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Pharm 1 - SP19 > lecture 15 > Flashcards

lecture 15 Flashcards

1
Q

Opioids inhib _ pathways and activate _ pathways

GABA receptors

A

inhib ascending pathways

activate descending pain relief pathways

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2
Q

a delta fibers

_ Adelta - low mechanical threshold
high heat threshold

A

Type 1 a delta

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3
Q

_ a delta - low heat threshold

- high mechanical

A

Type 2

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4
Q

A delta fibers

Type 1 _ stimuli
Type 2 _

A

Type 1 mechanical stimuli

Type 2 - heat

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5
Q

type A and C fibers are polymodal meaning

A

sense heat and mechanical stimmuli

C- dull burning poorly localized

Adelta - sharp

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6
Q

how does nociceptor signaling work

A

molecular sense of various stimuli

local depolarization and produces AP

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7
Q

mechanosensitive senors have been around a long time _ billion years

A

3.8 billion

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8
Q

_ mechano receptor

this is what we are causing pain because of these receptors

A

TRPV1

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9
Q

inflammation and nociceptive pain - related

how

A

Inflammation is why we have pain
That’s why we like anti-inflamm inside of opiods

cells release PG, substance P, TNFa ILs interacting with receptors and facilitate the transmission of pain signals

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10
Q

tissue injury can lead to sensitization of the pain response

how

A

inflammation makes it hurt more

Hyperalgesia - if someone is injury even a little touch can hurt it

Allodynia - something that doesn’t cause pain causes pain for some reason

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11
Q

a single neuron might receive multiple different APs but whether this happens is afftected by things like _ _ _

A

number and types of postsynaptic rececptors

synchrony and frequency of incoming signals - could be additive

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12
Q

pre or post synaptic

hyperpolarization diminishes Ca++ influx and NT release

depolarization enhances Ca++ influx and NT release

A

pre

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13
Q

pre or post

hyperpolarization diminished opening of Na channels and reinitiation

depolarisation enhances opening of Na channels and reinitiation of APs

A

post

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14
Q

4 endogenous opioids

Pro-opiomelanocortin peptides
pro-enkephalin peptides
prodynorphin
endomorphones

A

all have different receptors

beta endorphin - binds to mu receptor

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15
Q

3 important opioid receptors
Mu, kappa, delta

the are all _ receptors

A

g protein coupled
widely distrubted in CNS

activate G alpha -inhib

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16
Q

_ is the natural agonist of the mu receptor

A

beta-endorphin

17
Q

met-enkephalin and leu-enkephalin are the natural agonists of the _ opioid receptor

A

delta

18
Q

dynorphin A, B and alpha/beta neo-endorphin are agonist of the _ opioid receptor

A

kappa

19
Q

how do opioids work?

g protein coupled alphainhib receptors
Galpha inhib and G beta and Ggamma

A

they dont act as blockers

they make it more difficult to send synapses

Galpha Inhib - inhib of adenylate cyclase, reduced cAMP, reduce PKA, reduction of Ca++ entry from voltage sensitive Ca++ channels

GbetaGgamma - potassium channel - hyperpolarize - make K get outside easier

20
Q

opioids

postsynaptically, hyperpolarization will diminish _

presynatically, Ca is required to NT release and inhib of the Ca channel and hyperpolarization will each diminish Ca entry, thus will inhib synaptic transmission by _

A

postsynaptically - hyperpolarization diminish generation of AP

presynaptically - inhibit transmission by reducing NT release

21
Q

which receptors are not located in the midbrain

A

delta - might be new target to eliminate constipation/death

22
Q

3 forms of Mu receptors, _ and _ are physio important

found in periaqueductal gray region, superficial dorsal horn of spinal cord. - MAINLY PRESYNATPIC

A

majority of analgesic drugs act at Mu

mu 1 and mu 2 important

23
Q

are endogenous opioids were attenuating responses to pain

A

not sure but when give antagonist

it does not seem to modify base-line pain responses

24
Q

sites of action of opioids

_ of ascending pathway of pain inhibition

A

inhibit the ascending pathway to the brain - inhib excitatory NT release

25
Q

sites of action of opioids

_ of descending pathway of pain inhibitition

A

activation of descending pathway

inhibit release of GABA, inhib the inhibitor

having an activating effect

26
Q

A state of nociceptive sensization caused by exposure to opiods
The condition is characterized by a paradoxical response whereby the patient taking opiods for the tx of pain could actucvally become MORE SENSITIVE to certain painful stimuli

A

opioid-induced hyeranalgesia

27
Q

stimulation of the _ system produces emotional response to the physical stimulus of pain

A

limbic system

still hurts but doesn’t bother the patient - they feel something - but not pain

28
Q

clinical effects of opioids

all produce _

A 
analgesia with minimal sedation
respiratory depression
constipation
GI spasm
PHYSICAL DEPENDENCE
29
Q

morphine is a prototypic full agonist of the _ receptor

has to undergo metabolism by _ to get metabolites

A

mu

glucuronidation - why not that effective taken orally

M3 - not active - toxic - a lot more of this

M6 and IVmorphine get into brain - active analgesic not as much

30
Q

opioids more effective for dull aches or sharp pain

A

more effective against dull aches

31
Q

codeine is more effective than morphine as an analgesic when _

A

admined orally

32
Q

_ is currently the most widely used synthetic opioid in medicine

A

fentanyl

alone produces even less sedation than morphine

33
Q

fentanyl has a very high therapeutic index , 300- good drug

why , toxicity?

A
  1. more lipid soluable than morphine or heroin - aromatic ring

morphine as OH groups which reduce lipophilicity

  1. binds tighter to the mu receptor

skips the onset of sedation to show OD signs
goes from analgesia straight to respiratory distress

morphine goes from analgesia to sedation than to resp distress

Pharm 1 - SP19 (26 decks)

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