2. Physio Flashcards

1
Q

Resting membrane potential is determined by

A

distribution of K+, Na+, Cl-

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2
Q

where is AP generated

A

AP will only be generated if depolarisation reach threshold membrane potential at trigger point/ axon hillock

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3
Q

Describe rising phase in AP cycle

A

As neuron depolarises, voltage gated Na+ channels are opened.
Rapid entry of Na+ into the cell through voltage-gated Na channels depolarises the cell

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4
Q

Describe overshoot phase of AP cycle

A
  • at one point, the inside of the cell become more positive than outside → reverse membrane potential polarity → drop in voltage
  • at peak: no influx of Na+ and efflux of K+ through voltage gated channels
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5
Q

Describe falling phase of AP cycle

A
  • Inactivated voltage-gated Na channels
  • Open voltage-gated K channels (K more concentrated inside cell)
  • K+ moves out of cell → membrane rapidly repolarises
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6
Q

2 events that occur at Neuromuscular Junction

A

Receptive step and Translating/transmitting step

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7
Q

Receptive step

A
  • arrival of AP at presynaptic cell/ axon terminal → depolarisation of presynaptic neuron → opening of voltage-gated Ca channels → influx of Ca →
  • fusion of synaptic vesicle with presynaptic membrane → release of NT into synaptic cleft
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8
Q

Translating/transmitting step

A

binding of NT (eg acetylcholine) to postsynaptic ligand gated receptor (eg nicotinic receptor) → influx of Na into postsynaptic membrane

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9
Q

how does hypokalemia affect signalling

A

causes hyperpolarisation → impairs ability to generate AP at NMJ → skeletal muscle membrane becomes less excitable → muscle cannot contract → weakness and paralysis of skeletal muscles

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10
Q

how does hyperkalemia affect signalling

A

reduce efflux of K+ from inside to outside of the cell

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11
Q

sensory transduction

A

Transformation of an external stimulus to AP

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12
Q

describe the sensory transduction pathway

A
  1. Depolarisation of sensory receptor
  2. Generation of action potential
    • depolarisation at trigger point generate AP
    • Depolarisation from the receptor travels to the axon hillock/ tigger zone → generates AP
  3. Propagation to CNS
  4. Synaptic transmission
  5. Excitation of neuron in spinal cord/ CNS
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13
Q

types of sensory receptors and their stimuli

A
  • mechanoreceptor - mechanical energy (non-noxious)
  • nociceptor/free nerve ending - noxious stimuli
  • chemoreceptor - chemicals
  • photoreceptor - light
  • thermoreceptor - heat
  • proprioceptor - position of body in space
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14
Q

Afferent (nerve fiber)

A

carry signals from periphery to CNS

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15
Q

receptive field

A

area on skin where stimulus will excite a receptor

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16
Q

afferent eg 1

A
  • Pacinian corpuscle (touch): a type of afferent nerve fiber embedded in the skin
  • receptor in the receptive field will convey physical energy to signal → travels to CNS via Aß myelinated axon fiber
17
Q

afferent eg 2

A
  • Nociceptors/ free nerve endings (pain): pain receptors that respond to tissue damaging stimuli
  • Eg of nociceptor is TRPV1: opens when there is a painful stimuli → cations enter
  • signal travels via unmyelinated C axon fiber or thinly myelinated Aδ axon fiber to CNS
18
Q

type of fibers and their stimuli

A
  • Aß thickly myelinated axon fiber (largest diameter): for touch, non noxious stimuli
  • Aδ thinly myelinated axon fiber (bigger diameter than C): for pain
  • C unmyelinated axon fiber (smallest diameter): for pain
19
Q

how does myelination and size affects speed of conduction of signal

A

Aß (fastest) > Aδ > C (slowest)

20
Q

Significance of different fibers (eg loss/damage)

A
  • loss of Aß fibers: cannot feel touch/vibration but can still feel pain
  • absence of Aδ & C fibers (eg CIPA): cannot feel pain, touch sensation normal
21
Q

Postsynaptic target for excitatory and inhibitory

A
  • dendrite for excitatory synapse
  • soma for inhibitory synapse
22
Q

where is AP generated

A

AP generated in axon hillock/trigger zone

23
Q

how is NT released into synaptic cleft

A
  1. AP trigger opening of voltage-gated Ca2+ channels
  2. Influx of Ca2+ cause fusion of synaptic vesicles to membrane of axon terminal.
  3. NT released into synaptic cleft
  4. NT diffuse across synaptic cleft and bind to receptor on postsynaptic dendrite/soma membrane
24
Q

what happen when NT bind to receptor on postsynaptic neuron

A
  • on dendrite (excitatory): ligand-gated Na+ opens → Na+ enters → depolarisation
  • on soma (inhibitory): ligand gated K+ opens, ligand gated Cl- opens → K+ leaves, Cl- enters → hyperpolarisation
25
Q

2 forces acting on K+

A
  • concentration gradient - more K+ inside cell (favours movement of K+ out of cell)
  • electrical gradient - cell inside more negative (favours entering of K+)
26
Q

how does hypokalemia affects RMP

A
  • in hypokalemia (less K+ outside cell) → more K+ will move out of cell → neuron cell hyperpolarise (more negative inside)
  • moves RMP away from threshold (cell become less excitable) → cause muscle paralysis
27
Q

how does hyper-excitable neurons cause altered RMP

A
  • normally, inhibition of neurons by GABA cause hyperpolarisation
  • Decrease in GABA cause uncontrolled excitation → seizures/ epilepsy
28
Q

describe the generation of AP when touch is applied

A
  1. through pharmacological receptors (eg TRPV1/nociceptor open when exposed to heat) - receptors transduce external stimuli to an electrical charge
  2. mechanical pressure opens the channel → allows influx of cations → depolarisation
29
Q

what type of activities does the cortex control?

A

needed for all activities that need consciousness (aware and responsive to surrounding)

30
Q

what type of activities does the frontal lobe control?

A

personality trait

31
Q

what type of activities does the Broca’s area (in left hemisphere) control?

A

expressing language

32
Q

what type of activities does the Wernicke’s area (in left hemisphere) control?

A

comprehending language

33
Q

what type of activities does the Subgenual Anterior Cingulate Cortex (Subgenual ACC) control?

A

emotions
- hyperactivity of subgenual ACC leads to depression (sadness and lost of interest)

34
Q

what does the medial temporal lobe contain?

A

hippocampus and amygdala

35
Q

what type of activities does the Cortical and sub-cortical regions control?

A

cognition (learning and memory), emotions and mood

36
Q

what type of activities does the hippocampus control?

A

involved in declarative memory that involves recall (eg memory of events, names, numbers)
- lesion of hippocampus/ medial temporal → loss of memory (eg Alzheimer)

37
Q

what type of activities does the amygdala control?

A

for emotion and emotional memory

38
Q

eg of excitatory and inhibitory NT

A

excitatory: glutamate, epinephrine and norepinephrine
inhibitory: GABA