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Pharmacology > Autonomic Nervous System: Wk 2 > Flashcards

Autonomic Nervous System: Wk 2 Flashcards

1
Q

divisions of nervous system

A

divisions of nervous system
-Central Nervous System (CNS):
-Includes brain and spinal cord
-integrates all body activities
-Peripheral Nervous System:
-Somatic Nervous System
-Autonomic Nervous System (ANS):
-Parasympathetic nervous system
(PNS)
-Sympathetic nervous system (SNS)

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2
Q

somatic nervous system

A

somatic nervous system
-Activates skeletal muscle contraction
-Consists of motor neurons/sensory
neurons
-Sensory (afferent) – go TO CNS
-Motor (efferent) - go FROM CNS to
skeletal muscle
-Adjusts to external environment
-VOLUNTARY

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3
Q

ANS

A

-Further subdivided into PNS and SNS
-Regulates activity of smooth muscle,
exocrine glands, cardiac tissue and
certain metabolic activities
-Sensory neurons go from smooth
muscle & cardiac muscle TO CNS
-Motor neurons go to glands, smooth & cardiac muscle FROM CNS
-Adjust to internal environment
-INVOLUNTARY

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4
Q

enteric nervous system

A

enteric nervous system
-Aka 3rd division of ANS
-Network of autonomic nerves in
gut wall
-Receives innervation from SNS &
PNS and regulates gi motility and
secretion
-Responds to Neurotransmitters –
peptides and nitric oxide

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5
Q

neurotransmission of ANS

A

neurotransmission of ANS
-Preganglionic neuron – cell body in CNS, axon extends out of CNS
-Postganglionic neuron – innervate an
effector outside the CNS
-Ganglion – Small mass of nerve tissue containing the cell bodies of neurons
-Synapse – space b/w pre & post neurons or space b/w post neuron & effector where Neurotransmitter (NT) is released
-SNS – primary NT is Norepinephrine (NE) – may also be referred to as noradrenaline (NA)
-PNS- primary NT is ACh

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6
Q

neurotransmitters of the ANS

A

neurotransmitters of the ANS
-Acetylcholine (ACH)– Primary NT of PNS. Released at ALL autonomic ganglia (PNS & SNS), at PNS neuroeffector junction (nej), somatic neuromuscular junction (nmj), and some SNS nej
-Norepinephrine/Noradrenaline (NE/NA) – Primary NT of SNS. Released at most SNS nej
-Epinephrine (Epi) – released from adrenal medulla in response to activation of SNS
-Dopamine (DA)- important NT in CNS, and released at several peripheral SNS fibers

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7
Q

other neurotransmitters

A

other neurotransmitters
-Found in ANS nerves but they are nonadrenergic noncholinergic neurons (NANC)
-Primarily found in enteric nervous system of GI tract, genitourinary tract, airways and some blood vessels
-Includes peptides, ATP, GABA, substance P, nitric oxide, serotonin
-viagra- #1 drug that affects nitric oxide

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8
Q

ANS: general effects of PNS

A

-Responses are specific
-Rest & digest
-Miosis
-increase gi motility/salivation
-increase urination/defaction
-decrease HR
-Bronchoconstriction
-Erection

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9
Q

ANS: general effects SNS

A

-Responses are diffuse
-Fight or flight
-Mydriasis
-decrease gi motility/salivation
-decrease urination/defaction
-increase heart rate
-Bronchodilation
-Ejaculation

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10
Q

cholinergic (PNS) receptor effects

A

-PNS
-muscarinic
-pupil miosis
-HR decrease
-arteries/vein- dilation
-smooth muscles- increase motility
-gastric secretion- stimulate
-pancreas secretion- stimulate
-salivary secretion- stimulate
-liver- glycogenesis
-SLUDGE

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11
Q

cholinergic receptors (just know there are diff ones)

A

cholinergic receptors (just know there are diff ones)
-muscarinic 1
-muscarinic 2
-muscarinic 3
-nicotinic N
-nicotinic M

