Exam 2 Drugs

Question 1

sypmathomimetic subclasses:

Answer 1

direct acting
indirect acting

Question 2

midodrine

Answer 2

class: direct-acting (DA) sympathomimetic

receptor: alpha-1 agonist

indication: orthostatic hypotension

Question 3

clonidine

Answer 3

class: DA sympathomimetic
receptor: CENTRAL alpha-2 agonist; considered a PARTIAL AGONIST
indication:
* HTN (off label: adjuvant drug for sedation)
* diarrhea
* hot flashes
* hemodynamic instability intraOP
* ADHD, Tourettes, withdrawal symptoms
* OFF LABEL: anxiety, PTSD, adjunct to anesthesia (prolongs anesthesia)

MOA:
CENTRAL Alpha-2-Rs:
* Rostro Ventrolateral Medulla (RVLM) stimulated > INHIBITION of sympathetic outflow leads to decreased vasoconstriction, HR, and contractility
* Nucleus of the Tractus Solitarius (NTS) stimulated > leads to INCREASED FIRING ON VAGUS NERVE (CN X) > leading to INCREASED PARASYMPATHETIC OUTFLOW leads to slower HR
* overall effects of decrased HR and decreased SV will decrease BP

SE:
* may see initial transient increase in BP prior to decrease in BP d/t peripheral alpha-2 stimulation via oral route prior to crossing BBB
* dry mouth
* also has effect to induce sedation

Question 4

epinephrine

Answer 4

class: DA sympathomimetic
receptor: alpha + beta 1 + beta 2 agonist
indication: positive inotropic agent, positive chronotropic agent, dilation of skeletal muscles and bronchioles

Question 5

norepi (NE)

Answer 5

class: DA sympathomimetic
receptor: alpha + beta 1 agonist
indication: hypotension
MOA: increase in SBP + DBP; vagal reflex overcomes chronotropic effects (does not stimulate HR as much)

Question 6

isoproterenol

Answer 6

class: DA sympathomimetic
receptor: beta 1 + beta 2 agonist
indication: HTN
MOA:
* B1: will increase HR, CO, & contractility with a slight increase in SV; slight increase in pulse pressure but major effects will be to decrease DBP and a slight decrease in SBP
* B2: decrease vascular tone

Question 7

dopamine

Answer 7

class: DA sympathomimetic
receptor: D + beta 1 agonist
indication: cardiac
MOA:
* decreases peripheral resistance at LOW DOSES (induces diuresis)
* mimics action of epinephrine at HIGH RATES OF INFUSION (increase in HR, increase in contractility, increase in peripheral resistance, could be arrythmogenic)

Question 8

dobutamine (dobs)

Answer 8

class: DA sympathomimetic
receptor: beta 1 selective agonist
indication: cardiogenic shock, HF
MOA: positive inotropic/chronotropic effect

Question 9

phenylephrine

Answer 9

class: DA sympathomimetic
receptor: pure alpha agonist
indication: decongestant, hypotension

Question 10

midodrine

Answer 10

class: DA sympathomimetic
receptor: alpha-1 selective agonist
indication: postural/orthostatic hypotension

Question 11

ephedrine

Answer 11

class: DA && INDIRECT ACTING sympathomimetic
receptor: alpha and beta agonist
indication: nasal decongestant (pseudoephedrine)
MOA: mimics epi (direct-acting); crosses the BBB

found in plants; can be used to make meth

Question 12

dexmedetomidine

Answer 12

class: DA sympathomimetic
receptor: CENTRAL alpha-2-A selective agonist
indication: anxiolytic

MOA: induces anesthesia, analgesia, sympatholysis, sedation, anxiolysis, hypnosis, and increased congnition

Question 13

amphetamines

Answer 13

class: INDIRECT-acting sympathomimetics
effects: mood elevator, appetite suppresant, increased attention
MOA: readily enter CNS

methamphetamines have a higher ratio of CNS to PNS actions

Question 14

cocaine

Answer 14

class: indirect acting sympathomimetic
effects: amphetamine-like effects
MOA: inhibits dopamine reuptake into neurons in the “pleasure centers” of the brain

