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Foundations 2 > Drug List and Metabolism > Flashcards

Drug List and Metabolism Flashcards

1
Q

Neuromuscular Agents (categories)

A

Presynaptic drugs, toxins and venoms

Postsynaptic agents

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2
Q

Presynaptic drugs, toxins and venoms

A

Tetrodotoxin (TTX)

Mg2+ and other polyvalent cations

Botulinum Toxin Type A

Black Widow Spider Venom (latrotoxin)

Aminoglycoside antibiotics (side effect)

Hemicholinium

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3
Q

Postsynaptic agents (categories)

A

(1) Non-depolarizing blockers
(2) Depolarizing blockers
(3) Indirect-acting stimulants (anticholinesterases)
(4) Anticholinesterase antagonists
(5) Other peripherally-acting muscle relaxants

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4
Q

Non-depolarizing blockers

A

Tubocurarine

Pancuronium (PavulonR)

Vecuronium (NorcuronR)

Atracurium (TracriumR)

Cisatracurium (NimbexR)

Rocuronium (ZemuronR)

Agents with__curonium and _curium suffixes

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5
Q

Depolarizing blockers

A

Acetylcholine

Succinylcholine (AnectineR)

Nicotine

Carbachol

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6
Q

Indirect-acting stimulants (anticholinesterases)

A

Edrophonium (TensilonR)

Neostigmine (ProstigmineR)

Physostigmine (EserineR)

Pyridostigmine (MestinonR)

DFP (Diisopropylphosphorofluoridate)

Parathion

Malathion

Sarin

Ambenonium (MytelaseR)

Ecothiophate (PhospholineR)

VX

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7
Q

Anticholinesterase antagonists

A

oximes such as: Pralidoxime (2-PAMR ,ProtopamR)

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8
Q

Other peripherally-acting muscle relaxants

A

Dantrolene

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9
Q

Autonomic Agents - Cholinergic (categories)

A

Parasympathomimetics-direct action on Muscarinic Receptors

Parasympathomimetics: indirect-acting

Parasympathetic antagonists (anti-muscarinics)

Ganglionic blockers

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10
Q

Parasympathomimetics-direct action on Muscarinic Receptors

A

Acetylcholine

Methacholine

Bethanechol (UrecholineR)

Pilocarpine

Cevimeline (EvoxacR)

Carbachol

Muscarine

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11
Q

Parasympathetic antagonists (anti-muscarinics)

A

Atropine (and Homatropine)

Airways:

Ipratropium (AtroventR)

Tiotropium (SpirivaR)

Overactive bladder:

Tolterodine (DetrolR)

Fesoterodine (ToviazR)

Oxybutynin (DitropanR)

Solifenacin (VESIcareR)

Darifenacin (EnablexR)

Ocular:

Tropicamide (MydriacilR)

Cyclopentolate (CyclogylR)

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12
Q

Depolarizing ganglionic blockers

A

acetylcholine

nicotine

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13
Q

Direct acting Adrenergic receptor agonists (categories)

A

Non-selective prototypes

‘Selective’ α1 agonists

‘Selective’ α2 agonists

‘Selective’ β1 agonist

‘Selective’ β2 agonists

Dopamine receptor agonists

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14
Q

Non-selective prototypes

A

Norepinephrine

Epinephrine

Isoproterenol (IsoprenalineR, IsuprelR)

Dopamine (InotropinR)

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15
Q

‘Selective’ α1 agonists

A

Phenylephrine (NeosynephrineR)

Imidazolines such as: Oxymetazoline (AfrinR) Xylometazoline

Midodrine

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16
Q

‘Selective’ α2 agonists’

A

Clonidine (CatapresR)

α-Methyldopa (AldometR)

Guanfacine (TenexR)

Guanabenz (WytensinR)

Apraclonidine (IopidineR)

Brimonidine (AlphaganR)

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17
Q

‘Selective’ β1 agonist

A

Dobutamine (DobutrexR)

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18
Q

‘Selective’ β2 agonists

A

Albuterol (VentolinR)

Terbutaline (BrethineR)

Ritodrine (YutoparR)

Salmeterol (SereventR)

Formoterol (ForadilR)

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19
Q

Dopamine receptor agonists

A

Dopamine (IntropinR)

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20
Q

Autonomic Agents – Adrenergic (categories)

A

Direct acting receptor agonists

Indirect-acting sympathomimetic amines

Mixed (direct and indirect) acting sympathomimetic amines

Adrenergic receptor antagonists

Phosphodiesterase (PDE) inhibitors

Prostaglandin analogues

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21
Q

Indirect-acting sympathomimetic amines

A

Tyramine

Amphetamines

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22
Q

Mixed (direct and indirect) acting sympathomimetic amines

A

Ephedrine-Pseudoephedrine (SudafedR)

