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Exam 2 Flashcards

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1
Q

Most organs are innervated by both sympathetic and parasympathetic nervous system - what is the exception?

A

blood vessels = sympathetic only

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2
Q

Where do pre-ganglionic neurons original and what NT do they release?

A

Originate in the CNS and release ACh –> interacts with nicotinic cholingeric receptors on post-ganglionic

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3
Q

What are the second messengers (3) involved with activated GPCR?

A
  1. cAMP
  2. DAG
  3. IP3
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4
Q

What increases and decreases cAMP?

A

Gas - increases (PKA)

Gai - decreases

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5
Q

What increases DAG & IP3?

A

Gaq/11 - increases (PKC)

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6
Q

Postganglionic neurons (Parasympathetic)

A

Release ACh onto target organs w/muscarinic cholinergic receptors

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7
Q

Postganglionic neurons (Sympathetic)

A

Release EPI/NE (from adrenal gland) onto target organs w/adrenergic receptors

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8
Q

How are NT’s “turned off”?

A
  1. re-uptake
  2. diffusion
  3. degradation (AChE)
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9
Q

Which receptors have negative feedback?

A

Presynaptic receptors

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10
Q

Parasympathetics - distribution and ganglia

A
  • Cranio sacral distribution

- ganglia are in/near target organs (local regulation)

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11
Q

Parasympathetics - receptors

A

Muscarinic ACh:

  • M1 (Gaq)
  • M2 (Gai)
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12
Q

Sympathetics - distribution & ganglia

A
  • Thoracolumbar distribution

- ganglia along vertebral column in sympathetic chain –> coordinated activation of target organs

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13
Q

Sympathetics - main hormones

A

Catecholamines - EPI/NE

“fight or flight” response

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14
Q

Sympathetics - Receptos

A

ADRENERGIC (NE)

  • Alpha 1 (Gaq)
  • Alpha 2 (Gai)
  • Beta 1 (Gas)
  • Beta 2 (Gas)
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15
Q

Sympathetics - NT re-uptake

A

Re-uptake is common mechanism of inactivation for NE –>

  • repackaged/metabolized by MAO
  • metabolized by COMT in liver
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16
Q

Cholinergic agonists =

A

parasympathomimetics

  • mimic/enhance effect of parasympathetic ACh
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17
Q

Nicotinic Cholinergic receptors

A
  • inotropic ligand-gated cation channel

- ACh binding opens channel –> Na+ influx = depolarization

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18
Q

Muscarinic and Adrenergic receptors

A

All GPCR

Muscarinic cholinergic: M1-M5

Adrenergic: alpha 1 & 2; beta 1 & 2

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19
Q

G protein signaling

A

After dissociation from Gby, Ga subunits (s, i, q/11) either inc or dec the quantity of second messengers (signaling) molecules

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20
Q

cAMP

A

increased with Gas

decreased with Gai

*activates PKA

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21
Q

DAG

A

increased by Gaq/11

*activates PKC

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22
Q

IP3

A

increased by Gaq/11

*activates PKC

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23
Q

Muscarinic cholinergic signaling

A

Gaq/11 –> M1. 3. 5

Gai –> M2. 4

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24
Q

Alpha adrenergic signaling

A

Gaq/11 (alpha 1)

Gai (alpha 2)

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25
Q

Beta adrenergic signaling

A

Gas

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26
Q

Non-adrenergic, non-cholinergic (NANC) transmission

A

primarily inhibitory effects

*smooth mm innervated by ANS; some ANS effects in the presence of adrenergic and cholinergic blockade

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27
Q

NANC transmission

A

Purinergic neurotransmission

  • adenosine receptors (P1)
  • ATP receptors (P2X and P2Y)
    • ATP often released as a co-transmitter with ACh or NE

Nitric Oxide

  • aka endothelium-derived relaxation factor
  • nitrergic nerves
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28
Q

Heart

A

Sympathetic: inc CO
- B1
Parasympathetic: dec CO
- M2

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29
Q

Blood vessels

A

Sympathetic: arteries (general) constrict [dilates arteries in skel mm]
- a1 (general); b2 (skel mm)

Parasympathetic: dilates arterial endothelium via inc NO
- M3

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30
Q

Lungs

A

Sympathetic: dilation
- B2

Parasympathetic: bronchoconstriction & secretion from glands
- M3, M2

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31
Q

GI

A

Sympathetic: decrease fan
- a1 and a2

Parasympathetic: increase fan
- M3 and M2

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32
Q

Urinary bladder

A

Sympathetic: inhibit voiding
- a1 and b2

Parasympathetic: promote voiding
- M3

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33
Q

Eye

A

Sympathetic: mydriasis
- a1

Parasympathetic: mitosis
- M3, M2

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34
Q

Cholinergic agonists

A

Parasympathomimetics (aka cholinomimetics)

mimic/enhance the effect of endogenously released acetylcholine (parasympathetics)

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35
Q

Cholinergic agonists - heart

A

decreased CO via M2

  • bradycardia (decreased SA node automaticity)
  • decreased conduction (e.g. AV node
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36
Q

Cholinergic agonists - vasculature

A

vasodilation, M3 (inc NO)

