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Spring Semester 2014 > Med Neuro > Flashcards

Med Neuro Flashcards

1
Q

What does the anterior choroidal artery supply? (2)

A
  1. Choroid plexus

2. Hippocampus

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2
Q

What does the ACA supply?

A
  1. Anterior frontal lobe
  2. Medial aspect of the hemisphere
  3. Medial cortex - medial aspect of motor/sensory strip
  4. Basal ganglia
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3
Q

What main branch does the MCA give off and what does it supply?

A
  1. Lenticulostriate

2. Basal ganglia, internal capsule, and thalamus

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4
Q

What fissure does the MCA run through?

A

The lateral fissure of Sylvius

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5
Q

What does the MCA supply

A

Many deep and lateral structures of cerebrum

  1. Speech and language
  2. Swallowing
  3. Lateral motor and sensory strip
  4. Broca’s and Wernicke’s area
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6
Q

What does the anterior spinal artery supply?

A
  1. Medial medulla (medullary pyramids)

2. Anterior 2/3 of cervical spinal cord

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7
Q

What does the basilar artery supply? (3)

A
  1. Thalamus
  2. Midbrain
  3. Pons
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8
Q

What does the PCA supply?

A
  1. Occipital lobe
  2. Choroid plexus of 3rd and lateral v.
  3. Lower surface of temporal lobe
  4. Midbrain
  5. Thalamus
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9
Q

What else does the posterior inferior cerebellar supply?

A
  1. Cerebellum and

2. Lateral rostral medulla

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10
Q

What does a stroke in the PCA look like?

A
  1. Sense of smell
  2. Cranial nerve damage
  3. Visual problems
  4. Visual agnosia, hemianopsia and alexia
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11
Q

What does AICA supply?

A
  1. Inferior cerebellum

2. Lateral caudal pons

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12
Q

What does the superior cerebellar supply?

A
  1. Superior cerebellum
  2. Parts of midbrain
  3. Lateral pons
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13
Q

What do the internal auditory/labyrinthine arteries supply?

A

Inner ear

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14
Q

Where does the pericollosal artery run?

A

Curves across the corpus collosum in the collosal sulcus

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15
Q

Where does the collosamarginal artery run?

A

Follows the cingulate sulcus

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16
Q

What are two branches of the ACA?

A
  1. Pericollosal

2. Collosamarginal

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17
Q

What do the posterior communicating arteries supply?

A
  1. Optic chiasm
  2. Thalamus
  3. Parahippocampal gyrus
  4. Interpenduncular region
  5. Crus cerebri
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18
Q

Peripheral nerve regeneration requires _________.

A

Laminin

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19
Q

Schwann Cell growth promoting factors (3)

A
  1. Laminin
  2. NgCAM/L1 - cell adhesion
  3. NGF - maybe
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20
Q

Oligodendrocyte axonal inhibitors (4)

A
  1. Central myelin
  2. MAG
  3. NI-35
  4. Nogo gene & proteins
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21
Q

Ependymal cells have _____________, not tight junctions.

A

Desmosomes

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22
Q

Both Schwann cells and oligodendrocytes have ______ and ______, while only oligodendrocytes have _______.

A
  1. MBP
  2. MAG
  3. MOG
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23
Q

MBP is a major structural protein of CNS and PNS, located on the cytoplasmic face of myelin membrane or the _______________.

A

Major dense line

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24
Q

______ is a CNS autoimmune disease target - experimental allergic encephalomyelitis.

A

MBP

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25
Q

____ is on the surface of oligodendrocytes and is a target antigen in autoimmune aspect of CNS demyelinating diseases.

A

MOG

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26
Q

PNS nodes are ________, and CNS nodes are ________.

A
  1. Covered by schwann cell cytoplasm

2. Bare

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27
Q

At the nodes of Ranvier the _____________ is exposed to the extracellular environment.

A

Axolemma

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28
Q

Axon branching (collaterals) occur at ________________.

