Week 1 - Neuro Big Ideas Flashcards

1
Q

insults to developing embryonic nervous system

A

first 2 weeks = death, week 3-6 = neural tube defects, >6 weeks = mental retardation

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2
Q

neurulation

A

from middle in both directions, notochord induces thick neural plate, neural groove becomes neural tube from lateral plate cells, neural crest cell migrate, takes ~ 22 days, somites develop concurrently, derived from ectoderm

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3
Q

neurulation

A

neural plate –> neural folds –> neural groove –> neural tube and crest cells

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4
Q

neural tube

A

becomes brain and spinal cord

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5
Q

neural crest cells

A

becomes PNS, non-neuronal derivations like melanocytes and GI cells

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6
Q

neural canal

A

ventricular system in brain and canal in spinal cord

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7
Q

neuroepithelial cells

A

differentiate into neurons with cells bodies in CNS and macroglial cells, ventricular zone = neurons and ependymal cells, intermediate zone = gray matter, marginal zone = white matter

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8
Q

alar plate

A

becomes dorsal spinal cord, contains secondary sensory neurons, gives rise to afferent fibers

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9
Q

basal plate

A

becomes ventral spinal cord, contains motor neurons, nerve cell body grows neurites, axons in ventral horn synapse with skeletal muscle, neurons in lateral horn synapse with peripheral autonomic ganglia, gives rise to efferent fibers

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10
Q

roof and floor plates in neural tube

A

dorsal and ventral thin area with no neuroblasts, become regions of brain where axons cross

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11
Q

primary sensory neuron development

A

start as bipolar cells and become psuedounipolar

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12
Q

developing brain myelination

A

schwann cells in PNS, oligodendrocytes in CNS, from neural crest cells, continues throughout first year of life, schwann cell body wraps, oligodendrocyte extensions wrap

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13
Q

length of spinal cord

A

nerve roots lines up with matching vertebra at 8 wks, vertebra grow faster than spinal cord, newborn spinal cord ends at L2-3, adults spinal cord ends at L1-2, spinal tap below this level

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14
Q

neural tube closure

A

end 3rd week, creates primary vesicles of brain

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15
Q

primary vesicles of developing brain

A

forebrain (prosencephalon), midbrain (mesencephalon), hindbrain (rhombenceohalon)

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16
Q

forebrain vesicle (prosencephalon)

A

becomes telencephalon and diencephalon

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17
Q

midbrain vesicle (mesencephalon)

A

becomes mesencephalon

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18
Q

hindbrain vesicle (rhombencephalon)

A

becomes metencephalon and myelencephalon

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19
Q

caudal neural tube

A

becomes spinal cord

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20
Q

secondary vesicles of developing brain

A

telencephalon, diencephalon, mesencephalon, metencephalon, myelencephalon

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21
Q

telencephalon vesicle

A

becomes cerebral cortex, corpus striatum, olfactory bulbs, c shaped growth covers insula, convolutions develop, lateral ventricles, CN I

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22
Q

diencephalon vesicle

A

becomes thalamus, hypothalamus, epithalamus, subthalamus, third ventricle, CN II

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23
Q

mesencephalon vesicle

A

becomes tectum, tegmentum, basis pedunculi, superior and inferior colliculus, CN III, CN IV

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24
Q

metencephalon vesicle

A

becomes pons and cerebellum and fourth ventricle, CN V to XII

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25
Q

myelencephalon vesicle

A

becomes medulla and fourth ventricle, CN V to XII

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26
Q

cervical flexure

A

superior bend in secondary vesicles at base of myelencephalon

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27
Q

pontine flexure

A

inferior bend in secondary vesicles at metencephalon

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28
Q

cephalic flexure

A

superior bend in secondary vesicle at mesencephalon

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29
Q

choroid plexus

A

formed by modified ependyma, pia, and blood vessels, floor of fourth ventricles, roof of thrid and fourth ventricles, makes CSF

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30
Q

neural crest cell derivatives

A

dorsal root ganglia, sympathetic trunk ganglia, celiac ganglia, GI plexis, renal ganglia, suprarenal gland, melanocytes, odontoblasts, bones and cartilage of face

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31
Q

consciousness

A

wakeful (open eyes, motor arousal) and aware (thoughts, memories, emotions)

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32
Q

coma

A

unresponsive to internal and external stimuli, no reflexes, unarousable, no eye opening

