This document discusses different types of cataracts including age-related (senile) cataract, drug-induced cataract, and traumatic cataract. It provides details on the pathogenesis, clinical presentation, and histopathology of nuclear, cortical, and posterior subcapsular cataracts. Drug-induced cataracts caused by corticosteroids, phenothiazines, miotics, and amiodarone are described. Traumatic cataracts can result from mechanical injury, physical forces like radiation or electricity, or osmotic influences in diabetes. Radiation-induced and chemical-induced cataracts are also summarized.
This presentation describes the background of the cornea and the corneal diseases in general, also it describes in detailed manner how to manage the corneal ulcer with its different causes
Presbyopia/ Methods of Presbyopic Addition Determination (healthkura.com)Bikash Sapkota
DIRECT DOWNLOAD LINK ❤❤https://healthkura.com/presbyopia-near-addition/❤❤
Dear viewers Check Out my other piece of works at ❤❤❤ https://healthkura.com ❤❤❤
Presbyopia and techniques of measurement
A fantastic presentation in the topic "Presbyopia and techniques of measurement"
A detailed information about presbyopia, techniques of presbyopic add determination and different correction methods.
Informative slide presentation on presbyopia for ophthalmology residents, ophthalmologists, optometrists, ophthalmic assistants, ophthalmic technicians, ophthalmic nurses, medical students, medical professors, teaching guides.
Presentation Contents:
--Introduction to presbyopia
-Types of presbyopia
-Risk factors
-Symptoms and signs
-Refractive error and presbyopia
-Methods of determining near add.
-Management of presbyopia
In a nutshell..
- The evaluation and management of presbyopia are important because significant functional deficits can occur when the condition is left untreated
- Undercorrected or uncorrected presbyopia can cause significant visual disability and have a negative impact on the pt.'s quality of life
- Finally, every tentative addition should be adjusted according to the particular needs of the patient
For Further Reading:
-Clinical Procedures in Optometry by J.D. Bartlett, J.B. Eskridge, J.F. Amos
-Primary Care Optometry by Theodere Grosvenor
-Borish’s Clinical Refraction by W.J. Benjamin
-Clinical Procedures for Ocular examination by Carlson et al
-American Academy of Ophthalmology
-Optometric Clinical Practice Guideline by American Optometric Association
-Internet
Follow me to get in touch with optometric and ophthalmic updates.
This presentation describes the background of the cornea and the corneal diseases in general, also it describes in detailed manner how to manage the corneal ulcer with its different causes
Presbyopia/ Methods of Presbyopic Addition Determination (healthkura.com)Bikash Sapkota
DIRECT DOWNLOAD LINK ❤❤https://healthkura.com/presbyopia-near-addition/❤❤
Dear viewers Check Out my other piece of works at ❤❤❤ https://healthkura.com ❤❤❤
Presbyopia and techniques of measurement
A fantastic presentation in the topic "Presbyopia and techniques of measurement"
A detailed information about presbyopia, techniques of presbyopic add determination and different correction methods.
Informative slide presentation on presbyopia for ophthalmology residents, ophthalmologists, optometrists, ophthalmic assistants, ophthalmic technicians, ophthalmic nurses, medical students, medical professors, teaching guides.
Presentation Contents:
--Introduction to presbyopia
-Types of presbyopia
-Risk factors
-Symptoms and signs
-Refractive error and presbyopia
-Methods of determining near add.
-Management of presbyopia
In a nutshell..
- The evaluation and management of presbyopia are important because significant functional deficits can occur when the condition is left untreated
- Undercorrected or uncorrected presbyopia can cause significant visual disability and have a negative impact on the pt.'s quality of life
- Finally, every tentative addition should be adjusted according to the particular needs of the patient
For Further Reading:
-Clinical Procedures in Optometry by J.D. Bartlett, J.B. Eskridge, J.F. Amos
-Primary Care Optometry by Theodere Grosvenor
-Borish’s Clinical Refraction by W.J. Benjamin
-Clinical Procedures for Ocular examination by Carlson et al
-American Academy of Ophthalmology
-Optometric Clinical Practice Guideline by American Optometric Association
-Internet
Follow me to get in touch with optometric and ophthalmic updates.
Topic:- Astigmatic error
This presentation only explained about Definition, types, classification of astigmatism, It did not explained about correction.
Topic:- Astigmatic error
This presentation only explained about Definition, types, classification of astigmatism, It did not explained about correction.
Gross Anatomy & Physiology of Eye
Introduction to cataract
Epidemiology of cataract
The etiological factors
Pathophysiology
Clinical manifestations
Types
Diagnostic measures
Surgical measures
Pre and post operative nursing management
Complications after surgery.
Summary
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Title: Sense of Smell
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 primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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
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.
