Term
| What will α1 agonists produce? |
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Definition
-(+)TPR & BP
-*Potential reflex bradycardia
-No change in pulse pressure
-CO may be down, but offset by increased venous return |
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Term
| What does the reflex bradycardia? How would we block? |
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Definition
-Parasympathetic via the M2 receptor
-We would have to block either the M2 or Nn (ganglionic blockade) |
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Term
| What are two α1 agonists and uses? |
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Definition
1. Phenylephrine; *nasal decongestant and ophthalmologic use (to produce *mydriasis without cycloplegia*)
-Works by topical vasoconstriction in nose
2. Methoxamine; to treat paroxysmal atrial tachycardia caused by vagal reflex (atria super sped up) (not in use)
-Works because we raise bp, giving **reflex bradycardia
-Essentially, we don't use α1 agonist systemically (for hypotension, etc.) because we would have to worry about ischemia and *reflex bradycardia
-Instead we use it more topically |
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Term
| What will α2 agonists produce? What are two drugs and their use? |
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Definition
-Decreases *sympathetic outflow by stimulating prejunctional receptors in the CNS (inhibitory)
1. Clonidine
2. Methyldopa
-Both used to treat mild to moderate *hypertension
-Do not work acutely because they take time to effect synthesis etc. (no tracings)
-(more in cardiovascular section) |
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Term
| What will β agonists produce? |
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Definition
(+)HR
(-)BP
(+)Pulse pressure
-The β1 is acting to increase HR, SV, CO, and *systolic BP
-The β2 is acting to decrease TPR, and *diastolic BP
-Together they produce marked increase in pulse pressure
-TPR is a larger determinant of BP, so there is a **net drop in mean BP** |
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Term
| What are some β agonists drugs and uses (1 for both, 1 for β1, and 4 for β2)? What negative side effects do the selective drugs help avoid? |
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Definition
1. Isoproterenol (β1=β2); for brochospasms (β2), and heart block & bradyarrhythmias (β1)
-Can cause flushing, angina, and arrhythmias
-Better if we can target receptors so we don't give our asthma patient tachycardia
2. Dobutamine (β1>β2); for acute CHF (avoids flushing)
Selective β2 agonists (avoids tachycardia);
3. Salmeterol (slow, prophylactic), albuterol, terbutaline; for treating asthma
4. Ritodrine, prevent premature labor (uterine relaxation)
-Will cause fight or flight state, with anxiousness, tremors, etc. |
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Term
| What will NE produce and what does it act on? |
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Definition
-α1; (+)TRP & BP
-β1; (+)HR, SV, CO, pulse pressure (from +systolic BP)
-It acts on all but β2
-Has potential for *reflex bradycardia
-Remember, we can do a ganglionic blockade or an M2 antagonist to block the reflex action |
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Term
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Definition
-Never!!
-Because it cannot act on β2 receptors |
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Term
| What does Epi effect at different doses? What is the effect? What drug does it look like in each case? |
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Definition
LOW DOSE; only β effect (same as **isoproterenol)
-β1; (+)HR & pulse pressure
-β2; (-)BP (+)pulse pressure
MEDIUM DOSE; α1 and β2 cancel (same as **dobutamine)
-β1; (+)HR & pulse pressure
-β2; (-)BP (+) pulse pressure
-α1; (+)BP
-Overall; BP stays the same, and pulse pressure & HR rise (i.e. only the β1 effect)
HIGH DOSE; α1 overcomes β2 (same as **NE)
-α1; (+)BP
-β1; (+)HR & pulse pressure
-β2; (-)BP (+) pulse pressure
-Just as with NE, we can get reflex bradycardia
-Overall, the dose causes a switch from a *β2 to an α1* response, with β1 effects (+HR) always being present
-Remember that once the α1 response predominates, the reflex may also mask the β1 response |
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Term
| When really are reflexes possible? |
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Definition
-When we have a ++ or -- for HR & BP
-If they are going in the same direction, the reflex tries to switch the HR to the other direction, but if it is already in the opposite direction, the reflex will not be elicited |
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Term
| How would we be able to distinguish high dose Epi from NE? |
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Definition
-Epi; α1, β1, (β2)
-NE; α1, β1
-The Epi still has some β2 effect, and will cause some things not seen in NE; sm. muscle dilation, such as *bronchodilation, and increased glucose use/production
-Can also note an **epinephrine reversal |
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Term
| What is an epinephrine reversal? |
