Adrenergics Flashcards
Heart receptor?
B1
vessel receptor?
A1 = STRONGER = constrict
B2 = dilate (coronary/skeletal)
(a2=little effect)
Kidney receptor?
B1 = release renin
GI tract receptor?
a1 = stop secretion
Sex organs receptor
a1
Uterus receptors?
contract = a1 Relax = b2
Catecholamines
epi
NE
dopamine
NE released at
postganglionic sympathetic
Epi released from
adrenal medulla
Isoproterenol
ISUPREL
selective B ag
Stim the heart
Dopa
CNS transmitter
NE precursor
NE synthesis
Transporter sucks in Tyrosine
Tyr->Dopa->DA->NE->Epi
Inhibit NE release?
- presynaptic a2 receptor
- PGE2
*or degrade w/in terminals w/ MAO; reacumulate from synapse if cleaning
Enhance NE release?
angiotensin II
Most Cirulating Epi broken down by
MAO/COMT
Most of NE removed by
recycled into terminal by NET
receptors effects dependent on
g protein, kinases in target cell
Guanethidine
Mech
enters via NET, depletes NE
Reserpine
Mech
Enters terminal (lipid-solube), stops VMAT, NE can’t be recycled
MAOI inhibitors
Mech
accumulate intracellular NE, increased NE synapse levels
MAOI 8
Rx
Tranylcypromine (anti-depressant)
PARNATE
Amphetamine
Mech
Increase NET activity
more NE release
Faster kinetics than guanethidine/reserpine = gradual NE depletion
Large Tyramine load?
wine, cheese, beer, fava beans
- MAO cleans tyramine, so MAO taken up
- up NE = HTN
- NO MAOIs w/ large tyramine load
Block NET, Up synaptic NE
Rx
Cocaine
Imipramine TOFRANIL
Atomoxetine ASENDIN
Alpha Ag
Phenylephrine
Beta Ag
Isoproterenol ISUPREL
Apha blocker
Phentolamine REGITINE
Beta blocker
Propanolol
Chronic ag treatment causes
desensitization
Downregulation
Chronic blocker treatment causes
supersensitization
Upregulation
NE likes
1s
A1/B1
Isoproteranol likes
Betas
used to stimulate heart
Epi likes
low dose = betas b1 b2
High dose = everything
Dopamine likes
low: DA, b1
High: everything
Dobutamine likes
Low: b1 (UP contractility w/o effect HR)
HUGE AMINE SUBSTITUTION
High: may affect rate
B1 receptors like
Iso>epi=NE
B2 receptors like
iso> epi»NE
A1 receptors like
epi>NE »_space; iso
Normally will see NE
Catecholamine structure
OH on 3+4
amine side chain (LARGER = Up Beta receptor affinity)
Catecholamine Mech
How to increase CNS penetration
remove hydroxyl groups (3+4)
COMT ONLY breaks down
catecholamines
What blocks MAO metabolism?
substitute A carbon
Contractility (SBP/CO) stimulated by
B1
Also up O2 use
Down efficiency
Peripheral resistance (DBP) lowered by
B2
Epi effects timeline
- B1+B2 = up contractility up HR, down peripheral resistance
- then A1 = vasoconstriction
- up HR then reflex lowers
Epi effects
Blood pressure
B2 + A1
low: decrease (b2 dilation)
High: increase (a1 constriction)
Epi effects
Respiratory
B2 + A1
- Bronchioles dilated (B2)
- Secretions decreased (A1)
Epi effects
Metabolism
- glycogen breakdown (b2)
- DOWN glycogen synth (a1)
- DOWN insulin secretion (a2)
- UP free fatty acids (b3)
- Detruser muscle relax (b3)
Anaphylactic shock?
Epi
- Open airways (b2)
- Down histamines/leukotrienes (b2)
- Up BP (a1)
Epi uses
- anaphylactic shock
- Asthma (B2)
- topical hemostasis (a1)
- cardiac arrest (b1)
Epi S.E.
Arrythmia
CVA
emotional
NE
Effects
- Heart (b1)
- BP UP sys/dia/mean (a1)
- CO same or down (a1)
- DOWN Glyc synthase (a1)
Shock?
Neurogenic w/ spinal anesthesia
old-school Rx
NE (levophed)
Isoproterenol effects
- Heart (B1)
- DOWN BP (B2)
- Relax bronchi (B2)
Stimulate Heart in Heart block/pacemaker insertion?
Isoproterenol
Isoproterenol
S.E.
- Fatal Arrythmia
- Tachycardia
- Palpitations
- Anginal pain
Overactive bladder?
Mirabegron (b3) MIRBETRYQ
DA effects
DOSE-DEPENDENT
- heart rate (b1)
- BP = Low dose: DOWN (DA, B2) ;; High dose: UP (a1)
Shock? (cardiogenic)
DA
DA
S.E.
- Tachycardia
- anginal pain
- arrythmia
- N/V (DA @ CTZ)
NO CNS EFFECTS
Dobutamine
Effects
- heart (B1) CONTRACTILITY ONLY
* BP= high dose: UP (a1)
Heart failure w/ open heart surgery/MI?
Dobutamine
Dobutamine
S.E.
*arrythmia
NO CNS EFFECTS
A1 ag uses
- decongest mucous membranes
- Up BP
- Dilate Pupil
- Eye drops
- decongest mucous membranes
- Up BP
- Dilate Pupil
- Eye drops
A1 ag
A1 ag
S.E.
UP BP
Non-catecholamine A1 ag
Rx
- phenylephrine (replacing psuedoephedrine) - cold
- Phenylpropanolamine PPA (CVA risk-gone)
- Ephedrine (CNS, nasal decongest)
Non-catecholamine A1 ag broken down by
NOT COMT
Substituted A carb = NO MAO
= Longer t 1/2
B2 ags
Uses
- Bronchial asthma
- Anaphylactic shock (stops mast cells releasing)
- Relaxation of uterus/delay labor = many S.E.
- Bronchial asthma
- Anaphylactic shock (stops mast cells releasing)
- Relaxation of uterus/delay labor = many S.E.
B2 ags
Uses
B2 ags
effects
Skeletal, heart (high dose
Delay premature labor?
Ritodrine YUTOPAR (b2 selective) Terbutaline BRETHINE
COPD?
Formeterol (B2 ag) PERFOROMIST
Asthma?
- Albuterol/levalbuteraol
* Terbutaline
Nasal decongestant, release NE, CNS stimulant, pressor?
b2 ag
Epehdrine
Narcolepsy
*Amphetamine/ methamphetamine
CNS stim = Release NE
Weight reduction
Amphetamine
CNS stim
ADHD
- Methylphenidate (Concerta)
- Atomoxetine (Strattera) = NE reputake inhbitor NOT SCHEDULED
*Lisdexamfetamine dimesylate VYVANSE (amphet prodrug)
CNS side effects
Abuse
Cardio/CNS stimulation
Xanthines
ADENOSINE RECEPTORS
Resemble adrenergic stimulation but NOT binding adrenergic receptors (NO BETAS)
Xanthine effects
- CNS - all cortex
- Cardio- HR + contractility up
- Respiratory = relax bronchi
Xanthines
Rx
Caffeine = CNS
Theophylline = Heart, Bronchi
Theophylline
uses
Aminophylline = asthma
+B2 ag = chronic asthma