Neuro Test 2 Flashcards

1
Q

What is the NT for most sensory receptors?

A

glutamate

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2
Q

After stimulus of a depolarizing sensory receptor, what causes the change in membrane potential?

A

increase in nonspcific cation conductance in receptive area membrane

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3
Q

After stimulus of a hyperpolarizing sensory receptor, what causes the change in membrane potential?

A

closure of the receptive area cation channels

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4
Q

What are the 5 attributes of a stimulus that sensory systems convey information about?

A

modality, quality, intensity, duration or frequency, location

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5
Q

How do sensory systems convey information about the modality of a stimulus? ex. vision vs. hearing

A

which nerve cells are active; by specific neuronal connections from sensory organs through thalamus to the cortex.

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6
Q

How do long sensory receptor cells code stimulus intensity?

A

as an increase in AP firing frequency

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7
Q

What type of change in membrane potential in auditory receptor cells occurs as a result of an auditory stimulus?

A

oscillations in the membrane potential

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8
Q

What type of fibers innervate muscle spindle?

A

Aalpha fibers, the biggest diameter and fastest velocity: 60-120 m/sec

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9
Q

What type of nerve fiber innervates the mechanoreceptors of the skin?

A

A beta fibers

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10
Q

What type of nerve fibers detect sharp pain and cold temperature?

A

A deltas

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11
Q

What type of nerve fibers detect warm temperature, burning pain, itch, and crude touch?

A

C fibers

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12
Q

Do rapidly adapting mechanoreceptors stop firing even when the skin is still being pressed?

A

yes

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13
Q

Do slow adapting mechanoreceptors stop firing even when the skin is still being pressed?

A

no

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14
Q

What type of mechanoreceptor corresponds to rapidly adapting afferents with small receptive fields?

A

Meissner’s corpuscle

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15
Q

What type of mechanoreceptor corresponds to slow adapting afferents with small receptive fields?

A

Merkel’s disc

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16
Q

What type of mechanoreceptor corresponds to rapidly adapting afferents with large receptive fields?

A

Pascinian’s corpuscle

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17
Q

What type of mechanoreceptor corresponds to slow adapting afferents with large receptive fields?

A

Ruffini’s endings

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18
Q

What size receptive field do the mechanoreceptors involved in fine tactile sense of the fingertips have?

A

small receptive fields

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19
Q

Do hair follicle mechanoreceptors correspond to rapidly adapting or slow adapting afferents?

A

rapidly adapting

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20
Q

What type of afferent fibers do propioceptor receptors correspond with?

A

Aalpha

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21
Q

What cortical layer receives input from the thalamus?

A

layer IV

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22
Q

What cortical layer projects back to the thalamus?

A

layer VI

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23
Q

What does cortical layer V project to?

A

other subcortical structures

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24
Q

Where do cortical layers II and III project to?

A

other areas of the somatosensory cortex

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25
Q

Which somatosensory cortex area tends to have more complex stimulus requirements?

A

SII

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26
Q

Cells in what area is responsible for our perception of extrapersonal space (our “picture” of our own body)?

A

posterior parietal cortex

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27
Q

What temperature range do the cool receptors detect?

A

10-37 C

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28
Q

what temperature range do the warm receptors detect?

A

30-48 C

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29
Q

What temperature is the thermo-neutral point?

A

33 C= we neither sense coolness or warmth

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30
Q

What type of fibers are cool receptors associated with?

A

A delta fibers

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31
Q

Are there more cool receptors or warm receptors?

A

10X as many cool receptors as warm receptors

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32
Q

What type of fiber is associated with warm receptors?

A

C fibers

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33
Q

What is the name of the anterolateral system tract that conveys pain information to the thalamus?

A

spinothalamic tract

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34
Q

What is the name of the anterolateral system tract that conveys pain inputs that lead to forebrain arousal and elecits emotional/behavioral responses via connections to limbic system?