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12
Q

cholinergic receptors (ACh): muscarinic

A

-Activated by ACh and muscarine
-Located at PNS nej, some SNS nej (sweat glands), CNS, and autonomic ganglia
-Found in body in greater numbers than nicotinic receptors
-SLUDGE: salivation, lacrimation, urination, defecation, GI motility, erection
-Mediate smooth muscle contraction (except sphincter contraction)
-Stimulates gland secretion
-Decrease HR and conduction
-Bronchoconstriction
-Peripheral vasodilation
-Miosis

-“rest and digest activities”: slow HR, increase gland secretion in GI, stimulate smooth muscle activity - pee + poop

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13
Q

Effects of stimulating muscarinic receptors

A

-SLUDGE: salivation, lacrimation, urination, defecation, GI motility, erection
-Mediate smooth muscle contraction (except sphincter contraction)
-Stimulates gland secretion
-Decrease HR and conduction
-Bronchoconstriction
-Peripheral vasodilation
-Miosis

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14
Q

cholinergic receptors (ACh): nicotinic

A

-activated by ACh and nicotine
-Located at somatic neuromuscular junction-> activated mediates muscle contraction
-Nicotinic have some opposing effects of muscarinic (tachycardia, HTN)**

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15
Q

adrenergic receptors (NE and epi): alpha 1

A

-constricts blood vessels -> increase BP *
-constricts vascular smooth muscle
-pupil: mydriasis (dilation)
-Increase basal metabolic rate
-liver: glycogenolysis

-Located at SNS nej effector (primarily smooth muscle)
-> NEJ: neuroeffector junction, site where the postganglionic nerve meets the target effector cells to trigger physiological response

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16
Q

adrenergic receptors (NE and epi): alpha 2

A

-Inhibition of NE release from nerve endings at pre synaptic post ganglionic neuron (negative feedback)
-Also located on some postsynaptic tissue & blood platelets -> involved in blood clotting processes

-clinical relevance: targets for certain antihypertensive drugs

activation of alpha 2:
- INHIBITS further release of NE -> negative feedback
- alpha 2 located on PRE-SYNAPTIC post ganglionic neurons -> just before release of NT
- reduces SNS activity
- located on post-synaptic tissue and platelets: role in bloodclotting

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17
Q

adrenergic receptors (NE and epi): beta 1

A

-HEART muscle!!! - increase HR & contractility
-Located on SNS effector (cardiac muscle, vascular smooth muscle, renal cells - increase renin release)
-Increased lipolysis

clinical relevance: target for cardiac drugs - beta-blockers

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18
Q

adrenergic receptors (NE and epi): beta 2

A

-LUNGS!! - bronchodilation
-Mediates smooth muscle relaxation
-located on SNS effectors (bronchioles in lung, uterine smooth muscle and vascular smooth muscle)
-In liver and muscle – mediate glycogenolysis

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19
Q

non specific beta blocker

A

-works on beta 1 and 2
-ex. propanolol
-contraindicated in pts with asthma

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20
Q

Direct vs indirect autonomic drugs classification

A

-Can exert effects at any step in neurotransmission process depending on classification of drug
-PNS & SNS agonist- Direct or Indirect acting
-PNS & SNS antagonist- Direct or Indirect acting

-Direct: activates/deactivates the neurotransmitter receptor
-Indirect: something that stimulates/de-stimulates the neurotransmitter

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21
Q

direct/indirect agonist

A

-Direct agonists: Activate postsynaptic receptors

-Indirect agonists:
-Stimulate release of NT
-Inhibit reuptake of NT
-Inhibit metabolism of NT

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22
Q

direct/indirect antagonists

A

-Direct antagonists- Block postsynaptic receptors

-Indirect antagonists:
-Inhibit synthesis of NT
-Prevent vesicular storage of NT
-Inhibit release of NT

