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181 Cards in this Set
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IMMUNOLOGY: Definitions
-Name some characteristics of innate immunity -What are the main stimuli for innate immune reactions? -Is there molecular variation in the receptors for innate immunity? |
Definitions
-Innate immunity: antigen-independent, stereotyped/preprogrammed response to stimuli, nonspecific effector cells recruited, stimuli removed in nonspecific ways (phagocytosis, enzyme degradation) -Main stimuli: molecular motifs on triggering stimuli -Receptors of innate immunity are identical within all individuals of a species |
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IMMUNOLOGY: Definitions
-Name similarities and differences between the innate and adaptive immune responses |
Definitions
-BOTH: use WBC receptors to recognize offending stimuli (but different types of receptors used by each), trigger inflammation, use nonspecific effector cells to carry out functions -DIFFERENCES: triggers (adaptive - antigen; innate - toxins, cell debris of bacteria); recognition receptors, time of onset (adaptive is delayed, innate is fast), memory & specificity (only in adaptive immunity) |
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IMMUNOLOGY: Definitions
-What cells are increased in number in vernal keratoconjunctivitis? -What are the 3 main functions of monocytes/macrophages? |
Definitions
-Mast cells: increased number in conj of pts w/ VKC -Macrophages (tissue)/monocytes (blood): scavengers, APCs for T cells, inflammatory effector cells |
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IMMUNOLOGY: Definitions
-What are dendritic cells? -What are Langerhans cells? |
Definitions
-Dendritic cells: mononuclear cells distinct from monocytes/macrophages; involved in antigen presentation --> initiate responses in quiescent lymphocytes -Langerhans cells: subset of dendritic cells in conj & limbus --> the only cells in these areas to express MHC II |
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IMMUNOLOGY: Definitions
-Where do B & T cells mature, respectively? -What are 2 important lymphoid structures in the adaptive immune response? |
Definitions:
-B cells: mature in Bone marrow -T cells: mature in Thymus -Spleen & lymph nodes: important in adaptive immunity |
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IMMUNOLOGY: Definitions
-Describe the process by which an APC presents stimuli to T cells -What is the relationship b/w type of HLA molecule and different antigens |
Definitions
-APC phagocytoze antigen --> carry it to lymph node --> present Ag fragments within groove of HLA molecule on cell surface to T cells --> stimulation of T cells -Different HLA molecules are capable of binding to different antigen types (therefore the HLA type determines the repertoire of antigens capable of being presented to a T cell by an APC) -Note: this is why APCs from 1 individual cannot present to T cells from another individuals UNLESS the 2 individuals share HLA haplotype |
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IMMUNOLOGY: Definitions
-What cells carry class II MHC molecules? What cells are stimulated by class II cells? -What cells carry class I MHC molecules? What cells are stimulated by class I cells? |
Definitions:
-Class II MHC: present on macrophages, dendritic cells --> recognized by CD4 T cells -Class I MHC: present on all nucleated cells --> recognized by CD8 T cells |
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IMMUNOLOGY: Definitions
-What Ig's do naive B cells have on surface? What is the function of these Ig's? -Do B cells require Ag processing by APCs? -What is the difference b/w a naive and an activated B cell? What regulates the activities of active B cells? |
Definitions
-Naive B cells: have IgM & IgD on surface --> these serve at Ag receptors for the B cell -B cells DO NOT require Ag processing by APCs -Active B cells have ability to switch from IgM to another class --> this is regulated by cytokines released by CD4 cells |
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IMMUNOLOGY: Definitions
-What are the 2 antigen-specific effectors of adaptive immunity? -Describe the 2 exposures required for effector cells |
Definitions
-Ag-specific effectors of adaptive immunity: T cells, B cells + their Abs -2 exposures needed for these effector cells: 1) initial exposure --> priming/activation within lymph node; 2) second exposure --> restimulation in the peripheral tissue where initial Ag found |
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IMMUNOLOGY: Definitions
-What are differences b/w primary and secondary immune responses? -Why is the secondary immune response shorter? |