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33
Q

vegetative state

A

unresponsive wakefulness, sleep cycles, opens eyes, not aware of others, reflexes, smile/grimace, unresponsive to stimuli

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34
Q

minimally conscious state

A

sleep cycles, incomplete awareness, + = high level, - = low level

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35
Q

locked in syndrome

A

sleep cycles, aware, quadriplegia, unable to interact, brainstem lesion

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36
Q

neurological exam

A

H & P key, changes based on setting

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37
Q

mental status

A

assessing cortex, level of consciousness, speech, orientation (time and place), attention, calculation (world or months backwards, serial 7s), language, memory (naming, 3 words)

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38
Q

fundoscopic exam

A

blurring of disk, loss of venous pulse, color

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39
Q

parts of neurologic exam

A

mental status, cranial nerves, motor, sensory, reflexes, coordination, gait / station

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40
Q

mental status - level of consciousness

A

determine by observation

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41
Q

mental status - speech

A

determine by observation

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42
Q

mental status - orientation

A

determine with person / place / time, month / day / date, city / state / country

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43
Q

mental status - attention / calculation

A

world backwards, months of year backwards, serial 7s

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44
Q

mental status - language / memory

A

naming, 3 words (immediate, after distraction)

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45
Q

fundoscopic exam

A

look for - blurred optic disc, loss of venous pulse, color of optic nerve

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46
Q

testing CN I - olfactory

A

pass order, perceive not identify

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47
Q

testing CN II - optic (acuity, fields, pupils)

A

chart, confrontation, eye individually

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48
Q

testing CN III - occulomotor (pupils, eye movement)

A

direct, consensual, flashlight, conjugate gaze, nyastigma

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49
Q

CN of eye movement

A

CN III - occulomotor (MR, SR, IR, IO), CN IV - trochlear (SO), CN VI abducens (LR)

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50
Q

testinng CN V - trigeminal (facial sensation, corneal response, mastication)

A

cotton, pin, tuning fork, compare sides, bite down / open

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51
Q

testing CN VII - facial (facial muscle movements)

A

observe (palpebral fissures and nasolabial folds), squeeze eyes shut, smile, puff out cheeks, forehead spared = CNS lesion, forehead not spared = PNS lesion

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52
Q

testing CN VIII - vestibulocochlear (hearing, balance)

A

vestibulo - dizziness, cochlear - finger running, Weber, Rinne

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53
Q

Weber test

A

on forehead midline,conductive loss louder in affected ear, sensorineural loss louder in unaffected ear

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54
Q

Rinne test

A

mastoid, in air next to ear, air louder then bone

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55
Q

testing CN IX - glossopharyngeal

A

palate elevation, gag (coma), swallow, horseness / breathiness

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56
Q

testing CN X - vagus

A

palate elevation, gag (coma), swallow, horseness / breathiness

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57
Q

testing CN XI - accessory (sternoclidomastoid, trapezius)

A

turn head against resistance (tests opposite side), shoulder shrug

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58
Q

testing CN XII - hypoglossal (tongue)

A

listen for slurring, observe protrusion / deviation / slowness (will deviate to weak side)

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59
Q

testing motor

A

bulk (atrophy, diffuse = disuse, focal = denervated), tone (passive, decreased = flaccid, increased = spastic / rigid / paratonia), strength (grading 5-0, compare sides, compare proximal and distal, arm drift = upper motor neurons)

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60
Q

testing sensory

A

pain and temp (pin, tuning fork - spinothalamic tract), vibration and propioception (tuning fork - dorsal columns), light touch (cotton - both spinothalamic and dorsal columns)

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61
Q

Romberg test

A

sensory problems, close eyes and keep balance, positive = neuropathy in feet

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62
Q

testing reflexes

A

biceps - C5/6, brachioradialis - C6-7, triceps - C7/8, knees - L3/4, ankles - S1/2, Babinski, graded 4-0

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63
Q

clonus

A

upper motor neuron problem, hyperreflexive, flexed ankle shakes

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64
Q

hyporeflexive

A

radiculopathy (nerve root problem), neuropathy (sensory nerve problem), PNS

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65
Q

hyperreflexive

A

brain lesion, spinal cord lesion, upper motor neuron problem, CNS

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66
Q

testing coordination

A

finger - nose - finger and heel - knee - shin (cerebellum), rapid (frontal), fine finger and toe tapping (upper motor neurons)

