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N542 Physiology > Nervous System > Flashcards

Nervous System Flashcards

0
Q

Nucleus vs. Ganglion

A

Nucleus: neurons in CNS
Ganglion: neurons in PNS

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1
Q

White Matter vs. Grey Matter

A

White matter has high density myelin, few neurons, not metabolic, not much ATP, not too vascularized
Grey matter has high density of neurons and dendrites, highly vascularized, lots of ATP needed, highly metabolic (therefore gets more cerebral blood flow than white matter)

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2
Q

Spinal Cord functions

A

sensory input, reflex circuits, somatic and autonomic motor outputs

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3
Q

Reticular Formation, function and damage leads to what?

A

receives info entering brain stem and spinal cord, filters it
regulates arousal, wakefulness
when damaged, pt in vegetative state

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4
Q

Medulla: function, which cranial nerves, damage causes what?

A

Function: subconscious CV and respiratory, brainstem reflexes, early processing of information such as auditory, gustation, and balance
CN: 8-12
damage: pt unable to regulate vitals

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5
Q

Pons: function, cranial nerve #’s?

A

function: respiratory, urinary, and some CV control, motor of eye, motor/sensory of face (ventral: relay info to cortex, dorsal: taste, sleep, resp)
CN: 5-8

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6
Q

Midbrain: function, CN #

A

function: pain, pupil reflex, eye movement, acoustics, motor coordination (contains substantia nigra)
CN 3-4

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7
Q

What are the two pain centers in the brain?

A

Midbrain and thalamus

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8
Q

Cerebellum: function, CN #

A

function: coordination and equilibrium (input from spinal cord, cortex, inner ear), motor learning, sensory association of language
CN: 8

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9
Q

Thalamus: function, CN #

A

function: relays sensory information to the cortex, attention and consciousness (wakefulness), pain
CN: 2

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10
Q

diancephalon

A

hypothalamus and thalamus

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11
Q

hypothalamus

A

pleasure center of the brain, addiction is a huge problem here
autonomic, endocrine functioning, motivated behavior, circadian rhythms

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12
Q

what part of the brain has the superchiasmic nucleus, and what is this responsible for?

A

superchiasmic nucleus in the hypothalamus is responsible for circadian rhythms

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13
Q

basal ganglia functions?

A

thalamocortical motor inhibition patterns, controlling fine motor movements

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14
Q

amygdala

A

social behavior and emotion

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15
Q

hippocampus

A

memory

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16
Q

cerebral cortex: function and CN#

A

function: in order to work, it is dependent on lower brain to work, personality, learning, language, planning
CN: 1

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17
Q

4 lobes of cerebral cortex and functions

A

Frontal: personality, speech (Broca’s area), planning motor behavior, area that is important with pain tolerance
Parietal: sensory, spacial, Wernicke’s area
Temporal: sound, facial recognition, regulates ANS, emotions (limbic)
Occipital: vision, pupil constriction and accommodation

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18
Q

What part of the Circle of Willis, if occluded, has no collateral flow

A

Middle Cerebral Artery (if this is blocked on left side, Wernicke’s area/ speech comprehension is blocked)

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19
Q

Why is the Artery of Adamkiewicz important?

A

It supplies the lower 2/3 of the cord, it is a reticular artery branch of the aorta, in some procedures, the aorta is clamped, since this artery has no collateral flow, it can damage/paralyze the lower 2/3 of the spinal cord!

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20
Q

In spinal cord blood supply, what is the difference between the anterior and posterior arteries?

A

Posterior arteries have two branches of supply, ventral/anterior only has one, so it is a huge problem if this artery becomes occluded, motor control may be lost (bc ventral=motor and dorsal=sensory)

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21
Q

How much cerebral blood volume do we have (compared to brain tissue)?

A

0.5 mL/ 100 g brain tissue

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22
Q

What can impact blood flow to the brain

A

Artery blockages

Venous blockages, ex: positioning (head on one side, steep trendelemberg, positive flow ventilation, high peaks)

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23
Q

Where is ICP measured and what is the normal value?

