Busy. Please wait.
or

show password
Forgot Password?

Don't have an account?  Sign up 
or

Username is available taken
show password

why


Make sure to remember your password. If you forget it there is no way for StudyStack to send you a reset link. You would need to create a new account.
We do not share your email address with others. It is only used to allow you to reset your password. For details read our Privacy Policy and Terms of Service.


Already a StudyStack user? Log In

Reset Password
Enter the associated with your account, and we'll email you a link to reset your password.

Remove Ads
Don't know
Know
remaining cards
Save
0:01
To flip the current card, click it or press the Spacebar key.  To move the current card to one of the three colored boxes, click on the box.  You may also press the UP ARROW key to move the card to the "Know" box, the DOWN ARROW key to move the card to the "Don't know" box, or the RIGHT ARROW key to move the card to the Remaining box.  You may also click on the card displayed in any of the three boxes to bring that card back to the center.

Pass complete!

"Know" box contains:
Time elapsed:
Retries:
restart all cards




share
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.

  Normal Size     Small Size show me how

USMLE - Pharm

Kaplan Section 2 Chapter 3 Adrenergic Pharmacology

QuestionAnswer
a1 activation in the eye contraction of radial muscle --> mydriasis
a1 activation in arterioles (skin and organs) contraction of arterioles --> inc TPR --> inc diastolic BP --> inc afterload
a1 activation in veins contraction of veins --> inc venous return --> inc preload
a1 activation of bladder and sphincter contraction --> urinary retention
a1 activation of male sex organs contraction of smooth muscle in vas deferens --> ejaculation
a1 activation in liver inc glycogenolysis --> more glucose released to blood
a1 activation in kidney decreased renin release --> dec BP (opposite of the B1 effects)
When are a receptors dominant and when are B receptors dominant? B receptors are more sensitive to activators than a. With drugs that exert both effects, the B responses are dominant at low doses; at higher doses, the a responses will predominate.
a2 activation in nerve terminals decreased NE release and synthesis (negative feedback mechanism)
a2 activation in platelets aggregation (if bleeding, need to stop bleeding for fight or flight)
a2 activation in pancreas decreased insulin secretion --> leave more glucose in the blood
B1 activation of heart - SA node inc heart rate --> + chronotropy
B1 activation of heart - AV node inc conduction velocity --> + dromotropy
B1 activation of heart muscle inc force of contraction --> + inotropy; inc conduction velocity (+ dromotropy); inc cardiac output; inc O2 consumption
B1 activation of Bundle of His and Purkinje fibers inc automaticity and inc conduction velocity (+ dromotropy)
B1 activation in kidney increased renin release --> increase BP (opposite of a1 effect)
B2 activation in blood vessels vasodilation --> dec TPR --> dec diastolic BP --> dec afterload (opposite a1 activation in arterioles)
B2 activation in uterus relaxation of uterine muscle (don't want to have a baby if you're fighting or flighting)
B2 activation in bronchioles bronchorelaxation/dilation
What is different about B2 receptors as opposed to the other 3 adrenergic receptors? B2 receptors are mostly not innervated. They are activated by circulating compounds or compounds released into the post-synaptic space.
B2 activation in skeletal muscle increased glycogenolysis --> release glucose from the muscle into the blood --> increased contractility and tremor
B2 activation in liver increased glycogenolysis --> release glucose from the liver into the blood
B2 activation in pancreas increased insulin secretion --> extract glucose from the blood for storage (opposite the a2 actions in the pancreas)
D1 activation in the renal, GI, and heart vasculature Vasodilation. In the kidney, it increases GFR, RBF, and Na+ excretion.
What happens physiologically when you give a1 agonists? vasoconstriction --> inc mean BP --> REFLEX bradycardia (--> dec HR --> dec CO --> bring BP back down). BP = CO x TPR, CO = HR x SV. No change in pulse pressure (difference between systolic and diastolic BP).
Phenylephrine a1 agonist. Used as decongestant; causes mydriasis without cycloplegia.
Methoxamine a1 agonist. Used to treat paroxysmal atrial tachycardia by eliciting the reflex bradycardia.
What happens physiologically when you give a2 agonists? Due to the negative feedback at the presynaptic nerve junction, it decreases NE release --> dec mean BP. Used in mild to moderate HTN.