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67
Q

testing gait and station

A

walk - regular, heels, toes, tandem gait

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68
Q

wide, ataxia gait

A

cerebellum

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69
Q

wide, slapping gait

A

neuropathy

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70
Q

shuffling, stooped, multistep gait

A

basal ganglia, parkinsons

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71
Q

spastic gait

A

upper motor neuron

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72
Q

case - sensory and motor PNS problem, large fibers

A

dorsal columns, trouble sensing vibration, poor balance, bowel/bladder ok, foot slap, slight motor weakness, positive Romberg, no reflex on area

73
Q

case - left brain, motor pathways, language, likely left middle cerebral artery lesion in frontal / temporal area

A

right side of body affected, weakness, sudden, Hx hypertension, trouble speaking, right face weakness sparing forehead, decreased tone, slow finger tapping

74
Q

case - right side nerve root (C6)

A

neck / arm pain, weak arm, thumb and 1st finger affected, weak arm flexion, poor sensory in thumb, right biceps weaker then left

75
Q

brain disorders from most to least common

A

sleep, hearing, depressive, TBI, stroke, Alzheimer’s. schizophrenia, Parkinson’s, MS, spinal injury, Huntington’s

76
Q

neurovascular unit

A

coupled cerebral blood flow and cerebral metabolism, vasodilation in area that is most active, composed of neurons / synpases / astrocytes / capillaries

77
Q

brain fuel consumption

A

brain is 2% body weight, uses 25% of glucose and 20% of oxygen in body

78
Q

neuronal ATP consumption breakdown

A

44% synpatic transmission (including Ca2+ movement and nt recycling), 25% housekeeping (protein synthesis), 15% resting potential, 16% action potential

79
Q

fates of glucose in the brain

A

glycolysis and TCA cycle, 6-10% glycogen synthesis in astrocytes, 3-5% pentose phosphate shunt (makes NADPH for protein synthesis - more in babies)

80
Q

hexokinase

A

regulates glucose to glucose 6 phosphate step of glycolysis, inhibited by glucose 6 phosphate, uses ATP

81
Q

phosphofructokinase

A

regulates step from fructose 6 phosphate to fructose 1, 6 phosphate in glycolysis, activated by ADP / AMP / Pi, inhibited by ATP / PCr / citrate, uses ATP

82
Q

pyruvate kinase

A

regulates the phosphoenolpyruvate to pyruvate step of glycolysis, inhibited by ATP / acetyl-CoA, makes ATP

83
Q

phosphorylase

A

turns glycogen into glucose 1 phosphate so it can enter glycolysis, inhibited by cAMP

84
Q

pyruvate dehydrogenase

A

turns pyruvate into acteyl-CoA to enter TCA cycle, inhibited by ATP / NADH

85
Q

isocytrate dehydrogenase

A

regulates isocitrate to alpha ketoglutarate step of TCA cycle, activated by ADP

86
Q

alpha ketoglutarate dehydrogenase

A

regulates alpha ketoglutarate to succinyl-CoA step of TCA cyce, inhibited by ATP

87
Q

cerebral metabolic rate - glucose (CMR-G)

A

positive number because brain is consuming glucose, (A-V)F/W

88
Q

cerebral metabolic rate - oxygen (CMR-O)

A

positive number because brain is consuming glucose, (A-V)F/W

89
Q

cerebral metabolic rate - lactate

A

negative number because brain is producing lactate, (A-V)F/W

90
Q

cerebral metabolic rate - CO2

A

negative number because brain is producing CO2, (A-V)F/W

91
Q

cerebral metabolic rate - XXX equation

A

(A-V)F/W, A - arterial conc in mole/l, V venous conc in mol/l, F = blood flow in l/min, W = weight in grams, CMR unit = moles/g/min

92
Q

CMR-O2 vs CMR-G ratio

A

5:1, 156 to 31, 6 O per glucose to make ATP, some glucose not being oxidized and becoming lactate - that is why it is not a perfect 6:1 ratio (1 glucose + 6O2 –> 6CO2 + 6 H2O

93
Q

CMR-O2 and CMR-CO2 ratio

A

1:1

94
Q

drowning CMR-G and CMR-O

A

CMR-G up because making energy with glycolysis, CMR-O down because none available

95
Q

anesthetic CMR-G and CMR-O

A

depressants / less brain activity = less energy needed, CMR-G and CMR-O down

96
Q

epilepsy CMR-G and CMR-O

A

seizures = more energy needed, CMR-G and CMR-O up

97
Q

2-deoxyglucose (2-DG)

