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Neuro > Unit II week 2 > Flashcards

Unit II week 2 Flashcards

1
Q

Receptor (generator) potential

A

stimulus elicited change in membrane potential (depolarization or hyperpolarization) → release of NT from synaptic end (typically glutamate)

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2
Q

Short sensory receptor cells

A

(less than 0.1 mm or 100 um in length) → receptor potential spreads to synaptic end via passive electrotonic transmission

-Regenerative APs not necessary

EX) rod photoreceptor cells, auditory hair cells

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3
Q

Long sensory receptor cells

A

(>1mm in length) → regenerative AP used to carry info from receptive ending to synaptic release site

EX) skin mechanoreceptors

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4
Q

Depolarizing receptor potentials

EX) ?

A

increase in nonspecific cation conductance in receptive area membrane

EX) Muscle mechanoreceptors - mechanosensitive nonselective cation channels that open in response to stretch → depolarize sensory ending

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5
Q

Hyperpolarizing receptor potentials

EX) ?

A

substantial number of resting cation conductance channels open in receptive area → stimulus → receptive area cation channels close = hyperpolarization

EX) Rod photoreceptor

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6
Q

Rod photoreceptor resting state

A

resting membrane potential around -40mV due to high cGMP concentrations under resting conditions that maintain cGMP-gated cation channels open

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7
Q

What happens when light hits a rod photoreceptor?

6 steps

A

1) Light hits RHODOPSIN → 1-CIS-RETINAL bound to rhodopsin absorbs light → changes conformation to 1-TRANS-RETINAL
2) → causes rhodopsin to change conformation → METARHODOPSIN
3) Metarhodopsin stimulates TRANSDUCIN (g-protein) → activate cGMP PHOSPHODIESTERASE
4) → cGMP breakdown → closure of cGMP-gated nonselective cation channels
5) → HYPERPOLARIZATION
6) → Fewer NTs released

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8
Q

Transduction channel

-how is it different from voltage-dependent channel?

A

NOT voltage-dependent

Sensitive only to the adequate stimulus - allows channel to encode stimulus intensity as a graded increase in magnitude of receptor potential

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9
Q

Sensory systems convey information about what five attributes of a stimulus

A

1) Modality
2) Intensity
3) Quality
4) Duration/Frequency
5) Location

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10
Q

Modality is encoded how?

A

LABELED LINES

Conscious appreciation of sensory modality is determined by specific neuronal connections from sensory organs through thalamus to cerebral cortex

Separate pathways for different sensory systems → separate chain of neurons (separate labeled line) for each sensory system

Stimulus modality is coded by which nerve cells are active

EX) visual info relayed via LGN of thalamus → visual cortex in occipital lobe

EX) auditory info relayed via MGN of thalamus → auditory cortex in temporal lobe

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11
Q

All sensory information goes through the _______ except for __________

A

everything goes through THALAMUS, except for OLFACTION

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12
Q

How is Intensity coded?

A

the magnitude of the generator potential increases as intensity of stimulus is increased (more depolarized OR more hyperpolarized = increased generator potential)

The fraction of time the transduction channel spends in the open (or closed) state is a function of the intensity of the stimulus

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13
Q

C-fibers

A

small, unmyelinated axons, 1 um in diameter, slow conduction velocity

Warm temperature, burning pain, itch, crude touch

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14
Q

A-fibers

A

myelinated fibers

Alpha, Alpha
Alpha, Beta
Alpha, Delta

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15
Q

Alpha, Alpha fibers

A

most rapidly conducting, largest diameter
Ia → muscle spindle afferent
Ib → tendon organ afferent

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16
Q

Alpha, Beta fibers

A

slower and smaller diameter than Aa, but still fast

Mechanoreceptors of skin, secondary muscle spindle afferents

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17
Q

Alpha, Delta fibers

A

slower and smaller diameter than AB

Sharp pain, cool temperature, extreme hot temperature

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18
Q

Merkel’s Disk

A

Sensory Receptors of the Skin

  • slowly adapting, small receptive field
  • High density of receptors
  • Support fine tactile sense of fingertips

A-Beta fibers

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19
Q

Meissner’s Corpuscle

A

Sensory Receptors of the Skin

rapidly adapting, small receptive field
High density of receptors
Shallow depth in skin
Fine touch (fingertips)

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20
Q

Pacinian corpuscle

A

Sensory Receptors of the Skin

  • rapidly adapting, large receptive field
  • High sensitivity to skin deformation over a wide area
  • Very deep in skin
  • Vibratory stimuli
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21
Q

Ruffini Endings

A

Sensory Receptors of the Skin

slowly adapting, large receptive field

Free nerve ending,

Info on how skin is stretched

A-Beta fibers

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22
Q

Hair follicle receptors

A

Sensory Receptors of the Skin

bending of hair shaft activates nerve terminals

Rapidly adapting

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23
Q

Somatotopy

A

precise and orderly mapping of body surface onto cortex

Preservation of nearest neighbor relationships: neighboring cells in nucleus cuneatus or within thalamus have receptive fields near to one another in skin

Distorted “homunculus” due to differences in innervation density

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24
Q

Cortical Barrel

A

idea that cells innervating the same thing (e.g. one whisker) all project to the same place in somatosensory cortex

Circular arrangements of cells run throughout cortical depth

All cells within that barrel respond to movement of that “whisker”

Morphological specialization of cortex that reflects a functional organization

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25
Q

Columnar Organization

A

vertical arrangement of functionally related cells (barrels)

Seen in vertical segregation of cells by response to modality

6 layers of cortex within a column each project to different areas of brain → cortical columns serve as computational modules that transform information received from the thalamus and redistribute it to other brain regions

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26
Q

Dorsal Column/Lemniscal System

1) sensory cell receptors bodies in _________ → enters spinal cord → __________

2) → local branches project to ________ for spinal reflexes
→ ascending branches enter __________ = _________ (upper limbs) and __________ (lower limbs)

3) Ascending branches then…

A

1) Dorsal root ganglia, Bifurcate

2) dorsal horn
dorsal (posterior) columns
fasciculus cuneatus
fasciculus gracilis

3) → ascend spinal cord to nucleus cuneatus/gracilis in medulla

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27
Q

Dorsal Column/Lemniscal System

4) → second-order neurons ____________ after synapsing in _______ = __________ Pathway
5) → synapse in __________ complex of ___________

_____ nucleus = trunk and limbs
______ nucleus = head

6) → Ventrobasal complex projects to areas ____, ____ and _____ on posterior bank of ______ → primary motor cortex

A

4) cross midline, medulla, Medial Lemniscal
5) ventro-basal, thalamus

VPL nucleus = trunk and limbs
VMP nucleus = head

VPL + VPM = ventrobasal complex

6) 3, 1, and 2, Central sulcus

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28
Q

Trigeminal Lemniscal Pathway

A

lemniscal system for head

Afferent information regarding touch, proprioception, pain, and temperature on face and head flow through trigeminal nerve

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29
Q

Trigeminal Lemniscal Pathway

1) Cell bodies located in _______________ → synapse in _________
2) → second order cells then _________ and join __________ pathway
3) First-order afferents may also branch upon entering ______ and send a branch into ________ and other branch into nucleus
4) →_______ nucleus of thalamus → ______ area of somatosensory cortex

A

1) trigeminal ganglion
principal nucleus

2) cross midline
medial lemniscus

3) pons, descending spinal tract
4) VPM, face

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30
Q

Anterolateral System

includes what 3 tracts

A

ascending pathway for pain and temperature information, axons of dorsal horn second order neurons that cross midline and ascend anterolaterally