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23
Q

cholinergic agonists

A

-Direct agonists – bind and activate cholinergic receptors:
-Choline esters
-Plant alkaloids

-Indirect agonists – increase synaptic concentrations of ACH:
-Cholinesterase inhibitors (inhibits the metabolism of neurotransmitter)

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24
Q

direct cholinergic agonists (choline esters)

A

-ACh
-carbachol
-Betahanechol
-methacholine

-ACH and Carbachol – activate both nicotinic and muscarinic
-ACH has limited clinical indications
-Lack of specificity for muscarinic subtypes, therefore have a wide range of effects on many organ systems
-Bethanechol** and methacholine**: activates only muscarinic
-Methacholine not commercially available
-> main ones used in practice are bethanechol and carbachol

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25
Q

Bethanechol (urecholine)

A

Direct cholinergic - choline ester class
“Beth gave birth and can’t pee”

-acts at muscarinic only
-Stimulates bladder w/o significant effects on HR or BP
-TX of urinary retention post-op & post partum

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26
Q

choline esters: carbachol (isoptocarbachol, miostat)

A

-For chronic open-angle glaucoma
-Produce miosis during ophthalmic surgery
-not really used anymore

direct cholinergic agonist: muscarinic + nicotinic

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27
Q

direct cholinergic agonists: plant alkaloids

A

-Muscarine – no current medical use
-Nicotine – smoking cessation -> nicotine patches
-Pilocarpine (Isoptocarpine, Ocusert, Salagen)
-Higher affinity for muscarinic receptor
-Treats glaucoma: stimulate contraction of ciliary muscle fibers -> increase aqueous humor outflow -> decrease IOP
-Cevimeline (Exovac)- treat dry mouth associated with Sjogren’s syndrome!!!!!

-ceviMEline -> ME have Sjogren’s syndrome

28
Q

Cholinesterase inhibitors MOA

A

indirect cholinergic agonist
-MOA: Inhibit breakdown of ACH at all cholinergic synapses -> increase ACH concentration
-Reversible vs Irreversible binding agents

-Cholinesterase: enzyme that breaks down ACh

29
Q

cholinesterase inhibitors: reversible agents (increase ACh concentration)

A

DENPP
-donepezil
-edrophonium
-neostigmine
-pyridostigmine
-physostigmine

–
-Donepezil – Tx of Alzheimer’s Disease
-Edrophonium - very short DOA; Dx of Myasthenia gravis
-Neostigmine - Tx of Myasthenia gravis, antidote for skeletal muscle relaxants
-Pyridostigmine – Tx of Myasthenia gravis
-Physostigmine (Eserine) - Tx for Overdoses of drugs with anticholinergic effects (like atropine, TCAs)

-DONEpezil: “DONE with thinking -> Alzheimer’s ds tx
-stigmine = cholinesterase inhibitor (indirect agonist)

30
Q

cholinesterase inhibitors: irreversible agents

A

-Ecothiophate
-pesticides
-soman

-irreversible binds = organophosphates -> enzyme becomes permanently inactive -> long acting drug**

-Ecothiophate– Tx of chronic refractory glaucoma. long DOA of up to one week
-Pesticides (palathion and malathion)- parasites (lice + scabies)
-Soman (chemical warfare agent)

indirect cholinergic agonists

31
Q

organophosphate poisoning + Tx

A

-Augmented cholinergic neurotransmission at CNS and PNS synapses
-Produces all effects of muscarinic activation -> SLUDGE, spasm, bronchoconstriction, decrease HR & CO, miosis
-Cholinergic activation in CNS – seizures, respiratory depression, coma
-Excessive activation of nicotinic receptors- Neuromuscular blockade & muscle paralysis
-Treatment:
-Symptomatic - maintain vital signs
-Decontamination: remove contaminated clothes
-Antidotes – Atropine to counteract ACh and pralidoxime (2-PAM) to regenerate cholinesterase

32
Q

muscarinic receptor antagonists: categories and drug names

A

-plant alkaloids (“BellaDonna Alkaloids”): “ASH”
- atropine
- scopalamine
- hyoscyamine

