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Angeli - N929 Pharmacology > Exam 1: ANS Drugs > Flashcards

Exam 1: ANS Drugs Flashcards

1
Q

SNS neurons (location and length)

A 
o	Preganglionic thoracolumbar (short)
o	Postganglionic (long)
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2
Q

PSNS

A 
o	“around the SNS” above/below the thoracolumbar area - Cranial/sacral areas
o	Preganglionic (long)
o	Postganglionic (short)
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3
Q

key characteristics of ANS

A

o Regulates involuntary response—sm m, glands, heart
o 2-neuron pathways
o Diffuse vs. Discrete responses
o Dual Innervation–Opposing, antagonistic effects
 Will see reflex response that will oppose your drugs given
o Reflex responses
o Predominant, basal activity/control
 Basal activity = which system controls that tissue at the basal level (mostly PSNS)

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4
Q

exceptions to dual innervation

A

• Exceptions to Dual Innervation
o Adrenal Medulla
 Sympathetic only
o Most sweat glands
 Sympathetic only
o Blood vessels
 Sympathetic only
• But have cholinergic RECEPTORS on blood vessels (no PSNS innervation to the blood vessels)
 Basal tone – some vasoconstriction (SNS basal tone)
 Receptor distribution determines response
• Vessels in skeletal m, heart
o beta2 mediated vasodilation
o need more blood flow during fight or flight
• Vessels in skin, viscera
o alpha1 mediated vasoconstriction
o Most _______ in the body (missed this factoid)
• EPI stimulates both

other: piloerector muscle

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5
Q

unique glands: adrenal medulla

A 
	Sympathetic innervation 
	Only 1 neuron 
	Postsynaptic neuroendocrine cells 
	Secrete Epi/norepi into blood 
	Mimics sympathetic stimulation
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6
Q

unique glands: sweat glands

A

 Sympathetic innervation
 Post-ganglionic neuron is cholinergic (not adrenergic)
 Acetylcholine is NT
 Receptor at effector tissue is muscarinic (a cholinergic receptor)

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7
Q

nicotinic cholinergic receptor

A

o Ligand-gated, Na+ , K+ depolarizing channel
o 2 major subtypes
-NicN
-NicM

o	Location 
-Autonomic ganglia 
-Skel muscle innervated by somatic n 
-CNS 
o	ACh binds → Conformational changes; Channel opens and+ chgd ions pulled thru channel 
o	Depolarization of post-synaptic cell
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8
Q

M1, M4, M5 receptor location

A

CNS

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9
Q

M2 receptor location

A

heart

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10
Q

M3 receptor location

A

SEEG.
Also M1 = CNS, M2 = heart, so M3 = everything else!

smooth muscle, glands, endothelium, eye (circular, ciliary muscle)

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11
Q

Nic N receptor location

A

ANS ganglia (all of them), adrenal medulla, CNS

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12
Q

Nic M receptor location

A

skeletal muscle NMJ

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13
Q

3 subtypes of alpha adrenergic receptors

A

a1 - smooth muscle, eye
o a1 → excitatory - ^Ca++ → calmodulin activation → ^ actin-myosin interaction → sm muscle contraction (VSMC contr)

a2 - mainly presynaptic
o a2 → inhibitory - decrease cAMP → decrease norepinephrine release
-Eg. Clonidine is agonist for this receptor

ligands: NE, EPI, DA (in large doses)

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14
Q

beta adrenergic receptors

A

o β1 β2 β3
o GPCR, Gs
o Activation of adenyl cyclase → ^ cAMP → ^ kinase activation & phosphorylation
o Autonomic effector tissues
-heart, kidney, liver, smooth m, skel m; fat cells, B3
-receptor subtypes will cluster at certain tissues

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15
Q

a1 adrenergic receptor locations

A

alpha 1 - SEV

  • Smooth muscle: G-U sphincters (esp. bladder)
  • Most vascular (skin, splanchnic)
  • Eye –radial m
  • Heart, liver
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16
Q

a2 adrenergic receptor locations

A

(inhibitory)