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23
Q

Adrenergic receptor antagonists (categories)

A

Non-selective α blockers

α1 blockers

α2 blocker

Non-selective β blockers

β1 blockers

β2 blocker

α+ β blockers

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24
Q

Non-selective α blockers

A

Phenoxybenzamine (DibenzylineR)

Phentolamine (RegitineR)

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25
Q

α1 blockers

A

Prazosin (MinipressR)

Tamsulosin (Flomax)

Alfuzosin (UroXatralR)

Silodosin (RapafloR)

any other agents with an azosin suffix e.g. Terazosin (HytrinR), Doxazosin (CarduraR)

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26
Q

α2 blocker

A

Yohimbine (YohimexR)

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27
Q

Non-selective β blockers

A

Propranolol (InderalR)

Timolol (TimopticR)

various other agents ending in a vowel + lol (e.g. Nadolol, Alprenolol, Pindolol)

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28
Q

β1 blockers

A

Metoprolol (LopressorR)

Betaxolol (BetopticR)

Atenolol (TenorminR)

Esmolol (BreviblocR)

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29
Q

α+ β blockers

A

Labetalol (NormodyneR)

Carvedilol (CoregR)

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30
Q

Phosphodiesterase (PDE) inhibitors

A

Sildenafil (ViagraR)

Other ___afils such as Vardenafil (LevitraR),Tadalafil (CialisR) caffeine, theophylline and other _phyllines (generally better as adenosine receptor blockers than PDE inhibitors)

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31
Q

Prostaglandin analogues

A

Lananoprost (XalatanR) and other __oprosts such as Bimatoprost (LatisseR ) (These are PGF2a analogs)

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32
Q

Tetrodotoxin (TTX)

A

Presynaptic Blocking Agent Blocks Na+ channels in nerve terminals and in skeletal muscle responsible for AP upstroke

Puffer fish toxin

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33
Q

Mg2+, polyvalent cations

A

Presynaptic Blocking Agent Compete with Ca2+ at the external mouth of the Ca2+ channel

Reduces neurally-evoked ACh release, normal MEPPs, low EPPs

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34
Q

Aminoglycosides

A

Presynaptic Blocking Agent

Reduce Ca2+ entry through Ca2+ channels DO NOT USE WITH MG PTS – COULD KILL!!

Reduce ACh release, normal MEPPs, low EPPs (neomycin> kanamycin > amikacin > gentamicin > tobramycin)

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35
Q

Black Widow Spider Venom (alpha-latrotoxin)

A

Presynaptic Blocking Agent Forms Ca2+ channels in the membrane causing an asynchronous barrage of MEPPs and increased exocytosis of Ach

this is followed by a lack of vesicles &amp

increased of surface area of nerve terminal (overall effect: transmission block)

Fasciculations followed by dead post-synaptic membrane

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36
Q

Hemicholinium-3

A

Presynaptic Blocking Agent

Competitively inhibits uptake of choline via the choline transporter (thus inhibiting the synthesis of Ach)

MEPPs are extremely small, but sensitivity of muscle to Ach is normal

just smaller amount of Ach in the vesicles than usual

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37
Q

Tubocurarine

A

Postsynaptic Non-Depolarizing Blocker

Competitive inhibitor of Ach at nicotinic receptors, surmountable by increasing [Ach], Ach-like with stabilizing ring structure. Category prototype but obsolete clinically (except for So. American Indians)

RENAL clearance mostly (also in bile)

All neuromuscular blockers are used for: duration of sx’s muscle relaxation, initial phases of endotracheal intubation (masseter & lateral cricoarytenoid muscles), diagnostic procedures (-scopys)

Side Effects: 1. Histamine release (vasodilatation), 2. Ganglionic block @ higher doses (anti-hypertensives) -> fall in blood pressure

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38
Q

Pancuronium (Pavulon)

A

Postsynaptic Non-Depolarizing Blocker

2 AChs attached to steroid nucleus, favors non-depolarizing competitive inhibition, selective for neuromuscular junction

RENAL clearance

Pancuronium produces MG-like effects, DO NOT use with aminoglycosides (could kill pt)

Not used at NMH (might still be used in community hospitals & death row (cheap drug), long duration of action ~1 hr, 5-10X more potent than tubocurarine, no histamine release, minimal ganglionic block

Side effect: blocks parasympathetic vagal tone, causing tachycardia

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39
Q

Vecuronium (Norcuron)

