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Pharmocology > Autonomic nervous system drugs > Flashcards

Autonomic nervous system drugs Flashcards

1
Q

Sympathetic neuro-transmitters

A

Epinephrine (epi), norepinephrine (NE), dopamine

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2
Q

Parasympathetic neuro-transmitter

A

Acetylcholine (ACh)

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3
Q

Sympathetic receptors

A

Alpha-1, (alpha-2), beta-1, beta-2 adrenergic receptors

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4
Q

parasympathetic receptors

A

Cholinergic (nicotinic and muscarinic receptors)

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5
Q

Sympathetic physiological responses I

A

Vasoconstriction of vessel in skin and GIT→ moves blood to core organs
Increased BP
Increased HR and contractility
Increased RR
Bronchodilation

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6
Q

Parasympathetic physiological responses I

A

Relative vasodilation of peripheral blood vessels→ moves blood to skin +GI tract
Resting BP,HR, RR
(Bronchoconstriction)

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7
Q

Sympathetic Physiological responses II

A

Mydriasis (dilated pupils)
Decreased saliva, GI fluids, GI motility, urination

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8
Q

Parasympathetic Physiological responses II

A

Miosis (constricted pupils)
Increased saliva, GI fluids, GI motility, urination

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9
Q

3 mechanisms can occur for ANS drugs

A

Mimic neurotransmitters (and turn up a response; directly or indirectly)
Can increase the amount of naturally occurring neurotransmitter (enhance the natural response)
Some drugs bind to and block the receptors (turn off the response)

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10
Q

Drugs can be categorized by

A

Drugs act on either the SNS or PNS nervous system; never both
Also categorized as
Parasympathomimetics
Parasympatholytics
Sympathomimetics
Sympatholytic

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11
Q

4 classes of ANS drugs

A

Cholinergics
Anticholinergics
Adrenergics
Adrenergic blockers

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12
Q

Physiological effect of cholinergics

A

Turn up the PS response

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13
Q

physiological effects of anticholinergics

A

Turn down the PS response

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14
Q

Physiological effects of adrenergics

A

Turn up the sympathetic response

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15
Q

Physiological effects of adrenergic blockers

A

Turn down the sympathetic response

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16
Q

Cholinergic drugs do what

A

Drugs turn up the PS response by either
Mimic SCh (direct-acting)
Increase endogenous levels of ACh (indirect acting)
Action is increase binding to and turning on of cholinergic receptors

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17
Q

Overall effect of cholinergic drugs

A

Overall effect is to increase parasympathetic activity
Resting RR,HR,BP; decreased contractility, bronchoconstriction
Increased GI motility and GI secretions
Urination
Miosis, tearing

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18
Q

Ex of anticholinergics

A

Atropine
Glycopyrrolate

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19
Q

Ex of cholinergics

A

Organophosphates

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20
Q

Ex of adrenergics

A

Epinephrine sulphate
Epinephrine
Norepinephrine
Dobutamine

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21
Q

Ex of adrenergic blockers

A

Beta-blockers

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22
Q

Review of how the PSN response normally works

A

Electric signal moves down axon and causes ACh to be activated
ACh released in synapse
ACh binds to cholinergic receptors→ turns on cell→ PS response
The response is trend off when ACh-esterase (enzyme located in the synapse) breaks down ACh

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23
Q

Direct-acting cholinergic drugs

A

These drugs act like acetylcholine
They bind to and turn on cholinergic receptors
The drug eventually degrades or diffuses away from synapse

24
Q

Ex of Direct-acting cholinergic drugs

A

Bethanechol- drug used to stimulate urination
Cisapride- drug used to stimulate GI motility in cats with constipation

25
Q

Indirect acting cholinergic drugs stop what

A

These drugs block the activity of the acetylcholinesterase enzyme
This enzyme is normally located in the synaptic cleft and breaks down the neurotransmitter→ limits the PS response from going on too long or too much
Blocking this enzyme causes the naturally occurring ACh to stay around for longer

26
Q

Ex of Indirect acting cholinergic drugs

A

organophosphates

27
Q

How the indirect acting cholinergic work

A

Work by blocking ACh-esterase and preventing ACh breakdown
Result is ACh stays around longer (same as if increasing amounts of ACh that is present)
Example: organophosphates

28
Q

Organophosphates are

A

Class of incesticide
Indirect-acting cholinergic drug
If overdose or adverse reaction, can cause same effects in the host
Most common form of toxicity world-wide

29
Q

Organophosphates mechanism of action

A

(on the insect)
Triggers activation of nicotinic receptors at neuromuscular junctions→ muscle spasms (skeletal muscle) leading to rigid paralysis
Also increases PS tone→ severe bronchoconstriction

30
Q

Anticholinergics bind to and block what

A

Drugs bind to and block cholinergic receptors

31
Q

Anticholinergic drugs are

A

Commonly part of emergency drug kit
Examples: atropine, glycopyrrolate
Drug binds to cholinergic receptors and block ACh from binding
Because the PNS system cannot be turned on the SNS dominates

