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Derm > Wk 4 Neural Communication > Flashcards

Wk 4 Neural Communication Flashcards

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Dermatology Board Prep flashcards
1
Q

Hyperkalemia results

A

increased extracellular [K+] causes depolarization–>VG Na+ channels cannot be inactivated–> no AP

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2
Q

Tetrodotoxin function

A

blocks VG Na+ channels, found in pufferfish

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3
Q

Hyperkalemic periodic paralysis

A

mutation in VG Na+ channel, stay open during hyperkalemia causing transient paralysis

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4
Q

Absolute refractory period

A

stimulus produces no AP

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5
Q

Relative refractory period

A

stimulus produces but AP is not same amplitude

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6
Q

Why do APs not travel backward “up” axon?

A

A ==> B ==> C

A depol and brings Na+ into axon, diffusing in all directions and depolarizing B. B then repeats this for C, but cannot travel backwards because the ion channel upstream is still in its absolute refractory period

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7
Q

Spacing of Na+ channels in unmyelinated and myelinated fibers

A

close in unmyelinated, only at nodes of myelinated

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8
Q

Pathology of MS

A

demyelination of myelinated axons in CNS

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9
Q

Lidocaine–mechanism of action

A

blocks VG Na+ channels, affects C fibers (pain) most because only affects small area, most likely to disrupt C fibers because A and B fibers have VG Na+ channels only at nodes. reason we can move a muscle before we can feel it after being injected with lidocaine

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10
Q

How does diameter of an axon affect its ability to conduct a signal?

A

larger diameter ==> faster conduction

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11
Q

2 types of synapses

A

electrical

chemical

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12
Q

How often do synapses fail?

A

> 50% of the time

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13
Q

3 stages of chemical synapse signal transmission

A
  1. NT release
  2. NT binding
  3. Active termination (diffusion, degradation, reuptake)
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14
Q

Most secure synapse

A

auditory (then neuromuscular junction)

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15
Q

Describe the steps in depolarization of axon terminal/NT release

A
  1. AP travels down to axon terminal
  2. VG Ca2+ channels open
  3. Ca2+ enters nerve terminal
  4. NT vesicles fuse to membrane (exocytosis)
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16
Q

Botulinum toxin

A

destroys NT docking proteins on nerve terminal, no ACh released ==> flaccid paralysis

17
Q

Tetanus toxin

A

travels up to inhibitory neuron, block inhibitory glycine release ==> tetanic paralysis

18
Q

Dale’s Principle

A

neuromodulators affect primary NT release, each axon terminal releases same set of NT

19
Q

3 primary NT types

A
  1. “classic” like ACh, NE, Epi
  2. peptides like insulin
  3. gases like NO
20
Q

3 types of receptor activation

A
  1. autocrine
  2. paracrine
  3. hormonal
21
Q

Two types of NT receptors

A

ionotropic–fast

metatropic–slow

22
Q

ionotropic NT receptors

A

use ion channels, ligand and ion flow are coupled in same protein

23
Q

metatropic NT receptors

A

uses second messenger systems

24
Q

agonist

A

elicits same action as NT

25
Q

antagonist

A

blocks action of NT

26
Q

How many ACh molecules need to bind to a nAChR?

A

2

27
Q

What ions flow through a nAChR?

A

Na+, K+, Ca2+ (nonspecific cation channel)

28
Q

What is the role of Cl- in neurons?

A

stabilize membrane potential around -61 mV

29
Q

What type of membrane channels are Cl- channels?

A

GABA

30
Q

Why does Na+ flow through nAChR at beginning of AP?

A

the RMP is furthest way from its reversal potential

31
Q

How are nAChR self-limiting?

A

when Na+ enters, it decreases driving electrochemical gradient for Na+, allowing K+ to enter and hyperpolarizing the cell

32
Q

Myesthenia gravis pathology

A

autoimmune destruction of AChR

33
Q

AMPA recepter

  • -NT
  • -channel type
  • -action
  • -special notes
A
  • -glutamate
  • -nonselective cation channel
  • -excitatory in brain
  • -opens and closes quickly, desensitization
34
Q

NMDA receptor

  • -NT
  • -channel type
  • -action
  • -special notes
A
  • -glutamate
  • -nonselective cation channel
  • -learning/memory
  • -ligand and voltage gated, depolarization pushes Mg2+ away that normally blocks glutamate
35
Q

GABA receptor

  • -NT
  • -channel type
  • -action
  • -special
A
  • -GABA
  • -Cl-
  • -stabilization back to -61 mV, IPSP or EPSP depending on membrane potential
  • -nothing special
36
Q

Temporal summation

A

same axon releases multiple additive AP

37
Q

Spacial summation

A

multiple axons release additive AP

Derm (45 decks)

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