Pharacology Exam 2: Adrenergic Blockers Flashcards

Alpha
Terms Definitions
what is a non-selective alpha adrenergic blocker?
Phenoxybenzamine
Name the non-selective beta adrenergic blockers?
Propanolol- Nadolol- Timolol- Pindolol- Carteolol
name the alpha 1 selective blockers:
Prazosin: Terazosin and DoxazosinPDT
name the alpha 1A selective blocker:
Tamsulosin
Name the Beta1 aka cardio selective blockers:
Metoprolol- Atenolol- Betaxolol- Esmolol- Bisoprolol- Acebutolol
combined alpha and beta adrenergic blockers:
LabetalolCarvedilol
Labetolol is an___ blocker used in ___ ___.
- alpha and beta blocker- hypertensive crisis
___ _ antagonists are never used b/c you never want the bronchioles constricting.
beta 2
- sin =
alpha blocking
lol =
beta blocking
Alpha blockers are ____, meaning they have no ___ ___, however they do produce a physiologic change b/c they end up reducing the sympathetic tone.
- antagonists- no intrinsic activity
alpha adrenergic blockers:
block all agents that act directly or indirectly on alpha receptorsThey block the effects of any compound acting at a receptors (whether that compound acts directly or indirectly)Endogenous agonists (epinephrine; norepinephrine). Note: sympathetic tone explains why antagonists produce effects.Exogenously applied drugs (e.g. norepinephrine, phenylephrine, tyramine)
alpha 1 family:
alpha1A, alpha1B, alpha1D
alpha 2 family:
alpha2A, alpha2B, alpha2C
so a nonselective alpha blocker blocks:
- alpha 1A, alpha1B, alpha1D, alpha2A, alpha2B, alpha2C
an alpha 1 selective blocker blocks:
alpha1A, alpha1B, alpha1D
an alpha 2 selective blocker blocks:
alpha2A, alpha2B, alpha2C
Alpha 1 receptors are mostly ___ and mediate the effects on __ __ and ___.
- postsynaptic- smooth muscle and glands
Alpha 2 receptors, which are ___, are mostly ___ and are responsible for ___release of NE. When blocked the release of norepinephrine ___.
- autoreceptors- presynaptic - decreasing- increases
Some of the drugs differentiate a1 from a2 by family, but very few differentiate subtypes of receptors. The appearance of tamsulosin (see below) is particularly interesting in this regard.
Tamsulosin is specific for the ___ __ receptor. It is rare for a drug to be selective for a subtype, but this one is. KNOW IT.
alpha1A
alpha 1 receptors on arterioles and veins cause ___.
constriction
alpha 1 receptors in the eye cause:
- contraction of radial muscle leading to mydriasis aka dilation
alpha 1 receptors in the intestines cause:
- contraction of sphincters- decreased motility (hyperpolarization leads to relaxation)
___ ___ receptors are in the prostate and cause and promote what?
- alpha 1a- contraction- tissue growth
alpha 1 receptors in the urinary bladder sphincter causes:
constraction
what kind of blocker would you want to use for a man with BPH?
alpha1a blocker to reduce tone and cause relaxation of prostate so he doesn't have to pee as much
alpha __ is predominant in vasculature.
alpha 1b in vasculature
Alpha 2 autoreceptors are on __ ___ ___ and normally ___ outflow of NE.
- norepinephrine nerve terminals- decrease
alpha 2 autoreceptors are also in the ___ and ___ sympathetic outflow.
- CNS- decrease
prototype of nonselective alpha blockers:
Phentolamine/Phenoxybenzamine, this is also an agonist at muscarinic and histamine receptors
If you are looking at contraction of arterial strips, which is mediated by _ _ receptors and NE, and you add phentolamine, what would happen to the chart?
