain tumours: primary-intracerebral

A

astrocytoma
glioblastoma multiforme
pituitary adenoma

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52
Q

brain tumours: primary- extracerebral

A

meningioma
neurofibroma

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53
Q

brain tumours: metastatic - where?

A

lung
breast
skin
kidney

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54
Q

characteristics of tumors…types, what does it cause, what causes the local effects

A

-primary or metastatic
- cause local and generalized CM
- local effects caused by destruction or compression of the brain

55
Q

tumors: symptoms and generalized effects from

A
  • may include seizures, visual disturbances, unstable gait and cranial nerve dysfunction
  • generalized effects from raised ICP, hemorrhage or cerebral edema
56
Q

brain tumor: intracerebral: astrocytoma, rate of growth and from what

A

-slowly growing
- arises from astrocytes

57
Q

brain tumor: intracerebral: glioblastoma multiforme, growth rate and from what

A

-from more mature glial cells
- very rapidly growing

58
Q

brain tumor: intracerebral: pituitary adenoma- from what, resulting in

A

-pituitary cells
- resulting in secreting tumor

59
Q

brain tumor: extracerebral: meningioma-from what, and why a problem

A

-from arachnoid cells
- problems due to location

60
Q

brain tumor: extracerebral: neurofibroma- from what and where

A
  • arises from schwann cells
  • nerve sheath
61
Q

research metastatic disease

A
62
Q

cerebrovascular accidents (CVA)…what most cause of death, leading cause of…, 5-14% have what within a year

A
  • 3rd leading cause of death
  • leading cause of disability
  • 5-14% have a second stroke within a year
63
Q

CVA- highest incidence in what age group, what are the most severe outcomes, classified as?

A

-over 65 y/o
- severe outcomes are hemiplegia, coma, death
- classified as ischemic or hemorrhagic

64
Q

CVA risk factors

A
  • arterial hypertension (increased systolic and diastolic)
  • smoking
  • diabetes
  • insulin resistance
  • polycythemia (increase in all blood cells-blood disorder) and thrombocythemia (bone marrow makes too many platelets)
  • impaired cardiac function
  • atrial fibrillation
65
Q

ischemic (thrombotic) stroke: caused by and progressive over?

A

arterial occlusions due to thrombi (blood clots) in brain
- progressive over hours or days

66
Q

ischemic (thrombotic) stroke: conditions cause…that increase the risk?

A

inadequate cerebral perfusion (dehydration, hypotension, vasoconstriction)

67
Q

ischemic (thrombotic) stroke: transient ischemic attacks (TIA= mini stroke)…what is it and what happens to the neurologic deficits

A

intermittent blockage
- all neurologic deficits completely clear within 24 hours

68
Q

ischemic (thrombotic) stroke: completed stroke means

A

CVA reached its max destructiveness in producing neurologic deficits

69
Q

ischemic (thrombotic) stroke: embolic stroke involves and is often followed by

A

fragments of thrombi from outside the brain (or air, fat, tumors)
- often followed by another embolic stroke from same source

70
Q

hemorrahagic stroke occurs from

A

hypertension, ruptured aneurysms, bleeding into a tumor, bleeding disorders or anticoagulation, head trauma, illicit drug use

71
Q

hemorrahagic stroke: 20% is

A

subarachnoid
intracerebral

72
Q

hemorrahagic stroke: subarachnoid…what happens

A

uncontrolled bleeding on surface of brain (between brain and skull)

73
Q

diff size of hemorrhage

A

small: 1-2 cm in diameter
massive: several cm in diameter

74
Q

hemorrahagic stroke: intracerebral…what happens

A

an artery deep in brain ruptures, due to high BP

75
Q

what does the left side of your brain control

A

-spoken language
- reasoning
- number skills
- written language

76
Q

what does the right side of your brain control

A
  • creativity
  • music
  • spatial orientation
  • artistic awareness
77
Q

CVA-patho: cerebral infarction has 2 main pathological processes

A
  1. global process that affects neurons most susceptible to ischemia
  2. focal process with a central zone of cell loss surrounded by a zone of injured cells that could survive if re-perfused in one hour
78
Q

CVA-patho…cerebral infarction…someone can have ASK SENIOR ABOUT THESE 3 IM CONFUSED

A

-abrupt vascular occlusion-acute limb ischemia-sudden loss of limb perfusion
- gradual vessel occlusion
- partial occlusion

79
Q

CVA patho- hemorrhagic infarctions…can be a result of, may compromise?

