Adrenergics/Antiadrenergics

Question 1

What is the catecholamine synthesis pathway?

Answer 1

Tyrosine –> dopa –> dopamine –> norepinephrine –> epinephrine

Question 2

Which type of antiadrenergic causes the worst tachycardia?

Answer 2

Non-selective alpha blockers (worse than selective a1 blockers)

This is because blocking a1 drops BP and blocking a2 prevents feedback inhibition of NE release –> two factors that cause your HR to increase

Question 3

What enzymes metabolize catecholamines?

Answer 3

Monoamine oxidase (MAO) and catechol-o-methyl-transferase (COMT)

Both are in the liver, kidneys, and GI tract

Question 4

Discuss what happens with chronic adrenergic agonist/antagonist use.

Answer 4

Chronic adrenergic agonist use can lead to desensitization and downregulation, while chronic antagonist use can have the opposite effect

Question 5

What three drugs block the NET (norepinephrine transporter) to increase synaptic NE?

Answer 5

CIA - cocaine, imipramine, and atomoxetine

Question 6

Describe the mechanism of action of tyramine.

Answer 6

The large load of tyramine displaces NE from vesicles forcing NE out where it can be degraded by MAO (this is why you get hypertensive crisis if on MAOI and have tyramine)

*Tyra Banks is mean because she throws out and degrades excited models when their pictures suck, and then they all have hypertension because they’re depressed and have no skills because they’re models and it’s a midlife crisis.

Question 7

Describe the mechanism of action of guanethidine.

Answer 7

Enters via NET and concentrates in the vesicles blocking NE so MAO metabolizes it.

*Guanethidine is the ugly girl who wishes she was Tyra Banks but she’s fat and just gets physically in the way of excited models.

Question 8

Describe the mechanism of action of reserpine

Answer 8

It blocks VMAT (the transport protein that brings neurotransmitters into vesicles), depleting vesicular NE over time (gradual effect).

*Reserpine = no more reserve

Question 9

What are the xanthines and how do they work?

Answer 9

Caffeine and theophylline. They are antagonists at adenosine receptors causing CNS stimulation.

*THEY DON’T BIND ADRENERGIC RECEPTORS

Question 10

Where are B1 receptors located and what happens when stimulated?

Answer 10

In the heart; increase HR, contractility, conduction, and irritability

Question 11

What happens when you stimulate B2?

Answer 11

Vasodilation –> decreased BP, bronchodilation, increased glycogen breakdown

Question 12

What happens when you stimulate a1 receptors?

Answer 12

Decreased secretions, increased BP/automaticity/HR/conduction velocity/CO/oxygen consumption, decreased cardiac efficiency, decreased glycogen synthesis, bladder sphincter contraction

Question 13

What happens with B3 stimulation?

Answer 13

Increased free fatty acids, relaxation of the detrusor muscle

Question 14

What is the mechanism of action of epinephrine?

Answer 14

Agonist to it all, a1, a2, B1, B2, B3

Question 15

What drug interactions are relevant when giving epinephrine?

Answer 15

Any alpha blockers. It will cause a dip in blood pressure from B2 effects, which is called “epi reversal”

Question 16

What are the primary clinical uses of epinephrine?

Answer 16

Drug of choice for anaphylaxis, also used to support BP and in cardiac arrest to resuscitate the heart

Question 17

What is the mechanism of action and use of norepinephrine?

Answer 17

It is an a1 and B1 agonist used for shock

Question 18

What drug is a non-specific beta agonist?

Answer 18

Isoproterenol

*Iso, equal, likes both betas because equality.

Question 19

What is the clinical use of isoproterenol?

Answer 19

Used in emergencies to stimulate the heart in patients with heart block and when preparing to insert a pacemaker.

*Better start up your heart again before you turn to ice…

Question 20

Describe the mechanism of action and clinical use of dopamine.

Answer 20

It is an agonist at DA receptors, B1, B2, and at high doses a1. It’s used for cardiogenic shock.

Question 21

What is a common side effect of dopamine receptor agonists?

Answer 21

The stimulation of the chemoreceptor trigger zone (CTZ) which induces vomiting.

Question 22

Describe the mechanism of action and clinical use of dobutamine.

Answer 22

It is a B1 agonist, and at high doses a1 agonist. Used to treat heart failure associated w/ MI or open heart because it is mostly selective for B1 giving rise to unique inotropic qualities

Question 23

Describe the mechanism of action and clinical use of phenylephrine.

Answer 23

An alpha agonist used to treat rhinitis. Is a decongestant of mucous membranes, raises BP, dilates pupils (thus used in eye drops)

Question 24

Describe the mechanism of action and clinical use of ephedrine.

Answer 24

A weak alpha and beta agonist that also releases NE (CNS stimulant) used as a nasal decongestant and as a pressor agent.

Question 25

Name the selective B2 agonists and what they treat.

Answer 25

Albuterol and terbutaline, treat asthma.

*Terbutaline sounds like turtle, and they can’t breathe underwater so there ya go - asthma

Question 26

Describe the mechanism of action and clinical use of amphetamine.

Answer 26

A substrate for NET so it increases synaptic NE via facilitated exchange diffusion (risk of abuse, can cause excessive CNS stim). Used for narcolepsy and weight reduction

*well just think methamphetamine which makes you skinny and you can stay awake looking for drugs

Question 27

Describe the mechanism of action and clinical use of methylphenidate.

Answer 27

A CNS stimulation, used to treat ADD/ADHD.

Also called RITALIN AHHHH DUH.

Question 28

Describe the mechanism of action and clinical use of phenoxybenzamine.

Answer 28

An alpha blocker somewhat selective for a1 that is irreversible. Used for pheochromocytoma mgmt (medulla tumor), BPH (relaxes smooth muscle in bladder, prostate capsule, and prostatic urethra to improve flow)

*Pheno for your pheo and your peno…penis……

Question 29

Describe the mechanism of action and clinical use of phentolamine.

Answer 29

A non-selective alpha blocker used w/ propanolol for pheochromocytoma mgmt.

*remember that non-selective alpha blockers have worse reflex tachycardia

Question 30

How does a2 help regulate NE release?

Answer 30

There are presynaptic a2 receptors that exert feedback inhibition when stimulated by NE

Question 31

Describe the mechanism of action and clinical use of propanolol

Answer 31

A non-selective beta blocker that treats angina and SVT arrhythmias

*remember that B1 increases CO (cardiac output) so blocking that has the opposite effect, so drop in CO and all the other B1 things cause drop in BP and HR

Question 32

Describe the mechanism of action and clinical use of atenolol and esmolol.

Answer 32

Both are selective B1 blockers (so there’s reduced risk of bronchospasm). Esmolol has a short half-life good in emergencies. They decrease HR, myocardial O2 demand, etc.

Question 33

Describe the mechanism of action and clinical use of timolol.

Answer 33

A non-selective beta blocker (though it’s used for it’s B1 effects) to treat glaucoma by decreasing aqueous humor production

Question 34

Describe the mechanism of action and clinical use of prazosin.

Answer 34

An alpha blocker for htn and BPH

Question 35

What two drugs are a2 agonists and what is their effect?

Answer 35

Clonidine and methyldopa.

As a2 agonists they cause inhibition of NE release, useful in treating essential htn

Question 36

What side effects are associated with clonidine?

Answer 36

It is used to treat opioid withdrawal symptoms but ironically can have abrupt withdrawal itself when stopped causing hypertensive crisis

*Clonidine clobbers you with hypertension if you don’t take it.