A

Postsynaptic Non-Depolarizing Blocker

Same as pancuronium w/o a methyl grp

monoquaternary 85% BILIARY clearance 15% RENAL clearance

intermediate duration of action 30-40 min

no vagal block/tachycardia, no histamine release, devoid of CV effects

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40
Q

Atracurium (Tracrium)

A

Postsynaptic Non-Depolarizing Blocker

Prototype benzylisoquinolinium (benzyl + isoquino + Ach-like)

HOFFMAN ELIMINATION in plasma, rapid non-enzymatic dequaternization, pH/temp-dependent and by plasma esterases and ubiquitous carboxylases

NOT ELIMINATED BY KIDNEY or LIVER

Intermediate duration of action 20-30 min

no vagal block, no ganglionic block

Side Effects: some histamine release, may produce laudanosine in isomer mixture that causes seizures

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41
Q

Cisatracurium (Nimbex)

A

Postsynaptic Non-Depolarizing Blocker

Properties similar to atracurium, but is only one stereoisomer rather than 10 stereoisomers

Atracurium side effects minimized

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42
Q

Rocuronium (Zemuron)

A

Postsynaptic Non-Depolarizing Blocker

~~“very fast vecuronium”

Essentially 100% BILIARY clearance

Rapid onset, intermediate duration, no histamine release, very popular for intubation

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43
Q

Acetylcholine (Ach)

A

Postsynaptic Depolarizing Blocker

Nicotinic receptor agonists in exogenously high concentrations can block transmission

Ganglionic Blockers – Depolarizing:

@ high []s, PI-PII Block as in NMJ

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44
Q

Succinylcholine (SUX)

A

Postsynaptic Depolarizing Blocker

Nicotinic receptor agonist SUX = 2 Ach, hydrolyzed by ChE in 2 steps when used for long periods of time, can cause sustained depolarization and densensitization of nicotinic receptor/Na+ channel

RAPIDLY REVERSIBLE DO NOT USE FOR THE DURATION OF SURGICAL PROCEDURE – muscle damage caused by enormous fasiculations and continued release of pain producing substances (prostaglandins, potassium, ATP, etc) – remember story of 17 yo girl 1 wk of pain post-op rape accusation

Easy to control duration & intensity of effects; short duration & rapid onset (large doses can be used), used for early anesthesia & intubation to produce rapid by brief periods of block (generally Phase I); Fastest-acting for intubation, lasts increased serum K+ & CV collapse, arrhythmias, liver disease or

genetic ChE deficiency -> prolonged apnea due to Phase II block requires respirator HYDROLYZED in two stages by plasma CHE (Phase I, Hydrolysis)

45
Q

Nicotine

A

Postsynaptic Depolarizing Blocker Depolarizing blocker at neuromuscular junction, discussed later in CNS section PI-PII block

46
Q

Carbachol

A

Postsynaptic Depolarizing Blocker Nicotinic and muscarinic agonist

47
Q

Neostigmine (Prostigmine)

A

Indirect-acting Stimulants (anticholinesterases) / Parasympathomimetics – indirect-acting

Quaternary (no CNS effects), prevent degradation of Ach by binding to cholinesterase 2-4 hr duration, oral/parenteral @ skeletal NMJ: Treat MG patients, reverse residual non-depolarizing block after surgery

Autonomic: like pilocarpine – miotic & glaucoma tx; like bethanechol – tx for urinary retention and GI stasis

FYI Drug Metabolism: HYDROLYZED SLOWLY BY CHE (Phase I, Hydrolysis) and then Phase II glucuronide)

48
Q

Edrophonium (Tensilon)

A

Indirect-acting Stimulants (anticholinesterases) / Parasympathomimetics – indirect-acting

Short-acting, rapid onset Reversible anticholinesterases are hydrolyzed by liver cholinesterase

Quaternary agents have direct stimulatory action on the Ach receptor in addition to inhibiting cholinesterase

Test for MG –if injection causes pt to perk up briefly then MG (shown in “House” clip), else no effect and probably cholinergic crisis

Same contraindications as bethanechol

49
Q

Physostigmine (Eserine)

A

Indirect-acting Stimulants (anticholinesterases) / Parasympathomimetics – indirect-acting

Tertiary amine, can cross BBB, duration 1-2 hrs, oral/parenteral

In Calibar or ordeal bean-muscarinic control of emesis (if fast ingestion), death (if slow ingestion)

Used for glaucoma therapy (topically), antidote for atropine toxicity!! (the salicylate salt is known as Antilirium)

50
Q

Pyridostigmine Bromide (PB) (Mestinon)

A

Indirect-acting Stimulants (anticholinesterases) / Parasympathomimetics – indirect-acting

Same as neostigmine except slow release form has long-lasting 4-12 hr oral effect (useful @ bedtime)Most popular to treat MG

was given as a pretreatment in Persian Gulf war troops (doesn’t work with Sarin, made it worse!)

