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!
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 !
Professor Fink, you have helped me so much to grasp this material. Thank you for giving this gift to the world. I wish you and your family a happy holiday season
Thanks a lot professor Fink, the way you teach is glorious, superb, wonderful, splendid... thanks for all the videos ( anatomy, physiology, pharmaco and so on)👏🏾
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
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 .
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 ruclips.net/video/9zbA2PJ4e6Y/видео.html
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 RUclips Video describing these effects: ruclips.net/video/e5skmn5dokw/видео.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 🙏
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.
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
Professor Fink's Video Lecture on CORTICOSTEROIDS: ruclips.net/video/f6_eU2aw19A/видео.html Professor Fink's Video Lecture on NON-NARCOTIC ANALGESICS & NSAIDs: ruclips.net/video/EtbAvz-h2X8/видео.html
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.
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 !
you re by far the best pharmacology teacher who ever lived.
It's a good thing the internet can teach me, because my class lectures suck! Thanks for your very good lectures.
This is how pharmacology should be taught. Thank you for the great lecture professor.
Great explanation thank you. I was so lost in this topic. I love your teaching.
how wonderful, wish he was my teacher in my nursing school as well. this really helps thank you so much for this lecture.
Professor Fink, you have helped me so much to grasp this material. Thank you for giving this gift to the world. I wish you and your family a happy holiday season
Thanks a lot professor Fink, the way you teach is glorious, superb, wonderful, splendid... thanks for all the videos ( anatomy, physiology, pharmaco and so on)👏🏾
wow! what can i say? Best lecture series ever!!!!
Super simple way of teaching. Thank you, Professor! :)
Your concept map really helped me understand this topic. I hope it wins a Nobel Prize :)
You are the best.
Thanks Professor Fink for a clear understanding
Top Education!!! thankyou for posting. Gratefull
simple and amazing way of teaching .
Awesome lecture! Thank you so much! This made alot of sense to me after you explained it!
Thank you so much, Professor. I memorize and understand everything.
Thanks again for the lectures!!! Can I get the a copy of the table you were showing? I understand if not.
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!
Thank you. Now I have understood the ans ❤
is there any good quizlets for pharmacology????
Excellent. ALso, top marks for using an OHP!
Yes, thank you, because my class lecture doesn't teach this well at all....hungry for correct understandable information....thank you
excellent lecture.I learned lot. Thanks again for sharing.
Amazing lectures! Thank you so much for sharing these!!
wonderful lecture...thank you professor 👍
thank you for all these lectures
I am a student in dubai. love you're lecture and how you explain
Thank you so much. It helped me with NCLEX quest.
sir i didn't understand why we give phenylephrine after general anaesthesia
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
ruclips.net/video/9zbA2PJ4e6Y/видео.html
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 RUclips Video describing these effects:
ruclips.net/video/e5skmn5dokw/видео.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 🙏
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.
Thhank you so much! This help me out a lot...
This guy is amazing
thanx so much professor for this lectrure
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!
Thank you very much Sir
excellent!!
you are wonderful!
Sir, why can't we just use some other anti inflammatory instead of corticosteroid
Professor Fink's Video Lecture on CORTICOSTEROIDS:
ruclips.net/video/f6_eU2aw19A/видео.html
Professor Fink's Video Lecture on NON-NARCOTIC ANALGESICS & NSAIDs:
ruclips.net/video/EtbAvz-h2X8/видео.html
Interesting lecture ...:)
thnk u sir may god bless u
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.
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Mohammed Sumaidaee
Mohammed Sumaidaee