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VETM 443 Pharmacology > Autonomic (Cholinergic/Adrenergic) Drugs > Flashcards

Autonomic (Cholinergic/Adrenergic) Drugs Flashcards

1
Q

Compare the transmission of signals from the CNS to the target via the SNS and PSNS pathways

A

SNS signals are from the spinal cord. Sent via the short pre-ganglionic axon. Transmission to the longer post ganglionic axon is done via the nicotinic receptor and acetylcholine release. At the target organ, norepinephrine (or Ach or dopamine) bind to adrenergic receptors.

PSNS signals come from the brainstem or sacrum via a long pre-ganglionic axon. Signal transmitted via a nicotinic receptor and Ach to the shorter post-ganglionic axon. At the target organ, Ach is released and interacts with muscarinic (aka. cholinergic) receptors.

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2
Q

What are the steps of signal transmission at the ganglion level

A
  1. Acetyl-CoA + choline result in acetylcholine formation. In vesicles.
  2. Depolarization (influx of Na+) via an action potential.
  3. The Ca voltage gated ion channel open resulting in increased Ca2+. Influx results in vesicle fusion and release Ach.
  4. Ach binds nicotinic receptors via ligand gated ion channels which bind and depolarize the post synapse axon.
  5. Ach also binds the pre-synaptic nicotinic receptor. Negative feedback due to binding results in less Ach release
  6. Acetylcholinesterase degrades Ach in synaptic cleft
  7. Acetyl-CoA and choline resorbed
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3
Q

What are the steps of signal transmission from the SNS at the target tissue

A
  1. The post-ganglionic action potential causes release of norepinephrine
  2. NE bind the post-synaptic adrenergic receptor which is a G protein coupled receptor. This causes signal transduction and sympathetic effect.
  3. NE will also bind the pre-synaptic adrenergic receptor. Negative feedback will ensue resulting in less NE release and increased degradation.
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4
Q

How is norepinephrine degraded in neurons

A

Metabolism is done via catechol-o-methyltransferase (COMT). After absorption into the neuron it can be degraded in the mitochondria by monoamine oxidase (MAO). It could also diffuse away and be metabolism in plasma, liver, or kidneys.

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5
Q

What are the steps of signal transmission from the PSNS at the target tissue

A
  1. The post-ganglionic action potential causes release of Ach
  2. Ach bind the post-synaptic muscarinic/cholinergic receptor which is a G protein coupled receptor. This causes signal transduction and parasympathetic effect.
  3. Ach will also bind the pre-synaptic adrenergic receptor. Negative feedback will ensue resulting in less Ach release and increased degradation by AchE.
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6
Q

What is the structure of adrenal glands and the associated function?

A

There are 3 zones in the cortex.
1. zona glomeerulosa: salt - mineralocorticoids
2. zona fasiculata: sugar - glucocorticoid
3. zona reticularis: sex - androgens

Medulla: stress - cortisol

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7
Q

What is the function of the adrenal gland in the context of autonomic stimulation

A

The adrenal gland is a modified sympathetic ganglion. The chromaffin cells release NE which target alpha receptors resulting in a vascular effect. They can also release epinephrine which bind both alpha and beta receptors which results ini vasodilation of skeletal muscle, skin, and kidney. It also increases cardiac output. It may vasoconstrict some other vasculature.

If you have excess epinephrine it will have an preference for alpha receptors causing more vasoconstriction which increases blood pressure.

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8
Q

What are the consequences of PSNS overstimulation

A

DUMBBELLS

diarrhea
urination
miosis
bradycardia
bronchorrhea
emesis
lacrimation
lethargy
salvate/sweat

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9
Q

Compare the target organs of SNS and PSNS stimulation

A

SNS targets the radial smooth muscle around eye, salivary glands, arterioles, lung, heart,stomach, GI, kidney, and bladder.

PSNS targets the constricting circular muscle in eye, lacrimal gland, salivary gland, heart, lung, GI, bladder, penis, prostate. PSNS has no direct effects on vascular smooth muscle.