51
Q

DFP (Diisopropylphosphorofluoridate)

A

Indirect-acting Stimulants (anticholinesterases) / Parasympathomimetics – indirect-acting Irreversible anticholinesterase

phosphorylates esteratic site > 6 hrs, oily liquid well absorbed by every route, including skin. Effects similar to physostigmine Enzyme is stuck in phosphorylated state-resynthesis of the enzyme is necessary

52
Q

Sarin

A

Indirect-acting Stimulants (anticholinesterases) / Parasympathomimetics – indirect-acting

“weteye,” GB Examples of Japanese subway attack, US soldiers in Gulf War, Syria in 2013

53
Q

Parathion

A

Indirect-acting Stimulants (anticholinesterases) / Parasympathomimetics – indirect-acting

metabolized into paraoxon the toxic form that inhibits ChE Agricultural insecticide, Example of methyl derivative sprayed indoors in Chicago homes causing an environmental nightmare

FYI: CYP3A4 metabolizes parathion into paraoxon

54
Q

Malathion

A

Indirect-acting Stimulants (anticholinesterases) / Parasympathomimetics – indirect-acting

higher animals can metabolize drug faster than parathion; some selectivity towards insects Slightly safer than parathion as birds and mammals (but not fish) have carboxylase to inactivate. Examples of Medflies, spraying in suburban areas Tx use: in Prioderm lotion for head lice

55
Q

Oximes (Pralidoxime: 2-PAM/Protopam)

A

Anticholinesterase Antagonists

Enzyme reactivation, binds anionic site, lifts phosphorylated residue off esteric site

reverses skeletal muscle effects w/relief within 1-2 min

Antidote for anticholinesterase attack (SLUD syndrome)

56
Q

Dantrolene

A

Other Peripheral Muscle Relaxants

Blocks Ca2+ release from SR To treat malignant hyperthermia (such as caused by SUX)

57
Q

Acetylcholine

A

Parasympathomimetic – Direct

mimics parasympathetic stimulation by acting upon muscarinic receptors @ parasympathetic targets as well as sympathetic cholinergic targets (eccrine sweat glands), accommodation

CARDIAC:

  • SA node: 1) increased K+ current (via βγ subunits of G protein 2) inhibits If 3) inhibits L-type Ca2+ currents
  • AV node: increased gk and conductance, decreased BP -> vasodilatation via receptors on endothelium -> EDRF (NO) -> increased GMP in smooth muscle cells -> relaxation

Has 2 “faces” – muscarinic 4.4 A, nicotinic 5.9 A Non-specific, rapid hydrolysis, not used clinically

58
Q

Methacholine

A

Parasympathomimetic – Direct

Specific for muscarinic receptors, no hydrolysis by ChE but hydrolyzed slowly by AChE

Methacholine challenge test for bronchial asthma (no effect on normal people, intense bronchoconstriction & decreased vital capacity in asthmatics)

59
Q

Bethanechol (Urecholine)

A

Parasympathomimetic – Direct

Specific for muscarinic receptors, resistant to hydrolysis by esterases

Used for GI tract treatment of surgery/med-induced low bowel tone “adynamic ileus” to restore peristalsis

Also for treatment of urinary retention

Contraindications: IV/IM – could produce shock (like Ach+neostigmine), asthmatics, hyperthyroid b/c susceptible to arrhythmias, peptic ulcers, intestinal/bladder obstruction

60
Q

Pilocarpine

A

Parasympathomimetic – Direct

Tertiary amine w/4.4A selectivity for muscarinic receptors, not hydrolyzed by cholinesterases

Narrow angle: contracts circular muscle fibers, pulls iris toward center of eye & uncrowds angle

Open angle: improves trabecular tone by contracting circular and ciliary muscles, opening pores & increasing AH outflow

Tx of open angle glaucoma w/Ocusert 3rd line drug, for surgery of narrow angle glaucoma, pilocarpine is used as pretreatment along with anti-cholinesterase, acetazolamide/methazolamide/dichlorphenamide (carbonic anhydrase inhibitors inhibit AH synthesis), and mannitol/glycerol (osmotically decreases AH)

61
Q

Cevimeline (Evoxac)

A

Parasympathomimetic – Direct Muscarinic agonist

used orally to treat Sjogren’s syndrome (currently preferred to pilocarpine)

FYI:Metabolism: CYP3A4 and CYP 2D6 (Phase I)

