MYDRIATIC AND MIOTIC AGENTS AND DRUGS USED IN GLAUCOMA

A brief Pathophysiology Presentation on the topic " MYDRIATIC AND MIOTIC AGENTS AND DRUGS USED IN GLAUCOMA "
Includes Both Open Angle and Closed Angle Glaucoma , their Mechanism Of Onset , Pathophysiology and Treatment ( Drugs Used In Glaucoma )

1. MYDRIATIC AND MIOTIC AGENTS AND DRUGS USED IN GLAUCOMA :)

2. FIRSTLY , WHAT IS A MYDRIATIC AGENT ??? :) Agents that dilate the pupil. They may be either sympathomimetics or parasympatholytics.

3. MYDRIATIC AGENTS :- A mydriatic is an agent that induces dilation of the pupil. Drugs such as tropicamide are used in medicine to permit examination of the retina and other deep structures of the eye, and also to reduce painful ciliary muscle spasm. Normally, as part of the pupillary light reflex , the pupil dilates in the dark and constricts in the light to respectively improve vividity at night and to protect the retina from sunlight damage during the day. A mydriatic pupil will remain excessively large even in a bright environment. The excitation of the radial fibres of the iris which increases the pupillary aperture is referred to as a mydriasis.

4. USE OF MYDRIATICS :- More generally, mydriasis also refers to the natural dilation of pupils, for instance in low light conditions or under sympathetic stimulation. One effect of administration of a mydriatic is intolerance to bright light ( photophobia ).

5. CLASSIFICATION :-

6. ACTIONS OF AVAILABLE MYDRIATICS :-

7. DRUGS WHICH CAN CAUSE MYDRIASIS :- Mydriasis can be induced via modulation of adrenergic or cholinergic signalling. Drugs that can cause mydriasis include: Stimulants (typically monoaminergics) such as amphetamines , cocaine , MDMA , and mephedrone . Anticholinergics such as diphenhydramine , atropine , hyoscyamine , and scopolamine antagonize the muscarinic acetylcholine receptors in the eye. Blocking acetylcholine receptors, reduces the pupilary muscles' ability to constrict and causes dilation .The antimuscarinic, tropicamide , may be used as a mydriastic agent during surgery. Serotonergics such as LSD , psilocybin mushrooms , mescaline and 2C-B . . Similarly, selective serotonin reuptake inhibitors can cause mydriasis. Dissociatives such as dextromethorphan (an SSRI and sigma-1 agonist). Certain GABAergic drugs, such as phenibut and GHB . Adrenergic agonists , such as phenylephrine and cyclomydril .

8. WHAT ARE MIOTICS ?? Miotics (drugs that cause the pupil to contract) improve the outflow of aqueous as part of the treatment of glaucoma and reduce the risk of a posteriorly luxated lens entering the anterior chamber.

9. WHAT IS GLAUCOMA ?? Glaucoma is a disease that damages your eye’s optic nerve . It usually happens when fluid builds up in the front part of your eye. That extra fluid increases the pressure in your eye, damaging the optic nerve.

10. GLAUCOMA :- Glaucoma is a group of eye diseases which result in damage to the optic nerve and cause vision loss . The most common type is open-angle glaucoma , in which the drainage angle for fluid within the eye remains open, with less common types including closed-angle glaucoma and normal-tension glaucoma . Open-angle glaucoma develops slowly over time and there is no pain. Peripheral vision may begin to decrease, followed by central vision, resulting in blindness if not treated Closed-angle glaucoma can present gradually or suddenly. The sudden presentation may involve severe eye pain, blurred vision, mid-dilated pupil , redness of the eye, and nausea.

11. PATHOPHYSIOLOGY :OPEN-ANGLE GLAUCOMA

12. PATHOPHYSIOLOGY : CLOSED ANGLE GLAUCOMA

13. RISK FACTORS :- Vision loss from glaucoma, once it has occurred, is permanent. Risk factors for glaucoma include increased pressure in the eye , a family history of the condition, and high blood pressure . For eye pressures, a value of greater than 21 mmHg or 2.8 kPa is often used, with higher pressures leading to a greater risk. However, some may have high eye pressure for years and never develop damage. Conversely, optic nerve damage may occur with normal pressure, known as normal-tension glaucoma.

14. MECHANISM OF ONSET :- The mechanism of open-angle glaucoma is believed to be slow exit of aqueous humor through the trabecular meshwork , while in closed-angle glaucoma the iris blocks the trabecular meshwork. Diagnosis is by a dilated eye examination . Often, the optic nerve shows an abnormal amount of cupping .

15. MEDICATIONS /DRUGS USED IN TREATMENT OF GLAUCOMA :- Intraocular pressure can be lowered with medication, usually eye drops. Several classes of medications are used to treat glaucoma, with several medications in each class. The possible neuroprotective effects of various topical and systemic medications are also being investigated. Prostaglandin analogs , such as latanoprost , bimatoprost and travoprost , increase uveoscleral outflow of aqueous humor. Bimatoprost also increases trabecular outflow. Topical beta-adrenergic receptor antagonists , such as timolol , levobunolol , and betaxolol , decrease aqueous humor production by the epithelium of the ciliary body . Alpha2-adrenergic agonists , such as brimonidine and apraclonidine , work by a dual mechanism, decreasing aqueous humor production and increasing uveoscleral outflow.

16. Less-selective alpha agonists , such as epinephrine , decrease aqueous humor production through vasoconstriction of ciliary body blood vessels, useful only in open-angle glaucoma. Epinephrine's mydriatic effect, however, renders it unsuitable for closed-angle glaucoma due to further narrowing of the uveoscleral outflow (i.e. further closure of trabecular meshwork, which is responsible for absorption of aqueous humor). Miotic agents ( parasympathomimetics ), such as pilocarpine , work by contraction of the ciliary muscle , opening the trabecular meshwork and allowing increased outflow of the aqueous humour. Echothiophate , an acetylcholinesterase inhibitor, is used in chronic glaucoma. Carbonic anhydrase inhibitors , such as dorzolamide , brinzolamide , and acetazolamide , lower secretion of aqueous humor by inhibiting carbonic anhydrase in the ciliary body.

17. SUBMITTED TO :- DR . SUNANDA DASTIDAR MADE BY :- RISHABH SHARMA B.Sc CLINICAL RESEARCH

18. REFERENCES :- https://www.sciencedirect.com/topics/medicine-and-dentistry/mydriatic-agent https://www.aao.org/eye-health/diseases/what-is-glaucoma https://en.wikipedia.org/wiki/Glaucoma THANK YOU !!!!