A
  • result of reperfusion due to resumption of blood flow (ex from incomplete emboli)
  • may compromise recovery by accelerating the sequence of metabolically damaging events
80
Q

CVA patho- cerebral hemorrhage…primary cause, bleeding precipitated by, what forms

A

-primary cause: hypertension
- bleeding precipitated by aneurysms in smaller vessels or arteriolar necrosis(death of tissue)
- mass of blood forms

81
Q

CVA- diagnosis and when to have treatment/what is treatment

A

-Dx: primarily through CT and CM (physical exam)
- need to start tx within 6 hours at the latest
- usually done through stroke protocol with neurologist in central location

82
Q

treatment of CVA- ischemic

A
  • TPA (breaks up blood clot) needs to be administered within 4.5 hours
  • ASA (acetylsalicylic acid ex aspirin)
  • anticoagulant (heparin or coumadin)
  • BP controlled
  • anti-seizure meds
  • occasionally thrombectomy(procedure to remove blood clot)
83
Q

why use anticoagulant for the treatment of CVA-ischemic (the source)

A

for cardiac or carotid source

84
Q

treatment of CVA-hemorrhagic

A
  • BP control (much lower than ischemic)
  • tranexamic acid
  • antiseizure meds
  • surgery
85
Q

when do you use ct scans

A

dx tumors, internal bleeding or check for internal injuries or damage

86
Q

what is a seizure

A

sudden, explosive disorderly discharge of cerebral neurons

87
Q

what are seizures characterized by

A

sudden, transient alteration in brain function

88
Q

convulsion-meaning? (seizures)

A

clonic-tonic movement associated with some seizures

89
Q

what does epilepsy mean-seizures

A

general term for primary condition that causes seizures

90
Q

for seizures what are conditions associated…%

A

20%- genetic, especially if before 20 years old
33% from a known cause or disease

91
Q

etiologic factors associated with seizures

A

cerebral lesions, biochemical disorders, cerebral trauma, epilepsy

92
Q

what can epilepsy result from-seizures

A

metabolic defects
congenital malformation
perinatal injury
postnatal trauma
infection
brain tumor
vascular disease
drug or alcohol abuse

93
Q

triggers for seizures

A
  • hypoglycemia
  • fatigue
  • emotional or physical stress
  • febrile illness
  • excess H2O ingestion
  • constipation
  • use of stimulant drugs
  • withdrawal from depressant drugs
  • hyperventilation
    -environmental stimuli
94
Q

types of seizure disorders

A

generalized seizures
partial seizures

95
Q

types of seizure disorders- generalized seizures…what is it, what’s the onset, originates from and what happens to consciousness

A

-bilateral neuron involvement
-general onset
-originate from subcortical or deeper brain focus
- impaired or lost consciousness

96
Q

types of seizure disorders- partial seizures…what is it, what’s the onset, originates from and what happens to consciousness, stimuli?

A

-focal seizure
- unilateral neuron involvement
- originate from cortical brain tissue
- maintain consciousness if only unilateral but may become generalized (secondary generalization)
-may not respond to outside stimuli

97
Q

types of seizure disorders- status epilepticus

A

multiple seizures without regaining consciousness or seizure lasting more than 30 mins

98
Q

types of seizure disorders- post-ictal state…meaning

A

time period immediately following a seizure

99
Q

seizures patho-epileptogenic focus…what does this mean

A

group of neurons with more permeable plasma membranes that are hypersensitive to stimuli like hyperthermia, hypoxia and hypoglycemia

100
Q

seizures patho-primary abnormality

A

-may be a membrane defect leading to instability in resting potential or other defects

101
Q

seizures patho…what happens when neurons fire (the whole process)…watch a vid on this

A
  • more frequency and amplitude
  • reaches a threshold point
  • goes through contralateral cortex to subcortical areas of basal ganglia, thalamus and brain stem (tonic phase)
  • apnea may be present for a few secs
  • excitement spreads down spinal cord neurons
  • clonic phase as inhibitory neurons in cortex, anterior thalamus and basal ganglia inhibit excitation
  • inhibition interrupts seizure charge, alternation becomes less frequent until it stops
  • epileptogenic neurons are exhausted
102
Q

what happens in the tonic phase

A

muscle contraction with increased muscle tone

103
Q

what happens in clonic phase

A

alternating contraction and relaxation of muscles

104
Q

what does the maintenance of seizures activity require

A

250% increase in ATP
60% increase in cerebral O2 consumption
250% increase in cerebral blood flow