Includes: spinothalamic, spinoreticular, and spinomesencephalic tract

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31
Q

Spinothalamic tract

A

pain pathway to thalamus

Cell bodies in dorsal horn –> Projects to nuclei of ventrobasal thalamus (includes VPL) –> somatosensory cortex

Processes information related to localization of pain

-CONSCIOUS information on skin temperature

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32
Q

Spinoreticular tract

A

pain pathway that leads to forebrain arousal and elicits emotional/behavioral responses

second order axons end information via reticular formation to hypothalaumus

Connects to limbic system

Terminates in pons and medulla

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33
Q

Spinomesencephalic tract

A

projects to midbrain periaqueductal gray region (PAG)

Descending control of pain

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34
Q

Anterolateral system have cell bodies in the _______ or __________

A

DRG (trunk and limbs)

Trigeminal ganglia (head and neck)

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35
Q

primary neurons in anterolateral system synapse in __________ or __________

A

dorsal horn of spinal cord OR spinal trigeminal nucleus

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36
Q

Trigeminal System

A

pain and temperature input from head and neck

Axons enter CNS at level of pons, first synapse in spinal trigeminal nucleus

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37
Q

Cool receptors

A

(10-37 degrees C)

10x more than warm receptors

A-delta fibers

Decrease temp = increased AP frequency

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38
Q

Warm receptors

A

(30-48 degrees C)

C fibers

Increase temp = increased AP frequency

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39
Q

Within range of ____-___ degrees C we sense changes in skin as cooling/warming - outside this range = PAIN

Neutral ____ deg C, cold/warm receptor afferents have same firing rate

A

10-48

33

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40
Q

Are we wired to detect rapid change or gradual change in temperature?

A

RAPID change

Transient AP frequency followed by a steady state change after a rapid step change in temperature

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41
Q

Thermal nociceptors

fiber type?
stimulated by what?

A

extreme temperatures (less than 5C or >43C)

Ad = extreme hot, (opposite of normal)

C fibers = extreme cold, (opposite of normal)

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42
Q

Mechanical nociceptors

fiber type?
stimulated by what?

A

intense pressure (not touch)

Ad fibers

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43
Q

Polymodal Nociceptors

fiber type?

stimulated by what?

3 examples

A

high-intensity mechanical, chemical, or thermal stimuli (C fibers)

1) Vanilloid Receptors (e.g. VR1 Capsaicin receptor)
2) P2X receptors: ionotropic receptors opened by ATP
3) ASIC receptors: acid sensing channels

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44
Q

Types of nociceptors (3)

A

1) thermal nociceptors
2) mechanical nociceptors
3) Polymodal nociceptors

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45
Q

First pain

fiber type
localization
sensation

A

Ad fibers → detect tolerable, localized, “pricking pain”, tolerable

  • Alerts you, well-localized
  • Faster conduction velocity than C fibers

Smaller receptive field = better localized spatial discrimination

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46
Q

Second pain

fiber type
localization
sensation

A

intolerable, diffusely localized, “burning” pain

Slower conduction velocity than Ad fibers

Larger receptive field = dull, aching, poorly localized pain

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47
Q

As increasing pressure applied around arm, nerve fibers are lost in what order? (e.g. BP cuff)

A

Most metabolically active, large diameter Aa and AB fibers become nonconductive first → lose touch, vibration, joint position/movement

Next Ad fibers blocked → only burning sensation remains

Next C fibers blocked → no sensation remains

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48
Q

Anesthetics affect nerve fibers in what order and blocks what sensations?

A

Low dose → preferentially block small C fibers (suppress burning pain)

Higher doses → block pricking pain

Even high dose → block touch and motor

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49
Q

Pain activators (4)

A

Bradykinin
Potassium
Acid
Serotonin (5-HT)

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50
Q

Activators vs. sensitizers

A

Activators: lead to direct activation of nociceptors

Sensitizers: decrease threshold for activation of nociceptors

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51
Q

Bradykinin is an activator for ____ and ____ fibers and increases the synthesis of _______

A

→ Ad and C fiber activator

Also increases synthesis of prostaglandins (Sensitizer)

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52
Q

Primary hyperalgesia

A

sensitization of nociceptors

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53
Q

Allodynia

A

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

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54
Q

VR-1 Receptor

A

capsaicin receptor, non selective cation channel (activation = depolarization)

Strongly activated by capsaicin and weakly activated by acids

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55
Q

Modality Segregation

A

afferents conveying different modalities segregate to different positions within dorsal horn/trigeminal nucleus

EX) C fiber terminate in substantia gelatinosa (Rexed’s lamina II)

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56
Q

Referred pain

A

convergence of visceral and somatic inputs in dorsal horn neuron

Injury to internal organ perceived as injury to cutaneous site

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57
Q

Glutamate function at first synapse in pain pathway

A

primary NT released by nociceptive sensory neurons at site of first synapse in dorsal horn

Bind AMPA and NMDA ionotropic receptors → generate both fast and slower excitatory responses

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58
Q

Substance P role at first synapse in pain pathway

A

stored in vesicles in dorsal horn

Released by C fibers in response to strong repetitive stimulation in CNS at site of first synapse

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59
Q

What happens when substance P is released by C fibers at the first synapse in pain pathway?

A

→ binds Neurokinin 1 receptor (NK-1) → close K+ channel, depolarization

-Leads to enhancement and prolongation of glutamate actions

Takes longer to diffuse out of synapse → broad central sensitization at level of dorsal horn

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60
Q

Gate Control Theory

A

determine if you perceive pain based on balance of excitation and inhibition at the first synapse in dorsal horn

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61
Q

Why do you stroke or rub an area evoking pain?

A

Activation of non-nociceptive (A-Beta) fibers → activation of dorsal horn INHIBITORY INTERNEURONS that in turn inhibit synapses activated by nociceptive fibers

AB fibers excite inhibitory interneurons that decrease efficacy of nociceptive dorsal horn synapses

Elimination of AB fiber input → increase in pain sensitization (hyperalgesia)

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62
Q

Aspirin as an analgesic

A

COX inhibitor

Prevents conversion of arachidonic acid to prostaglandin → prevent nociceptor sensitization

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63
Q

Opiates as an analgesic (Morphine and Codeine)

A

Bind G-protein coupled opiate receptors → activation leads to inhibition of neuron on which they are found

High concentration of opiate receptors in PAG

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64
Q

What happens when PAG is activated?

A

PAG → nucleus raphe → spinal cord inhibitory interneuron

PAG especially sensitive to opiates → greater excitatory output from PAG → increased excitation of enkephalinergic inhibitory interneuron

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65
Q

Endogenous opiates include _________ and __________

A

Enkephalins, B-endorphin and Dynorphins (endorphins)

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66
Q

Naloxone

A

inhibitor of opiate receptor, blocks placebo effect too!

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67
Q

Cannabinoids effects

A

interact with opiate system (activate PAG) and immune system

→ Decrease secretion of proinflammatory cytokines, and increase secretion of anti-inflammatory cytokines

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68
Q

What kinds of things activate the PAG (midbrain)

A

1) cognitive factors (e.g. placebo effect) via frontal cortex and insular cortex
2) Systemic morphine
3) Stress (via hypothalamus)
4) Emotions (via amygdala)

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69
Q

Triple Response

A

occurs as a result of injury = reddening, wheal, and flare

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70
Q

What generates the redness and wheal during triple response?

