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BS IV, Module I > 8. Pain Mechanisms > Flashcards

8. Pain Mechanisms Flashcards

1
Q

Psychological Factors Affecting Pain Response

  • Cultural differences
  • Observational learning (modeling)
  • Fear and anxiety
  • Perceived control of events
  • Cognitive appraisal (the meaning of pain) • Coping style
  • Attention/distraction techniques
    • Big psychogenic component to pain
    • ____ descent - complain of their pain; ____ less likely to complain
    • Fear and anxiety ____ pain thresholds
    • Wiggle the cheek, listen to music
A

italian/jewish
asian/irish
lowers

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2
Q

ACUTE PAIN
• Provoked by an ____ cause, i.e., tissue damage with an expected course to resolution.
• Usually disappears in days or ____
•Behavioral responses: ____, restlessness,
increased sympathetic drive •Responds to routine ____/interventions
• Serves a protective biological function

A

identifiable
weeks
anxiety
analgesics

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3
Q

A big puss ball.

• Lidocaine is a weak \_\_\_\_, in acidic pH, won't penetrate well here because it's now \_\_\_\_; lacking \_\_\_\_ solubility
A

base
charged
lipid

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4
Q

CHRONIC PAIN

• Pain which:
Persists a ____ beyond the usual course of an acute disease or associated with a chronic
pathological process
• Behavioral Response : Quiet, ____, lack of emotion
• Routine ____/therapy do not relieve the pain
• Serves no ____ function

* Neuropathic pain syndromes fall into this
* Behavioral response is not as acute
* Addicting \_\_\_\_ don't work on chronic pain (inc. advil, motrin, etc.)
A 
month
depression
pain relievers
biological
opioids
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5
Q

• In effort to treat chronic pain go from HP to HP to find some pain relief
• ____ - more and more drug to get the same effect - downreg in receptors
• ____ - stop taking drug or give an antagonist, you will go into abstinence/withdrawal system - withdrawal is always opposite of what the drug does (CNS excitation vs. suppression)
○ Opioid withdrawal - muscle and joint achiness, diarrhea (opposite of constipation)
• ____ - psychological dependence, risky behaviors to yourself/others to get drug even though you know it’s risky

A

tolerance
physical dependence
addiction

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6
Q

Factors involved in the presentation of chronic pain

\_\_\_\_
Marital problems 
Problematic family relationship
Grief, personal loss
 \_\_\_\_ 
Personality disorder 
\_\_\_\_ rewards for complaining of pain 
Controlling others with pain behavior

AND

____ of injury
or disease

RESULTS IN

Presentation of ____ pain

* 10-15% of third molar patients are at risk of addiction, like the feeling of pain relievers
* If you don't address \_\_\_\_, they don't improve (TMD patients, for example)
A

drug abuse
depression
financial

history
chronic

depression

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7
Q

Total Pain Relief Index

* Developed at \_\_\_\_
* The higher the number, the more \_\_\_\_ the pain

Dental impactions (both full and partial) are very high on the index (____ > ____)

A

mcgill
intense
full
partial

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8
Q

Proposed Peripheral Mechanism of Non-narcotic analgesics action

* Membrane lipids become available to phospholipase A2 (ubiquitous enzyme) to generate AA > acted upon by COX > \_\_\_\_
* PG - at physiologic doses do not cause pain, but sensitize \_\_\_\_ in soft tissue, periosteum to histamine (from mast cells) and bradykinin (inactive precursor) ; maintain \_\_\_\_ BF, increase mucus layer in stomach
* Now with an influx of Na > AP generated > spinal cord medulla brain > perceive pain
* Advils etc. > analgesic effects by inhibiting \_\_\_\_; can cause GI ulcers which can lead to bleed, increase renal toxicity and increase \_\_\_\_ blood flow; all of these stem from blocking prostaglandin synthesis (COX inhibitors)
A 
PGE2
free nerve endings
renal
COX
renal
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9
Q