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37
Q

Cholinergic agonists - lungs

A

bronchoconstriction, increased secretions, M3 and M2

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38
Q

Cholinergic agonists - GI

A

increased motility, increased secretion (e.g. salivation), M3, M2

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39
Q

Cholinergic agonists - bladder

A

contraction (urination), M3

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40
Q

Cholinergic agonists - eye

A

lacrimation, mitosis, M3 and M2

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41
Q

Visible signs of excessive cholinergic stimulation…

A

SLUDE

salivation
lacrimation
urination
defecation
GI symptoms 
emesis (vomiting)
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42
Q

Endogenous cholinergic

A

Acetylcholine

  • rarely used clinically (ophthalmic)
    • muscarinic and nicotinic stimulation
  • rapid deviation by AChE and plasma butyrylcholinesterase
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43
Q

Direct acting cholinergic agonists - choline ester

A

Bethanechol (choline ester)

  • muscarinic stimulation, some GI/urinary bladder selectivity (M3)
  • promotes voiding by contraction of detrusor m. and relaxation of the trigone and sphincter
  • used to treat urinary retention when obstruction is absent
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44
Q

Direct acting cholinergic agonists - alkaloid (M)

A

Muscarine

  • stimulates muscarinic receptors!
  • not used clinically
  • found in certain mushrooms (contributes to mushroom poisoning)
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45
Q

Direct acting cholinergic agonists - alkaloid (P)

A

Pilocarpine

  • muscarine stimulation
  • topical ophthalmic use to induce pupil constriction and decrease intraocular pressure during glaucoma
  • rarely used systemically to promote salivation (sialogogue)
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46
Q

Indirect acting cholinergic agonists - AChE inhibitors

A
  • prevent hydrolysis of ACh to choline and acetate
  • accumulation of ACh sites of release –> autonomic effect organs and ganglia, skeletal m., cholinergic synapses in the CNS
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47
Q

AChE inhibitors - reversible

A

Physostigmine (crosses BBB)

Neostigmine

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48
Q

AChE inhibitors (reversible) - clinical use

A
  • smooth mm. atony (GI tract and UB)
  • glaucoma (topical)
  • reversal of competitive non-depolarizing neuromuscular blocking agents
  • myasthenia gravis (ACh receptor deficiency)
  • counter CNS symptoms of anticholinergic intoxication
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49
Q

Cholinergic antagonists

A

aka Anticholinergics

  • Block the effect of endogenous ACh at muscarinic receptors
  • little effect on ACh at nicotinic receptors
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50
Q

Cholinergic antagonists - Effects on heart, vasculature, and lungs

A

Heart: increase CO
- tachycardia (inc SA nodal automaticity), inc conduction (AV node)

Vasculature: little effect, no innervation

Lungs: bronchodilator, dec secretions

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51
Q

Cholinergic antagonists - Effects on GI, UB, eye

A

GI: dec motility and secretions (dry mouth)

UB: dec urination

Eye: dec lacrimation, mydriasis, cycloplegia (paralysis of ciliary mm - loss of focus on nearby objects)

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52
Q

What are the visible signs of Cholinergic antagonists

A

Anti-SLUDGE

Dec: salivation, lacrimation, urination, defecation, etc. etc.

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53
Q

Atropine

A

Cholinergic (parasympathetic) Antagonist

Competitively inhibits the binding and stimulation of muscarinic receptors by ACh and other muscarinic agonists

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54
Q

Can atropine enter the CNS? what are primary concerns with tx?

A

Yes, can enter the CNS (non-quaternary, possible toxicity, excitation followed by depression)

Primary concerns: tacharrhythmia, prolonged GI stasis, urine retention

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55
Q

How/why is atropine used during general anesthesia?

A

decreases salivary and airway secretions

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56
Q

Glycopyrrolate (cholinergic antagonists)

A

Similar to atropine, but:

  • quaternary
  • little CNS effects
  • Used as adjust to general anesthesia:
  • dec salivary and airway secretions
  • prevent vagally-mediated bradycardia
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57
Q

Ipratroium (cholinergic antagonists)

A
  • dec bronchoconstriction and airway secretions
  • quaternary: restricted distribution
  • administer via inhalation, limit systemic effects
  • Uses:
  • asthma (cats) and chronic bronchitis (dogs)
  • horses with recurrent airway inflammation
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58
Q

Propantheline (cholinergic antagonists)

A
  • dec detrusor contraction
  • inc trigone and sphincter contraction
  • promotes urine retention
  • Uses:
  • treat incontinence due to detrusor instability
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59
Q

NMJ blocking agents

A

Used as adjunct during general anesthesia (unconscious animals):

  • relax skel mm, NO sedative effects
  • especially the abdominal wall
  • given IV
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60
Q

NMJ - do all nACh- receptors have to be activated for mm contraction?