A

Nodes of Ranvier

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29
Q

Clefts of incisures are split between _________________.

A

Major dense lines

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30
Q

Dendrites experience both ___________ and __________ summation.

A
  1. Temporal

2. Spatial

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31
Q

Summation and length constant are __________ properties of neurons.

A

Passive (cable)

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32
Q

Length constant

A

The distance over which the potential falls by 63% of its original value

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33
Q

Active (Action Potential) properties of neurons

A
  1. Threshold
  2. All or none
  3. Latency
  4. Refractory Period
  5. Propagation
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34
Q

Latency

A

Time form onset of initial depolarization to the onset of action potnetial

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35
Q

Threshold

A

Reaching it causes majority of Na channels to open - more Na open - larger depol

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36
Q

Absolute refractory period

A

No AP - due to “inactive” Na channles

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37
Q

Relative refractory period

A

AP can be generated - but difficult - need more stimulus

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38
Q

AP propagation is _____________.

A

Unidirectional

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39
Q

Speed of propagation is determined by the ________________.

A

Length constant

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40
Q

The length constant can be increased by (2)

A
  1. Increasing the diameter of the neuron - reduce longitudinal resistance
  2. Myelination - Increasing the resistance of the axonal membrane
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41
Q

Hyperkalemic periodic paralysis

A

Cells are depolarized - can’t fire AP

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42
Q

What causes hyperkalemic periodic paralysis?

A

Mutation of voltage gated Na - can’t open or close - stuck as “inactive”

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43
Q

What does TTX (pufferfish) block?

A

Na channels of peripheral nerves

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44
Q

Active zones are a _______________ specialization.

A

Pre-synaptic

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45
Q

5 characteristics of Grey’s Type 1 Synapse

A
  1. Asymmetric
  2. Round
  3. Wide cleft
  4. Prominent PSD
  5. Excitatory
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46
Q

5 characteristics of Grey’s Type 2 Synapse

A
  1. Symmetric
  2. Flat
  3. Narrow cleft
  4. Less prominent PSD
  5. Inhibitory
47
Q

3 characteristics of monoaminergic synpases

A
  1. Dense-core vesicles
  2. Axonal varicosities
  3. Wide clefts and no PSDs
48
Q

Peptidergic Synapse characteristic

A
  1. Large dense-core vesicles
49
Q

Myasthenia Gravis

A

Autoimmune - destroys ACh receptors (nicotinic)

50
Q

How do you treat myasthenia gravis

A

AChE inhibitors

51
Q

Approach

A
  1. Synthesis of NT, channel proteins, and vesicles delivered to presyn. site
  2. AP propagated
52
Q

Attach

A
  1. Dephos’d synapsin 1 anchors vesicles to cytoskel
  2. Phos’d synapsin 1 releases vesicles from cytoskel
  3. RAB 3A helps propel vesicles to active zone
53
Q

Docking

A
  1. NSF (ATPase), SNAP and SNAREs help with vesicle membrane and presyn membrane interaction
  2. v-SNAREs bind to t-SNAREs - mediates fusion of vesicular membrane
54
Q

Fusion

A
  1. Ca dependent

2. Ca binds to synpatotagmin on the vesicle membrane to trigger rapid fusion

55
Q

Fusion is ____ dependent

A

Ca

56
Q

Fission (Opening)

A
  1. Nt released by exocytosis

2. Diffuse across cleft

57
Q

What triggers rapid fusion

A

Ca binding to synptotagmin

58
Q

Collapse and Retrieval

A
  1. Postsyn cell response w/ slow graded potentials/AP

2. termination of NT action by diffusion, AChE, negative feedback, reuptake

59
Q

4 ways NT action is terminated

A
  1. Diffusion
  2. AChE
  3. Negative feedback
  4. Reuptake
60
Q

Properties of chemical transmission (5)

A
  1. Amplification
  2. Plasticity
  3. Diversity (plurichem, chemical coding)
  4. Neuromodulation (neuropeptides)
  5. Synaptic delay
61
Q

Steps in NO/CO transmission

A
  1. Activation of nNOS with Ca/calmodulin and NADPH
  2. NO binds heme in guanylate cyclase
  3. cGMP made
  4. Altered gating of ion channels in postsyn
  5. Inactivation/removal of NO (spontaneous)
62
Q

Does glutamate cross the BBB?

