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Y1S1- Fundamentals of Medicine > Neural Function in Disease > Flashcards

Neural Function in Disease Flashcards

1
Q

law of dynamic polarisation

A

there is a preferred cell-to-cell direction in which currents move

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2
Q

soma

A

cell body

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3
Q

Dendrite

A

collects signals from other neurons

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4
Q

Node of Ranvier

A

exposed axon that allows ions to diffuse in and out of the neuron

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5
Q

myelin sheath

A

insulation that speeds up transmission

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6
Q

Astrocytes

A

fills spaces between neurons in brain and most numerous cell in organ, mop up chemical messengers that accidently diffuse into intercellular space to stop signal going to wrong cells

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7
Q

how can ions move across a membrane

A

through pumps (active) or channels (passive)

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8
Q

where are K+ and negatively charged proteins concentrated?

A

cytoplasm

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9
Q

where are Na+, Cl- and Ca2+ concentrated?

A

the ECF (extracellular fluid)

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10
Q

at rest, state of potassium and sodium channels?

A
  • At rest, leak potassium channels are open (not voltage dependant) and respond to pH, oxygen potential and mechanical stretch
  • At rest, sodium channels are closed
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11
Q

resting potential of cell

A

-65mv due to large negative proteins that can’t diffuse out of cell

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12
Q

action potentials

A

short pulses of electricity fired when a neurone is stimulated, they are propagated along its length carrying information

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13
Q

process of generating an action potential

A

Sodium channels and voltage gated potassium channels are closed
Sodium channels open (depolarisation)
Sodium channel inactivate and voltage gated potassium channels open (repolarisation)
Voltage-gates potassium channels gradually close (hyperpolarisation)

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14
Q

what does a sequence of APs show?

A

long stimulus

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15
Q

After-hyperpolarisation

A

when the K+ tries to reach its own equilibrium potential of -80mV after repolarisation, so membrane potential undershoots before K+ VGICs can close

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16
Q

Depolarisation

A

change in polarity in the membrane potential of a cell

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17
Q

mechanism of voltage gated ion channels

A
  1. Na+ VGIC are closed at rest to maintain the resting potential
  2. A stimulus depolarising the membrane to -40mV distorts the protein to open it specifically to Na+ ions
  3. This rapidly causes much faster depolarisation for 1ms
  4. The channel inactivates by covering the pore and then closes when the protein returns to its resting configuration after repolarisation of the membrane, the physical pore power is removed
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18
Q

why K+ VGIC are much slower to reopen after depolarisation ?

A

entry of K+ resets the membrane potential to resting, during the refractory period after an AP the cell cannon generate another AP so that depolarisations are discrete.

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19
Q

propagation in unmyelinated neurones

A

In unmyelinated neurones, depolarisation at one point of the membrane (production of an AP) sets up local circuits, so depolarisation continues as a wave down the length of the neurone

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20
Q

salutatory conduction in myelinated neurones

A

Between myelin, there are gaps called Nodes of Ranvier where there is a high density of ion channels. APs are initiated in an axon hillock (part of cell body of a neurone that connects to the axon) and jump from one node to the next

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21
Q

factors that increase conduction velocity

A

Myelin, increased axon diameter and higher temperatures

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22
Q

Mechanoreceptors

A

unmyelinated fibres in the skin sensitive to stretch/bend/pressure

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23
Q

Mechanosensitive ion channels

A

gates opened by stretching of membrane

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24
Q

dermatome

A

the area of skin with innervation supplied by one nerve

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25
Q

stimulus detected by free nerve endings

A

Pain, temperature, crude touch

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26
Q

stimulus detected by pacinian corpuscles

A

Deep pressure, vibrations

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27
Q

synapses

A

gaps between neurones

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28
Q

neurotransmitter

A

endogenous chemical messenger that conveys neuronal information from a pre-synaptic terminal to its post synaptic target

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29
Q

neurotransmission process- where are enzymes for the synthesis of NTs produced?

A

neurone cell body and move down the axon on microtubules

30
Q

neurotransmission process- what are NTs produced from?

A

precursors in the pre-synaptic terminal which is then stored in vesicles

31
Q

neurotransmission process after action potential reaches the pre synaptic terminal

A
  1. When an action potential reached the terminal, the membrane is depolarised which causes voltage gated calcium channels to open
  2. Ca2+ makes the NT vesicles fuse with the membrane (calcium sensing)
  3. The NT is released into the synaptic cleft (exocytosis)
  4. It binds to receptors on the post synaptic neurone
  5. Enzymes break down the NT and its constituents are taken up into the pre-synaptic terminal for re-use
  6. A new empty vesicle is pinched off the membrane into the pre-synaptic terminal (endocytosis)
  7. This is filled with NP (loading) for the next AP
32
Q

Ionotropic receptors

A

fast ligand-gated ion channels that open when the NT binds

33
Q

Metabotropic receptors

A

slow because they activate a second messenger system (via GPCRs)

34
Q

molecules that increase excitability of the post-synaptic neurone

A

acetylcholine, noradrenaline and glutamate

35
Q

molecules that decrease excitability of the post-synaptic neurone

A

GABA and glycine

36
Q

integration of signals allows

A

EPSPs to add up and if the threshold potential is met, generate an AP

37
Q

production of EPSPs

A

At an excitatory synapse, if sufficient NT binds to NA+ ionotropic receptors the membrane will depolarise to produce an excitatory post-synaptic potential (EPSP)

