How anticholinergics act? So many drugs are included in this category with wide variety of therapeutic applications. These drugs inhibit cholinergic transmission at muscarinic receptors Few of the drugs like pirenzepine and darifenacin are selective antagonist on M1 and M2 receptors respectively.
Hi everyone today in this video let us discuss about the anticholinergics what is the mechanism actions side effects and clinical use of anticoagulants we have so many types of and ecologics like the atropine hyoscine both of these drugs are coming from the natural source similarly dicyclobin propanethylene clidanium bromide all these redrocks are acting like
Antispasmodics cyclopentolate and tropicamide which are acting like materiatics eprotropium and tyotropium which are used as bronchodilators darifin acin tolterodine oxybutene flavoxate all these are acting like blood relaxants and pyranji pine propanethylene glycopyrolate act like antioxidants finally binge hexal and benzopine are acting like anti-parkinsonian agents
And one of the orphan adrenaline is centrally acting to decrease the muscle pain in our previous video we have already discussed all these and ecologic drugs and today in this video let us discuss how they are going to act and what is the pharmacology of these anti-colitics how they act now let us see how these anticholinergics are going to act anticholinergics
Are mainly acting at the mosconic receptors so at the cholegic nerve tempness on the post cinematic membrane the seven transmembrane g protein coupled receptors are present which are nothing but the muscanic receptors they may be either m1 m3 or m5 these muscanic receptors are g protein coupled receptors they’re coupled with the three subunits alpha beta and
Gamma now the acetylcholine which is present in the synaptic weight scales can be released by exocytosis so when the calcium is going to enter into the presynaptic nerve terminal the nerve terminal is going to be depolarized resulting in the release of the acetylcholine and this acetylcholine can act on the muscanic receptors now when it is acting on m1 m3 or m5
It can act through the alpha subunit such that it is going to stimulate the phospholipase system when this phospholipase is going to be activated it can cleave the fast watertill inositol biphosphate into two components one is the ip3 ionostal triphosphate and second was the daz diacyl glycerol this dicel glycerol can further activate the protein kinase c which
Are going to open the inward going calcium channels so through these calcium channels now the calcium can enter into the postsynaptic membrane and ip3 can directly increase the release of the calcium from the internal stores in this way the calcium levels are going to be increased within the postsynaptic membrane this calcium is responsible for few of the cellular
Actions for example within the cns it produces excitation on the smooth muscle it produces a contraction now the anticholinergics can act as antagonists at the mosconic receptors they can block the muscarinic receptors thereby they inhibit the action of this style collide in this way anticholinergis can block the m1 m3 or m5 receptors now that is the action of this
Anticholinergics on the other types of muscanic receptors at few of the organs we can observe another type of g protein coupled receptors which are the m2 or m4 receptors these are the muscanic is still chlorine receptors and again they are the g protein couple receptors associated with the three subunits alpha beta gamma but m2 and m4 are inhibitory nature and
They produce the inhibitory response through the alpha subunit so when this acetylcholine is going to be released by the exocytosis it can act on this m2 or m4 receptors and it act through the alpha subunit which is inhibitory in nature normally this alpha subunit is going to convert the atp into cyclic amp by activation of the adenylyl cyclase system but m2 and
M4 receptors are inhibitory nature so this adrenal cyclist is going to be inhibited such that the atp is not converted into cyclic amp which results in the decrease of the cyclic mp levels within the postsynaptic membrane now as the cyclic mp levels are going to decrease the protein kinase activation is going to be decreased which results in the decreased levels
Of the calcium within the post-synaptic membrane calcium is very important for contraction of the heart so when the calcium levels are going to be reduced the heart is unable to contract resulting in the in rate as well as force of contraction and these m2 and m4 receptors can also act through the beta gamma subunit which are going to open the potassium channels
When these potassium channels are going to open these channels are outward going so that the potassium is going outside resulting in the hyper polarization in this way m2 and m4 receptors are mainly produce the inhibited response now the anticholinergics can again block these m2 or m4 receptors thereby they prevent the inhibited response produced by acetylcholine