- Pre-synaptic nerve terminal Platelets, pancreatic beta cell

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17
Q

B1 adrenergic receptor locations

A
  • Heart
  • Kidney - juxtaglomerular cells Renin release *ppl usually forget this one

“you beta know that the heart and the kidney think they’re the most important 1”

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18
Q

B2 adrenergic receptor locations

A 
	Smooth m: bronchiolar, uterine, etc. 
	Vascular sm muscle: Skel m beds 
	Liver 
	Skeletal muscle 
	Heart
	(albuterol)
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19
Q

B3 adrenergic receptor locations

A

adipose tissue

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20
Q

adrenergic receptors -general info

A

o Adrenergic Receptors:
 GPCR (different signal transduction pathways)
 Alpha2 – inhibitory
 NT: Norepinephrine
 Other Ligands include -Epi, DA
 **Tip about smooth muscle receptors: alpha1 contracts; beta2 relaxes
 **Tip about beta receptors: 1 heart, 2 lungs
o Heart’s main receptor is B1, but has some B2

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21
Q

NE in the peripheral NS

A 
o	Roles in peripheral and CNS (excitatory) 
o	Catecholamine NT 
	aka noradrenaline 
o	Termination of action 
	reuptake back into presynaptic neuron 
	diffusion 
	Metabolism – minor role 
•	Monoamine oxidase (MAO) 
•	COMT
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22
Q

DA in the peripheral NS

A 
o	Roles in peripheral and CNS 
o	Catecholamine NT 
	Precursor of norepi, epi 
	At effector jxn –sympathetic, renal vascular sm m 
o	Termination of action 
	neuronal reuptake by DA transporter 
	MAO breakdown (remember that MAO breaks down DA also)
•	MAO-A – periphery 
•	MAO-B – CNS 
•	COMT – minor role
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23
Q

DA receptor

A

 GPCR, cAMP 2nd messenger
 D1 class (D1 , D5 ) - ^ cAMP
 D2 class (D2 , D3 , D4 ) - decrease cAMP
o Periphery
 D1 – Vasodilation in renal, mesenteric, coronary vasculature
 D2 – presynaptic; modulates NT release

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24
Q

DA drug effects (low, intermediate, high dose)

A
  • Low dose – vasodilation (D1 ) in renal, mesenteric, and coronary vascular beds
  • Intermediate - + inotrope (B1 )
  • High dose – vasoconstriction (a1)

Uses: shock, HF, increase blood flow to kidneys

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25
Q
  • Other Transmitters in autonomic, enteric, and NANC neurons
A 
o	Neurotransmitter and/or Co-transmitters in PNS – many postganglionic parasympathetic neurons utilize other transmitters, including 
	Nitric Oxide (NO) 
	Vasoactive intestinal peptide (VIP) 
	Calcitonin Gene Related Peptide (CGRP) 
	Neuropeptide Y (NPY) 
	Substance P 
	Serotonin 
	Others
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26
Q

Nitro-based vasodilators, PDE5 inhibitors, combined effect

A

o Nitro-based vasodilators
 Isosorbide
 NO
 NTG
 Nitroprusside
 (NTG and nitroprusside act in the same way)
o PDE5: phosphodiesterase 5; the enzyme that breaks down the 2nd messenger (cGMP)
-sildenafil/Viagra
-tadalafil/Cialis
o Nitro-based vasodilators + PDE5 inhibitor → pronounced vasodilation →
DEATH

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27
Q

ACh vs. other cholinergic agonists

A

o Ach

  • Quaternary ammonium
  • Short duration
  • Less therapeutic value
  • Both Nic & Musc activity

o Other drugs

  • ↑ muscarinic selectivity
  • Lack acetate ester fxn
  • AChE does not hydrolyze
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28
Q

Reversible AChE Inhibitor Drugs

A
  • Alcohol: edrophonium, short duration
  • Carbamate
    • neostigmine (quaternary) - medium-duration
    • also pyridostigmine, physostigmine, & donepezil