A

Tissue damage → Bradykinin local production → activator, vasodilator (heat, redness), increased permeability (edema)

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71
Q

Flare

A

pink zone around inflamed area

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72
Q

Generating a flare

A

Bradykinin → activate C fiber nociceptors → AP propagates in 2 directions

1) towards cell body
2) along collaterals toward peripheral sites in neighboring skin regions

→ Substance P released into surrounding wound region

→ vasodilation, sensitization

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73
Q

What is the adaptive benefit if the triple response?

A

These physiological changes promote behavioral changes that minimize contact with wound, and allow better repair of wounded area

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74
Q

Without innervation from the nervous system what happens to the triple response?

A

→ only get red center, and wheal, no flare, no sensitization

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75
Q

Substance P

A

Released by C fibers in response to repetitive stimulation in CNS at site of first synapse

Acts as a sensitizer
Released by collateral terminals in neighboring skin regions to tissue damage → Flare production

Causes vasodilation (less than bradykinin) → pink instead of red

→ Flare region shows enhanced response to noxious stimuli

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76
Q

What is the pathway that allows pain to be controlled by descending inputs?

1) __________ stimulated in midbrain
2) –> ___________ in medulla
3) → project to spinal cord via __________ and release ________ (NT)
4) ______ (NT) in spinal cord → inhibit second-order neurons by exciting __________________
5) Interneuron secretes NT _________ → presynaptic inhibition (block _______________) AND postsynaptic inhibition (open ____________)

A

1) Periaqueductal Gray Region (PAG) stimulated in midbrain
2) PAG –> nucleus raphe magnus in medulla
3) Nucleus raphe neurons → project to spinal cord via dorsal lateral funiculus and release serotonin
4) Serotonin in spinal cord → inhibit second-order neurons by exciting enkephalinergic inhibitory interneurons
5) Interneuron secretes NT enkephalin → presynaptic inhibition (block voltage gated Ca2+ channels) AND postsynaptic inhibition (open K+ channels)

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77
Q

When the PAG is stimulated what sensation is attenuated, and what sensation persists?

A

PAG stimulation in midbrain → analgesia (pain sensation attenuated) while touch, pressure and temperature sensation persists

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78
Q

Placebo Effect

A

physiologic response evoked by administration of inert drug

Activity in neocortex and/or limbic system → PAG activation via increased secretion of endorphins → inhibition of second-order neurons in dorsal horn of pain pathway

BLOCKED by nalaxone (opiate receptor blocker) –> indicates important role of PAG in this process

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79
Q

Stress-Induced Analgesia

A

adaptive response of individual to stressful conditions

Stress → increased limbic system activity (amygdala + hypothalamus) → activation of PAG

→ inhibition of second-order neurons in dorsal horn of pain pathway

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80
Q

Neuropathic pain

peripheral vs. central mechanism generally include what?

A

persistent pain syndrome resulting from peripheral or central nervous system damage

1) Peripheral = Na+ channels
2) Central = GABA content/receptors, sprouting/rewiring, glia and immune system

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81
Q

Peripheral mechanism for causing neuropathic pain

A

Following nerve damage, expression, distribution, and function of Na+ channels profoundly altered → spontaneous discharge of pain primary afferents

causes chronic pain patients to experience pain in absence of any stimuli

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82
Q

Types of sodium channels involved in neuropathic pain (3)

A

Na1.7 = TTX sensitive

Na1.8 and 1.9 = TTX resistant

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83
Q

What happens if you have a mutation in Na1.7 channel?

A

Na1.7 = TTX sensitive

Familial primary erythermalgia = mutation in SCN9A gene that encodes this channel → pain, warmth, redness in hands/feet

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84
Q

Familial primary erythermalgia

A

mutation in SCN9A gene that encodes this channel → pain, warmth, redness in hands/feet

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85
Q

What happens if you have a mutation in Na 1.8 or 1.9?

A

Na1.8 and 1.9 = TTX resistant

Lack this current → higher pain thresholds

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86
Q

Role of GABA in Central mechanism of neuropathic pain generation

A

Damage → neuronal loss, reduction in GABA content, decreased number of GABA and opiate receptors

→ reduce inhibition of dorsal horn neurons → increase their excitability (sensitization)

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87
Q

Role of sprouting and reqwiring in Central mechanism of neuropathic pain generation

A

Following injury to C fibers, AB afferents sprout and invade substantia gelatinosa (formerly region with only pain neurons synapse)

→ second-order neurons in SG that are normally activated only by pain input are now also activated by non-noxious stimuli (allodynia)

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88
Q

Role of glial and immune cells in Central mechanism of neuropathic pain generation

Macrophages in DRG secrete _________ which binds ____________ and activate __________

Microglia in spinal cord secrete ________ which causes what?

A

Inflammatory reaction to peripheral injury at lesion site, DRG, and spinal cord

Macrophages in DRG: secrete TNF → bind TNF-R1 on sensory neurons → activate TTX-resistant sodium channels

Microglia in spinal cord → secrete BDNF → change chloride reversal potential → GABA receptor activation = excitation, NOT inhibition

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89
Q

Epidemiology of headache

A

Complaint of more than half of patients seeking medical advice from physician

more common in women

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90
Q

Primary headache (3 kinds)

A

no known cause (e.g. migraines) (>90%)

Episodic (coming and going) or chronic (present most days for > 3 months)

Includes:

1) Migraine
2) Tension headache
3) Cluster headache

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91
Q

Secondary headache

A

attributed to a systemic or cephalic disorder

Constant

Associated with underlying cranial or systemic pathology in temporal relationship with onset of headache

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92
Q

Migraine criteria (3)

A

1) at least 5 recurring headaches that last 4-72 hours
2) with at least 2 of the following (unilateral in location, pulsating in character, moderate or severe intensity, pain increases with physical activity)
3) and must also be associated with nausea/vomiting or photo/phonophobia

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93
Q

Aura

A

neurologic symptoms preceding headache - visual, sensory, language, motor, brainstem, retinal changes

Migraine may or may not have aura associated

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94
Q

Abortive treatment of migraines (5)

A

1) Ibuprofen, Naproxen, *Acetaminophen
2) Combo: ibuprofen or acetaminophen + caffeine/ASA
3) Triptans (sumatriptan)
4) Ergotamine derivatives (Dihydroergotamine, DHE)
5) Dopamine receptor antagonists (for nausea and vomiting) = *Metoclopramide

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95
Q

Prophylactic treatment of migraines (6)

A

1-3) Antihypertensives: *B-blockers (propanolol), *Ca2+ blockers (verapamil), *ACEIs/ARBs (lisinopril / -sartans)

4) tricyclic antidepressants (SSRIs)
5) anti-epileptics/convulsants
6) botox

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96
Q

Pain pathway of migraine

_______ + ________ –> trigeminal activation at ____________

–> pain signal transduction to ____________ –> ________ then _________

A

Vasodilation + peptide release

→ trigeminal activation at trigeminal ganglion

→ pain signal transmission to trigeminal nucleus caudalis

→ thalamus and cortex

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97
Q

Cluster headache criteria (3)

aka Trigeminal autonomic cephalalgias

A

1) at least 5 episodes of severe, unilateral periorbital and/or temporal pain that lasts 15-180 min
2) Pain should recur at least every other day up to 8x per day
3) Ipsilateral, conjunctival injection, lacrimation, nasal congestion, rhinorrhea, eyelid edema, ptosis, miosis, facial swelling, ear fullness, restlessness/agitation

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98
Q

Tension type headache criteria (3)

