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 )
Mydiatics miotics Gloucoma Presented By: Miss. Pooja Dattatraya Kate
From: Vidya Niketan College Of Pharmacy, Lakhewadi
Definition- These are the pharmacological agents which when administered it produces Mydriasis, i.e. dilation of pupil.
Parasympatholytics
Atropine
Homatropine
Cyclopentolate
Tropicamide
Scopolamine
2) Sympathomimetics-
Adrenaline
Phenylephrine
Cocaine
Ephedrine
Mechanism of action-
Pupil is supplied by both sympathetic and parasympathetic nerve fibre. Parasympathetic nerve constricts the pupil, and sympathetic nerve dilates the pupil. When Mydriasis is administered it relaxes the pupil. Because of Mydriasis the focal length is increased i.e. the person can see the objects which are far away but fail to see near object. It is termed as cycloplegia.
Definition- These are the pharmacological agents which when administered it produces miosis, i.e. constriction of pupil.Classification-
1) Parasympathomimetics-
Acetylcholine
Methacholine
Carbacol
Pilocarpine
Physostigmine
2) Sympatholytics-
Tolazoline
Guanithidine
Dibenamine
Mechanism of action-
Pupil is supplied by both sympathetic and parasympathetic nerve fibre. Sympathetic nerve constricts the pupil, and parasympathetic nerve dilates the pupil. When miosis is administered it constricts the pupil. Because of Miosis the focal length is decreased i.e. the person can see the objects which are near but fail to see far away object. It is termed as spasm of accommodation.
Glaucoma- It is occular disease characterised by elevated intraoccular pressure, which causes damage to optic nerve head and produces visual loss.
Classification-
1)Miotics-
Carbacol
Pilocarpine
Physostigmine
2)Adrenergic drug-
Adrenaline and Pilocarpine mixture
3)Beta receptor blocker-
Timolol
4)Carbonic anhydrase inhibitor-
Acetazolomide
Dichlorphenamide
5)Osmotic agent-
Glycerine
Mannitol
Glaucoma types, Pathogenesis, Diagnosis and TreatmentPranatiChavan
Glaucomas are ocular disorders characterized by changes in the optic nerve head (optic disk) and by loss of visual sensitivity and field.
There are two major types of glaucoma: open-angle glaucoma, which accounts for most cases and closed-angle glaucoma.
Lecture covers the pharmacology of anticholinergic drugs. Includes classification, therapeutic uses, adverse effects of anticholinergics. Atropine has been described as prototype drug.
drug relative to eyes with their meiotic and mydriatic effect.
In the presentation discus about spasm of accommodation and cycloplegic action on eye . pharmacological action , dosage also discussed of condition developed on eye i.e. Glaucoma
Mydiatics miotics Gloucoma Presented By: Miss. Pooja Dattatraya Kate
From: Vidya Niketan College Of Pharmacy, Lakhewadi
Definition- These are the pharmacological agents which when administered it produces Mydriasis, i.e. dilation of pupil.
Parasympatholytics
Atropine
Homatropine
Cyclopentolate
Tropicamide
Scopolamine
2) Sympathomimetics-
Adrenaline
Phenylephrine
Cocaine
Ephedrine
Mechanism of action-
Pupil is supplied by both sympathetic and parasympathetic nerve fibre. Parasympathetic nerve constricts the pupil, and sympathetic nerve dilates the pupil. When Mydriasis is administered it relaxes the pupil. Because of Mydriasis the focal length is increased i.e. the person can see the objects which are far away but fail to see near object. It is termed as cycloplegia.
Definition- These are the pharmacological agents which when administered it produces miosis, i.e. constriction of pupil.Classification-
1) Parasympathomimetics-
Acetylcholine
Methacholine
Carbacol
Pilocarpine
Physostigmine
2) Sympatholytics-
Tolazoline
Guanithidine
Dibenamine
Mechanism of action-
Pupil is supplied by both sympathetic and parasympathetic nerve fibre. Sympathetic nerve constricts the pupil, and parasympathetic nerve dilates the pupil. When miosis is administered it constricts the pupil. Because of Miosis the focal length is decreased i.e. the person can see the objects which are near but fail to see far away object. It is termed as spasm of accommodation.
Glaucoma- It is occular disease characterised by elevated intraoccular pressure, which causes damage to optic nerve head and produces visual loss.