- 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
1. Age Related Cataract (Senile Cataract)
Drug Induced Cataract
Traumatic Cataract
By
Prof. Naimatullah Khan Kundi
Head, Department of Ophthalmology
Khyber Teaching Hospital
Peshawar
3. Lens & Cataract (Pathology)
Aging Chances
Age related cataract (Senile Cataract)
Very common cause of visual impairment in
older adults
50-70% between ages 60-75yrs
Pathogenesis:
Multifactorial and not completely understood.
As lens ages its wt. ↑
Thickness ↑
Accommodative power ↓
Lens Nucleus compressed and hardened (Nuclear
Sclerosis) as new layers of cortical fibers as formed
concentrically
4. Lens & Cataract (Pathology)
Lens proteins (Crystallines) – chemically modified and
aggregate into high molecular wt. proteins
The resulting proteins aggregates cause:
Abrupt fluctuations in refractive index
Scatter light rays
Reduce transparency
Chemical modification of nuclear lens proteins also produce
pigmentation (yellow/brownish hue with advancing ages)
↓ concentration of glutathione and K+, ↑conc. of Na+
and Ca++, ↑ Hydration
6. Lens & Cataract (Pathology)
Nuclear
In adults past middles ages some degree of nuclear sclerosis
and yellowing is considered physiologically normal. This
condition interferes minimally with visual function
7. Lens & Cataract (Pathology)
Nuclear
2. Excessive sclerosis and
yellowing (nuclear
sclerosis) cause central
opacity. Degree of
scleroses, yellowing and
opacifications evaluated
with SL bio-microscope
and examination of red
reflex (Pupil dilated)
8. Lens & Cataract (Pathology)
Nuclear (cont’d)
3.
Progression slow
4.
BL, (± asymmetric)
5.
Visual impairment greater of distance vision than
of near vision
6.
↑ refractive index and thus myopic shift in
refraction (Lenticular myopia). This myopic shift
transiently enables presbyopic individulas to
read without spectacles (second sight)
9. Lens & Cataract (Pathology)
Nuclear (cont’d)
7.
Monocular diplopia:
Abrupt change in the refractive index between the sclerotic
nucleus and the cortex
7.
Progressive yellowing of the lens causes poor hue
discrimination esp. at the blue end of the visible spectrum
8.
Photopic retinal function may ↓ with advanced nuclear
cataract
10. Lens & Cataract (Pathology)
10.
In very advanced cases the nucleus becomes opaque and brown
(brunescent)
11. Lens & Cataract (Pathology)
11.
Histopathology:
Nucleus homogenous with loss of celluler
laminations.
12. Lens & Cataract (Pathology)
Cortical Cataract
1.
Early changes:
2.
3.
4.
Changes in ionic composition + hydration + cortical
opacification
BL, often Asymmetrical
First visible signs of cortical cataract formation
(SL bio-microscope) are vacuoles & water clefts
in ant. And post. cortex
Cuneiform opacities (cortical spokes): wedge
shaped, form near the periphery the lens, with
pointed ends oriented toward the center
13. Lens & Cataract (Pathology)
5.
Cortical Cataract
The cortical spokes appear white when viewed with SL
bio-microscope and dark shadows when viewed by
retroillumination.
14. Lens & Cataract (Pathology)
Cortical Cataract (cont’d)
6.
Their effect on VA varies greatly, depending
upon the location of the opacity relative to the
visual axis
7.
Common symptom:
Glare from intense focal light sources (e.g. Car head
light)
8.
Monocular diplopia may also result
15. Lens & Cataract (Pathology)
Cortical Cataract (cont’d)
9.
Progression:
10.
11.
vary, some times unchanged for prolonged
periods, while others progress rapidly
The wedge shaped opacities may enlarge
and coalesce to form large cortical opacities.
Intumscent Cataract:
As lens continues to take up water it may swell
16. Lens & Cataract (Pathology)
12.
Mature Cataract:
When the entire lens from the capsule to the
nucleus becomes white and pacified
17. Lens & Cataract (Pathology)
13.
Hypermature Cataract:
when degenerated and
liquefied cortical
material leaks through
the lens capsule,
leaving capsule
wrinkled and shrunken
18. Lens & Cataract (Pathology)
14.
Morgagnian Cataract:
with further liquefaction
of the cortex allows free
movements of the
nucleus within the
capsular bag.
20. Lens & Cataract (Pathology)
Cortical Cataract (cont’d)
15.
Histopathology:
Hydropic swelling of the lens fibers
Globules (morgagnian) of eosinophilic
material observed in slit-like spaces
between lens fibers
21. Lens & Cataract (Pathology)
Posterior Subcapsular (cupuliform)
cataract (PSC)
1.
PSCs often seen in patients younger than
those presenting with nuclear/cortical
cataracts
2.
PSC located in the posterior cortical layer
and is axial in location
22. Lens & Cataract (Pathology)
Posterior Subcapsular (cupuliform)
cataract (PSC)
3.