A

1) at least 10 episodes of headache lasting 30min-7 days
2) each episode characterized by at least 2 of the following (pressing or tightening sensation, mild/moderate in severity, bilateral, not aggravated by physical activity)
3) Patients must NOT have nausea, vomiting, photophobia or phonophobia

**FEATURELESS headache

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99
Q

Trigeminal Neuralgia criteria (3)

A

primary or secondary headache

1) very brief pain in trigeminal nerve distribution lasting less than 1 second up to 2 min.
2) Intense, sharp, superficial, or stabbing pain
3) Triggered by sensory stimulation of particular area within trigeminal sensory innervation or by factor such as chewing/brushing teeth

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100
Q

Red flags indicating dangerous condition could be causing headache

A

SNOOP

1) Systemic symptoms (fever, weight loss) or secondary risk factors (HIV, systemic cancer)
2) Neurologic symptoms (confusion, impaired alertness/consciousness)
3) Onset sudden, abrupt
4) Older patient with new onset and progressive headaches
5) Previous history: Change in headache frequency, severity, or clinical features

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101
Q

Meningitis

features of headache + other signs

A

Acute pain (hours for bacterial, 1-2 days for viral)

Associated FEVER, stiff neck (meningismus), nausea/vomiting, altered consciousness, signs of meningeal irritation (Kernig, Brudzinski signs)

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102
Q

Traumatic injury to head

features of headache + other signs

A

Pain develops within 7 days of injury, resolves by 3 months

Dizziness, poor concentration, irritability and insomnia

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103
Q

Subarachnoid hemorrhage

features of headache + other signs

A

Severe “thunderclap” headache, sudden onset, +/- impaired consciousness or focal neurologic signs

Neck stiffness, photophobia, nausea, vomiting, neurologic signs, depressed arousal, obtundation

Aneurysm rupture accounts for 80% of cases

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104
Q

Giant cell arteritis symptoms

A

jaw claudication, temporal artery region scalp tenderness, joint pain, constitutional symptoms (fever, malaise, weight loss)

Usually in older patients (>60 years)

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105
Q

Giant cell arteritis diagnosis

A

Elevated ESR and CRP

Must biopsy temporal artery to confirm dx

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106
Q

Giant cell arteritis treatment

A

IMMEDIATE steroid treatment

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107
Q

Increased intracranial pressure

features of headache + other signs

A

headache that occurs/worsens with exertion, retro-orbital pain, nausea/vomiting, pulsatile intracranial noises, transient visual obscurations, photopsias, diplopia, vision loss

Headache worse when first awaking from sleep

  • 6th nerve palsies
  • Papilledema (edema of optic nerve), vision loss from optic nerve dysfunction
  • Possible neurologic exam findings
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108
Q

Idiopathic Intracranial Hypertension

A

1) normal CSF constituents
2) normal neuroimaging
3) normal neuro exam EXCEPT for PAPILLEDEMA and 6th NERVE PALSIES
4) no other causes to explain increased ICP

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109
Q

Cluster headache prophylaxis (3)

A

Lithium, methysergide (ergo), verapamil

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110
Q

Cluster headache abortive treatment (5)

A 
ergotamine (DHE)
glucocorticoids
lidocaine
oxygen
sumatriptan
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111
Q

Tension Headaches prophylaxis (2)

A

TCADs (amitriptyline)

SSRIs

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112
Q

Tension headaches abortive treatment (2)

A

NSAIDs

Acetaminophen

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113
Q

Medication overuse headache

A

dull or migraine-like headache present for at least 15 days a month, associated with overuse of analgesics

114
Q

High risk drugs that can cause medication overuse headache (3)

A

butalbital combinations
ASA-acetaminophen-caffeine
opioids

115
Q

Moderate risk drugs that can cause medication overuse headache (2)

A

triptans, ergots

116
Q

Low risk drugs that can cause medication overuse headache (1)

A

NSAIDs

117
Q

Pathogenesis of Migraine (5 steps)

A

1) Trigeminal Neurovascular Dysfunction
2) Trigeminal neurovascular activation
3) Release of vasoactive peptides (substance P + calcitonin and prostaglandins)
4) Neuroinflammation (including PG release) and Vasodilation of pial and dural vessels
5) Moderate to severe pain of migraine

118
Q

Serotonin in Migraines

A

serotonin=primary target in migraine treatment

5HT-1B receptors → Gi/o → Presynaptic inhibition, pulmonary vasoconstriction
Inhibits presynaptic release of vasoactive peptides

5HT-1D receptors→ Gi/o → Presynaptic decrease release, cerebral vasoconstriction
Inhibits vasodilation of pial/dural vessels

119
Q

“-triptans” (sumatriptan / zolmitriptan)

mechanism of action and 3 main effects that reduce migraine

A

Agonist activity at 5HT-1B/1D receptors →

1) Vasoconstriction of cerebral vessels → reverse vasodilation-induced throbbing headache
2) Inhibit release of vasodilatory, neuroinflammatory, and pain causing peptides
3) Prevent activation of pain fibers in trigeminal nerves

120
Q

Triptans should be avoided in which patients?

A

Avoid use in patients with uncontrolled HTN, cerebrovascular, coronary, or arterial disease

DO NOT use within 24 hrs of ergot alkaloid or concurrently with MAOI→ vasoconstriction additive

121
Q

Side effects of triptans (4)

A

1) Tingling, flushing dizziness, drowsiness, fatigue

2) Coronary vasospasm, angina MI, cardiac arrhythmia
- -> Heaviness/tightness/pressure in chest

3) Stroke and death
4) Increased risk of serotonin syndrome → too much serotonin activity → neuromuscular effects (clonus), ANS changes, mental status changes (Agitation, delirium, hypervigilance)

122
Q

Triptans are used for what?

A

first line drug for moderate/severe migraines

123
Q

NSAIDs (ibuprofen / naproxen / Celecoxib / ASA / Acetaminophen)

are used for what kinds of headaches?

A

mild/moderate episodes of migraine without nausea or disabling symptoms

124
Q

Mechanism of action of NSAIDs in headache

A

inhibits COX-2

Interrupts inflammatory mediator synthesis/release initiated by CGRP (calcitonin gene-related peptide)

125
Q

NSAIDs should be avoided in what kinds of patients?

A

should be avoided in patients with acute gastritis, peptic ulcer disease, renal insufficiency, and bleeding disorders

126
Q

Ergot alkaloids (dihydroergotamine, DHE) use for what kinds of headaches

A

terminating moderate/severe migraine attacks

127
Q

Ergot alkaloids (dihydroergotamine, DHE) mechanism of action

A

agonist at 5HT-1B/1D receptors

Similar to triptans

1) Vasoconstriction of cerebral vessels → reverse vasodilation-induced throbbing headache
2) Inhibit release of vasodilatory, neuroinflammatory, and pain causing peptides
3) Prevent activation of pain fibers in trigeminal nerves

128
Q

Side effects of Ergot alkaloids (dihydroergotamine, DHE)

A

More toxic and less effective than triptans - NOT FIRST LINE

Mild effects = nausea, vomiting → treat concurrently with antiemetic

Serious effects = vascular occlusion and gangrene due to stimulation of a1-adrenergic receptors

129
Q

Ergot alkaloids should NOT be used in what kinds of patients?