Question 15

tyramine

Answer 15

class: indirect sympathomimetic
effects: releases stored catecholamines; metabolized by MAO

MAOIs (monoamine oxidase inhibitor) inhibit the breakdown of NTs and are often prescribed as antidepressants; MAOis may increase blood pressure after eating fermented foods

ex) cheese, chicken liver, sausage (fermented), red wine, yeast

Question 16

phentolamine

Answer 16

class: reversible sympatholytic
receptor: competitive alpha-1, alpha-2 blocker
indication: HTN linked to pheochromocytoma, cardiac stimulant, ED (direct injection)
MOA:
* turns a pressor into a depressor
* if giving phentolamine BY ITSELF, very little effect
* if giving phentolamine AFTER pressor, will decrease some of the pressor agonists’ effects
* if giving phentolamine BEFORE pressor, GREATEST effect and decreases BP significantly

Question 17

prazosin

Answer 17

class: reversible sympatholytic
receptor: alpha-1 selective blocker (low affinity for alpha-2)
indication: HTN, BPH
MOA: relaxes arterial and venous smooth muscle

Question 18

labetalol

Answer 18

class: reversible sympatholytic
receptor: alpha & beta blocker
indication: HTN

Question 19

phenoxybenzamine

Answer 19

class: IRREVERSIBLE sympatholytic
receptor: non-specific alpha antagonist & covalently bonds, blocks H1, ACh, and serotonin receptors
indication: HTN linked to
pheochromocytoma
MOA: inhihbits NE reuptake

Question 20

-osin drug class

Answer 20

alpha-1 blockers

Question 21

what is the drug Yohimbine?

Answer 21

an alpha-2 selective antagonist which has little use clinically

allegedly helps ED patients

Question 22

propanolol

Answer 22

class: sympatholytic
receptor: non-specific beta blocker
indication: HTN
SE: bradycardia, rash, fever, CNS effects (sedation, sleep disturbances, depression), worsening of asthma (B2), hypoglyemia in diabetics (blocks glycogenolysis), must discontinue use gradually

Question 23

metoprolol

Answer 23

class: sympatholytic
receptor: beta-1 blocker
indication: HTN (safer in COPD, asthma, and diabetic patients)

Question 24

labetalol

Answer 24

class: sympatholytic
receptor: a1 **AND **b1, b2 blocker
indication: HTN, preeclampsia, pheochromocytoma

racemic mixture: 2 active forms and 2 inactive forms

Question 25

esmolol

Answer 25

**class:** sympatholytic **receptor:** beta-1 selective blocker **indication:** tachycardia intraop, supraventricular arrythmia **other facts**: ultra short acting, steady state infusion, terminated rapidly when discontinued, safer in critical care patients

Question 26

ACh

Answer 26

**class:** DA parasympathomimetic// cholinomimetic **subclass:** choline ester **indication:** miosis (pupillary constriction) *insoluble in lipids*

Question 27

methacholine

Answer 27

**class:** DA parasympathomimetic // cholinomimetic **subclass:** choline ester **indication:** *diagnostic drug for **asthma*** *insoluble in lipids*

Question 28

carbachol

Answer 28

**class:** DA parasympathomimetic// cholinomimetic **subclass:** choline ester **indication:** to decrease IOP *insoluble in lipids; resistant to hydrolysis*

Question 29

bethanechol

Answer 29

**class:** DA parasympathomimetic// cholinomimetic **subclass:** choline ester **indication:** bladder dysfunction, reflux disease *insoluble in lipids; resistant to hydrolysis*

Question 30

muscarine

Answer 30

**class:** DA parasympathomimetic// cholinomimetic **subclass:** alkaloid **effects:** mimics parasympathetic nerve discharge (saliva, bowel motility, urination, etc.) MOA: takes place at *effector cells*, not in ganglia **toxicity**: exaggeration of all symptoms of muscarinic agonism (**MYCETISM)**; can occur with high consumption of wild mushrooms **reversal for toxicity**: **ATROPINE 1-2mg IM**