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Definition
-Use an α1 blocker to reverse hypertension to hypotension when caused by too much epinephrine
-Basically, if it was Epi, the *β2 receptors will be unmasked*
-Would be good for someone who we treated for shock (hypotension) with too much Epi and they started getting reflex bradycardia and too high of BP
-Would not have a big reversal with NE (no β2) |
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Term
| What are the uses of NE and Epi? |
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Definition
-Cardiac arrest ; (β1 primarily)
-Adjunct to local anesthetic (significant vasoconstriction)
-Hypotension; (α1 & β1)
-Anaphylaxis and asthma (Epi only; β2) |
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Term
| What are three releasers and how do they act? What drug interaction do we have to be wary of? |
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Definition
-They displace NE from the mobile pool
-They may interact with MAOa inhibitors (for depression) and cause **hypertensive crisis (from α1 & β1 action)
1. Tyramine; found in wine, cheese and other foods
-A concern for those on MAOa inhibitors, especially because *MAOa in the gut metabolizes tyramine*
2. Amphetamines; illegal and prescribed
-Methyl phenidate is one used for narcolepsy and ADHD
3. Ephedrine; cold medication
-Ephedrine itself is no longer on the market in the US, but derivatives such as pseudoephedrine, also cannot be taken by a patient on a MAOa inhibitor |
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Term
| What are two reuptake inhibitors? |
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Definition
-Cocaine
-Tricyclic antidepressant (in part)
-When people snort cocaine, they get vasoconstriction, ischemia, and nasal septum perforation
-People usually smoke it however; which causes dilated cardiomyopathies, arrhythmias, and stroke
-People on tricyclic antidepressants also have to worry about the cardiotoxicity |
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Term
| Sidebar; What is shorthand for serotonin? |
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Definition
| -5-HT for 5-hydroxytryptamine |
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Term
| Where do we find MAOa & MAOb? |
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Definition
-MAOa is mostly in the liver but also Anywhere; metabolizes NE, 5-HT, & *tyramine
-MAOb is mostly in the Brain; metabolizes DA |
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Term
| What will α receptor antagonists produce and what are their uses? What would be some possible side effects and how would we deal with them? |
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Definition
-They will cause a decrease in TPR and BP
-May cause *reflex tachycardia and *salt and water retention from reflex renin system
-Can fix by also giving *β blockers and *diuretics (***classic hypertension treatment plan***)
-Used to treat;
-*Hypertension
-*Pheochromocytoma (adrenal tumor); α **nonselective
-Benign prostatic hyperplasia (BPH); α1 selective blocker |
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Term
| What are the two nonselective α blockers? What are they used for? |
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Definition
-Phentolamine; competitive (not used much)
-Phenoxybenzamine; noncompetitive**
-Again, the second can treat pheochromocytoma (where we have wayyyy too much Epi floating around)
-We need it to be noncompetitive, bc otherwise the Epi would kick it out |
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Term
| What are the selective blockers for both α1 (4) and α2 (2)? What are they used for? |
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Definition
-α1 blockers; prazosin, doxazosin, terazosin, tamsulosin
-Notice they all end in **-zosin or **-osin
-For treating *BPH; relaxes sphincters
-Also can treat the often comorbid *hypertension
-α2 blockers;
-Yohimbine; for *postural hypOtension and impotence
-*Mirtazapin; antidepressant |
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Term
| How do we use a β blockers together with an α blocker in treatment of pheochromocytoma? |
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Definition
-We would need to use the β blocker for the tachycardia that is caused by ++Epi and action on *β1 receptors
-We want to block the β1, but if we did it without first blocking the α1 receptor, we would make the hypertensive crisis worse by shifting all action to α1 receptors
-Therefore *phenoxybenzamine is always used **before the β blocker |
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Term
| Where do we see β1 receptors and what would we expect to see in their blockade? What are typical uses? What about reflex tachycardia? What about reflex renin? |
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Definition
β1 blockade;
-Heart; (-)HR, SV, & CO (decreases O2 demand)
-Kidney; (-) Renin release (decrease H2O & salt retention)
-Eye; (-) Aqueous humor production (glaucoma)
-The lower HR is good for *arrhythmias and tachycardia (esp. supraventricular tachycardias; SVTs - i.e. atrial)
-The lower 02 use is great for *angina and preventing MI
