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pharmacology > drugs acting on PNS > Flashcards

drugs acting on PNS Flashcards

1
Q

autonomic nervous system

A
  • innervates organs with involuntary functions
  • no direct control
  • most organs have dual sympathetic and parasympathetic innervation
  • resting level of activity in normal animal= resting tone
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2
Q

somatic nervous system

A
  • organs with voluntary/conscious control

- acts on neuromuscular junction

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3
Q

origin of PSNS

A
  • craniosacral

- long pre-ganglionic neuron, shorter post-ganglionic neuron

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4
Q

origin of SNS

A
  • thoracolumbar

- short pre-ganglionic neuron, longer post-ganglionic neuron

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5
Q

acetylcholine

A
  • released from pre-synaptic neuron (preganglionic neurons in SNS, PSNS)
  • post ganglionic terminal (SNS)
  • somatic terminal (NMJ)
  • broken down by cholinesterases- acetylcholinesterase (synapse), psuedocholinesterase (plasma/other tissues)
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6
Q

norepinephrine and epinephrine

A
  • norepinephrine released from synaptic nerve endings
  • epinephrine released from adrenal glands
  • tyrosine–>dopa–>dopamine–>norepinephrine–>epinephrine
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7
Q

receptors-Ach (agonist) (cholinergic)

A
  • nicotnic (ionotropic receptors)- Nm in neuromuscular junction, Nn in CNS and autonomic ganglia
  • muscarinic (metabotropic receptors)- 5 subtypes M1,3,5-stimulatory, M2,4- inhibitory
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8
Q

muscarinic receptors (cholinergic)

A
  • M1
  • GIT smooth muscle, increases gastric secretion, smooth muscle contraction
  • urinary bladder smooth muscle
  • myocardium- decrease heart rate
  • exocrine glands, increase exocrine secretions
  • SLUDD signs: salivation, lacrimation, urination, digestion, defecation
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9
Q

adrenergic receptors

A
  • catecholamines (epinephrine, norepinephrine, dopamine) are agonists
  • alpha and beta receptors
  • metabotropic g-coupled receptors
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10
Q

alpha 1 receptors

A
  • most common
  • vascular smooth muscle
  • vasoconstriction
  • increase blood pressure (MAP)
  • mydriasis
  • sphincter contraction (urinary bladder and GI tract)
  • glycogenolysis
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11
Q

alpha 2 receptors

A
  • brain and spinal cord
  • vascular endothelium
  • endocrine organs
  • decrease: insulin, renin, NE release, pancreatic secretion
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12
Q

beta 1 receptors

A
  • myocardium
  • adipose tissue
  • increase heart rate and cardiac contractility
  • lipolysis
  • smooth muscle relaxation
  • increase renin and blood pressure
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13
Q

beta 2 receptors

A
  • airway smooth muscle
  • vascular smooth muscle
  • bronchodilation
  • smooth muscle relaxation
  • blood to skeletal muscle
  • cycloplegia
  • glycogenolysis
  • increase insulin
  • increase NE release
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14
Q

autonomic drugs: mimetics

A
  • stimulate (mimic autonomic effects)

- parasympathomimetics, sympathomimetics

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15
Q

autonomic drugs: lytics

A
  • drugs that block autonomic effects
  • parasympatholytic (sympathetic signs)
  • sympatholytic (parasympathetic signs)
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16
Q

mechanism of action of autonomic drugs

A
  • autonomic drugs can be:
  • direct acting: agonists or antagonists, act directly on receptor
  • indirect acting: interact with substance other than receptor ex: enzymes–>Ach inhibitors
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17
Q

SNS- eye

A
  • relaxation of ciliary m. (far vision)
  • contraction of iris radial muscle (mydriasis)
  • decrease aqueous humor production
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18
Q

PSNS-eye

A
  • contraction of ciliary muscle (lens accommodation of near vision)
  • contraction of iris sphincter m.- miosis
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19
Q

SNS- heart (B-1)

A
  • increase heart rate (tachycardia)
  • increase contractility (positive ionotropism)
  • increase automaticity and conduction of AV node
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20
Q

PSNS-heart

A
  • decrease heart rate (bradycardia)
  • decrease contractility (negative ionotropism)
  • decrease AV node conduction
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21
Q

SNS-vasculature

A
  • alpha-1: vasoconstriction
  • B-2: vasodilation
  • alpha-2 various (vasodilation/constriction)
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22
Q