Definitions:
-Primary response: Ag must find the rare B/T cells specific to it --> these cells are then stimulated from a resting/naive state -Secondary response: B/T cells active during primary response are re-activated within 12-24 hours of repeat Ag exposure; more B/T cells specific for the Ag are present due to previous exposure (these cells may migrate to other sites of Ag encounter); low levels of Ag may persist in node/site so chronic low grade Ag stimulation may continually occur --> this is why secondary response is faster |
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IMMUNOLOGY: Ocular immunology
-What are immunologic features of the conjunctiva? |
Ocular immunology
-Immunologic features of conjunctiva: drainage to preauricular/submandibular nodes, APCs, foliclles, mast cells, IgE mediated degranulation of mast cells, IgA (most abundant Ab in tear film) |
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IMMUNOLOGY: Ocular immunology
-What is MALT (mucosa-associated lymphoid tissue)? -What are its immunologic features? |
Ocular immunology
-MALT: mucosal sites (GI/GU tracts, respiratory tract, ocular surface/adnexae) that are connected by specific immunologic features -Features: 1) rich in APCs, 2) specialized structures for localized Ag processing, 3) unique effector cells (i.e., mast cells) -Effector B & T cells have universal response to ALL MALT sites in response to immunization at one site -TH2 responses favored --> predominantly IgA & IgE antibodies produced |
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IMMUNOLOGY: Ocular immunology
-Since the eye does not contain lymphatics, how is particulate matter cleared? -What structures in the anterior segment contain APCs? -Where does immune processing by the APCs occur? -What are unique features of the vitreous compared to aqueous? |
Ocular immunology
-Clearance of particulate matter from inner eye depends on aqueous humor outflow channels, endocytosis by TM macrophages and endothelial cells -Immune processing does NOT occur locally --> APCs travel to spleen --> TH2 response favored -Vitreous: gel can bind charged proteins --> may serve as antigen depot for leukocyte adhesion |
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IMMUNOLOGY: Ocular immunology
-What is anterior chamber-associated immune deviation (ACAID)? What are its specific features? |
Ocular immunology
-ACAID: "deviant" immune response in AC --> robust systemic Ab response to an Ag but lack of delayed hypersensitivity response to that Ag -Features: decreased effectivity of TH1 DH cells, CD8/NK cells and complement in anterior uvea compared to elsewhere, presence of Fas ligand on iris/corneal endohtelium (induces lymphocyte apoptosis) |
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IMMUNOLOGY: Ocular immunology
-What are 5 factors that contribute to corneal graft rejection in experimental models? |
Ocular immunology: K graft rejection
-Central corneal vascularization -Stromal MHC molecule expression (usually very low) -Graft contamination w/ donor-derived APCs -MHC disparity b/w donor & recipient -Pre-immunization of recipient to donor transplantation Ags |
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IMMUNOLOGY: Innate effectors
-What is another name for endotoxin? Which component is responsible for most of the inflammatory effects of endotoxin? -What types of molecules are exotoxins? Examples? |
Innate effectors
-Endotoxin (LPS): component of gram negative bacterial cell walls --> lipid A is most important mediator of inflammation -Exotoxins: enzymes that cause tissue damage --> leads to inflammation (ex: streptolysin O, C. perfringens toxin, collagenases) |
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IMMUNOLOGY: Innate effectors
-Name 3 other triggers/modulators of innate immunity -What are the 2 most important receptors for phagocytosis of pathogens? |
Innate effectors
-3 other nonspecific modulators: complement, acute phase reactants, enzymes in tear film -Phagocytosis: mediated by antibody Fc receptors & complement receptors (pathogens complex w/ Abs or complement --> ingested by cell displaying one of these receptors) |
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IMMUNOLOGY: Innate effectors
-What are the functions of resting, primed, stimulated & activated macrophages (respectively)? |
Innate effectors: Macrophages
-Resting: scavengers -Primed: Ag-presentation (express MHC class II) -Stimulated: wound repair, angiogenesis, mild inflammation (incompletely activated) -Activated: severe inflammation, tumoricidal, bactericidal --> epitheliod cells & giant cells are terminally differentiated forms |