A

In the lateral ventricles in the supratentorium space, between occipital lobe and cerebellum
Normal 8-12

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24
Q

Intracranial volume (ICP measurements) is made up of 3 things, and what are the percentages?

A

Brain tissue/ICF 80%
Blood 12%
CSF 8%

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25
Q

Risk of herniation is increased when ICP is increased, what does this do to CPP, and how is MAP involved?

A

CPP decreases, unless you have a high enough MAP to compensate
CPP=MAP-ICP

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26
Q

What is intracranial elastance?

A

Change in ICP from a change in intracranial volume

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27
Q

What are some compensatory mechanisms involving intracranial elastance, when ICP increases?

A
  1. CSF moves from cranial to spinal compartment
  2. increased absorption of CSF (by arachnovilli)
  3. decreased CSF production
  4. decrease cerebral blood volume
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28
Q

What is normal CPP? Why is it important?

A

80-100 mmHg
(MAP-ICP)
This is how much O2 is reaching the brain

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29
Q

What is normal cerebral blood flow in ml/g/min and ml/min

A

50mL/100g/min

750mL/min

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30
Q

Relationship of neuronal activity (metabolism) and CBF

A

Increased metabolic by-products, increased blood flow

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31
Q

Relationship between H+ ions/ CO2 and CBF

Do H+ ions cross the blood brain barrier?

A

Increased CO2 will increase H+ ions (by increasing carbonic acid), and this will increase CBF, vasodilates (we hyperventilate, decrease PCO2, to decrease ICP, decrease CBF)
YES, H+ ions cross the blood brain barrier, this is why messing with a patient’s PCO2, changes pH quickly, but it doesn’t last long

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32
Q

When PCO2 changes by 1 mmHg, what is the EXACT change in CBF (ml/100g/min) and CBV (ml/100g)

A

Increased PCO2 will increase CBF
CBF changes 1-2ml/100g/min
CBV changes 0.05ml/100g of brain tissue

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33
Q

What is the average Cerebral Metabolic Rate (CMRO2)? How is it different in children?

A

3ml/100g/min

Children have twice the metabolic needs (5.2ml/100g/min)

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34
Q

Relationship of temperature and CBF?

A

Decreased temp decreases CBF/ EEG monitor shows less activity
Irreversible brain damage over 42 degrees C

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35
Q

The brain can’t store much glucose, what does this have to do with metabolism and CBF?

A

90% of brain tissue ONLY operates on AEROBIC conditions (34 ATP with O2/Krebs, 2 ATP without O2/glycolysis), within 3-8 minutes, the tissue will have irreversible damage with no oxygen (O2 coming from blood supply, so when vessels are occluded, “time is brain”)

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36
Q

What is the exact brain glucose consumption?

A

Brain glucose consumption: 5.5mg/100g/min

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37
Q

Relationship of PaO2 and CBF

A

When it drops to 50 mmHg (80-100 normal), it does a “hail mary” and CBF increases (makes sense: as we become hypoxic, we send more flow to the brain), this is not clinically useful

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38
Q

Autoregulation: What does intrinsic myogenic response of the arteries have to do with CBF?

A

They help maintain a constant CBF by adjusting based on pressures: when the vessels sense low pressures, vasodilation occurs, when they sense high pressures, vasoconstriction occurs

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39
Q

SNS role in CBF?

A

Autoregulation plays the main role in CBF, SNS only takes over in extreme BP rise (to prevent a stroke, it will constrict large vessels to keep from the small vessels receiving such a high pressure and occluding), therefore SNS works as a protective mechanism

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40
Q

Relationship of blood viscosity and CBF

A

decreased HCT will increase CBF, but decrease O2
Severe polycythemia will reduce CBF
(think: increased viscosity= increased HCT, means the blood is thicker, therefore the flow of blood will be slower)

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41
Q

What is the capacity of the brain and spinal cord? How much of that is filled with CSF? How much CSF is in the cerebral ventricles?

