This document discusses different types of cataracts, including age-related cataracts, traumatic cataracts, and cataracts caused by other factors like radiation, chemicals, and medical conditions. It describes the typical appearance and progression of nuclear, cortical, and posterior subcapsular cataracts. Traumatic cataracts are outlined including those caused by contusion, penetrating injuries, radiation, chemicals, electricity and intraocular foreign bodies. The lens' sensitivity to ionizing radiation is also summarized.
Ischemic optic neuropathy constitutes one of the major causes of blindness or seriously impaired vision among the middle-aged and elderly population.
Ischemic optic neuropathy is due to acute ischemia of the optic nerve. it can be classified into two, depending upon the part of the optic nerve involved:
1.Anterior ischemic optic neuropathy (AION)
-AION is due to acute ischemia of the front (anterior) part of the optic nerve (also called optic nerve head), which is supplied mainly by the posterior ciliary arteries.
-AION is divided into two types, depending on what causes it:
1.Arteritic AION: This is the most serious type and is due to a disease called giant cell arteritis or temporal arteritis.
2. Non-arteritic AION: This is the usual, most common type, with many different causes but not associated with giant cell arteritis.
2.Posterior ischemic optic neuropathy (PION). -
-PION is a much less common type. It is due to acute ischemia of the back (posterior) part of the optic nerve, located some distance behind the eyeball; this part of the optic nerve is NOT supplied by the posterior ciliary arteries
(Hayreh, 2009)
Gross Anatomy & Physiology of Eye
Introduction to cataract
Epidemiology of cataract
The etiological factors
Pathophysiology
Clinical manifestations
Types
Diagnostic measures
Surgical measures
Pre and post operative nursing management
Complications after surgery.
Summary
Ischemic optic neuropathy constitutes one of the major causes of blindness or seriously impaired vision among the middle-aged and elderly population.
Ischemic optic neuropathy is due to acute ischemia of the optic nerve. it can be classified into two, depending upon the part of the optic nerve involved:
1.Anterior ischemic optic neuropathy (AION)
-AION is due to acute ischemia of the front (anterior) part of the optic nerve (also called optic nerve head), which is supplied mainly by the posterior ciliary arteries.
-AION is divided into two types, depending on what causes it:
1.Arteritic AION: This is the most serious type and is due to a disease called giant cell arteritis or temporal arteritis.
2. Non-arteritic AION: This is the usual, most common type, with many different causes but not associated with giant cell arteritis.
2.Posterior ischemic optic neuropathy (PION). -
-PION is a much less common type. It is due to acute ischemia of the back (posterior) part of the optic nerve, located some distance behind the eyeball; this part of the optic nerve is NOT supplied by the posterior ciliary arteries
(Hayreh, 2009)
Gross Anatomy & Physiology of Eye
Introduction to cataract
Epidemiology of cataract
The etiological factors
Pathophysiology
Clinical manifestations
Types
Diagnostic measures
Surgical measures
Pre and post operative nursing management
Complications after surgery.
Summary
most common ophthalmic disorder seen in all over world. in India 2015 incidence of cataract patient was 62.6 % (9 million). so the awareness and the management is very important for this disease condition. i hope this presentation is very helpful to all the student and people to understanding the cataract refractive ophthalmic disease
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
3. AGE-RELATED CHANGES in the LENS
1. Change of crystallins (lens proteins) by chemical
modification and aggregation into high-
molecular-weight protein.
