The document summarizes the physiology of aqueous humour in the eye. It is produced by the ciliary body at a rate of around 2.5 μL/min and has a similar composition to plasma but with lower protein levels. It is replenished around every 100 minutes. Aqueous humour maintains intraocular pressure and provides nutrients to ocular tissues before draining through the trabecular meshwork. Increased pressure can lead to glaucoma, which involves damage to the optic nerve and visual field loss. Diagnosis involves measuring pressure, examining the optic nerve and drainage angle, and testing vision.
The retina is the sensory membrane that lines the inner surface of the back of the eyeball. It's composed of several layers, including one that contains specialized cells called photoreceptors.
Photoreceptor cells take light focused by the cornea and lens and convert it into chemical and nervous signals which are transported to visual centers in the brain by way of the optic nerve.
In the visual cortex of the brain (which, ironically, is located in the back of the brain), these signals are converted into images and visual perceptions.
The aqueous humour is a transparent, watery fluid similar to plasma, but containing low protein concentrations. It is secreted from the ciliary epithelium, a structure supporting the lens
Corneal metabolism
1. o Cornea requires energy for normal metabolic activities as well as for maintaining transparency and dehydration o Energy is generated by the breakdown of glucose in the form of ATP o Most actively metabolizing layer are epithelium and endothelium o Sources of nutrients : o Oxygen : mainly from atmosphere through tear film , with minor amount supplied by the aqueous and limbal vasculature o Glucose , amino acid, vitamins and other nutrients supplied to cornea by aqueous humor o Glucose also derived from glycogen stores in corneal epithelium o Epithelium consumes O2 10 times faster then stroma
2. o Three process or pathways – o Pentose shunt (Hexose monophosphate shunt) –occurs both in hypoxic and normoxic condition o Glycolysis (Embden meyerhof pathway) –anaerobic process , glucose / glycogen converted to pyruvate yeilding 2 ATPs o TCA or krebs or citric acid cycle- aerobic condition pyruvate is oxidized to yield 36 ATP, water, CO2.
3. o In normal conditions all the glucose consumed by the cornea o Glucose mostly come from aqueous humor o The rate of glucose consumption by the whole cornea is approx. 100 microgram/hr/cm2. o 1 mol. of glucose will be converted to the pyruvic acid and produced 2 molecules lactic acid and 2 mol. of ATP o In the krebs cycle, 1 mol. of glucose will utilize the pyruvic acid and O2 to produced 36 mol. ATP o Epithelium and endothelium will consume the oxygen
4. o The pentose phosphate pathway is used to metabolize five carbon sugars; one ATP and 2 NADH molecules are produced from oxidation of one glucose molecule o Produced intermediates for nucleic acid synthesis and some amino acids o This process will happen in hypoxic or normoxic condition o The purpose of glucose metabolism through the pentose shunt is the production of NADPH
The retina is the sensory membrane that lines the inner surface of the back of the eyeball. It's composed of several layers, including one that contains specialized cells called photoreceptors.
Photoreceptor cells take light focused by the cornea and lens and convert it into chemical and nervous signals which are transported to visual centers in the brain by way of the optic nerve.
In the visual cortex of the brain (which, ironically, is located in the back of the brain), these signals are converted into images and visual perceptions.
The aqueous humour is a transparent, watery fluid similar to plasma, but containing low protein concentrations. It is secreted from the ciliary epithelium, a structure supporting the lens
Corneal metabolism
1. o Cornea requires energy for normal metabolic activities as well as for maintaining transparency and dehydration o Energy is generated by the breakdown of glucose in the form of ATP o Most actively metabolizing layer are epithelium and endothelium o Sources of nutrients : o Oxygen : mainly from atmosphere through tear film , with minor amount supplied by the aqueous and limbal vasculature o Glucose , amino acid, vitamins and other nutrients supplied to cornea by aqueous humor o Glucose also derived from glycogen stores in corneal epithelium o Epithelium consumes O2 10 times faster then stroma
2. o Three process or pathways – o Pentose shunt (Hexose monophosphate shunt) –occurs both in hypoxic and normoxic condition o Glycolysis (Embden meyerhof pathway) –anaerobic process , glucose / glycogen converted to pyruvate yeilding 2 ATPs o TCA or krebs or citric acid cycle- aerobic condition pyruvate is oxidized to yield 36 ATP, water, CO2.
3. o In normal conditions all the glucose consumed by the cornea o Glucose mostly come from aqueous humor o The rate of glucose consumption by the whole cornea is approx. 100 microgram/hr/cm2. o 1 mol. of glucose will be converted to the pyruvic acid and produced 2 molecules lactic acid and 2 mol. of ATP o In the krebs cycle, 1 mol. of glucose will utilize the pyruvic acid and O2 to produced 36 mol. ATP o Epithelium and endothelium will consume the oxygen
4. o The pentose phosphate pathway is used to metabolize five carbon sugars; one ATP and 2 NADH molecules are produced from oxidation of one glucose molecule o Produced intermediates for nucleic acid synthesis and some amino acids o This process will happen in hypoxic or normoxic condition o The purpose of glucose metabolism through the pentose shunt is the production of NADPH
The tear film constitutes Three layers :- An outermost lipid (oily) layer An aqueous (watery) layer that makes up 90% of the tear film volume; and A mucin layer that coats the corneal surface.
