Biochemistry Flashcards
(25 cards)
Define neurotransmitters
Chemical compounds that communicate signals to adjacent cells (paracrine action)
Define hormones
Chemical compounds that communicate signals to distant cells (endocrine action)
Where are the receptors for neurotransmitters located
On the post-synaptic membrane (outside target cells)
Where are the receptors for hormones located
Either on the cell membrane (e.g. adrenoceptors) or inside the cell (e.g. steroid receptors)
Where are hormone secreting cells
Clusters of specialized cells in:
- Endocrine glands e.g. thyroid, adrenal
- Embedded within organs and tissues e.g. gastrin secreting cells in the stomach
How is the release of hormones triggered
- Signals from the CNS (HORMONAL)
- Signals from the CNS (NEURAL)
- By changes in homeostasis detected by a gland
How are hormones transported in the blood
Water soluble hormones
- In solution in plasma e.g. adrenaline
Non-water soluble hormones
- Bound to plasma proteins e.g. thyroxin, cortisol
What is myelin?
- Thin lipid sheath ‘rolled’ around axons
- Produced by glial cells
- Insulator and results in faster ‘saltatory’ transmission of AP
- White matter in the CNS
What cell produces myelin?
CNS - Oligodendrocytes
PNS - Schwann cells
Pathogenesis of MS
- Focal damage to the myelinated axons in the CNS
- Altered neurotransmission which alters function
Define Nociception
Signalling in the nervous system resulting from tissue damage
Define Pain
Consequence of nociception; it is subjective feeling - a perception
*Nociception can exist without pain if there is no psychological distress. Pain can exist without nociception if it is hypnotically induced or imagined although not to the same degree.
What happens after tissue damage
Signal generation - Nociceptors convert mechanical/ chemical signals into neural signals (AP)
Transmission - AP travels through ascending neural pathways
Perception/ conceptualisation - Higher brain levels
3 Classes of nociceptors
- Thermo
- Chemo
- Mechanical: Associated with sharp pricking pain
- Polymodal: Activated by a variety of stimuli (mechanical, chemical or extreme temp) <5 or >45 found in almost all tissues
What is receptor potential?
The degree of stimulus required to reach the threshold in order to generate an AP
What are the 2 pain pathways?
Slow - Paleospino-thalmic
Fast - Neospino-thalamic
Features of the fast, Neospino-thalamic pathway
- Sharp pricking pain from mechanical and fast thermal nociceptors
- Ad fibres (3-10 m/s) to superficial dorsal horn
- Transmission via Glu (rapid and precise action)
- Well localised, painful stimuli
Features of the slow, Paleospino-thalmic pathway
- Dull, burning, ache
- C fibres (0.5-2 m/s) to deeper dorsal horn
- Transmits via SUBSTANCE P (slow sustained action)
- Poorly localised and usually distressing pain
Most go to reticular formation producing increased alertness and arousal
Referred pain
- Pain causing damage to viscera is ‘referred’ to a somatic area
- Though to arise because of convergence of somatic and visceral nociceptor afferents in dorsal horn
Types of pain
- Nociceptive
- Inflammatory
- Dysfunctional
- Neuropathic
- Phantom and referred
Nociceptive pain
Stimulus dependent pain (No nervous system lesion or inflammation)
Inflammatory pain
- Caused by active inflammation
- Stimulus dependent pain causes sensory amplification of the already occurring inflammatory pain
Dysfunctional pain
- No known structural nervous system lesion or active peripheral inflammation
- Sensory amplification present with a lack of stimulus
E.g. - Primary erythermalgia (mutation in Na channel > increased excitability of nociceptors)
Neuropathic pain
- Nervous system lesion or disease
- Marked neuroimmune response
- Sensory amplification is cause by stimulus