2. Compression and hardening of lens nucleus
(nuclear sclerosis)
3. Decreased concentrations of glutathione and
potassium
4. Increased concentrations of sodium and calcium
5. Increased hydration
6. Progressive pigmentation (yellow or brownish
hue)
AGING CHANGES
5. Definition: Central lens opacity caused by
excessive amount of sclerosis and yellowing of
the lens nucleus
Natural course
1. Usually bilateral but asymmetric
2. Tend to progress slowly
Evaluation of the degree of sclerosis, yellowing
and opacification
1. Slit-lamp biomicroscope
2. Examining the red-reflex with pupil dilated
Histopathology: Homogeneity of lens nucleus
with loss of cellular laminations
NUCLEAR CATARACTS
6. CLINICAL APPEARANCE
1. Typically cause greater impairment of distance
vision than of near vision
2. In the early stages, the progressive hardening
of the lens nucleus commonly causes an
increase in the refractive index of the lens and
thus a myopic shift in refraction, sometimes
known as lenticular myopia.
3. In some cases, the myopic shift transiently
enables otherwise presbyopic individuals to
read without spectacles (second sight)
NUCLEAR CATARACTS
7. CLINICAL APPEARANCE
4. Occasionally, the abrupt change in refractive
index between the sclerotic nucleus and the
lens cortex can cause monocular diplopia.
5. Progressive yellowing of the lens causes poor
hue discrimination, especially at the blue end
of the visible light spectrum.
6. Decreased photopic retinal function (in
advanced cases)
7. Opacification of lens nucleus in very
advanced cases (brunescent cataract)
NUCLEAR CATARACTS
8. Pathogenesis: Changes in the ionic composition
of the lens cortex and subsequent changes in
hydration of the lens fibers
Natural course
1. Usually bilateral but asymmetric
2. Vary greatly in rate of progression; some
remain unchanged for prolonged periods,
while others progress rapidly.
Histopathology: Hydropic swelling of the lens
fibers
CORTICAL CATARACTS
9. Classification according to maturation
1. Mature cataract occurs when the entire
cortex from the capsule to the nucleus
becomes white and opaque
2. Hypermature cataract occurs when
degenerated cortical material leaks through
the lens capsule, leaving the capsule wrinkled
and shrunken
3. Morgagnian cataract occurs when further
liquefaction of the cortex allows free
movement of the nucleus within the capsular
bag
CORTICAL CATARACTS
11. CLINICAL APPEARANCE
1. Symptom: Glare from intense focal light
sources; monocular diplopia
2. Effect on visual function varies greatly,
depending on the location of the opacification
relative to the visual axis
3. First sign: Vacuoles and water clefts in the
anterior or posterior cortex
4. The cortical lamellae may be separated by
fluid.
CORTICAL CATARACT
12. CLINICAL APPEARANCE
5. Wedge-shaped opacities (cortical spokes or
cuneiform opacities) form near the periphery
of the lens, with the pointed end of the
opacities oriented toward the center
Appears as white opacities when viewed
with the slit-lamp biomicroscope, and as
dark shadows when viewed by
retroillumination
May enlarge and coalesce to form large
cortical opacities
May swell and become intumescent cortical
cataract as the lens continues to take up
water
CORTICAL CATARACT
13. ETIOLOGY
1. Age-related
2. Trauma
3. Systemic or topical corticosteroid use
4. Inflammation
5. Exposure to ionizing radiation.
Histopathology: Posterior migration of the lens
epithelial cells in the posterior subcapsular area,
with aberrant enlargement (Wedl or bladder
cells)
POSTERIOR SUBCAPSULAR CATARACT
14. CLINICAL APPEARANCE
1. Symptom: Glare and poor vision under bright
lighting conditions (because the posterior
subcapsular cataract obscures more of the
pupillary aperture when miosis is induced by
bright lights, accommodation, or miotics);
monocular diplopia.
2. Near visual acuity tends to be reduced more
than distance visual acuity.
3. Opacities are located in the posterior cortical
layer and are usually axial.
4. Subtle iridescent sheen in the posterior cortical
layers.