A

NO! there are “spare receptors” that provide a safety factor at the NMJ (consider the diaphragm)

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61
Q

Spare receptors and the NMJ

A

practical consequences:

- reversal of clinical blockage with drug still present
consider the diaphragm - lost safety factor

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62
Q

NMJ - Curare

A
  • Natural alkaloid found in S. America
  • Used to make arrow poison
  • toxin = tubocurarine
  • death from skeletal m paralysis

**Competitive ACh antagonist at nicotinic receptors in the NMJ

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63
Q

Competitive NMJ bockers

A
  • No motor end plate depolarization
  • aka: non-depolarizing NMJ blockers
  • initial mm weakness followed by –> flaccid paralysis
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64
Q

Competitive NMJ blockers - drugs (3)

A

1) Pancuronium (long-acting)
2) Atracurium (intermediate)
3) Mivacurium (short-acting)

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65
Q

Properties to consider - Competitive NMJ blockers:

A
  • duration of action
  • route of elimination
  • degree of ganglionic blockade
  • antagonize muscarinic receptors
  • propensity to release histamine from mast cells
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66
Q

Pancuronium - competitive NMJ blockers

A
  • long duration of action (2-3 hours)
  • renal elimination (half-life inc with renal dz)
  • little ganglionic blockade
  • no histamine release
  • blocks histamine release
  • blocks muscarinic receptors (tachycardia)
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67
Q

Atracurium - competitive NMJ blockers

A
  • intermediate duration (0.5-1h)
  • spontaneous degradation + hydrolysis by plasma enterases + renal elimination
  • spontaneous degradation is reduced with hypothermia and acidosis, leading to inc half-life and duration of action
  • little/no ganglionic blockade
  • promotes histamine release
  • half-life is NOT inc with renal dz
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68
Q

Mivacurium - competitive NMJ blockers

A
  • short duration of action (15 mins)
  • rapid hydrolysis by plasma enterases –> half-life not inc w/ renal dz
  • little/no ganglionic blockade
  • promotes histamine release
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69
Q

Competitive NMJ blockers - how to reverse?

A

Reverse with AChE-inhibitors

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70
Q

Depolarizing NMJ Blockers

A
  • Cause prolonged motor end plate depolarization by stimulation of NMJ nicotinic receptors
  • aka non-competitive NMJ blockers
  • initial m. fasciculation (uncoordinated contractions) followed by relaxation
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71
Q

Depolarizing NMJ Blockers - drugs

A

Only succinylcholine used clinically

  • two Act molecules linked together
  • essentially mimics ACh at the NMJ
  • resistant to AChE
  • NOT pharmacologically reversible
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72
Q

Two phases of Depolarizing NMJ Blockers

A

Early (phase 1): depolarization

  • persistent stimulation of nicotinic receptors
  • nicotinic receptors during this phase are incapable of transmitting further impulses
  • fasciculations (last less than 1 min) –> flaccid paralysis

Late (phase 2): depolarization

  • flaccid paralysis
  • resembles receptor desensitization
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73
Q

Succinylcholine - Depolarizing NMJ Blockers

A
  • rapid onset (1min)
  • ultra-short acting (5 min): rapidly hydrolyzed by butyrylcholinesterases
  • useful for rapid and short lived NMJ blockage (e.g. facilitate tracheal intubation)
  • some histamine release but does not generally cause ganglionic blockade
  • hyperkalemia from release of intracellular K+ from skeletal mm.
  • avoid in presence of extensive soft-tissue damage or burns
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74
Q

Potential problem with NMJ Block

A
  • Monitoring depth of anesthesia
  • Many signs of anesthesia are lost during NMJ blockade
  • *more difficult to assess the depth of anesthesia
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75
Q

NMJ blockade toxicity

A

Res paralysis

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76
Q

NMJ toxicity intervention - histamine

A

Toxicity interventions: histamine release from mast cells

  • bronchospasm, hypotension, bronchial and salivary secretion
  • minimize with antihistamine pre-tx (benadryl)
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77
Q

NMJ toxicity intervention - Vagal (parasympathetic) reflex

A
  • often procedure (not drug) induced
  • visceral manipulation
  • bradycardia, bronchospasm, hypotension, bronchial and salivary secretion
  • compounds many symptoms of histamine release
  • minimize with anticholinergic (e.g. atropine)
  • Note: some rabbits have high levels of plasma enterases which degrade atropine (polymorphism)
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78
Q

NMJ toxicity intervention - ganglionic blockade

A
  • hypotension

- can manage with sympathetic adrenergic agonists (adrenergic lectures)

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79
Q

NMJ toxicity intervention- MALIGNANT HYPERTHERMIA

A
  • life-threatening
  • excessive contracture and heat production from skeletal mm
  • initiated by the release of Ca2+ from the SR of skeletal mm
  • usually triggered by combination of halogenated anesthetics (e.g. halothane) and succinylcholine
  • prevalent in pigs, also reported in dogs (esp Greyhounds), cats, and horses
  • tx with dantrolene (limits SR Ca2+ release) plus supportive measures
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80
Q

Adrenergic Agonists

A

aka Sympathomimetics

  • mimic the effect of endogenous sympathetic catecholamines Its (NE and Epi)
  • excitation or inhibition of smooth mm or glandular activity
  • cardiac excitation
  • general catabolic state
  • glucose/FFA mobilization
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81
Q

Adrenergic Agonists - CNS stimulation or pre-junctional actions

A

CNS stimulation
- inc wakefulness, resp stimulation, etc

Pre-junctional (e.g. a2 receptors)

  • dec NT release
  • dec sympathetic outflow; CNS depression
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82
Q

General classification of agonists

A
  • Direct acting agonists
  • endogenous catecholamines
  • Indirect acting agonists
  • amphetamine
  • Mixed acting agonists
  • Phenylpropanolamine (PPA)
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83
Q

