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OU PDA > Exam 1 II > Flashcards

Exam 1 II Flashcards

1
Q

What are the components of the PNS?

A
  • afferent (somatic and visceral)

- efferent (motor)

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2
Q

What are the components of efferent PNS?

A
  • somatic (skeletal muscle)

- ANS

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3
Q

What are components of ANS?

A
  • symp. nervous system (thoracolumbar)
  • parasymp. nervous system (craniosacral)
  • enteric nervous system
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4
Q

Preganglionic symp. fibers

A

leave through the thoracic and lumbar spinal nerves

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5
Q

Preganglionic parasymp. fibers

A
  • leave through cranial nerves 3,7,9 and 10

- leave sacral spinal nerves 3 and 4

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6
Q

location of symp. ganglia

A

outside the CNS in the paravertebral symp. ganglia chain

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7
Q

location of parasymp. ganglia

A

inside target organs; some in head and neck

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8
Q

What does every pregang. nerve release?

A

ACh

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9
Q

Describe pre and post-ganglionic neurotransmitter release of parasymp. system

A
  • pregang. release ACh and synapse on nicotinic receptors

- postgang. release ACh and synapse on muscarinic receptors

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10
Q

Describe pre and post-ganglionic neurotransmitter release of symp. system

A
  • pregang. release ACh and synapse on nicotinic receptors
  • cardiac, smooth, gland cells: postgang. release NE and synapse on α and β receptors
  • renal: postgang. release dopamine and synapse on D1 receptors
  • sweat glands: postgang. release ACh and synapse on muscarinic receptors
  • adrenal gland: release Epi, NE
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11
Q

Describe ganglionic neurotransmitter release of somatic system

A

release ACh and synapse on nicotinic receptors on muscle cells

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12
Q

What kind of receptor is the muscarinic receptor?

A

GPCR

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13
Q

What kind of receptor is the nicotinic receptor?

A

ligand activated ion channels

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14
Q

What are the receptors that ACh synapse on?

A
  • muscarininc

- nicotinic

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15
Q

What are the receptors that NE and Epi synapse on?

A

α and β receptors

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16
Q

What is the trophotropic system?

A
  • parasymp. system

- rest and digest -> leads to growth

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17
Q

What is the ergotropic system?

A
  • symp. system

- fight or flight -> energy expenditure

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18
Q

Define autoreceptor

A

receptor that inhibits release of its own neurotransmitter; feedback inhibition

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19
Q

Define heteroceptor

A

inhibits synthesis and release of neurotransmitter that’s not its own transmitter

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20
Q

What are types of presynaptic neuromodulation?

A
  • autoreceptor

- hetroceptor

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21
Q

What are types of postsynaptic neuromodulation?

A
  • receptor upregulation

- receptor downregulation

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22
Q

Which steps in neurotransmission can we alter with drug?

A
  • action potential
  • synthesis of NT
  • storage of NT
  • release of NT
  • termination of action of NT
  • receptor binding
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23
Q

Describe the symp. innervation of the eye

A
  • α1 adrenoceptor activation -> contracts radial pupillary dilator muscle to cause mydriasis
  • β adrenoceptor activation -> increase secretion of aqueous humor -> intraocular pressure increases
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24
Q

Describe the parasymp. innervation of the eye

A
  • happens via ACh synapse on M3 receptors
  • contract circular pupillary constrictor muscle -> miosis
  • contract ciliary muscle -> aq. humor flow into canal of Schlemm
  • allows doe accommodation for near vision
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25
Q

What happens in glaucoma?

A
  • injury blocks canal and cannot drain fluid out of eye
  • increase in intraocular pressure -> damaged optic nerve
  • can be genetic; canal deteriorates
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26
Q

What is the main cause of the predominant tone?

A

the parasymp. system

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27
Q

In which instances does the symp. system determine the predominant tone?

A

blood vessels and sweat glands

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28
Q

What is a cholinergic neuron?

A

a neuron that synthesizes and release ACh

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29
Q

What does it mean when something is innervated?

A
  • when there is a neuron above the location that releases NT
  • receptors that are not innervated will get a response from that blood flow or drugs
30
Q

How is ACh synthesized?

A
  • CHT transports choline into cell

- AcetylCoA + Choline -> ACh

31
Q

Hemicholinium

A

blocks the action of CHT -> decreases levels of ACh

32
Q

What happens after synthesis of ACh?

A

VAT transports it into vesicle for storage

33
Q

Vesamicol

A

blocks activity of VAT

34
Q

What effect does intracell. Ca have on nerve terminals?