PSNS- vasculature

A

-indirect vasodilation through release of nitric oxide

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23
Q

SNS- lung

A

-B-2 bronchodilation

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24
Q

PSNS-lung

A
  • bronchoconstriction

- increased respiratory secretions

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25
Q

GI tract- SNS

A

(alpha-1, beta-1, beta2)

  • decrease motility
  • close sphincters
  • inhibit secretion
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26
Q

GI tract-PSNS

A
  • increase motility
  • relax sphincters
  • stimulate secretion
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27
Q

urinary bladder- SNS

A
  • Beta-2: relax detrusor muscle

- alpha-1: contract sphincter

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28
Q

urinary bladder-PSNS

A
  • contract detrusor

- relax sphincter

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29
Q

Ach effects

A
  • bradycardia
  • decreased bp
  • increased motility and secretion
  • smooth muscle contraction in: bladder, uterus, bronchioles, iris
  • increased secretions
  • convulsions in CNS
  • stimulation of autonomic ganglia and adrenal medulla
  • skeletal muscle contraction
  • SLUDD
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30
Q

Direct acting parasympathomimetics (muscarinic receptor agonists)

A

-Bethanechol

31
Q

Bethanechol

A
  • choline ester
  • some M3 receptor selectivity, minimal nicotinic activity
  • directly stimulates detrusor muscle, contraction of bladder
  • PO
  • indications: increase urinary bladder detrusor muscle contractility, increase GI motility, can stimulate uterine contractions
  • do not use in urethral/urinary tract/GI obstruction
  • in overdose: excessive muscarinic effects (SLUDD)
  • very high dose= life threatening cholonergic signs (bradycardia, bronchospasm, etc)
32
Q

Indirect acting parasympathomimetics (all reversible acetylcholinesterases)

A
  • Neostigmine
  • Pyridostigmine
  • Endrophonium (Tensilon)
33
Q

Neostigmine

A
  • oral tablets/injectable
  • onset and duration of action: relatively short, humans: effects in 10-30 mins, lasts 4 hrs
  • indications: rumen atony, increased GI motility and bladder emptying, reversal agent of choice for neuromuscular blockers, can be used to treat myesthenia gravis, but Pyridostigmine is drug of choice
  • precautions: SLUDD signs, may be more dramatic in patients with pre-existing high vagal tone)
  • contraindications: peritonitis, GI obstruction, late pregnancy, other cholinesterase inhibitors
34
Q

Pyridostigmine

A
  • oral tablet, extended release tablets, oral syrup, injectable
  • onset and duration: onset about 1 hr after oral dosing, more rapid with IV, longer lasting than neostigmine: 8-12 hours, why its used in maintenance of MG
  • indications: long term effect of MG in dogs
  • precautions: SLUDD signs, preexisting high vagal tone, any other contradictions/concerns with cholinergic agent apply
35
Q

Endrophonium (Tensilon)

A
  • injection
  • onset and duration: very fast acting–>onset within 1 min, short duration–>lasts about 10 mins
  • indications: tensilon test for MG, reversal of non-depolarizing NMBs
  • precautions: SLUDD signs (mild), less commonly, more severe cholinergic crisis (bronchoconstriction/secretions, bradycardia or tachycardia, hypotension, cardiac arrest)
36
Q

Parasympathomimetics- indirect acting- irreversible anticholinesterases

A

-organophosphate insecticides (toxicity)

37
Q

organophosphate toxicity-muscarinic effects

A
  • SLUDD

- DUMBBELL-diarrhea/dyspnea, urination, miosis, bronchospasm, bradycardia, emesis, lacrimation, salivation

38
Q

organophosphate toxicity- nicotinic effects

A
  • muscle tremors
  • muscle weakness
  • muscle paralysis (respiratory)
  • tachycardia and mydriasis due to stimulation of sympathetic ganglia and release of norepinephrine
  • CNS effects
39
Q

Parasympatholytics- direct acting-muscarinic agonists

A
  • atropine
  • glycopyrrolate
  • oxybutynin
  • propantheline
40
Q

atropine effects

A
  • tachycardia
  • mydriasis (dilated pupil)
  • dries secretions
  • reduces salivation
  • slows gut
  • bronchodilation
  • blurred vision
  • difficulty urinating
41
Q

