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PT 680 Clinical Medicine > Intro to CNS Disorders > Flashcards

Intro to CNS Disorders Flashcards

1
Q

what does the CNS control

A

behavior, thought, motor function

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2
Q

changes in ____ in the nucleus of the cell body alters gene expression resulting in abnormal production of harmful proteins that make the CNS more vulnerable to disease

A

DNA

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3
Q

give examples of how DNA can be altered, causing CNS disease

A
  • genetic predisposition
  • toxicity due to drug/alcohol abuse
  • environmental triggers
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4
Q

tissue death that occurs with severe injury or disease

A

necrosis

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5
Q

sets off cascade of inflammatory actions; leads to excitoxicity and release or free radicals; contributes to damage of surrounding tissues; cell is destroyed (membranes and structures)

A

necrosis

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6
Q

genetically programmed degradation of DNA

A

apoptosis

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7
Q

seen in development as neuronal pruning; does not lead to inflammatory action; may be triggered by free radicals resulting in cell death; may be pathologic (cancer cells); cell membranes generally intact

A

apoptosis

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8
Q

what are the two types of glial cell

A

macroglia and microglia

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9
Q

give examples of macroglia cells

A

astrocytes, oligodendrocytes, schwann cells

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10
Q

the connective tissue of CNS; support and maintain neuronal plasticity; most populous in CNS

A

macroglia cells

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11
Q

most numerous on all CNS cells (supporting cells)

A

astrocytes

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12
Q

associated with CNS deymylemination and what is a disease example

A

olgiodendrocytes
MS

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13
Q

associated with PNS demyelination and what is a disease example

A

schwann cells
diabetic peripheral neuropathy

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14
Q

the immune system of the CNS; 10% of glial population; respond when CNS tissue is damaged; act as phagocytes and can trigger astrocytes

A

microglia cells

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15
Q

when microglia are triggered, what s/s do they produce

A

fever, sleep, decreased appetite, lethargy, swelling

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16
Q

are usually transient, but aging cells are not deactivated by apoptosis and may contribute to pathogenesis of neurologic disease

A

microglia

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17
Q

made of epithelial cells that form a tight matrix that block diffusion between cells

A

blood brain barrier

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18
Q

how does glucose and amino acids cross the blood brain barrier

A

protein transport

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19
Q

give some examples of pathogens that are able to penetrate the blood brain barrier and lead to disease

A

meningitis
encephalitis
some metabolic disorders

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20
Q

cells that line the ventricles and spinal canal; produce CSF

A

ependymal cells

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21
Q

what can ependymal cells be implicated by

A

infectious diseases
stroke
TBI

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22
Q

shunt that drains CSF from the ventricles to the perineum (gut) to decrease ICP

A

ventriculoperitoneal shunt

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23
Q

what are the 3 main ways axons can be injured

A

shearing, compression, traction

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24
Q

damage to axons that occurs in TBI due to shearing forces during coup-countercoup injury (due to increased velocity)

A

diffuse axonal injury (DAI)

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25
Q

traction on a peripheral N that causes degeneration of the distal end of axon

A

wallerian degeneration

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26
Q

amines

A

serotonin, dopamine, acetycholine, norepinephrine

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27
Q

amino acids

A

GABA, glycine, glutamate

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28
Q

neuroactive peptides

A

enkephalins, endorphins, substance P

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29
Q

gaseous neurotransmitters

A

nitrous oxide, carbon monoxide

30
Q

how can pathology develop due to neurotransmitters

A
  • changes in the synthesis/availability of neurotransmitters
  • changes in target cells can cause abnormal responses to normal levels of transmitters
31
Q

nerve growth factor, BDNF, and other _______ contribute to maintenance and survival functions of neurons known as ______

A

neurotrophic factors
neuroprotective

32
Q

best way to increase neurotrophic factors

A

aerobic exercise

33
Q

aging

A

senescene

34
Q

nerve conduction velocity decreases by 15% in myelinated fibers by

A

8th decade (80 y/o)

35
Q

what can develop in the brain with aging

A

neurotic plaques, glial scar tissue, neurofibrillary tangles

36
Q

by how much does blood supply decrease to brain with aging and what does this mean