A

Capacity: 1600 mL
CSF: 150 mL
Cerebral ventricles: 30 mL
Remainder volume is brain and spinal cord

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42
Q

What forms CSF? How fast is it formed? How many times a day is it formed? What absorbs CSF?

A

forms: choroid plexus at 0.35mL/min, 3-4 times a day
absorbs: arachnoid villi

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43
Q

Where are the choroid plexuses? What do they do?

A

They are in lateral (not posterior horn), third, and fourth ventricles, they make CSF and use epedymal cells to transport the CSF

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44
Q

When looking at the difference of concentration of ions and constituents in the blood compared to lumbar CSF, what are the major difference? (hint: Na, K, Cl, glucose, protein, and pH)

A

Protein is much lower in CSF (30) than in blood (6,800)
K, glucose, and pH is a little LOWER in CSF than blood
Na and Cl are HIGHER in CSF than blood

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45
Q

What is the flow of CSF? (What parts does it travel to?)

A

LATERAL ventricles, through intraventricular foramen of Munro, to THIRD ventricle, down the (cerebral) aqueduct of Sylvius, into FOURTH ventricle, then goes out through 3 holes: 2 lateral foramen of Luschka, 1 middle foramen of Magendie, from those 3 holes, it enters the cisterna magna (behind medulla, under cerebellum), this flows to subarachnoid space (where we do lumbar punctures), then to arachnoid villi, to sinus/veins

46
Q

What does the blood brain barrier do? How? And how to astrocytes play a role?

A

It restricts movement of large molecules and highly charged particles through barrier action of capillary endothelial cells, they have tight junctions
Astrocytes help by taking up K ions

47
Q

What area of the brain does the blood brain barrier not exist? Why?

A

Not in hypothalamus, pituitary, and area postrema
They work by having receptors for feedback (tight junctions do not allow this to work, so it makes sense they these areas of the brain do not have the BBB)

48
Q

astrocytes

A

neuroglia in the CNS, help maintain normal ECF by acting as a buffer (takes up K ions), their foot processes surround capillaries and contact connective tissue, they are coupled by gap junctions

49
Q

What mylinates CNS? PNS?

A

CNS: oligodendrocytes
PNS: schwann cells
(One schwann cell mylinates one axon
One oligodendrocyte can mylinate many axons)

50
Q

Microglia

A

CNS immune cells that perform phagocytosis, they can release cytotoxic elements to kill a foreign invader

51
Q

Ependymal cells

A

In CNS, they line the ventricles. Ependymal cells of the choroid plexus secrete CSF

52
Q

What is common in the axon hillock?

A

There are more sodium voltage gated channels, so it is easier to initiate action potential, this is where the message starts to propagate down to synapse and have a motor response

53
Q

Multipolar vs. Unipolar cells, what is the function (sensory/motor?)

A

Multipolar: motor
Unipolar: sensory
The shape of the cell meets the need of conduction

54
Q

Kenesis vs. Dyenin

A

Kenesis: message from spinal cord to exterior
Dyenin: retrograde transport (signals from exterior to spinal cord)

55
Q

How does myelin effect capacitance

A

capacitance is the ability to store a charge

Myelin decreases capacitance (it hides the charge, other charges around it can’t see it)

56
Q

What is the difference between electrical and chemical junctions?

A

electrical: contains gap junctions, cytoplasm of cells are united through connexons (one from each cell unites the cells), aka. electrical coupling
chemical: only unidirectional flow is possible, the chemical must travel through the synapse to a postsynaptic membrane

57
Q

Where do chemical junctions occur?

A

it is usually axodendritic (from axon of one cell onto dendrite of another cell), there is also axoaxonic, dendrodendritic, and dendrosomatic

58
Q

How are the three classes of neurotransmitter released from the presynaptic cell?