A

AVOID USE WITH non-selective B-blockers or other vasoconstrictors (→ severe peripheral ischemia)

AVOID USE in patients with ischemic vascular disease

130
Q

When to use prophylaxis treatment of migraines? (7)

A

1) Severe
2) frequent (>4/month)
3) long lasting (>12 hours)
4) disabling
5) Failure-overuse of acute therapies
6) Contraindications to vasoconstrictor therapies
7) Adverse drug events

131
Q

Local anesthetics cause

A

Loss of sensation, particularly pain, in circumscribed region of body

No loss of consciousness

132
Q

Mechanism og local anesthetics

A

Block AP initiation and conduction via block of voltage-gated Na+ channels in peripheral nerve

133
Q

Method of application of local anesthetic determines ____

A

body region and size of region affected

134
Q

Where can local anesthetics block Na channels

A

Anywhere!

Including CNS and heart

135
Q

Tripartite structure of local anesthetics consists of:

A
  1. Lipophilic aromatic portions
  2. intermediate alkyl chain
    Hydrophilic amine portion
136
Q

What are the two types of local anesthetics?

A
  1. amide

2. ester

137
Q

What part of the tripartite structure do amide and ester local anesthetics differ in?

A

Intermediate alkyl chain

138
Q

Amides have how many i’s in their name?

A

2

Lidocaine, Bupivacaine

139
Q

Esters have how many i’s in their name

A

one

Cocaine, procaine, benzocaine, tetracaine

140
Q

Amide local anesthetics: duration of action and termination

A

Duration of action: A1-acid glycoprotein (plasma protein) → readily binds amide local anesthetics → amides typically have longer duration of action

Termination: Metabolized by liver → excreted via kidney

141
Q

Ester local anesthetic: Termination

A

Termination: Hydrolyzed in plasma by esterase (pseudo cholinesterase), also hydrolyzed in liver → excreted via kidney

142
Q

Effective of pH in determining effectiveness of local anesthetics

A

Local anesthetics = weak bases: pKa=7.7-9.0 → partly ionized at pH 7.4

  1. Cationic (+) form → bind better to local anesthetic binding site
  2. Neutral form → cross plasma membrane to reach site of action
    ii. In cases with increased tissue acidity (e.g. infection), need to give increased dose, because will decrease amount of neutral local anesthetic present
143
Q

binding of Neutral form of local anesthetics

A

a. Bind site when channel is OPEN via intracellular pore entrance
b. Can cross plasma membrane even when channel is closed/inactivated
c. Much slower rate

144
Q

binding of Cationic form of local anesthetics

A

a. Enters OPEN channel and binds
b. High affinity for Na+ channel pore
c. Enters/exits channel when channel is in OPEN state, but NOT when channel is closed or inactivated

145
Q

Local anesthetics exhibit ___ dependent blockage

A

use

146
Q

Use-dependent block

A

the more Nav channel is open/used, the greater degree of local anesthetic binding and block
i.UNBLOCK is also use dependent - channel must be open

147
Q

Which form (neutral or cationic) are needed for local anesthetic blockage of Na channel?

A

Both

148
Q

Local anesthetics and the inactivated state of Na channels

A

Local anesthetics can also increase stability of inactivated state of channel → prolong refractory period of nerve

149
Q

Local anesthetics preferentially block which fibers?

A

Preferential conduction block of small fibers: Conduction block occurs at LOWER DOSES for SMALL DIAMETER axons (shorter internodal distance, more rapid AP firing rate) than in large diameter axons

1.Best block conduction in small-diameter, myelinated and unmyelinated axons, such as C fibers → pain sensation first functionality lost

150
Q

Physicochemical properties of local anesthetics that determine potency

A

determined by lipid solubility→higher lipid solubility = higher potency

151
Q

Physicochemical properties of local anesthetics that determine speed of onset

A

determined by pKa

Lower pKa → more uncharged → more easily get across cell membranes → faster speed of onset

152
Q

Physicochemical properties of anesthetics that determine duration of action

A

determined by protein-binding capacity

More bound to plasma protein → longer duration of action

153
Q

Topical application of local anesthetics: 3 drugs, used for what, and disadvantage

A

tetracaine, lidocaine, cocaine

  1. Superficial anesthesia
  2. Disadvantage = considerable absorption into circulation
154
Q

Injection of local anesthetic into tissue: 3 drugs, uses, and disadvantage

A

lidocaine, procaine, bupivacaine

  1. Superficial anesthesia, function of underlying organ unaffected
  2. Disadvantage: need large dose, significant absorption into circulation
155
Q

Nerve block: what is it, two drugs used, what is it used for

A

injection of high concentration near peripheral nerve/nerve plexus

  1. Lidocaine (2-4 hours), bupivacaine (longer duration)
  2. Anesthetize larger body regions
156
Q

Intravenous regional anesthesia AKA ___?

What is it and drug used?

A

Bier’s block

tourniquet applied, inject anesthetic via catheter for limb anesthesia

1.Lidocaine

157
Q

Spinal anesthesia: 3 drugs used with duration of action

A

inject into CSF

  1. Anesthetize large body areas with low plasma level of drug
  2. Lidocaine (shorter procedures), Bupivacaine (intermediate), and tetracaine (long lasting, ester-linked drug)
    a. No plasma esterase activity in CSF → long duration of action
158
Q

Epidural anesthesia

A

inject just outside dura-enclosed spinal canal

  1. Allows repeated/continuous anesthetic application
  2. Higher plasma level of anesthetic than spinal anesthesia
  3. Lidocaine (shorter), bupivacaine (longer procedures)
159
Q

Often times, ____ are used with local anesthetics

A

vasoconstrictors

160
Q

Why are vasoconstrictors used with local anesthetics

A

prolongs duration of conduction blockade by reducing blood flow in vicinity of injection

i.Retards systemic absorption of anesthetic

EX) Epinephrine = vasoconstrictor

iii.Local anesthetics typically reduce SNS activity → vasodilation

161
Q

7 side effects of local anesthetics

A

i. OD → convulsions due to action on inhibitory interneurons of CNS (cross BBB)
ii. Interfere with ANS function (give with epinephrine to avoid this)
iii. Block cardiac Na channels → Cardiovascular effects, proarrhythmic
iv. Vasodilation via action on vascular smooth muscle
v. Can cross placenta and enter fetal circulation
vi. Inhibit neuromuscular transmission
vii. Allergic reactions - hypersensitivity reactions

162
Q

Tetrodotoxin

A

toxin found in puffer fish, newts, and frogs

i. Block extracellular entrance of voltage-gated Na+ channel
1. VERY high affinity for Nav channel
ii. Cause death by paralyzing respiratory muscles, not by action on heart

163
Q

Saxitoxin

A

toxin found in dinoflagellates (red tide) eaten by clams/shellfish

i. Block extracellular entrance of voltage-gated Na+ channel
ii. Cause death by paralyzing respiratory muscles, not by action on heart

164
Q

Paresthesia

A

abnormal sensation - burning, pricking, tickling, tingling, pins and needles

165
Q

Dysesthesia

A

impairment of sensation short of anesthesia

166
Q

Hyperesthesia

A

abnormal acuteness of sensitivity to touch, pain or other sensory stimuli

167
Q

Paresis

A

decreased strength

168
Q

Plegia

A

complete loss of strength

169
Q

Dermatome

A

cutaneous area served by an individual SENSORY ROOT

170
Q

Myotome

A

muscles innervated by an individual MOTOR ROOT

171
Q

Radiculopathy

A

sensory and/or motor dysfunction due to injury to a nerve root

172
Q

Myelopathy

A

disorder resulting in spinal cord dysfunction

173
Q

Nerve root

A

combined sensory (dorsal) and motor (ventral) rami of spinal cord

31 pairs of nerve roots (8 Cervical, 12 Thoracic, 5 Lumbar, 5 Sacral, 1 Coccygeal)

Vertebral body number is different from underlying cord segment

174
Q

Intervertebral foramen

A

opening formed by 2 adjacent vertebral bodies through which nerve roots travel

175
Q

Spinothalamic tract

A

(pain and temperature)

first synapse in substantia gelatinosa (dorsal horn of spinal cord) and crossing via anterior white commissure in spinal cord

176
Q

Posterior/Dorsal columns

A

(vibration and position)

first synapse in medulla at nucleus gracilis/cuneatus and crossing in medulla after synapse

177
Q

Lateral Corticospinal tract

A

motor (extremities, head/neck)

crossing in medulla at pyramid, first synapse in ventral horn of spinal cord on alpha motor neurons

178
Q

At what level do the nerve roots exit?