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10
Q

What are the factors impacting adrenergic activation

A

It depends on receptor subtype and the tissue it is expressed on. The effect of NT depends on what receptors are expressed and activated

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11
Q

How does autonomic innervation impact cardiovascular structures.

A

Heart is subject to PSNS and SNS impacts

Vasculature is only impacted by SNS. Vasoconstriction and dilation is controlled by the amount or frequency of SNS stimulation

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12
Q

What type of drug is a sympathomimetic?

A

adrenergic agonist

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13
Q

What are the potential mechanisms of action for adrenergic agonists?

A

It can be direct via endogenous catecholamines like norepi and epi or via specific adrenergic receptor agonists (dobutamine)

It could also be from indirect mechanisms like making them release more catecholamines or reducing catecholamine metabolism by inhibiting MAO/COMT or reducing reuptake

Drugs can act via both mechanisms

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14
Q

Discuss the pros and cons of alpha 2 agonists

A

It is a good pre-med and effective for large animal standing procedures

Some negative effects include
- reduced cardiac output which is independent of the dose (a reduction in dose will result in the same magnitude of effect and but for a shorter duration)
- it can cause persistent bradycardia
- it can cause paradoxical excitation

it is important to use it in healthy animals

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15
Q

What are the contraindications for uses of alpha 2 agonist

A
  • shock
  • cardiovascular disease
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16
Q

What is the mechanism of action for alpha 2 agonists

A

It causes sedation via inhibiting norepi release a the brainstem (initially acts as norepi resulting in reduced subsequent release)

It causes analgesia via reduced neurotransmitter release in afferent pathways

It reduces cardiac output via initial vasoconstriction causing increased blood pressure, this is followed by reflex bradycardia. The pre-synaptic effect is bradycardia

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17
Q

How is the sedation and analgesia effect of alpha 2 agonists enhanced

A

If it is paired with an opiod

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18
Q

What type of drugs are parasympathomimetics?

A

either cholinergics or cholinoreceptor stimulants

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19
Q

What is the mechanism of action for cholinergic drugs

A

either

Muscarinic receptors that target nerves/heart/glands

nicotinic receptors which target ganglions which is also neuromuscular but under somatic control

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20
Q

What is the mechanism of action for cholinoreceptor stimulant drugs

A

It can act either directly or indirectly

Directly it can act as an agonist via alkaloid or choline esters

Indirectly it can act as a reversible or irreversible AchE inhibitor that can affect both muscarinic or nicotinic receptors

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21
Q

What type of drug is xylazine?

A

alpha2 agonist

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22
Q

What species is xylazine used in primarily?

A

horses and ruminants

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23
Q

What are the negative effects and potential contraindications of xylazine?

A

It is an alpha 2 agonist and so it has the associated impacts

  • AV block
  • reduced GI motility
  • increased sweating
  • increased uterine tone resulting in a risk of birth in pregnant animals
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24
Q

Compare the use of xylazine in horses and ruminants

A

Ruminants require 1/10th the dose when compared to a horse dose

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25
Q

How is xylazine enhanced for sedation and analgesia?

A

It is usually combined with an opioid like butorphanol to increase its sedation and pain control effects

The analgesia effect is much shorter than the sedative effect

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26
Q

What drug class is detomidine

A

alpha 2 agonist

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27
Q

What species is detomidine used in primarily?

A

horses mainly and also ruminants

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28
Q

How is detomidine reversed?

A

atipamezole an alpha 2 antagonist

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29
Q

Compare detomidine to xylazine

A

they are both alpha 2 agonists but detomidine is 50-100x more potent and it also offers better pain control and sedation with a reduced likelihood of inducing birth

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30
Q

How is xylazine reversed?

A

atipamezole or yohimbine

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31
Q

What type of drug is romifidine and how does it compare to detomidine?

A

It is another alpha2 agonist and it will cause effects for a longer duration and result in less ataxia

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32
Q

What drug class is dexmedetomidine

A

alpha 2 agonist

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33
Q

What species is dexmedetomidine primarily used in

A

small animal sedation

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34
Q

What is/are the adverse effect(s) of dexmedetomidine

A

50% of cats vomit

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35
Q

How to reverse dexmedetomidine

A

atipamezole

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36
Q

Compare the effect of Dexmedetomidine and Metomadine and why is there a difference?