Direct acting adrenergic agonists

A
  • interact directly w/ a and b receptors to different degrees
  • endogenous catecholamines
  • catecholamine derivatives
  • add various substituents = alter activity and selectivity
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84
Q

Direct acting adrenergic agonists - Epinephrine

A

aka Adrenaline

  • potent a and b agonist
  • released by adrenal chromatin cells
  • complex action: summation of a and b agonist activity
  • cardiovascular effects (very important)
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85
Q

Direct acting adrenergic agonists - Epinephrine

Cardiac effects

A

Cardiac effects (b1)

  • inc contractility (positive ionotrope)
  • inc HR (positive chronotrope)
  • inc O2 consumption

General result: inc CO

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86
Q

Direct acting adrenergic agonists - Epinephrine

Vascular effects

A

Vascular effects:

  • low dose —> dec BP via b2 dominance
  • high dose —> inc BP via a1

*can be given IV, IM, or SQ (not orally active)

87
Q

Direct acting adrenergic agonists - Epinephrine

Respiratory effects (important)

A

Resp effects: important

  • powerful bronchodilator (b2)
  • especially if bronchioles pre-constricted
    (e. g. anaphylaxis or asthma)
  • small dec in bronchial secretions
88
Q

Direct acting adrenergic agonists - Epinephrine

Therapeutic Uses

A
  • rapid release of hypersensitivity reactions (e.g. anaphylaxis and asthma)
  • cardiovascular support and bronco dilation
  • restoring cardiac rhythm
  • cardiac arrest, AV node block
  • Topical hemostatic agent
  • control superficial bleeding of mucosal and SQ surfaces via vasoconstriction (a1)
  • Adjunct w/ local anesthetics (lidocaine)
  • vasoconstriction (a1) localizes anesthetic action and limits systemic absorption and toxicity
89
Q

Direct acting adrenergic agonists - Epinephrine

Toxicity

A
  • Extension of pharmacological action

- cardiac arrhythmias, hypertensive crisis, cerebral hemorrhage, restlessness, etc.

90
Q

Direct acting adrenergic agonists - NE

A
  • Major NT released by post-ganglionic sympathetic nerves

* Differs from Epi by lacking a single methyl group

91
Q

NE vs Epi - potencies

A

B1: Epi = NE

B2: EPI&raquo_space;»»> NE

A1: EPI > NE

92
Q

NE Effects and Toxicities

A

NE similar to Epi in most respects

  • differences result from lack of B2 stimulation
  • intense vasoconstriction and increase in blood pressure
  • initiates vagal reflex (baroreceptors) which slows HR
93
Q

Direct acting adrenergic agonists - NE

Therapeutic uses

A
  • limited use
  • cardiovascular support (maintain BP) during shock via a1 (vasculature) and B1 (heart) effects
  • NO B2 effect = no bronchodilation
94
Q

Direct acting adrenergic agonists - Dopamine

A
  • endogenous catecholamine
  • precursor to NE and EPI
  • given IV (infusion)
  • short half-life
95
Q

Direct acting adrenergic agonists - Dopamine

Dose dependent effects

A
  • Low dose:
  • vascular vasodilation
  • inc renal blood flow and Na excretion
  • stimulates cardiac B1 receptors –> positive inotropic effect

**Use low dose IV infusion for congestive heart failure w/compromised renal failure (short term only)

  • High dose:
  • a1 receptor stimulation –> vasoconstriction, dec renal blood flow, etc
96
Q

Non-selective B adrenergic agonists - Dobutamine

A
  • structurally related to dopamine

* complex agonist activity on B1, B2, and a1 receptors (B1 > B2 and a1)

97
Q

Non-selective B adrenergic agonists - Dobutamine

Cardiovascular effects

A
  • inc cardiac contractility (B1 agonist) w/minimal changes in HR
  • minimal change in BP as a1 and B2 agonist activities are weaker and counterbalance
  • use as positive inotrope during hear failure (short term only)
98
Q

Non-selective B adrenergic agonists

General adverse effects/toxicity

A
  • unwanted and/or excess B stimulation

e. g. inc HR (B1) when sued as bronchodilator (B2)

99
Q

Selective B adrenergic agonists

B1 and B2

A

BI:
- dobutamine is close from a functional perspective (B1 > B2 or a1)

B2:
- many examples; used as bronchodilators

100
Q

Selective B adrenergic agonists

B2

A

B2 agonist = bronchodilator

- Gas = inc cAMP = relax bronchial smooth mm

101
Q

Selective B2 adrenergic agonists - Albuterol

A

Albuterol (aka salbutamol)

- for bronchospasm in dogs, cats, and horses

102
Q

Selective B2 adrenergic agonists - Clenbuterol

A

Clenbuterol:

- used for allergic bronchitis, recurrent airway obstruction (“heaves”), and bronchoconstriction in horses

103
Q

Selective B2 adrenergic agonists

B receptor down-regulation

A
  • Minimize with proper dose, dosing schedule
  • following chronic, long-term administration of B agonists (esp with over-usage)
  • leads to loss of pharmacological efficacy
104
Q

Selective B2 agonists & repartitioning

A
  • repartitioning in livestock:
  • alter carcass composition by partitioning energy away from fat deposition and towards protein accretion (inc mm mass)
  • improve weight gain, leanness, etc.
  • repartitioning agents:
  • ractopamine, zilpaterol, clenbuterol
105
Q

Selective B3 adrenergic agonists

A

Toxic to dogs!!

