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
This presentation gives a brief idea about angle of anterior chamber along with its structures and diagnostic methods to grade and visualize the structures.
This presentation describes the background of the cornea and the corneal diseases in general, also it describes in detailed manner how to manage the corneal ulcer with its different causes
Uveitis is an interesting disease of the with such a varied and diverse pathogenesis, various systemic causes and Dangerous complications in relation to the eye which makes it difficult and challenging to treat in a proper way. I hope this share will help.
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
This presentation gives a brief idea about angle of anterior chamber along with its structures and diagnostic methods to grade and visualize the structures.
This presentation describes the background of the cornea and the corneal diseases in general, also it describes in detailed manner how to manage the corneal ulcer with its different causes
Uveitis is an interesting disease of the with such a varied and diverse pathogenesis, various systemic causes and Dangerous complications in relation to the eye which makes it difficult and challenging to treat in a proper way. I hope this share will help.
• 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
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
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Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
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This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
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Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
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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.
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
2. Presentation layout
Anatomy of uvea
Uveitis introduction
Classification of uveitis
Anterior uveitis introduction
Etiology of AU
Clinical features,complications and D/D
Investigations
Treatment of AU
3. Anatomy of uvea
UVEA constitutes- middle vascular coat
3 parts-
a)iris
b)ciliary body
c)choroid
Developmentally, structurally and functionally- indivisible
color varies from light blue to dark brown
4. Developmental milestones
9TH WEEK GESTATION-
12TH WEEK GESTATION-
5TH MONTH- all layers of choroid seen & iris fully developed
6TH MONTH- dilator muscle begins to form, sphincter muscle is fully formed
POSTNATAL PERIOD- dilator muscle fully formed by 5 years,
iris stromal pigment develops after birth
5. MACROSCOPIC APPEARANCE OF IRIS
TWO SURFACES
A)ANTERIOR SURFACE
Collarette- zigzag line, 2mm from pupil, thickest, represents attachment of pupillary
membrane
Divides surface into-
a) CILIARY ZONE- c/b
b) PUPILLARY ZONE-
Between collarette and pigmented frill
B)POSTERIOR SURFACE-
dark brown/black Contains-
A) Schwalbe’s contraction folds
B) Schwalbe’s structural furrows
C) Circular furrows
6.
7. FOUR LAYERS-
a)Anterior limiting layer-
b) Iris stroma-
•Forms main bulk
•Consists of collagenous tissue with mucopolysaccharide
C) Anterior epithelial layer
D)Posterior pigmented epithelial layer
Anterior continuation of non pigmented epithelium of ciliary body
8.
9. Ciliary body
Forward continuation of choroid at ora serrata
Triangular in cut section, ant side of its form part of angle, in
middle attached to iris and outer part lies against sclera
Triangle – two parts
a) Anterior part- ciliary processes (pars plicata) 2-2.5mm
b)Posterior part- smooth (pars plana) 5mm wide temporally
& 3mm nasally
10. Structure of ciliary body
MICROSCOPIC STRUCTURE
1.SUPRACILIARY LAMINA- outermost part
2. 2.STROMA-
Consists Ciliary muscle- non striated, triangular in cut section, 3 parts
a.Longitudnal/meridional fibres- origin from scleral spur, inserts into suprachoroidal lamina
b.Circular fibres- in inner portion, nearest to lens
c.Radial fibres- obliquely placed
3)Layer of pigmented epithelium- forward continuation of RPE
4)Layer of non pigmented epithelium- forward continuation of sensory retina
5)Internal limiting membrane-lines NPE Forward continuation of internal limiting
membrane of retina
11. Choroid
Posterior most part
Extension- optic disc to ora serrata
Inner surface- smooth, brown and in contact with RPE
Outer surface-rough and in contact with sclera
Thickness- posteriorly 0.22mm
anteriorly 0.10mm
12. Microscopic structure of choroid
1) Suprachoroidal lamina- lamina fusca
Thin layer, continues anteriorly with supraciliary lamina of ciliary
body
2) Stroma – plenty of pigmented cells, macrophages,mast and
plasma cells
3) choriocapillaris- rich capillary network
4)Basal lamina- Bruch’s membrane/lamina vitrae-Innermost
layer
13. Uveitis
Term uveitis- inflammation of uvea
However, clinically there is some association from the nearby
structures
14. Classification of uveitis
A. Anatomical classification
Acc to SUN, uveitis is classified anatomically :
a. Anterior uveitis
b. Intermediate uveitis
c. Posterior uveitis
d. Pan uveitis
16. Anterior uveitis
Inflammation of the uveal tract from the iris upto the plars plicata of ciliary body i.e …..