3. To form smooth optical surface on cornea. To keep the surface of cornea & conjunctiva moist It serve as lubricant It transfer oxygen Provide antibacterial action Wash debris out It provides a pathway for WBC in case of injury
4. Functions of lipid layer Retards evaporation of tear film Prevents the overflow of tears
5. Function of Aqueous Layer Flushes, buffers and lubricates the corneal surface Delivers oxygen and other nutrients to the corneal surface Wash out debris Delivers antibacterial enzymes and antibodies such as lysozyme.
6. Functions of Mucin Layer Spreads tears over corneal surface. Protects the cornea against foreign substances . Makes corneal surface smooth by filling in surface irregularities
Vitreous humour
1. Vitreous Humour
2. General features Vitreous humour is an inert ,transparent , colourless, jellylike, hydrophilic gel that serves the optical functions and also acts as important supporting structures for the eyeball. The vitreous cavity is bounded by anteriorly by the lens and ciliary body and posteriorly by the retina Its weighs nearly 4g Vitreous is an extacellular material composed of approximately 99 per cent water
3. Structure The vitreous body is the largest and simplest connective tissue present as a single piece in the human body Divided into three parts- 1. The hyaloid layer or membrane 2. The cortical vitreous and 3. The medullary vitreous
1-IT IS A MIDDLE VASCULAR COAT OF EYEBALL.
2-IT MAINLY CONSIST OF THREE PARTS IRIS, CHOROID, CILIARY BODY.
3- CILIARY BODY CAN HOLD THE LENS AND PLAY IMPORTANT ROLE IN ACCOMODATION.
INTRODUCTIONThe clear fluid filling the space in front of the eyeball between lens and cornea.The aqueous humour supplies nutrition and removes waste from the clear structure in the anterior eye(cornea and lens)The balance between aqueous production and outflow determines the intraocular pressure.
INTRODUCTION
The clear fluid filling the space in front of the eyeball between lens and cornea.
The aqueous humour supplies nutrition and removes waste from the clear structure in the anterior eye(cornea and lens)
The balance between aqueous production and outflow determines the intraocular pressure.
LIMBUS… • The limbus forms the border between the transparent cornea and opaque sclera, contains the pathways of aqueous humour outflow, and is the site of surgical incisions for cataract and glaucoma
2. Anatomical Limbus: Circumcorneal transitional zone of the conjunctivocorneal & corneoscleral junction Conjunctivo-corneal junction: • Bulbar conjunctiva is firmly adherent to underlying structures • Substantia propria of the conjunctiva stops here but its epithelium continues with that of the cornea. Sclero-corneal junction: • Transparent corneal lamellae become continuous • With the oblique, circular and opaque fibres of sclera
3. CONTINUE…. • In the area near limbus, the conjunctiva, tenon’s capsule & the episcleral tissue are fused into a dense tissue which is strongly adherent to corneo scleral junction.It is preferred site for obtaining a firm hold of the eyeball during ocular surgery. • The limbus is a common site for the occurrence of corneal epithelial neoplasm. • The Limbus contains radially oriented fibrovascular ridge known as the palisades of Vogt that may harbour a stem cell population. The palisades of Vogt are more common in the superior and inferior quadrants around the eye
Glaucoma is not a single disease process but a group of disorders characterized by a progressive optic neuropathy resulting in a irreversible visual field defects that are associated frequently raised intraocular pressure (IOP).
IOP is the most common risk factor but not the only risk factor for development of glaucoma.
The tear film constitutes Three layers :- An outermost lipid (oily) layer An aqueous (watery) layer that makes up 90% of the tear film volume; and A mucin layer that coats the corneal surface.
3. To form smooth optical surface on cornea. To keep the surface of cornea & conjunctiva moist It serve as lubricant It transfer oxygen Provide antibacterial action Wash debris out It provides a pathway for WBC in case of injury
4. Functions of lipid layer Retards evaporation of tear film Prevents the overflow of tears
5. Function of Aqueous Layer Flushes, buffers and lubricates the corneal surface Delivers oxygen and other nutrients to the corneal surface Wash out debris Delivers antibacterial enzymes and antibodies such as lysozyme.
6. Functions of Mucin Layer Spreads tears over corneal surface. Protects the cornea against foreign substances . Makes corneal surface smooth by filling in surface irregularities
Vitreous humour
1. Vitreous Humour
2. General features Vitreous humour is an inert ,transparent , colourless, jellylike, hydrophilic gel that serves the optical functions and also acts as important supporting structures for the eyeball. The vitreous cavity is bounded by anteriorly by the lens and ciliary body and posteriorly by the retina Its weighs nearly 4g Vitreous is an extacellular material composed of approximately 99 per cent water
3. Structure The vitreous body is the largest and simplest connective tissue present as a single piece in the human body Divided into three parts- 1. The hyaloid layer or membrane 2. The cortical vitreous and 3. The medullary vitreous
1-IT IS A MIDDLE VASCULAR COAT OF EYEBALL.