-Enzyme active site is carbamylated (when its stuck on there, the ACh cannot bind)

• can be insecticides as well

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29
Q

Irreversible AChE Inhibitor Drugs

A

organophosphates; long duration

  • Echothiophate
  • Think covalent bond to the enzyme, NONcompetitive

requires synthesis of new AChE to overcome

30
Q

AChE inhibitor drug effects

A

o Autonomic

  • ↑ secretions (salivary, lacrimal, bronchial, GI)
  • ↑ GI motility
  • Bronchoconstriction
  • Bradycardia
  • Hypotension
  • Miosis; accommodation for near vision

o Neuromuscular junction

  • Reverses NM block by nondepolarizing blocker
  • Improves transmission – myasthenia gravis
  • Large doses—depolarizing block
o	CNS (if it can get into the CNS system)
-Therapeutic – dementia tx/Alzheimer’s  
-Toxicity 
•	Excitation (possible convulsion) 
•	Depression follows (unconsciousness)
31
Q

Toxicity mnemonic: Cholinergic crisis “DuMBBELLS”

A 
o	Diarrhea, Diaphoresis 
o	Urination 
o	Miosis 
o	Bradycardia 
o	Bronchoconstriction 
o	Excitation (skel m; CNS)*   + Emesis 
o	Lacrimation 
o	Salivation Sweating 
o	*paralysis of skel m/depression of CNS follows initial excitation

o Examples - pesticide, Sarin nerve gas
o Muscarinic toxicity
-Antidote: atropine
o AChE Inhibitor toxicity
- Antidote
• Atropine (prototype muscarinic receptor antagonist)
• Pralidoxime – regenerates active AChE enzyme (PAM?)

32
Q

Muscarinic agonist drug effects “parasympathomimetic”

A

o Think about where you have muscarinic receptors in the body – these drugs are still going to have broad effects in the body
o Cardiovascular
- ↓ HR
- ↓ CO & arterial pressure
- vasodilation (via NO – stimulated by endothelium musc receptors)
o GI - ↑ motility
o Bladder - contracts
o Lungs – bronchoconstriction
o ↑ Secretions
-sweat, lacrimation, salivation, bronchial
o Eye
-miosis, accommodation for near vision, ↓ intraocular pressure

33
Q

SLUDGE mnemonic

A

o Salivation
o Lacrimation
o Urination
o Diarrhea
o GI Upset
o Emesis
o Limited list bc skeletal muscle part
o Note: this mnemonic is good for GI-GU effects, but does not include effects on: heart, lungs, eye effects from muscarinic receptor activation.
o What effects would you expect on these organs?
o What drug could be used to oppose toxicity of muscarinic agonists? ATROPINE

34
Q

drugs affecting the nAChR

A

o Different nicotinic subunits – so that’s how you target certain receptor types despite them being nicotinic receptors
o Ganglionic stimulators are not particularly useful, bc then you just excite all those cells
o Mecamylamine, trimetaphan, hexamethonium, a-conotoxin more useful for lab than medical use

35
Q

muscarinic blockers, in general

A

Most muscarinic blockers are non-selective – so you’ll just be blocking ALL muscarinic receptors.

Some newer ones are selective for M3 receptor – for incontinence

36
Q

muscarinic ANTAGONIST effects on systems

A 
Heart - ↑ 
Bronchi – broncodilate
GI – decrease 
GU – decrease
Glands – decrease
Sweat glands – decrease 
Eye – mydriasis, paralysis of accommodation, atropine can ↑ IOP in pts with glaucoma
CNS – sedation (receptors in the brain are excitatory), cycloplegia

No effects on blood vessels, or skeletal muscles (uses NAchR)
Parkinsons – imbalance between DA and ACh, so they’ll block muscarinic receptors and increase the DA [ ]

