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stupid brain CA > physiology > Flashcards

physiology Flashcards

1
Q

movement of signal

A

sensory/visceral stimuli -> afferent division -> CNS -> efferent division -> somatic NS (motor behaviour) or autonomic NS (regulate visceral structures)

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2
Q

what are afferent and efferent nerves part of

A

peripheral nervous system (PNS)

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3
Q

types of myelin fibres

A

1) alpha beta fibre: thick, myelinated
2) alpha delta fibre: thin, myelinated
3) C fibre: unmyelinated

  • C slowest, alpha beta fastest
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4
Q

examples of afferent nerves

A

1) pacinian corpsucle (touch receptor, alpha beta)
2) free nerve ending pain receptor (C, alpha delta)

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5
Q

pacinian corpuscle

A
  • respond to non-noxious stimulus (non-painful)
  • skin receptors -> enclosed nerve ending -> myelinated axon -> cell body -> spinal cord -> break into collaterals -> axon terminal
  • function of components
    1) axon terminal: communicate with spinal cord
    2) receptor: generate electrical signals to external stimuli
    3) receptive field: area of skin wherereceptors are embedded in for stimulus to excite
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6
Q

free nerve ending pain receptor

A
  • respond to noxious stimulus
  • free because not covered by connective tissue
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7
Q

structure of neuron

A

soma (cell body), dendrite, axons (split into axon terminals)

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8
Q

synapse

A
  • consists of presynaptic axon, synaptic cleft, postsynaptic part of neuron
  • if postsynaptic connect to dendrite -> likely to be excitatory
  • if postsynaptic connect to soma -> likely to be inhibitory
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9
Q

terminology for electrical signalling

A

1) action potential

  • change in electrical potential

2) resting membrane potential (RMP)

  • -ve value
  • caused by unequal distribution of charges -> inside membrane more negatiev than outside

3) voltage gated channels

  • respond to changes in membrane potential
  • only opens when threshold reached
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10
Q

tldr process of signal generation by membrane

A

1) resting membrane potential
2) depolarisation
3) depolarisation until threshold (action potential)
4) recovery back to RMP

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11
Q

process of depolarisation (signal generation)

A

happen within CNS, triggered by synaptic transmission

  • action potential generated by afferent (axon terminal) -> trigger opening of voltage gated Ca channel -> influx of Ca -> fusion of synaptic vesicle with membrane of axon terminal -> release neurotransmitter into synaptic cleft -> neurotransmitter diffuse and bine to receptor on postsynaptic membrane -> receptor open
  • difference in effect once receptor opens
    ** excitatory: influx of cation -> inside more positive -> depolarisation
    ** inhibitory: influxof anion -> inside more negative -> hyperpolarisation (further from threshold potential)
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12
Q

process of depolarisation until threshold (signal generation)

A

1) upstroke of action potential until peak

  • initial depolarisation trigger opening of voltage gated Na channel -> membrane more permeable to Na+ -> Na+ concentrate outside cell -> rapid Na+ entry through voltage gated channel -> depolarise cell

2) overshoot phase

  • inside cell more positive than outside = reverse membrane potential polarity

3) downstroke of action potential

  • inactivation of voltage gated Na channel
  • opening of voltage gated K channel -> membrane more permeable to K+ -> K+ move out of cell -> repolarise membrane potential
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13
Q

recovery back to RMP (signal generation)

A
  • voltage gated K+ closed
  • membrane potential back to normal
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14
Q

how hypoK affect RMP

A
  • forces acting on K+

1) concentration gradient
2) electrical gradient

  • hypoK -> lower K outside -> favour movement of K from outside to inside -> hypoerpolairsation
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15
Q

component of CNS roles and damage consequences - cortex

A

1) roles

  • sensation and perception (both cortices)
  • voluntary control of movement
  • personality trait (frontal lobe)
  • learning and memory
  • language

