AUTONOMIC DRUGS; PART 3; Alpha & Beta Adrenergic Agonists by Professor Fink
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- Опубліковано 17 лип 2024
- This is Part 3 of 4 Video Lectures on AUTONOMIC DRUGS by Professor Fink. In this Video Lecture, Professor Fink describes the location of Alpha, Beta-1 & Beta-2 Adrenergic Receptor Sites and their Effects. (The use of a simplified "branching diagram" is used to help understanding.) Also presented are "Orally-Active Non-Catecholarmine" Sympathomimetics, including Ephedrine & Amphetamine. Examples of commonly used AGONIST drugs in each of the pharmacologic categories and identified and their clinical uses described.
Check-out professor fink's web-site for additional resources in Biology, Anatomy, Physiology & Pharmacology: www.professorfink.com
Down-loadable e-Books of the Lecture Outlines by Professor Fink can be purchased from the WLAC Bookstore at: wlac.redshelf.com/
“Hard Copy” Lecture Outlines can be purchased from the WLAC Bookstore at: onlinestore.wlac.edu/fink.asp
I have been watching your videos for 3 years since I first started my journey to become an RN. You have helped me pass Anatomy & Physiology 1&2, Biology, Microbiology and Pharmacology 1 with A's. I'm now in Pharmacology 2 and back again. I just wanted to say a huge THANK YOU for your amazing lectures. Your passion for these subjects and ability to make the information understandable is truly a gift. I am very grateful for you. God bless you, Professor Fink!
Thank you for your kind words, Shandi. My sincere Best Wishes for your Success!
حشContraction of amphetamine blood vessels
Same here, professor fink’s lecture help me complete ADN, now I am watch his lecture to write my NCLEX-RN, I can’t walk so far without his lecture; he is a God send professor !
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Thanks for sharing.professor some question. Also there is tow type alpha receptor alpha1,2 which a little bit diffrient from each other also dopamine receptors is exist you didn't mention it.).is the action of epi and nor epi the same if be the same why we don't use nor epi ?and is nor epi available in market? Also epi and nor epi acts as hormone and as a neurotransmitter is both action occurs Samiltaneusly during stress?.and action of epi on heart vessel it self is dilation for increasing blood flow .
Thanks, I understand this a lot better, do you have any examples of antagonists?? So beta blocker for beta 1 but not sure of any for beta 2. Thanks
Beta 2 Blockers are not used clinically (because they block bronchodilation, among other things). You can watch Part 4; AUTONOMIC DRUGS; PART 4; Orally Active Sympathomimetics & Adrenergic Blockers
ua-cam.com/video/9zbA2PJ4e6Y/v-deo.html
sir i didn't understand why we give phenylephrine after general anaesthesia
is there any good quizlets for pharmacology????
never understood better than this Sir....thanks a lot
but derez a doubt abt OraVerse.... other than blocking the effect of adrenaline , does it affect local anesthetic solution function... i mean wat will happn to PAIN??
Purnata Manohar OraVerse blocks the action of the vasoconstricting action of epinephrine in the Local Anesthetic preparation. As a result, the local vessels dilate, "carrying away" the lidocaine local anesthetic and terminating its anesthetic action more quickly.
Amazing thank you
Since the Betas have no action on the other blood vessels except those to the heart and skeletal muscle, and sometimes to some extent to those in the skin (hence the flushing), I assume the drop in BP is just partial ? i.e, a small drop in BP, and isn’t it gonna trigger more Tachycardia ? The beta drug itself increases heart rate. I’m asking because under « cautions & contraindications » it says same as those happening with Epi, but Epi increases BP (through alpha-activation and generalized vasoconstriction/increased TPR), and it won’t trigger a reflex bradycardia because the drug’s pozitive chronotropic effect (through beta1-activation) outweighs the CV reflex centre effect. So the question is, is the tachycardia a result of ONLY the action of the drug itself (beta1), or, is it due to the reaction of the body (CV reflex center) to the drop in BP as well (does it add) ? Or there is no reflex tachy to that « partial » drop in BP ?