A

No

63
Q

How is glutamate synthesized?

A
  1. Major - recycled from Gln in astrocytes using glutamate/glutamine synthase and glutaminase
  2. Minor - de novo from α-KG via GluDH
64
Q

How is Glu stored?

A

In vesicles via active transport via VGluT

65
Q

How is Glu released

A

Increase in intracellular Ca

66
Q

What inhibits Glu release?

A

Autoreceptors that inhibit release or reduce synthesis

67
Q

How is Glu inactivated?

A

High expression of receptors in astrocytes

Co-transport of Na - 2˚ active transport

68
Q

What are the 4 types Glu receptors?

A
  1. AMPA - conducts Na opens and closes quickly
  2. Kainate - conducts Na
  3. NMDA - conducts Ca - needs glycine cofactor - opens and closes slowly
  4. mGluR
69
Q

NMDA is a ________________ channel

A

High conductance

70
Q

NMDA receptors play a role in (2)

A
  1. Long term potentiation

2. Memory formation and synaptic plasticity

71
Q

Long term potentiation needs

A
  1. Ca

2. NMDA

72
Q

NMDA is almost always found with _____.

A

AMPA

73
Q

Overactive glutaminergic systems occur when _______________ and lead to __________.

A
  1. Brain deprived of O2 or glucose

2. Hyperexcitability (can’t keep Glu low) - seizures

74
Q

What are two examples of overactive glutaminergic disease

A
  1. Huntingtons

2. Amyotrophic lateral sclerosis (ALS)

75
Q

What does receptor does 2-AG bind?

A

Cannabinoid: CB1

76
Q

Where is 2-AG found?

A
  1. Cerebellum
  2. Hippocampus
  3. Amygdala
  4. Limbic cortex
77
Q

How is 2-AG synthesized?

A
  1. Phospholipase C: PIP2 -> DAG and IP3

2. DAG lipase: DAG -> 2-AG (~40%)

78
Q

How and where is 2-AG synthesized?

A

It is made on demand on the postsynaptic side

79
Q

What is the regulated step in 2-AG synthesis?

A

DAP lipase - requires PLC & increase in intracellular Ca

80
Q

How is 2-AG inactivated?

A

Monoacylglycerol lipase: glycerol and arachadonic acid

81
Q

What type of a receptor is CB1and where is it found?

A

GPCR - on the presynaptic nerve terminal

82
Q

What is CB1’s mechanism of action?

A

Inhibits opening of voltage operated Ca channels - inhibits NT release

83
Q

What are 2-AG’s effets

A

Fat, dumb and happy; calm, cool, and collected

84
Q

2-AG is activated by _________ and is also turned on by ____________.

A
  1. Glutamate (modulate)

2. Stress

85
Q

What is the lifetime prevalence of major depression?

A

15%

86
Q

What are risk factors of major depression? (4)

A
  1. 2x more common in women
  2. Family hx
  3. Mean age - 40
  4. Inc. risk after significant relationship loss
87
Q

What is the recurrence risk of MDD?

A

1/3 - never
1/3 - spaced out
1/3 - frequent

88
Q

How long does an episode last?

A

Untreated: 6-12 months
Treated: ~ 2months

89
Q

What are symptoms of major depression? (8)

A
  1. Change in sleep/appetite
  2. Decrease energy
  3. Suicidal
  4. Anhedonia
  5. Decreased concentration/memory
  6. Feeling worthless, helpless, excessive guilt
  7. Irritability/tearfulness
  8. Psychosis?
90
Q

To be considered major depression a patient must exhibit ________________.