A

Metomadine contains both isomers of the drug but only one isomer is the active one

Dexmedetomidine contains only the active isomer of the drug

They are essentially the same but dexmedetomidine is more potent

37
Q

What drug class is dobutamine

A

beta 1 agonist

38
Q

What are the adverse effects of dobutamine

A

It precipitates with bicarbonate

At high doses it can cause tachycardia

It must be given as a CRI

in cats it can induce seizures

39
Q

What is the mechanism of action of dobutamine? How does this impact its use?

A

It is a positive inotrope and there is no change in heart rate at a normal dose

It is important to fix any hypovolemia before administration

40
Q

What is the drug class of clenbuterol

A

beta 2 agonist

41
Q

What species is clenbuterol used in

A

horses

42
Q

What species is clenbuterol not used in

A

production animals

43
Q

How is clenbuterol used? in what scenario?

A

as a treatment for equine asthma but now there are newer treatments like steroids, albuterol, and ciclesonide that are better

44
Q

What drug class is epinephrine?

A

It is a non selective adrenergic agonist

45
Q

When is epinephrine used in veterinary medicine and what is its mechanism of action

A

Low dose epinephrine is used for CPR to increase coronary perfusion and increase arterial blood pressure
- increasing cardiac output will also increase cardiac oxygen demands

It is used to treat anaphylaxis by inducing vasoconstriction

46
Q

What route of administration is epinephrine given

A

IM
SC
IV
IT

47
Q

What class of drug is prazosin

A

alpha 1 antagonist

48
Q

What species is prazosin used in

A

small animals

49
Q

What is prazosin used for primarily?

A

It was used for blocked cats but it isnt anymore

It now may increase the risk of these cats re-blocking

50
Q

What is the mechanism of action for prazosin?

A

It causes vasodilation which reduced arterial and venous blood pressure

97% of it is protein bound

51
Q

What drug class is atipamezole?

A

alpha 2 antagonist

52
Q

What species is atipamezole used in?

A

small animals and horses

53
Q

What is atipamezole used for and how is it administered?

A

It is used to reverse sedation and analgesia

It is administered IM
- in horses you can administer half the dose IM and the other half IV (inject slowly)

54
Q

What should you consider/be aware of when reversing dexmedetomidine, ketamine, and butorphanol after a cat neuter (for example)? How would you reverse these drugs?

A

an alpha 2 antagonist like atipamezole

Ensure that you wait long enough for the ketamine to wear off

Also consider that when you are reversing sedation you are also reversing the analgesic effects as well

55
Q

What drug class is esmolol?

A

beta 1 antagonist

56
Q

What species is esmolol used in?

A

Cats

57
Q

What is esmolol used for?

A

Primarily used in CPR and anesthesia of cats

58
Q

What is the mechanism of action for esmolol and what are the associated adverse effects?

A

It acts to reduce heart rate and contractility (chronotropy and inotropy) resulting in reduced myocardial oxygen demand and reduced systolic and diastolic blood pressure

The adverse effects are hypotension and bradycardia

59
Q

What drug class is neostigmine?

A

cholinergic

60
Q

What is the mechanism of action of neostigmine?

A

It is a reversible acetylcholinesterase inhibitor which results in the reduced breakdown of Ach

61
Q

What is neostigmine used for?

A

Used to treat myasthenia gravis but pyridostigmine is now the preferred treatment because it has less impact on the GI

It increases GI motility

62
Q

What toxins is neostigmine similar to? How is it different?

A

It is similar to organophosphates and sarin gas

They both bind AchE receptors

Neostigmine reversibly binds these receptors and the toxins irreversibly bind them

63
Q

What drug class is atropine?

A

anticholinergic

64
Q

What drug class is glycopyrrolate?

A

anticholinergic

65
Q

What is the mechanism of action of both atropine and glycopyrrolate? What are the effects?