2-IT MAINLY CONSIST OF THREE PARTS IRIS, CHOROID, CILIARY BODY.
3- CILIARY BODY CAN HOLD THE LENS AND PLAY IMPORTANT ROLE IN ACCOMODATION.
INTRODUCTIONThe clear fluid filling the space in front of the eyeball between lens and cornea.The aqueous humour supplies nutrition and removes waste from the clear structure in the anterior eye(cornea and lens)The balance between aqueous production and outflow determines the intraocular pressure.
INTRODUCTION
The clear fluid filling the space in front of the eyeball between lens and cornea.
The aqueous humour supplies nutrition and removes waste from the clear structure in the anterior eye(cornea and lens)
The balance between aqueous production and outflow determines the intraocular pressure.
LIMBUS… • The limbus forms the border between the transparent cornea and opaque sclera, contains the pathways of aqueous humour outflow, and is the site of surgical incisions for cataract and glaucoma
2. Anatomical Limbus: Circumcorneal transitional zone of the conjunctivocorneal & corneoscleral junction Conjunctivo-corneal junction: • Bulbar conjunctiva is firmly adherent to underlying structures • Substantia propria of the conjunctiva stops here but its epithelium continues with that of the cornea. Sclero-corneal junction: • Transparent corneal lamellae become continuous • With the oblique, circular and opaque fibres of sclera
3. CONTINUE…. • In the area near limbus, the conjunctiva, tenon’s capsule & the episcleral tissue are fused into a dense tissue which is strongly adherent to corneo scleral junction.It is preferred site for obtaining a firm hold of the eyeball during ocular surgery. • The limbus is a common site for the occurrence of corneal epithelial neoplasm. • The Limbus contains radially oriented fibrovascular ridge known as the palisades of Vogt that may harbour a stem cell population. The palisades of Vogt are more common in the superior and inferior quadrants around the eye
Glaucoma is not a single disease process but a group of disorders characterized by a progressive optic neuropathy resulting in a irreversible visual field defects that are associated frequently raised intraocular pressure (IOP).
IOP is the most common risk factor but not the only risk factor for development of glaucoma.
Glaucoma is an eye disease that is often associated with elevated intraocular pressure, in which damage to the eye (optic) nerve can lead to loss of vision and even blindness. Glaucoma is the leading cause of irreversible blindness in the world.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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
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
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
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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
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.
2. Physiology of aqueous humour
• Aqueous humor is an optically clear, slightly alkaline ocular fluid
that is continuously formed (~ 2.5 μL/min in humans) from plasma
by epithelial cells of ciliary body.
• similar to plasma, but containing low protein concentrations.
• Three different processes diffusion, ultrafiltration and active
secretion contribute to the chemical composition and formation
of aqueous humor.
• It is estimated that the entire aqueous humor is replaced in
approximately 100 min
• ciliary body : The ciliary body is the tissue which covers the inner
part of the anterior segment of the eye coating. It is composed of
the ciliary muscle.
• On the surface of the ciliary body is the black ciliary epithelium,
which produces the aqueous humour,
5. • aqueous humour fills both the anterior and
the posterior chambers of the eye.
• Aqueous humor produced and secreted into the posterior eye
segment passes through the pupil into the anterior chamber.
It is drained into the venous blood circulation
via the trabecular
meshwork and
the canal of Schlemm
8. • FUNCTION:
• Maintains the intraocular pressure and inflates the globe of the eye.
• It is this hydrostatic pressure which keeps the eyeball in a roughly
spherical shape and keeps the walls of the eyeball tight.
• Provides nutrition (e.g. amino acids and glucose) for the avascular ocular
tissues; posterior cornea, trabecular meshwork, lens, and anterior
vitreous.
• May serve to transport ascorbate in the anterior segment to act as an
antioxidant agent.
• Presence of immunoglobulins indicate a role in immune response to
defend against pathogens.
• Provides inflation for expansion of the cornea and thus increased
protection against dust, wind, pollen grains and some pathogens.
• for refractive index.
9. • Drainage
• The drainage route for aqueous humour flow is first through
the posterior chamber, then the narrow space between the
posterior iris and the anterior lens (contributes to small resistance),
through the pupil to enter the anterior chamber. From there, the
aqueous humour exits the eye through the trabecular
meshwork into Schlemm's canal (a channel at the limbus, i.e., the
joining point of the cornea and sclera, which encircles the cornea[)
• It flows through 25–30 collector canals into the episcleral veins. The
greatest resistance to aqueous flow is provided by the trabecular
meshwork (esp. the juxtacanalicular part), and this is where most of
the aqueous outflow occurs. The internal wall of the canal is very
delicate and allows the fluid to filter due to high pressure of the
fluid within the eye.
11. Aqueous humour
• Drainage:
• The secondary route is the uveoscleral drainage, and
is independent of the intraocular pressure, the
aqueous flows through here, but to a lesser extent
than through the trabecular meshwork (approx. 10%
of the total drainage whereas by trabecular
meshwork 90% of the total drainage).
