Autonomic Pharm Flashcards

1
Q

NEpi has activity on the heart, if stimulated the clinical effect is?

A

Increased HR

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2
Q

What is NE effect on blood vessels?

A

Constriction leading to higher BP

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3
Q

Sympathetic N.S. describe

A

Fight or flight. Involved with exercise, activation, arousal

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4
Q

Parasympathetic describe

A

Rest and digest, recovery.

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5
Q

2 systems of ANS

A

Sympathetic and Parasympathetic

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6
Q

NT has to be synthesized where?

A

In the cell

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7
Q

Name the 3 main 2nd messenger systems

A
  1. Phospholipase C
  2. Adenylyl Cyclase
  3. Guanylyl Cyclase
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8
Q

What do 2nd messenger systems do?

A

They get signal across so stimulation can occur. They are triggered when NT hits receptor, they are bystanders. They do the grunt work. They do all the work and help signal transmission

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9
Q

Are 2nd messengers intra or extracellular?

A

Intracellular

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10
Q

Which is not a 2nd messenger system?

  1. Guanylyl cyclase
  2. Phenyl A esterase
  3. Adenylyl cyclase
  4. Phospholipase C
A

Phenyl A esterase (made up)

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11
Q

This drug is given in emergency and is an anti chollenergic. It works specifically on M2 (muscarinic 2) So when it is given it blocks M2 to decrease HR.

A

Atropine

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12
Q

Drugs that bind directly to muscarinic receptor are called?

A

Agonists

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13
Q

______ bind to the muscarinic or nicotinic receptors resulting in activation

A

Direct binding agents

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14
Q

______inhibit AChE(E is for estherase), therefore resulting in an increase of Ach in the synaptic cleft

A

Indirect acting agents

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15
Q

_____is an enzyme designed to break down Ach so if you prevent breakdown you _____ amount cause there is no where to go

A

Ach, Increase

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16
Q

If more Ach at receptor it should cause _______ but if you prevent it from being broken down that should cause more _______ too b/c it should be broken down and recycled and whole process started over again

A

More activation, more activation

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17
Q

m1-m5 all activated by what?

A

Ach

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18
Q

Drug that is specific for N(m) for example _____ Ach and ____ muscle movement

A

blocks, prevents

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19
Q

Which muscarinic receptor is directly innervated with the myocardium?

A

M2

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20
Q

What are the 5 steps in synaptic transmission? (test)

A
  1. Transmitter synthesis
  2. Transmitter storage
  3. Transmitter release
  4. Receptor binding
  5. Termination of transmission
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21
Q

NT dissociates from receptor and is removed from synaptic gap by: (3 ways)

A
  1. Reuptake (recycled)
  2. Enzymatic degradation (got digested by another enzyme system)
  3. Diffusion (goes from high concentration to low)
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22
Q

If depleted NT being made (synthesized) then impact on receptor is ________

A

decreased

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23
Q

What happens if binding to receptor is blocked? (test)

A

Shouldn’t be activated as much if blocked, so decreased

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24
Q

Inhibiting neurotransmitter release from presynaptic nerve terminal will ____ receptor activation (test)

A

Block or decrease. (simple concept, if you have more, you have more activation. if you have less, then you have less activation)

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25
Q

Increased synthesis of neurotransmitters will ______ receptor activation

A

increase

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26
Q

Inhibiting neurotransmitter breakdown will ______ receptor activation

A

increase (example: if sitting there at end of receptor but prevent it from being broken down and starting process over it should increase the activation which makes sense cause can’t reset whole cycle and start over if its still sitting there).

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27
Q

_____ mediates responses at cholinergic receptors

A

Acetylcholine (Ach) “CH”

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28
Q

_____ mediates responses at adrenergic receptors

A

Norepinephrine (NE) “NE” or Epinephrine (similar to NE)

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29
Q

_____ mediates responses at dopaminergic receptors

A

Dopamine (DA)

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30
Q

Adrenergic receptors have 5 subtypes, what are they?