A

glucose analogue, glucose transporter into cells, phosphorylated by hexokinase to glucose 6 phosphate, then gets stuck in glycolysis pathway, use to locate areas of high glucose metabolism by marking it with radioactive fluroine-18 (often used in PET scans)

98
Q

PET scan of Alzheimer’s brain

A

low metabolic activity in parietal / temporal / occipital lobes

99
Q

PET scan of frontal temporal dementia

A

shows decreased metabolism in frontal / temporal lobes

100
Q

effect of visual stimulation on brain

A

increased blood flow / glucose / O2 to occipital area, but not increase O2 usage because brains uses aerobic respiration to meet the needs of momentary visual stimulation

101
Q

aerobic glycolysis

A

glycolysis in the presence of O2, when excess pyruvate is made it is shunted to lactate

102
Q

astrocyte-neuron lactate shuttle

A

astrocytes take up 80% of the glucose in brain and shuttle it to neurons, glutamate and Na+ through GLAST / GLT1 triggers alpha subunit of Na/K - ATPase –> glucose uptake through GLUT1 –> glycolysis to lactate with LDH5 –> release of lactate via MCT1 / 4 –> reuptake of lactate in neuron by MCT2 –> LDH1 converts lactate back to pyruvate –> TCA cycle

103
Q

glutamate / glutamine shuttle

A

glutamate and Na+ are cotransported from neuron to astrocyte, Na+ influx triggered Na/K ATPase in astrocyte, glycolysis occurs making lactate to meet ATP needs of ATPase and glutamate to glutamine conversion, glutamine trasported to neuron via GLAST/GLT1 and used as glutamate neurotransmitter, lactate transported to neuron via MCT1/4/2 and turned back into pyruvate by LDH1 then enters TCA cycle

104
Q

acetoacetate and D-3-hydroxybutyrate

A

ketone bodies, three conditions when the brain can use for TCA cycle –> suckling newborn, fasting adult, ketogenic diet adult, hibernation, product of fatty acid break down in the liver mitochondrion

105
Q

ketones + antioxidants + hypothermia

A

common therapy for blood loss, stroke, and cardiac arrest, because it requires 28% less O2 to sustain the brain with ATP

106
Q

case - 4 month old baby, odd eye movements, limb jerking, CSF glucose low (should be 2/3 of plasma glucose), head circumference low

A

mutated glucose transporter in endothelial cells prevents glucose from entering and brain can’t grow, normal diet causes seizures, need to be on ketogenic diet

107
Q

blood brain barrier

A

dye put into veins shows up in all body tissues but brain tissue, dense capillary network, endothelial cells joined by tight junctions, tight junctions promoted by pericytes, astrocyte end feet on capillaries, anything that gets into the brain must go through endothelial cells by crossing the luminal and abluminal membranes and diffusing through the cytoplasm

108
Q

tight junction

A

form blood brain barrier, transmembrane proteins with extracellular loops made of claudin and occludin and junctional adhesion molecules (JAM)

109
Q

paracellular aqueous pathway

A

not a usual pathway into the brain by water soluble agents due to blood brain barrier, through tight junction

110
Q

transcellular lipophilic pathway

A

rare pathway into the brain across enodothelial membrane by lipid soluble agents, ex: steroids, alcohol, and drugs of abuse

111
Q

transport protein pathway

A

common way into the brain, transport proteins move glucose, amino acids, and nucleosides

112
Q

monocarboxylate transporter 1 (MCT1)

A

12 transmembrane segments, moves lactate and H+, pyruvate, acetate, and butyrate during times of exercise and hypoglycemia; moves ketones during times of fasting and ketogenic diets; in membrane of endothelial cells, number of transporters changes based on conditions ex: more in suckling infants and in ketogenic diet adults

113
Q

GLUT1

A

transports glucose via endothelial cells into / out of brain

114
Q

MCT1

A

transports lactic acid and ketone bodies via endothelial cells into / out of brain

115
Q

LAT1

A

transports amino acids vie endothelial cells into / out of brain

116
Q

ENT1, CNT2

A

transports adenosine via endothelial cells into / out of brain

117
Q

FATP1

A

transports fatty acid via endothelial cells into / out of brain

118
Q

CT1

A

transports creatine via endothelial cells into / out of brain

119
Q

aquaporins

A

transport H2O in / out of brain across the epithelium in the choroid plexus

120
Q

p-glycoprotein, Mdr1, Bcrp1

A

12 transmembrane segments, only in lumenal membrane of endothelial cells, efflux transporter, substrate non-specific, pumps xenobiotics back into blood making it hard to treat the brain directly with drugs, ex: erlotinib a tyrosine kinase inhibitor for cancer can enter the brain better in mice that have had efflux transporters knocked out