62
Q

Non-depolarizing ganglionic blockers

A

Trimethaphan (ArfonadR) Mecamylamine (InversineR) Tubocurarine

63
Q

β2 blocker

A

Butoxamine (you are not responsible for this; it is just to let you know that such a drug exists)

64
Q

Atropine (Hyoscyamine, Levsin, Levbid, Nulev)

A

Parasympathetic Antagonists

MUSCARINIC RECEPTOR BLOCKER Alkaloid from Atropa belladonna prototype, competitive inhibitor of Ach at muscarinic receptors

tertiary TOXICITIES (Jimson Weed):

  • DRY as a bone - decreased secretions, urinary retention
  • HOT as a stove - increased body temp by decreased eccrine sweating
  • RED as a beet – histamine release -> cut. Vasodil.
  • BLIND as a bat – mydriasis and cycloplegia
  • MAD as a hatter – delirium, hallucinations
  • …eventually coma and death

Effects, uses, and contraindications: predictable from ANS effects (oppose parasympathetics, produce sympathetic effects) – mydriasis and cycloplegia,** **bronchiolar tx of COPD and asthma, GI and urinary colic, block secretions (respiratory, acid, adjunct to surgery by blocking autonomic effects of neostigmine), increases HR during stage 2 and spinal anesthesia, antidote for anti-ChE poisoning, Parkinsonism (as an adjunct to L-dopa) Tx of toxicities – emesis, gastric lavage, activated charcoal ANTIDOTE for severe neuro effects: salicylate salt of PHYSOSTIGMINE (aka ANTILIRIUM)

65
Q

Homatropine (Novatran) / Eucatropine (Euphthalmine)

A

Parasympathetic Antagonists MUSCARINIC RECEPTOR BLOCKER

Shorter duration of action Drug of choice at NU for ciliary spasm due to injury

66
Q

Scopolamine (1-hyoscine)

A

Parasympathetic Antagonists MUSCARINIC RECEPTOR BLOCKER

Similar to atropine, w/more CNS depressant effects @ usual therapeutic doses

Remember muscarinic blockers produce anti-emesis via vestibular nucleus and vomiting center, sedation via basal forebrain and mesopontine nuclei, amnesia via septo-hippocampal projection Tx of motion sickness

Previously used for “twilight sleep” during labor

67
Q

Tolterodine (Detrol)

A

Parasympathetic Antagonists MUSCARINIC RECEPTOR BLOCKER

Active by itself but also metabolized to another active drug-5-OHmethyltolterodine by CYP2D6

Tx of overactive bladder (OAB) and bladder spasms / urinary incontinence and enuresis, reduced sedation, and dry mouth

Contraindications: urinary retention, GI retention, narrow-angle glaucoma

FYI Metabolism: Phase I via CYP3A4, Phase II by glucuronide

68
Q

Fesoterodine (Toviaz)

A

Parasympathetic Antagonists MUSCARINIC RECEPTOR BLOCKER

INACTIVE by itself but metabolized to same active drug 5-OHmethyltolterodine as tolterodine but by non specific esterases

Tx OAB and bladder spasm glaucoma

FYI Metabolism: active metabolite further metabolized by Phase I via CYP3A4and CYP2D6, Phase II by glucuronide

69
Q

Solifenacin (Vesicare)

A

Parasympathetic Antagonists MUSCARINIC RECEPTOR BLOCKER

Superior to tolterodine

Tx OAB and bladder spasms

FYI Metabolism for _fenacins: Phase I via CYP3A4 and CYP2D6, Phase II by glucuronide

70
Q

Darifenacin (Enablex)

A

Parasympathetic Antagonists MUSCARINIC RECEPTOR BLOCKER

Tx for bladder spasms

71
Q

Oxybutynin (Ditropan)

A

Parasympathetic Antagonists MUSCARINIC RECEPTOR BLOCKER

Just another uninteresting drug to treat OAB and bladder spasms

72
Q

Tropicamide (Mydriacyl)

A

Parasympathetic Antagonists MUSCARINIC RECEPTOR BLOCKER

Ocular effects (b/c atropine is too long-lasting) For older patients

73
Q

Ipratropium (Atrovent)

A

Parasympathetic Antagonists MUSCARINIC RECEPTOR BLOCKER

Quaternary (also blocks ganglia), effective bronchiolar dilation w/o impairing mucociliary clearance – muscarinic receptors are located in larger, more centrally-located airways while

2 adrenoreceptors are located in fine branchelets of the bronchioles 1st line tx for COPD

M1 and M2!