2) consequences

  • damage to frontal lobe = drastic change in personality
  • damage to left cortex (Brocas, Wenickes) = aphasia (affect written & spoken language)
  • damage to prefrontal cortex (subgenual ACC) = affect emotions
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16
Q

components of CNS roles and damage consequences - limbic structures

A

1) hippocampus

  • role: declarative memory (recall)
  • damage: alzheimer

2) amygdala

  • role: emotion, emotional memory important for mood change
  • damage: express emotion on face but can’t recognise other people’s facial expression of emotion
17
Q

principles regarding underlying sensory processing

A

(LAYMEN)
- each stimulus pick up specific stimulus and a specific signal produced by that stimulus is passed along a specific path that regions a specific region on brain
- n order means the number of neuron that the signal is passed to from the receptor
- more intense stimuli = more signals produced = stronger sensation

18
Q

types of pain

A

1) spontaneous: activation of pain pathway only for that period of time
2) hyperalgesia: increased pain to given noxious stimulus (inflammation or tissue damage)
3) allodynia: pain to normally non-painful stimulus (normally sensed as touch), reduced threshold to invoke pain

19
Q

identifying type of pain on pain sensation x stimulation graph

A

1) normal curve
- pain threshold basically the amt of stimulation where pain sensation starts to increase

2) allodynia curve

  • any point on non normal curve before normal threshold is reached

3) hyperalgesia pain

  • any amt of pain sensation more than normal
20
Q

normal pain pathophysiology

A

1) touch receptors: movement of alpha beta neurons

  • spinothalamic-tract pathway
    ** nociceptive signals synapse with second order neurons in dorsal horn of spinal cord -> relay pain signals to higher brain centre -> perception of pain
  • dorsal column pathway
    ** nociceptive signals move up dorsal column -> synapse with inhibitory neuron -> modulate/suppress transmission of pain signals -> don’t perceive pain when we sense touch

2) pain receptors

  • associated with C first order neuron
  • spinothalamic tract pathway ^
21
Q

allodynia pathophysiology

A
  • stimulus evoke more AP than normal = hyperexcite more and more stuff along the pathway until it overcomes the inhibitory portion
  • possible effects of tissue damage
    1) loss of inhibitory neuron in spinal cord -> side branch of alpha beta excite pain pathway
    2) sensitisation/hyperexcitability of excitatory relay form C fibre to spinothalamic tract neuron
    ** how hyperexcitation/sensitisation work: increase number of receptors, decrease threshold to excite, release chemicals at damage site -> hyperexcite nociceptors -> generate more AP -> hyperexcite second order neuron
22
Q

pain modulation

A
  • regulate signal along pain pathway
  • PAG
  • process

1) stuff that excite PAG
2) neuron in PAG excite neuron in medulla -> excite inhibitory neuron in spinal cord -> inhibit transfer of signal from 1st order C fibre to 2nd order spinothalamic neuron

  • segmental modulation (gate theory)
    ** stimualte larger afferent for touch -> excite inhibitory neuron -> decrease transmission of pain
23
Q

types of motor behaviour generated

A

1) reflex: involuntary
2) rhythmic motor pattern: require voluntary initiation and termination
3) voluntary: goal directed

24
Q

hierarchial features of motor control

A

1) Cortex

  • voluntary

2) brain stem

  • postural reflex, rhythmic motor pattern

3) spinal cord (efferent)

  • site of motor neuron
  • control of muscle activity

4) brainstem pathway

  • long descending axon pathyway from brain stem to ventral horn
25
Q

role of cerebellum in motor function

A
  • bring about coordinated movement
  • adjust output of efferent via cortex and brainstem
  • if damaged: can’t do coordinated movement like walking in a straight line or touching nose quickly
26
Q

role of basal ganglia in motor function

A
  • initiation of movement
  • selection of motor program
  • if damaged: disorder of movement (even at rest) or disorder of posture (rigidity)

stupid brain CA (5 decks)

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