105
Q

what can severe seizures cause…and it progresses to and may result in

A

-deficiency of ATP, phosphocreatine and glucose
- secondary hypoxia, acidosis and lactate accumulation
- may result in progressive brain tissue injury/destruction

106
Q

seizures-CM: aura…what is it

A

partial seizure that immediately precedes a generalized seizure

107
Q

seizures-CM: prodoma…what is it

A

early manifestation that can occur hours to days before a seizure

108
Q

seizures-acute treatment

A

-benzodiazepines (depressant for sedation/hyponosis that reduces seizures)
- phenytoin (control some types of seizures, treat and prevent)
- valproic acid (treats epilepsy)
- carbamazepine (manage and treat epilepsy)
- phenobarbital (anti-seizure management)
- levetiracetam (control certain types of seizures: myoclonic, tonic/clonic or partial)

109
Q

for diagnosing seizures…what is most important, look for what during what, rule out, use an EEG to, why use imaging

A

-health history
-physical exam and lab tests to look out for systemic diseases
- rule out neurologic diseases
- EEG to assess type of seizure and ID cause
- imaging for mass lesions CT scan or MRI

110
Q

how are benzodiazepines administered

A

IV, IM (intramuscular), SC (subcutaneous?)

111
Q

how is phenytoin administered

A

loading dose IV

112
Q

seizures- chronic treatment

A
  • phenytoin
  • valproic acid
  • carbamazepine
  • levetiracetam
  • lamotrigine (controls certain seizures: partial, tonic-clonic, lennoz-gastaut syndrome)
  • topiramate( treat and manage epilepsy)
  • clonazepam (for panic disorder, epilepsy and nonconvulsive status epilepticus)
113
Q

symptoms of meningitis

A

rash, stiff neck, chills

114
Q

two most common types of meningitis

A

meningococcal and streptococcus

115
Q

the main causes of meningitis

A

viral infection, bacteria, fungi, parasites

116
Q

where does this occur

A

in CSF through subarachnoid space, starts in body and crosses blood-brain barrier

117
Q

how do you treat meningitis

A

antibiotics

118
Q

what is the age demographic more likely to get meningitis and how quickly it is over (no matter the outcome)

A

20-40 y/o
over in 24 hours

119
Q

what is MS, can you see in on diagnostic imaging

A

demyelinating disease with white matter plaques
- cant see MS on CT scan

120
Q

treatments for MS

A

steroids for acute
interferons for chronic…this makes you feel like shit bc works on immune system

121
Q

how do they realize that its MS

A

neurological findings then another neurological finding then they realize its MS

122
Q

which hemisphere is ms more common in

A

northern hemisphere

123
Q

what is myasthenia gravis

A

chronic autoimmune disease mediated by anti-acetylcholine receptor antibodies

124
Q

where does myasthenia gravis occur

A

at neuromuscular junctions

125
Q

what is the first sign of myasthenia gravis and how to test for it

A

tossus…eyelid drooping unilaterally or bilateral
- tell patient to look up and eye will droop in 30secs to 1 min

126
Q

how to test using diagnostic testing for myasthenia gravis

A

EMG (electromyogram)…tests muscles/measure how fast muscles are firing

127
Q

guillain-barre syndrome….what is it

A

inflammatory disease that results in demyelination of peripheral nerves

128
Q

guillain-barre syndrome symptoms and what is it preceded by

A

-leg paralysis then whole body
- ventilation till body gets better

129
Q

what is Alzheimer’s and what is the diagnsis

A

progressive dementia…loss of cognitive mental function
- diagnosis is clinical

130
Q

what tests are used to see if you are testing for Alzheimers

A

sage test…clock drawing test(can do for short-term dementia-like delirium
- quick 3 point recall…say 3 random words then say it twice more then later ask what the 3 words were
-moca test
-mmse

131
Q

what treatment is used for Alzheimers

A

-cholinesterase inhibitors like aricept or reminyl (tries to keep the person at the level they are at…so they dont deteriorate)

132
Q

parkinson disease…what is it and age demographic

A

degenerative disease of dopamine pathway in the substantia nigra (dark part of brain turns white)
-usually after 40, peaking in onset around 60

133
Q

SYMPTOMS OF PARKINSONS and type of diagnosis

A

resting tremor
rigidity (cogwheel)
bradydyskinesia
postural instability
-clinical diagnosis (can’t see this on any imaging)

134
Q

treatment of parkinsons

A

dopamine agonists

patho-pharm (3 decks)

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