• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

76 Cards in this Set

  • Front
  • Back
effects of Epi on BP, HR, PVR

low dose vs. high dose
low dose: ↑pulse pressure, little to no ∆ in BP, ↑HR, ↓PVR
β effects dominant

high dose: α dominates, so ↑BP, ↑PVR
also see ↑blood glucose & renin
effects of NE on BP, HR, PVR
effects of isoproterenol on BP, HR, PVR
what drug is used for dry mouth, with few side effects?
what class & receptor?

what drug is a worse choice (due to side effects) for dry mouth?
cevimeline (evoxac)

direct acting cholinergic agonist
M3 receptors

worse choice: pilocarpine ⇒ profuse sweating
what choline ester, quaternary amine is used for GI? what are the indications?
what class & receptor?
bethanechol - stimulate peristalsis (decr bowel act w/o obstruction, post-op ileus, congenital megacolon)
also facilitates urine voiding

direct acting cholinergic agonist
M receptors
what are the contraindications for direct acting cholinergic agonists?
peptic ulcers, coronary insufficiency, asthma, hyperthyroid
what are the uses of pilocarpine?
what are the side effects?
used for:
open angle glaucoma
narrow angle if used w/ AChE inhibitor
dry mouth

side effects:
blurred vision
what is use for carbachol?
what class & receptor?
use in eye ⇒ decreased pressure & miosis

direct acting cholinergic agonist
M & N receptors
what happens w/ nicotine stimulation?
what happens w/ nicotine OD?
initial stim of skeletal mm.
not broken down quickly, so ⇒ desensitization of NMJ ⇒ flaccid paralysis

OD: vomiting, convulsions followed by coma & respiratory arrest, paralysis, HTN, cardiac arrhythmia
what drug is used for smoking cessation?
how does it work?
what subtype of receptor is it acting on?
what are the side effects?
varenicline (chantix)

partial agonist of N receptor in the brain - α4β2 subtype
it substitues for nicotine to relieve craving & blocks action of nicotine if they do smoke (b/c partial agonist)

SE: N/V, CNS sx - sleep disturbances, nightmares, psychosis, mania, anxiety, suicide ideation
what drug can be used to dx MG or determine if med dosing is correct?
what is another use of this drug?

what class?
edrophonium - short duration of action

can also reverse NMJ blockade after surgery

AChE inhibitor
what drug is given PO for MG?
what class?
given PO even though it is a quaternary amine (poor absorption)

AChE inhibitor
it also has some direct stimulatory effect on NMJ, making it a good choice for MG
what is the use for physostigmine?
why isn't it used very often?

what class?
can be used for narrow angle glaucoma
rarely used b/c of side effects - it's a tertiary amine, so it gets into the CNS

AChE inhibitor
what drug is good for long-term control in glaucoma emergencies? why?

what class?
it is an organophosphate w/ a long duration of action - irreversible biding

AChE inhibitor
why do you have to give 2-PAM quickly w/ organophosphates? how does 2-PAM work?

what other drug do you apply w/ 2-PAM? what do you look for?
organophosphates phosphorylate AChE
in the early stages, it is reversible, but the bond undergoes "aging" and becomes irreversible

2-PAM is a strong nucleophile that can be added before the aging process to remove the organophsophate, preventing aging

also give atropine and watch for pupils to dilate
what is the use of donepizil?

what class?
used for alzheimer's

AChE inhibitor
what is the little saying to remember the effects of atropine?

what class is atropine?
dry as a bone
blind as a bat
mad as a hatter
red as a beet

cholinergic (muscarinic) antagonist
what are the indications for atropine?
reverse bradycardia due to excessive vagal tone
reverse AV block
treatment of cholinergic poisoning
treatment of muscarine poisoning
what are the effects of increasing dose of atropine? (i.e. what order are the tissues affected - the stair step diagram)
1 - dry mouth & decreased sweating
2 - increased HR, very dry mouth, thirst
3 - blurred vision, tachycardia, palpitations
4 - GI effects, urinary retention, hot & dry skin, restlessness, fatigue
5 - rapid & weak pulse, ataxia, hallucinations, delirium, coma
what drug is used for motion sickness?
how is it applied?
what are side effects of this drug?

what class?

excitement, euphoria, hallucinations, coma w/ high dose (it enters the CNS ⇒ sedation & amnesia)

cholinergic (muscarinic) antagonist
what is the preferred drug for overactive bladder in the elderly? why?