Thanks in advance ! 🙏
Excellent Question. The actual effects of different Adrenergic Agents will depend upon their relative intrinsic actions on alpha vs beta receptors, the dose that is used, & the particular patient. If you have my Pharmacology Lecture Outline, There is a relevant chart on Page D-28.
It shows that Epinephrine will usually raise Heart Rate (directly), and raise Systolic Blood Pressure, Diastolic Blood Pressure remains unchanged, and mean arterial BP increases a little. In contrast Isoproterenol (a Beta Agonist) raises Heart Rate significantly, raises Systolic BP a little, but significantly lowers Diastolic BP (because of decreased Peripheral Resistance from generalized VASODILATION.
Here is a LINK to a Journal describing these effects:
academic.oup.com/bmb/article-abstract/19/2/132/262139
Here is a LINK to a UA-cam Video describing these effects:
ua-cam.com/video/e5skmn5dokw/v-deo.html
Unfortunately, I don’t have access to your pharmacology lectures outline Sir. Where can I find them please ?
Professor Fink, thank you much Sir for the links, the valuable content, and for taking the time to reply to our messages.
Much appreciated 🙏
where Can We get the book of guide the professor use in her class?
Down-loadable e-Books of the Lecture Outlines by Professor Fink can be purchased at: wlac.redshelf.com/
“Hard Copy” Lecture Outlines can be purchased from the WLAC Bookstore at: onlinestore.wlac.edu/fink.asp
thanks for write! greetings from venezuela!
27:59
"you can just use a 4% _________ solution" Professor, what is the alternative here? I really can't hear or spell that medication.
I should have said a 2% mepivacaine (Carbocaine) with 1:20,000 levonordedrin (Neo-Cobefrin) (which is an Alpha-Adrenergic Agonist vasoconstrictor) OR a 4% mepivacaine with no vasoconstrictor
@@professorfink Thank you so much for taking your time to respond. Wishing you a wonderful long life!
Sympathomimetic drugs cause mydriasis by dilation of the pupil and thus lowering Intraoccular pressure and relieves glaucoma. Why is he saying contraindication glaucoma?
isn't the reason for a glaucoma a dilatation of the muscle due to muscarinic receptor-antagonist?... you use muscarinic-agonist (parasympathomimetics against glaucoma
Sympathomimetic drugs are used (1) in the treatment of open-angle glaucoma by decreasing aqueous humour secretion and increase the outflow through the trabecular meshwork thus reducing the intraocular pressure (e.g. adrenaline (epinephrine), apraclonidine, dipivefrine hydrochloride, brimonidine tartrate), (2) dilate the pupil without affecting accommodation (e.g. phenylephrine) and (3) constrict conjunctival blood vessels (e.g. naphazoline, tetrahydrozoline).
+Collins Santha
I know this is an old post but I was hoping this was resolved by now. Intraoccular pressure is actually increased, in glaucoma, with dilated pupils because the canals of schlem become blocked with a relaxed iris. This explains why pts have attacks of acute angle glaucoma in dark environments. Something that induces miosis is the preferred medication to allow continued flow of aqueous humor. Timoptic or timolol opthic drops are beta blocker. MOA constricts pupils and decreases production of aqueous humor. Being a year out im sure youve found this.
Sir, why can't we just use some other anti inflammatory instead of corticosteroid
Professor Fink's Video Lecture on CORTICOSTEROIDS:
ua-cam.com/video/f6_eU2aw19A/v-deo.html
Professor Fink's Video Lecture on NON-NARCOTIC ANALGESICS & NSAIDs:
ua-cam.com/video/EtbAvz-h2X8/v-deo.html
Chingada madre paolaaaaaaaa!
Mohammed Sumaidaee
Mohammed Sumaidaee