Peripheral Targets for Analgesia

* 5HT - serotonin - at site of injury it’s a \_\_\_\_ provoker, but in CNS it's important in \_\_\_\_ and \_\_\_\_ - depends on where it's released
* TNF - embrol, remicade - inhibit, \_\_\_\_ patients are taking these - immunosuppressives
* NO coming out of BV (NT) - natural \_\_\_\_ in body - knock it out, half the people will have \_\_\_\_ rising - NO-cGMP pathway affected resulting in \_\_\_\_ dysfunction
* ATP - cells dump when \_\_\_\_ - \_\_\_\_ receptor antagonist  - may work better for \_\_\_\_ pain and not acute
A 
pain
mood
analgesic
RA
vasodilator
BP
male erectile
damaged
purinergic
chronic
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10
Q

• Drugs that block before COX - glucocorticoidss - ____, ____, to reduce post-op ____ from dental impaction surgery
○ Limits ____
• They are also ____
• Raise blood sugar; taken chronically cause ____
• Suppress hypothalamic-pituitary-adrenal axis - when into emotional stressful situation - going into cold, release of cortisol, makes symp work better, but on drugs you don’t get naturally cortisol release, and you get ____ and unconscious - ____

A 
pregnazone
cortizone
swelling
trismus
immunosuppressant
cataracts
hypoglycemic
acute adrenal crisis
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11
Q

Biosynthesis of Endoperoxides, PGG2 and PGH2

• Acted on upon by \_\_\_\_ - the intermediate PG don't have \_\_\_\_ importance (PGG, PGH)
A

COX

physiological

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12
Q

Arachidonic Acid Metabolism

• Alt pathway - lipoxygenase > \_\_\_\_: pro-inflam, big players in \_\_\_\_ including asthma; \_\_\_\_ (singulair) - pill, prevent asthmatic attacks, and apporved for seasonal allergies
	○ Drugs that block lipoxygenase - liver toxicity
• PGI2 (prostacyclin) - found in endothelium of BV - released, \_\_\_\_ and inhibits platelet \_\_\_\_
• Thrombaxin A2 - \_\_\_\_, stiulates platelet \_\_\_\_
	○ Balnce bt these two
• Baby aspirin is selective at KO \_\_\_\_ and sparing \_\_\_\_
	○ Platelets have no nucleus, aspirin irreversibly binds \_\_\_\_, the platelet is non-functional - always forming new platelets
	○ Endo cells have a \_\_\_\_ - can make new COX easily
	○ Relatively selective effects
A 
leukotrienes
AID
montoleukist
vasodilator
aggregation
vasoconstrictor
aggregation

thrombaxin 2
PGI2
COX
nucleus

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13
Q

Salicylates

• Aspirin irreversibly inhibits COX; other NSAIDs eventually let go
	○ Dosed every 4 hr; drugs are dosed base on half-life (1-2 hr), and first mebtaolite SA (half-life of 3 hours); dosed based on \_\_\_\_ half-life of parent and metabolite
• SA manipulated into SS - comes on a little \_\_\_\_
• SA - no longer has \_\_\_\_ activity, still have pain relief; cannot used for \_\_\_\_ protection
• \_\_\_\_ - aspirin derivative - new generation NSAID - more powerful and better in post-surg pain than maximum doses of aspirin; trade name is Dolabid (taken twice per day)
A 
combined
quicker
anti-platelet
cardio
diflunisol
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14
Q

