Biochemistry Flashcards

(25 cards)

1
Q

Define neurotransmitters

A

Chemical compounds that communicate signals to adjacent cells (paracrine action)

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2
Q

Define hormones

A

Chemical compounds that communicate signals to distant cells (endocrine action)

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3
Q

Where are the receptors for neurotransmitters located

A

On the post-synaptic membrane (outside target cells)

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4
Q

Where are the receptors for hormones located

A

Either on the cell membrane (e.g. adrenoceptors) or inside the cell (e.g. steroid receptors)

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5
Q

Where are hormone secreting cells

A

Clusters of specialized cells in:

  • Endocrine glands e.g. thyroid, adrenal
  • Embedded within organs and tissues e.g. gastrin secreting cells in the stomach
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6
Q

How is the release of hormones triggered

A
  • Signals from the CNS (HORMONAL)
  • Signals from the CNS (NEURAL)
  • By changes in homeostasis detected by a gland
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7
Q

How are hormones transported in the blood

A

Water soluble hormones
- In solution in plasma e.g. adrenaline

Non-water soluble hormones
- Bound to plasma proteins e.g. thyroxin, cortisol

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8
Q

What is myelin?

A
  • Thin lipid sheath ‘rolled’ around axons
  • Produced by glial cells
  • Insulator and results in faster ‘saltatory’ transmission of AP
  • White matter in the CNS
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9
Q

What cell produces myelin?

A

CNS - Oligodendrocytes

PNS - Schwann cells

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10
Q

Pathogenesis of MS

A
  • Focal damage to the myelinated axons in the CNS

- Altered neurotransmission which alters function

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11
Q

Define Nociception

A

Signalling in the nervous system resulting from tissue damage

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12
Q

Define Pain

A

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.

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13
Q

What happens after tissue damage

A

Signal generation - Nociceptors convert mechanical/ chemical signals into neural signals (AP)

Transmission - AP travels through ascending neural pathways

Perception/ conceptualisation - Higher brain levels

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14
Q

3 Classes of nociceptors

A
  • 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
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15
Q

What is receptor potential?

A

The degree of stimulus required to reach the threshold in order to generate an AP

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16
Q

What are the 2 pain pathways?

A

Slow - Paleospino-thalmic

Fast - Neospino-thalamic

17
Q

Features of the fast, Neospino-thalamic pathway

A
  • 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
18
Q

Features of the slow, Paleospino-thalmic pathway

A
  • 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
19
Q

Referred pain

A
  • 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
20
Q

Types of pain

A
  • Nociceptive
  • Inflammatory
  • Dysfunctional
  • Neuropathic
  • Phantom and referred
21
Q

Nociceptive pain

A

Stimulus dependent pain (No nervous system lesion or inflammation)

22
Q

Inflammatory pain

A
  • Caused by active inflammation

- Stimulus dependent pain causes sensory amplification of the already occurring inflammatory pain

23
Q

Dysfunctional pain

A
  • 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)

24
Q

Neuropathic pain

A
  • Nervous system lesion or disease
  • Marked neuroimmune response
  • Sensory amplification is cause by stimulus
25
What cardiovascular abnormalities may cause heamorrhagic stroke
- Hypertension - Aneurysms - Arterio-venous malformations - Head injuries - Blood dyscrasias