Classification-
1)Miotics-
Carbacol
Pilocarpine
Physostigmine
2)Adrenergic drug-
Adrenaline and Pilocarpine mixture
3)Beta receptor blocker-
Timolol
4)Carbonic anhydrase inhibitor-
Acetazolomide
Dichlorphenamide
5)Osmotic agent-
Glycerine
Mannitol
Glaucoma types, Pathogenesis, Diagnosis and TreatmentPranatiChavan
Glaucomas are ocular disorders characterized by changes in the optic nerve head (optic disk) and by loss of visual sensitivity and field.
There are two major types of glaucoma: open-angle glaucoma, which accounts for most cases and closed-angle glaucoma.
Lecture covers the pharmacology of anticholinergic drugs. Includes classification, therapeutic uses, adverse effects of anticholinergics. Atropine has been described as prototype drug.
drug relative to eyes with their meiotic and mydriatic effect.
In the presentation discus about spasm of accommodation and cycloplegic action on eye . pharmacological action , dosage also discussed of condition developed on eye i.e. Glaucoma
some people are affected with this problem they want to know about the glaucoma causes, risk factor, pathophysiology, signs and symptoms, treatment and complication, etc and they get more knowledge and they will avoid the complication especially loss of vision.
INTRODUCTION
ETIOLOGY
RISK FACTORS
PATHOPHYSIOLOGY
CLASSIFICATION
CLINICAL FEATURES
DIAGNOSTIC MEASURES
MANAGEMENT
Medical
Surgical
Nursing
CONCLUSION
BIBLIOGRAPHY
POST TEST
GLAUCOMA
,dignosis , types of glaucoma , risk factors oo glaucoma and treatment , the clasis of drugs that use in treatment of glaucoma.
prepared by : Hardi Sdiq
university of sullaimani
collage of pharmacy
DIFFERENT METHODS OF PROTEIN ESTIMATION - PROTEINS AND ENZYMES ASSIGNMENTRishabh Sharma
A brief PROTEINS AND ENZYMES ASSIGNMENT on the topic - " DIFFERENT METHODS OF PROTEIN ESTIMATION " . Includes Methods, Applications, Uses and different techniques of protein estimation and separation . Separation on the basis of charge
ACID PHOSPHATASE - PROTEINS AND ENZYMES ASSIGNMENT Rishabh Sharma
A brief PROTEINS AND ENZYMES ASSIGNMENT on the topic - ACID PHOSPHATASE . Includes Properties, Reactions and Classification of Acid Phosphatases . Includes significance and functions of Aid Phosphatases as well.
(Monitoring Of Clinical Trial Assignment ) " Write about the factors that de...Rishabh Sharma
"Write about factors that determine the strategy of monitoring of Clinical Trials (Monitoring Of Clinical Trial Assignment )
Includes Extent and nature of monitoring , components of a monitoring plan , Documentation / Monitoring activities , Procedures of Monitoring , Importance of Monitoring Report , Factors to consider when developing a monitoring plan
Biopharmaceutics Presentation - A brief presentation on the topic- BCS Classification and it's role in formulation development . Includes uses of BCS Classification
CLINICAL BIOCHEMISTRY PRESENTATION ON HPLC- HIGH PERFORMANCE LIQUID CHROMATOG...Rishabh Sharma
A brief presentation of CLINICAL BIOCHEMISTRY on the topic HPLC- HIGH PERFORMANCE LIQUID CHROMATOGRAPHY
Includes :- Origin, Uses, Mechanism, Drawbacks,
A brief presentation of pharmacology on the topic " ANTICHOLINESTERASES " .
Includes Origin,USES, MECHANISM OF ACTION, SIDE EFFECTS , ADVERSE REACTIONS ,
A brief Presentation of Pharmacology on the Drug " Physostigmine " . Includes origin ,Indication, uses, treatment, trade name pharmacodynamics, side effects,
References -https://en.wikipedia.org/wiki/Physostigmine
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
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Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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).
10. 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.
11. 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.
12. 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.
13. 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.
18. 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.
19. 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.
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26. 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.
27.
28. ● 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.
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36. SUBMITTED TO :- DR . SUNANDA DASTIDAR
MADE BY :- RISHABH SHARMA
B.Sc CLINICAL RESEARCH