Drug List and Metabolism Flashcards

Question

α1 blockers

Answer 1

Prazosin (MinipressR) Tamsulosin (Flomax) Alfuzosin (UroXatralR) Silodosin (RapafloR) any other agents with an azosin suffix e.g. Terazosin (HytrinR), Doxazosin (CarduraR)

Answer 2

Yohimbine (YohimexR)

Answer 3

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

Answer 4

Metoprolol (LopressorR) Betaxolol (BetopticR) Atenolol (TenorminR) Esmolol (BreviblocR)

Answer 5

Labetalol (NormodyneR) Carvedilol (CoregR)

Answer 6

Sildenafil (ViagraR) Other \_\_\_afils such as Vardenafil (LevitraR),Tadalafil (CialisR) caffeine, theophylline and other \_phyllines (generally better as adenosine receptor blockers than PDE inhibitors)

Answer 7

Lananoprost (XalatanR) and other \_\_oprosts such as Bimatoprost (LatisseR ) (These are PGF2a analogs)

Answer 8

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

Answer 9

Presynaptic Blocking Agent Compete with Ca2+ at the external mouth of the Ca2+ channel Reduces neurally-evoked ACh release, **normal MEPPs, low EPPs**

Answer 10

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)

Answer 11

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 & increased of surface area of nerve terminal (overall effect: transmission block) Fasciculations followed by dead post-synaptic membrane

Answer 12

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

Answer 13

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

Answer 14

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

Answer 15

Postsynaptic Non-Depolarizing Blocker Same as pancuronium w/o a methyl grp monoquaternary **85% BILIARY clearance 15% RENA**L clearance intermediate duration of action *30-40 min* **_no vagal block/tachycardia, no histamine release, devoid of CV effects_**

Answer 16

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

Answer 17

Postsynaptic Non-Depolarizing Blocker Properties similar to atracurium, but is only one stereoisomer rather than 10 stereoisomers **_Atracurium side effects minimized_**

Answer 18

Postsynaptic Non-Depolarizing Blocker ***~~“very fast vecuronium”*** **Essentially 100% BILIARY clearance** _Rapid onset, intermediate duration, no histamine release, very popular for intubation_

Answer 19

Postsynaptic Depolarizing Blocker Nicotinic receptor agonists in exogenously high concentrations can block transmission _Ganglionic Blockers – Depolarizing_: @ high []s, PI-PII Block as in NMJ

Answer 20

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)

Answer 21

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

Answer 22

Postsynaptic Depolarizing Blocker Nicotinic and muscarinic agonist

Answer 23

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)}

Answer 24

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

Answer 25

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)

Answer 26

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!)

Answer 27

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***

Answer 28

Indirect-acting Stimulants (anticholinesterases) / Parasympathomimetics – indirect-acting “weteye,” GB Examples of Japanese subway attack, US soldiers in Gulf War, Syria in 2013

Answer 29

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}

Answer 30

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

Answer 31

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)

Answer 32

Other Peripheral Muscle Relaxants **Blocks Ca2+ release** from SR To treat _malignant hyperthermia_ (such as caused by SUX)

Answer 33

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

Answer 34

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)

Answer 35

***_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

Answer 36

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)

Answer 37

Parasympathomimetic – Direct Muscarinic agonist used orally to treat **_Sjogren’s syndrome_** (currently preferred to pilocarpine) _{FYI:Metabolism: CYP3A4 and CYP 2D6 (Phase I)}

Answer 38

Trimethaphan (ArfonadR) Mecamylamine (InversineR) Tubocurarine

Answer 39

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

Answer 40

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)*

Answer 41

Parasympathetic Antagonists MUSCARINIC RECEPTOR BLOCKER **Shorter duration of action** Drug of choice at NU **_for ciliary spasm_** due to injury

Answer 42

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

Answer 43

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}

Answer 44

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}

Answer 45

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}

Answer 46

Parasympathetic Antagonists MUSCARINIC RECEPTOR BLOCKER Tx for bladder spasms

Answer 47

Parasympathetic Antagonists MUSCARINIC RECEPTOR BLOCKER Just another uninteresting drug to treat OAB and bladder spasms

Answer 48

Parasympathetic Antagonists MUSCARINIC RECEPTOR BLOCKER Ocular effects (b/c atropine is too long-lasting) **For older patients**

Answer 49

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!**

Answer 50

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

Answer 51

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)

Answer 52

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

Answer 53

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

Answer 54

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**

Answer 55

‘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}

Answer 56

‘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}

Answer 57

‘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}

Answer 58

‘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}

Answer 59

‘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.

Answer 60

‘Selective’ alpha2 Agonist **Inhibit secretion of AH** *2nd line drug* for stubborn glaucoma (remember pilocarpine is 3rd line drug)

Answer 61

‘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}

Answer 62

‘Selective’ beta2 Agonist **Prototype, most selective** Rescue inhaler _{FYI: Metabolism: Phase II Sulfation}

Answer 63

‘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}

Answer 64

‘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}

Answer 65

‘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

Answer 66

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)

Answer 67

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

Answer 68

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}

Answer 69

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}

Answer 70

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),

Answer 71

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

Answer 72

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

Answer 73

alpha1 Blocker **Selective alpha1A antagonists** Very useful **_treatment for BPH_** _{FYI Metabolism: Phase I via CYP3A4, Phase II by glucuronide (silodosin also uses CYP2D6)}

Answer 74

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

Answer 75

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***

Answer 76

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**

Answer 77

beta1 Blocker Equipotent w/propanolol for cardiac arrhythmias, htn, & angina **“propanolol for asthmatics”** ***Metabolism: Phase I via CYP2D6 -- important!***

Answer 78

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***

Answer 79

beta1 Blocker Was very popularly prescribed, now **very much out of favor** (little to no metabolism)

Answer 80

beta1 Blocker **Short duration of action** (hydrolyzed by esterases) Metabolism: plasma esterases (Phase I)

Answer 81

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

Answer 82

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***

Answer 83

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}

Answer 84

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

Answer 85

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*

Drug List and Metabolism Flashcards

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