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Flashcards in Neuro Test 2 Deck (154)
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1

What is the NT for most sensory receptors?

glutamate

2

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

increase in nonspcific cation conductance in receptive area membrane

3

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

closure of the receptive area cation channels

4

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

modality, quality, intensity, duration or frequency, location

5

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

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

6

How do long sensory receptor cells code stimulus intensity?

as an increase in AP firing frequency

7

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

oscillations in the membrane potential

8

What type of fibers innervate muscle spindle?

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

9

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

A beta fibers

10

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

A deltas

11

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

C fibers

12

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

yes

13

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

no

14

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

Meissner's corpuscle

15

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

Merkel's disc

16

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

Pascinian's corpuscle

17

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

Ruffini's endings

18

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

small receptive fields

19

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

rapidly adapting

20

What type of afferent fibers do propioceptor receptors correspond with?

Aalpha

21

What cortical layer receives input from the thalamus?

layer IV

22

What cortical layer projects back to the thalamus?

layer VI

23

What does cortical layer V project to?

other subcortical structures

24

Where do cortical layers II and III project to?

other areas of the somatosensory cortex

25

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

SII

26

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

posterior parietal cortex

27

What temperature range do the cool receptors detect?

10-37 C

28

what temperature range do the warm receptors detect?

30-48 C

29

What temperature is the thermo-neutral point?

33 C= we neither sense coolness or warmth

30

What type of fibers are cool receptors associated with?

A delta fibers

31

Are there more cool receptors or warm receptors?

10X as many cool receptors as warm receptors

32

What type of fiber is associated with warm receptors?

C fibers

33

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

spinothalamic tract

34

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?

spinoreticular tract

35

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

cingulate gyrus and insular cortex

36

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

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

37

How does the insular cortex contribute to pain information processing?

it processes information related to autonomic components of pain

38

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

43 C

39

What type of fibers do HOT thermal nociceptor cells have?

A delta fibers

40

What type of fibers do COLD thermal receptor cells have?

C fibers

41

What type of fibers do mechanical nociceptors have?

A delta fibers

42

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

C fibers

43

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?

VR-1

44

How does capsaicin work as a long-term analgesic?

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

45

What type of channel is VR-1 coupled to?

non-selective cation channel

46

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

P2X

47

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

ASICs

48

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

4

49

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

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

50

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

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

51

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

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

52

In what order do anesthetics block different sensory fibers?

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

53

What factors do damaged cells release that influence pain modulation?

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

54

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

serotonin, other chemicals

55

How is bradykinin produced?

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

56

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

bradykinin, K+, acid, and serotonin

57

What are some compounds that sensitize nociceptors?

prostaglandins, sub P, ATP, ACh, serotonin

58

How does aspirin work?

inhibits COX-2, which converts arachadonic acid to prostaglandins

59

What is hyperalgesia?

sensitization of nociceptors --> increased sensitivity to pain

60

What is allodynia?

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

61

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

referred pain

62

What input dominates in referred pain?

cutaneous input so it is the site that is recognized

63

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

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

64

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

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

65

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

AMPA Rs, NMDA Rs, NK1 Rs

66

What NT binds to NK1 receptors?

substance P

67

What type of channels are the NK1 receptors coupled to?

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

68

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

AMPA Rs only really

69

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

AMPA, NMDA, and NK1 receptors

70

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

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

71

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

increase in phosphorylation of NMDA receptors via PKC

72

What happens with NMDA R phosphorylation?

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

73

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

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

74

How are glutamate and substance P removed from the synapse?

glutamate by reuptake, but Substance P by diffusion

75

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

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

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?

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

77

How do opiates produce analgesia?

inhibit inhibitory neurons in the PAG

78

What endogenous compounds bind the receptors that opiates do?

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

79

How does the inhibitory interneuron inhibit the efferent pain fibers?

both pre-synaptically and post-synaptically.

