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Pharmacology > Ch. 8: Intro to Autonomic Drugs > Flashcards

Ch. 8: Intro to Autonomic Drugs Flashcards

1
Q

Pharmacology

A

the study of histories, sources, chemical properties, biological actions, biological handling and therapeutic uses of drugs in living organisms

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2
Q

main fxs of ANS (3)

A
  • maintains homeostasis of visceral tissues
  • regulates the functions of 3 primary cell types: smooth m, cardiac m, and secretory glands
  • provides a means for the body to alter the functions of many tissues in response to external or internal changes (i.e. senses, body temp, pain, BP, fear, dz)
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3
Q

pharmacotherapeutic uses of autonomic drugs (3)

A
  • re-establish “normal” function in dysfunctional organs (i.e. CV, GI, resp., urinary tract, etc. disorders)
  • offset visceral changes secondary to CNS disorders or treatment with CNS-acting drugs
  • treat poisonings and hypersensitivity reactions
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4
Q

classification of phenylephrine

A

alpha-1 adrenergic agonist

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5
Q

What are the effects of phenylephrine administration**

A

(alpha-1 agonist)

  • vasoconstriction
  • increase BP
  • increase total peripheral resistance
  • DECREASE in heart rate
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6
Q

Why does phenylephrine cause DECREASE in heart rate?**

A

Vasoconstriction/Increased BP activates baroreceptors/stretch receptors, which results in reflex arc from receptors –> CNS –> cardiac output/HR falls to try to compensate for increased BP

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7
Q

Integration centers at brainstem or above control which functions?

A

baroreceptor, GI secretion, sweating

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8
Q

Integration centers on spinal cord control which functions?

A

vasomotor tone
bladder emptying
defecation
GI motility

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9
Q

main fx of afferent nerves

A

relay status of heart/lungs/kidney/vascular stability back to CNS where it is processed/integrated

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10
Q

Drugs we use primarily target where on autonomic reflex circuit?

A

postganglionic nerves (for both sympathetic and parasympathetic)

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11
Q

Ach primarily acts on which type of receptors?

A

nicotinic ganglionic receptors

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12
Q

What type of drugs target integration centers (forebrain, brainstem, etc.)

A

tranquilizers, sedatives, anesthetics, stimulants

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13
Q

What type of drugs target autonomic ganglion?

A

nicotinic (i.e. nicotinic cholinergic antagonist) and anti-AChE drugs

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14
Q

What type of drugs target neuroeffector junction?

A

adrenergic, cholinergic, and anti-AChE drugs

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15
Q

Why do we rarely target autonomic ganglion?

A

because all the ganglia utilize a similar primary mech. of neurotransmission utilizing ACh acting on nicotinic receptors

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16
Q

Primary intended site of action for ANS drugs***

A

neuroeffector junction

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17
Q

T/F: nearly all visceral tissue receive dual innervation by sympathetic and parasympathetic neurons

A

T

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18
Q

T/F: neuroeffector junctions are located at many sites throughout the body

A

T

19
Q

pharmacological antagonism

A

blockade of an agonist by an atagonist

20
Q

physiological antagonism

A

opposing actions produced by two drugs via actions on different receptors or via distinct mechs.

21
Q

How does atenolol work?

A

blocks EP at cardiac beta-1 receptors

22
Q

Histamine causes constriction/dilation of bronchiole smooth muscle?

A

constriction

23
Q

What causes dilation of bronchiole smooth muscle? via what receptors?

A

epinephrine on beta-2 adrenergic receptors

24
Q

Advantages of physiological antagonism

A
  • allows for different pharm. approaches for management of numerous disorders
  • allows for complimentary txs that target branches of the ANS (ie. to speed up HR, you can either block parasympathetics, or stimulate sympathetics)
25
Q

does isoproterenol stimulate or block sympathetic input to heart?

A

stimulate

26
Q

does atropine stimulate or block parasympathetic input to heart?

A

block. Thereby stimulating heart

27
Q

Sympathetic postganglionic neurons utilize what NT? What receptors do they act on? **

A

NE and EP. Act on alpha-1/2 and beta-1/2 adrenergic receptors

28
Q

Parasympathetic postganglionic neurons utilize what NT? What receptors do they act on?

A

Ach. Act on muscarinic receptors

29
Q

Sites of drug action in parasympathetic neurons**

A 
Ach synthesis
Ach release
presynaptic receptors
postsynaptic receptors***
Ach elimination (AchE)***
30
Q

Sites of drug action in sympathetic neurons**

A 
NE biosynthesis
NE storage and release (from vesicles)
presynaptic receptors***
postsynaptic receptors***
NE and EP elimination***
31
Q

Preganglionic neurons use what NT for parasympathetic side? Sympathetic side?***

A

ACh for both!

32
Q

Preganglionic neurons use what receptor types for parasympathetic side? Sympathetic side?***

A

Nicotinic for both!

33
Q

Postganglionic neurons use what transmitter for para. side? Sym. side?***

A

Para: Ach

Sym.: NE and EP

34
Q

Postganglionic neurons use what receptor type for para. side? Sym. side?

A

Para: muscarinic
Sym: alpha-1,2 beta-1,2

35
Q

T/F: There is NO uptake (transport) process for Ach elimination in parasympathetic neurons***

A

TRUE. Ach elimination is via AChE only!

36
Q

how does botulinum toxin work?

A

inhibits Ach release in motor neurons

37
Q

Name 3 drugs that act on postsynaptic receptors in parasympathetic neurons, either as agonists or antagonists**

A

bethanechol (agonist of AchE)

atropine, glycopyrrolate (antagonists of AchE)

38
Q

Name 3 drugs that act on Ach elimination (via AchE) in parasympathetic neurons**

A

edrophonium
physostigmine
parathion

39
Q

major target for therapeutic control of parasymp. function**

A

postsynaptic receptors

40
Q

On sympathetic side, drugs primarily target receptors pre/postsynaptically

A

postsynaptically

41
Q

How do drugs act on presynaptic receptors on sympathetic neurons?

A

increase or decrease NT release from nerve terminals

42
Q

major target for drug action on sympathetic neurons

A

postsynaptic (alpha or beta) receptors

43
Q

In sympathetic neurons, how is NT (EP or NE) eliminated?**

A

2 ways:

1) uptake (most important; inhibited by ketamine)
2) enzymatic degradation (via multiple enzymes, such as MAO)

Pharmacology (21 decks)

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