Atropine sulfate

A
  • direct acting parasympatholytic- anticholinergic, antimuscarinic
  • tertiary compound, can cross BBB
  • injectable solution*, oral tablets, opthalamic drops
  • indications: systemic uses: treatment of bradyarrythmias/bradycardia, cardiac arrest (asystole or pulseless electrical activity), treatment of acetylcholinesterase inhibitor toxicity (organophosphates, carbamates), treatment of cholinergic crisis/anticholinesterase overdose
  • precautions: initial drop in HR after injection then increase, may cause tachycardia/exacerbate tachyarrythmias, don’t use in rabbits
  • contraindications: glaucoma, tachycardia/tachyarrythmias, hypothermic bradycardic patients, certain GI diseases, obstructive uropathy, MG
42
Q

glycopyrrolate

A
  • quarternary compound, does not cross BBB
  • slower onset, longer duration than atropine
  • indications: anywhere atropine is indicated but slower kinetics favorable (bradyarrythmias), pre-med anesthesia, decreased hypersialism, rabbits
  • precautions: same as atropine, less likely to cause CNS does not cross BBB
  • generally less arrythmogenic than atropine
  • duration of action longer
43
Q

Oxybutynin and Propantheline

A
  • MOA: GI or urinary antispasmodic agents–>relax detrusor and allow bladder to fill, oxybutynin widely distributed, crosses BBB, propantheline does not readily cross BBB, oral tablet, ER tablet, syrup, topical (human)
  • indications: main use: urinary antispasmodic to treat detrusor instability (overactive bladder), propantheline used to treat certain bradyarrythmias
  • precautions and contraindications: may cause other parasympatholytic signs as for atropine, however at normal doses bladder and GI most effected, avoid in glaucoma, tachycardia, ileus
44
Q

other direct acting parasympatholytics

A
  • Aminopentamide- antispasmodic for GI indications, approved in cats and dogs
  • N-butylscopal ammonium bromide- antispasmodic for colic in horses, used to treat bradycardia
45
Q

D1 receptor (adrenergic dopamine receptor)

A
  • smooth muscle of blood vessels in most organs
  • JG apparatus and renal tubules
  • direct vasodilation
  • natriuresis- diuretic response due to increased RBF and GFR
46
Q

D2 receptor (adrenergic dopamine receptor)

A
  • post ganglionic, sympathetic nerve terminals
  • glomeruli, renal cortex, and renal tubules
  • adrenal cortex- zona glomerulosa cells
  • chemoreceptor trigger zone in brain
  • indirect vasodilation- inhibits NE release from sympathetic nerve terminals (pre-junctional)
47
Q

sympathomimetics

A

-adrenaline response–>fight/flight

48
Q

catecholamines

A
  • direct acting sympathomimetics
  • poorly absorbed orally, give by injection (first pass effect)
  • readily absorbed from respiratory tract (inhalation is second best route)
  • SQ absorption slower for alpha 1 agonists
  • does not readily cross BBB
  • rapid onset of action and inactivation- good for emergency use
  • action terminated by removal from site of action -uptake by pre-85% or post 5% synaptic nerve terminal, cleared about 8% by kidney and lung (norepinephrine removal)
  • made in adrenal medulla
49
Q

General adverse effects of catecholamines

A
  • potent with narrow safety margin, risk of toxicity
  • very short half life–> minutes, given as IV injection commonly and as CRI
  • predispose myocardium to tachycardia and tachyarrhythmias
  • anxiety, restlessness, tremors
  • altered perfusion–> preferential bloodflow to flight tissue, vasoconstriction to other organs esp, kidneys, norepi causes most vasoconstriction
  • extravasation of norepi/dopamine can cause tissue damage and sloughing
  • cerebral hemmorhage not common in vet patients
  • specific indications only, not for everyday use
50
Q

degradation of catecholamines

A
  • when released from nerve endings (norepinephrine), actively uptaken, diffusion, or destruction by MAO and COMT
  • in circulation (norepinephrine and epinephrine)- destroyed by diffusion into tissues containing COMT liver is primary organ, effect peaks 10-30 seconds, absent by 1 min
51
Q

epinephrine

A
  • direct acting catecholamine sympathomimetic
  • competitive agonism on all alpha and beta adrenergic receptors
  • B1 causes cardiac constriction
  • B2 causes bronchodilation, vasodilation to flight tissue, more pronounced in low doses
  • alpha 1 vasoconstriction is dose dependent, increase venous return to heart during CPR by this mechanism
  • routes of administration: IV, IM, SQ, inhaled, IO, not PO, injectable diluted
  • indications: systemic effects: cardiopulmonary arrest, anaphylaxis- used as vasopressor, + ionotrope if given IV, increase MAP by increasing systemic arterial pressure
  • local effects: used with local anesthetic (lidocaine) to produce regional vasoconstriction, can be used topically to treat local hemorrhage
  • precautions and contraindications: causes massive sympathetic output by increasing myocardial workload and oxygen demand, can cause myocardial ischemia or cardiac arrest, only use in emergency
52
Q

