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Pharmacology test 2 > Adrenergic Receptor Antagonists > Flashcards

Adrenergic Receptor Antagonists Flashcards

1
Q

alpha1 antagonist

A 
(Remember: alpha1 located vascular smooth muscle: blood vessel, sphincters, bronchi; Iris, Pilomotor sm, Prostate, Uterus, Heart)
ANTAGONIST so..
relax
miosis
bladder/prostate relax
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2
Q

alpha2 antagonist

A

(remember: located on platelets, presynaptic: neg feedback, CNS, GI)
ANTAGONIST so…
Increased NE from nerve terminals
blocking neg feed back

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3
Q

Phentolamine

class, causes, uses, does, DOA

A

nonselective alpha blocker
causes vasodilation, decrease BP, increased HR/CO
used in: Hypertensive emergencies, pheocromocytoma or autonomic dysreflexia, local infiltration for extravascular admin of sympathomimetics
(*not first choice for HTN bc get increase HR)
30-70 mcg/kg IV
Onset 2 minutes; DOA 10-15min

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4
Q

Phenoxybenzamine

receptors, causes/uses, e1/2t,

A

binds covalently
more alpha1 than 2 (less tachyc)
decreased SVR, vasodilation
pro-drug w/1hr onset time:LONG acting E1/2, 24hrs
used for: pheochromocytoma, Raynaud’s disease

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5
Q

Prazosin

receptors, uses, CV effects

A

Selective alpha1 blocker (minimal alpha2)
Control BP in pheochromocytoma
Less reflexive tachycardia (remember alpha2 is inhibitory to NE release)

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6
Q

Yohimibine

receptors, uses

A

Alpha2 selective blocker
Increases the release of NE from post-synaptic neuron
Used w/ orthostatic hypotension (pt that needs more SNS for postural changes) impotence

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7
Q

Terazosin and tamulosin

receptors uses

A

selective alpha 1
long acting
effective in prostatic smooth muscle relaxation

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8
Q

Beta adrenergic antagonist

A

remember beta1 located: Heart, kidneys
beta2 located: visceral sm:resp,uterine, vascular, GI, GU; mast cells, skeletal muscles, liver, pancreas, adrenergic nerve terminal
ANTAGONIST
improve O2 supply and demand balance
bronchospasm (2)
vasoconstriction in skeletal muscle, PVD symptoms increase
decreased renin release (indirect way of decreasing BP)

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9
Q

Beta-adrenergic receptor antagonist MOA

A

Selective binding to beta receptors (influence inotropy, chronotropy)
Large doses of agonists will completely overcome antagonism
Chronic use is associated with increase in the # of receptors (up-regulation) so have massive response bc of all the receptors

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10
Q

beta agonist derivatives

A

beta isoproterenol
substitution on benzene ring
possessing some sympathomimetic effects

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11
Q

Propranolol
class, receptors
how to give

A 
prototype
no selective
pure antagonist
equal B1 and 2
give in stepwise manner until goal lf 55-60 HR
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12
Q

Propranolol cardiac effects

A

Decreased HR, contractility, CO
especially during exercise and sympathetic outflow
Blockade of β2 receptors-increased PVR, increased coronary vascular resistance
*decreased HR and CO oxygen demand is lowered, compensating for the increased PVR
Sodium retention due to renal
system response to drop in CO

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13
Q

Propranolol pharmacokinetics

A

goes through firsts effect (90-95%)
therefore PO dose much larger
0.05mg/kg IV or 1-10mg *give slowly q5min
protein bound 90-95%
metablized in liver E1/2 2-3hrs–will be increased in low hepatic blood flow states
decrease clearance of amide LA due to a drop in hepatic blood flow/metabolism inhibition
decrease pulm 1st pass effect of fentanyl

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14
Q

Timolol receptor, use

A

Non selective beta blocker
Used to tx glaucoma-decreases intraocular pressure by ↓ production of aqueous humor
Eye drops can cause ↓BP, ↓HR and ↑ airway resistance (can get systemicly absorption)

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15
Q

Nadolol receptor, metabolism

A

Non selective beta blocker
No significant metabolism (renal/biliary elimination)
E1/2t of 20-40hrs take 1X daily *LONG 1/2life

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16
Q

Metoprolol

receptor, causes, first pass, dose, e1.2t

A 
Selective beta 1 blocker (better for asthma than propranolol bc selective)
Prevents inotropy and chronotropy
Selectivity is dose related
About 60% goes thru first pass effect
PO 50-400mg
IV 1-15 mg
E1/2t of 3-4hrs
17
Q

Atenolol

receptor, causes, metabolism, e1.2t

A

Most selective beta 1 antagonist and thought to have the least CNS
effects (polar, doesn’t cross BBB)
E1/2t is 6-7hrs
Not metabolized in liver, excreted via renal system (polar), sticks around active until kidney gets rid of it.
therefore E1/2t is increased in renal disease
Very useful in cardiac patients with CAD

18
Q

Betaxolol

e1/2t, use, receptor

A

Cardioselective beta 1 blocker
E1/2t is 11-22hrs
Single dose daily for HTN
Topical useful for glaucoma, with less risk of brochospasm than Timolol,
so good alternative choice in asthmatics with glaucoma

