(Glycogenolysis)
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Glycogen degradation (glycogenolysis) involves breaking the alpha 1-4 glycosidic bonds between glucosyl residues to produce glucose 1-phosphate. Glucose is also released from alpha 1-6 linkages. This process involves: 1) Glycogen phosphorylase shortening chains by cleaving alpha 1-4 bonds until limit dextrins are reached. 2) A debranching enzyme removes outer glucosyl residues from branches and transfers them to other chains. Its glucosidase activity releases glucose from alpha 1-6 linkages. 3) Glucose 1-phosphate is converted to glucose 6-phosphate, which can be released from the liver or used in glycol
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Glycogen breakdown
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Bifunctional enzyme
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Vitreous (Attachments, age changes, vitreous hemorrhage, Vitreous Detachment)
Vitreous
Vitreous is an inert, avascular, transparent, jelly like structure.
Serve as one of refractive media of the eye and has optical functions.
It gives structural integrity to eye and provide nutrients to the lens, ciliary body and retina.
Constitute 80% volume of the eye.
Contain collagen fibrils, mucopoly-saccharides and hyaluronic acid.
It’s a hydrophilic gel which become ‘’fluid’’ when protein coagulates.
Reasons for coagulation of proteins could be,
• Advancing senile age
• Degenerations, e.g. as in high myopia
• Chemical and mechanical trauma
Internal limiting membrane on inner surface of retina separate it from vitreous. There is potential space ‘subhyaloid space’ between two.
Figure 1 structures of vitreous
Vitreous attachments
1. Anteriorly to the lens and ciliary epithelium in front of ora serrata. Part of vitreous about 4mm across ora serrata is called as ‘base of vitreous’. Here, attachment is strongest.
2. Posteriorly to the edge of optic disc and macula lutea (foveal region) forming ring shaped structure around them.
Figure 2 vitreous attachments
Age changes in Vitreous
Vitreous undergo certain physical and biochemical changes with aging.
1. At birth_ the Cloquet’s canal runs straight from lens to optic disc. It contains primary vitreous.
2. In young persons_ vitreous gel is homogenous but its fibers become coarse with process of advancing age.
3. In old age and high myopes_ secondary vitreous liquified (syneresis) and shrinks, producing a vitreous detachment, vitreous and retinal hemorrhage and retinal break.
Figure 3 Vitreous at birth Figure 4 Vitreous in young adults.
Figure 5 vitreous detachment in old age
Vitreous Hemorrhage
Vitreous hemorrhage is the extravasation, or leakage, of blood into the areas in and around the vitreous humor of the eye.
TYPES
There are two types of vitreous hemorrhage.
1. Peripheral or subhyaloid hemorrhage _ occurs between retina and vitreous.
Blood remains fluid, red in color
Blood moves with gravity forming boat-shaped figure in macular area.
Figure 3 subhyaloid hemorrhage
2. Intravitreal hemorrhage_ the hemorrhage may get absorbed or degenerate to form a white fibrous tissue mass.
Etiology
Common causes of vitreous hemorrhage are;
i. Trauma_ by contusion or penetrating injury
ii. Vitreous retraction_ vitreous fibrous bands or membrane retraction
iii. Eale’s disease_ due to retinal vasculitis and periphlebitis
iv. Blood dyscrasias_ leukemia, sickle cell anemia, purpura.
v. Diabetes mellitus_ common in diabetic proliferative retinopathy
vi. Central retinal vein thrombosis
vii. Malignant hypertension_ often results in large intravitreal hemorrhage.
Symptoms
I. Black spots or clouds maybe seen in front of eye.
II. Impaired vision maybe up to perception of light.
Signs
1. Fundus examination
a) Faint or no red reflex seen
b) Grey opacities maybe present in vitreous
Figure 4 (A) Fundus exami
VISUAL FIELD (Classification, neurological and glaucomatous visual fields)
The visual field refers to the total area in which objects can be seen in the side (peripheral) vision as you focus your eyes on a central point.
OR
The island of vision surrounded by a sea of blindness is known as visual field.
Normal field of vision
upwards = 60
inwards = 60
downwards = 70
outwards = > 90
Normal visual field
The island of vision surrounded by a sea of blindness is known as visual field.
Point of fixation
Area of maximum VA in normal visual field.
It corresponds to fovea of retina.
Blind spot
Area of absolute scotoma within the boundaries of normal VF.
It corresponds to optic nerve head where no rods and cones are present.
Locate 15° temporal to point of fixation.
Overview of visual pathway
Glaucomatous Visual Fields Neurological Visual Fields
Result from lesions of nerve fiber bundles 1. Toxic amblyopia
Bilateral Central scotoma_ as in tobacco amblyopia, alcohol amblyopia, nutritional amblyopia, lead poisoning or digitalis toxicity
Peripheral depression_
Contraction_ as in poisoning by quinine, arsenic, chloroquine or salicycate.
Centrocecal scotoma_ scotoma of tobacco or alcohol amblyopia
Figure 3 optic nerve head in optic neuropathies
Defects occur as a result of diminished blood flow in anterior optic nerve in region of lamina cribrosa, arterial circle of zinn-Haller and peripapillary choroidal circulation. 2. Optic nerve diseases
Optic neuritis_ is an inflammation of the optic nerve. Causes include infections and immune-related illnesses such as multiple sclerosis. Sometimes the cause is unknown.
Optic nerve atrophy_ is damage to the optic nerve. Causes include poor blood flow to the eye, disease, trauma, or exposure to toxic substances.
Optic nerve head drusen_ are pockets of protein and calcium salts that build up in the optic nerve over time.