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IMMUNOLOGY: Adaptive effectors
-What is an immune hypersensitivity reaction? -In an immunoglobulin, what part defines the specific isotype? -What is the name for the Ag-recognition part of the Ig molecule? -What is the name for the effector cell-binding part of the Ig molecule? |
Adaptive effectors
-Immune hypersensitivity reaction: inflammation due to adaptive immune response -Heavy chain: defines specific Ab isotype -Fab region (hypervariable region): contains Ag-recognition domain -Fc region: attachment site for effector cells |
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IMMUNOLOGY: Adaptive effectors
-What are idiotopes and epitopes on an antibody molecule? -Distinguish b/w a monoclonal and polyclonal antibody response |
Adaptive effectors
-Idiotope: region of antibody itself that is antigenic (idiotypes are antibodies to idiotopes) -Epitope: antigenic site on foreign molecule -Polyclonal: population of all ag-specific Abs to various epitopes (Abs are derived from different B cell clones) -Monoclonal: products of 1 specific B cell (i.e. myeloma) |
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IMMUNOLOGY: Adaptive effectors
-What are functions of Ag-Ab complexes in the intravascular space? -What is the classic clinical setting in which immune complexes cause disease? |
Adaptive effectors
-Intravascular Ag-Ab complexes: 1) neutralization of pathogen ability to bind cells; 2) opsonization (facilitates clearance of pathogen); 3) agglutinization (complex precipitates out of solution); 4) cytolysis via complement activation -Classic example: serum sickness |
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IMMUNOLOGY: Adaptive effectors
-What are the features of Ag-Ab complexes in peripheral tissues? -Which Ig subclass can passively leak into peripheral tissues? |
Adaptive effectors
-Ag-Ab complexes in peripheral tissues: complement-mediated cell lysis via MAC, production of anaphylotoxins (complement fragments) in Arthus reaction, stimulation of target cells (Graves disease) -IgG subclass can passively leak into peripheral tissues |
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IMMUNOLOGY: Adaptive effectors
-How is an Arthus reaction different from intravascular Ag-Ab complexes? -What is a chronic Arthus reaction? |
Adaptive effectors
-Arthus reaction caused by LOCALLY formed Ag-Ab complexes (not formed in blood) -Chronic Arthus reaction: lymphocytes, plasma cells, granulomatous features --> caused by persistence of Ag within the site |
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IMMUNOLOGY: Adaptive effectors
-What disease states are produced by TH1 reactions? -What disease states are produced by TH2 reactions? |
Adaptive effectors
-TH1: classic delayed hypersensitivity reaction (i.e., PPD), intracellular infection, fungal infection, transplant rejection, most severe forms of inflammation -TH2: atopic disease, parasitic infections |
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IMMUNOLOGY: Adaptive effectors
-What disease states are associated with CD8 T cells? -What is the ideal CD8 T cell antigen? -What cell assists in differentiation of CD8 T cells? |
Adaptive effectors
-Involved in tumors, viruses, graft rejection -Ideal antigen: intracellular protein -Requires CD4 T cells to fully differentiate |
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IMMUNOLOGY: Adaptive effectors
-What are the 2 mechanisms by which CD8 T cells kill cells? -What is one similarity and one difference b/w NK cells and CD8 T cells? |
Adaptive effectors
-CD8 killing mechanisms: 1) assassination (lysis of target cell w/ perforin); 2) suicide induction (apoptosis of target cell w/ Fas ligand) -NK cells: kill using same mechanisms as CD8 cells but do not have a specific Ag receptor (unlike CD8 cells) |
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IMMUNOLOGY: Adaptive effectors
-What are lymphokine-activated T cells? |
Adaptive effectors
-Lymphokine-activated T cells: T cells that are nonspecifically activated by iatrogenic administration of immune cytokines (i.e., IL-2) |
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IMMUNOLOGY: Amplifiers of immune response
-By which pathway is complement activated in active and innate immunity, respectively? -What are the 4 basic functions of complement? -What are the principal complement-derived mediators? |
Amplifiers of immune response
-Complement activated by classic pathway in adaptive immunity, alternative pathway in innate immunity -4 functions: 1) enhance phagocytosis, 2) promote cell membrane lysis; 3) recruit neutrophils, induce inflammation; 4) modulates Ag-specific immune responses -Principal complement-derived mediators: anaphylotoxins (induce chemotaxis and change in cell adhesiveness) |