Phenylpropionic Acid Derivatives

* Better tissue \_\_\_\_ and \_\_\_\_ penetration for left two
* Some component of pain-relieiving is central - penetrate CNS better than aspirin
* Side effect profile is better (full analgesic doses of aspirin)
A

penetration

CNS

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15
Q
  • Rx prescription to Over the counter
    • Has to work at ____ dose, ____ and ____ onset and decent duration
    • Safe because people are ____
A

lower
safe
quick
self-medicating

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16
Q

Role of Prostaglandins

* PG > \_\_\_\_ (painful menstrual cramps); ibuprofein penetrates uterus better than \_\_\_\_, works better
* Acetominophen is not a weak \_\_\_\_
* High levels of PG in brain > contribute to fever (\_\_\_\_ effects); after dental surgery, is having anti-pyretic a good thing? No > fever is early sign of post-op infection
* Constitutively made in certain regions; stomach: \_\_\_\_, break on HCl secretion and increase mucus; kidney: good guys, increase renal \_\_\_\_ (PGI2), increase \_\_\_\_ of water and sodium (retention if drug blocking this)
A 
dismenuria
acetominophen
acid
anti-pyretic
cyto-protectants
BF
excretion
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17
Q

Mechanism of Action of NSAIDs: Old Theory

* Reported how aspirin did its thing, blocking COX
* \_\_\_\_ isoforms of COX
A

two

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18
Q

• All these drugs end in coxib, all selective
• Problem giving someone that’s old w/ cardiovascualr disease and giving a pure COX-2 inhibitor > unopposed ____ and platelet ____
○ This ultimately hit increased ____ and strokes
• [NOTES]

A

vasoconstriction

aggregation

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19
Q
  • Only one that is still on market is celebrex (which one???)
    • Valdecoxib = bextra
    • [NOTES]
A

???

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20
Q

PGs and Pain

* PG are senstizing \_\_\_\_ > hyper-algesic, more sensitive to pain provoking things
* \_\_\_\_ - sunburn, doesn't hurt until you press on it
* \_\_\_\_ involved in eventual painr esponse
A

free nerve endings
hyperalgesia
Ach

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21
Q

Peripheral Nerve Fibers

* Doesn't have to be chemical; \_\_\_\_ (TRPV1/2 receptors that respond to \_\_\_\_), \_\_\_\_ receptors (H+), \_\_\_\_-sensitive receptors (extracting a tooth)
* Polarization of NF > AP make way centrally (\_\_\_\_); EFFERENT is going outside the CNS
A 
heat
capsacian
acid-sensitive
pressure
afferent
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22
Q

Types of NF Associated with Nociceptive (Pain) Impulses

• Adelta - lighlty \_\_\_\_ > conduct pretty quickly
	○ Pain - \_\_\_\_, not just quick, can figure out where it hurts
• C - \_\_\_\_, slowly conducting
	○ Pain - not as well defined, the \_\_\_\_ from finger to hand
A

myelinated
localized
unmyelinated
spreading

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23
Q

Type A Delta Fiber Characteristics

  • Small, ____
  • Faster than ____
  • Much slower than ____ myelinated
  • ____ pain
A

myelinated
C fibers
large
sharp

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24
Q

Type C Fiber Characteristics

  • ____ diameters
  • ____
  • ____ conduction velocities
A

small
unmyelinated
slow

25
Q

Amides I

* Local anesthetic - ends in caine - blocks \_\_\_\_ channels
* Look similar
* \_\_\_\_ in the middle - metabolized in the \_\_\_\_
* Local anesthesia wares off - drug moving away from the site; if you want to keep it there you use \_\_\_\_
* Amino terminus end - \_\_\_\_ solubility; carpules are full of water
* Aromatic group - gives drug \_\_\_\_ solubility (penetrate nerve sheets and nerve membranes)
* Low \_\_\_\_ at adminster site - makes it hard to get in
A 
Na+
amides
liver
epinephrine
water
lipid
pH
26
Q

The effects of lidocaine on the compound AP

* Same experiment with \_\_\_\_, used in intractable chronic pain syndromes, AP never comes back > toxic; prolonged \_\_\_\_
* If slow down recovery, add \_\_\_\_; wears off bc vasculature picks it up and moves it away and processes it in the bdoy
A

alcohol
neurotoxicity
Epi

27
Q

Blockade of all sodium channels in 3 consecutive nodes of ranvier

• Critical length hypothesis
• To kkncok out myelinated nerve > you need to deliver enough aneasthtic that's as long as \_\_\_\_ consectuive nodes of ranvier
• Bc sensory nerves like \_\_\_\_; the nodes are closer together than big nerves like motor fibers; they knock out quicker but recover quicker
	○ In real world, depends on where nerve fibers are in nerve trunk; \_\_\_\_ on outside, they'll be exposed first and KO first
A