80

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

It closes calcium channels presynaptically so reducing vesicle release

81

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

it opens potassium channels

82

What is the mechanism of stress-induced analgesia?

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

83

Does naloxone block stress-induced analgesia?

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

84

Does naloxone block the placebo effect?

yes

85

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

higher inflammatory pain thresholds

86

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

pain, warmth, and redness

87

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

cardiac issues, MORE

88

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

GABA

89

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

damaged neurons secreting less factors for survival and maintenance

90

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

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

91

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

TTX-resistant ones

92

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

activation of microglial cells which secrete BDNF

93

What does BDNF signaling in the spinal cord cause?

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

Where is intrathecal space?

within either the subarachnoid or the subdural space

95

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

amides

96

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

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

97

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

they increase the stability of the inactivated state of the channel

98

What property of local anesthetics correlates best with its potency?

lipid solubility

99

What property of local anesthetics determines their speed of onset?

pKa.

100

How does pKa affect the lipid solubility of an anesthetic?

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

101

What property of anesthetics primarily determines their duration of action?

their protein-binding capacity

102

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

increases

103

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

amides

104

What 3 anesthetics can be applied topically?

tetracaine, lidocaine, and cocaine

105

What is EMLA cream?

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

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

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

107

What anesthetics are injections into tissue to cause infiltration anesthesia?

lidocaine, procaine, bupivacaine

108

What is the advantage of infiltration anesthesia?

function of underlying organs is unaffected.

109

what is the disadvantage of infiltration anesthesia?

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

110

What is the advantage of nerve block anesthesia?

larger body regions can be anesthetized as compared to infiltration anesthesia

111

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

lidocaine

112

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

bupivicaine

113

How is Bier's block performed?

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

114

How long can Bier's block be performed?

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

115

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

lidocaine, because bupivicaine is more cardiotoxic.

116

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

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

117

What anesthetics are used for longest duration procedures?

tetracaine

118

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

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

119

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

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

120

How do TTX and saxitoxin block NA+ channels?

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

121

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

age 24-35

122

What types of head injury can contact injury cause?

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

123

What type of head injury results in diffuse axonal injury?

rotational forces in an acceleration/deceleration injury

124

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

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

125

What is a subdural hematoma?

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

126

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

cortical atrohpy

127

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

24 hrs after injury, can see axonal spheroids

128

What is pathology of diffuse axonal injury seen on MRI?

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

129

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

mannitol

130

What are the 2 signs of increased intracranial pressure?

progressive lethargy and poor responsiveness

131

What cranial nerves does the pupillary reflex test?

2 and 3, also midbrain

132

What cranial nerves does corneal blink reflex test?

5 and 7, also pons

133

What cranial nerves do cold caloric testing and "doll's eyes" test?

8,6,3 pons

134

What cranial nerves does gag reflex test?

9 and 10, medulla

135

What are the 3 main categories of glasgow coma scale?

eyes, best motor response, best verbal response

136

What are the clinical features of herniation?

headache, nausea, vomiting, progressive lethargy and poor responsiveness

137

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

subfalcine

138

What can occur as a result of a subfalcine herniation?

a stroke due to kinking of anterior cerebral artery

139

Herniation of what structures cause transtentorial herniation?

uncal herniation across tentorial edge

140

What does transtentorial herniation cause?

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

141

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

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

142

What is Kernohan's notch?

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

143

What is central herniation?

central bilateral uncal herniation downward

144

Into what foramen do the cerebellar tonsils herniate into?

foramen magnum

145

Into what structure do the uncus herniate?

posterior fossa

146

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

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

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

delirium

148

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

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

149

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

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

150

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

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

151

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

low-dose atypical antipsychotics such as quetiapine or risperidone

152

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

drugs that worsen mental status such as benzos and anticholinergic drugs

153

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

haldol or an atypical neuroleptic

154

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

cholinesterase inhibitors and memantine