what class & receptor?
tolderodine (detrol)
it is not lipid soluble & has few CNS effects, so good for elderly

cholinergic (muscarinic) antagonist
M3 receptor selective
what is oxybutynin (ditropan) used for?

what class?
prevent bladder spasm after prostate surgery

cholinergic (muscarinic) antagonist
what is the use for glycopyrrolate (robinul)?

what class?
used in surgery to prevent vagal response when viscera is handled
decrease M side effects when using neostigmine for MG

cholinergic (muscarinic) antagonist
what is dicyclomine (bentyl) used for?

what class?
inhibits motility & secretions of GI tract
used as GI antispasmodic

cholinergic (muscarinic) antagonist
what is solifenacin (vesicare) used for?
what makes it a good choice?

what class?
used for overactive bladder & urinary frequency
it's good b/c it has little effect on salivation

cholinergic (muscarinic) antagonist
M3 selective
what is ipratropium (atrovent) used for? what about its structure makes it a good choice? what are the side effects?

what class?
used to treat asthma & COPD
it works well b/c it is a quaternary amine and is not absorbed well. when inhaled, it stays in the lungs

SE: dry mouth

cholinergic (muscarinic) antagonist
what is tropicamide (mydriacil) used for? what is the contraindication?

what class?
mydriasis & cycloplegia
used for eye exam

don't use w/ narrow angle glaucoma

cholinergic (muscarinic) antagonist
what is the opioid that is combined with atropine? what is it used for?

what class?
diphenoxylate-atropine (lomotil) is used to treat diarrhea

cholinergic (muscarinic) antagonist
what is seen in the "train of four" for non-depolarizing NMJ blockers?

what about depolarizing?
non-depol: see fade represented by reduced twitch height; undergo post-tetanic potentiation

depol: size of each twitch is reduced, but no fade; NO post-tetanic potentiation
which non-depol NMJ blocker has a rapid onset & intermediate duration of action?
what is its use?
rocuronium (zemuron)
use for intubation
which non-depol NMJ blocker is most commonly used? why is a good choice?
cisatracurium (nimbex)

it is spontaneously hydrolyzed and had low toxicity
also, it does not cause histamine release (unlike d-tubocurarine)
what is the onset/duration of action of pancuronium (pavulon)?

how about vecuronium (norcuron)?
these are both non-depolarizing NMJ blockers

pan - slow onset & long duration

vec - slow onset & intermediate duration
what is the order of muscles affected by non-depol NMJ blockade?
what is the order of recovery?

what is the prototype of this class?
1st - small muscles (eye, jaw, larynx)
2nd - larger muscles
last - diaphragm & intercostals

recover in the opposite order

d-tubocurarine is prototype
what class is succinylcholine?
describe phase I & phase II blockades.
depolarizing NMJ blocker

phase I - prolonged depol; fasciculations followed by flaccid paralysis; effects are NOT reversed w/ AChE inhibitors; proper clinical use produces phase I blockade

phase II - occurs w/ prolonged exposure (should not occur clinically); membrane is repolarized and desensitized - looks like block seen w/ non-depol (i.e. PTP, AChE inhib may reverse)
what things increase the effects of succinylcholine?
aminoglycoside antibiotics (enhance due to Ca channel blockage)
tetracyclines (enhance due to Ca chelation)
Ca channel blockers also enhance
what are the contraindications for succinylcholine?
severe trauma
spinal cord injury
muscular dystrophy
kids <8yo unless emergency

causes release of K+ into blood - cardiac arrest
what are the ganglion blockers?
what receptor is in the ganglia?

what are the effects in the eye, BVs, heart, GU, skin, and reflexes? what do these things have to do with tone?
mecamylamine (inversine)

Nn receptor

eye: cycloplegia, mydriasis (blocked PNS tone, so see SNS effect)
BVs: vasodilation, orthostatic hypotension (blocking SNS tone)
heart: decr contractility, tachycardia (blocking vagal tone)
GU: urinary retention, can't get erection or ejaculation
skin: no sweating, have to control temp by vasodilation (red face)
decreased autonomic reflexes
what are the indications for use of Epi?
anaphylactic shock
cardiac arrest & complete heart block
vasoconstriction to decrease diffusion of local anesthetic
asthma emergency (rare)
which receptors does epi act on?