• The fluid is normally 15 mmHg (0.6 inHg) above
atmospheric pressure, so when a syringe is injected the
fluid flows easily. If the fluid is leaking, due to collapse
and wilting of cornea, the hardness of the normal eye
is therefore corroborate
12. Maintenance of normal intraocular
pressure
• Definition: Intraocular pressure is determined by the production
and drainage of aqueous humour by the ciliary body and its
drainage via the trabecular meshwork and uveoscleral outflow.
• The eye is a closed ball filled with clear jelly (vitreous humor) in the
back behind the lens and clear fluid (aqueous humor) in the front,
between the iris and the cornea. Aqueous humor is created just
behind the iris and is in continuous circulation throughout the front
part of the eye before it drains out just in front of the iris where it
meets the cornea. This fluid helps keep the eye "inflated" just like
air inside a balloon.
• Pressure in the human eye, known as intraocular pressure, varies
throughout the day with "normal" pressure being anywhere
between 10 and 21 mmHg.
13. Intraocular pressure
• Measurements:
• We can measure pressure of the eye just like you can gauge
how full a balloon is by poking the balloon with your
finger. The less air or pressure in the balloon, the easier it
will be to poke and conversely, the more air or pressure in
the balloon, the stiffer the balloon will be and the harder it
will be to poke it.
• We measure pressure in the eye the same way; by gently
touching the cornea with special instruments to see how
hard it is to "poke." The unit of measurement is
millimeters of mercury, or mmHg.
• Intraocular pressure is measured with a tonometer as part
of a comprehensive eye examination.
15. IOP Can be determined by using this formula
Po=(F−U)/C+Pv
Where:
• Po is the IOP in millimeters of mercury (mmHg)
• F the rate of aqueous humour formation in microliters per
minute (μL/min)
• U the resorption of aqueous humour through the
uveoscleral route (in μL/min)
• C is the facility of outflow in microliters per minute per
millimeter of mercury (μL/min/mmHg)
• Pv the episcleral venous pressure in millimeters of mercury
(mmHg).
16. Classification
• Current consensus among ophthalmologists and
optometrists define normal intraocular pressure as
that between 10 mmHg and 20 mmHg. The average
value of intraocular pressure is 15.5 mmHg with
fluctuations of about 2.75 mmHg.
• Ocular hypertension (OHT) is defined by intraocular
pressure being higher than normal, in the absence
of optic nerve damage or visual field loss.
• Ocular hypotension, Hypotony, or ocular hypotony, is
typically defined as intraocular pressure equal to or
less than 5 mmHg. Such low intraocular pressure could
indicate fluid leakage and deflation of the eyeball.
17. Factors influencing
intraocular pressure
The normal level of IOP is essentially maintained by a dynamic
equilibrium between the formation and outflow of the aqueous
humour.
LOCAL FACTORS:
• 1. Rate of aqueous formation influences IOP levels such as
permeability of ciliary capillaries and osmotic pressure of the blood.
• 2. Increased episcleral venous pressure may result
in rise of IOP.
• 3. Resistance to aqueous outflow (drainage).
• 4. Dilatation of pupil in patients with narrow
anterior chamber angle may cause rise of IOP
owing to a relative obstruction of the aqeuous
drainage by the iris.
18.
19. Factors influencing
intraocular pressure
GENERAL FACTORS:
• Heredity. It influences IOP, possibly by multifactorial modes.
• Age. The mean IOP increases after the age of 40 years, possibly due to reduced
facility of aqueous outflow.
• Postural variations. IOP increases when changing from the sitting to the supine
position.
• Blood pressure. As such it does not have longterm effect on IOP. However,
prevalence of glaucoma is marginally more in hypertensives than the
normotensives.
• Osmotic pressure of blood. An increase in plasma osmolarity (as occurs after
intravenous mannitol, oral glycerol or in patients with uraemia) is associated
with a fall in IOP, while a reduction in plasma osmolarity (as occurs with water
drinking provocative tests) is associated with a rise in IOP.
• General anaesthetics and many other drugs also influence IOP e.g., alcohol lowers
IOP, tobacco smoking, caffeine and steroids may cause rise in IOP.
20. Glaucoma
• Glaucoma is a progressive optic neuropathy where retinal
ganglion cells and their axons die causing a corresponding
visual field defect.
• An important risk factor is increased intraocular
pressure (pressure within the eye) either through increased
production or decreased outflow of aqueous humour.
• Increased resistance to outflow of aqueous humour may
occur due to an abnormal trabecular mesh work or to
obliteration of the meshwork due to injury or disease of the
iris.
• although it is a major risk factor. Uncontrolled glaucoma
typically leads to visual field loss and ultimately blindness.
21. Glaucoma
• Definition: Glaucoma is a group of eye
conditions that damage the optic nerve, the
health of which is vital for good vision. This
damage is often caused by an abnormally
high pressure in your eye. (IOP)
• Glaucoma is one of the leading causes of
blindness for people over the age of 60.
22. سبزموتیا Glaucoma
• Causes:
• Glaucoma is the result of damage to the optic nerve. As this nerve
gradually deteriorates, blind spots develop in your visual field.
• This nerve damage is usually related to increased pressure in the
eye.