Question 31

nicotine

Answer 31

**class:** DA parasympathomimetic// cholinomimetic **subclass:** alkaloid **MOA:** stimulates autonomic ganglia and skeletal muscle NMJ, not effector cells release of *dopamine, serotonin, GABA, and NE* **SE**: in larger doses -- tremors, emesis, stimulates respiratory center, convulsions, fatal coma (OD ingestion), addiction *crosses BBB; lipid soluble* *the antidote for nicotine OD is 2-PAM*

Question 32

arecoline

Answer 32

**class:** DA parasympathomimetic// cholinomimetic **subclass:** alkaloid stimulant; from betel nut

Question 33

pilocarpine

Answer 33

**class:** DA parasympathomimetic// cholinomimetic **subclass:** alkaloid **effects:** N/V/D, salivation, sweating, bronchial constriction

Question 34

edrophonium

Answer 34

**class:** INDIRECT-acting parasympathomimetic// cholinomimetic **subclass:** simple alcohol **indication:** diagonist drug for myasthenia gravis **onset:** 5-15 mins

Question 35

neostigmine

Answer 35

**class**: INDIRECT-acting parasympathomimetic// cholinomimetic **subclass**: carbamate **indication**: MG, surgical paralysis reversal agent **MOA**: inhibits the effects of **AChE**

Question 36

pyridostigmine

Answer 36

**class**: INDIRECT-acting parasympathomimetic// cholinomimetic **subclass**: carbamate **indication**: MG **MOA**: inhibits the effects of **AChE**

Question 37

echothiophate

Answer 37

**class**: INDIRECT-acting parasympathomimetic// cholinomimetic **subclass**: organophosphate **indication**: glaucoma **MOA**: increases the drainage of intraocular fluid

Question 38

atropine

Answer 38

**class**: parasympatholytic // anticholinergic **subclass**: antimuscarinic **indication**: organophosphate poisoning (with pralidoxime), bradycardia * effects occur d/t racemix mixture * competitively inhibits muscarinic responses to ACh

Question 39

scopolamine

Answer 39

**class**: parasympatholytic // anticholinergic **subclass**: antimuscarinic **indication**: motion sickness, excessive salivation

Question 40

tropicamide

Answer 40

**class**: parasympatholytic // anticholinergic **subclass**: antimuscarinic **indication**: mydriasis and cycloplegia (diagnostic drug)

Question 41

ipratropium bromide

Answer 41

**class**: parasympatholytic // anticholinergic **subclass**: antimuscarinic **indication**: asthma

Question 42

succinylcholine

Answer 42

**class**: parasympatholytic // anticholinergic **subclass**: antinicotinic && choline ester **indication**: DEPOLARIZING muscle relaxant **MOA:** * resembles ACh; it is considered a n-ACh-R **AGONIST** * blocks n-ACh-R on motor end plate of skeletal muscle * depolarization PERSISTS * continuous end-plate depolarization causes muscle relaxation (prolonged depol = delayed repolarization of cell) * this depolarizing agent causes a PHASE I BLOCK (depol w/ lack of repolarization) which will then lead to a phase II block **SE:** * fasciculations * muscle pain (when drug is bound for too long) * hyperK+ * MH * apnea

Question 43

curare derivatives (i.e. rocuronium)

Answer 43

**class**: parasympatholytic // anticholinergic **subclass**: antinicotinic **indication**: NON-depolarizing NMBA **MOA: ** * competitive with ACh at n-ACh-Rs; acts as a **COMPETITIVE** **ANTAGONIST** * does NOT depolarize motor end plate * excessive [ ] = channel blockade *the reversal for **ROCURONIUM & VECURONIUM** is **SUGGAMADEX***

Question 44

suggamadex

Answer 44

reversal agent for **NON-DEPOLARIZING NMBAs: ROCURONIUM & VECURONIUM** a cyclic molecule that cycles around the non-depolarizing blocking agent to prevent binding at the receptor site

Question 45

methyldopa

Answer 45

**class**: sympathoplegic **subclass**: centrally acting alpha 2 agonist **indication**: pregnancy induced HTN, (*does NOT cross placental barrier*); not first-line for normal HTN **MOA:** *CENTRAL Alpha-2-Rs:* * **Nucleus of the Tractus Solitarius (NTS)** stimulated > leads to INCREASED FIRING ON VAGUS NERVE (CN X) > leading to ***INCREASED** **PARASYMPATHETIC** OUTFLOW* leads to **slower HR**