B3 agonist = mirabegron
- relax the detrusor in the bladder, increase bladder capacity (in humans)

106
Q

Selective a1 adrenergic agonists

A
  • primary effect of a1 stimulation is constriction of vascular smooth muscle –> increased blood pressure (pressor agents)
  • a1 agonist = vasoconstrictor
  • Gaq = inc DAG and IP3 = inc Ca2+ = contract arterial smooth muscle
107
Q

Selective a1 adrenergic agonists - Phenylephrine

A
  • prototypical a1 agonist
  • topical, oral, parenteral
  • decongestant, vasopressor

Toxicity = excess a1 activity (hypertension)

108
Q

Selective a2 adrenergic agonists

A
  • Effect primarily central (CNS) and pre-synaptic inhibition of sympathetic neurons:
  • sedation, analgesia
  • decreased sympathetic outflow from brain
  • decreased NE release
109
Q

Selective a2 adrenergic agonists - (Dex)medetomidine & xylazine

A
  • a2 agonists = CNS depression
  • widely used as adjunct for sedation, anesthesia, and analgesia
  • pre-anesthetic, light anesthesia by itself
  • relatively high safety profile (therapeutic index)
  • allows for a lower dose of other anesthetic/analgesic agents with lower safety profiles
  • overall effect is a dec in BP (and sedation/analgesia)
110
Q

a adrenergic agonists - summary

a1 and a2

A

a1 = vasoconstrictor (phenylephrine)

a2 = sedative (medetomidine)
- also dec sympathetic outflow

111
Q

Misc adrenergic agonists

(pseudo)ephedrine

phenypropanolamine

A
  • direct a and B agonist activity
  • promotes release of NE from sympathetic neurons (indirect)
  • mixed acting adrenergic agonists
  • rarely used as decongestant
  • PPA - used for urinary incontinence
112
Q

Adrenergic agonist review

A
  • a1 = vasoconstriction (EPI, NE, phenylephrine)
  • a2 = presynaptic inhibition (medetomidine)
  • B1 = inc HR and contractile force (EPI, NE, dopamine, dobutamine)
  • B2 = bronchodilator (EPI, albuterol, clenbuterol)
113
Q

Adrenergic antagonists

A

Aka Sympatholytics

  • block the effect of endogenous sympathetic catecholamine Its
  • NE and EPI
  • effects dependent on sympathetic activity (tone)
  • vary with state of the animal
  • vary between tissues (e.g. heart and GI tract)
114
Q

General classification of antagonists

A
  • Direct acting competitive antagonists
  • reversibility block the stimulation of a and B receptors by endogenous Its
  • varying degree of selectivity at different receptors
  • phentolamine
  • MOST ADRENERGIC ANTAGONISTS
  • Direct acting non-competitive antagonists
  • irreversibly blocks a1 and a2 receptors
  • phenoxybenzamine
  • Indirect acting antagonists
  • reserpine
  • Non-selective a antagonists
  • Phenoxybenzamine, phentolamine
  • non-selective a antagonists
  • reduces urethral sphincter tone
  • manage urethral blockage
115
Q

a1 Adrenergic antagonists

A
  • primary effect of a1 stimulation is constriction of vascular smooth mm
  • antagonism: block endogenous NE and EPI
  • fall in BP from decreased TPR
  • magnitude dependent on sympathetic tone (e.g. frightened, injured, hypovolemic, etc)
116
Q

Selective a1 adrenergic antagonists

A
  • major effect is to relax arterial AND venous smooth mm = vasodilation
  • decrease in TPR (after load)
  • decrease in venous return (pre-load)
117
Q

Selective a1 adrenergic antagonists - Prazosin

A

Prazosin

  • used as antihypertensive and in congestive heart failure (dec pre- and after-load)
  • produce less reflex tachycardia than other vasodilation agents
118
Q

Selective a2 adrenergic agonists

A

Effect primarily center (CNS) and pre-synaptic inhibition

  • sedation, analgesia,
  • decreased sympathetic outflow from brain
  • decreased NE release
119
Q

Selective a2 adrenergic antagonists

A

Antagonist effect primarily relieving central (CNS) and pre-synaptic inhibition

  • less sedation, analgesia
  • increased sympathetic outflow from brain
  • increased NE release
120
Q

Selective a2 adrenergic antagonists - Atipamezole

A

used to reverse sedative and analgesic effects of (dex)medetomidine (a2 agonist)

also increases sympathetic activity –> do NOT use in patients with cardiac and respiratory dz or other conditions where excessive sympathetic stimulation is contraindicated

121
Q

a adrenergic antagonists - summary

A
  • a1 antagonist = vasodilation (prazosin)
  • a2 antagonist = reverse a2 agonists (atipamezole reverses dexmedetomidine)
  • non-selective a antagonists
  • phenoxybenzamine (non-comp, irreversible)
  • phentolamine (comp, reversible)
122
Q

B adrenergic antagonists

A

Primary result of B1 stimulation is positive cardiac inotropic and chronotropic effects