121
Q

diseases affected by the blood-brain barrier

A

MS, Alzheimer’s, epilipsy, creatine transporter defect, pathogenic infections - when an endothelial cell is dysfunctional all the ones around it are too resulting in neurological disease

122
Q

transcytosis

A

receptor on lumenal surface binds things like insulin and transferin allowing them to be endocytosed into the brain

123
Q

LRP receptor

A

peptide binding protein, allows agent endocytosis into brain across endothelium, drugs linked to a peptide will also be endocytosed, called trojan horse approach

124
Q

immune cell migration

A

immune cells can get into the brain by passing through endothelial cells, called diapedesis, happens in response to chemokines that are released by MS (is an autoimmune disease), stroke, TBI - could be used as a form of brain immunotherapy to target cancer cells

125
Q

formation of blood brain barrier

A

forms in first few weeks of embryonic development, neuropil expresses Wnt which causes endothelial cells to migrate into neuropil and establish vasculature

126
Q

blood-CSF barrier in choroid plexus

A

blood vessels in choroid plexus are leaky and the epithelial cells tight junctions, has aquaporins, Na+ and H+ inverse transporter, and bicarbonate and Cl- reverse transporter are all on the ECF side of the choroid plexus, Na+ / K+ / and 2 Cl- ATPases on CSF side move ions into CSF, aquaporins move H2O into CSF, ions and bicarbonate make CSF high osmolarity so water follows, bicarbonate is also made by carbonic anhydrase in epithelial cell, there are also nutrient transporters but not as key as in blood-brain barrier

127
Q

neurons

A

transmit impulses

128
Q

astrocytes

A

CNS - react to injury, create blood brain barrier, many cellular extensions, large spotted nucleus

129
Q

oligodendrocytes

A

CNS - produce myelin, dark small nucleus

130
Q

microglia

A

CNS - phagocytize intruders, elongated squished nucleus

131
Q

ependymal cells

A

CNS - line ventricles in single layer, have cilia

132
Q

acute injury

A

neuron reaction to injury, red = dead, often from lack of blood flow, cells not as plump

133
Q

subacute / chronic injury

A

neuron reaction to injury, like degeneration - neurons seem to disappear

134
Q

axonal reaction

A

neuron reaction to injury, axonal spheroids from swelling, trying to make proteins to fix things

135
Q

inclusions

A

neuron reaction to injury, can be viral or degenerative, Cowdry A, Negri,

136
Q

Cowdry A inclusion

A

red center, white halo, basophilic ring, viruses in cell, herpes

137
Q

Negri body

A

eosinophilic circle in cell body with sharp edges, seen with rabies

138
Q

neurofibrillary tangles

A

Alzheimer’s cell dying, dark lines

139
Q

Lewy body

A

pink circle, fuzzy edges, Parkinson’s

140
Q

gliosis

A

accumulation of astrocytes after injury, “scar” in CNS, astrocytes are numerous and bigger

141
Q

gemistocytic astrocytes

A

astrocytes that look big, plump, pink - reacting

142
Q

rosenthal fibers

A

long eosinophilic astrocyte processes where there has been longterm gliosis

143
Q

corpora amylacea

A

degenerative change, aging, carbohydrates in round purple cells

144
Q

microglia

A

proliferate, long nuclei, form nodules around dead cells, necrosis, bacteria, infection, and injury

145
Q

nerve reaction to axon transection

A

distal nerve function lost –> resealing of cut axons (hours), retrograde and anteretrograde transport stops

146
Q

retrograde transport in cut axon

A

transport up axon to cell body stops

147
Q

anteretrograde transport in cut axon

A

distal stump Wallerian degeneration, rapid fragmentation after 2-3 day latent phase, myelin disintegrates, macrophages and Schwann cells removel remnants in PNS only, neuron chromatolysis, target cell atrophy

148
Q

PNS axon regeneration

A

Schwann cells redifferentiate, proliferate, and release factors that stimulate axon regrowth and recruit macrophages, increased expression of growth related genes in neurons like GAP43, axon cuts in PNS prime CNS for repairing axon cuts, connective tissue forms supportive bridge (more with crush, less with cut), lack of axonal growth inhibitors that are present in CNS, strength and sensation a little reduced because axons don’t hit target perfectly - can form traumatic neuroma, 2-4mm/day with crush