-semi synthetic: “BIT POD”
- Benztropine
-Ipratropium
- Tolterodine
- Propantheline
- Oxybutynin
- Dicyclomine

-Belladonna: dilated eyes

33
Q

Nicotinic receptor antagonists

A

-ganglionic blockers: trimethaphan
-limited use due to adverse effects
-used rarely for hypertensive emergency

-neuromuscular blockers:
-1) depolarizing neuromuscular blocker- succinylcholine
-2) non-depolarizing neuromuscular blocker: “-curium”

34
Q

muscarinic receptor antagonist: ocular effects

A

-Relax iris sphincter -> mydriasis (dilated)
-Inhibits lacrimal gland –> dry eyes
-Tx use – mydriatic to facilitate eye exams (atropine, scopolamine; Tropicamide drops)

35
Q

muscarinic receptor antagonist: cardiac effects

A

-increase HR and AV conduction
-Tx: atropine -> fix sinus bradycardia & AV block

36
Q

muscarinic receptor antagonist: respiratory effects

A

-increase Bronchodilation
-Therapeutic Uses: COPD, emphysema, bronchitis
-ipratropium
-tiotropium

37
Q

muscarinic receptor antagonist: GI and urinary tract effects

A

-Relax gi muscle
-reduce intestinal motility
-inhibit gastric acid secretion
-increase urinary retention

-Therapeutic Uses:
-TX of intestinal spasms/pain – Hysosamine, Donnatal, Dicyclomine
-TX of dysuria & urinary incontinence: oxybutynin, tolterodine, darifenacin, solifenacin

“Working OT or playing on DS -> want to hold in pee longer
Oxybutynin
Tolterodine
Darifenacin
Solifenacin”

DAR
SOL
-ifenacin

38
Q

muscarinic receptor antagonist: CNS effects

A

-TX of motion sickness by blocking cholinergic transmission from vestibular apparatus to vomiting center (Scopolamine patch)
-TX of Parkinson’s Disease – reduce tremor (benztropine & trihexyphenidyl)
-CNS side effects include: sedation*, confusion, altered mental status

39
Q

nicotinic receptor antagonists

A

-1. ganglionic blockers
-limited use due to adverse effects
-trimethaphan- used rarely for hypertensive emergency
-2. neuromuscular blocking agents
-nondepolarizing
-depolarizing

40
Q

Nondepolarizing neuromuscular blocking agent

A

-nicotinic receptor antagonists: competetitve antagonist of ACh
-Causes muscle relaxation and paralysis
-Used for surgery, intubation, ventilators

-aka curariforms: “-curium”
-Atracurium, pancuronium, vecuronium, rocuronium

-Effects reversed by cholinesterase inhibitors**

41
Q

atropine poisoning

A

Red- rapid flushing
Eyes dilated- blurred vision
Very dry
CNS delirium

Red as a beet, blind as a bat, dry as a bone, mad as a hatter

tx: physostigmine -> cholinesterase inhibitor

42
Q

depolarizing neuromuscular blocking agent

A

nicotinic receptor antagonists

-Succinylcholine
-Causes “persistent” depolarization- muscle relaxant during surgery
-Used for surgery, RSI kits
-Effects NOT REVERSED by cholinesterase inhibitors therefore no antidote** if overdose
-short duration of action
-good for rapid emergency situation

43
Q

adrenergic agonists

A

-1. Direct Acting Agonists:
-Catecholamines (epi, NE, isoproterenol, dopamine and dobutamine)
-Non-catecholamines (albuterol, clonidine, phenylephrine)
-2. Indirect Agonists:
-Amphetamine, cocaine, tyramine
-3.Mixed direct/indirect agonists:
-pseudoephedrine

44
Q

nasal decongestant

A

-dont need to know
-afrin - great vasoconstrictor- used for nasal surgery
-sudafed is good for decongestant -> not phenylephrine