37
Q

Muscarinic antagonists: atropine

A

tertiary amine, lipophilic, CROSSES BBB

half-life: 4 hrs (10 hrs in elderly), eye effects last days

IV, IM, or opthalmic

Uses:
opthalmic, CV - for bradycardias, antidoe vs cholinergic agonists, preop - to inhibit secretions, adjunct for NMBD reversal

38
Q

Muscarinic antagonists: scopolamine

A

tertiary amine, CROSSES BBB, ++++CNS effects, such as amnesia and sedation

half-life: 1-4 hrs

onset: 10 minutes
duration: IV, 2 hrs

Transdermal patch, IV, or IM

Uses:
motion-sickness, PONV, preop - for amnesia, sedation, antiemetic, or to decrease secretions

39
Q

Muscarinic antagonists: glycopyrrulate

A

**quaternary amine, less CNS SEs. (charged, so won’t cross BBB)

half-life: 1 hr

onset: 1 min (IV)
duration: 7 hrs

IV, PO

Uses:
preop, cardiac dysrhythmias (vagal reflex association), and as an adjunct to reverse NMBD blockade

40
Q

anticholinergic mnemonic:

“Dry as a bone, hot as a pistol, red as a beet, blind as a bat, mad as a hatter”

A

Dry as a bone = urine retention

hot as a pistol, red as a beet = hyperthermic/no sweating

Mad = confusion/delirium from CNS effects

41
Q

antimuscarinic concerns

A

o Hyperthermia risk (esp. infants, children)
o Glaucoma – relative contraindication, esp. closed-angle (antimuscarinics ↑ IOP)
o GU obstruction
o Prostatic hypertrophy – relative contraindication
o CV – esp myocardial ischemia, HF, certain arrhythmias, HTN, etc.
o GI-ileus, ulcerative colitis, etc.

think about what muscarinic receptors do, then the opposite

42
Q

meds with anticholinergic activity

A

o Antihistamines (e.g., diphenhydramine, hydroxyzine)
o Antispasmodics
o Antiparkinson drugs (e.g., benztropine)
o Skeletal muscle relaxants
o Antipsychotics
o Antidepressants (e.g., tricyclic class) – replaced by SSRIs, sometimes they block adrenergic receptors too, “they’re just really dirty drugs”
o Antimuscarinics for urinary incontinence
o Note: elderly are especially susceptible to anticholinergic toxicity – often on (Beers?) list to avoid in elderly
- 1st gen antihistamines – Benadryl, _____,

43
Q

Nicotinic M antagonists: effects and clinical use

A

effects:
competitive antagonism at skeletal muscle
“non-depolarizing”

clinical uses include:
skeletal muscle relaxation for surgical, intubation, ventilation control

44
Q

Nicotinic N antagonists: effects and clinical use

A

effects:
blocks ganglionic output

uses:
historically used for HTN emergency

45
Q

endogenous catecholamines, and when they’re administered as drugs

A

Dopamine
Epinephrine
norepinephrine

o When catecholamines are administered as drugs:

  • Rapid onset
  • Brief duration (MAO, COMT metabolism)
  • No oral admin – why??
  • Poor CNS penetration– why??

o Most adrenergic drugs are NON-catecholamines:

  • Longer acting
  • Oral administration
46
Q

Ephedrine, pseudoephedrine - indirect or mixed action?

A

MIXED

  • Displaces/releases stored catecholamine NT
  • Some agonist activity - alpha and B- adrenergic receptors
  • Non-catecholamine – extended duration (won’t be readily metabolized)
  • Herbal source - ma huang
47
Q

amphetamine

A

 Displaces/ releases stored catecholamine NT
 Secondary–Inhibits catecholamine reuptake (NET, DAT)
 Uses in ADHD, narcolepsy, appetite suppression (not as much used for this anymore bc of potential for abuse)

48
Q

cocaine

A

 Blocks NE reuptake (inhibits NET & DAT transporters) into presynaptic neuron
 Blocks sodium channels – local anesthetic actions