74
Q

Tiotropium (Spiriva)

A

Parasympathetic Antagonists

MUSCARINIC RECEPTOR BLOCKER In the bronchioles, there are presynaptic inhibitory M2 autoreceptors as well as postsynaptic M1s. Blocking M2 inhibitory synapses will increase Ach release (defeating the purpose of muscarnic block). Tiotropium blocks only M1s; Ipratropium blocks both M1s and M2s so not as effective Superior to ipatropium for COPD tx

75
Q

Norepinephrine (Levophed)

A

Non-selective Autonomic Adrenergic Receptor Agonist - Direct-acting

Orally ineffective, poor absorption from SQ, usually given by IV but quickly inactivated

Good stimulant of alpha & beta1, essentially no beta2

For tx of severe hypotension in ICU (only clinical use of NE)

76
Q

Ephinephrine

A

Non-selective Autonomic Adrenergic Receptor Agonist - Direct-acting

Oral absorption satisfactory, but metabolized by MAO by gut/liver, so oral EPI has little effect

Good stimulant of alpha, beta1, & beta2

EPI inhaler for asthma attacks, intracardiac EPI is useful for cardiac arrest (for both alpha & beta1 vasoconstriction + cardiac stimulatory effects to increase perfusion), to treat anaphylactic shock-see the antihistamine lecture

77
Q

Isoproterenol (Isoprenaline, Isuprel)

A

Non-selective Autonomic Adrenergic Receptor Agonist - Direct-acting

Poor substrate for MAO so longer-acting Good stimulant of beta1 & beta2, essentially no alpha

Inhaler for asthma attack, but not selective

78
Q

Dopamine (Inotropin)

A

Non-selective Autonomic Adrenergic Receptor Agonist - Direct-acting

Low dose increases cardiac output; high dose may cause tachycardia & vasoconstriction

Direct vasodilator effect to relieve oliguria Also used for cardiogenic shock if systolics <80

79
Q

Phenylephrine

A

‘Selective’ alpha1 Agonist

Identical to EPI minus 4-OH (resistant to COMT for longer duration of action), selective but not very potent (need high doses), little effect on myocardium “get the red out” vasoconstrictor mechanism or nasal decongestants, also marketed for pupillary dilation

FYI: MAO metabolism

80
Q

Imidazolines (Naphazoline, Tetrahydrozoline, Oxymetazoline)

A

‘Selective’ alpha1 Agonist

5-membered rings, not catechol or amine. Long-acting because not substrates for MAO or COMT, @ low doses alpha1 agonists, @ high doses alpha2 agonists

Nasal spray or eye drops May cause severe depressant effects in kids! alpha2 constriction can cause structural damage to nasal mucosa due to loss of blood flow

FYI Metabolism: Phase I via CYP2D6

81
Q

Midodrine

A

‘Selective’ alpha1 Agonist

Metabolized by unknown peptidase to desglymidodrine, alpha1 constriction, increased BP in severe liver or kidney disease, occasionally used for postural hypotension

FYI Metabolism: Phase I via CYP2C19, Phase II by glucuronide

82
Q

Clonidine (Catapres)

A

‘Selective’ alpha2 Agonist

Reduces sympathetic tone in medulla & hypothalamus, decreasing sympathetic activity from CNS to periphery @ higher doses -> stimulate peripheral post-syn alpha2 receptors w/initial vasoconstriction decreased HR & decreased TPR (decreased NE)

Used in past as anti-hypertensive, with diuretic/direct vasodilator

CLONIDINE SUPPRESSION TEST: distinguish essential Htn from pheochromocytoma

Abrupt discontinuation – risk of rebound Htn

Side effects: sedation, constipation, sexual dysfxn

FYI: Metabolism:excreted largely unchanged in urine

83
Q

alpha-methyldopa (Aldomet)

A

‘Selective’ alpha2 Agonist

Produces alpha methyl NE that acts as an alpha2 agonist

An anti-hypertensive of choice for pregnancy (but not at NMH)

FYI: Metabolism: metabolized by Sulfation.

84
Q

Apraclonidine (Iodpidine) & Brimonidine (Alphagan)

A

‘Selective’ alpha2 Agonist

Inhibit secretion of AH 2nd line drug for stubborn glaucoma (remember pilocarpine is 3rd line drug)

85
Q

Dobutamine (Dobutrex)

A

‘Selective’ beta1 Agonist

Catecholamine that looks like dopamine w/bulky grp on N atom. increased Cardiac contraction w/minimal effect on HR

@ low []s mechanism complex-see Katzung for details. Useful for CHF or cardiogenic shock to increased CO, can also be used as chemical agent for stress echo Initial agent of choice for systolic >80mmHg; for MI when you don’t want alpha1 effects

FYI Metabolism: via COMT

86
Q

Albuterol (Ventolin)

