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Flashcards in Autonomic Pharm Deck (102):
1

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

Increased HR

2

What is NE effect on blood vessels?

Constriction leading to higher BP

3

Sympathetic N.S. describe

Fight or flight. Involved with exercise, activation, arousal

4

Parasympathetic describe

Rest and digest, recovery.

5

2 systems of ANS

Sympathetic and Parasympathetic

6

NT has to be synthesized where?

In the cell

7

Name the 3 main 2nd messenger systems

1. Phospholipase C
2. Adenylyl Cyclase
3. Guanylyl Cyclase

8

What do 2nd messenger systems do?

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

9

Are 2nd messengers intra or extracellular?

Intracellular

10

Which is not a 2nd messenger system?
1. Guanylyl cyclase
2. Phenyl A esterase
3. Adenylyl cyclase
4. Phospholipase C

Phenyl A esterase (made up)

11

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.

Atropine

12

Drugs that bind directly to muscarinic receptor are called?

Agonists

13

______ bind to the muscarinic or nicotinic receptors resulting in activation

Direct binding agents

14

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

Indirect acting agents

15

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

Ach, Increase

16

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

More activation, more activation

17

m1-m5 all activated by what?

Ach

18

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

blocks, prevents

19

Which muscarinic receptor is directly innervated with the myocardium?

M2

20

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

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

21

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

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

22

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

decreased

23

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

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

24

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

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

25

Increased synthesis of neurotransmitters will ______ receptor activation

increase

26

Inhibiting neurotransmitter breakdown will ______ receptor activation

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).

27

_____ mediates responses at cholinergic receptors

Acetylcholine (Ach) "CH"

28

_____ mediates responses at adrenergic receptors

Norepinephrine (NE) "NE" or Epinephrine (similar to NE)

29

_____ mediates responses at dopaminergic receptors

Dopamine (DA)

30

Adrenergic receptors have 5 subtypes, what are they?

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

31

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

decreased, nicotinic n, nicotinic m and muscarinic

32

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

neurotransmitter

33

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

Increased stimulation, heart rate increases

34

X vagus nerve acts on what?

Heart, GI tract

35

Ach is produced in neuron from ______

Acetyl-CoA

36

Acetyl-CoA synthesis occurs in the _____

Mitochondria

37

Ach storage and release phenomena can occur at a ______

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

38

When Ach is activated on vagus nerve is can ______ HR

decrease. direct stimulation=decrease heart rate

39

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

Exocytosis

40

What is eliminated by enzymatic hydrolysis via AchE?

Ach, its the main way it's degraded

41

What causes a versicle to open up?

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

42

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

MAO-Mono amene oxidase

43

What is a catecholamine?

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

44

Catecholamine release is triggered by?

Action potential or charge

45

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

Ca, exocytosis

46

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

COMT

47

MAO is __________

intracellular

48

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

MAO

49

What is NET?

Norepinephrine transporter. basically is reuptake back into neuron.

50

What is an agonist?

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

51

What is an antagonist?

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

What is an anticholinesterase?

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

AchE does what?

breaks down Ach

54

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

Anticholinesterase (AchE)

55

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

Neostigmine-has direct and indirect action

56

____ blocks Ach

Atropine (atropine is antichollenegic)

57

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

Answer: increase HR
(Stimulation causes decrease HR)

58

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

contraction of skeletal muscle

59

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

broncoconstriciton and increase flow of secretions

60

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

decrease HR, bradycardia

61

Epinephrine works on what receptors?

a1, a2, b1, b2

62

Norepinephrine works on what receptors?

a1, b1

63

Dopamine works on what receptors?

b1, dopamine

64

Alpha 1 when activated does what?

Vasoconstriction, leading to increase BP

65

________ is a direct adrenergic agonist

Epinephrine

66

Couple examples that block NE reuptake _____

Cocaine, tricyclic antidepressants

67

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

A: NE has none, epi should cause bronchodilation

68

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

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

69

a1 receptor location?

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

70

a2 receptor location?

CNS, peripheral vasculature

71

b1 location?

Heart, kidney

72

b2 location?

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

73

Domapine is in the _____

cns

74

Name 3 endogenous catecholamines (endogenous means in body)

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

75

_____ is mainly in adrenal medulla

Epinephrine

76

______ is mainly in sympathetic nerve endings

NE

77

a1 stimulation causes ______

Mydriasis, widening of the pupil.

78

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

constrict, increased blood pressure

79

a2 decreases release of ____ (exception to the rule)

NE

80

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

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

81

b2 when stimulated _______ up airways in lungs.

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

82

In blood vessels b2 ______ vessels

dilates for increased blood flow

83

A b1 agonist will do what on the heart?

Increase HR and force of contration

84

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

constrict, increased BP

85

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

Dilates and lowers BP. Also causes constriction of pupil.

86

Stimulating a1 receptor would cause what in eye?

Eye-Contraction of radial muscle of iris (mydriasis)

87

Stimulating a1 receptor in arterioles would do what?

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

88

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

Inhibition of transmitter release

89

Stimulation of b1 receptor in heart does what?

Increased rate, increased force of contraction, increased conduction velocity

90

Stimulation of b1 receptor in kidney does what?

Renin release

91

Stimulation of b2 in arterioles does what?

Dilation. Heart, lungs, skeletal muscle.

92

Stimulation of b2 in bronchi causes what?

Dilation, increased breathing

93

Stimulation of dopamine in kidney does what?

dilation of kidney vasculature

94

Miosis is what?

Pupil constriction muscarinic stimulation

95

Midriasis is what?

Pupil dialtion a1 receptor stimulation

96

Nicotinic N is located where and what does stimulation do?

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

97

Nicotinic M are located where and what does stimulation do?

Located: Neuromuscular junctions
Stimulation: contraction of skeletal muscle

98

Stimulation of muscarinic in the eye causes what?

Contraction of ciliary, leading to miosis "constriction" decreased pupil diameter

99

Stimulation of muscarinic receptor in heart does what?

Decreased HR

100

Stimulation of muscarinic receptor in lung does what?

Constriction of bronchi & promotes secretion

101

Stimulation of mucarinic receptor in bladder does what?

Promotes voiding

102

Stimulation of muscarinic receptor in GI tract does what?

Salivation, gastric secretions, defecation