In this way most of the anticoagulants are non-selective they can block any type of muscanic receptors but m1 m3 m5 are exerted in nature and m2 and m4 are inhibitory nature so anticholinergics can inhibit the excited response mediated by m1 m3 m5 and they can prevent the inhibited response produced by m2 and m4 now that is the form castle actions now let’s see
What is the effect of these anticholinergics on the different types of organs so let us start with the first one heart what is the action of this anticholinergics on the heart on the heart m2 receptors are present now the anticholinergics are going to block the m2 receptors these m2 receptors are inhibitory nature so normally they are going to decrease the rate
As well as force of contraction and since the anticholinergics are going to block these m2 receptors they can increase the rate of contraction so that’s why anticholinergics can produce the tachycardia as one of the side effect so atropine is one of the drag which can produce a tachycardia and since it is going to produce a tachycardia this drug can be used in
The treatment of sinus bradycardia so he here you should not confuse that atropine produce the tachycardia that’s why it is indicated for the bradycardia second one is on the eye again the smooth muscles of the eye are equipped with the m3 receptors now the anticholinergics are going to block these m3 receptors which are excited in nature and responsible for
The pupillary constriction since anticholinergics are going to block these empty receptors they produce the pupillary dilatation that’s why these drugs are going to produce the media assays and they can be used as matriarchs particularly cyclopentylate and tropicamide are used as mediatics and they can also produce a cycloplesia cycloplease is the perils
Of accommodation the vision is going to be fixed at a particular distance and it is not responding to the release of the style collide as the anticoagulants are going to block the cholinergic receptors so particularly atropine is one of the drag which produce the both materials as well as the cycloplesia whenever both of these actions are required we can use
Atropine particularly in the children during the eye examination cycloplasic effect is required in order to fix the vision to a particular distance so atropine can be administered in the children for eye examination but whenever we require only pupillary dilatation cyclopentlate and tropomide can be used as mediatix and because of the pupillary dilatation as
Well as cycloplesia the anticholinergics can increase the intraocular pressure which may prescribe the glaucoma in susceptible patients so anticholinergic should be carefully given in the patients who are having the increase in droplet pressure third one is the bladder again the bladder is equipped with the m3 receptors now the anticholinergics are going to block
The m3 receptors thereby they produce a relaxation of the bladder and this resistant decrease in the urination as well as frequency of urination that’s why these drugs are used in the treatment of urinary incontinence so in those patients who are unable to control the urination these anticholinergics can be given as bladder relaxants and since they are going
To decrease the urination these decks can produce the urinary retention as one of the side effect we have a few other drugs like the dairy financing as well as solely financing which are the two select two m3 blockers which can be used as bladder relaxants and other drugs like the tall terrorism oxybutynine and flavoxate are the non-selective anticholinergics
Which again used as bladder relaxants next one is the git the g8 is equipped with the different types of muscanic receptors it is equipped with the m1 m3 as well as m2 receptors so mixed effects can be observed at the gi tract so one of the important effect of anticholinergics is to decrease the gm motility normally style colon can increase the ga motility so
The anticholinergics can decrease the ga motility since they are going to decrease the mobility of the gi tract they can be used as anti-spasmodics because they produce a relaxation of the gi smooth muscle and the gastric varietal says the m1 receptors are present which are responsible for the gastric acid secretion so anticholinergics can also decrease the
Acid secretion thereby they can be used as anti-ulcerations but these drugs can decrease acid secretion that is stimulated by parasympatic system only normally the gastric acid secretion can be stimulated by mediators like the histamine or gastrin which is not controlled by anticholinergics and here we can also find one of the side effects of anticholinergics
Since the anticholinesis are going to decrease the ga modality they can produce one other side effect constipation next one is the lungs lungs are equipped with the m3 receptors so when these empty receptors are going to block they produce the bronchodilation particularly we have drugs like the protropium and diotropium which produce a bronchodilation that’s why