A

spinoreticular tract

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35
Q

What are the 2 other cortical regions involved in processing of pain information

A

cingulate gyrus and insular cortex

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36
Q

How does the cingulate gyrus play a role in pain information processing?

A

it is part of the limbic system and contributes to the emotional component of pain sensation

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37
Q

How does the insular cortex contribute to pain information processing?

A

it processes information related to autonomic components of pain

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38
Q

What is the range of temperatures that thermal nociceptors respond to?

A

43 C

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39
Q

What type of fibers do HOT thermal nociceptor cells have?

A

A delta fibers

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40
Q

What type of fibers do COLD thermal receptor cells have?

A

C fibers

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41
Q

What type of fibers do mechanical nociceptors have?

A

A delta fibers

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42
Q

What type of fibers do polymodal nociceptor cells that detect high-intensity mechanical, chemical, or thermal stimuli have?

A

C fibers

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43
Q

What is one type of receptor of polymodal nociceptor cells that is strongly activated by capsaicin and weakly activated by acids and also activated by moderate heat of 43 C?

A

VR-1

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44
Q

How does capsaicin work as a long-term analgesic?

A

it causes intense activation of capsaicin receptors which results in massive secretion and eventual depletion of sub P from sensory fibers

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45
Q

What type of channel is VR-1 coupled to?

A

non-selective cation channel

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46
Q

What type of receptor of polymodal nociceptor cells is activated by ATP?

A

P2X

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47
Q

What type of receptor of polymodal nociceptor cells are activated by acids?

A

ASICs

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48
Q

How many different ASIC genes are expressed in C fiber nociceptors?

A

4

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49
Q

Why is there a 1st pain and a 2nd pain?

A

in a painful stimulus, A delta fiber signals are detected first –> pricking pain. then C fiber signals detected –> intolerable, diffuse burning pain

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50
Q

With increasing pressure, what type of fibers will be the first to become nonconductive?

A

A alpha and A beta fibers because they are the most metabolically active ones. then A deltas, then Cs

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51
Q

When electrical stimulation is applied to activate peripheral sensory nerves, what is the order in which different fiber types will be activated?

A

A alpha and A beta –> A delta –> C fibers

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52
Q

In what order do anesthetics block different sensory fibers?

A

C fibers first! –> A deltas –> A alpha and A beta: touch afferents and motor axons

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53
Q

What factors do damaged cells release that influence pain modulation?

A

K+, ATP, prostaglandins, acid (H+)

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54
Q

What do mast cells secrete in areas of damaged tissues that influences pain modulation?

A

serotonin, other chemicals

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55
Q

How is bradykinin produced?

A

cleavage of an inactive precursor, kininogen, which is present in serum

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56
Q

WhAT are some compounds that can lead to direct activation of nociceptors?

A

bradykinin, K+, acid, and serotonin

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57
Q

What are some compounds that sensitize nociceptors?

A

prostaglandins, sub P, ATP, ACh, serotonin

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58
Q

How does aspirin work?

A

inhibits COX-2, which converts arachadonic acid to prostaglandins

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59
Q

What is hyperalgesia?

A

sensitization of nociceptors –> increased sensitivity to pain

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60
Q

What is allodynia?

A

when sensitization is extreme enough to allow non-noxious stimuli to trigger a painful sensation

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61
Q

What does a dorsal horn neuron receiving inputs from cutaneous as well as visceral pain afferents cause?

A

referred pain

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62
Q

What input dominates in referred pain?

A

cutaneous input so it is the site that is recognized

63
Q

If one performed repetitive stimulation of a nociceptive neuron, would one see the triple response?

A

no, would only get flare. No cut, so no BK to cause redness and wheal.

64
Q

If one performed botox injection to an area before cutting it, would one see the triple response?

A

no, only redness and wheal. no flare because no synaptic vesicle release of substance P.

65
Q

What types of receptors does a 2nd order dorsal horn neuron have?