- alpha 1 - the curve would shift to the right b/c phentolamine is a competetive antagonist to NE. Phentolamine is a nonselective alpha blocker, so it would take more NE to get same effect
So if we are looking at the relaxation of bronchial smooth muscle which is mediated by _ __ receptors and ____. And if we added propanolol, what would happen to the curve and why?
- beta 2- isoproterenol- the curve would shift to the right b/c propanolol is a nonselective beta blocker and is a competitive antagonists, so it would take more isoproterenol to get same effect
So if we are looking at contraction of the heart which is mediated by ___ __ receptors, and we add _____, what will happen to the curve and why?
- beta 1- propanolol- the curve will shift to the right b/c propanolol is a competetive antagonist and is a nonselective beta blocker
Phenoxybenzamine is a ___ ___ blocker. Thus it binds ____ to __ _ and ___ _ adrenergic receptors.
non-competitive aka non-equillibriumcovalentlyalpha1 and alpha2
Phenoxybenzamine is non-competitive nonselective blocker of alpha receptors. It has a __ onset b/c it takes several minutes to form ___ ___, and a ___ offset b/c the elimination half life is __ hours, so ___ ___ must be synthesized.
- slow- covalent linkages- slow- 24 hours- new receptors
Phenoxybenzamine:
non-competitive alpha blockerbinds covalently/irreversible to active site on alpha receptorscannot be overcome by adding more agonist
so if add phenoxybenzamine to NE and looking at vascular smooth muscle contraction, what will happen to curve and why?
it will shift to the right but not go up as high b/c this is a non-competitive blocker of alpha receptors. this cannot be overcome by adding more agonist.
effect of phenoxybenzamine on blood pressure and how?
- reduces blood pressure b/c block effects of NE
clinical uses of phenoxybenzamine:
1. Pre-op for Pheochromocytoma: when this tumor is operated on it tends to dump out NE and Epi> blood pressure goes out the roof and can lead to stroke- so 24-48 hours before surgery phenoxybenzamine is given since it is a non-competitive antagonist so it will block effect of NE and Epi on alpha receptors, also will give patient beta blocker to protect the heart
Name the alpha 1 selective blocker:
Prazosin
Prazosin:
alpha 1 selective blocker
uses of Prazosin:
- Prazosin is an alpha1 selective blocker- used to treat BPH to relax prostate around bladder, used less now due to b.i.d dosing and orthostatic hypotension- hypertension treatment
why is Prazosin used less now?
- it is an alpha 1 selective blocker (used to be used often for BPH and HTN) but there are also alpha 1 receptors in veins, so there was vein constriction, decreased venous return> decreased cardiac output> orthostatic hypotension
Doxazosin and Terazosin are similar to ____ in that they are ___ _ selective blockers, these two just have a ___ half life so only have to be taken once a day. However, these are also not used often b/c they also cause ___ ___.
- Prazosin- alpha 1- longer- orthostatic hypotension
The preferred alpha 1 selective blocker that does not cause orthostatic hypotension is:
Tamulosin
Tamulosin is a ___ alpha blocker (binds mostly alpha1a and a little alpha 1b). It is highly efficacious in treating ____ and has very little vascular effects since it has little ____ activity.
- competitive- BPH - alpha 1b
KNOW TAMSULOSIN- ALPHA 1A AGENT- does not cause orthostatic hypotension, may get a little nose stuffiness b/c blocking alpha1a in nose, but side efefcts not really bad.
3 familiesb1b2b3All use Gs second message system
Beta 1 receptors are on the heart and cause:
Increases rateIncreases contractilityEnhances conduction through the AV node
the uterus has ___ __ that cause ___.
beta 2relaxation
bronchioles have ___ __ receptors that cause ___.
beta 2 relaxation
arterioles have __ _ receptors that cause ___ which result in ____ blood pressure decreasing.
- beta 2- relaxation- diastolic
skeletal muscle has __ _ receptors that promote ___ ___ and increase ___ ___ __.
- beta 2- potassium uptake- high energy compounds
The liver has ___ __ receptors that promote ____.