direct acting catecholamine sympathomimetic

A
  • epinephrine
  • norepinephrine
  • isoproterenol
  • dopamine
  • dobutamine
53
Q

norepinephrine

A
  • MAO: mostly alpha-1 agonism, some alpha2, little B-1
  • indications: used when vasopressor support of CV is needed, treatment of hypotension due to inadequate vascular tone (septic shock), sepsis, vasopressor support during anesthesia
  • main clinical effects: vasoconstriction (a-1 agonism), important vasopressor (increase cardiac afterload), less increase of myocardial oxygen than with epinephrine, no significant bronchodilation, no vasodilatory effects counteracting vasoconstriction (can cause stronger vasoconstriction, and cause increased systemic vascular resistance= reflex bradycardia
  • precautions and contraindications: cardiac arrythmias/tachyarrythmias, hypertension
54
Q

Isoproterenol

A
  • MOA- synthetic amine, potent non-specific Beta agonist, no alpha agonism
  • indications and main clinical effects: cardiac stimulation, positive ionotrope, increase coronary, skeletal, renal, and mesenteric blood flow, bronchodilation (human asthma), not as commonly used
  • precautions and contraindications: side effects similar to dopamine and dobutamine (tachycardia, anxiety, tremors, arrythmias), IV infusion (CRI)–titrate, ECG and arterial BP monitoring
55
Q

Dopamine

A
  • MOA- acts on dopamine receptors, dose dependent effects on alpha and beta receptors, indirect stimulation of norepi release
  • dose dependent effects: low dose: agonize D receptors, dilation of renal, mesenteric, coronary, and intercerebral vascular beds, med-low dose: beta-1 agonist, positive ionotrope, med-high dose- B-1 agonist, positive chronotrope, increase cardiac automaticity, high dose- alpha-1 agonist, vasoconstriction, no b-2
  • indications and clinical effects: vasopressor support, treatment of hypotension due to decreased vascular tone, post-arrest vasopressor of choice
  • precautions and contraindications: can cause necrosis if extravasation occurs, monitor ECG and arterial bp for tachyarrythmias, tachycardia, fluctuations in BP, contraindicated in hypertensive
56
Q

Dobutamine

A
  • MOA: synthetic B-1 agonist, minimal B-2 and a-1 agonism, no dopamine activity
  • indications and main clinical effects: positive ionotrope, used in CHF, dilated cardiomyopathy (dogs), moderate positive chronotrope, treatment of anesthesia associated hypotension when ionotropic support is needed to maintain cardiac output and tissue/organ perfusion
  • increase coronary, skeletal, renal, mesenteric blood flow
  • precautions and contraindications: side effects similar to other catecholamines (tachycardia/tachyarrythmias), twitching/seizures, tachyphylaxis, don’t use when there is left atrial rupture or where myocardial integrity is concern
57
Q

non-catecholamine direct acting sympathomimetics

A

-phenylephrine

58
Q

phenylephrine

A
  • MOA- direct acting a-1 selective agonist only
  • indications/main clinical effects: increased peripheral vascular resistance through systemic vasoconstriction, treat reflex bradycardia, treat hypotension in dogs and cats, vasopressor effects immediately IV, lasts less than 20 minutes, local/topical use–> when vasoconstriciton needed to control hemorrhage, mydriatic for glaucoma
  • administration: wide variety of formulations
  • precautions and contraindications: may not want to cause vasoconstriction in kidney and GI tract, chronic use can rebound nasal congestion, contraindicated with hypertension
59
Q

non-selective sympathomimetic B-agonists

A
  • ractopamine

- zilpaterol

60
Q

ractopamine/zilpaterol

A
  • “partitioning agents”
  • non-selective B receptor agonists
  • cause increased weight gain, feed efficiency, leanness in food animals
61
Q

selective B-2 agonists from most to least

A
  • bronchodilators in lower airway disease (asthma, COPD), may be cilia augmenters
  • Albuterol/Salbutamol- in inhaler, human approved
  • Tetrabutaline- tablet/injectable
  • Clenbuterol- vet approved oral syrup in equine, contraindicated in food animals
  • Isoxsupine- not as commonly used, vasodilator/uterine relaxant in large animals, treat laminitis
62
Q

precautions/contraindications of selective B-2 agonists

A
  • cardiac stimulation- tachycardia
  • vasodilation
  • uterine relaxant
  • relative contraindications: patients with CV disease
  • nervousness, sweating, muscle tremors, weakness, vomiting
  • receptor downregulation with chronic use
  • may be prohibited by some equine associations
63
Q