19
Q

Esmolol

class, receptor, dose, infusion, e1/2t, hydrolyzed

A

Selective beta 1 antagonist
Rapid onset, short acting ( good for hemodynamic response to noxious stimuli)
dose: 0.5mg/kg IV (10-180mg IV)
DOA= <15mins
Can start infusion 50-300 mcg/kg/min
Small does: effects HR without decreasing BP significantly
In doses used, it does not occupy sufficient beta receptors to cause negative inotropy (decreased contractility)
E1/2t is 9 min
rapidly hydrolyzed by plasma esterases
*not the same as the cholinesterase that does succ, so no effect on such

20
Q

Beta blockers side effects

A

CV: decrease HR, Contractility, BP
worsens PVD (block of beta-2 vasodilation)
Airway: bronchospasm
Metabolism: alter carbohydrate and fat metabolism, mask the increase in HR caused by hypoglycemic
Distribution of ec K: inhibit uptake of K into skeletal muscles
Interaction with anesthetics: may have ↓BP with IAs
Nervous system: fatigue, lethargy
N/V/D

21
Q

Beta blockers relative contrindications

A

Pre-existing AV heart block or cardiac failure
Reactive Airway Disease
Diabetes Mellitus (without BS monitoring)
Hypovolemia

22
Q

Clinical uses of B-blockers

A 
HTN
mgmt Angina
decrease mortality in tx of post MI
periop/postop of pts at risk of MI
suppression of tachyarrythmias
prevention of excessive SNS activity (stage fright)
23
Q

Labetalol

receptors, metabolism, CO effects, dose, SE

A

Selective at alpha 1, beta 1 and 2 receptors; more beta 7:1 (no alpha 2 so still get neg feedback)
Metabolism conjugation of glucuronic acid; <5% in the urine
E1/2t of 5-8 hrs, prolonged in liver disease
↓ BP, SVR, HR.
CO is unaffected
Maximum drop in BP is 5-10 min after given
Dose 0.1-0.5mg/kg IV
Usually 5mg at a time for mild hypertension in the OR
Can cause orthostatic hypotension, bronchospasm, heart block, CHF, bradycardia

24
Q

Antimuscarinic MOA, natural vs semi-synthetic

A

Competitively antagonize Ach at muscarinic receptors ONLY
Cation portion of the drug fits into Ach’s place on mus receptor and reversibly inhibits Ach binding
**Allow sympathetic responses to predominate
This competitive inhibition can be reversed if Ach concentration is ↑
Natural (atropine & scopolamine) are tertiary amines – alkaloids of belladonna plants (can get into brain)
Semi-synthetic (glycopyrrolate/Robinal) - quaternary ammonium derivative (canNOT get into brain)

25
Q

Atropine

DOA, e1/2t, metabolism, dose

A

Sedation, mydriasis and motion induced nausea +
increased HR+++, most effective
relax sm ++
Anti-sialagogue +
IV onset fast, 1min
DOA 30-60 min
E1/2t 2.3hrs
18% unchanged via urine rest undergoes hydrolysis
DOSE: 0.2-0.4 mg IV (pre-op)
0.4-1.0 mg IV (bradycardia)
2mg in 5ml NS via nebulizer (bronchodilate)

26
Q

Scopalamine

metabolized, causes, dose

A

Sedation, mydriasis and motion induced nausea +++ most effective for N/V
increased HR +
relaxed sm +
Anti-sialagogue +++
extensiverly metabolized with only 1% excreted unchanged in urine
DOSE: 0.3-0.5 mg or 5mcg/kg IM (pre-op)
1.5mg transdermal (5mcg/hr X 72 hrs - nausea)

27
Q

Glycopyrrolate

causes, DOA, dose e1/2t, metabolized

A

Sedation, mydriasis and motion induced nausea 0
increased HR ++
relax sm ++
Anti-sialagogue ++
IV slower nose of 2-3 minutes
DOA 30-60 min
E1/2t 1.25hrs
80% unchanged via urine–renal disease sticks around longer
DOSE: 0.1-0.2 mg IV (pre-op and bradycardia)

28
Q

when would you use antimuscarinic? 6

A

1Pre-op: antisialagogue or sedation, nausea
prevention
2Tx of bradycardiac especially vagal stimulation related
Magnitude of effect depends on baseline vagal tone:
young pt has High tone so inhibit it was these drugs and they get more tachycardia
Elderly pt has low tone, less pronounced tachycardia
3With anti cholinesterase drugs–ALWAYS given when antagonizing NMB
4Promoting amnesia in unstable pts. (pts who can tolerated IA)
5Mydriasis and cycloplegia (ophtho cases) may be dangerous in pt with narrow angle glaucoma–increases IOP
6reduce biliary and ureteral spasm related to opioids

29
Q

Ipratropium
receptor
dose onset uses

A 
antimuscarinic 
Bronchodilation 
MDI 40-80 mcg 2 puffs
0.25-0.5mg via nebulizer
Onset 30-90 minutes
Consider in asthmatics, COPD, and smokers prior to airway instrumentation
30
Q

Central Anticholinergic Syndrome

A

Scopolamine and atropine (unlikely with glycopyrrolate)
Restlessness, hallucination
Somnolence and unconsciousness
Delayed emergence/recovery in PACU
Physostigmine 15-60 mcg/kg IV repeated as needed q1-2 hour

31
Q

Tiotropium (spiriva)

A

COPD bronchodilator

32
Q

Oxybutynin (Ditropan), tolterodine (Detrol)

A

overactive bladder

nonspecific M-rec

33
Q

Darifenacin (Enablex), solifenacin (Vesicare)

A

overactive bladder

M3 specific

Pharmacology test 2 (6 decks)

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