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STEP 1 (3) > Neurology- Anatomy and Physiology > Flashcards

Neurology- Anatomy and Physiology Flashcards

1
Q

Describe neurons

A

these are the signal-transmitting cells of the nervous system. They are permanent, and do not divide in adulthood.

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2
Q

What are functional parts of neurons?

A

dendrites (receive input), cell bodies, and axon (send output)

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3
Q

Cell bodies and dendrities can be seen on what?

A

Nissle staining (stains RER)

NOTE: RER is not present in the axon so cant be seen this way

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4
Q

What is Wallerian degeneration?

A

injury to an axon causes degeneration distal to the injury and axonal retraction proximally; allows for potential regeneration of axon (if in PNS)

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5
Q

What is this and what are its roles?

A

Astrocyte- phsyical support; repair; K+ metabolism; removal of excess neurotransmitters; component of BBB; glycogen fuel reserve buffer

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6
Q

What is the main astrocyte marker?

A

GFAP

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7
Q

What are microglia?

A

phagocytic scavenger cells of the CNS activated in response to tissue damage

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8
Q

What is the role of myelin?

A

it increases the space constant and conduction velocity of signals transmitted down axons, with saltatory conduction of action potentials at the nodes of Ranvier, where there are high conc of Na+ channels

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9
Q

Each Schwann cell myelinates ___ PNS axon

A

only 1

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10
Q

Schwann cells may be injured in what disease?

A

Guillain-Barre syndrome

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11
Q

What is acoustic neuroma?

A

a type of schwannoma, typically located in the internal acoustic meatus (CN VIII).

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12
Q

BILATERAL acoustic neuroma is strongly associated with what?

A

neurofibromatosis type II

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13
Q

What do olgiodendroglia do?

A

myelinate axons of neurons in the CNS. Each oligodendrocyte can myelinate many axons (~30). This is the predominant type of glial cell in white matter

Below: “fried egg” appearance

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14
Q

Oligodendrocytes can be injured in what diseases?

A

MS, progressive multifocal leukoencephalopathy (PML), and leukodystrophies

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15
Q

What are the main types of sensory receptors?

A
  • free nerve endings
  • Meissner corpuscles
  • Pacinian corpuscles
  • Merkel discs
  • Ruffini corpuscles
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16
Q

What are the types of free nerve endings?

A

C-slow, unmyelinated fibers

A(delta)- fast, myelinated

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17
Q

What do free nerve endings sense?

A

pain and temp

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18
Q

Meisnner and Pacinian corpuscles and Merkel discs are all described as ‘large, myelinated fibers that adapt quickly. Where are Meissner corpuscles found?

A

glabrous (hairless) skin

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19
Q

Meisnner and Pacinian corpuscles and Merkel discs are all described as ‘large, myelinated fibers that adapt quickly. Where are Pacinian corpuscles found?

A

deep skin layers, ligaments, and joints

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20
Q

Meisnner and Pacinian corpuscles and Merkel discs are all described as ‘large, myelinated fibers that adapt quickly. Where are Meckel discs found?

A

fingers tips and superficial skin

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21
Q

What do Meissner corpuscles sense?

A

dynamic fine/light touch, position sense

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22
Q

What do Pacinian corpuscles sense?

A

vibration and pressure

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23
Q

What do Meckel discs sense?

A

pressure, deep static touch (e.g. shapes, edges), position sense

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24
Q

What are Ruffini corpuscles?