Indirect/mixed acting sympathomimetics

A
  • generally used for CNS effects, behavior modification (antidepressant in humans)
  • tricyclic antidepressants- Clomipramine (5-HT), Doxepin (5-HT/NE, antihistamine)
  • monoamine oxidase inhibitors- selegiline, coicaine (blocks NE reuptake), amphetamine (increase NE release)
  • Phenylproanolamine
  • Ephedrine
64
Q

Phenylpropanolamine

A
  • MOA: mixed (direct/indirect acting) sympathomimetic, indirect increase in NE in bladder neck/urethra (primary action), direct alpha-1 agonist
  • indications: small dogs to treat urinary incontinence due to urethral sphincter hypotonus/incontinence
  • drug-drug interactions- synergism with estrogens
  • precautions: restlessness, urinary retention, tachycardia, hypertension, possible anorexia
65
Q

ephedrine

A
  • MAO: mixed (direct and indirect acting) sympathomimetic, indirect and increased NE release (major action), direct alpha 1 and beta activation
  • indications and main effects- used as CRI to maintain bp under anesthesia increase blood pressure–>vasoconstriction and direct cardiac stimulation, bronchodilation, urinary sphincter contractions (urinary retention), mydriasis
  • precautions- hypertension, arrythmias
66
Q

direct acting sympatholytics

A
  • Phenoxybenzamine

- Prazosin

67
Q

Phenoxybenzamine

A
  • MOA- non-specific alpha antagonist, binds reversibly to receptors lasts for lifetime of receptors (3-4 days)
  • indications: SAM to treat: urinary retention due to urethral hypertonicity (relax internal sphincter), pheochromocytoma (used prior to surgery to treat associated hypertension)
  • precautions: excessive alpha blockage: hypotension, reflex tachycardia, miosis and changes in IOP, GI signs
68
Q

Prazosin

A
  • MOA: alpha-1 antagonist: urinary smooth muscle relaxation, vasodilation, may have more dramatic effects and faster onset of action then phenoxybenzamine, only oral in humans
  • indications: SAM: urinary retention due to urethral hypertonicity- feline urinary tract disease, feline idopathic cystitis, adjunctive treatment of CHF, systemic/pulmonary hypertension, less common than other anti-hypertensive drugs
  • precautions and contraindications: caution in patients with chronic renal failure, relatively contraindicated in certain types of heart disease (hypertrophic obstructive cardiac myopathy in cats), may cause bradycardia, bronchospasm (careful in feline patients), GI effects, CNS effects in people (can cause ataxia in animals), nicitans elevation
69
Q

sympatholytics- class II antiarrhythmics

A
  • non-selective B antagonists- propanolol

- selective B-1 antagonists- atenolol, esmolol

70
Q

propanolol

A
  • MOA- decrease SA node firing (bradycardia), decrease AV conduction (decrease cardiac output and myocardial oxygen demand), increase airway resistance, readily cross BBB, significant first pass effect, half life: 1-2 hours, most excreted in urine as metabolites, oral or injectable
  • indications- used to treat tachyarrythmias- superventricular tachyarrhythmias, chocolate toxicosis, feline hyperthyroidism
  • precautions and contraindications: bradycardia, hypotension, bronchospasm, receptor desensitization and increased regulation (taper dose to reduce this), contraindicated with overt heart failure, sinus bradycardia, heart block, hypertrophic cardiac myopathy in cats, contraindicated with bronchspastic lung disease, caution in hepatic/renal disease, hypoglycemia or on digitalis
71
Q

atenolol

A
  • longer half life than propanolol and more selective for B-1 receptors
  • lack of B-2 effects–> potentially safer if bronchoconstriction is concern
  • overall less side effects
  • only oral
72
Q

esmolol

A
  • ultra short acting B-1 antagonist

- IV control of supraventricular arrythmias

73
Q

indirect acting sympatholytics- reserbpine

A
  • blocks NE uptake into vesicles which reduces storage of NE and leads to mediator depletion
  • calming for equines on long term stall rest
74
Q

direct acting on SNS

A
  • co-transmission- ATP (common in vesicles containing NE), may be responsible for some fast sympathomimetic response with NE later
  • NANC (non-adrenergic, non-cholinergic transmission): NO- potent vasodilator, GABA- main inhibitory NT in CNS< serotonin 5-HT, dopamine

pharmacology (5 decks)

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