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Neuroendocrine > Neuro Test 2 > Flashcards

Neuro Test 2 Flashcards

1
Q

What are common clinical findings for lower motor neuron (anterior horn) paralysis?

A

Atonia, areflexia, fasciculation, and flaccid paralysis.

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2
Q

What tract contains upper motor neurons?

A

The corticospinal tract.

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3
Q

What are common clinical findings for a CST lesion?

A

Contralateral spastic hemiplegia, hyperreflexia, hypertonia, paralysis, and disuse atrophy

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4
Q

What resulted in supranuclear facial palsy?

A

Unilateral lesions of the uncrossed corticobulbar tract results in contralateral supranuclear facial palsy.

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5
Q

Where do corticobulbar fibers decussate?

A

In the lower pons and descend in the lower brainstem as crossed CBT.

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6
Q

What does a lesion in the crossed CBT result in?

A

Ipsilateral cranial nerve palsies.

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7
Q

What part of the internal capsule do corticobulbar fibers pass through?

A

Genu

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8
Q

Where does the corticospinal tract decussate?

A

In the medulla at the base of the pyramids

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9
Q

What is another name for a serotonin receptor?

A

5HT

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10
Q

What are the main serotonin receptors and the specific role for each of them?

A

5HT3 - Area postrema
5HT6 - Anti-depressant effect
5HT7 - Limbic system

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11
Q

What does a vesicular ACh transporter protein (VAChT) do?

A

Moves ACh into the vesicle

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12
Q

What does diamine oxidase do?

A

Catabolizes histamine

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13
Q

What does monoamine oxidase do?

A

Catabolizes epi, norepi, dopamine, and serotonin

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14
Q

What does acetylcholinesterase do?

A

Binds to the post-synaptic cell membrane and removes ACh from the synaptic trough

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15
Q

Where is norepinephrine found and what is its role?

A

Locus ceruleus and other pontine/medullary areas.

It is important in wakefullness/alertness

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16
Q

Where is epinephrine found and what is its role?

A

Medulla

Its role is modulatory

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17
Q

What is the amino acid is responsible for creating epinephrine?

A

Tyrosine

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18
Q

What are the stages forming epi from tyrosine?

A

Tyrosine –(Tyrosine hydroxylase(RLS), cytoplasm)–> L-DOPA –(cytoplasm)–> Dopamine –(Vesicle)–> norepinephrine –(PNMT, Outside of vesicle)–> epinephrine

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19
Q

What inhibits ACh transport into vesicles?

A

Reserpine

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20
Q

What helps transports norepi into the vesicle?

A

VMAT

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21
Q

Where is dopamine found and what role does it play in these specific locations?

A

Basal Ganglia - motor control
Hypothalamus and limbic system - Endocrine and emotional control
Cortex

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22
Q

What are the 5 receptor types for dopamine and what do they do?

A

D1 and D5 - Increase cAMP
D2 - decrease cAMP which leads to a potassium efflux
D3 and D4 - decrease cAMP

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23
Q

Where is serotonin (5HT) found and what role does it play in these specific locations?

A

Hypothalamus and limbic system - Mood
Cerebellum - Modification of motor activity
Brainstem Raphe nucleus - Modification of motor and sensory activity)

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24
Q

What amino acid is serotonin derived from?

A

Tryptophan

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25
Q

What enzyme turns tryptophan into serotonin?

A

Tryptophan hydroxylase

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26
Q

Where do you find histamine and what is its role in this location?

A

Tuberomammillary nucleus of the hypothalamus - Wakefulness

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27
Q

How is histamine made?

A

Histadine –(Histidine decarboxylase)–> Histamine

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28
Q

What are the different groups of histamine receptors and what do they do?

A

H1: PLC activation (involved in wakefulness)
H2: Increases cAMP (associated with gastric acid release)
H3: presynaptic, decrease histamine release

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29
Q

What are GABAs major roles?

A

Consciousness, motor control, and vision (retina)

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30
Q

How is GABA made?

A

Glutamate –(glutamate decarboxylase)–> GABA

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31
Q

What are VGAT and GAT?

A

Vesicle GABA transporter - transports GABA into the vesicles
GAT - GABA transporter - removes GABA from synapse
- GAT1 - on the presynaptic terminal
- GAT2 - on glial cells surrounding the synapse

32
Q

What type of receptor is a GABA A receptor?

A

Ionotropic (Cl conductance)

33
Q

What does GABA A receptor activate?

A

IPSP

34
Q

Where are a lot of GABA A receptors found and what are they used for?

A

Large number of extra-synaptic GABA A receptors that are believed to be the site of action for a number of general anesthetics including Propofol.

35
Q

What type of receptors are GABA B receptors?

A

Metabotropic - Gi/Go activate K+ channel and inhibit Ca++ channel

36
Q

Where is Glycine found?

A

Spinal cord, brainstem

37
Q

What type of receptor is glycine?

A

Ionotropic - chloride -> influx of chloride leading to IPSP

38
Q

What do lesions to the MCA produce?

A

Tactile loss over the contralateral upper body and face

39
Q

What do lesions of the ACA produce?

A

Tactile loss of the contralateral lower limb

40
Q

What artery supplies the VPL and VPM?

A

Thalmogeniculate branches of the posterior cerebral artery.

41
Q

What artery supplies the spinal trigeminal nucleus?

A

PICA

42
Q

What artery supplies the principle sensory nucleus for the trigeminal nerve?

A

Superior cerebellar artery and long circumferential branches of the basilar artery.

43
Q

What Is lateral medullary syndrome?

A

An occlusion of PICA or branches of PICA

44
Q

What sx are present in medullary syndrome?