It may be sub divided into
A. Iritis
B. Iridocyclitis
C. Anterior cyclitis
Aetiology
Uveitis (anterior)
Anterior uveitis (the most common form of uveitis: 75% of all cases of uveitis). Annual
incidence 12 per 100,000 population
it may affect all ages, although it is most common in individuals in the third and fourth
decades.
(https://www.college-optometrists.org/guidance/clinical-management-guidelines/uveitis-anterior-acute-and-recurrent-
.html)
(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6095364/)
17. Etiology of uveitis/AU
Depending upon the offending agent of uveitis,
A. infectious
i. exogenous
ii.secondary
iii.endogenous
B.non infectious
i.auto-immune
a.HLA-associated
b.others
ii.Atopic
iii.Toxic
iv.Idiopathic
specific
nonspecific
19. Clinical features
Clinically it may be present as acute or chronic uveitis:
Acute: Symptoms more severe like photophobia, redness,
lacrimation and decreased vision
Chronic: Signs more severe than symptoms, however eye may
be presented white as that of very minimal symptoms
20. Symptoms
Pain:
complain of skull aching which typically Worsen at night
Acute Severe Radiates along V1 nerve distribution
dominant symptom of AAU
Redness:
feature of AAU, and occur due to circum corneal congestion, as a result of
hyperemia of anterior ciliary vessels due to the effect of toxins, histamines
and histamine like substances and axon reflexes.
Photophobia and Blepharospasm:
in AAU, due to reflex between sensory fibers of fifth CN {WHICH ARE
IRRITATED} and motor fibres of seventh CN supplying the orbicularis oculi
21. Lacrimation
occurs as a reflex of Vth CN (afferent) and secretomotor
of seventh CN(efferent)
Diminution of vision
a. Ciliary spasm –induces ?
b. Vitreous exudates
c. Exudates in pupillary area {pupillary block}
d. CME
e. Sec. glaucoma
f. Turbid aqueous
g. Complicated Cataract
22. Signs
A . Lid Edema
Mild, may accompany a severe attack of AAU
B . Ciliary congestion
ccc is marked in AU, it may be differentiated from superficial
congestion occurring in acute conjunctivitis
23.
24. C. Corneal signs
1.KPs:
KPs are pathogenic sign of AU.
Are proteinaceous cellular deposits occurring at the back of the cornea
mostly arranged in triangular fashion occupying the centre and inferior part of the
cornea due to convetion currents in the aqueous humour.
Different morphology of KPs are
Mutton fat KPs
in granulomatous iridocyclitis and composed of epitheloid cells and macrophages
Large,thick ,fluffy and lardaceous KPs ,having greasy or waxy appearance
usually a few -10-15 in no
Small and medium KPs
small,discrete,dirty white KPs arranged irregularly at the back of cornea
they may be numerous
these are pathognomic of nongranulomatous uveitis and are composed of
lymphocytes
25. Fine KPs :
also also called as ‘satellite’ KPs,typically cover entire corneal endothelium and form the so
called endothelial dusting.
Are seen in Fuchs heterochromic iridocyclitis,herpetic iritis and CMV retinitis.