A

dendritic endings with capsules, adapt slowly

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25
Where are Ruffini corpuscles found and what do they sense?
finger tips and joints and sence pressure, slippage of objects along the skin, and joint angle change
26
What are the protective layers around nerves?
Endoneurium (invest singulr nerve fibers) Perineurium (surrounds a fascicle of nerve fibers) Epineurium (dense CT that surrounds the entire nerve)
27
What neurotransmitter levels change in anxiety?
nor elevated 5-HT, GABA decreased
28
What neurotransmitter levels change in depression?
nor, dopamine, 5-HT decreased
29
What neurotransmitter levels change in Huntington disease?
dopamine elevated ACh, GABA decreased
30
What neurotransmitter levels change in Parkinson's?
dopamine decreased ACh elevated
31
What neurotransmitter levels change in Alzheimer?
ACh decreased
32
Where is nor made in the brain?
locus ceruleus (pons)- activated in states of stress and panic
33
Where is dopamine made in the brain?
ventral tegmentum and substantia nigra pars compacta (midbrain)
34
Where is nor made in the 5-HT?
raphe nuclei (pons, medulla, and midbrain)
35
Where is ACh made in the brain?
Basal nucleus of Meynert
36
Where is GABA made in the brain?
nucleus accumbens- the 'reward' center, activated in pleasure, **addiction**, and fear
37
What forms the BBB?
- tight junctions between nonfenestrated capillary endothelial cells - BM - Astrocyte foot processes
38
What are some other notable barriers in the body?
- blood-testes - maternal-fetal bloof barrier of the placenta
39
Notes about the BBB
40
Do any parts of the brain lack a BBB?
A few specialized brain regions have fenestrated capillaries and no BBB to alow molecules in blood to affect brain function (e.g. vomiting after chemo; OVLT- osmotic sensing) or neurosecretory products to enter circulation (e.g. ADH)
41
What are the main functions of the hypothalamus?
**TAN HATS** **T**hirst and water balance **A**denohypophysis control (regulates anterior pituitary) **N**eurohypophysis **H**unger regulation **A**utonomic regulation **T**emp regulation **S**exual urges
42
What are the inputs from the brain to the hypothalamus that dont have BBB?
OVLT (organum vasculosum of the lamina terminalis- senses changes in osmolarity) area postrema (responds to emetics)
43
What part of the hypothalamus makes ADH?
supraoptic nucleus
44
What part of the hypothalamus makes oxytocin?
paraventricular nucleus
45
What does the lateral area of the hypothalamus do?
promotes hunger (destruction= anorexia, failure to thrive)
46
The action of the lateral area of the hypothalamus cna be inhibited by what?
leptin
47
What does the ventromedial area of the hypothalamus do?
promotes satiety (stimulated by leptin)
48
What does the anterior hypothalamus do?
promoting body cooling and parasympathetic action
49
What does the posterior of the hypothalamus do?
heating and sympathetic
50
What does the suprachasmatic nucleus of the hypothalamus do?
regulates circadian rhythm
51
What regulates sleep?
Circadian rhythm, which is driven by suprachiasmatic nucleus (SCN) of the hypothalamus. Circadian rhythm promotes nocturnal release of ACTH, prolactin, melatonin, and nor Basically, light promotes the SCN to release nor which acts on the pineal gland to promote melatonin release
52
What are the stages of sleep?
REM (rapid eye-movement) and non-REM
53
What causes REM?
activity of PPRF (paramedian pontine reticular formation/conjugate gaze center).
54
How frequent is REM sleep?
~every 90 minutes during sleep, with increasing duration as the night continues
55
What things decrease REM sleep?
alcohol, benzodiazepines, barbituites, and nor
56
How can sleep enuresis (bedwetting) be tx?
desmopressin (ADH analog) (preferred over imipramine b/c of less AEs)
57
What is a good tx option for sleepwalking or night terrors?
benzodiazepines
58
What is the predominant EEG waveform seen when awake with eyes open?
Beta (highest frequency, lowest amplitude **B**ATS Drink Blood
59
BATS Drink BloodWhat is the predominant EEG waveform seen when awake with eyes shut?
Alpha B**A**TS Drink Blood
60
What are the stages of non-REM sleep?
N1 (5%)-light sleep N2 (45%)-deeper, when bruxism (teeth-grinding) occurs N3 (25%)-deepest, slow-wave sleep; when sleepwalking, night terrors, and betwetting occur
61
What is the major EEG waveform in N1 sleep? N2? N3?
N1: theta N2: Sleep spindles and K complexes N3: Delta (lowest frequency; highest amplitude) BA**TS D**rink Blood
62
How much of the night is spent in REM sleep?
25%
63
What things occur in the body during REM sleep?
loss of motor tone, increased brain O2 use, varibale pulse and BP
64
What waveforms are seen during REM sleep?