49
Q

tyramine

A

 Displaces/releases stored catecholamines
 Not a drug, in fermented foods (red wine, aged cheese, pickled things); role in drug-food interactions of MAO inhibitors
-Can be taken up by storage vesicles and pushes NE out. And when they take MAOI inhibitors, can have massive NE response – hypertensive crisis

50
Q

indirect acting:

A

o Tricyclic antidepressants, serotonin-norepinephrine reuptake inhibitors
- Block NE reuptake (inhibits NET transporter)

51
Q

indirect acting:

A 
o	Monamine oxidase inhibitors (MAOIs) 
-	Prevents breakdown of catecholamines in presynaptic terminal— catecholamine accumulates in vesicles 
•	MAO-A – metabolizes NE 
•	MAO-B –metabolizes DA  
-	Nonselective – inhibits MAO-A & MAO-B 
•	Tranylcypromine, phenelzine, etc. 
	Selective MAO-B inhibitors 
•	Selegiline, rasagiline
52
Q

Adrenergic receptor agonists predominant effects, uses, adverse effects - alpha 1

A

• Vasoconstriction (skin/splanchnic beds)
• Smooth muscle
o contracts (except GI)
o Trophic effect - BPH
• GI/GU sphincters-contract
• Eye- mydriasis
My dry eyes DILATE with the radial muscle, uses alpha 1 receptors.

  • increases vasc tone, PVR (peripheral vasc resistance), BP, EYE - mydriasis (redness also disappears bc of vasoconstriction)
  • phenylephrine

Uses:
shock
(OTC) decongestant, opthalmic hyperemia

53
Q

Adrenergic receptor agonists predominant effects, uses, adverse effects - alpha 2

A
  • Decrease NE release (presynaptic) – mostly found pre-synaptic
  • CNS- inhibit sympathetic outflow from the brain to lower BP (clonidine)
  • Platelet aggregation
  • Pancreas- ↓ insulin
  • ↓ sympathetic outflow from brain
  • AE: in the brain, will have high degree of sedation bc decreasing NE which is stimulatory in the brain. So those drugs would be given at nighttime.

*clonidine

Uses:
HTN (central effects)

54
Q

Adrenergic receptor agonists predominant effects, uses, adverse effects - B1

A
  • ↑ HR, contractility
  • Effects on rhythm - AV node conduction force
  • Kidney – renin
  • Trophic effect- hypertrophy (another reason why we use B-blockers in CHF)

Uses:
acute CHF

55
Q

Adrenergic receptor agonists predominant effects, uses, adverse effects - B2

A
  • Bronchodilation
  • Vasodilation (esp skel m beds)
  • Most sm muscle - relaxes
  • Skeletal m contracts-tremor
    • Hypokalemia/Incr K+ uptake
  • GI/GU-relaxation
  • Uterine sm muscle relaxation
  • Glycogenolysis (raise BG)
  • Think about fight or flight responses

Uses:
asthma, COPD, preterm labor

AE: increased glucose, cardiac stimulation

56
Q

(NE vs. Epi vs. ISO) - NE

A

o NE will induce reflex bradycardia

  • Causes ↑ SBP and DBP bc of alpha activation
  • Increases peripheral vasc resistance

Receptors: a1, B1 (little effect on B2).
Use: shock

57
Q

(NE vs. Epi vs. ISO) - EPI

A
  • Increase HR – all alphas and betas
  • B2 receptors in skeletal muscle/liver – dilate - decreases DBP
  • Α1, partially B1 - increased SBP
  • Mix effects – net decrease in peripheral vasc resistance

ALL adrenergic receptors: a1, a2, B1, B2, B3
Low doses: B effects
High doses: alpha effects
Uses: anaphylaxis, use with local anesth’s (vasoconstricts locally, keeps LA in that area to extend DOA, and prevent systemic effects), cardiac arrest

58
Q

(NE vs. Epi vs. ISO) - ISO

A
  • Nonselective B-agonist - B1, B2
  • Increase force (B1) – increase SBP
  • vascular size – vasodilate (B2) – decrease DBP
  • Net decrease in peripheral vasc resistance