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IMMUNOLOGY: Amplifiers of immune response
-What are the effects of kinins? What is the best known kinin? -What are the effects of fibrin? What is fibrin deposition a clinical sign of? -What are the effects of vasoactive amines? What are the sources of each type? |
Amplifiers of immune response
-Kinins: vasodilation, pain, increased vascular permeability, Arachidonic acid metabolism stimulation (bradykinin = best known kinin) -Fibrin: hemostasis, fibrosis, angiogenesis, leukocyte adhesion (clinical sign of delayed hypersensitivity) -Vasoactive amines (serotonin and histamine): increase vascular permeability and blood flow, mediate allergic reactions -Serotonin: found in platelets -Histamine: mast cell, basophil granules |
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IMMUNOLOGY: Tolerance
-What are mechanisms of immunologic tolerance? -What is a mechanism of autoimmunity? |
Tolerance
-Mechanisms of tolerance: CLONAL DELETION (destruction of self-reactive T cells by thymus), ANERGY (Ag-specific B/T cells rendered incapable of mounting inflammatory response), REGULATION (regulatory T cells to balance population of inflammatory T cells), NON COMPLEMENT-FIXATING ABS (anti-self Abs that are unable to fix complement so do not cause inflammatory response) -Mechanism of autoimmunity: molecular mimicry (immunologic cross-reaction b/w epitopes of unrelated foreign Ag and self-epitopes w/ similar structures) |
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IMMUNOLOGY: HLA
-What are HLA molecules and what is their function? |
HLA
-HLA molecules are major histocompatibility complex proteins (MHC) expressed on surface of APCs -Type of HLA haplotype determines repertoire of Ags to which individual can respond (not all HLA molecules can bind all Ags) --> some HLA haplotypes will be unable to mount a T cell response response to certain Ags if unable to bind these Ags |
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IMMUNOLOGY: HLA
-What % of pts w/ acute anterior uveitis have HLA-B27 haplotype? -What is the proposed pathophysiology of HLA-B27 associated uveitis? |
HLA
-50% of pts w/ anterior uveitis are HLA-B27+ (pathogenesis unknown) -HLA-B27 assoc uveitis: individuals w/ specific HLA molecule type are predisposed to processing certain Ags that also cross-react w/ certain self Ags --> uveitis occurs |
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UVEITIS: Classification
-What is the etiology of most types of anterior uveitis? posterior uveitis? -What is intermediate uveitis? |
Classification
-Anterior uveitis --> mostly sterile, inflammatory reactions -Posterior uveitis --> usually infectious -Intermediate uveitis --> inflamm of posterior ciliary body, pars plana (floaters, CME, cataract may occur) |
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UVEITIS: Classification
-What are the most common causes of panuveitis? |
Classification
-Panuveitis: Tb, syphilis, Lyme, sarcoidosis, sympathetic ophthalmia, Bechet's, VKH |
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UVEITIS: Symptoms
-What are consequences of chronic uveitis? -What is the definition of recurrent uveitis? -What is the most common cause of eye pain in uveitis? |
Symptoms
-Chronic uveitis: complicated by cyclitic membrane (w/ secondary CB detachment, hypotony), calcific band keratopathy, cataract, CME --> decreased vision -Recurrent uveitis: periods of inactivity for >3 months off all meds, followed by return of sx -Pain in uveitis is secondary to iris inflammation, secondary glaucoma or ciliary spasm --> may radiate over trigeminal nerve (V) distribution |
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UVEITIS: Signs
-What is the predominant intraocular inflammatory cell in uveitis? -What are signs of anterior uveitis? -Name 3 types of iris nodules and their location |
Signs
-Lymphocyte = predominant inflammatory cell in uveitis -Signs of anterior uveitis: KP, cells, flare, fibrin, hypopyon, pigment dispersion, iris nodules, miosis -3 types of iris nodules: Koeppe (pupillary border), Busacca (mid-iris), Berlin (iris angle) |
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UVEITIS: Signs
-What are 4 types of AC reaction and what are the predominant cell types in each? |
Signs
-Serous (aqueous flare, protein influx) -Purulent (PMNs, necrotic debris, hypopyon) -Fibrinous (plasmoid) -Sanguinoid (inflammation + RBCs) |
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UVEITIS: Signs
-How are AC cells and flare graded? |
Signs