A

Alpha(1) Alpha (2) Beta (1) Beta (2) Dopamine (DA)

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31
Q

If Ach is blocked you will have a ____ activity on these receptors ______

A

decreased, nicotinic n, nicotinic m and muscarinic

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32
Q

Receptor is specific to the ______ they are one in the same

A

neurotransmitter

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33
Q

Epinephrine is released and activates b1 receptor, beta 1 receptor is on the heart, what is the clinical outcome? (test)

A

Increased stimulation, heart rate increases

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34
Q

X vagus nerve acts on what?

A

Heart, GI tract

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35
Q

Ach is produced in neuron from ______

A

Acetyl-CoA

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36
Q

Acetyl-CoA synthesis occurs in the _____

A

Mitochondria

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37
Q

Ach storage and release phenomena can occur at a ______

A

very fast speed. Storage and release are mili seconds. Enzyme system is quick at digesting and starting process over again.

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38
Q

When Ach is activated on vagus nerve is can ______ HR

A

decrease. direct stimulation=decrease heart rate

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39
Q

Fancy term means vesicles got to end of neuron and opened up

A

Exocytosis

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40
Q

What is eliminated by enzymatic hydrolysis via AchE?

A

Ach, its the main way it’s degraded

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41
Q

What causes a versicle to open up?

A

change in charge causes vesicle to open and NE is released then goes to receptor to bind

42
Q

_____ is an enzyme responsible for breaking down catecholamines, one of those responsible for breaking it down and recycling the whole process

A

MAO-Mono amene oxidase

43
Q

What is a catecholamine?

A

Included among catecholamines are epinephrine (adrenaline), norepinephrine (noradrenaline), and dopamine.

44
Q

Catecholamine release is triggered by?

A

Action potential or charge

45
Q

Action potential results in influx of ____ in the nerve terminal and fusion of granules resulting in _____ of NE

A

Ca, exocytosis

46
Q

enzyme system outside the neuron responsible for degradation of NE is ______(test)

A

COMT

47
Q

MAO is __________

A

intracellular

48
Q

Enzyme system inside responsible for degrading NE is _______(test)

A

MAO

49
Q

What is NET?

A

Norepinephrine transporter. basically is reuptake back into neuron.

50
Q

What is an agonist?

A

An agonist is a chemical that binds to a receptor and activates the receptor to produce a biological response.

51
Q

What is an antagonist?

A

A receptor antagonist is a type of receptor drug that blocks or dampens a biological response by binding to and blocking a receptor rather than activating it like an agonist.

52
Q

What is an anticholinesterase?

A

Drug that prevents Ach metabolism, maintain ach concentration at each effector site ach is released. It’s a drug that blocks AchE. Drugs that block acetylcholinesterase (achE)

53
Q

AchE does what?

A

breaks down Ach

54
Q

A way to increase Ach activity is to give an ______, can give these after surgery to restore muscle function

A

Anticholinesterase (AchE)

55
Q

Main anticholinesterase given at controlled dose that is most effective at restoring neuromuscular function after a blockade?

A

Neostigmine-has direct and indirect action

56
Q

____ blocks Ach

A

Atropine (atropine is antichollenegic)

57
Q

If Ach is blocked @ the muscarine receptor of the heart what should be the clinical effect be? (test)

A

Answer: increase HR

Stimulation causes decrease HR

58
Q

The neuromuscular system Nm when its activated with Ach it should cause ______

A

contraction of skeletal muscle

59
Q

If muscarinic receptors in the lung m3, if stimulated should cause ______

A

broncoconstriciton and increase flow of secretions

60
Q

When Ach is activated on muscarinic receptor in heart stimulation translates to __________

A

decrease HR, bradycardia

61
Q

Epinephrine works on what receptors?

A

a1, a2, b1, b2

62
Q

Norepinephrine works on what receptors?

A

a1, b1

63
Q

Dopamine works on what receptors?

A

b1, dopamine

64
Q

Alpha 1 when activated does what?