Question 46

hydralazine

Answer 46

**class**: oral vasodilator **indication**: HTN **MOA:** * induces NO production in endothelium to relax smooth muscle of arterioles * reduces peripheral vascular resistance * reduces MAP **pharmacokinetics:** well abosrbed, rapid first pass metab, *tachyphylaxis* **SE:** HA, nausea, sweating, flushing, worse in slow ACETYLATORS (phase II metabolism); symptoms resemble **LUPUS**

Question 47

minoxidil

Answer 47

**class**: oral vasodilator **indication**: HTN, hair growth (rogaine) **MOA:** * opens K+ channels in smooth muscles; stabilizes potential which will decrease likelihood to fire AP * dilates arteries and arterioles **pharmacokinetics:** well absorbed, typically rogaine **SE:** HA, sweating, palpitations, tachycardia, angina, **hypertrichosis (hair growth)**

Question 48

nitroprusside

Answer 48

**class**: vasodilator **indication**: HT emergency, cardiac failure **MOA:** * relaxes vascular smooth muscle * breaks down in blood to release NO * NO > increased cGMP > vasodilation of arteries and veins **SE:** * rapidly lowers BP * higher rates cause toxicity: CN accumulation will occur (met acidosis, arrhythmias, death -- worse in renal insufficiency patients) ***sodium thiosulfate **facilitates metabolism of cyanide*

Question 49

fenoldopam

Answer 49

**class**: vasodilator **subclass:** **D1 agonist** **indication**: HTN emergencies, post-op HTN **MOA:** peripheral arteriolar dilator; increases renal blood flow to promote diuresis

Question 50

calcium channel blockers

Answer 50

**class**: CCBs - vasodilators **indication**: HTN, anti-anginal, anti-arrhythmic **MOA:** blocks mostly L-type Ca2+ channels in the heart and inhibits Ca2+ influx in arterial smooth muscle ex) verapamil, diltiazem, dihydropyridines (-dipines, i.e. nicardipine) | **class IV **vaughn-williams classification for arrythmia drugs

Question 51

ace inhibitors

Answer 51

**class**: anti-angiotensins **indication**: HTN **MOA:** inhibits the synthesis of **angiotensin I** to convert to **angiotensin II** by blocking the ACE enzyme * decreaes PVR * CO & HR are not significantly changed * eliminated via kidneys **SE:** * severe hypotension * **teratogenic**: contraindicated in pregnant women and especially those in their first trimester * altereed sense of taste * rashes drug interactions: * K+ supplements can lead to hyperK+ * NSAIDS block some effects * **DRY COUGH (d/t bradykinin build up; ACE converts bradykinin to its inactive metabolites, so inhibiting ACE would cause a build up of bradykinin** ex) -prils (i.e. captopril, lisinopril, enalapril)

Question 52

ARBs

Answer 52

**class**: anti-angiotensin **indication**: HTN **MOA:** * ARBs block ATII from binding to receptor sites at sites where vasoconstriction would occur, as well as on the adrenal cortex where aldosterone gets secreted; **by blocking vasoconstriction** as well as **aldosterone secretion**, the overall effect is **decreased PVR and decreased sodium/water retention**, lowering overall BP ex) -sartans (i.e. losartan, valsartan) *no effect on bradykinin, since ACE is not being inhibited, therefore NO cough symptoms associated*

Question 53

bosentan (tracleer)

Answer 53

**class**: endothelin receptor antagonist **indication**: PAHTN **MOA:** * blocks ET-1 from binding to ETa and ETb * ET-1 is the active form of an endogenous product created in the lungs; normally ET-1 when bound to ETa receptors will cause vasoconstriction and increased cell proliferation * when ET-1 is **blocked** from binding to ETa-Rs, there will be an increase in **vasodilation** in the pulmonary circulation as well as **decreased cell proliferation** to help with vascular remodeling **SE:** HA, edema, rash, hepatotoxicity, teratogenic