These drugs can be used in the treatment of copd chronic obstructive pulmonary disorder and anticholinergics can also increase the mucoceleric clearance but this action is mainly observed with the atropine hypnotropium and diotropium are not showing this mucoceleric clearance but eutropine is only showing the mucocelery clearance next is the glandular secretions
Normally acetylcholine is going to increase the glandular secretions through the m3 receptors now the anticholinergics are going to block the empty receptors thereby they inhibit the glandular secretions particularly the lacrimal secretion is going to be inhibited which results in the blood vision because the lacrimal fluid is important for the lubrication of
The eye similarly they can decrease the salivary secretion which results in the dry mouth and you can also decrease the sweat secretion which may result in the hyperthermia this hyperthermia is observed with anticholinergics at a toxic dose because they are going to inhibit the sweat secretion even the sweat glands are connected with the sympathetic system but
The receptors are cholinergic receptors that’s why anticholinergics can block these cholinergic receptors thereby they can decrease the sweat secretion so here all of these three form causal actions are mainly observed as the side effects of anticholinergics and finally the central actions so one of the drug is the high ocean which can decrease the embassies
That’s why it is used as an anti-ametake and few of the anticholinergics can decrease the eps extrapyramidal side effects that are produced by antipsychotics so particularly the two drugs like benzotropine and benzoxol are used to decrease the extrapyramidal side effects and m1 receptors are present within the cns which are responsible for the increase in the
Memory and when these receptors are going to be blocked the anticholinergis can decrease the memory which may result in that dementia loss of memory hyacinth is one of the drag which can produce the dementia and similarly they can produce a cns excitation this cns excitation results in the agitation hyperactivity disorientation and at a very toxic dose they can
Also produce a hyperthermia so here we have two important beneficial action at the center level they can be used as antimatics as well as they can be used as anti-parkinsonian agent to decrease the extra pyramidal side effects now let’s see what are the side effects of the anticholinergics four important side effects we have to always remember the first one is
The dry mouth this is because of the inhibition of the salivary secretion blood vision because of inhibition of lacrimal secretion constipation because of decrease in the ga motility and urinary retention because of the bladder relaxation these are the four important side effects of the anticholinergics and you can also produce a tachycardia because they’re
Going to block the m2 receptors and at toxic dose they can produce restlessness agitation hyperthermia and disorientation in the patients clinical uses sandy cholinergics are used in the various clinical conditions they can be used as pre-analystics particularly atropine and hyacinth can be used as pre-enastics in order to decrease the secretions and they can be
Used as anti-spasmodics we have so many types of drugs like the dicyclomine propanethylene clidanium bromide they can be used as anti-spasmodics mediatix cyclopentellate and tropicomide mainly used as madriatics but if cycloplesia is required atropine can be used as a materiatic they can be used as bladder relaxants particularly dairy financing solely financing
Polterodine oxybutine all these drugs can be used as blood relaxants in the treatment of urinary incontinence as bronchodilators particularly the treatment of copd we have two drugs like the protropium and diotropium they can also be used as anti-mtx hyosine is used as an anti-amtrak in the treatment of motion sickness as an anti-ulcerations like glycopyrolate
Propanethylene and pyringerpine can be used anti-parkinsonian agents benzexol and benzopine can be used finally for treatment of sinus bradycardia atropine can be used as well as in the treatment of physostic mean poisoning physosigmine is a a still cholinesterase inhibitor which increase the ester colon levels thereby increase the mescanic actions and for this
Physical stigma poisoning we can use the atropine so these are the various clinical use of the anticholinergics so that’s about the pharmacology of anticholinergics we have number of drugs acting like anticholinergics but many of these anticholinergies are non selective they can block any type of muscanic receptors m1 m3 m5 are excited in nature and m2 and m4 are
Inhibitory in nature so now these anticholinergics can inhibit both exaggeratory as well as inhibited response mediated by these mechanical receptors because of their wider actions on the mescanic receptors these decks are used in the multiple clinical conditions so that’s for today if you like this video please subscribe to our channel share this video with your
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Transcribed from video
Anticholinergics – Mechanism, actions, side effects & uses By egpat