A

Vasoconstriction, leading to increase BP

65
Q

________ is a direct adrenergic agonist

A

Epinephrine

66
Q

Couple examples that block NE reuptake _____

A

Cocaine, tricyclic antidepressants

67
Q

What’s the difference on B2 activity of Epi vs NE? (test)

A

A: NE has none, epi should cause bronchodilation

68
Q

Albuterol is b2 agonist so when inhaled it activates _____receptors and b2 causes _______

A

activates b2 receptors, and b2 causes bronchodilation or opening of the lungs

69
Q

a1 receptor location?

A

eye, peripheral vasculature (prodominatly concentrated in arteries and veins)

70
Q

a2 receptor location?

A

CNS, peripheral vasculature

71
Q

b1 location?

A

Heart, kidney

72
Q

b2 location?

A

Skeletal muscle, lungs, uterus, liver (know cardiac related)

73
Q

Domapine is in the _____

A

cns

74
Q

Name 3 endogenous catecholamines (endogenous means in body)

A

NE, EPI, DA. Catecholamines directly stimulate adrenergic receptors and activate effector tissues

75
Q

_____ is mainly in adrenal medulla

A

Epinephrine

76
Q

______ is mainly in sympathetic nerve endings

A

NE

77
Q

a1 stimulation causes ______

A

Mydriasis, widening of the pupil.

78
Q

If a1 is stimulated on blood vessels they should _____ and the clinical outcome is______

A

constrict, increased blood pressure

79
Q

a2 decreases release of ____ (exception to the rule)

A

NE

80
Q

b1 is predominately on the _______ , also related to renin release on _____

A

heart, kidney

Increases HR and increase force of contraction (main effects of b1 stimulation)

81
Q

b2 when stimulated _______ up airways in lungs.

A

opens up airways. Albuterol is b2 agonist, its effects on the lungs are to dilate so patient can breathe better

82
Q

In blood vessels b2 ______ vessels

A

dilates for increased blood flow

83
Q

A b1 agonist will do what on the heart?

A

Increase HR and force of contration

84
Q

Epi and NE when they act on a1 should ______ the veins so it translates to ____ BP

A

constrict, increased BP

85
Q

If a1 antagonist what affect would that have on the blood vessels and what affect on bp?

A

Dilates and lowers BP. Also causes constriction of pupil.

86
Q

Stimulating a1 receptor would cause what in eye?

A

Eye-Contraction of radial muscle of iris (mydriasis)

87
Q

Stimulating a1 receptor in arterioles would do what?

A

constriction

skin, viscera, mucous membranes, veins. Stimulating a1 in sex organ=ej

88
Q

Stimulation of a2 receptors located in presynaptic nerve terminals does what?

A

Inhibition of transmitter release

89
Q

Stimulation of b1 receptor in heart does what?

A

Increased rate, increased force of contraction, increased conduction velocity

90
Q

Stimulation of b1 receptor in kidney does what?

A

Renin release

91
Q

Stimulation of b2 in arterioles does what?

A

Dilation. Heart, lungs, skeletal muscle.

92
Q

Stimulation of b2 in bronchi causes what?

A

Dilation, increased breathing

93
Q

Stimulation of dopamine in kidney does what?

A

dilation of kidney vasculature

94
Q

Miosis is what?

A

Pupil constriction muscarinic stimulation

95
Q

Midriasis is what?

A

Pupil dialtion a1 receptor stimulation

96
Q

Nicotinic N is located where and what does stimulation do?

A

Located: All ANS nervous system ganglia
Stimulation: Of nerves causes Epi release from adrenals

97
Q

Nicotinic M are located where and what does stimulation do?

A

Located: Neuromuscular junctions
Stimulation: contraction of skeletal muscle

98
Q

Stimulation of muscarinic in the eye causes what?

A

Contraction of ciliary, leading to miosis “constriction” decreased pupil diameter

99
Q

Stimulation of muscarinic receptor in heart does what?

A

Decreased HR

100
Q

Stimulation of muscarinic receptor in lung does what?

A

Constriction of bronchi & promotes secretion

101
Q

Stimulation of mucarinic receptor in bladder does what?

A

Promotes voiding

102
Q

Stimulation of muscarinic receptor in GI tract does what?

A

Salivation, gastric secretions, defecation