A

CL loss of pain and thermal sense on body (ALS), Ipsilateral loss of pain and thermal sense on face and in the oral cavity (spinal trigeminal tract/nucleus), dysphagia, soft palate paralysis, hoarseness, diminished, gag reflex (nucleus ambiguus, roots CN IX/X), Ipsilateral Horner syndrome (hypothalamospinal fibers), Nausea, diplopia, tendency to fall to upsilateral side, nystagmus (vestibular nuclei), Ataxia to the ipsilateral side (restiform body, spinocerebellar fibers)

45
Q

What does a syringomyelia damage and what symptoms are present?

A

Damage to ALS and anterior horn. Results in loss of pain and temperature over her arms, shoulders, upper chest, and upper back. There is also weakness, atrophy, and fasciculations of muscles.

46
Q

What sx are associated with Wallenburg Syndrome?

A

CL loss of pain and thermal sensation.

47
Q

What is another name for Wallenburg Syndrome?

A

Lateral medullary syndrome.

48
Q

What are the sx associated with lateral pontine syndrome?

A

CL loss of pain and thermal sensation.

49
Q

What is hypersensitivty?

A

An increased response to nociceptive neurons to their normal input.

50
Q

What is hyperaesthesia?

A

Increased sensitivity to stimulation not special senses.

51
Q

What is hyperalgesia?

A

Increased pain from something that normally evokes pain.

52
Q

What is allodynia?

A

Pain due to stimulus does not normally cause pain (e.g. sun burn)

53
Q

What type of motorneuron innervates the intrafusal muscle fibers?

A

Gamma motorneuron

54
Q

What fiber goes to the spinal cord go to the golgi tendons?

A

1b fibers

55
Q

What are key indicators of Brown-Sequard syndrome?

A

The combination of weakness on one side and a loss of pain sensation on the opposite side.

56
Q

What are the main differences between lateral medullary and lateral pontine syndrome?

A

PICA and dysphagia in LMS

AICA and facial involvement in LPS

57
Q

What do the pharyngeal arches become?

A

Arch 1 - CN V - muscles of mastication
Arch 2 - CN VII - muscles of facial expression
Arch 3 - CN IX - Stylopharyngeus muscle
Arch 4 - CN X - muscles of the pharynx, larynx, and upper esophagus

58
Q

What are the vestibular nuclei related to?

A

Balance, equilibrium, and control of eye movement

59
Q

What is another name for lateral medullary syndrome?

A

Wallenburg syndrome

60
Q

What does the AICA supply?

A

Lateral and inferior cerebellar surface and pons

61
Q

What does the superior cerebellar artery supply?

A

Superior surface and much of the cerebellar nuclei and midbrain

62
Q

What does the posterior spinal artery supply?

A

The posterior columns and their nuclei

63
Q

Where do fibers from the posterior columns decussate?

A

In the internal arcuate fibers within the medulla

64
Q

What does the PICA supply?

A

The lateral area of the medulla that contains the ALS, spinal trigeminal tract, and the nucleus ambiguus.

65
Q

What does the posterior spinal artery supply?

A

The posterior column nuclei in the medulla.

66
Q

What does the anterior spinal artery supply?

A

The pyramid, medial lemniscus, and exiting roots of the hypoglossal nerve.

67
Q

Collateral fibers from which brainstem nuclei enter the trigeminal motor nucleus to initiate the motor response?

A

Mesencephalic

68
Q

What is a Rinne test?

What makes it positive or negative?

A

Application of a tuning fork to the mastoid process and then putting the tuning fork next to the external ear once the patient can no longer hear the sound conducted through the mastoid process.

The test is positive if the patient is able to hear the sound through the mastoid process and then again once the fork is held at the external ear.

The test is negative if the sound is not able to be heard in the external ear after hearing the sound in the mastoid process.

This is a way to test hearing loss by testing bone conduction with air conduction.

69
Q

What is Weber’s test?

A

You place the tuning fork on to of the head at the midline and ask the patient if they hear the sound better on either side or hear it right in the middle.

This is a way to test hearing loss.

70
Q

What type of cells are vestibular receptors?

A

Neuroepithelial cells?

71
Q

What is the main ganglion associated with the vestibular system and what types of neurons are associated with it?

A

Vestibular (Scarpa’s) Ganglion

Bipolar Neurons

72
Q

What is the Romberg test and what is it testing for?

A

It is where the patient stands up and closes their eyes and tries to remain still. This test is to see if there is a possible vestibular injury/lesion resulting in sensory ataxia. A positive test will result in the patient falling or them unable to maintain balance while trying to stand with their eyes closed.

If the patient is ataxic but has a negative Romberg test, this could suggest cerebellar ataxia.

73
Q

What are some visceral symptoms of a vestibular system disturbance and what sends these signals?

A

Nausea, vomiting, and pallor sent from disturbances in the reticular formation.

74
Q

What is INO, how does it develop and what are the signs?

A

INO is internuclear ophthalmoplegia. It results from a unilateral lesion of the MLF superior to the abducens nerve. It results in a contralateral disturbance of horizontal gaze. For example, if there is a right lesion, looking left will cause inability to adduct the right eye and nystagmus of the left eye; looking to the right would be normal for both eyes (named Right INO). Accommodation is still in tact (able to cross eyes). INO is named for the side that the eye cannot ADduct.

75
Q

What does the paramedian pontine reticular formation include?

A

Lateral gaze center.

76
Q

What does a lesion to the PPRF cause?

A

Inability to perform horizontal gaze to the SAME side of the lesion.

Neuroendocrine (8 decks)

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