• 1- Elevated eye pressure is due to a buildup of a fluid (aqueous
humor) that flows throughout the inside of your eye. This internal
fluid normally drains out through a tissue called the trabecular
meshwork at the angle where the iris and cornea meet. When fluid
is overproduced or the drainage system doesn't work properly, the
fluid can't flow out at its normal rate and eye pressure increases.
• 2- Genetics: Glaucoma tends to run in families. In some people,
scientists have identified genes related to high eye pressure and
optic nerve damage.
23. • Pathophysiology:
• The space between the clear front surface of the eye (the cornea) and the lens
inside the eye is filled with a clear fluid called the aqueous humor. This fluid
nourishes the inside of the anterior part of the eye. It also maintains the shape of
the eye by keeping the eyeball properly pressurized.
• The aqueous humor is constantly being produced by a structure called the ciliary
• body that surrounds the lens, and it drains from the eye through a mesh-like
channel called the trabecular meshwork that's located in the angle formed inside
the eye where the cornea and iris meet.
• If something causes this "drainage angle" to close down or the trabecular
meshwork to become clogged, the aqueous humor cannot drain from the eye
fast enough, and pressure inside the eye (IOP) increases.
• Glaucoma usually occurs when too much pressure inside the eye causes damage
to the optic nerve at the back of the eyeball, leading to permanent vision loss.
• Recent studies also have implicated low intracranial pressure (the pressure that
surrounds the brain) as one of the risks for glaucoma
24.
25. Types of glaucoma
Open-angle glaucoma
• Open-angle glaucoma is the most common form of the
disease. The drainage angle formed by the cornea and iris
remains open, but the trabecular meshwork is partially
blocked.
This causes pressure
in the eye to gradually
increase. This pressure
damages the optic nerve.
It happens so slowly that
you may lose vision before
you're even aware of a problem.
26. • Angle-closure glaucoma
• Angle-closure glaucoma, also called closed-angle glaucoma, occurs when the iris
bulges forward to narrow or block the drainage.
angle formed by the
cornea and iris. As a
result, fluid can't
circulate through the
eye and pressure
increases. Some
people have narrow
drainage angles,
putting them at
increased risk of
angle-closure
glaucoma.
27. • Normal-tension glaucoma
• In normal-tension glaucoma , optic nerve becomes damaged even though
eye pressure is within the normal range. No one knows the exact reason
for this. You may have a sensitive optic nerve, or you may have less blood
being supplied to your optic nerve. This limited blood flow could be
caused by atherosclerosis — the buildup of fatty deposits (plaque) in the
arteries or other conditions that impair circulation.
• Pigmentary glaucoma
• In pigmentary glaucoma, pigment granules from your iris build up in the
drainage channels, slowing or blocking fluid exiting your eye. Activities
such as jogging sometimes stir up the pigment granules, depositing them
on the trabecular meshwork and causing intermittent pressure elevations.
• Primary glaucoma - this means that the cause is unknown.
• Secondary glaucoma - the condition has a known cause, such as
a tumor, diabetes, an advanced cataract, or inflammation.
28. • Sign & Symptoms:
• The most common type of glaucoma has no early warning signs
and can only be detected during a comprehensive eye exam. If
undetected and untreated, glaucoma first causes peripheral vision
loss and eventually can lead to blindness.
• By the time you notice vision loss from glaucoma, it's too late. The
lost vision cannot be restored, and it's very likely you may
experience additional vision loss, even after glaucoma treatment
begins.
• the signs and symptoms of glaucoma vary depending on the type
and stage of your condition. For example:
• Open-angle glaucoma
• Patchy blind spots in your side (peripheral) or central vision,
frequently in both eyes
• Tunnel vision in the advanced stages
29. • Symptoms of Acute angle-closure glaucoma
• Severe headache
• Eye pain
• Nausea and vomiting- due to occulocardiac reflex
• Blurred vision
• Halos around lights
• Eye redness
• The oculocardiac reflex is one of several trigeminal
nerve reflexes. Noxious stimulation of trigeminal nerve
afferents activates the paratrigeminal nuclei in the
medulla with secondary stimulation of the vagus nerve.
30. Glaucoma
• Risk factors
• Having high internal eye pressure (intraocular pressure)
• Being over age 60
• Being black, Asian or Hispanic
• Having a family history of glaucoma
• Having certain medical conditions, such as diabetes, heart
disease, high blood pressure and sickle cell anemia
• Having corneas that are thin in the center
• Being extremely nearsighted or farsighted
• Having had an eye injury or certain types of eye surgery
• Taking corticosteroid medications, especially eyedrops, for
a long time
31. • Diagnosis:
• doctor will review medical history and conduct a
comprehensive eye examination.
• He or she may perform several tests, including:
• Measuring intraocular pressure (tonometry)
• Testing for optic nerve damage with a dilated eye
examination and imaging tests (CT-Scan)
• Checking for areas of vision loss (visual field test)
• can detect central and peripheral vision problems caused
by glaucoma, stroke and other eye or brain problems.
• Measuring corneal thickness (pachymetry)
• Inspecting the drainage angle (gonioscopy)
32. Pachymetry
• The instrument used for this purpose is known as a pachymeter.
• It can be done using either ultrasonic or optical methods
• This devices that display the thickness of the cornea, usually in
micrometres, when the ultrasonic transducer touches the cornea.
