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biological psychology > topic 5 - pain and pain suppression > Flashcards

topic 5 - pain and pain suppression Flashcards

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1
Q

types of nociceptors

A

Highly myelinated axons (Aδ fibres) convey mechanical pain very quickly and precisely: early pain. This is informative about location.

Unmyelinated axons (C fibres) convey different kinds of pain more slowly and less precisely: late pain. This is vague about location.

  • C fibres can be sensitive to pungent irritants (mustard oil) and capsaicin
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2
Q

prostaglandis

A
  • molecules that help with inflamation and fight off invaders
  • senstise the free nerve endings therefore pain perceived in that area is stronger
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3
Q

Somatosensory pathways

A
  • incoming nociceptor has a cell body in the dorsal root ganglion and they make a synapse in the dorsal horn of the spinal cord. Glutamate is the main neurotransmitter used in that synapse and substance P as a co-neurotransmitter (substance p used as an amplifier)
  • that first CNS sensory neuron’s axon runs across other side of spinal cord, through medulla and through the mid brian and makes a synapse in the thalamus (ventral posterior nucleus)
  • neurons from the thalamus make synapses onto the neurons in the primary somatosensory cortex which tells us where the pain is
  • pathway that it comes through tells us there is pain - if it doesn’t make it to the brain it is not pain.
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4
Q

phantom limb

A

feeling of pain in a lost limb due to it still being represented in the brain

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5
Q

Dual brain mechanisms

A

Pain sensation (physical) - coded in the primary somatosensory cortex.
Unpleasantness perception (emotional) - anterior cingulate cortex.

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6
Q

how to treat phantom limb pain

A

mirror with good limb seeing it being treated

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7
Q

hypnosis induced analgesia

A

pain with sticking ur hand in rly hot water
hypnosis reduced pain of uncomfortablness by reducing activity in the anterior cingulate cortex

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8
Q

pain suppression - non-drug approach

A
  • direct stimulation of the PAG
  • stressful situations (soldiers etc)
  • placebo effect
  • acupuncture (tested using naloxone)
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9
Q

what blocks opiate receptors

A

naloxone, also used for heroin overdoses

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10
Q

Capsaicin

A
  • used topically on skin for muscle relief (deep heat)
  • hot sensation depletes substance p
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11
Q

NSAID

A

anti-inflamatory drugs
inhibit the enzymes that make prostaglandins - reduction in prostaglandins production

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12
Q

NSAID side effects

A

COX1 - involved in blood clotting: aspirin prevents blood clotting. involved in protection of stomach lining from acid: NSAID bad for stomach

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13
Q

paracetamol

A

works through CB-1 receptors (cannabis)

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14
Q

morphine usage and half life

A

half life - 3/4 hours only 20% crosses blood-brain barrier

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15
Q

heroin usage and half life

A

0.1-0.25 hours half life, lipid soluble so easily crosses blood-brain barrier

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16
Q

morphine usage and half life

A

3-4 hours half life, 20% crosses barrier

17
Q

oxycodon half life

A

4.5 hours half life

18
Q

Fentanyl half life

A

3-7 hours

19
Q

opiates short term effects

A
  • relieve pain
  • relieve cough
  • relieve diorhea
  • induce hypothermia
  • induce sleep
  • stimulate pleasure
20
Q

opiates physiological action (how do they work)

A
  • mimic the action of endogenous opioids: endorphins
21
Q

opioid receptors

A

3 major subtypes:
- delta
- kappa
- mu
maybe learn where they are and what for

22
Q

opioids on the periaqueductal gray matter in mid brain ( in the descending analgesia circuit DAC)

A

the inhibit activity of inhibitory neurons

23
Q

opioids on the spinal cord in the DAC

A

block the incoming pain signals

24
Q

opiates long term effect

A

mild as long as taken.
you will be:
- constipated
- reduced libido
- pupil constriction
- menstrual irregularity
But you will have withdrawals
You get all the pleasure you need so might not take care of yourself etc

25
Q

Heroin withdrawal effects

A

begin 6-12 hours after last dose, stop after around 7 days
Includes:
- restlessness
- runny nose
- sweating
- muscle spasms
- tremor
- vomitting
- sweating

26
Q

how to deal with heroin withdrawals

A
  • avoid drug-related context
  • take more drugs
  • methadone
  • acupuncture
27
Q

opiate addictiveness

A

in Ventral tegmental area (VTA):
- opiates inhibit GABA-ergic interneurons
- this releases inhibition from neurons which project to nucleus accumbens
- more dopamine release
In nucleus Accumbens:
-effects independent from but similar to dopamine from VTA

28
Q

cannabis usage

A
  • 20-50% taken up from smoke, less from ingested (6%)
  • very lipid soluble and easily crosses the blood-brain barrier
  • easily stored in fat tissue, half life of 7 days
29
Q

cannabis short term effects

A

Recreational use:
- reduction in anxiety
- dissociation in ideas
- heightened sensations
- distorted sense of time (goes slower)
- intense emotional experiences
- hallucinations (infrequent)
Medical use:
- reduces nausea
- increase in appetite
- dilation of bronchioles
- blocks seizures
- decreases severity of glaucoma
pain relief:
- as effective as opiates for acute pain
- greater potency and efficiency than opiates for chronic pain (but side effects)
- sites of action include:
peripheral nerves
direct spinal chord activity
descending analgesia circuit
anterior cingulate cortex

30
Q

cannabinoid receptors

A

highest concentration exist in the hippocampus

31
Q

function of endocannabinoids

A
  • released from the POST synaptic side of synapse and bind with pre synaptic side
  • work in close vicinity of other synapses
  • suppresses the pre-synaptic release of neurotransmitters
  • in the hippocampus, this affects GABA, hence suppressing inhibition: depolarisation-induced suppression of inhibition (DSI)
32
Q

DSI

A

-endogenous cannabinoids released from post-synaptic terminal when depolarised
- cannabinoids sit on pre-synaptic terminals of other synapses
( i dont rly get this)

33
Q

person who doesnt feel pain

A
  • burns herself on stove without realising
  • defect in the FAAH enzyme (breaks down anandamine (linked with cannabinoids))
34
Q

cannabis long-term effects

A
  • problems associated with smoking
  • impairments in memory recall
  • impairments in attention
  • slower decision making
  • if taking skunk - increased odds of psychosis by up to 5x
  • decline in IQ with persistent use (age 13-39)
  • especially vulnerable if starting in adolescence
35
Q

physical dependance on cannabis

A
  • tolerance develops during extended use but withdrawls are rare
  • long-term users may experience sensitization of the desired effect
36
Q

what drugs work on the CNS

A

cannabis and opiates

37
Q

cocaine usage and half-life

A
  • reaches peak in blood in blood at 30-60 mins
  • half life of 30-90 mins
  • easily penetrates blood-brain barrier
38
Q

what does cocaine increase

A
  • euphoria
  • energy
  • confidence
  • talkative
  • active
  • attention
  • alertness
39
Q

mono-amines

A
  • seratonin
  • dopamine
  • noradrenaline
  • adrenalin
    cocaine acts at the mono-aminergic synapse

biological psychology (8 decks)

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