3
aDelta
aDelta

28
Q

Local anesthetic mechanisms

Sodium channel blockade
Membrane expansion

* Either directly plugging up the \_\_\_\_, or entering the lipid phase and \_\_\_\_ it and squeezing the channel closed
* Charged vs uncahrged form????
* In order to get in, it must be \_\_\_\_; in the actoplasm, the pH is down so it \_\_\_\_ up and binds within the membrane and closes the channel
A

channel
expand
uncharged
charges

29
Q

Esters

• Ester, chewed up in BS by \_\_\_\_ (different from succinhyl choline)
• Doesn't have \_\_\_\_ end - to get it in solution - it's dissolved in \_\_\_\_ - do not want to shoot into a nerve, good for \_\_\_\_  pain
• Gives off \_\_\_\_ after metabolized, where people have allergic reactions to these
	○ Not observed with \_\_\_\_
• \_\_\_\_ - goes up the nose (in covanaise)
• \_\_\_\_ - add carbons to locals - make powerful and icnrease duration of action; this doesn't work for other drugs; opioids, the most powerful have shortest duration of action
A 
cholinesterases
amino
polyethylene glycol
topical
PABA (para-amino-benzoic acid)
amides
tetracaine
procaine
30
Q

Clinical Presentation of Toothache Patient

Definitive therapy is RCT (endo) or extraction and not ____

A

analgesics

31
Q

Placebo vs. Benzocaine

• Placebo = \_\_\_\_ (must compare to the vehicle); the placebo is not totally \_\_\_\_, can potentially block AP if given enough - Benzo is more effective, DUH
A

polyethylene glycol

inactive

32
Q

The Lidocaine Transmucosal Patch (Dentipatch)

• Good for topical \_\_\_\_ anesthesia, not for teeth procedures
A

soft tissue

33
Q
  • [NOTES]

* Vasoconstrictor - oxymetazolene

A

YEAH CMON

34
Q

Target area for nasal mist anesthesia

	• 2nd \_\_\_\_ to 2nd \_\_\_\_
	• \_\_\_\_ and \_\_\_\_ alveolar nerves
	• 1s molar
		○ Mesial buccal root - \_\_\_\_ alveolar nerve
		○ 2 roots - \_\_\_\_ alveolar nerve
		○ Doesn't catches those well
A 
bicuspid
bicuspid
anterior
middle superior
mesial superior
posterior superior
35
Q
  • Success - ability to complete filling without giving the injection
    • 1st bicuspid forward - ____%
    • 2nd bicuspid dropoff - in 25-35% of individuals they don’t have middle superior alveolar nerve, the 2nd bi is innervated by the ____ alveolar nerve, which is when the nasal can’t get to it
A

95-100

posterior superior

36
Q

Tetrodotoxin

• Toxin in the \_\_\_ and \_\_\_\_ of fish
• Local molecule - absorbed \_\_\_ and knocks out \_\_\_ channels all over the body
	○ Muscles affected - \_\_\_ muscle - not beating
A 
gonads
ovaries
readily
Na+
cardiac
37
Q

Primary afferent (1st order) neuron synapsing on 2nd order neuron in spinal dorsal horn