A

10-15%
decreased glucose and decreased brain metabolism

37
Q

changes in PNS associated with age

A

diminished vestibular, vision, and somatosensation

38
Q

changes in ANS due to age

A

decreased ANS reactivity
alterations in BP, RR, HR, blood flow, organ function

39
Q

by 60 y/o, we lose what percent of hair cells in vestibular system

A

40%

40
Q

neurological disorders associated with age

A

muscular dystrophy
down syndrome
parkinson’s
alzheimer’s

41
Q

neurological disorders associated with race/ethnicity

A

tay-sachs
neural tube defects

42
Q

neurological disorders associated with genetic history

A

duchenne’s muscular dystrophy
huntington’s chorea
spinal muscle atrophy

43
Q

neurological disorders associated with familial history

A

DM
charcot marie tooth

44
Q

CT markers placed for tracking dopamine uptake

A

DaTScan

45
Q

used to identify disruption of white matter

A

diffusion tensor imaging

46
Q

evaluates function of CN 8 - auditory component and integrity of brainstem in coma

A

brainstem auditory evoked potentials (BAEP)

47
Q

determines O2 saturation in brain tissue

A

near-infrared spectroscopy

48
Q

how/where is CSF analysis taken

A
  • via percutaneous puncture in subarachnoid space
  • between L3-4 or L4-5
49
Q

why would a CSF analysis be performed

A
  • evaluate inflammatory diseases of CSF
  • rule out CNS infection
  • confirm otherwise undiagnosed CNS conditions
50
Q

what does pink/clear/yellow/cloudy CSF each indicate

A

clear = normal
yellow = old RBC
pink = active bleeding
cloudy = infection

51
Q

example of diseases for evaluation of CSF

A

meningitis, encephalitis, MS, parasitic/fungal infections, rabies, syphyilis

52
Q

when is CSF analysis contraindicated

A

ICP is elevated or presence of focal neurologic signs –> brain would leak into back

53
Q

evaluates changes in glucose, proteins, WBC, or identified bacteria in blood samples which may indicated infectious pathologies

A

CBC and diff, cytology, bacteriology

54
Q

most common ordered lab test; provides info on size, availability, # of blood cells in peripheral circulation; ratio of RBC, WBC, plasma

A

CBC

55
Q

measures relative volume of RBC’s; quick screen of anemia/polycythemia

A

hematocrit

56
Q

normal hematocrit values for M and F

A

M 42-52%
F 37-47%

57
Q

measures oxygen carrying capacity of RBC

A

hemaglobin

58
Q

normal hemoglobin levels for M and F

A

M: 14-18
F: 12-16

59
Q

____ level changes cause brain/nerve tissue to shrink/swell which may alter consciousness, induce coma, or intracranial hemorrhage

A

sodium

60
Q

must have ____ and ____ levels WNL for neuromuscular transmission of action potentials

A

potassium and calcium

61
Q

high or low levels of _____ may result in diabetic ketoacidosis, insulin shock, or diabetic coma

A

glucose

62
Q

normal adult values and critical values for sodium, potassium, calcium, fasting glucose

A
  • Sodium: 134-142; 110
  • Potassium: 3.7-5.1; <3.2 or >5.1
  • Calcium: 8.6-10.3; <7 = tetany; >12 = coma
  • Fasting Glucose: 70-100; over 60 y/o 90-130
63
Q

sedative-hypnotic drugs and side effects they can cause

A

barbituates, benzodiazepines
- drowsiness, changes in motor performance the next day, antegrade anmesia, physical dependance, sleeping while driving, GI discomfort

64
Q

anti-anxiety, anti-depressant, affective disorder drugs and side effects they can cause

A

xanax, buspar, ativan, klonopin, elavil, cymbalta, prozac
- dizziness, HA, nausea, drowsiness, addiction, abuse, orthostatic hypotension, cardiac arrhythmias, seizures

65
Q

anti-epiletic drugs and aide effects they can cause

A

pehnobartial, valium, ativan, tegretol, neurontin (gabapentin)
- usually take across the lifespan - withdrawal has to be gradual and controlled by physician

66
Q

anti-coagulation medications (stoke) and side effects

A

coumadin, herparin, asprin (ASA)
- hemorrhage most common negative effect, easily bruised

67
Q

drugs to tx:
parkinsons
seizures/spasticity
spasticity
and side effects

A
  • PD: levadopa/sinemet
  • Seizures/spasticity: neurontin/gabapentin
  • Spasticity: balcofen
    sedation, dizziness, nausea, ataxia, fatigue
68
Q

initial period of neural shock and disruption of neural connectivity in undamaged areas of brain due to connection to damaged portions of brain

A

diaschisis

69
Q

cortical reorganization via collateral sprouting; regenerative synaptogenesis via pharmacological, novel tasks, and aerobic activity

A

neuroplasticity

70
Q

3 main interventions to help improve neuroprotection

A

exercise
diet
sleep

PT 680 Clinical Medicine (18 decks)

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