45
Q

direct adrenergic agonists: catecholamines

A

-norepinephrine, epinephrine, dopamine, dobutamine, isoproterenol

-Rapidly metabolized by monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT) enzymes in gut, liver and other tissues
-must give parenterally**

“NEDDI goes to CAl TECH”
ned loves his wife -> wants to be PARENT(erally) administered”

46
Q

epinephrine

A

-class: direct adrenergic agonists - catecholamines
-Epinephrine – can bind to ALL the adrenergic receptors:
-Vasoconstriction & increase BP (alpha1)
-Cardiac stimulation (beta1)
-Bronchodilation & skeletal muscle vasodilation (beta2)
-Used in anaphylactic shock and cardiac arrest

47
Q

norepinephrine

A

-direct adrenergic agonists: catecholamines
-Vasoconstriction & increase BP (alpha1)
-Cardiac stimulation (beta1)
-Used in hypotension and shock
-no lung involvement

48
Q

dopamine + dobutamine

A

both are direct adrenergic agonists: catecholamines
-Dopamine: D1, B1, A1
- precursor to epi, NE
-Renal vasodilation (D1)- at a low dose -> at a long term dose it will cause kidney constriction
-Cardiac stimulation (beta1)
-increase BP (alpha1)
-Used to TX cardiogenic shock, septic shock, heart failure and adjunct to fluid administration in hypovolemic shock

-Dobutamine
-Highest affinity for beta1 receptor
-Less activity at alpha1 receptor
-Used to Tx cardiogenic shock, cardiac arrest and heart failure
-no affect on kidney -> better for a longer term dose

49
Q

direct adrenergic agonists: non-catecholamines drugs

A

direct adrenergic agonists: non-catecholamines:
- Phenylephrine (Neosynephrine)
- Albuterol (Proventil)
- Clonidine (Catapres)
- Terbutaline (Brethine

non-catecholamines: “ppl who didn’t get into Cal Tech form a PACT”

50
Q

isoproterenol

A

-class: direct adrenergic agonists catecholamines
-Isoproterenol (Isoprel)
-Cardiac stimulation (beta1) & Bronchodilation (beta2)
-Used to TX asthma, AV block and bradycardia

51
Q

Phenylephrine

A

-class: direct adrenergic agonists: non-catecholamines
-Phenylephrine (Neosynephrine)
-Vasoconstriction, increase BP and mydriasis (alpha1)
-Used as nasal decongestant, ocular decongestant and maintenance of BP during surgery
-given IV or topical

52
Q

Albuterol

A

-class: direct adrenergic agonists: non-catecholamines
-Albuterol (Proventil)
-Bronchodilation (beta2)
-Used in asthma
-has alpha1 affect -> increase HR -> doesnt last though

53
Q

Clonidine

A

-class: direct adrenergic agonists: non-catecholamines
-Clonidine (Catapres)
-Inhibits NE release from nerve terminal of postganglionic neuron (feedback inhibition: alpha2)
-Used to treat chronic hypertension
-Can cause CNS - sedation -> not a good drug bc of this

54
Q

Terbutaline

A

-class: direct adrenergic agonists: non-catecholamines
-Terbutaline (Brethine)
-Bronchodilation and uterine relaxation (beta2)
-Used to TX asthma and premature labor (tocolytic)
-great for children
-case reports for learning disability for premature labor use -> not proven

55
Q

amphetamine

A

class: indirect adrenergic agonists

-INCREASES THE RELEASE of NE & dopamine (DA) from SNS neurons
-Vasoconstriction, cardiac stimulation and increase BP
-Penetrates to CNS through the blood brain barrier: CNS stimulation -> increases mood and alertness (but decreases appetite)

56
Q

indirect adrenergic agonists drugs

A
  • Amphetamine
  • Cocaine
  • Tyramine

“Indirect ppl too high on cocaine they don’t know how to ACT”