- beta 2 - glycogenolysis
Fat cells have ___ __ receptors that increase ___.
beta 3lipolysis
Note: no drugs are available that selectively stimulate or block b3 receptors
Prototype of beta adrenergic blocker:
Propanolol
Propanolol is a _____ ____ antagonist at __ _ and __ _ receptors. High therapeutic doses may also have a non- receptor related ___ ___ effect.
- non-selective competitive- beta 1 and beta 2- membrane stabilizing
Propanolol effects on the heart:
- decreased cardiac output- decreases HR (negative chronotropic effects)- decreases spontaneous pacemaker activity- used as antiarrhythmic drug
Propanolol effects on blood vessels:
- decreased renin release (b/c renin release is controlled by beta1 receptors on kidneys) leading to decreased angtiotensin and decreased aldosterone- slowly developing decrease in peripheral resistance
Propanolol effects on bronchial smooth muscle:
- blocks relaxationHUGE CONTRADINDICATION FOR ASTHMA
Metabolic effects of propanolol:
- blocks lipolysis and glycogenolysis
Following oral administration of propanolol, up to ___ may be inactivated by ___ ___ ___, thus it has a __ bioavailability.
- 2/3- first pass effect- low Large inter-individual variationVariation is relatively constant for a given patientTitrate the dose upward for each patient.
Clinical uses of propanolol and why:
1. Angina pectoris- reduces cardiac work and oxygen consumption2. Hypertension- decreases peripheral resistance by decreasing renin release3. Migraine headaches (prophylactic treatment)
angina pectoris is same as:
exertional angina
Increasing propanolol over weeks, and we see the heart rate comese down (beta 1 blockade). Systolic and diastolic come down slightly, and renin release decreases. Decreased bp.
more clinical uses for propanolol:
4. Arrhythmias5. Pheochromocytoma (but give alpha blocker first)6. Thyrotoxicosis7. anxiety adjunct treatment8. reduce mortality post MI
Thyroitoxicosis- when thyroid way over stimulating body,
side effects of Propanolol:
common CNS effects: - dizziness- tiredness- nausea- depression- vivid dreams- impotence
In insulin dependent diabetics, propanolol ___ recovery from ____ b/c blocking ___ __ inhibits ____.
- delays- hypoglycemia- blocking beta 2 inhibits glycogenolysis
sudden withdrawal from propanolol:
- may see rebound hypertension and possibly anginal attacks- beta receptor synthesis is increased by beta blocker use (up-regulation)
contraindications to propanolol use:
- asthma- COPD- cardiogenic shock- acute treatment of heart failure- 2nd degree heart block- 3rd degree heart block3r
3rd degree heart block:
SA node is firing but not getting to the ventricles b/c the AV node is NOT firing this is made worse by beta blockers- propanolol
2nd degree heart block:
not all SA firings are causing the AV node to fire
2nd degree heart block the AV node is not going off every time the SA node does. With third degree heart block the AV is not firing at all. Both of these are contraindications for beta blockers.
propanolol drug interactions:
Additive with hypotensive agentsProlongs hypoglycemia in patients taking hypoglycemic agents. Masks signs of hypoglycemia.Mask symptoms of hyperthyroidism
Diabetics recognize they are getting hypoglycemic b/c they get shaky>symp acitve> beta 2 on muscles are stimulated. They need sugar. So do not want to block beta receptors with diabetics.
___ is another non-selective beta blocker that may be preferred over propanolol b/c of its ___ duration of action.
Nadolol
____ is a non-selective beta blocker in eye drops in patients with glaucoma b/c it decreases production of aqueous humor.
Timolol
what is the cardio/beta 1 selective antagonist:
Metoprolol
beta 1 selective blockers:
Metoprolol as prototypeAtenolol (Tenormin)hypertension, stable anginaEsmolol (Brevibloc)Very short-acting – used in management of myocardial infarction
still dont give beta 1 selective blockers to asthmatics.
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