• Using this technology
the user can capture an
ultra-high definition
echogram of the cornea,
somewhat like a corneal A-scan.
• Pachymetry using the
corneal waveform process allows
the user to more accurately
measure the corneal thickness,
and measure structures within the cornea such as micro bubbles.
33. Gonioscopy
• Gonioscopy is an eye examination to look at the front part of your eye (anterior
chamber) between the cornea and the iris.
• Gonioscopy is a painless examination to see whether the area where fluid drains
out of your eye (called the drainage angle) is open or closed. It is often done
during a regular eye examination, depending on your age and whether you are at
high risk for glaucoma.
• Process
• cleaning and sterilising the front (curved) surface of the goniolens
• applying lubricating fluid to the front surface if appropriate
• anaesthetising the patient's cornea with topical anaesthetic
• preparing the slit lamp for viewing through the goniolens
• gently moving the patient's eyelids away from the cornea
• slowly applying the goniolens to the ocular surface, forming suction
• fine-tuning the slit lamp to optimise the view
• interpreting the gonioscopic image
• swivelling the goniolens to view each section of the iridocorneal angle
• when satisfied, very carefully breaking suction via the eyelids
34.
35. • Treatment
• The damage caused by glaucoma can't be reversed. Glaucoma is treated
by lowering your eye pressure (intraocular pressure). Depending on your
situation, your options may include prescription eyedrops, oral
medications, laser treatment, surgery or a combination of any of these.
• Eyedrops
• Glaucoma treatment often starts with prescription eyedrops. These can
help decrease eye pressure by improving how fluid drains from your eye
or by decreasing the amount of fluid your eye makes.
• Prostaglandins. These increase the outflow of the fluid in your eye
(aqueous humor), thereby reducing your eye pressure. Medicines in this
category include latanoprost (Xalatan), travoprost (Travatan Z), tafluprost
(Zioptan), bimatoprost (Lumigan) and latanoprostene bunod (Vyzulta).
• Possible side effects include mild reddening and stinging of the eyes,
darkening of the iris, darkening of the pigment of the eyelashes or eyelid
skin, and blurred vision. This class of drug is prescribed for once-a-day use.
36. • Beta blockers. These reduce the production of fluid in your eye, thereby
lowering the pressure in your eye (intraocular pressure). Examples include
timolol (Betimol, Istalol, Timoptic) and betaxolol (Betoptic).
• Possible side effects include difficulty breathing, slowed heart rate, lower
blood pressure, impotence and fatigue. This class of drug can be
prescribed for once- or twice-daily use depending on your condition.
• Alpha-adrenergic agonists. These reduce the production of aqueous
humor and increase outflow of the fluid in your eye. Examples include
apraclonidine (Iopidine) and brimonidine (Alphagan P, Qoliana).
• Possible side effects include an irregular heart rate, high blood pressure,
fatigue, red, itchy or swollen eyes, and dry mouth. This class of drug is
usually prescribed for twice-daily use but sometimes can be prescribed for
use three times a day.
37. • Carbonic anhydrase inhibitors. These medicines reduce
the production of fluid in your eye. Examples include
dorzolamide (Trusopt) and brinzolamide (Azopt). Possible
side effects include a metallic taste, frequent urination, and
tingling in the fingers and toes. This class of drug is usually
prescribed for twice-daily use but sometimes can be
prescribed for use three times a day.
• Rho kinase inhibitor. This medicine lowers eye pressure by
suppressing the rho kinase enzymes responsible for fluid
increase. It is available as netarsudil (Rhopressa) and is
prescribed for once-a-day use. Possible side effects include
eye redness, eye discomfort and deposits forming on the
cornea.
38. • Miotic or cholinergic agents. These increase the outflow of fluid
from your eye. An example is pilocarpine (Isopto Carpine).
• Side effects include headache, eye ache, smaller pupils, possible
blurred or dim vision, and nearsightedness. This class of medicine is
usually prescribed to be used up to four times a day. Because of
potential side effects and the need for frequent daily use, these
medications are not prescribed very often anymore.
• Because some of the eyedrop medicine is absorbed into your
bloodstream, you may experience some side effects unrelated to
your eyes. To minimize this absorption, close your eyes for one to
two minutes after putting the drops in. You may also press lightly at
the corner of your eyes near your nose to close the tear duct for
one or two minutes. Wipe off any unused drops from your eyelid.
39. • Surgery and other therapies
• Other treatment options include laser therapy and
various surgical procedures. The following techniques
are intended to improve the drainage of fluid within
the eye, thereby lowering pressure:
• Laser therapy. Laser trabeculoplasty is an option if you
have open-angle glaucoma. It's done in your doctor's
office. Your doctor uses a small laser beam to open
clogged channels in the trabecular meshwork. It may
take a few weeks before the full effect of this
procedure becomes apparent.
40. • Filtering surgery. With a surgical procedure called a
trabeculectomy, your surgeon
creates an
opening in the white of the
eye (sclera) and removes
part of the trabecular meshwork.
Drainage tubes. In this
procedure, your eye
surgeon inserts a small
tube shunt in your eye to
drain away excess fluid to
lower your eye pressure.