Old KPs
are sign of healed uveitis
either of the abive described KPs with healing process shrink,fade,become pigmented and
irregular in shape(crenated margin)
old mutton fat KPs usually have a ground glass appearance due to hyalinization
2.cornea edema
toxic endothelitis and raised IOP when present
3.Posterior corneal opacity
may be formed in long standing cases of iridocyclitis
28. D.ANTERIOR CHAMBER SIGNS:
Aqueous cells
Early sign
On oblique illum.:1 mm long 1mm wide slit with max light and
magnifications
Grading:
29. Aqueous flares
D/t leakage of protein into the aqueous humor from the leaky vessels
On oblique illumination: a point of beam projected on the iris plane
Protein particles seen floating the beam of light: Tyndall phenomenon
Grading:
Hypopyon:
sterile pus in AC
Changes in depth and shape of AC
Changes in the angle of anterior chamber
32. E.Iris signs
1. Loss of normal pattern
2. Muddy in color in active stage & hyper/ hypopigmented
3. Iris nodules: Aggregations of lymphyocytes and epitheloid
cells.
Koeppe’s nodules ….
Busacca’s nodules….
4. Posterior synechiae
Adhesion of posterior surface of iris to anterior surface of
cornea
a. Segmental
b. Annular
c. Total
38. G.Lens signs
1. Pigment dispersion on lens surface
2. Fibrin exudates on lens surface
3. Complicated cataract: Polychromatic lusture
4. Bread crumb appearance
5. Cyclitic membrane:
retrolental, fibrovascular membrane which stretches across the back of the lens
42. I.Changes in IOP
1. Normal
2. Increased (sec glaucoma)
3. Decreased (in acute iridocyclitis - acute ciliary shock
chronic,longlasting iridocyclitis -atrophy of ciliary process
leading to phthisis bulbi)
55. INVESTIGATIONS
A.Hematological Examination
It includes following tests:
• TLC/DLC: Gross idea of inflammatory response of body
• ESR: r/o Chronic infection
• Blood sugar: r/o DM
• Blood Uric Acid: r/o Gout
• Seological Test: Syphilis, toxoplasmosis & histoplasmosis
• Test for: Anti Antinuclear Antibodies CRP Rh factor Anti-
streptolysin O LE cells
56. B.Urine Examination:
For WBC, Pus cells, RBS
Culture : r/o Urinary tract infection
C.Stool Examination ;
For Cysts & ova to r/o parasitic infestations.
D . Radiological Investigation :
CXR , Paranasal sinus, Sacroiliac joints , Lumbar spine.
E. Skin Tests:
Tuberculin test, Kveims test & Toxoplasmin test
57.
58. Treatment of iridocyclitis
I. Non specific treatment
a.Local therapy
b.systemic therapy
c.Physical measures
II. Specific treatment for the cause
III. Treatment complications
1) Cycloplegics
2) Corticosteroids
3) Broad spectrum antibiotics.
1. Corticosteroids
2. Non-Steroidal Anti inflammatory Drugs(NSAIDS)
3. Immunosupressives
70. C. Physical Measures
1. Hot fomentation
more antibodies are brought and toxins are drained
2. Dark goggles
helps in photophobia,lacrimation and blepharospasm
74. Just as different fads that seize the imagination of the general public are often carried to
excess, so diagnostic or therapeutic fads may take over in the practice of medicine.
Analysis of 33 surveys of the causes of uveitis reported by ophthalmologists over the
course of 120 years shows how some diagnoses such as syphilis and tuberculosis fell from
favor because tests ruled out these diseases, whereas others such as toxoplasmosis
became popular because of the finding of the organism in a few cases by a famous
ophthalmic pathologist. Yet others (pars planitis, sarcoidosis) were not even causes of
disease, but rather merely descriptive, or the ocular component of a systemic disease
whose etiology and pathogenesis remain unknown. We will examine the waxing and
waning of these diagnostic categories and the impressive confidence of some clinicians in
their own diagnostic acumen as they made diagnoses often unsupported by objective
evidence.
(https://pubmed.ncbi.nlm.nih.gov/9657289/)
75.
76. 1. Comprehensive ophthalmology by AK Khurana
2. Kanski’s clinical ophthalmology 8th edition
3. Parson’s eye disease
4. Americal Academy of ophthalmology(AAO)
5. American Optometric Association(AOA)
6. https://www.college-optometrists.org/guidance/clinical-management-
guidelines/uveitis-anterior-acute-and-recurrent-.html