A

AMPA Rs, NMDA Rs, NK1 Rs

66
Q

What NT binds to NK1 receptors?

A

substance P

67
Q

What type of channels are the NK1 receptors coupled to?

A

GIRK channel: sub P binding –> closes K+ channel –> depolarization (PLC mechanism)

68
Q

What receptors are activated after a single stimulus to a 2nd order dorsal horn neuron?

A

AMPA Rs only really

69
Q

What receptors are activated after repetitive stimulation to a 2nd order dorsal horn neuron?

A

AMPA, NMDA, and NK1 receptors

70
Q

What do NMDA and NK1 receptor activation cause in a 2nd order dorsal horn neuron?

A

direct increase in depolarization by NK1, which leads to increased intracellular calcium; NMDA also increasing intracellular calcium

71
Q

Increased intracellular calcium in a 2nd order dorsal horn neurons results in what?

A

increase in phosphorylation of NMDA receptors via PKC

72
Q

What happens with NMDA R phosphorylation?

A

it no longer has the requirement for depolarization to be activated. just like AMPA

73
Q

SO then what does a single stimulation of a nociceptice neuron cause after a period of repetitive stimulation?

A

potentiation of the synapse, sensitivity of the area. = hyperalgesia

74
Q

How are glutamate and substance P removed from the synapse?

A

glutamate by reuptake, but Substance P by diffusion

75
Q

How does transcutaneous electrical nerve stimulation lead to a reduction in pain sensation?

A

because it involves stimulation of large-diameter A beta fibers that are in the inured area that synapse onto the inhibitory enkephalinergic interneurons in the dorsal horn

76
Q

What is the name of the disease in which A beta fiber inputs to the interneurons in the dorsal horn are eliminated due to damage of the large diamter primary afferents?

A

tabes dorsalis, associated with the advanced stages of syphilis. results in hyperalgesia

77
Q

How do opiates produce analgesia?

A

inhibit inhibitory neurons in the PAG

78
Q

What endogenous compounds bind the receptors that opiates do?

A

enkephalins, beta-endorphins, dynorphins. all collectively known as endorphins.

79
Q

How does the inhibitory interneuron inhibit the efferent pain fibers?

A

both pre-synaptically and post-synaptically.

80
Q

How does the inhibitory interneuron inhibit efferent pain fiber activation pre-synaptically?

A

It closes calcium channels presynaptically so reducing vesicle release

81
Q

How does the inhibitory interneuron inhibit efferent pain fiber activation postsynaptically?

A

it opens potassium channels

82
Q

What is the mechanism of stress-induced analgesia?

A

increased activity in the limbic system –> activation of the PAG

83
Q

Does naloxone block stress-induced analgesia?

A

some, but not all. so it involves both opioid and non-opioid mediated mechanisms

84
Q

Does naloxone block the placebo effect?

85
Q

What symptoms do mouse mutants of the TTX resistant NA+ channels have?

A

higher inflammatory pain thresholds

86
Q

What symptoms do humans who have SCN9A mutations (TTX senstive Na+ channel) have?

A

pain, warmth, and redness

87
Q

What symptoms are important to watch for in patients that are taking Na+ channel blockers to treat neuropathic pain following nerve injury?

A

cardiac issues, MORE

88
Q

What is the main inhibitory NT in the dorsal horn of the spinal cord?

89
Q

How does injury to the dorsal column results in decreased GABA and GABA receptors?

A

damaged neurons secreting less factors for survival and maintenance

90
Q

Following injury of C fibers, what do A beta afferents do?

A

sprout and invade the normally forbidden territory of the substantia gelatinosa –> hyperalgesia

91
Q

In which of the 2 types of Na+ channels does ATP binding of purinergic receptors occur preferentially?

A

TTX-resistant ones

92
Q

What does ATP binding of purinergic receptors in the dorsal horn cause?