First indication: subtle iridescent sheen in the
posterior cortical layers (SLB exam)
Later stages:
Granular opacities and
A plaque like opacities of posterior subcapsular
cortex appear
23. Lens & Cataract (Pathology)
Posterior Subcapsular (cupuliform)
cataract (PSC)
Patient complains of
glare and
↓ vision
PSC obscures more of the pupillary area when
In bright light
miosis is induced by:
Bright light
Accommodation
Miotics
24. Lens & Cataract (Pathology)
Posterior Subcapsular (cupuliform) cataract
(PSC)
5.
6.
7.
Near VA tends to be decreased more than
distance VA
Some patients experience monocular diplopia
Other causes of PSC:
1.
2.
3.
4.
5.
Age related – main type
Trauma
Corticosteroids
Inflammations
Ionizing radiations
25. Lens & Cataract (Pathology)
Posterior Subcapsular (cupuliform) cataract
(PSC)
8.
Histopathology
1.
Posterior migration of lens epithelial
cells in the posterior sub-capsular area,
with aberrant enlargement
2.
These swollen epithelial cells are called
Wedl (Bladder) cells
29. Drug induced cataracts
Corticosteroids (cont’d)
Cataract Formation:
Nasal spray
Systemic / Topical / Sub-conjunctival
Eye lid dermatitis (steroids treatment)
Histopathology:
Similar to senescent PSC changes
Some steroid-induced PSCs in children may
be reversible with cessation of the drug
30. Drug induced cataracts
Phenothiazines
Chloropromazine, Thioridazine
Phenotiazines, a major group of Psycho-tropic medications, can cause
pigmented deposits in the anterior lens epithelium in an axial configuration
Deposits appear to be affected by dose and duration
Visual changes associated with phenothiazine are usually insignificant
31. Drug induced cataracts
Miotics
Anticholinesterases (Ecothiophate, demacrium)
pilocarpine, phospholine lodide
These can cause cataracts
Cataract dose and duration related
Cataract may progress to posterior cortical and
nuclear
First appears as small vacuoles within and
posterior to the anterior lens capsule and
epithelium (Best appreciated by retroillumiunation)
32. Drug induced cataracts
Miotics
Visually significant cataracts common in
elderly patients (Topical
anticholinesterase)
Progressive cataract not reported in
children (Echothiophate for
accommodative esotropia)
35. Traumatic Cataract
Traumatic lens damage may be caused by:
1.
Mechanical injury
2.
Physical forces
Electrical current
3.
Radiation
Chemicals
Osmotic influences (diabetes mellitus)
36. Traumatic Cataract
Contusion (Blunt injury)
Vossius ring
Blunt trauma to eye can sometimes cause
pigment from pupillary ruff to be imprinted on
anterior lens surface in a ring shape
It is visually insignificant
It indicates previous trauma
38. Traumatic Cataract
Contusion (Blunt injury)
Blunt, non perforating injury
may cause lens opacification
(acute event / late sequela)
Cataract may involve a
portion or entire lens
Often the initial manifestation
is a stellate / rosette-shaped
opacification, axial in location
(PSC)
39. Traumatic Cataract
Contusion (Blunt injury)
Rosette cataract may progress to
opacification of entire lens
In some cases lens capsule may be
ruptured by the force of blunt trauma,
with subsequent hydration and rapid
opacification of the lens
40. Traumatic Cataract
Contusion (Blunt injury)
Perforating and penetrating injuries
Penetrating injury of lens often results in
opacification of cortex at site of rupture,
progressing rapidly to complete opacification
A small perforating injury of the lens capsule
may heal, resulting in a small focal cortical
cataract
41. Radiation-induced cataracts
Ionizing radiations
Lens is extremely sensitive to ionizing
radiations
Cataract clinically apparent after period
of up to 20 yrs
Latency related to:
Dose and
Age of patient
A young patient with more actively growing lens
cells is more susceptible
42. Radiation-induced cataracts
Ionizing radiations (cont’d)
Clinically:
Punctate opacities within posterior
capsule and feathery anterior subcapsular opacities that radiate towards
the equator of the lens
These may progress to complete
opacification
43. Radiation-induced cataracts
Infra-red radiations (Glasses blower’s
cataract)
Intense heat and infra-red radiations
cause outer layer of the anterior capsule
to peel off as a single layer (true
exfoliation)
May be associated with cortical cataract
Rarely seen today
45. Radiation-induced cataracts
Micro-wave Radiations
Non-ionizing radiations with wavelength
between IR and short waves on the
electromagnetic spectrum
No evidence of cataract by microwaves
Biological effect – thermal
Microwaves could theoretically cause
cataract:
Dose levels would be so high as to induce
hyperthermic brain damage
46. Chemical injuries
Alkalis and Acids
Alkalis injuries to ocular surface result in cataract
Alkalis compounds penetrate eye readly causing:
1.
↑ Aqueous pH
2.
↓ Aqueous Glucose
3.
↓ Aqueous Ascorbate
Cortical cataract:
Acutely or delayed effect
Associated injuries:
Damage to cornea,
conjunctiva, iris etc.
Acids: Tends penetrate eye less easily than alkali
Acid injuries are less likely to result in cataract formation