A

5 or more symptoms for 2+ weeks

91
Q

What else is on a differential for major depression?

A
  1. Bipolar
  2. Dysthymia - chronic, personality related
  3. Grief
  4. Substance abuse - chronic cocaine depletes catecholamines
  5. Hypothyroidism or adrenal disorder
  6. Stimulant withdrawal
  7. Congestive Heart Failure
  8. Parkinsons, HIV
92
Q

What can depression be misdiagnosed as?

A

Alzheimer’s or dementia

93
Q

What is the suicide risk in patients with MDD?

A

10-15%

94
Q

How do you treat MDD?

A

SSRI, SNRI, tricyclics, MAOIs

95
Q

How is serotonin synthesized?

A
  1. Trp-hydroxylase: Trp -> 5-hydroxyTrp

2. Amino acid decarb: 5-hydroxyTrp -> Serotonin (5-HT)

96
Q

How is serotonin broken down?

A
  1. Monoamine oxidase

2. Aldehyde DH

97
Q

How do SSRI’s function?

A

Block reuptake of serotonin

98
Q

What clinical observation implies there is a 2˚ mechanism to SSRI and MAOI action?

A

There is a 2-8 week delay

99
Q

What is the lifetime prevalence of schizophrenia?

A

1-2%

100
Q

When do females and males tend to present with it?

A

Females: early 20’s
Males: late adolescence

101
Q

What are symptoms of schizophrenia? (8)

A
  1. Delusions
  2. Paranoia
  3. Hallucinations
  4. Disorganized thought process
  5. Blunted affect
  6. Social isolation
  7. Lack of motivation
  8. Anhedonia
102
Q

What doe you need to be considered with schizophrenia?

A
  1. 2 or more of the 5 major categories of systems for a couple weeks
103
Q

What will a person with schizophrenia experience throughout their life/

A
  1. Recurrent psychotic exacerbations
  2. Negative symptoms
  3. 10% suicide risk
104
Q

What is on your differential with schizophrenia? (6)

A
  1. Bipolar mania - more grandiosity in delusions
  2. Substance induced
  3. Depressive - morbid psychotic episodes
  4. Schizoidal PD - hermits - not psychotic
  5. Schizotypal PD - atypical thinking, not quite psychotic
  6. Delirium - seen w/ dementia, hospitalized patients
105
Q

What is the dopamine theory for schizophrenia?

A
  1. Too much in mesolimbic area

2. Too little in mesocortical/prefrontal

106
Q

How do you treat schizophrenia?

A

D2 blockers - treats psychotic - worsens negative symptoms

Atypical: D2/4 blockers, 5-HT blockers

107
Q

What are risk factors for schizophrenia?

A

Genetic - identical twin - 66% chance

108
Q

A watershed area of an artery is _______________.

A

An area where the vascular beds of two arteries overlap

109
Q

What does hemisection of the spinal cord lead to?

A
  1. Loss of fine touch, vibration, and propioception ipsilateral to/below lesion
  2. Loss of pain and temp contra/below lesion
  3. Spastic paralysis ipsi/below lesion
110
Q

Ventral root lesions result in (3)

A
  1. Weakness,
  2. Flaccid paralysis
  3. Atrophy
    - possible autonomic dysfunction
111
Q

Dorsal root lesions result in _______________.

A

Hypothesia or anesthesia

112
Q

If a lesion hits the posterior funiculus what is the result?

A

Ipsilateral loss of fine touch, proprioception and vibration

113
Q

If a lesion hits the lateral corticospinal tract what is the result?

A

Spastic ipsilateral paralysis

114
Q

If a lesion hits the spinothalamic tract what is the result?

A

Contralateral loss of pain, temp and crude touch

Spring Semester 2014 (6 decks)

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