E: α, β1, β2

NE: α, β1
[no lung effects]

I: β1, β2
[no α, so no BV effects]
what are the effects of low dose dopamine?

high dose?
low: activate D1 receptor in renal vascular beds ⇒ vasodilation, ↑renal blood flow (↑GFR & Na excretion)
also dilates coronary & mesenteric aa

higher: stimulate β1 in the heart ⇒ +inotropic & chronotropic effect
may release NE to stimulate α1 (⇒ vasoconstriction & ↑BP like high Epi dose)
what is the indication for dopamine?
how is it applied?

side effects?
IV treatment for cardiac shock

SE: N/V, tachycardia, angina, arrhythmias, HA, peripheral vasoconstriction
what is the class & receptor for phenylephrine (neo-synephrine)?

what are its uses?
α1 agonist

causes vasoconstriction
-use as nasal decongestant (can get rebound effect)
-use in hypotensive emergency to ↑BP
-mydriasis w/o affecting accomodation - eye exam
what is the class & receptor of pseudoephedrine?

what is the use? who needs to be careful w/ its use?
α agonist

OTC decongestant
use caution w/ HTN
what drug can be applied orally or w/ a patch for HTN?
what class & receptor?
how does it work?
other uses?
α2 agonist
decrease NE release by acting on PREsynaptic terminals in CNS ⇒ ↓BP & HR

also used for addiction/alcoholism, menopause (↓hot flashes), pre-anesthetic (sedates)
what is the use for apraclonidine?
what class & receptor?
used in eye to ↓pressure by reducing formation of aqueous humor (via vasoconstriction)

α2 agonist
what is the class & receptor for ritrodine (yutopar)?
what is it used for?
β2 agonist

relax uterus and suppress pre-term labor
what 2 β2 agonists are used for asthma?
side effects?
terbutaline (brethine)

SE: HA, tremors, tacycardia (b/c they can have small effect on β1, too)
what class & receptor for dobutamine (dobutrex)?

what does it do?
when is it used?
β1 agonist

↑renin release
+inotrope, chrontrope
↑CO w/ little effect on PVR

1/2 life is 2 min, so can be used for cardiac stress test if pt can't exercise
incr CO for cardiogenic shock & CHF
what is ephedrine?
a MIXED acting adrenergic stimulant - denervation will ↓ its effect

acts on α & β receptors

it is similar to epi but is less pronounced and has longer duration
it is a CNS stimulant
how does amphetamine act?
what can it be used to treat?
what are the side effects?
indirect acting - displaces NE & DA from vesicles, ↑ their release from neurons; CNS stimulant

tx enuresis - strong contraction of urinary bladder sphincter

SE - tremor, tachycardia, HTN, psychosis, dizziness, restlessness, irritability, fever, aggression, HA, cerebral hemorrhage, convulsions, coma
why does methylphenidate (ritalin) work for ADHD?
it has a paradoxical effect in someone w/ ADHD ⇒ decrease in activity
how does cocaine act?
what can it be used for?
what are the side effects?
indirect acting
inhibits reuptake of NE & DA into nerve terminal
has amphetamine-like effect that is shorter acting & more intense

used in nasopharyngeal surgery to ↓blood flow & local anesthesia

SE: addiction; severe HTN, stroke, tachycardia, arrhythmia, MI, psychosis
how does tyramine act?
what can happen w/ a large dose?
what are the contraindications?
indirect acting - increases release of catecholamines from nerve
gets taken up into vesicles & displaces NE w/ false NT (octopamine)

w/ large dose get massive release ⇒ tachyphylaxis

CI - MAOIs ⇒ severe HTN crisis
what is fendolopam (corlopam)?
what are its uses?
DA agonist - D1 receptor

causes dilation of vascular beds & ↓BP
used short-term to ↓BP in severe HTN
what class is phentolamine?


side effects?

α blocker (1 & 2)
↓BP & PVR - used for short-term tx of HTN crisis in pheochromocytoma
or HTN crisis due to tyramine or abrupt clonidine withdrawal

SE: tachycardia, myocard ischemia, abd pain, arrhythima, low BP

CI: peptic ulcer, CAD (caution); viagra-absolute
what class is phenoxybenzamine?


side effects? CI?
α blocker (1 & 2)

IRREVERSIBLE - good for use in pheochromocytoma b/c their high secretion of catecholamines can overcome reversible blockade

postural hypotension, tachycardia, nasal stuffiness, inhibition of ejaculation

CI - viagra absolute
what class is prazosin (minipress)?
uses? how often do you give it?

what about giving it to someone w/ CHF?