-The lower renin will lead to lower TPR (via lower angiotensin II); good for *hypertension & *CHF
-Would also reduce *edema
-*Reflex tachycardia is not possible*
-*Reflex renin is also not possible*
-Remember that both of these were a problem if we were to block *α1 alone to treat hypertension
-This means β blockers are a good initial treatment in *mild hypertension (HTN) (may have to add in α1 block down the road) |
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Term
| What would we see in a β blocker overdose? how do we treat? |
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Definition
-We would see an *AV block
-Can use **glucagon to reverse effect
-Can't use β agonists, because β receptors get unregulated in chronic β blocker use, and an agonist would produce too strong an effect
-Glucagon will increase cAMP in a more controlled manner
-WIll also help with metabolic effects of β blockade |
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Term
| What would we expect to see in a β2 blockade? |
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Definition
β2 blockade;
-*Bronchospasm (in asthmatics)
-*Vasospasm (in vasospastic disorders; like *prinzmetal)
-*Metabolic effects; blocked glycogenolysis and gluconeogenisis, increased LDLs & TGs (problems fasting; will get hypoglycemia, esp. if on **diabetic drugs)
-β2 blockade has no clinical use
-β2s are mostly only stimulated when needed
-These are simply unwanted effects of using β blockers which can be selective for β1, but **not perfectly so |
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Term
| So then, what are the three contraindications of using β blockers? |
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Definition
1. Asthmatics
2. Vasospastic diseases (esp. *prinzmetal angina)
3. Diabetics
-If treating angina, β blockers are great, but they may actually cause an MI in prinzmetal angina patients!
-Instead, we use Ca2+ channel blockers |
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Term
| What are some beta blocking drugs? How do we tell they are beta blocking based on the name? How do we tell if they are β1 selective or not? (remember, none are β2 selective) |
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Definition
-Acebutolol
-Atenolol
-Metoprolol
-Pindolol
-Propranolol
-Timolol
-All drugs ending in **-olol are β blockers
-If the first letter is A-M, they are β1 selective; these would be safER for those contraindicated for β blockers |
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Term
| Which of the β blockers were ISM, and what does that mean? What is an advantage? |
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Definition
-*Acebutolol & **pindolol are both intrinsic sympathomimetic drugs (mimic NE/Epi effect)
-Means they are **partial agonist
-This is good because they will help support necessary basal levels of action
-Less worry about overdose (bradycardia), *hyperlipidemia (from blocked lipolysis), etc.
-The pindolol in particular will help promote slight **bronchodilation and vasodilation via its partial agonist action on the β2 receptor |
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Term
| Which of the β blockers will not enter the CNS? |
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Definition
-Atenolol; is water soluble and won't cross BBB
-Means, it will have less **sedative effects than others |
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Term
| Which one of the β blockers can actually be used as a sedative? What do we have to worry about? |
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Definition
-Propranolol has a highly sedative effect
-All of the B blockers can depress CNS function
-For this reason, we have to worry about mixing β blockers with other depressants such as alcohol or sedatives |
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Term
| Which are the class II antiarrhythmic β blockers (3)? |
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Definition
-Propranolol, acebutolol, esmolol
-Pro-ace-esmo |
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Term
| Which can we use for glaucoma? |
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Definition
-Timolol
-Think of Tim Ward's bulging eyes (from glaucoma lol) |
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Term
| What can we use for thyrotoxicosis? Why? What else can it be used for? |
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Definition
-Propranolol
-Because it inhibits the associated tachycardia, but also inhibits deiodinase (T4-->T3)
-It is a "propra" good drug (bc of dual action)
-Also used for migraine & performance anxiety
-Cops think it's "propra" to use it on the job lol |
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Term
| What are the two with combined α1 & β blocking? What do they treat? |
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Definition
-LabetAlol, and carvedilol (notice they aren't -olol)
-Used in CHF |
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Term
| What is the combined K+ and β blocking drug? |
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Definition
-SotAlol (again, not -olol)
-Used as antiarrhythmic (class III)
-Sought a laugh out loud (lol) |
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