Figure 4 Optic neuritis
Result from lesions of nerve fiber bundles 1. Toxic amblyopia
Bilateral Central scotoma_ as in tobacco amblyopia, alcohol amblyopia, nutritional amblyopia, lead poisoning or digitalis toxicity
Peripheral depression_
Contraction_ as in poisoning by quinine, arsenic, chloroquine or salicycate.
Centrocecal scotoma_ scotoma of tobacco or alcohol amblyopia
Figure 3 optic nerve head in optic neuropathies
Defects occur as a result of diminished blood flow in anterior optic nerve in region of lamina cribrosa, arterial circle of zinn-Haller and peripapillary choroidal circulation. 2. Optic nerve diseases
Optic neuritis_ is an inflammation of the optic nerve. Causes include infections and immune-related illnesses such as multiple sclerosis. Sometimes the cause is unknown.
Optic nerve atrophy_ is damage to the optic nerve. Causes include poor blood flow to the eye, disease, trauma, or exposure to toxic substances.
Optic nerve head drusen_ are pockets of protein and calcium salts that build up in the optic nerve over time.
Figure 4 Optic neuritis
Blind spot & Bjerrum scotoma: in early stage of Open-angle glau
Uveitis (Classification, Panuveitis, Endophthalmitis, Panophthalmitis, Synech...
Uveitis
• Inflammation of uveal tissue.
• Associated inflammation of adjacent structures, such as Retina, Vitreous, Sclera and Cornea.
Figure 1 uveitis
Anatomical classification
Clinical classification
Pathological classification
Etiological classification
(Duke Elder’s)
1. Anterior uveitis
Can be divided as follow;
1) Iritis_ inflammation mainly the iris
2) Iridocyclitis _iris and pars plicata involved
3) Cyclitis_ pars plicata is affected
Acute uveitis
Onset is sudden,
Last for less than 3 weeks Granulomatous uveitis
Infective nature
Inflammation is insidious in onset
Chronic in nature with minimum clinical features Infective uveitis
2. Intermediate uveitis
Inflammation of pars plana, peripheral retina and choroid.
Also called as “pars planitis”. Chronic uveitis
Onset is insidious
Duration is more than 3 weeks
Non-granulomatous uveitis
due to allergic or immune related reaction
acute onset
short duration
Allergic uveitis or immune related uveitis
3. Posterior uveitis
Inflammation of choroid(choroiditis)
Associated inflammation of retina (chorioretinitis) Recurrent uveitis
uveitis keeps reoccurring periodically
Toxic uveitis
4. Panuveitis
Inflammation of whole uveal tract Traumatic uveitis
5. Uveitis associated with non-infective systemic diseases
6. Idiopathic uveitis
7. Neoplastic
Figure 2 anatomical classification of uveitis
Panuveitis
Endophthalmitis
Panophthalmitis
Inflammation of all layers of uvea of eye
Can also affect lens, retina, optic nerve and vitreous causing reduced vision or blindness. Inflammation of internal structures of the eye, I;e choroid, retina and vitreous Purulent inflammation of all structures of eye
Including all the three coats and Tenon’s capsule as well.
Etiology
1. Idiopathic
After ruling out other causes
2. Infectious
Tuberculosis
Syphilis
Lyme disease
Leptospirosis
Infectious endophthalmitis
3. Immune related
Sarcoidosis
Vogt-koyanagi-Harada syndrome
Sympathetic ophthalmitis
Behcet syndrome
Etiology
Acute process 1-7 days following intraocular surgery such as Cataract surgery and filtering operation
Commonly caused by Bacteria-staphylococcus, pseudomonas, pneumococcus, streptococcus, E. coli,
Fungus -aspergillus fumigatus, candida albicans, fusarium,
Etiology
1.Exogenous
Due to infected wounds
Common pathogens are pneumococcus, staphylococcus, pseudomonas, pneumococcus, streptococcus, E. coli.
2.Endogenous
Due to metastasis of infected embolus in retinal artery and choroidal vessels.
Clinical Features
• Sudden onset of unilateral pain, redness, photophobia
• Maybe associated with lacrimation
• Visual acuity is usually good at presentation except in eyes with severe hypopyon.
• Low IOP
• Fibrinous exudate
• Posterior synechiae
• Miosis
• Aqueous flare and cells
• Endothelial dusting
Clinical Features
Bacterial endophthalmitis
• Sudden onset with severe pain
• Redness
• Visual loss
• Lid oedema, chemosis, corneal haze
• Low
Management of trauma Ropper Hall classification system (Preventive ophthalmol...
Ocular Trauma:
• Eye trauma refers to damage caused by a direct blow to the eye.
• The trauma may affect not only the eye, but the surrounding area, including adjacent tissue and bone structure.
• There are many different forms of trauma, varying in severity from minor injury to medical emergencies.
• It involves lids trauma, orbital trauma, chemical burns, orbital fractures and corneal foreign bodies.
Ropper Hall classification for chemical injuries
Ropper Hall classification system
Grade Prognosis Limbal ischemia Corneal involvement
i good none Epithelial damage
ii good <1/3 Haze, but iris details visible
iii guarded 1/3 – 1/2 Total epithelial loss with haze that obscure iris details
iv poor >1/2 Cornea opaque with iris and pupil obscured
Preventive measures of Ocular Trauma
1. Primary prevention:
• Reduction or elimination of exposure to factors associated with disorders.
• Prevention of work related complain is done by reducing exposure to physical, personal and psychosocial stressors.
2. Secondary prevention:
• Reducing disability
• Hastening of recovery
3. Tertiary prevention:
• Prevention of recurrence in Pt
• Job task and person-job fit evaluation
• Job or task modification
• Workstation changes
• Repetitions, abnormal postures (as corrective lenses in presbyopes) and other ergonomic problems should be addressed.