5. Granular (plaque-like) opacities of the
posterior subcapsular cortex
POSTERIOR SUBCAPSULAR CATARACT
16. Immature cataract Mature cataract
Hypermature cataract Morgagnian cataract
Classification according to maturity
SENILE CATARACT
17. HARDNESS of the NUCLEUS
Grade Color Type of cataract Red reflex
1 Transparent or pale
gray
Cortical or recent
subcapsular
High
2 Gray or gray-yellow Subcapsular posterior Marked
3 Yellow or yellow-
gray
Nuclear, cortico-nuclear Good
4 Yellow-amber or
amber
Cortico-nuclear, dense Poor
5 Dark brown or black Totally dense Absent
18. CORTICOSTEROIDS
Posterior subcapsular
cataracts may be induced
depending on:
1. Dose and duration of
corticosteroid treatment
2. Individual susceptibility to
corticosteroid
PHENOTHIAZINES
Pigmented deposits in the
anterior lens epithelium in
an axial configuration →
affected by both dose and
duration of medication
DRUG-INDUCED LENS CHANGES
19. MIOTICS (ANTICHOLINESTERASES)
(echothiopate and demecarium Br)
Cataracts may be induced depending on dose
and duration of treatment.
1. First appear as small vacuoles within and
posterior to the anterior lens capsule and
epithelium (by retroillumination).
2. May progress to posterior cortical and
nuclear lens changes.
AMIODARONE
Stellate anterior axial pigment deposition
DRUG-INDUCED LENS CHANGES
21. TRAUMA to the LENS
1. Contusion
2. Perforating and penetrating injury
3. Radiation-induced cataracts
4. Chemical injuries
5. Electrical injury
6. Intralenticular foreign bodies
7. Metallosis
TRAUMA
22. VOSSIUS RING
1. Imprinting of pigment from the pupillary ruff
onto the anterior surface
2. Indicator of prior blunt trauma
3. Visually insignificant; resolves gradually with
time
CONTUSION
23. TRAUMATIC CATARACT
1. Lens opacification may occur as an acute event
or as late sequela and may involve only a
portion of the lens or the entire lens.
Common initial manifestation: Stellate or
rosette-shaped opacification that is axial in
location, involves the posterior lens
capsule and may progress to opacification
of the entire lens
2. Lens dislocation
CONTUSION
24. DISLOCATION and SUBLUXATION
1. Pathogenesis: Compression of the globe →
rapid expansion in an equatorial plane →
disruption of zonular fibers → dislocation or
subluxation.
2. Traumatic lens subluxation
CONTUSION
Fluctuation of vision,
impaired accommodation,
monocular diplopia, and
high astigmatism
Iridodonesis or
phacodonesis
Zonular disruption
25. IONIZING RADIATION
1. The lens is extremely sensitive to ionizing
radiation
2. Dose of radiation: Ionizing radiation in the x-ray
range (0.001-10 nm wavelength) can cause
cataracts in dosages as low as 200 rads in one
fraction → A routine chest x-ray equals 0.1 rads
exposure to the thorax
3. Patient’s age: Younger patients are more
susceptible because of more actively growing
lens cells.
4. First appear as punctate opacities within the
posterior capsule and feathery anterior
subcapsular opacities that radiate toward the
equator of the lens and may progress to
complete opacification of the lens.
RADIATION-INDUCED CATARACT
26. INFRARED RADIATION
(GLASSBLOWER’S CATARACT)
May cause the outer layers of the anterior lens
capsule to peel off a single layer.
ULTRAVIOLET RADIATION
Long-term exposure of UV-B (290-320 nm) from
sun exposure → increased risk of cortical and
posterior subcapsular cataracts
MICROWAVE RADIATION
1. Non-ionizing radiation with wavelengths
between infrared and shortwave on the
electromagnetic spectrum
2. No evidence that microwaves cause cataracts in
humans. The only biological effect of
microwaves is thermal.
RADIATION-INDUCED CATARACT
27. ALKALI INJURIES to the ocular surface
1. Often result in cortical cataract as an acute
event or as late sequela
2. Alkali compounds penetrate the eye readily,
causing an increase in aqueous pH and a
decrease in the level of aqueous glucose and
ascorbate.