A

They are competitive muscarinic antagonists resulting in

increased chronotropy
mydriasis
reduced secretions
bronchodilation

The effects are dose dependent

66
Q

What are the adverse effects of atropine and glycopyrrolate?

A

tachyarrhythmias
ileus in horses

If used in combination with an alpha 2 agonist it increases the risk for myocardial hypoxia (increases cardiac work)

high doses of atropine are associated with mania

67
Q

What is atropine and glycopyrrolate used for?

A

It is an emergency treatment for bradyarrhythmias

Treats equine recurrent uveitis and acute recurrent airway obstruction (RAO)

Used for opthalmic exam

When you need to increase heart rate
- when there is a risk for vagal bradycardia (eye sx)
- opioid use
- brachycephalic breeds with high vagal tone

68
Q

How does atropine compare to glycopyrrolate?

A

Atropine does cross the BBB and glycopyrrolate does not

There are more neurologic effects associated with atropine vs glycopyrrolate

69
Q

What is another name(s) for N-butylscopolammorium bromide? What drug class is it?

A

Hyoscine butylbromide aka buscopan

anticholinergic

70
Q

What species is N-butylscopolammonium bromide used in?

A

horses only

71
Q

What is the mechanism of action of hyoscine butylbromide? What are its effects?

A

It is similar to atropine

It is a competitive muscarinic antagonist
- increase chronotropy
- mydriasis
- reduced secretion
- bronchodialation

72
Q

What is hyoscine butylbromide used for?

A

To treat spasmodic or gas colic
To treat choke
- relaxes the smooth muscle in the intestines and esophagus

To treat acute equine asthma
- bronchodilation

73
Q

After administration of buscopan you ascult the horse to monitor heart rate. The heart rate is notably increased. What does this mean?

A

It it a normal response to the drug

You cannot use heart rate as a measure of pain when administering buscopan/hyoscine butylbromide/N-butylscopoammonium bromide

74
Q

List 2 cholinergics commonly used in vet med

A

neostigmine
pyridistigmine

75
Q

List 3 anticholinergics commonly used in vet med

A

atropine
glycopyrrolate
N-butylscopoammonium bromide/hyoscine butylbromide

76
Q

List 3 alpha 1 antagonists commonly used in vet med

A

prazosin
acepromazine
carvedilol

77
Q

List 5 alpha 2 agonists commonly used in vet med

A

xylazine
detomidine
dexmedeomidine
medetomidine
romifidine

78
Q

List 1 beta 1 agonist commonly used in vet med

A

dobutamine

79
Q

List 1 beta 1 antagonist commonly used in vet med

A

esmolol

80
Q

List 2 beta 2 agonists commonly used in vet med

A

clenbuterol
albuterol

81
Q

List the primary non selective adrenergic agonist used in vet med

A

epinephrine

82
Q

What is the overall impact of alpha 1 receptors on the body

A

No impact on the heart

vasoconstriction systemically

reduced GI motility

increased muscle tone in the GI, bladder, uterus

83
Q

What is the overall impact of alpha 2 receptor stimulation on the body

A

Initially:
vasoconstriction of the viscera and the muscle

reduced motility and secretion in GI

increased smooth muscle tone in the uterus

There is a pre-synaptic effect of alpha 2 receptors that reverse the initial effects resulting in sedation and analgesia

84
Q

What are the overall effects of beta 1 receptor stimulation on the body

A

increased chronotropy and inotropy of the heart

85
Q

What are the overall effects of beta 2 receptor stimulation on the body

A

Vasodilation of the viscera and muscles

reduced GI motility

increase lung secretion

Reduced tone in bronchioles, bladder, and uterus

86
Q

What is the effect of stimulating dopamine receptors on the body?

A

vasodilation of the viscera and kidneys

87
Q

What is the effects of muscarinic receptor stimulation on the body

A

Reduced chronotropy and inotropy

Increased GI motility and secretion

Reduced tone in GI sphincters

Increased tone in the bladder, uterus. and bronchioles

Increased lung secretion

88
Q
A

VETM 443 Pharmacology (11 decks)

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