A
  1. small molecule neurotransmitters: diffuse across synaptic cleft and bind to postsynaptic receptor
  2. Neuropeptides: bind to G-protein receptors (for secondary response)
  3. Gaseous: diffuse across membrane
59
Q

What is a neurotransmitter? (What criteria must be met)

A

Substances that mediate chemical signaling between neurons
Criteria: They must be present on presynaptic terminal, where they are released by depolarization, receptors for it must be on postsynaptic membrane, and they must be able to be synthesized by the substance

60
Q

What are some examples of small-molecule/classic neurotransmitters

A 
Class 1: acetylcholine
Class 2 (biogenic amines): norepi, epi, dopamine, histamine
Class 3 (amino acids): GABA, glutamate, aspartate
61
Q

What are some examples of neuropeptides? What do they do?

A

opioids (leucine enkephalin and methionine enkephalin): inhibit pain perception
Substance P: promotes pain perceptions

62
Q

How do vesicles release neurotransmitters?

A

Active zones on the presynaptic membrane are rich in calcium channels, when Ca is released, Synaptotagmin senses this
V-snares (Synaptobrevin) connected to the vesicle zip up with T-snares (Syntaxin and SNAP25) to bring the vesicle to the end of the membrane, causing the neurotransmitter to release into the synapse

63
Q

Compare/Contrast the two theories on vesicular recycling: 1. Vesicular collapse/fusion vs. 2. Transient fusion/kiss and run

A
  1. vesicular collapse: plasma membrane pinches off to form vesicle, vesicles lose their coats
  2. transient fusion: a pore is formed, this is where the transmitter is expelled, the pore can reseal quickly
64
Q

How are the different types of calcium voltage gated channels different? L,P,N,T,Q/R

A

L: long lasting, in skeletal muscle, doesn’t need much activation to work
P (Purkinje) and N (Nerve): have slow inactivation, found in presynaptic membranes (works on releasing transmitters)
T: Transient, require weak depolarization, but have strong inactivation, found in cardiac cells and neural cell bodies
Q/R: similar to P/N, found in granule cells, slow inactivation to release transmitters

65
Q

Glutamate: what is it, how does it work, how is it broken down

A

It is an amino acid functioning as a neurotransmitter, it is the major excitatory transmitter in the CNS
With limited ATP and hypoxia, concentration gradients can’t be restored, so too much glutamate is a big problem
Glutamate synthase is the enzyme that turns glutamate into glutamine, this is very energy/ATP costly

66
Q

How is acetylcholine recycled?

A

Acetyl CoA (from mitochondria) + choline = ACh (acetylcholine)
Acetylcholinesterase hydrolyzes/ breaks down ACh into acetate and choline
Choline is recycled to make more ACh (uses active transport)
In general, ACh is not as energy/ATP costly bc choline is recycled

67
Q

What is the equation that shows current has to do with conductance and driving force of an ion?

A

Ix = (Gx) (Vm-Ex)
Ix: current, Gx: conductance, Vm: membrane potential, Ex: Nerst
Vm-Ex is the driving force
For example, at resting potential, Na has a high driving force bc it is far from its Nerst, K has a small driving force, K nerst is close to membrane potential

68
Q

What is the EPSP response? Which ions travel which way?

A

In excitatory, there is Na coming into the cell, depolarization occuring

69
Q

What is IPSP response? Where is it occurring? Which ions are acting?

A

Cl coming into the cell or K leaving the cell in presynaptic (3 ways: 1. autoinhibition at presynaptic terminal, 2. synapse from another axon, 3. hormone release) or postsynaptic, this hyperpolarizes the cell, making it harder to elicit a response
IPSP usually hyperpolarizes, but it can also depolarize a cell

70
Q

Temporal vs. Spacial Summation

A

Temporal: same synapse firing over and over to get to threshold
Spacial: multiple synapses firing to get to threshold
Both Summations occur to get to threshold

71
Q

How does acid/base effect synaptic transmission? How does hypoxia effect it?