α1 blocker

used for HTN - BID
also BPH

CHF - half life is 2x

SE: first dose phenomenon; inhibit ejaculation; dizziness; nasal stuffiness
CI: viagra absolute
what are terazosin & doxazosin used for? why are they good?
sim to prazosin - α1 blockers

used for BPH
good b/c long 1/2 life (qd) & ↓prostate size by causing apoptosis
what is tamsulosin (flomax)?
what is its use?
why is it more selective?
α1 blocker
used for BPH, works rapidly
more selective for α1A (prostate) than α1B (BVs), so little BP effect
what the class of yohimbine?
what was it marketed as?
what drug does it interact with?
α2 blocker
claimed to be natural alternative to viagra

antagonizes clonidine
why do you have to use caution when giving a β1-blocker to COPD or asthma pts?
selectivity is not absolute - high dose can block β2 as well
what is the class of propanolol?
what are its effects?
β-blocker (1&2)
• – chronotrope, dromotrope, inotrope
• ↓renin release
• ↓aqueous humor production
• ↓glycogenolysis & mask sx of hypoglycemia (caution in DM type I)
• chronic use ⇒ ↑VLDL & ↓HDL
• interfere w/ K+ buffering by catecholamines - ↑plasma [K]
• local anesthetic
what things affect the effectiveness of propanolol?
metabolized by liver - varies in each pt

metabolism reduced by: cimetidine (causes increase in the antihypertensive effect)
metab increased by: barbiturates, phenytoin, rifampin, smoking

Ca channel blockers have additive effect
what is timolol (timoptic) used for?
what are the contraindications?
β-blocker (1&2)
used for open angle glaucoma

CI - pheochromocytoma (must give α-blocker to prevent vasoconstriction); asthma; type I DM (caution); Ca channel blockers
what is metoprolol (lopressor) used for?
used for HTN, ↑life expectancy w/ MI, migraine prophylaxis
have better exercise tolerance b/c don't block β2
also ↓risk of causing hypoglycemia
what is atenolol (tenormin)?
sim to metoprolol, but w/o anesthetic effect
↑risk for developing type II DM
what is esmolol (brevibloc)?
use via IV when you want a short β blockade (duration ~8min)
what is betaxolol (betoptic)?
open angle glaucoma w/ fewer side effects than timolol
what is nebivolol (bystolic)?
what makes it a good drug?
most selective β1 antagonist on the market
causes vasodilation due to ↑NO release
significantly ↓C, TAGs, glucose
what are the 2 β-blockers w/ intrinsic sympathetic activity?
pindolol (visken)
acebutolol (sectral)

used for HTN, angina
↓risk of bradycardia b/c don't ↓HR much

acebutolol is local anesthetic, don't use for gualcoma
what are the 2 combined bockers?
what do they do?
which is used w/ CHF & why?
lebetalol (normodyne)
carvedilol (coreg)

both ↓BP w/o ↑HR (compensatory increase is blocked)

use carvedilol w/ CHF b/c it inhibits vascular sm mm mitogenesis
what is guanethidine (ismelin)?
how does it act?
side effects?
NT release blocker
transported into terminal & replaces NE to gradually deplete NE stores

SE: complete loss of SNS ⇒ postural hypotension, ↓blood to brain & heart
what is reserpine?
how does it act?
NT release blocker
interferes w/ uptake & storage of biogenic amines in nerve terminal - depletes NE, DA, 5-HT in brain

low doses ↓BP (not used clinically)

SE: severe diarrhea, depression, sedation, parkinson-like
what is metyrosine (desmer)?
how does it act?
synthesis inhibitor - tyrosine analogue
blocks tyrosine hydroxylase (rate limiting) ⇒ ↓DA, NE, E synthesis

pre-surgical tx in pheochromocytoma (combined w/ phenoxybenzamine)
what are the 4 β-blockers w/ local anesthetic effects?
what is the contraindication for these?

don't use w/ glaucoma - don't want to anesthetize the cornea
(the other β-bockers [esp. timolol & betaxolol] are used for glaucoma b/c they ↓humor production)
match the receptors to their second messenger system
sodium channel

M1, M2, M3
Nn, Nm
β1, β2, β3
α1, α2
D1, D2, D3, D4, D5
Gs (stimulate AC ⇒ ↑cAMP)
β1, β2, β3, D1, D5

Gi (inhibit AC ⇒ ↓cAMP)
M2, α2, D2, D3, D4

Gq (PLC, IP3, DAG, ↑Ca2+)
M1, M3, α1

sodium channels
Nn, Nm