Clonidine a2 agonist. Binds to a2 receptor (in nerves and medulla) --> decrease release of NE into the synapse --> dec TPR --> dec mean BP. Used to treat HTN and addictions (opioids, nicotine).
a-methyldopa a2 agonist. pro-drug that eventually forms a methyl dopa --> binds to a2 receptor --> decrease release of NE into the synapse --> dec TPR --> dec mean BP. Used in mild to mod HTN; dec LV hypertrophy.
What happens physiologically when you give B1 agonists? increase HR, SV, and CO
What happens physiologically when you give B2 agonists? decrease TPR
What happens physiologically when you give agonists that activate both B1 and B2? decrease TPR, decrease mean BP, increase HR; diastolic P falls more than systolic --> widens the pulse pressure
Isoproteranol B1 = B2 agonist; Used for bronchospasm, heart block, and bradyarrhythmias
Dobutamine B1 > B2; increase HR, SV, and CO (like only effects of B1); no change in TPR, GFR, or RBF. Used in congestive heart failure (causes tachyphylaxis)
Name 4 B2 agonists used in asthma Asthma AL META SALMon and TERp. Albuterol, Metaproteranol, Salmeterol, Terbuterol.
Ritodrine B2 agonist used in premature labor.
Name all the a agonists PMCM. a1 = PM --> Phenylephrine, Methoxamine; a2 = CM --> Clonidine, a-methyl-dopa
Name all the B agonists Get RID of asthma AL, who META SALMon and TERp. Ritodrine (B2), Isoproterenol (B1=B2), Dobutamine (B1>B2), B2 for asthma: Albuterol, Metaproterenol, Salmeterol, Terbuterol
Norepinephrine a1, a2, B1. Increased TPR and both systolic and diastolic BP (pulse pressure increases). Reflex bradycardia.
Epinephrine a1, a2, B1, B2.
Low-dose epinephrine increase HR (B1), but TPR and diastolic pressure decrease (B2), so you get a slight decrease in BP overall, and an increase in the pulse pressure
Medium dose epinephrine increase HR (B1), increase in BP overall, and an increase in the pulse pressure
High-dose epinephrine a activation dominates --> increased TPR, increased diastolic BP, and increased mean BP. You get a reflex change in HR (B1), and a2 stimulation dominating over B2.
What would you use epinephrine for? 1. Anaphylaxis 2. Cardiac arrest 3. Glaucoma 4. Adjunct to local anesthetics
MAO Type A Anywhere, but mostly in liver. Metabolizes NE, 5HT (serotonin), and tyramine.
MAO Type B In brain. Metabolizes dopamine.
Name the drugs that inhibit MAO MAO is inhibited by the PHoNE call from TRANsylvania. Phenelzine and tranylcypromine. They block MAO and therefore, increase prejunctional NE levels.
Name the drugs that release NE from the mobile pool. You can EAT in the mobile pool. Ephedrine, amphetamine, and tyramine. They increase the prejunctional levels of NE.
Cocaine Block reuptake of NE into the presynaptic junction --> prolong NE action in the nerve junction --> vasoconstriction. In CNS, blocks reuptake of NE, DA, and 5HT. Also used as local anesthetic because blocks voltage-dependent Na+ channels.
Tricyclics Block reuptake of NE into the presynaptic junction --> prolong NE action in the nerve junction --> vasoconstriction.
Low-dose Dopamine D1 activation --> increases RBF and GFR
Medium-dose Dopamine B1 activation --> increased cardiac output
Very high-dose Dopamine a1 activation --> increased BP
Tyramine High levels --> displaces NE from mobile pool --> increased NE --> vasoconstriction. Metabolized in GI tract and liver by MAO Type A.
Amphetamine Releases NE from mobile pool --> increased NE --> SANS stimulation and reflex bradycardia. Used for ADHD, short term weight loss, narcolepsy.
What is special about the indirect-acting adrenoceptor agonists? Act only on tissues innervated by SANS (don't act on the denervated receptors) because these effect the release and uptake of NE. Doesn't attach to any receptors themselves.
Name the a receptor antagonists Angry a said, "YO MIRTA! PRAise PHEN PHEN!" a2: Yohimbine and Mirtazapine; a1: Prazosin (+ other -osins); a: Phentolamine, Phenoxybenzamine
What are the effects of a receptor antagonists? a1 antagonism: dec TPR, dec BP --> reflex tachycardia and salt and water retention; a2 antagonism --> more NE release.
Phentolamine a antagonist. Increases gastric acid secretion, short acting. Used in pheochromocytoma (tumor that secretes lots of NE and epi) and vasoconstrictor OD.
Phenoxybenzamine a antagonist. Irreversible. Short-term use in pheochromocytoma (tumor that secretes lots of NE and epi).
Prazosin a1 selective antagonist. dec TPR, dec BP; less reflex tachycardia because a2 receptors are not blocked and negative feedback still in play. However, because no reflex mechanism, causes postural HTN. Used for mild to moderate HTN and for BPH.
Yohimbine a2 selective antagonist. Increase NE outflow. Used to treat postural HTN and impotence.
Mirtazapine a2 selective antagonist. Increase NE outflow. Used to treat depression.