-AC cells graded by looking at # of cells in 1x1mm slit beam: if < 15 (0-1+), 15-50 (2-3+), > 50 (4+) -AC flare graded by visibility of iris/lens detail: if details clear (0-2+), if hazy (3+), if fibrin or plasmoid aqueous (4+) |
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UVEITIS: Signs
-What is the mechanism for low and high IOP in uveitis? |
Signs
-Low IOP (more common): decreased aqueous production or increased alternative outflow -High IOP: inflammatory cells/debris clog TM or trabeculitis (inflammation of TM itself) |
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UVEITIS: Testing
-What are the differences b/w type I and type 2 patterns on ICG? |
Testing - ICG
-Type 1 pattern: early and late multifocal areas of hypofluorescence (MEWDS) -Type 2 pattern: early hypofluorescence, late hyperfluorescence (sarcoid, SO, birdshot, VKH) |
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UVEITIS: Medical mgmt
-Why are mydriatics and cycloplegic agents used in uveitis? -What is the utility of topical NSAIDS? Side effects? |
Medical mgmt
-Mydriatics/cycloplegics: prevent posterior synechiae formation, relieve photophobia associated w/ ciliary spasm -NSAIDs: reduce prostaglandin synthesis in inflammation; useful for postop inflammation/CME but unclear utility for endogenous anterior uveitis -Side effects of NSAIDs: GI bleeding/ulceration, hepatotoxicity, nephrotoxicity |
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UVEITIS: Medical mgmt
-How should steroid tx be initiated? -What are indications for periocular steroids? -When should periocular steroids be avoided? |
Medical mgmt
-Initiation of steroids: start high dose --> taper as inflammation subsides -Periocular steroid indications: need for more posterior effect than that provided by topicals, poor response to topical/systemic steroids -Avoid periocular steroids in necrotizing scleritis or infectious uveitis |
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UVEITIS: Medical mgmt
-What are indications for systemic steroids? -What are indications for starting immunomodulatory therapy? |
Medical mgmt
-Systemic steroid indications: vision threatening chronic uveitis w/ insufficient control w/ topical meds, need for treatment of systemic disease -Immunomodulatory therapy indications: pt requires dose of steroids > 10 mg/day for chronic treatment, if pt needs steroids > 3 months, failed tx w/ steroids, contraindicated steroids, reversible disease |
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UVEITIS: Medical mgmt
-What are indications for the sustained release fluocinolone implant? What are the most common side effects? |
Medical mgmt
-Sustained release fluocinolone implant: for chronic noninfectious posterior uveitis --> releases drug for median of 30 months -side effects: cataract (seen in nearly all phakic pts), glaucoma (60% of pts) |
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UVEITIS: Medical mgmt
Name drugs in each category... -Antimetabolites -Inhibitors of T-cell signaling -Alkylating agents -Biologics |
Medical mgmt
-Antimetabolites: MTX, azathioprine, mycophenolate mofetil -T cell signaling inhibitors: cyclosporine, tacrolimus, sirolimus -Alkylating agents: cyclophosphamide, chlorambucil -Biologics (cytokine inhibitors): etanercept, infliximab, daclizumab, etc |
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UVEITIS: Medical mgmt
-What is the first line drug of choice in immunomodulation with children? Which disease has been studied for this? -What drug category is used only if other drugs fail? For which disease are these drugs first line? |
Medical mgmt
-Methotrexate: first line immunomodulatory agent in children (long success record in JIA/JRA) -Alkylating agents (cyclophosphamide, chlorambucil) are used only if other drugs fail --> increased risk of malignancy **Note: alklyating agents are 1st line tx for necrotizing scleritis assoc w/ systemic vasculitides |
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AUTOIMMUNE: Anterior uveitis
-What are the 2 most common patterns of acute anterior uveitis? -What are the seronegative spondyloarthropathies associated with HLA-B27 uveitis? |
Anterior uveitis
-2 patterns: 1) acute, unilateral, recurrent in either eye; 2) acute, bilateral, assoc w/ tubulointerstitial nephritis -HLA-B27 associated uveitis: assoc w/ spondyloarthropathies (ankylosing spondylitis, Reiter syndrome/reactive arthritis, psoriatic arthritis, IBD) |
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AUTOIMMUNE: Anterior uveitis
-What are the typical symptoms of ankylosing spondylitis? Xray findings? -Mainstay of treatment? -Drug that reduces ocular recurrences? -What % of pts have +HLA-B27? |
Anterior uveitis