Sclera (scleritis and episcleritis, staphyloma)
Sclera
• Strong, opaque, white fibrous layer which forms 5/6th of external tunic of eye.
• Avascular, therefore infections rarely affect it.
• Blue in childhood, yellow in old age (due to fat deposition)
• 1mm thick
• Thinnest at attachment of EOMs.
Scleral Attachments
• The sclera provides a tough housing for intraocular contents and maintains the shape of the eye.
• The sclera comes to an end anteriorly where it attaches to the limbus of the cornea.
• Posteriorly the sclera fuses with the sheath of the optic nerve.
Scleral Apertures
• There are 3 sets of apertures namely;
1. Anterior
o Anterior ciliary vessels
o Perivascular lymphatics
o Nerves
2. Middle
o Four vena vorticosa exit 4mm behind the equator
3. Posterior
o Optic nerve exit 3mm to the medial side and just above the posterior pole
o Long and short ciliary vessels and nerves
Figure 2 posterior aspect of right eye
Scleritis
Episcleritis
Inflammation of deep scleral tissues Inflammation of subconjunctival and episcleral tissue
More severe Transient, self-limited
Can occur as anterior (95%) and posterior (5%) scleritis benign in nature
Etiology
1. Associated connective tissue diseases such as,
o Rheumatoid arthritis
o Polychondritis
o Polyarteritis nodosa
2. Associated herpes zoster and gout. Etiology
o Allergic reaction to endogenous proteins or toxin
o Maybe a collagen disease associated with Rheumatoid arthritis
o Associated with herpes zoster and gout.
Types/Classification
1. Anterior scleritis
Nodular scleritis
Diffuse scleritis
Necrotizing scleritis
With inflammation
Without inflammation
2. Posterior scleritis Types
1. Simple diffuse episcleritis
2. Nodular episcleritis
Incidences
o Women are affected commonly
o Bilateral usually Incidences
o Common in women
o Bilateral usually
o Peek age incidence is in 4th decade
Pathology
o Extend more deep
o Dense lymphocytic infiltration Pathology
o Lymphocytic infiltration of subconjunctival and episcleral tissue
Symptoms
o Localized redness
o Discomfort
o Mild to moderate pain Symptoms
o Localized redness in nodular episcleritis
o Discomfort
o Mild to moderate pain
Signs
o One or more nodules (nodular scleritis)
o Multiple hard, whitish nodules about pin size in inflamed area (diffuse scleritis)
o Dead tissue appearance and exposure of uveal pigment through thin sclera with anterior uveitis (necrotizing scleritis)
o Inflamed area behind equator with macular oedema, exudative retinal detachment, proptosis and limited ocular movements (posterior scleritis)
Signs
o Nodule like lentil situated 2-3mm away from limbus
o Hard, immovable and tender
o Conjunctiva move freely over nodule
o Conjunctiva looks purple as deep episcleral vessels traverse it.
Staphyloma
Ectatic condition of sclera in which uveal tissue is incarcerated.
Etiology:
Due to raised intraocular tension, staphylomas are formed due to thinni
Retina (Define ,anatomy of retina, examination of retina, classification of ...
Retina
The retina is a layer tissue at the back of the eye that senses light and sends images to the brain. In the center of this nervous tissue is the macula, that allows to focus the view toward the center and provides the needed sharpness to read, drive and clearly see details.
The retina processes light through a layer of photoreceptor cells. These are essentially light-sensitive cells, responsible for detecting qualities such as color and light-intensity. The retina processes the information gathered by the photoreceptor cells and sends this information to the brain via the optic nerve. Basically, the retina processes a picture from the focused light, and the brain is left to decide what the picture is.
Layers of Retina
The retina can be divided into 11 layers including
1. the inner limiting membrane
2. the nerve fiber layer
3. the ganglion cell layer
4. the inner plexiform layer
5. the inner nuclear layer
6. middle limiting layer
7. the outer plexiform layer
8. the outer nuclear layer
9. the outer limiting membrane
10. the photoreceptor layer
11. The retinal pigmented epithelium (RPE) monolayer.
Ora serrata
Anterior termination of retina where it continues with epithelium of Ciliary body.
Macula lutea (yellow spot)
1.5mm diameter area at post. Pole about 3mm temporal to optic disc.
Fovea centralis
Small depression in centre of macula
Cones predominate in this area
Most sensitive part of retina
Figure 1 Normal fundus Vessels emerge from nasal side of disc. Arteries are narrower than veins
Examination of Retina
Direct & indirect Ophthalmoscopy
1. Darken room, ask patient to look at the same point as far as possible in the room (this will help to dilate the pupil).
2. Wedge scope against your cheek with hand and then head/hand/scope should move as one unit.
3. Use your right hand & your right eye to look at the patient’s right eye. (Less important if using the PanOptic.)
4. Look through the ophthalmoscope, if you are nearsighted and have taken off your glasses, you may need to adjust the focusing wheel towards the negative/red until what you see at a distance is in focus.
5. Direct the ophthalmoscope 15 degrees from center and look for the red reflex (see video). Simply follow the red reflex in until you see the retina. If you lose the red reflex, come back until you find it again and repeat.
6. To look around the retina using a traditional direct ophthalmoscope, you should "pivot" the ophthalmoscope, angling up, down, left and right. If using the PanOptic, you can slightly "pivot" or ask the patient to look up to see upper retina, down to see lower retina, medial to see medial, latereral to see lateral and finally to look at the light to visualize the macula.