ACID INJURIES to ocular surface
Less likely to result in cataract formation
because acid tends to penetrate the eye less
easily than alkali.
CHEMICAL INJURIES
28. 1. Can cause protein coagulation and cataract
formation. This cataract may regress, remain
stationary, or mature to complete cataract over
months or years
2. Lens manifestations are more likely when the
transmission of current involves the patient’s
head
3. Initially, lens vacuoles appear in the anterior
midperiphery of the lens, followed by linear
opacities in the anterior subcapsular cortex
ELECTRICAL INJURY
29. Opacification of the cortex at the site of the
rupture that usually progresses rapidly to
complete opacification
PERFORATING and
PENETRATING INJURY
30. INTRALENTICULAR FOREIGN BODIES
1. May cause cataract formation but do not
always lead to lens opacification.
2. Foreign body is sometimes retained within the
lens if the foreign body is not composed of a
ferric or cupric material, or the anterior lens
capsule seals the perforation site.
PERFORATING and
PENETRATING INJURY
31. SIDEROSIS BULBI
1. Deposition of iron molecules in the trabecular
meshwork, lens epithelium, iris and retina
2. The epithelium and cortical fibers of the
affected lens at first show a yellowish tinge,
followed later by a rusty brown discoloration
METALLOSIS
32. CHALCOSIS
1. Occurs when an intraocular copper-containing
foreign body deposits copper in Descemet’s
membrane, the anterior lens capsule, and other
intraocular basement membranes.
2. Sunflower cataract (petal-shaped deposition of
yellow or brown pigmentation in the lens
capsule that radiates from the anterior axial
pole of the lens to its equator) usually causes
no significant loss of visual acuity
METALLOSIS
34. PATHOGENESIS
1. As the blood sugar level increases, so also does
the glucose content in the aqueous humor.
Because glucose enters the lens by diffusion,
glucose content in the lens will be increased.
2. Some of the glucose is converted by aldose
reductase to sorbitol, which is not metabolized
but remains in the lens. Subsequently, osmotic
pressure causes an influx of water into the lens,
which leads to swelling of the lens fibers.
Change of refractive power of the lens
(most commonly myopic).
Decreased amplitude of accommodation
Presence of presbyopia at a younger age
DIABETES MELLITUS
35. DIABETIC CATARACT (SNOWFLAKE CATARACT)
1. Bilateral, widespread subcapsular lens changes
of abrupt onset and acute progression, typically
in young people with uncontrolled diabetes
mellitus
2. Multiple gray-white subcapsular opacities that
have a snowflake appearance are seen initially in
the superficial anterior and posterior lens cortex
3. Vacuoles in the lens capsule; clefts in the
underlying cortex
4. Intumescence and maturity of the cortical
cataract follow shortly thereafter
Any rapidly maturing bilateral cortical cataracts
in a child or young adult should alert the clinician
to the possibility of diabetes mellitus.
DIABETES MELLITUS
36. SENESCENT CATARACT
1. Accumulation of sorbitol within the lens
2. Subsequent hydration changes
3. Increased glycosylation of proteins in the
diabetic lens
→ Increased risk of age-related lens changes which
tend to occur at a younger age
DIABETES MELLITUS
37. DEFINITION
Autosomal recessive inherited inability to
convert galactose to glucose. Consequently,
excessive galactose accumulates in body
tissues, with further metabolic conversion of
galactose to galactitol (dulcitol)
ETIOLOGY
Defects in one of three enzymes – galactose-1-
phosphate uridyl transferase, galactokinase, or
UDP-galactose-4-epimerase
GALACTOSEMIA
38. CLASSIC GALACTOSEMIA
(caused by a defect in transferase)
1. Malnutrition, hepatomegaly, jaundice, and
mental deficiency present within the first few
weeks of life
2. Cataract develops in 75% of cases, usually
within the first few weeks of life
3. Oil-droplet bilateral cataract (opacification of
the nucleus and deep cortex) that may
progress to total opacification of the lens
TREATMENT
Elimination of milk and milk products from the
diet
GALACTOSEMIA
39. 1. Usually bilateral punctate iridescent opacities
in the anterior and posterior cortex that lie
beneath lens capsule and separated from it by
a zone of clear lens.