32
Q

effect of anticholinergics

A

Effect is PS responses cannot be tuned on; result is sympathetic response dominate
Increased HR, contractility
Peripheral vasoconstriction (increases BP)
Bronchodilation
Decreased GI motility, decreased GI secretions
Urine retention
Decreased secretions (tears, saliva, bronchosecretions)

33
Q

Atropine is

A

Anticholinergic drug
Binds to and blocks ACh receptors→ blocks PNS response

34
Q

Physiological effects of atropine

A

Increased HR
Blocks peripheral vasodilation (skin and GI) which results in increased BP and moves blood to support heart, lungs, kidney and brain
Bronchodilation
Mydriasis, decrease secretions

35
Q

Clinical use of atropine

A

CPR drug (give IV)
Given SQ as aprt of premedication or intra-op
Supports heart rate and blood pressure
Decreases airways secretions so easier to intubate
Treating organophosphate toxicity
Ophthalmic drops dilate pupils, decreases tearing

36
Q

Glycopyrrolate is

A

Synthetic anticholinergic
Mechanism of action is similar to atropine, but longer acting and less pronounced effects

37
Q

Glycopyrrolate is used for

A

Used as part of pre-med or intra-op
Supports HR and BP
Decrease salivation and bronchial sections to easier to intubate
Decreases gastric fluids so lessens reflux

38
Q

How adrenergic drugs work

A

These drugs turn up the sympathetic response
Works by binding to and turning on the adrenergic receptors
Effect depends on which receptors are targeted

39
Q

What does alpha-1 receptor do

A

blood vessels in skin and GIT; when activated, causes vasoconstriction of these vessels→ shifts blood flow so there is increased BP to heart/lung/brain

40
Q

What does alpha-2 receptor do

A

Alpha-2: sedatives discussed in anesthesiology

41
Q

What does beta-1 receptor do

A

Beta-1: heart muscle; increases HR and stroke volume

42
Q

What does beta-2 receptor do

A

Beta-2: bronchioles; causes dilation to increase airflow and increases RR

43
Q

2 classes of adrenergic drugs and what they do

A

Non-selective adrenergics
-Bind to more than one adrenergic receptor→ broader effects
-Ex. epinephrine, ephedrine
Selective adrenergics
-Only bind to one receptor→ more limited effects
-Ex. beta-blockers

44
Q

Epinephrine is

A

Non-selective adrenergic agonist
Exact same as endogenous neurotransmitters
Epinephrine has slight increased beta-1 activity compared to its activity on the other adrenergic receptors

45
Q

Effect of epinephrine

A

Main effect: increased HR
Also: causes peripheral vasoconstriction, increases airway diameter, pupil dilation

46
Q

Clinical indications for epinephrine

A

CPR drug
Cardiac resuscitation
High dose
IV, intratracheal every 2-5 min
Anaphylaxis
Low dose
IV, SQ or IM depending in how emergent and what symptoms of anaphylaxis are
Too rapid IV can cause arrhythmias

47
Q

Ephedrine sulfate works on

A

Indirectly turns on sympathetic receptors
By increasing amounts of norepinephrine in the body
Longer lasting and less pronounced effects than epinephrine

48
Q

Clinical indications of ephedrine sulfate

A

Use to produce bronchodilation (beta-2)
Use to treat nasal congestion (alpha-1)
Use for hypotension during anesthesia (alpha-1)

49
Q

Adrenergic blockers are and work for

A

Drugs that bind to and block adrenergic receptors from being turned on
Block sympathetic activation; parasympathetic responses dominate as a result
Adrenergic blockers can be nonselective or selective

50
Q

Effects of adrenergic blockers

A

Decreed HR, contractility, RR, vasodilation
Bronshoconstriciton, increased bronchial secretions
Increased GI motility and GI secretions
Urination
Miosis, tearing

51
Q

Side effects of the ANS drugs occur if

A

Drug binds receptors in non-targeted tissues
Ex. want to see its effect in the bladder, but drug also goes to the heart
Drug binds more than one type of receptor
Cholinergic drugs can also bind to nicotinic receptors at neuromuscular junction
Selective adrenergic drugs may also bind unintentionally to other adrenergic receptors
Ex. an alpha-1 specific adrenergic blocker may also block beta-1 and/or beta-2 receptors
Most common at high doses

52
Q

Side effects of cholinergics

A

Usually undesired or excessive parasympathetic responses
Ex. cisapride is a cholinergic that increases GI motility. Side effects may include bradycardia or bronchoconstriction
Also, unwanted activation of neuromuscular junctions

53
Q

Side effects of anticholinergics

A

Usually undesired or excessive sympathetic response
Includes; tachycardia, constipation, urine retention, dry mouth
Also, unwanted inhibition of neuromuscular junctions

54
Q

Side effects of adrenergics

A

Usually undesired or excessive sympathetic response
Includes: tachycardia, arrhythmias, hypertension anxiety, excitability

55
Q

Side effects of adrenergic blockers

A

Usually undesired or excessive parasympathetic responses
Includes: bradycardia, hypotension, syncope, nausea, vomit, diarrhoea

Pharmocology (10 decks)

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