  • antagonism: block endogenous NE and EPI resulting in decreased HR and cardiac contractility
  • magnitude dependent on sympathetic tone (consider exercise and stress)
123
Q

B1 adrenergic antagonists

Cardiac

A

dec HR and contractility
* dec CO, dec cardiac O2 demand

  • dec BP
  • dec cardiac arrhythmias
124
Q

B2 adrenergic antagonists

A

Primary effect of B2 stimulation is bronchodilator

antagonism:
* inc bronchoconstriction
- this is not generally a desirable effect

125
Q

Nonselective B adrenergic antagonists

Propranolol

A

Prototypical B antagonist with equal affinity for B1 and B2 receptors

  • dec CO (B1 blockade)
  • more pronounced during exercise (inc sympathetic tone)
  • anti arrhythmic action from decreased sympathetic stimulation
  • limited use because of B2 blockade and availability relatively selective B1 inhibitors
126
Q

Nonselective B adrenergic antagonists

Timolol

A

ocular use to decrease aqueous humor production during glaucoma

127
Q

Carvedilol

A

used in vet med

  • CHF
  • valvular disease

Unique non-selective B antagonist

  • blocks B1 (heart) and B2 receptors (not good)
  • blocks a1 (vasculature) receptors
  • antioxidant properties
128
Q

Atenolol

A

Selective B1 adrenergic antagonist

  • potentially useful in feline hypertonic cardiomyopathy (dec HR, oxygen demand, etc)
  • dec HR
  • counteract anticholinergic tachycardia
129
Q

B adrenergic antagonists summary

A

B1 antagonists: dec HR

  • propranolol (non-sel), atenolol (sel)
  • dec HR, reduces cardiac oxygen demand

B2 antagonists: bronchoconstriction

  • propranolol (non-sel)
  • not helpful, limitation of non-self agents
130
Q

Hypotension during anesthesia

A

Very common during general anesthesia

  • induced by anesthetics (IV and inhalational)
  • cardiovascular and central sympathetic depression
  • parasympathetic reflexes
  • NMJ blocker: histamine release
131
Q

Pronounced hypotension often assoc’d with…

A
  • Volume depletion (hypovolemia)
  • e.g. injured animal
  • give fluids
  • cardiac insufficiency
  • e.g. heart failure
132
Q

Hypotension during anesthesia - autonomic pharmacological interventions

A
  • increase HR (thus CO) with anticholinergic
  • potential problem with cardiac insufficiency
  • increase HR, contractility, and vasoconstriction with a sympathomimetic
  • potential problem with cardiac insufficiency
133
Q

Shock

A
  • circulatory system fails to maintain adequate blood flow

***Poor delivery of oxygen and nutrients to vital organs

  • hypotensive state
134
Q

Analgesia

A

Lack of pain

135
Q

Anesthesia

A

Lack of sensation

  • anesthesia is usually accompanied by analgesia
136
Q

Three types of shock

A
  1. Hypovolemic: intravascular volume deficit (e.g. hemorrhage)
  2. Distributive: peripheral vasodilation; septic, anaphylactic, and neurogenic shock
  3. Cardiogenic: myocardial pump failure
137
Q

Hypotensive state

A

Increase in sympathetic outflow –> restore BP and preserve perfusion to vital organs

138
Q

What does an increase in sympathetic outflow (hypotensive state) do?

A

inc HR and contractility

Vasoconstriction –> redistributes blood to vital organs

139
Q

Sympathomimetics

A

inc CO (B1 stimulation)

inc TPR (a1 stimulation)

Inc BP (MAP = CO x TPR)

140
Q

Shock assoc’d vasoconstriction

A

maldistribution of blood flow

141
Q

When there is shock assoc’d vasoconstriction, which sympathomimetics do you choose?

A

B1 stimulation

inc CO –> raise BP

142
Q

Two basic types of shock?

A

Primarily vascular

Primarily myocardial

143
Q

Primarily vascular shock

what drugs do we give?

A

e.g. hypovolemia following trauma

Strategy: promote vasoconstriction

Dopamine, NE, Epi, phenylephrine

144
Q

Anaphylactic shock

Drug?

A

Allergic/hypersensitivity response

  • mast cell degranulation = histamine release
  • vasodilation and bronchoconstriction

EPINEPHRINE is primary therapy
- bronchodilator (B2)

145
Q

Primarily myocardial insufficiency (shock)

drugs?

A

Strategy: increase CO via B1 stimulation

Dobutamine

146
Q

Mix of myocardial insufficiency and vasodilation? Strategy? drugs?

A

Strategy: increase CO by stimulation B1 receptors and promote vasoconstriction via a1 (balanced)

  • moderate infusion of dopamine often considered appropriate in this setting
147
Q

Goal in treating shock?

A

Establish and maintain perfusion

BP does NOT equal perfusion

148
Q

Glaucoma

A

Disease in which the pressure in the eye is too high

  • inc in intraocular pressure
  • leads to loss of vision (damage to optic n, etc)
149
Q

Glaucoma - tx goals

A

Autonomic drugs:

  • can be used to manage primary glaucoma
  • adjunct to surgical tx for primary and secondary glaucoma
  • goal is to lower intraocular pressure
150
Q

Glaucoma - drugs

A

Beta antagonists (e.g. timolol)

Cholinergic agonists

  • lower pressure
  • opposite with anticholinergics
151
Q

Where does cardiac electrical activity come from?