41. Anatomy & physiology of Lens
• Definition Lens is a unique transparent, biconvex, avascular intraocular
structure along with the cornea, helps to refract (To change the
direction) light to be focused on the retina.
• Topography (A precise description of place)
The center of the anterior surface is called anterior pole and it is situated
3mm away from the posterior (endothelial) surface of cornea. The center
of the posterior surface is called posterior pole. The distance between
these poles is measured as lens thickness. The thickness of lens is 3mm at
birth, which increases to 6mm in older age.
• The marginal circumferences of the lens, where anterior and posterior
surface meet, are known as equator. The equatorial diameter of lens is 6.5
mm at birth, which reaches to 9-10 mm in adult life.
• Synonym: aquula (Latin, a little stream, of aqua, water) or crystalline
lens.
• Location:
The Lens is situated behind the iris and in front of the vitreous.
42.
43.
44. • Structure:
• The lens is part of the anterior segment of the human eye.
• In front of the lens is the iris, which regulates the amount
of light entering into the eye.
• The lens is suspended in place by the suspensory ligament
of the lens, a ring of fibrous tissue that attaches to the lens
at its equator and connects it to the ciliary body.
• Posterior to the lens is the vitreous body, which, along with
the aqueous humor on the anterior surface, bathes the
lens.
• The lens has an biconvex shape.
• The anterior surface is less curved than the posterior.
45. • Microanatomy
• The lens has three main parts: the lens capsule, the lens epithelium,
and the lens fibers.
• Lens capsule is the smooth, transparent outermost layer of the
lens,
• while the lens fibers are long, thin, transparent cells that form the
bulk of the lens.
• Capsule is synthesized by the lens epithelium
• The capsule is very elastic and so allows the lens to assume a more
globular shape when not under the tension of the zonular
fibers (also called suspensory ligaments)
• The capsule varies from 2 to 28 micrometres in thickness, being
thickest near the equator and thinnest near the posterior pole.
46. • 2- lens epithelium
• The lens epithelium, located in the anterior portion of the
lens between the lens capsule and the lens fibers, is
a simple cuboidal epithelium. The cells of the lens
epithelium regulate most of the homeostatic functions of
the lens. As ions, nutrients, and liquid enter the lens from
the aqueous humor, Na+/K+-ATPase pumps in the lens
epithelial cells pump ions out of the lens to maintain
appropriate lens osmotic concentration,
• Lens fibers
• The lens fibers form the bulk of the lens. They are long,
thin, transparent cells, firmly packed, with diameters
typically 4–7 micrometres and lengths of up to 12 mm long
47.
48. • Blood supply & innervation:
• The lens has no blood supply or innervation after fetal development, and
it depends entirely on the aqueous humor to meet its metabolic
requirements and to carry off its wastes.
• Refractive power: (refractive=change direction as result of entering in
mdium fom another medium)
The diopteric power of human eye is approximately 58 diopters. The
refractive power of crystalline lens is about 15 diopters. Though lens has
less refractive power than cornea, it has the ability to change its shape
with the help of cilliary muscle, by which it can change its diopteric power,
allowing the distant and near vision. However this property changes with
age. Lens has a refractive index of 1.39 (1.36 in periphery and 1.40
centrally - a property which is termed as grading refractive index)
• Optical power (also referred to as dioptric power, refractive
power, focusing power, or convergence power) is the degree to which
a lens, mirror, or other optical system converges or diverges light
49. • Function:
• Accomodation: The lens is flexible and its curvature is controlled
by ciliary muscles through the zonules (ligaments). By changing the
curvature of the lens, one can focus the eye on objects at different
distances from it. This process is called accommodation.
• The inherent elastic property of the lens allows it to become more or less
spherical depending on the amount of tension exerted by the zonular
fibers on the lens capsule. Zonular tension is controlled by the action of
the parasympathetically innervated ciliary muscle
• When cilliary muscles contracts, relaxation of zonular tension occurs. The
lens then assumes a more spherical shape, resulting in increased dioptric
power which helps to bring nearer objects into focus.
• Ciliary muscle relaxation causes the zonular tension to increase. As a
result, lens flattens, which helps in bringing more distant objects into
view.
50. Crystallins and transparency
• Crystallins are water-soluble proteins that
compose over 90% of the protein within the lens.
• The three main crystallin types found in the
human eye are α-, β-, and γ-crystallins.
• Crystallins tend to form soluble, high-molecular
weight aggregates that pack tightly in lens
fibers,
• thus increasing the index of refraction of the lens
while maintaining its transparency.
51. Cataract eye
• Definition: cataract is a clouding of the normally
clear lens of your eye
• C= clear C= clouding C= cataract
• cloudy lenses is a bit like looking fogged-up window
• cataracts can make it more difficult to read, drive a car (especially at night) or
recognize face.
52. Types of cataracts
• Types of cataracts include:
• A subcapsular cataract occurs at the back of the lens. right in the path of
light. People with diabetes or those taking high doses of steroid
medications have a greater risk of developing a subcapsular cataract.
• A nuclear cataract forms deep in the central zone (nucleus) of the lens.