Slit Lamp Binocular Indirect Ophthalmoscopy
The use of slit lamp BIO is an increasingly popular form of fundoscopic examination. Minimum a dilated fundus examination with an indirect lens should be carried out on those presenting with photopsi
Retinoblastoma (Preventive measures for retinoblastoma)
Retinoblastoma
• Retinoblastoma (Rb) is a rare form of cancer that rapidly develops from the immature cells of a retina, the light-detecting tissue of the eye.
• It is the most common primary malignant intraocular cancer in children, and it is almost exclusively found in young children.
Preventive measures for retinoblastoma
1. Primary actions
• In adults, the risk for many cancers can be reduced by avoiding certain risk factors, such as smoking.
• Children born to a parent with a history of retinoblastoma should be screened for this cancer starting shortly after birth because early detection of this cancer greatly improves the chance for successful treatment.
2. Secondary actions
• Screening offspring of retinoblastoma survivor
• Indirect ophthalmoscopy for fundus examination
• OCT
Figure 1: indirect ophthalmoscopy fundus examination for retinoblastoma
Figure 2: OCT findings for retinoblastoma
3. Tertiary actions
• Prevent local / systemic tumor spread
• Prevent loss of an eye or vision
RETINOPATHY OF PREMATTURITY (ROP) PREVENTIVE MEASURES
RETINOPATHY OF PREMATTURITY (ROP)
RETINOPATHY OF PREMATTURITY (ROP)
• It is seen in premature infants who have been given high concentration of Oxygen.
• High concentration of oxygen at birth cause obliteration of peripheral retinal arteries and veins, resulting in release of vascular endothelial growth factors (VEGF) leading to neovascularization.
Preventive measures for ROP
1. Primary actions
• Parents are informed about retinopathy of prematurity (ROP),
• screening,
• treatment and outcomes (including the importance of breastfeeding for the prevention of ROP.)
2. Secondary actions
• Develop and implement a unit guideline on prevention and management of ROP.
• Develop information material on ROP for parents.
• Develop fail-safe systems for the identification of infants at risk of ROP.
• Develop formalized programs for education in oxygen saturation targets.
• Develop formalized programs for promotion of mother’s own milk feeding
3. Tertiary actions
• Developing and implementation of national guideline on prevention and management of ROP
• Consider telemedicine support for screening for retinopathy of prematurity (ROP).
• treatment of ROP.
• improve patient adherence to ophthalmological follow-up during screening and after treatment.
Onchocerciasis
• Onchocerciasis also known as ‘’river blindness’’ and ‘’Robles disease.’’
• It is a parasitic disease caused by infection by Onchocerca volvulus, a nematode (roundworm).
• It is the world's second-leading infectious cause of blindness.
• The parasite is transmitted to humans through the bite of a black fly of the genus Simulium.
• The larval nematodes spread throughout the body
Figure 1 Onchocerciasis
CAUSES
The disease is caused by filaria of O Volvulus.
Figure 2 O Volvulus.
LIFE CYCLE OF O. VOLVULUS
1. A Simulium female black fly takes a blood meal on an infected human host, and ingests microfilaria
2. microfilaria enter the gut and thoracic flight muscles of the black fly
3. progressing into the first larval stage.
4. The larvae mature into the second larval stage
5. move to the proboscis and into the saliva in its third larval stage
6. Maturation takes about 7 days.
7. After maturing, adult male worms mate with female worms in the subcutaneous tissue to produce Simulium female black fly takes a blood meal on an infected human host, and ingests between 700 and 1,500 microfilaria per day.
8. the black flies only feed in the day
Figure 3 LIFE CYCLE OF O. VOLVULUS
SIGNS AND SYMPTOMS
Skin involvement
• Typically consists of intense itching, swelling, and inflammation.
• Skin atrophy - loss of elasticity, the skin resembles tissue paper 'lizard skin' appearance.
• Depigmentation
• Nodules under the skin form around the adult worms.
Ocular involvement
• may involve any part of the eye from conjunctiva and cornea to uvea and posterior segment, including the retina and optic nerve
• cornea: Punctate keratitis
• can lead to visual impairment and permanent blindness
Figure 4 'lizard skin'
Onchocerciasis – the disease and its impact
Onchocercal skin disease also has an important socio-cultural impact. People with the disease often have low self esteem, experience social isolation, and worry that they will never marry. Children are distracted in school due to constant itching.
Blindness is caused when microfilariae migrate to the eye and die, causing an inflammatory response. Over time the affected area becomes opaque, leading to impaired vision and eventually blindness.
TREATMENT
• infected people can be treated with two doses of ivermectin,
• six months apart, repeated every three years
• Ivermectin treatment is particularly effective because it only needs to be taken once or twice a year
PREVENTION
Primary prevention:
• Vector control- applications of environmentally safe insecticides to the black flies breeding areas during rainy seasons.
• Mass treatment with Ivermectin.
• Various control programs aim to stop Onchocerciasis from being a public health problem
• larvicide spraying of fast-flowing rivers to control black fly populations
• The disease can be controlled by actions at the primary level with the village health worker administering the drug according to t
Primary, Secondary and Tertiary Eye Care Services
Primary Eye care
Primary eye care (PEC) is an integral part of comprehensive eye care.
It is targeted not only towards preventing blindness and visual impairment, but also towards providing services to redress ocular morbidity.
PEC is a frontline activity, providing care and identifying disease before it becomes a serious medical condition.
Primary eye care is delivered in many different ways. However, it all aims at making eye care services available within reach of the community. In the long run this allows each better penetration of services and reduced cost for the patient.
Components of primary eye care
Eye health education
Symptom identification
Visual acuity measurement
Basic eye examination
Diagnosis
Timely referral
Secondary Eye care
Includes acute care
• necessary treatment for a short period of time for a brief but serious illness,
• Injury or other eye health condition.
• Such as management of diseases like cataract, glaucoma, trachoma etc at secondary level i.e. hospitals.