A

arises from diverse population of ions channels throughout heart

152
Q

3 major ions in membrane potential:

A

Na, Ca, K

153
Q

Reversal potential

A

Each ion with “drive” the cell membrane potential towards its own reversal potential it it is allowed to move freely in or out of the cell

154
Q

RMP - ions

A 
Na = +50 
Ca = 150+ 
K = -90
155
Q

Sodium channel - VG Na channels –> threshold for activation

A

-60 mV

156
Q

Ion responsible for plateau phase

A

Ca channels open - Ca enters cell (imitation of contraction)

K exits the cell also

157
Q

Ca channel - VG Ca channels –> threshold for activation

A

-40 mV

Inactivate slowly –> allows Ca influx to trigger contraction

158
Q

Pacemaker (SA nodal) AP

A

Phase 0 depolarization is slow

  • no fast opening VG Na
  • only slow opening VG Ca channels

**No plateau phase (phase 2)

Phase 3
- K channel repolarization

Phase 4

  • no true RMP
  • continuous slow depolarization
  • results from activation of “funny” current
  • *slowly depolarizing inward current activated by hyperpolarization
159
Q

Electromechanical Coupling

A
  • Ca2+ influx via Ca channels
  • trigger Ca release from internal stores (jSR)
  • stimulates the opening of intracellular Ca channels called RyR
  • *Ca induced Ca release (CICR)
160
Q

Electromechanical coupling - Ca removal

A

pumped back into SR by Ca ATPase

shunted out of the cell by Na/Ca exchanger

161
Q

P wave

A

atrial depolarization

162
Q

QRS complex

A

ventricular depolarization

163
Q

T wave

A

ventricular repolarization

164
Q

Arrhythmias

A

Results from disorders of

Impulse formation

Conduction

or both

165
Q

Disorders of impulse formation involve:

A

either a change in the normal pace make (SA node) or the development of a new ectopic pacemaker (e.g. in the ventricles)

166
Q

Multiple potential pacemaker sites in the heart

A

SA node, atrial foci, AV node, ventricular foci

Dominant pacemaker will be the one with the highest frequency (normally the SA node)

167
Q

Conduction arrhythmias

A

Disorders of impulse conduction can cause either bradycardia or tachycardia

brachycardia: from AV nodal block
tachycardia: from a re-entrant circuit

168
Q

Atrial fibrillation

A

too much depolarization going through the AV node to the ventricles

169
Q

Reentrant arrhythmias

A

Accessory pathway: supra ventricular tachycardia

170
Q

Does complete arrhythmia suppression eliminate the risk for subsequent lethal arrhythmia?

A

NO! all anti arrhythmic drugs can induce arrhythmias

171
Q

Antiarrhythmic drugs - Class 1

A

Na channel blockers

Class 1A: moderate conduction slowing = procainamide
* prolongs refractory period

Class 1B: little conduction slowing = lidocaine
* shortens refractory period

Class 1C: profound conduction slowing = flecainide
* little change refractory period

172
Q

Antiarrhythmic drugs - Class 2

A

beta blockers

173
Q

Antiarrhythmic drugs - Class 3

A

AP prolonging

174
Q

Antiarrhythmic drugs - Class 4

A

Ca channel blockers

175
Q

Class 1A: procainamide

A

slows conduction velocity

prolongs refractory period

Use: supraventricular tachycardia
* “break” the reentrant circuit and allow SA node to take over

176
Q

Class 1B: lidocaine

A

little change in conduction velocity

shortens the refractory period

binds to inactivated Na channels

  • keeps them in the inactivated state
  • depolarization –> inactivation
  • effect is inc in depolarized tissues
  • dec automaticity in depolarized cells

Use: ventricular tachycardia

177
Q

Class 1C: flecainide

A

little change in refractory period

Profound decrease in conduction velocity

Use only in life-threatening ventricular tachycardia or fibrillation and for the tx of refractory supra ventricular tachycardia

*Cast = cure is worse than the dz

178
Q

Class 2: beta blockers

A

Too much sympathetic activity is arrhythmogenic = manage w/ a beta blocker

179
Q

Congestive heart failure (CHF)

A

heart fails as a pump

dec CO (poor tissue perfusion)

blood does not circulate properly (congested)

180
Q

Causes of CHF

A

pressure/volume overload

  • pulmonary, renal, vascular dz
    e. g. hypertension secondary to renal failure

myocardial damage, valvular insufficiency

  • idiopathic cardiomyopathies, nutritional deficiencies, toxic, infection, neoplastic
    e. g. touring def in cats
181
Q

Two basic tx approaches for heart failure

A
  1. reduce workload of the heart

2. increase performance

182
Q

3 basic ways to inc cardiac performance (tx heart failure)

A
  1. inc B1 adrenergic (sympathetic) stimulation
  2. cardiac myocyte intracellular Ca2+
  3. enhance the contractile process directly
183
Q

Adrenergic (sympathetic) stimulation - baroreceptor reflex

A

Happens automatically when CO (and BP) drops during heart failure through baroreceptor reflex

184
Q

B1 adrenergic stimulation (heart failure)

A

inc sympathetic tone during heart failure (hyperadrenergic state)

Limits the use of adrenergic agonists

  • cardiac B1 adrenergic pathways are already stimulated
  • “ceiling effect” of B1 receptor stimulation
185
Q

B1 adrenergic stimulation (heart failure) - drugs

A

Dopamine and dobutamine (best)

  • stimulate cardiac B1 receptors to inc CO (with less vasoconstriction)
  • often last ditch effort to keep patient alive

Epi and NE not that useful: too much vasoconstriction via a1 receptor stimulation in the vasculature

186
Q

Inc cardiac myocyte intracellular Ca

A
  • increase Ca influx

or

  • decrease Ca efflux
187
Q

What degrades cAMP?