Question 54

nitroglycerin

Answer 54

**class**: vasodilator **indication**: angina, HTN **MOA:** * NO release in vascular smooth muscle * increases guanylyl cyclase * increases cGMP * cGMP will dephosphorylate myosin-LC-PO4 and will be left with myosin-LC * this will cause relaxation in the *vascular smooth muscle* **SE:** orthostatic hypotension, syncope, **HA**, reflex tachycardia, hemoglobin interactions (NO2- reacts with Hgb to form methemoglobin > can cause pseudocyanosis at extremely high levels, but will ALSO have a high affinity for CN in the case of CN poisoning) mononitrate form: isosorbide dinitrate

Question 55

digoxin

Answer 55

**class**: cardiac glycoside **indication**: positive inotropic agent **MOA:** * blocks Na+/K+/ATPase pump * leads to increased ICF [Na+] > lowers AP duration * slows the NCX > increases ICF [Ca2+] * increases more forcible contractility **SE:** * has a very low therapeutic index * pro-arrythmogenic * increases PR int & decreases QT int * toxic doses = tachycardia, fibrillation, cardiac arrest * hyperK+, hyperCa2+, and hypomg2+ can occur

Question 56

milrinone

Answer 56

**class**: PDE3 inhibitor **indication**: HF **MOA:** * PDE3 is an enzyme that inactivates cAMP/cGMP * when PDE3 is inhibited, increases cAMP/cGMP * more cAMP = more foricble contraction (positive inotropic effect) * more cGMP = more vasodilation * also increases/prolongs Ca2+ effects

Question 57

levosimendan

Answer 57

**class**: calcium sensitizer **indication**: positive inotropic agent; vasodilation **MOA:** * binds troponin * stabilizes Ca2+ bound conformation * opens K+ channels (vasodilation) * not approved in US yet

Question 58

class I antiarrythmics

Answer 58

**sodium channel blockers** works on **phase 0** of the cardiac cycle

Question 59

class IA drugs (3)

Answer 59

1. quinidine 2. procainamide 3. disopyramide * these drugs **prolong AP duration** * have an effective refractory period * depresses PM rate * lengthens QT int (2-8% Torsades de Pointes) * depresses conduction and excitability, especially in depolarized tissue

Question 60

class IB drug

Answer 60

1. lidocaine * shortens AP duration * decreased ERP * low toxicity; high efficacy * acts exclusively on Na+ channel * suppresses abnormal cardiac activity * recovery from block between APs d/t rapid dissociation * no effect on conduction

Question 61

class IC drugs

Answer 61

1. flecainide * minimnal effects on APD * slows dissociation; not enough sodium channels reset before next AP * suppresses abnormal firing channels * no effect on ERP (but sodium channels are still bklocked) * some beta blocking properties

Question 62

class II anti-arrythmics (2)

Answer 62

**sympatholytics (beta blockers)** * suppresses ventricular ectopic depolarization * prevents infarction and sudden death in patients recovering from acute MI 1. esmolol 2. sotalol works on **phase 4** of the cardiac cycle

Question 63

class III anti-arrythmics

Answer 63

**K+ channel blockers** * prolongation of repolarization and refractoriness by increased AP duration 1. amiodarone +has all V-W class effects; only categorized in class II d/t the nature of the receptors it works on 2. dronedarone these drugs work at **phase 3** of the cardiac AP cycle

Question 64

amiodarone

Answer 64

**class**: potassium channel blocker **v-w class**: class III antiarrythmic indications: VT/Vfib/Afib/Aflutter **MOA**: * lengthens APs well in tachycardias * weak CCB * non-competitive inhibitor of beta receptors * inhibits normal automaticity **SE:** * dilation in peripheral vasculature * can precipitate HF; fatal in pulm fibrosis patients * [ ] in tissues; found in almost every organ * VERY LONG HALF LIFE

Question 65

class IV antiarrythmics

Answer 65

**CCBs** 1. verapamil **MOA**: * blocks both activated/inactivated Ca2+ channels * prolongs AV node conduction * slows SA node * useful in supRAventricular arrythmias * (adenosine has become first line agent for SVT) * can reduce ventricular rate in afib/flutters but rarely converts to NSR these drugs work on **phase 2** of the cardiac cycle