Tertiary Eye Care
Carries specialized consultative health care,
• usually for in patients and on referral from a primary or secondary health professional,
• In a facility that has personnel and facilities for advanced medical investigation and treatment, such as tertiary referral hospitals.
• Centralized at a major health care complex.
• A medical teaching hospitals, eye hospitals or eye centers.
Optometry and Orthoptics (Laws and Acts)
Optometry is a health care profession that involves examining the eyes and applicable visual systems for defects or abnormalities as well as the correction of refractive error with glasses or contact lenses and treatment of eye diseases.
Definition of optometry and optometrist
The World Council of Optometry, World Health Organization and about 75 optometry organisations from over 40 countries have all over the world adopted the following definition, to be used to describe optometry and optometrist.
Optometry is a healthcare profession that is autonomous, educated, and regulated (licensed/registered).
Optometrists are the primary healthcare practitioners of the eye and visual system who provide comprehensive eye and vision care, which includes refraction and dispensing, detection/diagnosis and management of disease in the eye, and the rehabilitation of conditions of the visual system.
Competencies
• refractive error,
• ocular disease management,
• medical therapeutics,
• binocular vision,
• sports vision,
• vision therapy,
• contact lenses
Laws of optometry
Currently, optometrists can…
1. Prescribe Schedule II (hydrocodone products only), III, IV, and V narcotics (including oral antivirals, oral steroids, etc)
2. Order imaging, such as MRIs, CT scans, and x-rays
3. Remove foreign bodies
4. Perform post-operative care after 90 days with referral from a physician
5. Treat glaucoma with topicals and orals
6. Treat anterior uveitis
7. Perform dilation and irrigation
8. Perform scraping, debridement, or removal of corneal epithelium
9. Deliver injections limited to anaphylaxis
Optometrists cannot…
1. Perform surgical procedures (Any procedure that involves mechanical or laser means to cut, alter, or infiltrate human tissue is included here. This restriction includes refractive surgery, any laser procedure, or chalazia removal/eyelid or conjunctival cyst lancing procedures, to name a few) (Colorado is one of a few states with verbage to explicitly exclude surgery-most statutes maintain that the license to practice optometry does not include the right to practice medicine)
2. Deliver injectables, except for in the case of anaphylaxis
3. Treat posterior uveitis
4. Prescribe Schedule I or II narcotics
Acts of optometry
1. Health Professions Procedural Code
The Health Professions Procedural Code shall be deemed to be part of this Act.
Definitions
“College” means the College of Optometrists of Ontario; (“Ordre”)
“Health Professions Procedural Code” means the Health Professions Procedural Code set out in Schedule 2 to the Regulated Health Professions Act, 1991; (“Code des professions de la santé”)
“member” means a member of the College; (“membre”)
“profession” means the profession of optometry; (“profession”).
IOP measurements
Intraocular pressure
Intraocular pressure (IOP) is the fluid pressure inside the eye. . IOP is an important aspect in the evaluation of patients at risk of glaucoma.
Tonometry is the method eye care professionals use to determine this. Most tonometers are calibrated to measure pressure in millimeters of mercury (mmHg).
Physiology
• 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 reason for this is because the vitreous humour in the posterior segment has a relatively fixed volume and thus does not affect intraocular pressure regulation.
• The intraocular pressure (IOP) of the eye is determined by the balance between the amount of aqueous humor - that the eye makes and the ease with which it leaves the eye.
The Goldmann equation states:
Po = (F/C) + Pv
Po is the IOP in millimeters of mercury (mmHg),
F is the rate of aqueous formation,
C is the facility of outflow,
Pv is the episcleral venous pressure.
Measurements
Intraocular pressure is measured with a tonometer as part of a comprehensive eye examination.
Types of Tonometry
1. Applanation tonometry
Applanation tonometry is based on the Imbert-Fick principle, which states that;
‘’The pressure inside an ideal dry, thin-walled sphere equals the force necessary to flatten its surface divided by the area of flattening’’
P = F/A
where P = pressure, F = force and A = area
In applanation tonometry, the cornea is flattened and the IOP is determined by varying the applanating force or the area flattened.
Goldmann and Perkins applanation tonometry
Equipment
• Tonometer, either Goldmann (used on slit lamps) or Perkins (hand-held)
• Applanation prism
• Local anaesthetic drops
• Fluorescein strips
• Clean cotton wool or gauze swabs.
Method
• The Goldmann applanation tonometer measures the force necessary to flatten an area of the cornea of 3.06mm diameter. At this diameter, the resistance of the cornea to flattening is counterbalanced by the capillary attraction of the tear film meniscus for the tonometer head.
• The IOP (in mm Hg) equals the flattening force (in grams) multiplied by 10. Fluorescein dye is placed in the patient’s eye to highlight the tear film. A split-image prism is used such that the image of the tear meniscus is divided into a superior and inferior arc. The intraocular pressure is taken when these arcs are aligned such that their inner margins just touch.
• Applanation tonometry measurements are affected by the central corneal thickness (CCT). When Goldmann designed his tonometer, he estimated an average corneal thickness of 520 microns to cancel the opposing forces of surface tension and corneal rigidity to allow indentation. It is now known that a wide variation exists in corneal thickness among individuals. Thicker CCT may give an artificially high IOP measurement, whereas thinner CCT can give an arti
Keratoconus
KERATOCONUS
• Progressive thinning of cornea usually bilateral condition at puberty in girls.
• May result in blurry vision, diplopia, astigmatism, light sensitivity and myopia.
• In severity, scarring or circle seen in cornea.