A

activation of microglial cells which secrete BDNF

93
Q

What does BDNF signaling in the spinal cord cause?

A

a change in the chloride reversal potential such that GABA receptor activation produces excitation rather than inhibition. in part mediated by changes in KCC2 expression

94
Q

Where is intrathecal space?

A

within either the subarachnoid or the subdural space

95
Q

What type of local anesthetic is metabolized primarily by the liver?

96
Q

How does the use-dependent entry and exit of local anesthetic from a sodium channel impact its duration of action?

A

anesthetics can get trapped in closed receptors! will have effect for longer

97
Q

How do local anesthetics increase the refractory period of sodium channels?

A

they increase the stability of the inactivated state of the channel

98
Q

What property of local anesthetics correlates best with its potency?

A

lipid solubility

99
Q

What property of local anesthetics determines their speed of onset?

100
Q

How does pKa affect the lipid solubility of an anesthetic?

A

the lower the pka, the higher the lipid solubility of the anesthetic

101
Q

What property of anesthetics primarily determines their duration of action?

A

their protein-binding capacity

102
Q

Does protein binding increase or decrease the duration of actio n of an anesthetic?

103
Q

Which type of anesthetic is contraindicated in patients with hepatic insufficiency?

104
Q

What 3 anesthetics can be applied topically?

A

tetracaine, lidocaine, and cocaine

105
Q

What is EMLA cream?

A

mixture of lidocaine and prilocaine that has a melting point lower than the two alone, exists as oil at RT, can produce anesthesia up to 5 mm deep

106
Q

Why can benzocaine be directly applied to wounds without a risk of toxicity?

A

it lacks the terminal amino groups, so has low water solubility, low absorption.

107
Q

What anesthetics are injections into tissue to cause infiltration anesthesia?

A

lidocaine, procaine, bupivacaine

108
Q

What is the advantage of infiltration anesthesia?

A

function of underlying organs is unaffected.

109
Q

what is the disadvantage of infiltration anesthesia?

A

have to use a lot and might be significant absorption into the circulation

110
Q

What is the advantage of nerve block anesthesia?

A

larger body regions can be anesthetized as compared to infiltration anesthesia

111
Q

Which anesthetic is used in nerve block anesthesia for 2-4 hr periods?

112
Q

Which anesthetic is used in nerve block anesthesia for periods longer than 4 hrs?

A

bupivicaine

113
Q

How is Bier’s block performed?

A

blood squeezed out a limb. anesthetic injected with catheter. limb anesthesia within 5-10 min.

114
Q

How long can Bier’s block be performed?

A

up to 2 hrs, because tissue can’t be unperfused for longer

115
Q

Which drug is used for Bier’s block the most? why not use bupivicaine?

A

lidocaine, because bupivicaine is more cardiotoxic.

116
Q

Why are the effects of ester-linked local anesthetics prolonged in spinal anesthesia (injected into the CSF)?

A

because there is little to no plasma esterase activity in the CSF

117
Q

What anesthetics are used for longest duration procedures?

A

tetracaine

118
Q

What is the advantage of epidural anesthesia compared to spinal anesthesia?

A

injection just outside the dura-enclosed spinal cord allows the use of catheters for repeated bolus or continuous application of anesthetic

119
Q

How does a vasoconstrictor prolong the duration of conduction blockade by an anesthetic?

A

reduces blood flow in the viscinity of injection, retarding systemic absorption

120
Q

How do TTX and saxitoxin block NA+ channels?

A

by binding to the extracellular entrance. no use dependence. block channels everywhere. die of suffocation

121
Q

What is the peak age group in which head injuries occur?

122
Q

What types of head injury can contact injury cause?

A

skull fractures, epidural hematoma, subgaleal hematoma: between the periosteum and the scalp. cerebral contusions

123
Q

What type of head injury results in diffuse axonal injury?

A

rotational forces in an acceleration/deceleration injury

124
Q

What type of injury do translational forces to the head normally cause?