What are the general effects of B blockers? On heart, eyes, lungs, and metabolism. Heart - dec contractility, HR, CO, O2 demand, & BP (no ortho hypoTN bc a2 not blocked); eyes - dec ciliary secretions --> dec intraocular P --> used in glaucoma; lungs - bronchospasm in asthma; metab - dec glycogenolysis --> delay recovery frm hypoglycemi
Propranolol prototype B blocker, nonselective.
What happens with chronic use of propranolol? increased LDL and/or TG's
What happens with chronic use of B blockers in general? B receptors are upregulated --> need to taper dose when withdrawing the medication to avoid rebound CV effects
In what pts would you want to use a B1-specific blocker instead of a nonselective B blocker? Asthma - to avoid bronchospasm; Diabetes - less effects on metabolism --> B2 promotes glycogenolysis so B2 blocker would delay recovery from hypoglycemia; Peripheral vascular disease -- B2 causes vessel dilation so you wouldn't want to block that in these
Which B blockers do NOT enter the CNS? atenolol and nadolol. NADir stands at Attention when you tell him that he can't enter the CNS war room.
Which B blockers have the longest half lives? Carvedilol and nadolol. It takes NADir a LONG time to CARVE the turkey.
Which B blockers have combined a and B blocking activities? Carvedilol and labetalol. At alpha beta supermarket, they CARVE and LABEl the turkey.
Sotalol K+ channel blocker as well as a B blocker
Increase in the cytosolic [ ] of NE in sympathetic nerve endings leads to A. activation of dopa decarboxylase B. inc release of NE C. inhib of tyrosine hydroxylase D. stimulation of MAO E. none of above C. inc NE in cytosol inhibits tyrosine hydroxylase, the rate limiting step of NE production
Administration of hexamethonium will cause A. abolition of the circulatory reflex, B. cycloplegia, C. reduction of bladder tone, D. xerostomia, E. all of the above PANS dominates in the ANS, so hexamethonium will oppose all PANS tone. All autonomic reflexes are blockes, cycloplegia because of M3 block in ciliary muscle in eye, GI/GU smooth muscle relaxes because you stop wanting to pee or poop, decrease in salivati
Reflex tachycardia is most likely to occur after the systemic administration of A. albuterol, B. methoxamine, C. phenylephrine, D. propranolol, E. mecamylamine A. albuterol is B2 agonist --> decrease TPR --> reflex tachy. Methoxamine and phenylephrine are a1 agonists --> reflex bradycardia. Propranolol --> can't have reflex tachy because B1 is blocked. Mecamylamine -- all ANS reflexes are blocked.
Side effects of propranolol 1. inc blood lipids (TG, LDL) 2. AV block, 3. CHF, 4. bradycardia, 5. impotence, 6. CNS - sleep and sedation
Can topical use of nonselective B blockers for glaucoma worsen asthma in a patient? yes.
Side effects of a-methyldopa sedation, dizziness, dec libido, edema, + Coombs hemolysis
For which type of HTN pts should you consider a-methyldopa? Those with renal dysfunction and pregnancy.
Where are a1 receptors in the body? Eye, vessels, liver, kidney, bladder, vas deferens
Where are a2 receptors in the body? Nerve terminals, platelets, pancreas
Where are B1 receptorsin the body? Heart and kidney
Where are B2 receptorsin the body? Vessels, skeletal muscle, bronchioles, liver, pancreas, uterus
Side effect of clonidine Dry mouth, sedation/insomnia, edema, bradycardia. Severe rebound HTN if withdraw suddenly.
Reserpine destroys NE storage granules in the nerve endings --> dec NE outflow --> dec CO and dec TPR. In CNS, dec NE, 5HT, and DA outflow.
Side effects of reserpine mild orthostatic hyPOtension, fluid retention, sedation, severe depression, inc GI secretions
Guanethidine Binds to storage granules in nerve endings to inhibit NE release.
How do tricyclics affect guanethidine? decrease guanethidine uptake and effectiveness.
Side effects of guanethidine diarrhea, fluid retention (need diuretics), orthostatic hyPOtension, sexual dysfunction
What is the mechanism of prazosin in treating BPH? a1 blocker --> dec sphincter tone --> better voiding of the bladder --> dec frequency of urination. Doesn't change prostate size much.
Side effects of prazosin/doxazosin/terazosin first-dose syncope (because block the vasoconstriction of a1), orthostatic hypotension (lose the reflex tachy with blocking of a1), urinary incontinence (esp in women); no adverse effects on lipids
What would you use dopamine for? acute heart failure
what is the side effect of dopamine? tachyphylaxis when used to increase cardiac contractility
What do you use carvedilol for? Use in heart failure patients to slow the remodeling that accompanies increased SANS stimulation in CHF. Can also use for pts with angina for its vasodilation effects (equivalent to the nitrate, Isosorbide)
Created by: christinapham