A

Alkalosis increases neuronal excitability
Acidosis depresses neuronal activity
Hypoxia decreases neuronal excitability

72
Q

Mechanoreceptors:
Type 1 vs Type 2
slow adapting vs fast adapting

A

Type 1: high density, small area, to know exactly where stimulus is coming from
Type 2: dull feeling from large receptive area
Slow adapting: important, such as pain
Fast adapting: not important, such as leg resting on chair

73
Q

Pacinian corpuscle

A

A mechanoreceptor, FA2, it is the deepest of the 4 types of mechanoreceptors (FA: stimulus doesn’t really matter, Type 2: not really sure where it’s coming from)
It has many layers, it senses a stretch or change in permeability, and it sends an action potential

74
Q

Labeled line principle

A

Each sensory nerve tract ends in a specific location, no crossover occurs, for example, pressure can become more intense, but it can not be perceived as pain

75
Q

Difference between DCML (dorsal column medial lemniscal) and Anterolateral (spinothalamic) sensory pathways
hint: which sends faster largely myelinated signals, which gives more/less spacial orientation

A

DCML: A alpha, A beta, fast, high quality, high localized, fine touch, pressure, large myelinated fibers send faster signals, more spacial orientation, synapse in medulla
Anterolateral: pain, tickle, itch, crude touch/pressure, smaller myelinated fibers send slower signals, less spacial orientation, synapse in spinal cord

76
Q

Spinocerebellar Proprioceptive Tract

A

Sends proprioceptive info to cerebellum and cerebral cortex for body awareness

77
Q

Differences in types of cortical motor areas of the brain

A

Primary Motor Cortex: where movements are elicited
Supplementary Motor Area: need high amount of stimulus to activate, higher order processes including posture and vocalization
Premotor Cortex: monkey-see-monkey-do (mirroring), also complex
Cingulate Motor: planning of movement, also complex

78
Q

Basal Ganglia vs. Cerebellum

A

Both involve motor response, but cerebellum deals more with muscle memory and basal ganglia has more to do with active excitatory and inhibitory response

79
Q

Lateral vs. Medial motor pathways
Lateral: lateral corticospinal, lateral corticobulbar, and rubrospinal
Medial: reticulospinal, vestibulospinal, and tectospinal

A

Lateral: terminate in lateral spinal cord grey matter, can excite interneurons and motor neurons, influence reflex arc
Medial: terminate in medial ventral horn interneurons, these interneurons control axial muscles (balance, posture) and limb muscles

80
Q

memory traces

A

increased sensitivity of synapses allows us to remember things easier, the more firing, the more memory

81
Q

Habituation vs facilitation in memory

A

Habituation: you are accustomed to hearing something, over time, the presynaptic calcium channel closes, the signal is not sent
Facilitation: noxious stimulus causes serotonin to be released, secondary messengers are involved, the impulse is continually sent

82
Q

pregangliotic vs postgangliotic

A

preganglionic: cell body in CNS
postgangliotic: cell body outside CNS in autonomic ganglia

83
Q

Where are the sympathetic preganglionic neurons located? Where are the parasympathetic preganglion neurons located?

A

SNS: “thoracolumbar” T1-L2/L3
PSNS: “cranial-sacral” CN 3,5,7,9,10, S2-4

84
Q

SNS vs PSNS: Which has long preganglionic and short postganglionic neurons?

A

Long preganglionic, short postganglionic: PSNS

Short preganglionic, long postganglionic: Sympathetic

85
Q

summary of SNS vs PSNS functions

A

SNS: fight or flight, self preservation, maintain vasomotor tone
PSNS: rest and digest (digest is active excitation of digestion organs)

86
Q

The effect a neurotransmitter has on a tissue depends on what 3 things?

A

Type of receptor stimulated, receptor density in a tissue, what second messengers activate in the cell

87
Q

Parasympathetic pre- and post- ganglionic and Sympathetic preganglionic secrete what? Sympathetic postganglionic secretes what?

A

PSNS pre/post and SNS preganglionic secrete Acetylcholine (have cholinergic receptors)
SNS postganglionic secrete norepinephrine (have adrenergic receptors)

88
Q

Adrenal medulla, when activated by the SNS releasing Acetylcholine, secretes what?