Classification:
1. Keratometry classification
a) Mild <48 D
b) Moderate 48-54 D
c) Severe >54 D
2. Morphological classification
a) Nipple cones
• Small size(5mm)
• Steep curvature
• Thick apical center
• Displaced inferonasally
b) Oval cones
• Larger(5-6mm)
• Ellipsoid
• Displaced infer-temporally
c) Globus cones
• Largest (>6mm)
• May involve 70% cornea
Figure 1 Morphological classification of keratoconus
Symptoms
• Impaired vision due to progressive myopia
Signs
a) Early signs
“Oil droplet” reflex in ophthalmoscopy
Irregular “scissor reflex” in retinoscopy
Mires cannot superimpose and principal meridians are no longer 90° apart in Keratometry
b) Late signs
Conical shape of cornea
Apex of cornea situated below center of cornea
Placido disc show distortion of corneal reflex
Figure 2 uneven spacing of rings
Munson’s sign indentation or acute bulge of lower lid, when Pt looks down.
Figure 3 Munson’s sign
Slit-lamp examination
I. Vogt’s lines-
Fine, parallel lines seen at apex which are vertical folds at deep Stroma & Descment’s membrane.
II. Fleischer ring-
Brownish ring at base due to haemosiderin pigment.
III. Acute hydrops-
Oedema and opacity of stroma due to rupture in Descement’s membrane.
Figure 10 Slit-lamp examination of the left eye.
(A) Corneal irregularity with marked thinning of the central cornea
(B) diffuse cloudiness of the corneal graft with stromal oedema
(c)epithelial defect on the central cornea,
(d) no sign of infection after the second repeat keratoplasty
Assessment of keratoconus (Evaluation and diagnosis)
History and family history
Follow up evaluation
Slit-lamp exams
o Keratoscopy – keratometry
o Corneal thickness- pachymetry
o Topography- orbscan – pentacam
Corneal Diseases.docx
• Cornea is an avascular, transparent tissue that is an important component of the ocular refractive system.
• It is one of the most densely innervated tissues in the body.
Behind the precorneal tear film there are five layers of cornea:
1. Epithelium and basal lamina
2. Bowman’s layer
3. Stroma
4. Descemet’s membrane
5. Endothelium
Corneal Transparency
The cornea transmits nearly 100% of the light that enters it.
Transparency achieved by Arrangement of stromal lamellae.
Other factors:
Epithelial non-keratinization
Regular & uniform arrangement of corneal epithelium
Junctions between cells & its compactness
Corneal avascularity
Non-myelinated nerve fibers
Once the damaged corneal epithelia are invaded by offending agent, the sequence of pathological changes which occur during development of corneal ulcer can be described under four stages:
1. Progressive infiltration
Grey zone
Localized necrosis
Saucer-shaped ulcer with overhanging edges
2. Active ulceration
Dead material material thrown off
Oedema subsides
Floor and edges are smooth and transparent
3. Regression
From limbus, minute vessels grow in
4. Cicatrization
Formation of fibrous tissue which fill the gap
Opacity generated
Glaucoma Preventive Measurements.pptx
Glaucoma
• A chronic, progressive optic neuropathy caused by a group of ocular conditions which leads to damage to optic nerve with loss of visual function.
• Risk factor is raised IOP above 25mmHg
Interventions for Prevention:
1. Primary level:
• Recognition of acute red eye with pain
• VA examination
• Cloudy cornea examination
• Examination of dilated pupil
• Examination of depth of anterior chamber
2. Secondary level:
• Identification of people with glaucoma
• Determination of IOP after 40 years of age
• Positive family history
• Refractive error examination (myopia)
• Associated DM, HTN consideration
• Alcohol and smoking consideration
3. Tertiary level:
• As Vision lost due to glaucoma cannot be regained. Early detection and proper treatment is the key to preventing blindness from this disease.
• Pt screening
• Determination of IOP after 40 years of age
• Fundus examination
• Visual field examination
COMMUNITY OPHTHALMOLOGY.pptx
Community ophthalmology:
• Community ophthalmology, also known as public health ophthalmology or preventive ophthalmology.
• Delivery of eye care involves preventive, curative, promotive, and rehabilitative activities, making it a holistic approach.
• It is foreseen as a health-management approach in preventing eye diseases, lowering eye morbidity rates and promoting eye health through active community participation at the ground level.
Classification
The United States Commission of Chronic Illness proposed the original classification system for prevention in the public-health field. It contained three types of prevention interventions, in terms of primary goals related to the disorder or illness. These stages of prevention and control of a disease are also true for community eye health.
1. Primordial health promotion
In community ophthalmology, this is achieved through health education, environmental hygiene, and healthy dietary practices.
The promotive component (mainly health education and promotion) consists of
a. provision of information, education, communication (IEC) materials on simple personal hygiene,
b. detecting visual disturbances in children,
c. eradication of myths and misconceptions on eye care,
d. advice on proper diet such as adding dark-green, leafy vegetables high in betacarotene to the diet of young children,
e. increasing awareness on the availability of surgery to restore sight of those blind because of cataract,
f. as well as other existing health services.
Community ophthalmology
1. promotive
• Nutrition education
• Improved maternal and child nutrition
• Health education
• Face washing
• Good antenatal care
• Safe water
• Improved environmental sanitation
2. Preventive
• Ocular prophylaxis(treatment given or action taken to prevent disease.) at birth
• Vitamin- A doses
• Measles vaccine
• Perinatal (time immediately before and after birth) care
• Avoid hypoxia at birth
• Avoid medication in pregnancy
• Neonatal examination
3. Rehabilitative
• Provision of services on low vision
• Community-based rehabilitation
• Counseling of the incurably blind
• Certification of blindness by eye surgeon
• Sensitize about concessions
4. Curative
• Vision screening
• Treatment for vitamin-A deficiency
• Referral for surgery
• Emergency management
• Treatment for trachoma
• Treatment for other common eye diseases
2. Primary prevention of diseases
It seeks to decrease the number of new cases of a disorder or illness
In eye care, it can be through
• measles immunization in childhood,
• vitamin-A supplementation for pregnant women,
• awareness campaigns for preventing unhealthy birth practices.
