Neurology Flashcards

1
Q

Intracerebral Bleed Incidence Associated with

A

HTN, anticoagulation therapy or coagulopathy, drug and alcohol abuse, neoplasia, amyloid angiopathy, infection

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2
Q

aneurysm etiologies

A

trauma, inflammation, atherosclerosis, congenital, peak age 35-50

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3
Q

ischemic stroke risk factors

A

increasing age, underlying atherosclerotic disease, hx TIA’s, associated with CV disease

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4
Q

patients at risk for stroke anesthetic implications

A

control DM, HTN, coagulation therapy

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5
Q

SAH risk factors

A

HTN, DM, CAD

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6
Q

oligodendrocytes

A

form myelin around CNS axons (schwann cell in PNS)

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7
Q

astrocytes

A

help regulate composition of ISF in CNS, provide glucose to and remove ammonia from neurons
-repair after neuronal injury and maintain metabolic environment

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8
Q

microglia cells

A

specialized macrophages that phagocytize neuronal cells

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9
Q

CSF emptying

A

from saggital sinus to superior jugular vein to SVC

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10
Q

CSF pathway

A

made in ependymal cells in lateral and 3rd ventricle, then goes to 4th ventricles, then foramen of magendie, then cerebellar versus spinal pathway

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11
Q

which artery carries 80% of blood to the brain

A

MCA

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12
Q

susceptibility to aneurysm formation

A

structural abnormalities, genetics, atherosclerosis, HTN, coarctation of aorta, connective tissue DO’s

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13
Q

where are most AVM’s

A

75% supratentorial

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14
Q

3rd leading cause of death in US

A

ischemic stroke

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15
Q

thrombus formations associated with these risk factors

A

atherosclerosis, hyper coagulation, sickle cell disease, polycythemia vera, decreased BF

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16
Q

TBI: extradural hematoma

A

usually arterial source of bleeding, can lead to herniation because bleed is compressing veins

17
Q

TBI: subdural hematoma

A

usually torn bridging vein or venous sinus, increased ICP compresses tear, can lead to herniation

18
Q

TBI: intracerebral bleed

A

small blood vessel trauma- shearing or penetration. increased ICP and brain compression, brain edema. dont have effect on CSF movement like the others

19
Q

what can predispose to seizures

A

hyperthermia, hypoxia, hypoglycemia, hyponatremia, repeated sensory stimulation, sleep phases

20
Q

tonic phase of seizures

A

muscle contraction/increased muscle tone. occurs when neuronal excitation spreads to subcortical, thalamic, and brainstem areas

21
Q

clonic phase

A

alternating muscle contraction and relaxation. this is essentially periodic interruption of tonic phase. occurs when inhibitory neurons (in cortex, thalamus, and basal ganglia) begin to inhibit neuronal (cortical) excitation

22
Q

seizure risk factors

A

genetic-idiopathic
genetic predisposition for disorder associated with DiGeorge syndrome- hypoparathyroidism and hypocalcemia
tumor, trauma, infection, fever
sah, stroke damage
metabolic origin (fever, uremia, hypoxemia, hyperglycemia, hyponatramia, hypocalcemia)
hypoxia, hyperventilation (resp alkalosis)
drugs or alcohol OD or withdrawal
fatigue or stress
excessive sensory stimuli

23
Q

cytotoxic edema

A

ischemia induced neuronal ion influx that facilitates cell swelling. no net increase in fluid, brain ISF goes to ICF

24
Q

vasogenic edema

A

ischemia- damages endothelial cells, BBB breakdown in 2-3 days, BBB breach means plasma protein moves into ISF

25
hydrostatic edema
cerebral auto regulation disrupted, CBF increased, capillary hydrostatic pressure increased
26
osmotic edema
dilution of blood, pressure decreases, more plasma volume goes to brain interstitium ex)liver failure, lack of albumin
27
interstitial edema
transependymal movement of CSF to interstitium from ventricles
28
communicating hydrocephalus
no CSF absorption at saggital sinus, extraventricular
29
non communicating
intraventricular
30
Parkinsons Pathophysiology
DA at SN inhibits GABA so movement can occur, but there is less dopamine being released to inhibit GABA at the substantial niagra and allow for movement. Ach modulates GABA neurons, so Ach exacerbates parkinsons since the cholinergic and dopaminergic receptor balance is screwed. Usually, Ach inhibit DA input to the GABA neurons, so now Ach transmission is favored. This is why anticholinergic meds may help.
31
Alzheimers pathophysiologu
extracellular neuritic plaques that contain amyloid protein and deform the synaptic terminal, and you lose you Ach NT. most prominent in hippocampus (memory, navigation)
32
alzheimers risk factors
genetic, chronic HTN, head injury, female, TIA
33
sx of cross clamping
preload increases because its a reduced container, SVR increases, RAAS and catecholamines
34
each segment of the SC will receive blood from how many anterior and how many posterior spinal arteries that stem from which artery
1 anterior 2 posterior stem from vertebral artery
35
tx if hypotension occurs when you unclamp from cross clamping
partial or complete re application of cross clamp recommended
36
possible reasons for ALS
heavy metal exposure, glutamate excitotoxicity, oxidant stress, hereditary component
37
MD anesthesia risks
acute respiratory depression, rhabdomyolysis, hyperkalemic cardiac arrest (esp c succ), heart failure/arrhythmias
38
scoliosis associated with increased risk of
mitral valve prolapse, pulmonary resistance, pulmonary hypertension