A

fuses VAMPs and SNAPs -> exocytosis of vesicle -> release of ACh

35
Q

Botulinum Toxin

A

inhibits fusion of VAMPs and SNAPs

36
Q

What are drugs / toxins that can increase release of ACh?

A
  • Latratoxin

- Carbachol

37
Q

Toxins you should be aware of

A
  • Latrotoxin

- Tetrodotoxin

38
Q

Tetrodotoxin

A

inhibits action potential of cholinergic neurons

39
Q

Acetylcholinesterase (AChE)

A
  • breaks down ACh into acetate and choline

- located on post-synpt. cell

40
Q

PseudoAChE

A

in the blood to break down any access ACh into acetate and choline

41
Q

Cholinomimetics

A

drugs that bind on receptors that act as ACh

42
Q

Anticholinergics

A

drugs that bind on receptors to block cholin. pathway

43
Q

What are the types of cholinoceptors?

A
  • Muscarinic receptors

- Nicotinic receptors

44
Q

M2 are on which tissues?

A
  • myocardium
  • smooth muscle
  • CNS neurons
45
Q

M3 are on which tissues?

A
  • exocrine glands
  • vessels
  • CNS neurons
46
Q

Mechanism of M2

A
  • opening of K channels

- inhibit adenylyl cyclase

47
Q

Mechanism of M3

A
  • formation of IP3 and DAG

- increased intracell. Ca

48
Q

Drugs that work on muscarinic receptors do what?

A

favor parasymp. system

49
Q

nicotinic receptors

A

ion channel that causes depol. of neurons and muscles

50
Q

nicotinic receptors tissue distribution

A
  • postgang. neurons

- skeletal muscle neoromuscular end plates

51
Q

How many molecules of ACh needs to be bounded to nicotinic receptors?

A

two; after the first one binds, it is must easier for the second one to bind

52
Q

Myasthenia gravis

A
  • patient develops antibodies against their own receptors

- up to 80% of nicotinic receptors are reduced

53
Q

Alzheimer’s disease

A

loss of cholinergic neurons in temporal lobe and entorhinal cortex brain

54
Q

Where are nicotinic(m) receptors located?

A

skeletal muscle

55
Q

Properties of ACh with respect to drug development

A
  • non-selective
  • hydrolyze quickly
  • poor bioavailability
56
Q

What is the effect of the acetylated choline in ACh?

A

quick hydrolysis

57
Q

What is the effect of the quaternary amine in ACh?

A

poor permeability -> poor absorption

58
Q

properties of muscarine

A
  • cross BBB
  • natural alkaloid found in mushrooms
  • used in poison darts in which the antidote is atropine
59
Q

What are the responses to mAChR agonists?

A
  • smooth muscle contraction
  • vasodilation
  • increased secretion of exocrine
  • miosis
  • decreased heart rate
60
Q

What can you alter in ACh to slow down hydrolysis?

A

add a carbamyl group at the ester end

61
Q

effect of physostigmine

A
  • Carbamylated AChE increases half life from 0.2ms to 15 min
  • slows down hydrolysis of ACh
  • reversible
62
Q

effect of diethylphosphate

A
  • half life is 8 hours
  • irreversible
  • phosphorylates AChE
63
Q

What does MAO do?

A

metabolizes NE

64
Q

How did the classification of alpha and beta come about?

A

classification based on response to NE, E, or isoproterenol

65
Q

Effects of excessive ACh

A
  • Salivation/ secretion/ sweating
  • Lacrimation/ low bp
  • Urination
  • Defecation
  • GI distress
  • Emesis
66
Q

Cholinergic agonists

A
  • can cross BBB
  • produce arousal and cortical activation
    affects:
  • cognitive function
  • motor control
  • appetite suppression
  • nociception
67
Q

ACh as a choline ester

A
  • charged molecule, cannot cross BBB
  • in low doses, high affinity for M receptors
  • in high doses, affinity for both M and N receptors
  • 1% solution in eye to produce miosis during ophth. surgery
68
Q

Bethanechol as a choline ester

A
  • increases GI motiliy and urinary system
  • tight closure of LES will prevent acid reflux
  • resistant to activation by AChE
69
Q

Methacholine as a choline ester

A
  • used for diagnostic tool for asthma (back in the day; induces asthma)
  • partially resistant to AChE inactivation
70
Q

Carbachol as a choline ester

A
  • resistant to AChE inactivation
  • not selective
  • releases ACh from nerve endings

OU PDA (8 decks)

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