2. May either remain stable or mature into
complete cortical cataract
HYPOCALCEMIC CATARACT
(TETANIC CATARACT)
40. DEFINITION
Autosomal recessive inherited disorder of
copper metabolism
CLINICAL APPEARANCE
1. Kayser-Fleischer ring (golden brown
discoloration of Descemet’s membrane around
the periphery of the cornea)
2. Characteristic sunflower cataract – Deposition
of reddish brown pigment (cuprous oxide) in
the anterior lens capsule and subcapsular
cortex in a stellate shape → usually does not
produce serious visual impairment
WILSON DISEASE
(HEPATOLENTICULAR DEGENERATION)
41. DEFINITION
Autosomal dominant inherited
condition characterized by delayed
relaxation of contracted muscles,
ptosis, facial musculature
weakness, cardiac conduction
defects, and prominent frontal
balding in affected male patients.
OCULAR MANIFESTATIONS
Polychromatic iridescent crystals
(whorls of plasma-lemma from the
lens fibers ultrastructurally) in the
cortex, with sequential posterior
subcapsular cataract progressing
to complete cortical opacification.
MYOTONIC DYSTROPHY
42. CLINICAL APPEARANCE
1. Posterior subcapsular cataract that may
progress to a mature cataract
2. Posterior synechiae formation, often associated
with thickening of the anterior lens capsule and
development of a fibrovascular membrane
across it and the pupil (pupillary membrane)
CATARACT associated with UVEITIS
3. Calcium deposits on the
anterior capsule or within
the lens substance
43. TRUE EXFOLIATION
1. Pathogenesis: Intense exposure to infrared
radiation and heat causes the superficial lens
capsule to delaminate and peel off in scrolls
2. Occurs primarily in glassblowers and blast
furnace operators
EXFOLIATION SYNDROME
44. EXFOLIATION SYNDROME (PSEUDOEXFOLIATION)
CLINICAL APPEARANCE
1. Unilateral or bilateral disorder; onset often occurs
in the seventh decade
2. Basement membrane-like fibrillogranular white
material is deposited on the lens, cornea, iris,
anterior hyaloid face, ciliary processes, zonular
fibers, and trabecular meshwork. These deposits
arise from basement membranes within the eye,
and appear as grayish white flecks that are
prominent at the pupillary margin and on the lens
capsule
3. Atrophy of the iris at the pupillary margin
4. Deposition of pigment on the anterior surface of
the iris
EXFOLIATION SYNDROME
46. Cataract may develop in up to 25% of cases
1. Usually bilateral (70%)
2. Onset occurs in the second to third decade
3. Typically anterior subcapsular opacities in the
pupillary area that resemble shieldlike plaques.
CATARACT and ATOPIC DERMATITIS
47. PHACOANTIGENIC (PHACOANAPHYLACTIC UVEITIS)
DEFINITION: Immune-mediated granulomatous
inflammation initiated by lens proteins released
through a ruptured lens capsule
PATHOGENESIS: Liberation of a large amount of lens
protein into the anterior chamber disrupts the
normal immunologic tolerance and may trigger a
severe inflammatory reaction
CLINICAL APPEARANCE
1. Usually occurs days to weeks following traumatic
rupture of the lens capsule or following cataract
surgery when cortical material is retained within
the eye
2. Secondary glaucoma
LENS-INDUCED UVEITIS
48. PHACOANTIGENIC (PHACOANAPHYLACTIC UVEITIS)
HISTOPATHOLOGY: Zonal granulomatous
inflammation surrounding a breach of the lens
capsule.