A

‘Selective’ beta2 Agonist

Prototype, most selective

Rescue inhaler

FYI: Metabolism: Phase II Sulfation

87
Q

Terbutaline (Brethine)

A

‘Selective’ beta2 Agonist

Resorcinol w/more selectivity, only one available for parenteral & oral use

‘TERB’ - Successful bronchodilator (orally) -> poor MAO substrate

Uterine relaxation during premature labor @ NU

FYI Metabolism: Phase II Sulfation as described in the Drug Metabolism lectures

88
Q

Ritodrine (Yutopar)

A

‘Selective’ beta2 Agonist

Not very selective

Highly popularized in media, only one currently approved for prevention/delay of premature labor

Potential for serious metabolic/CV effects (fetal and maternal HR), Not used at NMH

FYI Metabolism: Phase II Sulfation

89
Q

Salmeterol (Serevent) & Formoterol (Foradil)

A

‘Selective’ beta2 Agonist

As selective as albuterol but long-lasting (12+ hours, inhaler), not as rapid onset

Do not use alone -> caused deaths in asthmatics! Used in combination with corticosteroids

FYI Metabolism: Phase I CYP3A4

90
Q

Dopamine (Intropin)

A

Dopamine Receptor Agonist

increased CO beta1 effect, some increased HR, dilate renal beds via D1 dopamine receptors, vasoconstrictive alpha1 effects

@ high doses Systolics <80 mmHg, oliguria (but tachycardia & increased TPR may worsen myocardial ischemia)

91
Q

Tyramine

A

Sympathomimetic Amine – Indirect

Enters nerve terminal via Uptake 1, displacing NE (increased release of NE), degraded by MAO

Found in aged cheese, ripe fruit, processed meat, etc. Tachyphylaxis, inhibitors of uptake can block effects

MAO inhibitors like Phenylzine (Nardil) can potentiate & produce hypertensive crisis Uptake 1 inhibitors: cocaine, tricyclic antidepressants, methylphenidate Metabolism: MAO

92
Q

Amphetamines

A

Sympathomimetic Amine – Indirect

Release of biogenic amines (NE, dopamine, serotonin) from nerve endings Tachyphylaxis, inhibitors of uptake can block effects,

FYI Metabolism: Phase I via CYP2D6, Phase II by glucuronide. MAO inhibitors like Phenylzine (Nardil) can potentiate

93
Q

Ephedrine-Pseudoephedrine (Sudafed)

A

Sympathomimetic Amine – Mixed Direct

agonist on alpha & beta receptors (esp. beta2), indirect release of NE from nerve terminals; resistant to COMT & MAO

“oral EPI,” less potent than EPI, CNS stimulant effect, tolerance develops (tachyphylaxis), long duration OTC nasal decongestants (alpha1) OTC anti-asthma preps (beta2)

Toxicity: peripheral vasoconstriction, cardiac stimulation, CNS (nervousness, anxiety, tremor, irritability, insomnia)

@ very high doses -> HTN (possibly leading to stroke), tachycardia, nausea & vomiting, fever, psychosis, respiratory depression, convulsions, & coma

FYI Metabolism: as much as 74% unchanged in urine , some (unknown) CYP mediated N-dealkylation

94
Q

Phenoxybenzamine (Dibenzyline)

A

Non-selective alpha Blocker

Has some selectivity for alpha1; irreversibly alkylates receptors, decreased BP

Used to manage pheochromocytoma, tx of sexual dysfunction (increased NO, mediator of NANC release),

95
Q

Phentolamine (Reglitine)

A

Non-selective alpha Blocker

alpha1 = alpha2 selectivity; short-acting, competitive; v. good against circulating catecholamines Used to test for pheochromocytoma (decreased BP if injected), but less useful than testing urinary metabolites

tx of sexual dysfunction (but must be injected into the corpus cavernosum—ouch…also nonselective & causes priapism due to blocking detumescence so phenylephrine is needed)

Drug of choice for hypertensive crisis induced by tyramine + MAOI

96
Q

The ___azosins Prazosin (Minipress), also Terazosin Doxazosin & Trimazosin

A

alpha1 Blocker

All are non-selective alpha1 blockers - decreased BP w/o persistent tachycardia, decreased urinary outflow resistance in bladder neck, prostate, & urethra Rare use for Htn (combine with diuretic + beta blocker for moderate htn)

Also used to treat BPH, but not really used anymore because of severe orthostatic hypotension (block of alpha1B on blood vessels FYI Metabolism: Phase I via CYP3A4, Phase II by glucuronide

97
Q

Tamsulosin (Flomax), Alfuzosin (Uroxatral), Silodosin

A

alpha1 Blocker

Selective alpha1A antagonists Very useful treatment for BPH

FYI Metabolism: Phase I via CYP3A4, Phase II by glucuronide (silodosin also uses CYP2D6)