A

C1,2,3,4,5,6,7 exit ABOVE same numbered vertebra
(Only have 7 cervical vertebrae, but 8 cervical roots)

–>
C8 and below exit BELOW same numbered vertebra

179
Q

Anterior cerebral artery

A

supplies ventral spinal cord

(created by two branches of vertebral artery that come together to form single midline artery)

Gets contributions from radicular branches at each level

180
Q

Spinal cord level each vertebral body overlies

Upper cervical
Lower cervical
Upper thoracic
Lower thoracic/lumbar
Conus medullaris
A

Upper cervical: vertebra # overlies same cord segment #
EX) C2 vertebra overlies C2 spinal cord segment

Lower cervical: vertebra # overlies cord segment # + 1
EX) C6 bone, C7 cord

Upper thoracic: vertebra # overlies cord segment # + 2
EX) T4 bone, T6 cord

Lower thoracic/lumbar: vertebra # overlies cord segment # + 2-3
EX) T11 bone → L1-2 cord

Lower edge of L1 vertebral body overlies cord tip (conus medullaris)

181
Q

Somatotopic organization of tracts

Dorsal column: _____ is most medial, _______ is most lateral

Corticospinal and spinothalamic tracts: ______ is most medial, _______ is most lateral

A

Dorsal column: sacral (medial) → cervical (lateral)

Corticospinal and spinothalamic tracts: sacral (lateral) → cervical (medial)

182
Q

Signs/symptoms of radiculopathy

A

Pain = shooting, burning, tingling, numbness
-Radiates to dermatome or myotome

Spurling’s sign
Lasegue’s sign

183
Q

Spurling’s sign

A

foraminal compression test

Turn head towards a narrowed neural foramen → tight foramen can cause acute pinching of nerve root → pain radiates out with nerve root into arms

sign of radiculopathy

184
Q

Lasegue’s sign

A

straight leg raising test

Sciatic nerve test - if sciatic nerve roots are under compression → shooting shock like sensation down legs

sign of radiculopathy

185
Q

Common causes of radiculopathy

A

compression by degenerative joint disease or herniated disc (posterior/lateral direction) near intervertebral foramen

186
Q

Lhermitte’s symptom

A

pain syndrome arising due to disease of spinal cord

Neck flexion results in “electric shock” sensation down back and/or arms

Due to posterior column disease

Indicative of myelopathy

187
Q

Polyradiculopathy

A

impingement of collection of nerve roots within cauda equina (in lumbosacral spine below conus medullaris) → can cause problems with bowel/bladder function

188
Q

Spinal shock

A

physiologic disruption of all spinal cord function
Loss of all neurological activity below level of injury, including loss of motor, sensory, reflex, and autonomic function

-no bulbocavernosus reflex

189
Q

Bulbocavernosus reflex

A

indicates when spinal shock has resolved

Tug on the tip of the dick, if your asshole squeezes tightly, then reflex is present

If BC reflex is present and patient still is not moving/no sensation → anatomic transection of fibers

190
Q

Neurogenic shock

A

disruption of descending sympathetic outflow

No sympathetic response and unopposed vagal tone

Cardiovascular instability

Treated with dopamine drip

191
Q

Extramedullary lesions

A

arise from outside cord

EARLY PAIN and UMN signs

Pain and temperature sensation evolves in ASCENDING fashion (affects sacral, lumbar, then thoracic, etc.)

192
Q

Intramedullary lesions

A

arise within cord

Cause early bladder dysfunction with only LATE development of PAIN

Loss of pain and temperature progresses in DESCENDING fashion (Cervical → thoracic early, then lumbar → sacral later)

193
Q

Upper motor neuron signs (3 reflex signs)

A

hyperreflexia

  • Babinski sign
  • Hoffman’s sign
  • Crossed adductor response
194
Q

Babinski sign

A

Plantar response: normal = flexion of toes

Babinski sign = extension of big toe, fanning of other toes → HYPERREFLEXIA

195
Q

Hoffman’s sign

A

hyperreflexia in upper extremity

196
Q

Complete Cord Transection

tracts affected?
deficit?

A

Tracts: all ascending and descending

Deficit: sensory + motor levels below lesions

→ Spinal shock, followed by UMN signs

197
Q

Central lesions

tracts affected?
deficit?

A

EX) syringomyelia (fluid filled cavity in cord)

Tracts: initially involve CROSSING SPINOTHALAMIC tract

Deficit: pain/temp loss at level of lesion with sparing of position sensation
→ “Cape-like” distribution if in C-spine

198
Q

Posterior Column Syndrome

tracts affected?
deficit?

A

EX) Tabes dorsalis (neurosyphilis)

Tracts: DORSAL (posterior column)

Deficit: bilateral loss of position and vibration sensation

199
Q

Combined anterior horn cell-pyramidal tract syndrome

tracts affected?
deficit?

A

Tracts: CORTICOSPINAL and LMN cells in cord

Deficit: loss of bilateral strength + UMN/LMN signs
-Fasciculations, atrophy, decreased or increased deep-tendon reflexes, normal sensation

200
Q

Brown-Sequard (hemi-section)

tracts affected?
deficit?

A

Tracts: crossed spinothalamic, uncrossed dorsal column, crossed corticospinal

Deficit:
Below lesion, loss of: contralateral pain/temp, ipsilateral, position and strength

201
Q

Posterolateral column syndrome

tracts affected?
deficit?

A

EX) B12 deficiency

Tracts: DORSAL column, CORTICOSPINAL tract

Deficit: bilateral loss of position, vibration, strength

202
Q

Anterior Horn Cell Syndrome

tracts affected?
deficit?

A

Tract: none - lower motor neurons only

Deficit: bilateral loss of strength
-Fasciculations, decreased tone, decreased deep-tendon-reflexes

*Spares sensory tracts and bladder functions

203
Q

Anterior Spinal Artery Occlusion

tracts affected?
deficit?

A

Tracts: SPINOTHALAMIC and CORTICOSPINAL tract

Deficit: bilateral loss of strength, pain/temp

*Spare position sense

204
Q

Pyramidal Tract Syndrome

tracts affected?
deficit?

A

Tract: CORICOSPINAL tract

Deficit: bilateral UMN weakness with spastic gait
-Increased deep-tendon-reflexes

*Complete sparing of all sensory tracts and bladder function

205
Q

Myelopathy with Radiculopathy

tracts affected?
deficit?