57
Q

Cocaine

A

-indirect adrenergic agonists
-Local anesthetic
-Simulates SNS by BLOCKING RE-UPTAKE of NE & DA in the PNS & SNS
– SNS: increase BP, cardiac stimulation

58
Q

tyramine

A

-indirect adrenergic agonists:
-Normal by-product of tyrosine amino acid metabolism in body
-food sources: fermented foods like certain cheeses, beers, red wine, certain cured meats (salami & pepperoni)
-Indirect sympathomimetic b/c it causes the release of stored catecholamine -> increase BP and HR
-Normally metabolized by monoamine oxidase (MAO)
-if taking an MAO inhibitor must avoid tyramine-containing foods -> prevents breakdown of tyramine -> hypertensive crisis

59
Q

mixed acting adrenergic agonist

A

-Nasal decongestants – Pseudoephedrine (sedofed) -> cant take it long term
-Cause vasoconstriction by binding to alpha1
-Increase release of NE from SNS neurons

60
Q

adrenergic antagonists

A

-alpha adrenergic receptor antagonists (alpha blockers):
-Nonselective alpha-blockers: phenoxybenzamine, phentolamine
-Selective a1-blockers (-“azosin”)

-beta adrenergic receptor antagonists (-“olol”):
-Nonselective beta blockers: ex - propanolol, timolol,nadolol
-Selective beta 1 blockers: metropolol, atenolol

-Mixed and adrenergic receptor antagonists: carvedilol, labetalol

61
Q

nonselective alpha-blockers

A

-Block alpha1 and alpha2 receptors
-Phenoxybenzamine
-Phentolamine

62
Q

Phenoxybenzamine

A

-nonselective alpha-blockers
-Noncompetitive, irreversible*
-TX: hypertensive episodes associated w/ pheochromocytoma
- pheochromocytoma: tumor in adrenal medulla that secretes catecholamines

“Phenoxybenzamine longer name than Phentolamine -> NON-competitive and IR-reversible (longer words)”

63
Q

Phentolamine

A

-nonselective alpha-blockers
-Competitive, reversible*
-DX and TX hypertensive episodes from pheochromocytoma
-Tx necrosis and ischemia from extravasations of epinephrine -> counteracts vasoconstriction from accidental tissue extravasation

64
Q

selective alpha 1-blockers

A

-relaxes smooth muscle: bladder + prostate + vascular
-Produce vasodilation -> decrease BP
-Used to treat hypertension and urinary retention due to benign prostatic hyperplasia (BPH)
-Agents include: “-ZOSIN”
-Doxazosin
- Prazosin (Minipress)
- Terazosin (Hytrinon)
-Tamsulosin + Alfuzosin (TA) – only for BPH not for HTN
-not really our go to drug for HTN
-can cause phantom ejaculation

65
Q

nonselective beta-blockers

A

-Propranolol
-Nadolol
-Timolol

-Block beta1 receptors in heart and beta 2 in smooth muscle, liver and other tissues
-beta1 blockade: decrease BP , decrease cardiac output, decrease renin release and decrease aqueous humor secretion
-beta 2 blockade: bronchoconstriction, decrease glycogenolysis (dont give to pts with diabetes), mask signs of hypoglycemia

-TX HTN, angina, arrhythmias, MI, migraine, glaucoma

66
Q

selective beta1-blockers

A

-Selective for beta1 receptors (primarily in cardiac tissue) -> -Aka cardioselective beta-blockers
-Produce less bronchoconstriction and other beta2 receptor mediated effects6
-TX HTN, angina, MI
-Agents include: Metoprolol (Lopressor), Atenolol (Tenormin)

“MAs are needed for cardiac (cardioselective beta blockers) health”

67
Q

mixed alpha and beta receptor antagonists

A

-Block both alpha and beta receptors
-Carvedilol – Tx HTN and CHF
-Labetalol – Tx HTN -> this can be used IV in emergency
-not reaching their goals with just beta blocker

Pharmacology (15 decks)

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