98
Q

Yohimibine (Yohimex)

A

alpha2 Blocker

Disinhibition of synaptic transmission – similar effects as nerve stimulation -> persistent tachycardia, increased GI motility

Popular in drug culture b/c of CNS stimulatory effects + aphrodisiac quality; used to treat impotence in diabetics (decreased inhibition of presyn relaxation -> increased release of NANC -> increased vasodilation

99
Q

Propanolol (Inderal)

A

Non-selective beta Blocker

Prototype blocker of cardiac beta1 receptors: decreased HR, decreased CO, generally less or no change in BP after prolonged use

Main currently accepted mechanism as an antihypertensive is a block of renin release (recall rennin produces Angiotensin II, which is one of the most potent vasoconstrictors) Anti-arrythmic, anti-anginal, antihypertensive, pheochromocytoma (+ phenoxybenzamine), stage fright, prophylaxis of migraines.

Contraindications: asthmatics, diabetics (masks signs of severe hypoglycemia & decreased glycogenolysis), in past, disorders in which cardiac contractility is depressed. Now this drug category useful to treat heart failure.

Side effects: fainting lightheadedness, fatigue

Metabolism: Phase I via CYP2D6 and CYP2C19, Phase II by sulfation or glucuronide

100
Q

Timolol (Timoptic)

A

Non-selective beta Blocker

Decreases secretion of aqueous humor by ciliary body

Useful to treat all forms of glaucoma, better than pilocarpine b/c no cyclospams, miosis, or impaired vision

Metabolism: Phase I via CYP2D6

101
Q

Metoprolol (Lopressor)

A

beta1 Blocker

Equipotent w/propanolol for cardiac arrhythmias, htn, & angina “propanolol for asthmatics”

Metabolism: Phase I via CYP2D6 – important!

102
Q

Betaxolol (Betoptic)

A

beta1 Blocker

Can be used in place of timolol to treat glaucoma in pts with airway disease “timolol for asthmatics”

Metabolism: Phase I via CYP2D6

103
Q

Atenolol (Tenormin)

A

beta1 Blocker

Was very popularly prescribed, now very much out of favor (little to no metabolism)

104
Q

Esmolol (Brevibloc)

A

beta1 Blocker

Short duration of action (hydrolyzed by esterases)

Metabolism: plasma esterases (Phase I)

105
Q

Labetalol (Normodyne, Trandate)

A

alpha1 + beta Blocker

Blocks the pressor amines at alpha1 (increased TPR) & beta1 (increasedHR)

Treatment of hypertensive crisis & pheochromocytoma. The current drug of choice for hypertension during pregnancy.

Metabolism: only Phase II via glucuronide demonstrated

106
Q

Carvedilol (Coreg)

A

alpha1 + beta Blocker

alpha block to produce vasodilatation, alpha block to decrease adverse effects of sympathetic stimulation -> overall decreased afterload & increased CO in pts w/heart failure

Tx for pts w/mild to moderate heart failure, w/no signif hypotension or pulmonary congestion, already on ACEI, diuretic, & digoxin

Metabolism: Phase I via CYP2D6, Phase II via glucuronide

107
Q

Sildenafil (Viagra)

A

Phosphodiesterase (PDE) Inhibitor

Selective inhibitors of phosphodiesterase type 5, the PDE that breaks down cGMP; leads to increased cGMP accumulation

Under Revatio label, used to treat pulmonary hypertension Used to treat erectile dysfunction (along with the other –afils)

_Contraindications: _oral/transdermal nitrates b/c synergy leads to potentiation of hypotension; use with alpha1B blockers leads to bad hypotension; Also, increased cGMP by inhibition of PDE type 6 in retina leads to visual problems

FYI: For all three of these agents-Drug Metabolism: CYP3A4

108
Q

Lananoprost (Xalatan), and other __oprosts

A

Prostaglandin Analogue

PGF2alpha agonist increases AH outflow by uveal scleral route

Another 1st line drug tx for glaucoma

Major side effect: production of irreversible darkening of iris + eyelashes in 33% of hazel eyes, also dry eyes & conjunctivitis

109
Q

Trimethaphan (Arfonad)

A

Ganglionic BLocker - Non-depolarizing

Block the predominant tone, which is largely PARASYMPATHETIC so effects similar to atropine (don’t forget sweat is sympathetic cholinergic)

used as antihypertensives as sympathectic tone to bvs unopposed

Htn crisis, Dissecting aortic aneurysm, bloodless field

Foundations 2 (33 decks)

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