38
Q

production of IPSPs

A

occur at inhibitory synapses because Cl- channels are opened instead, further polarising the membrane (making it more negative instead of reversing the voltage, so it is harder to generate an action potential)

39
Q

Spatial summation

A

when a neurone combines multiple EPSPs from different synapse connections

40
Q

Temporal summation

A

when a neurone combines multiple consecutive EPSPs from the same synapse

41
Q

Nicotinic receptors

A

ionotropic receptors that respond to acetylcholine (Ach), are agonised by nicotine and antagonised by curare

42
Q

Muscarinic receptors

A

metabotropic Ach receptors, are agonised by muscarine and antagonised by atropine

43
Q

GABA inhibitory receptors

A

agonised by ethanol and other depressants that reduce stimulation

44
Q

Somatic motor fibre

A

one nerve fibre that connects CNS to the skeletal muscle it innervates

45
Q

relationship of axial and distal muscle neurones

A
  • Axial muscle neurones are medal to those of distal muscles
46
Q

relationship of flexor and extensor muscle neurones

A
  • Flexor muscle neurones are dorsal to extensor muscle neurones
47
Q

The motor end plate

A

pre-synaptic terminal for one skeletal muscle fibre. Many motor end plates split off from one nerve so that it can innervate the whole muscle and coordinate its contraction

48
Q

Motor unit

A

alpha motor neurone form the spine and fibres of the muscle that it innervates (causes to contract) which then splits into many synapses (motor end plates)

49
Q

Motor neurone pool

A

set of alpha motor neurones that innervate one muscle, so damage to a single motor unit will not prevent normal muscle activity

50
Q

what does the autonomic nervous system do?

A

controls involuntary reactions and innervates smooth muscle, cardiac muscle and gland cells

51
Q

where are the cell bodies of ANS neurones?

A

cluster in ganglia which run down beside the spinal cord

52
Q

Components of the autonomic nervous system

A

sympathetic and parasympathetic nervous systems

53
Q

adrenaline pathway

A
  • Pre-ganglionic neurones release Ach and post-ganglionic release noradrenaline (NA) so receptors in the ANS are known as adrenoreceptors
54
Q

Ach pathway

A
  • All neurones in this system release Ach and neurones travel long distances to target organs since most original in the cranial (neck) spinal cord
55
Q

Contraction of muscles leads to

A

shortening of muscle fibres

56
Q

areas where smooth muscle is present

A

in blood vessel wall and the digestive tract lining

57
Q

Neuromuscular junction-

A

synapse between the neurone and the muscle fibre

58
Q

action of acetylcholine to imitate contraction and degradation

A

Ach crosses NMJ and stimulates receptors to initiate contraction then is degraded by acetylcholinesterase enzymes so that acetic acid and choline (products) diffuse back to the pre-synaptic neurone to be resynthesized into Ach.

59
Q

muscle contraction- movement of myosin and actin

A
  1. The EPSP generated in the post-synaptic membrane (sarcolemma) travels through T-tubules (transverse tubules) into the fibre
  2. This causes Ca2+ of the sarcoplasmic reticulum to open up
  3. Ca2+ diffuses into the sarcoplasm and binds to troponin C so that the myosin heads are free to attach to binding sites on the actin filament
  4. This binding causes a conformation change in the heads which pivot and slide the actin filament along the myosin filament to shorten the sarcomere
  5. ATP is hydrolysed so the head detaches and swings back into its original position, ready to repeat the process for as long as APs and Ca2+ are present
60
Q

Reflex

A

involuntary movement in response to a stimulus, instead of being processed by the brain and producing a conscious response, they travel through a reflex arc as far as the spinal cord and back

61
Q

Myotatic reflex

A

in antagonist pairs of muscles, they are innervated so that one is inhibited when the other is excited to allow movement eg. in knee reflex jerk so that extensors contract, flexors relax

62
Q

Cross extensor reflex

A

one leg extends when one flexes so gives stability when one leg is moved from pain

63
Q

Vestibulo-ocular reflex

A

when the head is rotated, extraocular muscles (around the eyes) are inhibited on one side and excited on the other to fix the position of eyes- line of sight

64
Q

hyponatremia

A

Less Na+ so less excitability, can be caused by diuretics cirrhosis ect., symptoms= cramps, fatigue, weakness

65
Q

hypernatremia

A

More Na+ so more excitability, causes: water loss, renal failure ect. symptoms: Tremor, seizures, hyper-reflexia, thirst

66
Q

hypokalaemia

A

Less K+ so less excitability Causes: Diuretics, cirrhosis, renal disease, malnutrition, malabsorption in GI tract,
Symptoms: Mild: weakness, fatigue, constipation, arrhythmias
Sever: paralysis of muscles including vital systems

67
Q

hyperkalaemia

A

Less K+ so less excitability

causes: drug interactions with kidney function, symptoms: Impaired vital organ systems

68
Q

channelopathies

A

diseases which affect ion channels (eg. mutations) and thus depolarisation/repolarisation of cells

69
Q

demyelinating diseases examples

A

damage the Schwann cell insulation of neurones so lower AP conduction eg. multiple sclerosis, Guillain Barre syndrome (autoimmune)

70
Q

myasthenia gravis

A

the immune system attacks Ach receptors so signals can’t be sent at the neuromuscular junction leading to weakness and fatigue

Y1S1- Fundamentals of Medicine (11 decks)

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