Beta BATS Drink **B**lood
65
What is the major location for relay of all ASCENDING sensory info except olfaction?
the thalamus
66
What are the five major nuclei of the thalamus?
VPL VPM LGN MGN VL
67
What is the input into the VPL of the thalamus?
spinothalamic and dorsal columns medial lemniscus
68
What info does the VPL of the thalamus process?
pain, temp, pressure, touch, vibration, and proprioception
69
Where does info into the VPL and VPM of the thalamus go to?
primary somatosensory cortex
70
What is the input into the VPM of the thalamus?
trigeminal and gustatory pathways
71
What info does the VPM preceive?
face sensation, and taste
72
What is the input into the LGN of the thalamus and where does it transmit to?
from CN II to the calcarine nucleus
73
What info does the LGN of the thalamus perceive?
vision
74
What is the input into the MGN of the thalamus and where does it transmit?
input via the superior olive and inferior colliculus of the tectum to the auditory cortex of the temporal lobe
75
What info does the MGN of the thalamus perceive?
hearing
76
What is the input into the VL of the thalamus and where does it transmit?
input via the basal ganglia and cerebellum to the motor cortex transmitting **motor function**
77
What is the limbic system?
a collection of neural structures involved in emotion, long-term memory, olfaction, behavior modulation, and ANS function
78
What structures are included in this limbic system?
hippocampus, amygdala, fornix, mammillary bodies, and the cingulate gyrus
79
What is the Limbic system responsible for?
**the 5 F's**: **F**eeding, **F**leeing, **F**ighting, **F**eeling, and **F**ucking
80
What are the symptoms of osmotic demyelination syndrome (aka central pontine myelinolysis)?
acute paralysis, dysarthria, dysphagia, diplopia, and syncope. Can cause 'locked in syndrome'
81
What causes osmotic demyelination syndrome (aka central pontine myelinolysis)?
massive axonal demyelination in pontine white matter secondary to osmotic changes. Commonly iatrogenic, caused by **overly rapid correction of hyponatremia**
82
While correcting hyponatremia too quickly might lead to osmotic demyelination syndrome (aka central pontine myelinolysis), what might correcting HYPERnatremia too quickly lead to?
cerebral edema/herniation
83
Mnemonic for correcting serum Na+ too fast:
"from low to high, your pons will die" (osmotic demyelination syndrome (aka central pontine myelinolysis)) 'from high to low, your brain will blow' (cerebral edema/herniation)
84
What does the cerebellum do?
modulates movement and aids in coordination and balance
85
What is the input into the cerebellum?
the contralateral cortex via the middle cerebellar peduncle, and ipsilateral priproceptive info via the inferior cerebellar peduncle from the spinal cord
86
Where does info from the cerebellum go?
- contralateral cortex to modulate movement via output nerves called Purkinje cells - deep nuclei
87
How does info get from the cerebellum to the contralateral cortex?
Perkinje cells, to the deep nuclei of the cerebellum to the contralateral cortex via the superior cerebellar peduncle
88
What are the deep nuclei of the cerebellum from lateral to medial?
**D**entate, **E**mboliform, **G**lobose, **F**astigial | ('Dont Eat Greasy Foods')
89
Lateral lesions of the cerebellum can lead to what?
voluntary movement of extremities issues; when injured, there is a propensity to fall toward the injured side
90
Medial lesions of the cerebellum affect what?
lesions involving midline structures (vermal cortex, fatigial nuclei) and/or flocculonodular love can lead to **truncal ataxia (a wide-based cerebellar gait), nystagmus, and head tilting.** Generally, midline lesions reuslt in bilateral motor deficits affecting axial and proximal limb musculature
91
What are the roles of the basal ganglia?
voluntary movements and making posterual adjustments It receives corticol input and provides negative feedback to the cortex to modulate movement
92
What is the excitatory pathway of the basal ganglia?
Corticol input stimulates the striatum (putamen (motor) + caudate (cognitive)), stimulating the release of GABA, which disinhibits the thalamus via the GPi/SNr (increasing motion) Modulator: **D1** Dopamine binding (aka direct pathway)
93
What is the inhibitory pathway of the basal ganglia?
corticol input stimulates the striatum, which disinhibits the STN (Subthalamic nucleus) via the GPe (globus pallidus externus), and STN stimulates GPi (globus pallidus internus)/SNr to inhibit the thalamus (decreasing motion) Modulator: **D2** Dopamine binding (aka indirect pathway)

STEP 1 (3) (16 decks)

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