Nuclear cataracts usually are associated with aging. But with time, the lens
gradually turns more densely yellow. As the cataract slowly progresses,
the lens may even turn brown. Advanced yellowing or browning of the
lens can lead to difficulty distinguishing between shades of color
• A cortical cataract it effects edges of lens, is characterized by white,
wedge-like opacities that start in the lens and work their way to the center
in a streak fashion. This type of cataract occurs in the lens cortex, which is
the part of the lens that surrounds the central nucleus.
53.
54. Cataract
• Mechanism:
• The lens focuses light that passes into your eye, producing clear, sharp
images on the retina the light-sensitive membrane in the eye that
functions like the film in a camera.
• As you age, the lenses in your eyes become less flexible, less transparent
and thicker.
• Age-related and other medical conditions The lens is mostly made of
water and protein. The protein is arranged in a precise way that keeps
the lens clear and lets light pass through it.
• But as we age, some of the protein may clump together and start to cloud
a small area of the lens. This is a cataract, and over time, it may grow
larger and cloud more of the lens, making it harder to see.
• As the cataract continues to develop, the clouding becomes denser and
involves a bigger part of the lens. A cataract scatters and blocks the light
as it passes through the lens, preventing a sharply defined image from
reaching your retina. As a result, your vision becomes blurred.
55. • Causes:
• Age: Age is the most common cause, Lens proteins denature and degrade over
time, and this process is accelerated by diseases such as diabetes
mellitus and hypertension.
• Trauma: Blunt trauma causes swelling, thickening, and whitening of the lens fibers.
While the swelling normally resolves with time, the white color may remain. In
severe blunt trauma, or in injuries that penetrate the eye, the capsule in which the
lens sits can be damaged. This damage allows fluid from other parts of the eye to
rapidly enter the lens leading to swelling and then whitening
• Radiation
• Cataracts can arise as an effect of exposure to various types of radiation. X-rays,
one form of ionizing radiation, may damage the DNA of lens cells. Ultraviolet light,
specifically UVB, has also been shown to cause cataracts, and some evidence
indicates sunglasses worn at an early age can slow its development in later life.
The protein coagulation caused by electric and heat injuries whitens the lens.This
same process is what makes the clear albumen of an egg become white and
opaque during cooking.
56. • Genetics: The genetic component is strong in the
development of cataracts. The presence of cataracts in
childhood or early life can occasionally be due to a
particular syndrome. Examples of chromosome
abnormalities associated with cataracts include 1q21.1
deletion syndrome
• 1q21.1 deletion syndrome
• is a syndrome caused by the deletion of a small
segment of chromosome 22. While the symptoms can
vary, they often include congenital heart problems,
specific facial features, frequent infections,
developmental delay, learning problems
58. • Skin diseases
• The skin and the lens have the same embryological origin and so can be affected
by similar diseases.Those with atopic dermatitis and eczema occasionally develop
shield ulcer cataracts. Ichthyosis
• Smoking and alcohol
• Cigarette smoking has been shown to double the rate of nuclear sclerotic cataracts
and triple the rate of posterior subcapsular cataracts. Evidence is conflicting over
the effect of alcohol. Some surveys have shown a link, but others which followed
people over longer terms have not.
• Post-operative
• Nearly every person who undergoes a vitrectomy without ever having had cataract
surgery—will experience progression of nuclear sclerosis after the operation. This
may be because the native vitreous humor is different from the solutions used to
replace the vitreous. This may also be because the native vitreous humour
contains ascorbic acid which helps neutralize oxidative damage to the lens and
because conventional vitreous substitutes do not contain ascorbic acid.
59. • Medications
• Some medications, such as systemic, topical,
or inhaled corticosteroids, may increase the
risk of cataract development. Corticosteroids
most commonly cause posterior subcapsular
cataracts.
60. • Sign & Symptoms:
• Your vision is cloudy or blurry
• Colors look faded
• You can’t see well at night
• Lamps, sunlight, or headlights seem too bright
• You see a halo around lights
• You see double (this sometimes goes away as the
cataract gets bigger)
• You have to change the prescription for your
glasses often
61. • Risk factors
• Increasing age
• Diabetes
• Excessive exposure to sunlight
• Smoking
• Obesity
• Previous eye injury or inflammation
• Previous eye surgery
• Prolonged use of corticosteroid medications
• Drinking excessive amounts of alcohol
• Diagnosis: An eye doctor can check for cataracts as part of a dilated
eye exam. The exam is simple and painless your doctor will give
you some eye drops to dilate (widen) your pupil and then check
your eyes for cataracts and other eye problems.
62. • Treatment:
• When symptoms begin to appear, you may be able to improve your vision for a
while using new glasses, strong bifocals, magnification, appropriate lighting or
other visual aids.
• Think about surgery when your cataracts have progressed enough to seriously
impair your vision and affect your daily life.
• Many people consider poor vision an inevitable fact of aging, but cataract surgery
is a simple, relatively painless procedure to regain vision.
• During surgery, the surgeon will
remove your clouded lens and in
most cases replace it with a clear,
plastic intraocular lens (IOL).
IOL blocks both ultraviolet radiation
and high-energy visible blue light,
which research indicates may damage
the retina.