A

Tracts: any or all 3 tracts

Deficit: bilateral UMN syndrome with spastic gait
-Increased DTRs + ipsilateral or contralateral root signs

*Possible bladder dysfunction

206
Q

Conus medullaris syndrome

  • pain = early vs. late
  • muscle weakness where?
  • symmetric vs. asymmetric?
  • early vs. late bladder/bowel dysfunction
A

S3-S5, tip of cord
Supplies bladder, rectum, and genitalia

LATE pain in thighs and buttocks

Pelvic floor muscle weakness

SYMMETRIC “saddle” anesthesia numbness

EARLY bladder dysfunction
EARLY bowel and sexual dysfunction

207
Q

Cauda equina

  • pain = early vs. late
  • muscle weakness where?
  • symmetric vs. asymmetric?
  • early vs. late bladder/bowel dysfunction
A

ROOTS L1-S5

EARLY root pain radiating to legs

Leg weakness and decreased DTRs (LMN sign)

Patchy, ASYMMETRIC “saddle”

LATE bladder dysfunction
LATE bowel and sexual dysfunction

208
Q

Detrusor (smooth) muscle innervated by what?

A

activated by preganglionic parasympathetic outflow from S2-S4 (pelvic nerve)

209
Q

Involuntary (smooth) sphincter innervated by what?

A

controlled by sympathetic outflow, T10-L2 (hypogastric nerve)

210
Q

Skeletal (voluntary) muscle of pelvic floor innervated by what?

A

innervated by alpha motor neurons, S2-S4 (Pudendal nerve)

211
Q

Forebrain (medial frontal) role in micturition

A

voluntary inhibition of pontine center AND relaxation of voluntary sphincter

212
Q

Pontine micturition center

A

coordination of sympathetic and parasympathetic centers in spinal cord

213
Q

Flaccid Bladder

A

bladder does not contract → overflow incontinence

Parasympathetic lower motor neuron injury, axon compression/disruption

214
Q

Spastic Bladder

A

Descending pathways cut or injured (BILATERALLY) → UMN injury = initial flaccidity of bladder, then spasticity

Problems with coordination between sympathetic outflow (inhibited during voiding) and parasympathetic outflow (activated during voiding)

Urinary frequency and urgency

215
Q

What dermatome covers the nipple line?

A

T4 dermatome

216
Q

What dermatome covers the xiphoid process?

A

T6 dermatome

217
Q

What dermatome covers the umbilicus?

A

T10 dermatome

218
Q

C5 nerve root

motor function
reflex
usual disc involved

A

motor function = deltoid, infraspinatus, biceps

reflex = biceps

usual disc involved = C4-C5

219
Q

C6 nerve root

motor function
reflex
usual disc involved

A

motor function = wrist extension, biceps

reflex = biceps, brachioradialis

usual disc involved = C5-C6

220
Q

C7 nerve root

motor function
reflex
usual disc involved

A

motor function = Triceps

reflex = triceps

usual disc involved = C6-C7

221
Q

L4 nerve root

motor function
reflex
usual disc involved

A

motor function = Psoas, quads

reflex = patellar

usual disc involved = L3-4

222
Q

L5 nerve root

motor function
reflex
usual disc involved

A

motor function = foot dorsiflecion, big toe extension, foot eversion and inversion

reflex = none

usual disc involved = L4-L5

223
Q

S1 nerve root

motor function
reflex
usual disc involved

A

motor function = foot plantar flexion

reflex = achilles

usual disc involved = L5-S1

224
Q

C5 nerve root

sensory zone

A

shoulder, upper/lateral arm

225
Q

C6 nerve root

sensory zone

A

1st and 2nd digits of hand

226
Q

C7 nerve root

sensory zone

A

3rd digit (middle finger)

227
Q

L4 nerve root

sensory zone

A

Knee

medial leg

228
Q

L5 nerve root

sensory zone

A

dorsum of foot

great toe

229
Q

S1 nerve root

sensory zone

A

lateral foot
small toe
sole of foot

230
Q

Opioid indications/uses (5)

A

1) Relief of moderate to severe pain (best for NOCICEPTIVE pain - NOT effective for NEUROPATHIC pain)
2) Cough suppression (lower dose)
3) Diarrheal conditions (Loperamide - local GI tract actor)
4) Pulmonary edema associated with cardiac dysfunction
5) Effects on cardiovascular system: MI → analgesia, decrease cardiac load

231
Q

Opioid contraindications (7)

A

1) Respiratory dysfunction of any cause: emphysema, asthma, sleep apnea, severe obesity

Pathological:

2) Suspected head injury (opioids cause cerebral vasodilation → problem if pt has increased ICP)
3) Hypotension → lower BP even more
4) Shock → makes shock worse
5) Histamine release
6) Hypothyroidism
7) Impaired hepatic function → increased bioavailability and accumulation of toxic metabolites

232
Q

Behavioral effects of opioids (4)

A

1) Euphoria
2) Dysphoria (hallucinations)
3) Sedation, lethargy, confusion
4) Behavioral excitation (sign of acute toxicity)
- Due to buildup of toxic metabolites)

233
Q

Adverse interactions of opioids with other drugs (3)

A

1) CNS Depressants:
- Barbiturates: additive or synergistic CNS depression

2) Antipsychotics (Phenothiazines)
- Increase opioid analgesia, but increase respiratory depression
- Increase hypotensive effect of opioids

3) MAO Inhibitors and Tricyclic Antidepressants:
- Increase respiratory depression
- Can induce CNS excitation, delirium, and seizures

234
Q

Major/life-threatening side effects of opioids (5)

A

1) Respiratory depression = **MOST dangerous side effect of opioids
* *Avoid by avoiding use with head injury patients, and patients with compromised respiratory function

2) Nausea and vomiting
3) Pupillary Constriction (Miosis) - pinpoint pupils
4) Constipation

5) Anaphylaxis (rare)
- Cause histamine release (typically managed with antihistamines)

235
Q

μ , mu receptor

endogenous agonists?
Agonist drugs?

A

target of most clinically useful drugs - e.g. morphine

endogenous agonist = B-endorphin

236
Q

Three types of opioid receptors

A

1) μ , mu
2) d, delta
3) K, kappa

237
Q

μ , mu receptor activation causes ______ and ______.

This is accomplished what what 3 mechanisms?

A

analgesia (central) and respiratory depression

DECREASE neuronal excitability

1) Inhibit presynaptic voltage-gated Ca2+ channels → inhibit NT release
2) Activate potassium channels → membrane hyperpolarization
3) Inhibit cAMP synthesis

238
Q

Opioid Analgesics produce analgesia through what three mechanisms?

A

1) Inhibit spinal cord/ascending pain pathway
2) Activate “descending” pain pathway
3) Reduce subjective response to pain

239
Q

How do opiates inhibit the ascending pain pathway?

A

Inhibit spinothalamic “ascending” output neurons

Inhibit presynaptic excitatory NT release from primary afferent terminals in dorsal horn of spinal cord (substance P, glutamate)

240
Q

How do opiates activate the “descending” pain pathway?

A

Activate descending inhibitory output system in medulla, PAG, and locus coeruleus mediated by 5-HT and NE

Inhibiting GABA-ergic neurons → increase descending output

241
Q

Tolerance

A

Decreased response to drug as a result of previous exposure

  • Need increased dose to produce same pharmacological effect
  • Does not develop to all opioid effects equally (pupillary constriction, and constipation issues do not develop tolerance - resp depression does)

Tolerance can “generalize” to similar drugs (all mu agonists)

Tolerance reverses following withdrawal

242
Q

Dependene

A

physical and psychological

Produced by opioids in patients abusing opioid drugs and long-term therapy to treat chronic pain

Continued use of drug to prevent withdrawal

Different mechanism than tolerance

243
Q

Withdrawal

A

Occurs with cessation of opioid following prolonged use

Symptoms of withdrawal: OPPOSITE to those caused by acute opioids
–> “Flu-like”, dilated pupils, insomnia, restlessness, yawning, rhinorrhea, sweating, diarrhea, nausea, cramps, chills

Withdrawal not life-threatening with opiates

Clonidine (a2-agonist) can be used to treat withdrawal symptoms

244
Q

What are the main sites of opioid action?