3. Secondary prevention:(early diagnosis and treatment)
It seeks to lower the rate of established cases of a disorder or illness in the population, is intended for those with existing disease.
In eye care, it can be achieved through a screening system where cases like cataract can be diagnosed early and treated to preve
contact lens solution
Different types of solutions are use in contact lens practice. Some solutions are only for hydrophobic rigid contact lenses and some for hydrogel soft contact lenses. While few of them may be used for both types of lenses. Various solutions available can be grouped as follow:
• Wetting agents
• Cleaning agents
• Storage (soaking agents)
• Rewetting agents
Multifunctional solutions are combination of two or more of the above solutions that enhance compliance by reducing number of solutions the pt has to use.
Components of solutions
All solutions contain certain components that are peculiar to particular function of the solution at varying concentration.
Cleaning agent
Buffering agent
Vehicle
Surfactant cleaner
Enzymatic cleaner
Soaking solution
Heat for disinfection
Chemical disinfecting
Preservatives
Preservative conc. is usually low in CL solutions in order to reduce risk of any eye irritation.
Range of preservatives includes:
Benzalkonium chloride
Chlorobutanol
Thiomesal
Chlorhexidine
Ethylene diamine tetra-acetic acid (EDTA)
Sorbic acid
Potassium sorbate
1. Wetting solution
An agent that coats the contact lens with a film intends to minimize the friction of CL against pelpebral conjunctiva and cornea. It act as
buffer
Cushioning agent
It disintegrates to be replaced by lacrimal fluid. It must meet standards as regard to sterility, isotonicity, nonirritabilty and stability.
Should be buffered at pH of tears.
Essential characteristics of a Wetting agent
1. Wet thoroughly and spread over an entire surface of lens, rendering it hydrophilic.
2. Should form a film sufficiently tenacious so that it’ll not be washed away during the wearing period by tears.
3. Nonirritating and nonsensitizing
4. No residue existence (pure)
5. Cleaner, antiseptic and self-preserving
6. Viscous
7. Lubricant and preserving agent
8. Allow lens sticking on fingertip during insertion and sallow no oil of finger to get on lens
Not interfere with wetting
Contact Lens Deposits, Contact lens Aftercare, Overview of care and Maintenance
Conatct lens deposit
Any lens surface coating or lens matrix formation which is not flushed or rinsed from the lens by tears during blinking. In effect, anything that remains on the surface despite blinking is deposit.
Deposit Formation:
Tear protein(lysozyme) are attached to the lens
Tear evaporates and leave residue on the lens
After protein are deposited, other components of the tear film (such as mucin) may adhere to protein
Over time, Layers build up and structural changes take place(e.g. Denaturation)
Factors influencing lens deposition:
o Individual difference in tears
o Lens materials
o Care system
o Wearing schedule
o Environment
o Patient hygiene
Types of Deposits:
1. TEAR RELATED:
• Protein
• Lipid
• Jelly bumps
2. NON-TEAR RELATED:
• Fungi
• Lens discoloration
• Mercurial deposits
• Cigarette residues
• Surface combination
• Rust spots
1. Protein deposits:
• Are a semi-opaque or translucent film usually thin whitish and superficial
• Have a frosted glass appearance
• may cover lens surface partially or full
• Cause the lens surface to become hydrophobic
• Can crack and peel if thick
Factors favoring a buildup of protein on a contact lens:
• short BUT
• Ionic binding capacity
• Inadequate cleaning especially of the lens periphery
• Altered blinking
• Heat disinfection
• Tear deficiency or altered tear composition
• Chronic allergies and GPC
2. Lipid Deposits
• Appears as greasy, smooth, and shiny adherent films on both RGP and soft contact lenses
• Best observed between blinks
• Appears as a thick
• oily coating
Lipids involved includes:
• phospholipids,
• neutral fats,
• triglyceride,
• cholesterol,
• cholesterol esters,
• fatty acids
Origin: mainly from meibomian gland
Predisposing factors:
• Tear film quality
• Slow blink pattern
• Poor lens compliance
• Careless use of inappropriate cosmetics/lotions
3. Jelly Bumps
• Appear as a clump of raised translucent mulberry like deposits
• Typically form in inferior
• exposed portion of lens
• Occur more frequently in high water, ionic, EW lenses
Predisposing factors
• Quality of tear film
• Poor blinking
• Lens surface contamination
• Aphakia cleaning consequences
• Large and numerous jelly bumps lead to wearer discomfort
• Large deposits can cause the lens to attach to the upper lid so that each blink causes excessive lens movement
• When located within pupil zone-visual acuity can fluctuating
• Maya also cause mechanical irritation of tarsal conjunctiva
• In extreme case, may cause CLPC
4. Inorganic Deposits
• Calcium carbonate deposits
• Calcium phosphate deposits
Appearance:
• White crystalline specks
• Can be small or large
• Rough surface
• Penetrate lens surface if severs
5. Fungal Deposits
Appearance:
• Filamentary growth on and into lens
• Usually white, brown or black
Fungal formation
• Spores on lens surface from eye or environment
• Proliferates to large visible growth
Contact Lens Intro.ppt
INTRODUCTION
HISTORY
CL is an artificial device whose front surface substitutes the anterior surface of cornea.
