Neuro Test 2 Flashcards
(154 cards)
1
Q
What is the NT for most sensory receptors?
A
glutamate
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
3
Q
After stimulus of a hyperpolarizing sensory receptor, what causes the change in membrane potential?
A
closure of the receptive area cation channels
4
Q
What are the 5 attributes of a stimulus that sensory systems convey information about?
A
modality, quality, intensity, duration or frequency, location
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.
6
Q
How do long sensory receptor cells code stimulus intensity?
A
as an increase in AP firing frequency
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
8
Q
What type of fibers innervate muscle spindle?
A
Aalpha fibers, the biggest diameter and fastest velocity: 60-120 m/sec
9
Q
What type of nerve fiber innervates the mechanoreceptors of the skin?
A
A beta fibers
10
Q
What type of nerve fibers detect sharp pain and cold temperature?
A
A deltas
11
Q
What type of nerve fibers detect warm temperature, burning pain, itch, and crude touch?
A
C fibers
12
Q
Do rapidly adapting mechanoreceptors stop firing even when the skin is still being pressed?
A
yes
13
Q
Do slow adapting mechanoreceptors stop firing even when the skin is still being pressed?
A
no
14
Q
What type of mechanoreceptor corresponds to rapidly adapting afferents with small receptive fields?
A
Meissner’s corpuscle
15
Q
What type of mechanoreceptor corresponds to slow adapting afferents with small receptive fields?
A
Merkel’s disc
16
Q
What type of mechanoreceptor corresponds to rapidly adapting afferents with large receptive fields?
A
Pascinian’s corpuscle
17
Q
What type of mechanoreceptor corresponds to slow adapting afferents with large receptive fields?
A
Ruffini’s endings
18
Q
What size receptive field do the mechanoreceptors involved in fine tactile sense of the fingertips have?
A
small receptive fields
19
Q
Do hair follicle mechanoreceptors correspond to rapidly adapting or slow adapting afferents?
A
rapidly adapting
20
Q
What type of afferent fibers do propioceptor receptors correspond with?
A
Aalpha
21
Q
What cortical layer receives input from the thalamus?
A
layer IV
22
Q
What cortical layer projects back to the thalamus?
A
layer VI
23
Q
What does cortical layer V project to?
A
other subcortical structures
24
Q
Where do cortical layers II and III project to?
A
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