Analgesia (3 sites)

Limbic and motor CNS regions (3 sites)

Reinforcement regions (2 sites)

Gut (1)

A

Analgesia:

1) Periaqueductal gray (descending pain)
2) Medulla nuclei (side effect respiratory depression)
3) Spinal cord dorsal horn (ascending pain)

Limbic and motor CNS regions:
Amygdala, hippocampus, striatum (affective response to pain)

“Reinforcement” Regions in CNS:
Ventral tegmentum, nucleus accumbens (addiction-abuse)

Gut: myenteric plexus (side effect-complication)

245
Q

Classes of endogenous opioids

A

1) Enkephalins = NT in brain/spinal cord
2) Endorphins = NT and neurohormone
3) Dynorphins
4) Endomorphins

246
Q

μ agonists include…(9)

A

1) Morphine
2) Heroin
3) Hydrocodone
4) Oxycodone
5) Codeine
6) Tramadol
7) Fentanyl
8) Loperamide
9) Dextromethorphan

247
Q

Morphine

A

μ agonists

Use: severe post-op pain and in acute trauma (IV/IM), also available in oral sustained release for chronic pain

248
Q

Heroin

A

μ agonists

not medicinal, schedule 1 drug

249
Q

Hydrocodone

A

μ agonists

aka Vicodin

Use: antitussive, weak analgesic, similar to codeine

250
Q

Oxycodone

A

μ agonists

aka Oxycontin, Percocet

Use: equipotent to morphine

oxycontin has highly abused currently

251
Q

Codeine

A

μ agonists

most commonly used opioid analgesic, also an antitussive

Less potent than morphine

Often combined with acetaminophen or ASA

10% metabolized to morphine by CYP2D6 metabolism, but some patients don’t have CYP2D6 → not effective in everyone

252
Q

Tramadol

A

μ agonists AND monoamine re-uptake inhibitor (potentiate descending pain pathway)

253
Q

Fentanyl

A

μ agonists

Extremely potent - 100x more potent than morphine

Use: perioperative and postoperative pain management

Adjunct to surgical anesthesia

Requires mechanical ventilation at high doses

254
Q

Loperamide

A

μ agonists

Anti-diarrheal (oral)
Low abuse potential

255
Q

Dextromethorphan

A

μ agonists

aka robitussin DM

cough suppresant

256
Q

Bupenorphine

A

Partial μ agonist

can precipitate mild withdrawal because partially antagonizes effects of morphine

257
Q

Naloxone

A

aka narcan

μ antagonist

Competitive antagonist

Short duration, may require readministration in tx of OD with long-acting agonists

258
Q

Drugs to treat constipation side effects (4)

A

Bisacodyl-senna (stimulant laxative)

Docusate (stool softener)

Magnesium hydroxide (osmotic laxative)

Polyethylene glycol (osmotic laxative)

259
Q

Methadone

A

mu agonist

used to alleviate symptoms of withdrawal

260
Q

Acute pain

A

short duration, resolves

Primarily NOCICEPTIVE (somatic more common than visceral)

261
Q

Chronic pain

A

pain that persists for longer than would be expected

Pain persists beyond normal healing time for acute injury → NEUROPATHIC

Related to a chronic disease → NOCICEPTIVE

Without identifiable organic cause → FUNCTIONAL

Associated with cancer

262
Q

Nociceptive pain

A

“normal” pain from activation of nociceptive nerve fibers

either somatic or visceral

263
Q

Somatic pain

A

arising from skin, bone, joint, muscle or CT

Throbbing, well-localized

264
Q

Visceral pain

A

arising from internal organs

Can be referred pain or well-localized

265
Q

NSAIDs use in nociceptive pain

A

inhibit COX-2 and PG synthesis → reduce peripheral and central sensitization

Reduce PG synthesis from tissue damage

Reduce PG release in central sensitization

266
Q

Celecoxib

A

COX-2 reversible inhibitor (can be used for analgesic and anti-inflammatory injury)

May increase risk of clotting

267
Q

Acetaminophen

A

COX-2 reversible inhibitor, CNS ONLY (no anti-inflammatory action, only analgesic)

Risk of hepatotoxicity

Safest one for patients with kidney dysfunction or gastric ulcers

268
Q

Ibuprofen

A

COX-½ reversible inhibitor

→ can have GI side effects

269
Q

Aspirin

A

COX-½ irreversible inhibitor
→ causes antiplatelet (bleeding)
→ can have GI side effects

270
Q

Local anesthetics (lidocaine) use in nociceptive pain

A

block voltage-sensitive Na+ channels → reduce nociceptive stimuli AP

Block noxious mechanical pain transmitted via Ad fiber and noxious heat/chemical pain in C fiber

(as well as non-noxious mechanical stimuli of AB fibers)

271
Q

NMDA receptor antagonists (Ketamine) use in nociceptive pain

A

block glutamate receptor depolarization at 2nd order neuron → decreased transmission of nociceptive stimuli

272
Q

Mu opioid receptor agonists (morphine) use in nociceptive pain

A

block glutamate-substance P release from primary neuron

AND

hyperpolarizes 2nd order neuron → reduce excitation of 2nd order neuron → decreased transmission of nociceptive stimuli

273
Q

A2-adrenergic receptor agonists (clonidine) use in nociceptive pain

A

block glutamate-substance P release from primary neuron → reduce excitation of 2nd order neuron → decreased transmission of nociceptive stimuli

274
Q

Neuropathic Pain/Functional pain (whats the difference?)

A

persists, disengaged from noxious stimuli or healing process

Typically chronic

Burning, tingling, shock-like/shooting

Hyperalgesia + allodynia

Neuropathic → result of nerve damage

Functional → abnormal operation of nervous system (fibromyalgia, IBS, tension type headache)

275
Q

Multimodal management of acute pain

A

Use of different classes of analgesics that act via different pathways

→ greater analgesic efficacy from synergistic actions of agents with different mechanisms

→ Synergism allows LOWER DOSES → REDUCE dose-related SIDE EFFECTS

Typically have comparable EFFICACY (equal analgesia) within a mechanistic class

276
Q

Mechanistic approach to treatment of chronic pain (neuropathic mostly):

A

Non-opioid and adjuvant medications emphasized for treatment of chronic-persistent pain

→ NSAIDs, Acetaminophen

→ Anticonvulsants, antidepressants, and local anesthetics (neuropathic pain only)

→ Tricyclic antidepressants

Opioid analgesics reserved for moderate to severe pain that adversely impacts function or quality of life

277
Q

Brodmann’s areas 3, 1, and 2

A

make up somatosensory cortex

3b → primary somatosensory cortex
3a → proprioception (contralateral information)
1 and 2 → receive input from 3b, and detect complex features of somatosensory stimulation

278
Q

________ stroke is most likely to transform into homorrhage

A

embolic

279
Q

Stroke protocol for evaluation and treatment

A

Noncontrast head CT –> look for contraindication for TPA

Perfusion CT (with IV contrast) to determine complete infarct of penumbra

Give TPA in less than 4.5 hours, consider IA thrombolytics (mechanical intracranial embolectomy)

280
Q

Perfusion CT imaging:

shows decreased blood volume = ?
shows normal or increased blood volume = ?

A

shows decreased blood volume = complete infarct

shows normal or increased blood volume = brain at risk (penumbra)

Neuro (8 decks)

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