A

Phosphodiesterase 3 (found in myocardium) decreases cAMP –> decreases PKA stimulation of Ca channels

188
Q

PDE 3 - inhibitors

A

PDE 3 inhibition increases cAMP levels –> increases Ca –> increases contraction

Ex: Milrinone

  • mimics the effect of B1 stimulation by increasing cAMP
  • *can be used along with beta blockers
189
Q

Decrease Ca efflux

A

*limit Na/Ca exchanger function indirectly

Ex: digoxin

190
Q

Cardiac glycosides: digoxin

A
  • inhibit the Na/K ATPase
  • lowers intracellular K
  • increases intracellular Na
  • Na/Ca exchanger
  • activity is regulated SOLELY by the concentration of Na and Ca
  • increase Na in the cell will dec Ca efflux through the exchanger

*Narrow therapeutic index

191
Q

Frank-Starling law of the heart

A

the heart pumps what it receives

192
Q

Enhance the contractile process directly (heart failure)

A

“Ca sensitizers”

Ex. Pimobendan

  • inc cardiac contraction by sensitizing the contractile machinery to Ca
  • related to an increased affinity of troponin C for Ca
  • “positive inotropic” effect
193
Q

Pimobendan

A

Enhances the contractile process directly

  • approved for CHF in dogs`
194
Q

Vasdilators

A

Disrupt excitation-contraction coupling in vascular smooth mm

Results in less vasoconstriction (or more vasodilation)

195
Q

E-C coupling:

A

translation of smooth muscle cell electrical stimulation into contraction

vascular smooth mm contraction is ultimately regulated by levels of intracellular Ca

  • inc Ca = contraction
  • dec Ca = relaxation
196
Q

3 vasoconstrictors

A

NE, Epi, Ang II

197
Q

Arterial vs venous dilators

A

Arterial dilation = dec after load

Venous dilation = dec preload

198
Q

Main player of RAAS - and outcome

A

Ang II

Water and salt retention. Effective circulation volume increases

199
Q

ACE inhibitors

A

Ex. Enalapril

Competitive antagonists of ACE (prevent conversion of Ang I to Ang II)

200
Q

Angiotensin receptor antagonists

A

Ex. Losartan

Competitive antagonists at AT1 receptors
- Angiontesin receptor type 1

  • Blocks pro-hypertensive effects of Ang II
201
Q

Renin inhibitors

A

Ex: aliskiren

Renin antagonist

Prevents conversion of angiotensinogen to Ang I

202
Q

Effect of Ang II inhibition

A
  • dec sympathetic NS activity
  • dec vasoconstriction (inc vasodilation)
  • dec tubular Na and water retention (dec aldosterone)
  • dec collecting duct water absorption (dec antidiuretic hormone)
203
Q

What is the primary mech for maintaining BP - ANS?

A

Baroreceptor reflex (stretch receptors in carotid a and aortic arch)

204
Q

Alpha adrenergic antagonists - vasculature

A

vasodilation

205
Q

Alpha adrenergic antagonists - Prazosin

A

Competitive antagonists at alpha receptors

  • vasodilation
206
Q

Ca2+ channel antagonists - vasculature

A

inhibit arterial smooth mm Ca2+ channels –> dec vasoconstriction (promote vasodilation)

207
Q

Ca2+ channel antagonists - Amlodipine

A

Promote vasodilation

208
Q

Nitric oxide - GC - cGMP - PKG

A

PKG –> promotes smooth m relaxation

209
Q

Exogenous NO donors

A

Nitroglycerin

Sodium Nitroprusside

Promote smooth mm relaxation - vasodilation

210
Q

Exogenous NO donors - Nitroglycerine

A
  • venous dilation
  • dec preload
  • Uses:
  • acute carcinogenic pulmonary edema
  • CHF

Problem: tolerance develops over time

211
Q

Exogenous NO donors - Nitroprusside

A

Arterial and venous dilation!

  • dec preload (CO)
  • dec after load (TPR)
  • profound dec in BP

Uses:
- hypertensive emergencies, acute CHF

(light sensitive)

212
Q

Inhibition of PDE-5

A

enzyme that converts cGMP to 5’GMP

Inhibition = increased levels of cGMP –> inc PKG ==> VASODILATION

213
Q

Inhibition of PDE-5 - drugs

A

Sildenafil

214
Q

K+ channel activators

A
  • inc K conductance hyperpolarizes the smooth m cell membrane-
  • hyper polarization dec the opening of Ca channels
  • Promotes vasodilation

spanish (5 decks)

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