Use: acute asthma (obsolete), cardiac stimulant

59
Q

dexmedetomidine

A

“agonist that shuts off NE”
o Selective alpha2 receptor agonist – CNS actions
- Suppresses sympathetic NS activity
- Sedative effects (locus coeruleus); activates endogenous sleep pathways
- Analgesic effects (spinal cord)
- CV—infusion decrease HR (up to 42%), decrease SVR, hypotension (up to 56%); transient HTN (28%) with bolus dose; bradycardia may be significant (fatal cases reported); elderly may be more sensitive
- Respiratory—less decrease in resp rate; some decr in tidal vol; some resp flr
- Tolerance, tachyphylaxis, withdrawal symptoms
- Uses include ICU sedation, premed, adjunct to general anesthesia (decreases dose requirements)

60
Q

• Adrenergic Agonists Some potential concerns

A

o CV disease
o Cerebrovascular disease
o Other vasoconstriction related
o Diabetes (incr blood glucose)
o IV extravasation risks
o Thyroid disease – general SNS stimulation
o *depending on receptor activity profile of drug

61
Q

beta receptor antagonists effects, clinical SEs, adverse effects

A

decreased HR/force of contraction, renin release by kidneys, anti-dysrhythmic effects (some)

Uses:
HTN, angina, MI, arrhythmia, thyrotoxicosis, CHF (only for chronic and stable, and only select agents. Decreases morbidity and mortality)

Other uses: infantile hemangioma, glaucoma topical, migraine prophylaxis/anxiety - propanolol

AEs:
R- bronchoconstriction
CV - bradycardia
CNS - sedation 
decreased sexual fn
DM - nonselective blocks B2 response of glycogenolysis, and blocks typical sx's of hypoglycemia (tachycardia and anxiety)
62
Q

Comparison of AChE inhibitors: edrophonium

chemical structure
onset, DOA, dose

A

only alcohol chemical structure of the 3. Quaternary amine, VERY polar (won’t cross BBB).

reversible blockade
IV, IM

Use: reversal of nondepolarizing block

Onset 30-60 sec, DOA 10 minutes

Dosage 1-1.5 mg/kg (from pharm 1)

63
Q

Comparison of AChE inhibitors: neostigmine

chemical structure
onset, DOA, dose

A

carbamate, quaternary amine, moderately polar (won’t cross BBB).

Hydrolyzed by AChE; labile covalent bond

IV, “orally active”
Use: reversal of nondepolarizing block

Onset 10-30 minutes, DOA 2-4 hours

64
Q

Comparison of AChE inhibitors: physostigmine

chemical structure
onset, DOA, dose

A

carbamate, tertiary amine**
(Crosses BBB!)

Hydrolyzed by AChE; labile covalent bond

PO, IM, IV
use for tx of anticholinergic toxicity

Onset 3-8 minutes, DOA 1 hr

65
Q

DBA receptor/use

A

B1 primarily

use: acute HF

66
Q

MYDRIASIS

A

My dry eyes DILATE - SNS response - iris radial muscle - alpha 1 ARs

alpha 1 AR also causes ciliary eye muscle to constrict

67
Q

MIOSIS

A

My, OH the circle CONSTRICTs, sis - PSNS response -iris circular - M3 muscarinic

M3 also causes ciliary eye muscle to accommodate for “near vision”

68
Q

ejaculation

A

“AAAAH - alpha 1”

SNS - alpha 1 receptor

69
Q

erection

A

PSNS - M3 (if not CNS or heart, is going to be the M3 muscarinic receptor)

70
Q

B3 cells cause

A

glycolysis (glucose broken down into pyruvate/pyruvic acid)

71
Q

ciliary body - SNS and PSNS effects

A

SNS - ↑ IOP by ↑ secretion of aqueous humor, B2 receptors

PSNS - ↓ IOP by ↑ outflow of aqueous humor (unknown receptor)

Angeli - N929 Pharmacology (12 decks)

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