A

80% epinephrine, 20% norepinephrine

89
Q

Mechanism of Action: G alpha S

A

Adenylate Cyclase activates cAMP (smooth muscle dilates/relaxes)
cAMP causes vasodilation, increased cardiac contractility, increases HR

90
Q

Mechanism of Action: G alpha I

A

decreased cAMP leads to vasoconstriction, increases K conduction therefore hyperpolarizes

91
Q

Mechanism of Action: G alpha Q

A

PLS activates IP3 & DAG, increases PKC, INCREASES CALCIUM, (therefore causes contraction)= vasoconstriction (smooth muscle)

92
Q

Which G protein is a receptor for M1, M3, and Alpha1

A

G alpha q

93
Q

Which G protein is a receptor for M2 and Alpha2?

A

G alpha i

You have 2 eyes=i’s, so i lines up M2/alpha2

94
Q

Which G protein is a receptor for Beta1,2,3?

A

G alpha s

95
Q

What are the receptors for Acetylcholine Nn and Nm, what is their mechanism of action and physiologic response?

A

Receptors are ligand gated ion channels, causes increased sodium and potassium permeability and results in depolarization

96
Q

What is innervated out of alpha1, alpha2, beta1, and beta2, and what does this have to do with norepinephrine?

A

All are innervated EXCEPT beta2, therefore beta2 barely responds from norepinephrine (NE is secreted from nerve terminal)
(Hint: This is why we don’t give high doses of NE, beta2 receptors don’t get stimulated and beta2 is responsible for vasodilation.. with high doses of NE, ischemia is possible)

97
Q

Why do dopamine, norepinephrine, and epinephrine all act on the same receptors (except beta2)?

A

They come from the same biosynthetic pathway (tyrosine hydroxylase is rate limiting step)
Tryosine -> DOPA -> Dopamine -> NE -> Epi

98
Q

How is norepinephrine’s action terminated?

A

Reuptake: 80% can be reused
Metabolism: enzymes MAO in cytoplasm, and COMT in liver

99
Q

How is epinephrine’s action terminated?

A

MAO and COMT (like norepinephrine, but relies more on COMT because it has a longer halflife)

100
Q

Which receptor constricts vessels, dilates pupils, erects hair (piloerector contraction), contracts prostate/uterus, decreases insulin secretion of pancreas, and increases force of contraction slightly?

A

Alpha1

101
Q

Which receptor does platelet aggregation, presynaptic dilation of vessels, postsynaptic contraction of vessels, GI relaxation, and CNS sedation

A

Alpha2

102
Q

Which receptor increases the force and rate of contraction, and stimulates renin release in the kidneys (leads to more Angiotensin2 vasocontriction)

A

Beta1

103
Q

Which receptor bronchodilates, relaxes uterine, vascular, GI, and GU, speeds skeletal muscle contraction by increasing potassium uptake, gluconeogenesis/glycogenolysis of the liver, insulin secretion of the pancreas, and releases NE?

A

Beta2

104
Q

What is the difference between dopamine D1/D2 receptors?

A

D1 works on smooth muscle at postsynaptic location, dilates vessels
D2 works on nerve endings at presynaptic location, releases neurotransmitters and causes nausea/vomiting

105
Q

Which fibers are sensory fibers (A,B,C?)

A

A-alpha, A-beta, A-delta, C

106
Q

Which fibers are motor (A,B,C)?

A

A-alpha, A-gamma, B, and C

107
Q

Which is the largest fiber (has the fastest conductance)? (A,B,C?)

A

A-alpha

108
Q

Which fiber is involved in sensing pain, temperature, and touch (important for anesthesia practice)? (A,B,C?)

A

A-delta

109
Q

Which fiber is important for sensing slow, dull, chronic pain? (A,B,C?)

A

C fibers

110
Q

What two areas of the brain regulate respiratory control?

A

Pons and medulla

111
Q

What two areas of the brain are involved in wakefullness?

A

Thalamus and reticular formation

112
Q

What are the first/second/third order neurons in sensory?

A

first: peripheral, primary afferent fibers
second: where it synapses, more diverse response than primary (medulla/spinal cord)
third: where it sends info to the cortex, small receptive fields (thalamus)

N542 Physiology (9 decks)

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