* AP generated, travel up \_\_\_\_, and reach a synapse (\_\_\_\_ neuron) with a \_\_\_\_ neuron; crosses to other \_\_\_\_ of the spinal cord/medulla
* To stimulate 2nd order neuron, something is released at 1st order
A

adelta
1st order
2nd order
side

38
Q

• NT in packets of vesicles
○ ____, ____ (calcitonin gene realted peptide), and ____ (excitatory AA)
○ When released, receptors on ____ order neuron to become activated, channels open and depolarization
• ____, 5 AA containing peptides, body’s natural opioids - break on the release of NT
• Drugs with ____ have the least organ toxicity
○ Opioids don’t cause ____ - bc we have natural opiods in our body

A 
Substance P
CGRP
glutamate
2nd
enkephalin
natural receptor
organ toxicity
39
Q

Transmission of Nociceptive Impulses Dorsal Horn Synapse of the Afferent Pathway

• Enkephalins can exist \_\_\_\_- and \_\_\_\_-synaptically
	○ When bind to their receptor on nerve terminal of first neuron, they prevent the release of SP, CGRP, or glutamate
	○ When they bind to receptors on 2nd order neurons - cause \_\_\_\_ - \_\_\_\_ channels open and leave the neuron
• First order nerve terminals within dorsal horn of spinal cord or medulla (substantia gelatinous) - have \_\_\_\_ receptors - if stim : with clonidine, block release of NE, and can block release of itself; NE/clonidine can block release of some of the pain-provoking NT; other use of clonidine, useful for some \_\_\_\_ syndrome (worn on patches), can inhibit release of these pain NT
• Post-synpatically, 2nd order neurons have \_\_\_\_ receptors - GABA is inhibitory causes hyperpolarization by increasing \_\_\_\_ inward; drugs that affect this > \_\_\_\_ (valium) don't bind directly to GABA receptor, bind their own receptor which increases \_\_\_\_ of GABA for its receptor; drugs have sedative and \_\_\_\_ effects, but no \_\_\_\_ effects
A 
pre
post
hyperpolarization
K
alpha 2 arenergic
pain
GABA
Cl-
benzo's
affinity
anti-anxiety
pain/analgesic
40
Q

Neuropeptides

READ THE SLIDE

* Substance P - 10 AA, \_\_\_\_ protein, but bigger than \_\_\_\_ or NE
* Small NT, primary place of synthesis is \_\_\_\_; big molecules that are NT are in \_\_\_\_ and travel via \_\_\_\_ direction
* Thought that SP was only in CNS, but it's also found in the \_\_\_\_, some is traveling in wrong direction (\_\_\_\_ direction)
* Can be a \_\_\_\_ - to Ach it can tamp up its effects, it can also tamp down depending on the NT
* In periphery, contirbutor to peripheral \_\_\_\_ and inflammation; and in \_\_\_\_
A 
small
Ach
nerve terminal
nerve cell bodies/ganglia
enterograde
periphery
retrograde
neuromodulator
pain
osteoarthritis
41
Q

Substance P: Distal nerve effects

* Substance P is also located in free nerve endings in \_\_\_\_, along with the \_\_\_\_ order neurons in ganglia
* When spilled out, accelerates release of pain-proviking chemicals like \_\_\_\_, serotonin, enhanced released of \_\_\_\_ - plays a role in pain generation out in periphery
* Drug that you can buy OTC that depletes SP - topical oitnments containing \_\_\_\_
A 
periphery
first
histamine
PG
capsaicin
42
Q

Capsaicin

* \_\_\_\_ (brand name)
* Rub on initially, a lot of burning - due to SP release - but if you keep applying it - deplete the free nerve endings of SP - \_\_\_\_ and \_\_\_\_ effects (reduced joint swelling in \_\_\_\_)
* Allows you to \_\_\_\_ the treatment, little blood levels - but if high blood levels > destroys \_\_\_\_ selectively - localization is safer
A 
zostrix
analgesic
anti-inflam
osteoarthritis
localize
C fibers
43
Q