149
Q

CNS axon regeneration

A

more limited, aborted after 1 month, myelin produces inhibitors of axon growth (nogoA and myelin associated glycoprotein MAG), oligodendrocytes don’t clean up myelin and macrophages are hard to recruit, astrocyte proliferation forms glial scar that produces inhibitory chondroitin sulfate proteoglycan CSPG, CNS neurons have receptors for inhibtors and change gene expression not favoring plasticity

150
Q

CNS plasticity in adults

A

neurogenesis in two regions - hippocampus and olfactory nerves

151
Q

strategies to promote axonal regeneration in CNS

A

neutralize myelin inhibitors (nogoA and MAG), enzyme chondoitinase degrades CSPG from glial scar, enhance growth signaling pathway by increasing cAMP

152
Q

strategies to promote cell replacement in CNS

A

growth factors to recruit progenitor cells, transplant embryonic stem cells or induced pluripotent stem cells, transplant supportive cells like oligodendrocytes

153
Q

strategies to promote CNS plasticity

A

remaining axons can sprout new connections or increase synaptic strength, Tx to increase plasticity = chondroitinase to inhibit CSPG and physical therapy

154
Q

critical period in brain plasticity

A

up to 5 years old, ends with maturation of inhibitory neurons like GABA neurons and effects of CSPG

155
Q

two sources of skull embryologically

A
  1. paraxial mesoderm –> occipital somites –> base of skull, 2. neuroectoderm –> neural crest –> mesenchyme in pharyngeal arches –> bones of face and skull
156
Q

somitomeres

A

somites 1-7, from paraxial mesoderm, contribute to head myotome, neuromere, and sclerotome

157
Q

embryological head

A

derived from somitomeres 1-7 and occipital somites 1-4

158
Q

neurocranium

A

brain case, forms around rostral end of neural tube, neural tube induced, cartilaginous and membranous ossicifcation

159
Q

viscerocranium

A

face, taste / sight / smell organs, forms around gut tube rostral to notochord

160
Q

cartilaginous (endochondral) ossification in neurocranium

A

ethmoid, sphenoid, occipital base, petrous temporal, temporal-mastoid; skull base

161
Q

intramembranous ossification in neurocranium

A

flat bones - parietal, frontal, squamous occipital; occurs in a radial pattern

162
Q

bones of skull from neural crest (pharyngeal arch) mesenchyme

A

frontal, squa. temporal, sphenoid, bones of face, hyoid

163
Q

bones of skull from paraxial mesoderm (somites / somitomeres) mesenchyme

A

pet. temporal, occipital, parietal

164
Q

bones of skull from lateral plate mesoderm mesenchyme

A

laryngeals

165
Q

cartilaginous (endochondral) ossification in viscerocranium

A

malleus, incus, stapes, hyoid, styloid, temporal

166
Q

membranous ossification of bones in viscerocranium

A

premaxilla, maxilla, zygomatic, squamous temporal, mandible; form from mesenchyme in pharyngeal arches

167
Q

pharyngeal arches

A

mesenchymal cells migrate from neural crest

168
Q

newborn skull

A

1/4 of body length, becomes less with age

169
Q

newborn skull sutures

A

frontal / metopic, coronal, sagittal, lambdoid - dense connective tissue

170
Q

newborn skull fontanelles

A

anterior (becomes bregma), posterior (becomes lambda), posterolateral / mastoid, anterolateral / sphenoidal

171
Q

skull molding

A

overlapping of skull bones at sutures during birth, returns to normal in 24 hours

172
Q

frontal / metopic suture

A

begins closing at 2 years, done closing by 8 years

173
Q

changes to developing skull after birth

A

brain and cranial vault growth (midline moves from brow to center of eyes), growth of sinuses, eruption of teeth, growth of mandible

174
Q

CT without contrast

A

good for blood and bone imaging of head, sensitive to fine fractures (over x-ray),contrast turns things white and blood looks white = bad

175
Q

MRI

A

good for imaging brain itself, tumors, abcesses, etc.

176
Q

imaging contrast

A

avoid using in pt with renal failure and in pt with possible brain bleed (can’t see blood)

177
Q

retrograde

A

traveling up an axon toward neuronal cell body

178
Q

anteretrograde

A

traveling from neuronal cell body to axon terminal