A

1) contusions. low mortality. coup-contracoup= frontal/occipital contusions
or 2) subdural hematoma

125
Q

What is a subdural hematoma?

A

stretching and tearing of the veins between the brain and dura. high mortality rate

126
Q

What causes a brain to be more susceptible to subdural hematoma formation?

A

cortical atrohpy

127
Q

When can diffuse axonal injury first be detected with a light microscope?

A

24 hrs after injury, can see axonal spheroids

128
Q

What is pathology of diffuse axonal injury seen on MRI?

A

nothing! sometimes there might be punctate hemorrhages in large white matter tracts like CC. mortality as high as 80%

129
Q

What diuretic is used to draw water back into the vasculature to treat cytotoxic edema?

130
Q

What are the 2 signs of increased intracranial pressure?

A

progressive lethargy and poor responsiveness

131
Q

What cranial nerves does the pupillary reflex test?

A

2 and 3, also midbrain

132
Q

What cranial nerves does corneal blink reflex test?

A

5 and 7, also pons

133
Q

What cranial nerves do cold caloric testing and “doll’s eyes” test?

A

8,6,3 pons

134
Q

What cranial nerves does gag reflex test?

A

9 and 10, medulla

135
Q

What are the 3 main categories of glasgow coma scale?

A

eyes, best motor response, best verbal response

136
Q

What are the clinical features of herniation?

A

headache, nausea, vomiting, progressive lethargy and poor responsiveness

137
Q

What is the name of the herniation in which the cingulate gyrus herniates laterally into the falx cerebri?

A

subfalcine

138
Q

What can occur as a result of a subfalcine herniation?

A

a stroke due to kinking of anterior cerebral artery

139
Q

Herniation of what structures cause transtentorial herniation?

A

uncal herniation across tentorial edge

140
Q

What does transtentorial herniation cause?

A

ipsilateral 3rd nerve palsy and contralateral hemiparesis or hemiplegia due to compression of midbrain and ipsilateral cerebral peduncle

141
Q

What is the name of the hemorrhage in which the uncus punches the brain stem?

A

duret hemorrhage, which is bad because reticular activating system located here, so consciousness is messed with!

142
Q

What is Kernohan’s notch?

A

when uncal herniation compresses all the way to the contralateral cerebral peduncle

143
Q

What is central herniation?

A

central bilateral uncal herniation downward

144
Q

Into what foramen do the cerebellar tonsils herniate into?

A

foramen magnum

145
Q

Into what structure do the uncus herniate?

A

posterior fossa

146
Q

What can tonsilar herniation cause due to compression of the medulla?

A

cardiac and respiratory responses , including cushing’s reflex: bradycardia and hypertension in the setting of high intracranial pressure (due to compression of the medulla)

147
Q

What is the acute confusional state in which a disorder of attention cahracterized by an inability to maintain a coherent line of thought called?

148
Q

In order for a patient to be classified as having dementia, he/she must have deficits in at least 3 of what 5 categories?

A

memory. language, visuospatial skills, emotion and personality, and complex cognition

149
Q

What is most important to keep in mind during the evaluation of dementia?

A

try to detect the reversible etiologies so pt can be treated as quickly as possible.

150
Q

What are the tests to run in a patient exhibiting dementia?

A

history and PE, CMP, CBC, TSH, B12, RPR, and MRI or CT scan

151
Q

What type of drug should be given for disruptive psychiatric syndromes in a patient with irreversible dementia?

A

low-dose atypical antipsychotics such as quetiapine or risperidone

152
Q

What types of drugs should be avoided in patients with irreversible dementia?

A

drugs that worsen mental status such as benzos and anticholinergic drugs

153
Q

What type of drug should you start with in treating patients with delirium?

A

haldol or an atypical neuroleptic

154
Q

What drugs have been shown to slow progression of certain dementias?

A

cholinesterase inhibitors and memantine