• Crosses over to other of cord; pain on right side is crossing to the ____ side
• ____ containing enkephalins
• At the synapse, the 2nd order synapses with 3rd order in the ____
• Pathways that go in opposite direction - descending analgesic pathways - ____ pain signals - some start in ____ > drop down to neurons containing enkephalins and turn them on; some NT from the descending neuron is ____ and ____ (where ____ activity is also occurring) - a break on the system
○ Not usually turned on enough to turn off pain
○ Not feeling any pain in ____ individuals, may be bc these pathways turned on
○ ____ also stimulate descending pathways

A 
left
interneurons
thalamus
dampen
medulla/midbrain
NE
ST
alpha2

PTSD
opioids

44
Q

Trigeminal Nociceptive Pathways

• Input from mouth and from face - comes in via \_\_\_\_ - the ganglia (gasieron); neurons come in from \_\_\_\_, from first synapse and drop into the \_\_\_\_, and synapse \_\_\_\_ horn, releases synapse P or glutamate or CGRP, stimulate second order neuron, crosses over to other \_\_\_\_ of medulla, synapses in \_\_\_\_, and then synapses with 3rd order but the NT are unknown
A 
trigeminal nerve
pons
medulla
dorsal
side
thalamus
45
Q

Poppy Plant: contains opiates (narcotics)
§ Morphine
§ Codeine
§ Thebaine > oxycodone

Synthetic opioids 
§ Meperidine
§ Hydrocodone
§ Oxycodone
§ Methadone 
§ Heroin
• Opiate - a natural product of poppy plant
	○ Morphine > can form \_\_\_\_, in the body it metabolites into morphine
	○ Codeine - \_\_\_\_ contains codeine
	○ Thebaine converted into \_\_\_\_
• Opiod - partially or totally synthesized in lab
	○ Hydrocodone - major in \_\_\_\_
	○ Oxycodone - in \_\_\_\_ and perc's
	○ Methadone - comes on \_\_\_\_, but prevents the craving and stimulates same receptors; can be abused; not a cure, used in \_\_\_\_ to stop the shooting behavior and craving, and have to then wean them off - drug has a very long \_\_\_\_
	○ Heroin
A 
heroin
tylenol
oxycodon
vicodin
oxycotin

slower
rehab
half-life

46
Q

Opioid Receptors also Located in Periphery!!!

• Thought only a CNS thing
• Major side effect - \_\_\_\_, not a central effect
• \_\_\_\_ opiod receptors in stomach and GI > stimulate > decreases peristalsis (more powerful then anticholinergic)
• Chronic cancer, chronic pain - require opioids, being constipated all the time is not a good thing
	○ Develop a slick molecule - \_\_\_\_, opioid receptor antagonist, major use in opoiod rehab, pure antagonist (v diff from methadone), wean off opiod and introduce naltrexone, blocks opioid receptors for \_\_\_\_ hours, if give it to them quickly the'll go into withdrawal
	○ Cant take drug with on naltrexone; perc will block it
	○ Deal with constipation - add a \_\_\_\_ - cannot cross BBB, doesn't go into the brain, so only treats the constipation
• Atropine gets in, but glycopyrolate doesn't
A 
constipation
mu
trexone
48
charge
47
Q
  • Diff types of opioid receptors
    • [NOTES]
    • ____ are smaller than enkephalin (4 AA, endogenous)
    • ____ - partial agonist - similar to chantix - issue: need a weaning off period, and like methadone it’s abused > major fomrulation is ____ (subutrex), some people absorb and mix with valium it’s a nother way to get high; made ____ (pinch of naloxone in there) > sends them right into opioid withdrawal, when used sublingual, very little naloxone gets to receptors
    • Ways to treat opioid withdrawal - ____, partial ____ and ____
    • ____ - after market for five years, claimed not to be addicting but ended up being addicting; at one opioid receptor it simtulates and the other it blocks
A 
endomorphin
buprenorphine
sublingual
saboxone
agonist
agonist
antagonist
pentazocine
48
Q

• Beta-endorphin - released in ____ (like epi from adrenal medulla) and released into ____
• Within the structure is ____; a bigger molecule pro-opioid ____ gets cleaved into beta-endorphin
They all arise from ____