Correct refractive errors
Correct irregularities of front surface of cornea
CL was developed by Leonardo de vinci who conceived the idea of
‘neutralizing cornea by substituting it with a new refracting surface.’
INTRODUCTION
HISTORY
First lens was made up of Polymethyl methacrylate (PMMA )
Then soft lenses were introduced made up of hydroxyethyl methacrylate (HEMA)
Rigid gas permeable lenses (RGP) developed in the same period.
CL Terminology
Classification
CL design
Lens material properties
1. Classification
CL has been variously classified as follow;
Depending upon the
Anatomical position occupied
Nature of material used for manufacturing
Mode of wear
Water content
i) Anatomical position occupied
a) Scleral CLs
cover the cornea and conjunctiva overlying sclera
b) Semi scleral CLs
cover cornea and bridge the limbus to lie partially on conjuctiva
c) Corneal CLs
confirm to cornea
Scleral CLs
ii) Nature of material used for manufacturing
a) Rigid non-gas permeable CLs
Made up of PMMA
b) RGP CLs
made up of cellulose acetate butyrate (CAB)and silicone lenses
c) Soft CLs
Hydrogel CLs made up of hydroxyethyl methacrylate (HEMA)
iii) Mode of wear
Daily wear CLs
Extended wear CLs
Disposable CLs
iv) Water content
Depending upon the H2O content, hydrogel lenses can be
a) Low H2O content (0-40%)
b) Medium H2O content (40%-55%)
c) High H2O content (>55%)
2. CL Design
Single-cut lenses
Lenticular cut lenses
A) Single-cut lenses
Front surface has a single continuous curve
Back surface consist of base curve and peripheral curves as desire
B) Lenticular cut lenses
Front surface has a central optical portion surrounded by a peripheral carrier portion.
Peripheral carrier portion is thinner than central optic portion.
Radius of curvature is flatter than radius of central optical portion.
Back surface of lenticular lens has same curve as single-cut lenses
i;e base curves and peripheral curves as
desired.
3) CL Material Properties
Wettability
Water content
Oxygen permeability
Oxygen transmissibility
Light transmission
Refractive index
Heat resistance
Dimensional stability
Flexure
1. Wettability
Adherence of liquid to solid surface despite the cohesive forces holding the liquid together.
Wetting angle is inversely proportional to
wettability.
Complete wetting- wetting angle 0˚
Partial wetting- wetting angle 70˚
Nonwetting- wetting angle 150˚
2. Water content
Percentage of CL that is constituted by water.
CL has pores that are formed by cross linking of monomers.
These pores absorb water, forming the water content of lens.
water content, oxygen transmissibility
If H2O content increase by 20%, oxygen permeability is doubled.
Intro databases (Table, Record, Field)
Intro databases
Data – a collection of facts made up of text, numbers and dates: Ali 35000 7/18/86
Information - the meaning given to data in the way it is interpreted:
Mr. Ali is a sales person whose annual salary is $35,000 and whose hire date is July 18, 1986.
A structured collection of related data
An filing cabinet, an address book, a telephone directory, a timetable, etc.
Google and your email is a database
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(Glycogenolysis)
- 1. DEGRADATION OF GLYCOGEN (GLYCOGENOLYSIS) Maryam Fida (o-1827) Source: Lippincott
- 2. • When glycogen is degraded, the primary product is glucose 1-phosphate, obtained by breaking α (1→ 4) glycosidic bonds • In addition, free glucose is released from each α (1→ 6)- linked glucosyl residue
- 3. Steps A. Shortening of chains B. Removal of branches C. Conversion of glucose 1-phosphate to glucose 6- phosphate D. Lysosomal degradation of glycogen
- 4. A. Shortening of chains • Glycogen phosphorylase sequentially cleaves the α (1→ 4) glycosidic bonds between the glucosyl residues at the nonreducing ends (producing glucose 1- phosphate) until four glucosyl units remain on each chain before a branch point • Pyridoxal phosphate (PLP) is required as a coenzyme • Resulting structure is called a limit dextrin and phosphorylase cannot degrade it any further
- 5. B. Removal of branches Branches are removed by the two enzymic activities of a single bifunctional protein, the Debranching Enzyme: • DEBRANCHING ENZYME 4:4 transferase activity • DEBRANCHING ENZYME 1:6 glucosidase activity
- 8. DEBRANCHING ENZYME 4:4 transferase activity • Removes the outer three of the four glucosyl residues attached at a branch • It next transfers them to the non-reducing end of another chain, lengthening it accordingly
- 9. DEBRANCHING ENZYME 1:6 glucosidase activity • The remaining single glucose residue attached in an α (1→ 6) linkage is removed hydrolytically by (1→ 6)- glucosidase activity, releasing free glucose • The glucosyl chain is now available again for degradation by glycogen phosphorylase until four glucosyl units from the next branch are reached
- 10. C. Conversion of glucose 1-phosphate to glucose 6- phosphate • In the liver, glucose 6-phosphate is converted to glucose by glucose 6-phosphatase and released into the blood to help maintain blood glucose levels • In the muscle, glucose 6-phosphate cannot be dephosphorylated because of a lack of glucose 6- phosphatase. Instead, it enters glycolysis, providing energy needed for muscle contraction Interconversion of glucose 6- phosphate and glucose 1-phosphate by phosphoglucomutase
- 11. D. Lysosomal degradation of glycogen • A small amount (1–3%) of glycogen is continuously degraded by the lysosomal enzyme, α (1→ 4)- glucosidase (acid maltase)
- 14. REGULATION OF GLYCOGEN SYNTHESIS AND DEGRADATION Note: • The Active form of Glycogen synthase is dephosphorylated • The active form of Phosphorylase kinase and Glycogen phosphorylase is Phosphorylated