COMPLICATION
Cyclitic membrane, synechiae formation, phthisis
bulbi.
TREATMENT: Lens extraction
LENS-INDUCED UVEITIS
50. GLAUKOMFLECKEN
1. Gray-white epithelial and anterior cortical lens
opacities that occur following an episode of
markedly elevated IOP, as in acute ACG.
2. Histopathology: Necrotic lens epithelial cells,
degenerated subepithelial cortex
LENS-INDUCED GLAUCOMA
51. PATHOGENESIS
1. Complication of a mature or hypermature
cataract
2. Denatured, liquefied high-molecular-weight lens
proteins leak through an intact but permeable
lens capsule. An immune response is not elicited;
rather, macrophages ingest these lens proteins.
The trabecular meshwork can become clogged
with both the lens proteins and the engorged
macrophages.
PHACOLYTIC GLAUCOMA
52. CLINICAL APPEARANCE
1. Abrupt onset in a cataractous eye that has had
poor vision for some time
2. White flocculent material in the anterior
chamber and adheres to lens capsule
3. Open angle glaucoma
TREATMENT
1. Initial treatment: Control of IOP with
antiglaucoma medications, and of the
inflammation with topical corticosteroids.
2. Definitive treatment: Surgical removal of the
lens
PHACOLYTIC GLAUCOMA
53. PATHOGENESIS
Liberation of lens cortex into the anterior
chamber following penetrating lens injury, ECCE
with retained cortical material, or Nd:YAG
capsulotomy → obstruction of aqueous outflow
through trabecular meshwork
CLINICAL APPEARANCE
1. Usually occurs days or weeks after the surgical
event or lens injury
2. White, fluffy, cortical lens material in the
anterior chamber
3. Open angle glaucoma
LENS-PARTICLE GLAUCOMA
54. TREATMENT
1. Medical therapy to lower IOP and to reduce
intraocular inflammation
2. Surgical removal of the retained lens material
LENS-PARTICLE GLAUCOMA
55. PATHOGENESIS
Intumescent cataractous lens → pupillary block
and shallowing of the anterior chamber →
secondary ACG.
CLINICAL APPEARANCE
1. History of decreased vision (cataract formation
prior to acute event)
2. Angle-closure glaucoma
TREATMENT
1. Initial treatment: Medical therapy to lower IOP;
laser iridotomy
2. Definitive treatment: Cataract extraction
PHACOMORPHIC GLAUCOMA
56. 1. Takayasu arteritis
2. Thromboangiitis obliterans
3. Anterior segment necrosis
Posterior subcapsular cataract may develop and
may progress rapidly to total opacification of the
lens
ISCHEMIA
57. Retinitis pigmentosa
Essential iris atrophy
Chronic hypotony
Absolute glaucoma
Usually begins as posterior subcapsular cataracts
and may progress to total lens opacification.
CATARACTS associated with
DEGENERATIVE OCULAR DISORDER
58. 1. Anterior
capsulotomy
3. Expression of
nucleus
5. Care not to aspirate
posterior capsule
accidentally
2. Completion of
incision
4. Cortical cleanup
6. Polishing of posterior
capsule, if appropriate
Extracapsular cataract extraction
CATARACT EXTRACTION
59. Extracapsular cataract extraction ( cont. )
7. Injection of
viscoelastic
substance
9. Insertion of inferior
haptic and optic
11. Placement of haptics
into capsular bag
and not into ciliary
sulcus
8. Grasping of IOL and
coating with viscoelastic
substance
10. Insertion of superior
haptic
12. Dialing of IOL into
horizontal position
CATARACT EXTRACTION
60. Phacoemulsification
1. Capsulorrhexis
3. Sculpting of nucleus
5. Emulsification of
each quadrant
2. Hydrodissection
4. Cracking of nucleus
6. Cortical clean-up and
insertion of IOL
CATARACT EXTRACTION