A 
posterior pituitary
BS
metenkephalin
melanocortin
precursors
49
Q
  • Oxy to heroin? Why?
    • ____ + ____ > stop responding to CO2, don’t want to breath
    • Naloxone - ____ , taken opioid and stretch it out, now has higher ____ for receptor but doesn’t activate it
A

heroin
fentanxyl
antagonist
affinity

50
Q

Opioid Agonist

____ (Duramorph®), heroin, ____ (Sublimaze®), methadone, oxycodone (in Percocet®), and ____ (in Vicodin®)
are opioid receptor agonists.

• Opioid receptors are \_\_\_\_
A

morphine
fentanyl
hydrocodone
GPCR

51
Q

Drug Antagonist

____ (Narcan®) and naltrexone are opioid receptor antagonists.

* Higher \_\_\_\_ for receptor than the drug, and covers the \_\_\_\_ site and not activating
* \_\_\_\_ gets into brain; \_\_\_\_ does not get into the brain
A 
naloxone
affinity
activity
naltrexone
methylnaltrexone
52
Q

Intranasal Naloxone

* Different from intranasal local; here, spray, get into BS and reverse \_\_\_\_
* Most have \_\_\_\_mg naloxone - deliver as plume; injectible dose is 0.4, but sytemic absorption \_\_\_\_ is not as good as \_\_\_\_
A

opioid overdose
4
intranasally
injection

53
Q

Peripheral Pain Pathway

• Primary \_\_\_\_ nerve is stimluated, pressure, incisonal pain, fracture > AP > NT release > SP, CGRP, glutamate > upstrairs crosses \_\_\_\_ of spinal cord
A

afferent

side

54
Q

Convergence of Multiple Inputs

• Can have multiple \_\_\_\_ fibers synapsing on same second order neuron > convergence may explain \_\_\_\_ pain; toothache but complaining about pain in \_\_\_\_ region > all stimulating second order neuron
A

presynaptic
referred
ear

55
Q

Mechanism for Gate Control of Pain Transmission

• Breaks postsynaptically - ____, opening up ____ channels, but there are breaks ____ also

A

hyperpolarization
K
pre-synaptically

56
Q
  • 1st order n neuro with Sub P that can s timulate 2nd order neuron
    • Nerve fiber from descedning coming from brain into spinal cord - some of these chemicals released are ____ and ____ (in periphery, pain producing, in CNS may be part of analgesic pathways), stimulate ____ neuron to release enks and blocks rleease of SP on 1st order neuron
    • Large myelinated nerve fibers that carry ____ (not pain) from periphery that synapse on enk neuron that can be break - stimulated by ____, or by ____
A 
ST
NE
enkephalin
propioception
acupuncture
rubbing
57
Q
  • Beta-endorphin released from ____ is similar to EP released from adrenal medulla (backup system)
    • From here, it’s a neurohormone, the drug can move around systemically like a ____; has ____ solubility; stimulates ____ receptors systemically
A

posterior pituitary
catecholamine
lipid
opioid

58
Q
  • Some free nerve ending, instead of synasping with 2nd order, it can directly or indirectly synapse with ____ NS out of cord, specifically the ____ NS; in ____ pain, this is why the symp NS gets turned on
    • Some free nerve endings, it can also synapse via efferent fibers of ____ NS; people with ____, and the free nerve endings are getting stimulated, you can have muscle ____ in area which makes the pain syndrome even worse
A 
efferent
sympathetic
acute
somatic
TMD
contraction
59
Q
  • Stimulate symp in acute pain > ____, inc HR/contraction, ____, some constrict and dilate (depending on ____ receptors); ____ is turned off
    • Sympathetic - shorter, and ____ exit
    • Para - ____ and ____ exit
A 
mydriasis
BV
A1/B2
GI
thoracic-lumbar
cranial
sacral

BS IV, Module I (9 decks)

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