Analgesics: treatment of pain
13 important questions on Analgesics: treatment of pain
What are the phases of nociceptive pain? (5)
2. Conduction (neuron fires)
3. Transmission (activation of the spinal cord)
4.
5. Modulation (inhibition or facilitation of pain) (in danger pain doesnt compromise function)
What are the three noxious stimuli?
Therminal: > 43 or <0
Chemical:
- Chemokines: inflammation
- ATP by damage cells
- Prostanoids: lipids
- Bradykinin:
- Serotonin
- Histamine: mastcells
- Hydrogen: activate ion channels
What is the difference between neurotransmitters and neuropeptides? Name different neuropeptides
- Substance P
- Somatostatin
- Calcitonin gene related peptide (CGRP)
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How are neurons that sense pain called? And what kind of receptors are this? (5)
- Pseudounipolar.
- Dendrites receive the imput > relay into the soma > to the axon
- First order neuron (input and than the output in the spinal cord neurons)
- Do nothing when not stimulated (all or nothing neurons)
- Are excitatory (glutamate = AMPA)
- Can release neuropeptides are related to them: substance P, somatostatin and calcitonin gene related peptide (CGRP)
- How bigger the diameter of the neuron the faster the conduct that signal
Which two types of pain transduction are there?
Chronic: (arthritis > inflammation > cytokines etc > have also receptors > pain) GPCR activation (neuropeptide)
What are the differences between neuropathic and nocicpetive pain?
Neuropathic: damage in nervous
So we have nociceptors. Neurons that sense pain. What receptors are on these neurons?
Ion channels
TRP channels: heat and capsaicin (hot food)
ASIC channel: H+ ions (acid)
Purinergic receptors: ATP (damaged cel) P2X receptor
G-couple protein receptors
Purinergic receptors: P2Yreceptor activated by ATP (damaged cel)
Bradykinin receptor B2: Bradykinin
ER receptor: prostagandin E2
Receptor tyrosine kinase
NGF that activated tyrosine kinase receptors
(nerve growth factor) => when neurons become activated to much they becoming more sensitive over time.
During transduction a stimulus activates a receptor a nociceptor. In which two way can this happen? And what is the goal?
- Direct activation: ion channel
- Indirect activation: GCPR
- Goal: depolarization > glutamate
What is hyperalgesia? And how does this start?
Start after
- chronic inflammation
- chronic opioid use
Normale pijn stimulus > veel pijn
Peripheral pain (nociceptive pain). How is the pathway?
We have steroid and non-steroid anti-inflammatory drugs. Which one is which?
Steroid: Glucocorticoids
What kind of NSAID's (non-steroids) are there? In what situations are these used?
Anti-Inflammatory, Antipyretic (against fever), and Analgesic
We have two kind of COX. Which ones? And why is this interesting?
COX2 more in people that are at risk for internal bleeding.
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