-AS: low back pain/stiffness after inactivity -Xray: sclerosis, narrowing of joint space, fusion of vertebrae on sacroiliac views -NSAIDS = mainstay of tx -Sulfasalazine: may reduce frequency of iritis recurrences -HLA-B27+ in 90% of pts |
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AUTOIMMUNE: Anterior uveitis
-What is the triad of Reiter syndrome? -What 2 other conditions are considered major diagnostic criteria? |
Anterior uveitis
-Reiter syndrome triad: urethritis, polyarthritis, conjunctivitis + iritis -Other important conditions: 1) keratoderma blennorrhagicum (scaly eruptions on palms/soles); 2) circinate balanitis (circumferential rash of distal penis) |
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AUTOIMMUNE: Anterior uveitis
-What % of pts w/ Reiter syndrome have +HLA-B27? -What are organisms assoc w/ triggering infections? -Most common population of pts w/ disease? -Most common eye finding in Reiter's syndrome? |
Anterior uveitis
-85-95% have +HLA-B27 -Triggering infections: Shigella, Salmonella, Yersinia, Chlamydia, Ureaplasma -Epi: young adult males -Most common ocular finding: mucupurulent, papillary conjunctivitis (nongranulomatous iritis in 5-10% of pts) |
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AUTOIMMUNE: Anterior uveitis
-What % of pts w/ IBD have HLA-B27+? -What are features of psoriasis-assoc uveitis? (compared to other forms of HLA-B27 assoc uveitis) -Clinical features of psoriasis? |
Anterior uveitis
-60% of pts w/ IBD have HLA-B27+ -Psoriasis-assoc uveitis: older mean age of onset, bilateral, more chronic, requires PO NSAIDs -Psoriasis features: sausage digits, erythematous hyperkeratotic rash, nailbed pitting, subungual hyperkeratosis |
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AUTOIMMUNE: Anterior uveitis
-What population gets tubulointerstitial nephritis uveitis (TINU)? -Diagnostic criteria? -Mgmt? |
Anterior uveitis - TINU
-Adolescent girls (11-120), women (early 30s) -Diagnosis: 1) abnl serum Cr or decreased Cr clearance; 2) abnormal U/A; 3) systemic illness (constitutional sx, abnl LFTs, etc) -Mgmt: high dose PO steroids |
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AUTOIMMUNE: Anterior uveitis
-What is the clinical presentation of Poser-Schlossman syndrome? What meds should be used and avoided in mgmt? |
Anterior uveitis - Posner-Schlossman
-Presentation: unilateral, mild acute iritis w/ markedly elevated IOP, K edema, fine KP, low grade cell/flare -Mgmt: topical steroids & IOP lowering meds --> avoid Pilo (may exacerbate ciliary spasm) |
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AUTOIMMUNE: Anterior uveitis
-How does lens-associated uveitis occur? -How does the uveitis present? -Histologic appearance? -Mgmt? |
Anterior uveitis - Lens-associated uveitis
-Pathophysiology: altered tolerance to lens proteins --> immune reaction to lens material released via leakage from capsule in hypermature cataract OR following trauma to capsule -Uveitis: KPs present; may be granulomatous OR nongranulomatous, no fundus lesions -Mgmt: surgical removal of all lens material (curative) |
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AUTOIMMUNE: Anterior uveitis
-Pathophysiology of phacolytic glaucoma? -Are KPs present? Other features of the uveitis? |
Anterior uveitis - Phacolytic glaucoma
-Pathophysiology: leakage of lens protein thru capsule in hypermature cataracts --> TM clogging by lens material & engorged macrophages --> acute IOP rise -Uveitis: NO KPs, no synechiae, presence of refractile bodies in AC (lipid laden macrophages) |
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AUTOIMMUNE: Anterior uveitis
-What are mechanisms of IOL-associated uveitis? -What is the most severe form of IOL-assocaited uveitis called? |
Anterior uveitis - IOL-associated uveitis
-Mechanisms: retained lens material, effect of surgery itself, iris chafing by IOL, K touch by IOL --> endothel decompensation & inflammation -UGH = most severe form of IOL-associated uveitis |
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AUTOIMMUNE: Anterior uveitis
-Name some medications that are associated w/ uveitis |
Anterior uveitis - Drug-associated
-Rifabutin -Bisphosphonates -Sulfonamides -OCPs -Diethylcarbamazine (anti-filarial) -Topicals: prostaglandin analogs, anticholinesterase inhibitors, metipranol (beta blocker) |
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AUTOIMMUNE: Anterior uveitis
-What is the most common systemic disease assoc w/ anterior uveitis in children? -What are the 3 subtypes of this disease? Risk of uveitis w/ each type? |
Anterior uveitis - JIA/JRA associated
-JIA/JRA = most common systemic disease assoc w/ iritis in pediatric age group -Definition: arthritis beginning before age 16, lasting at least 6 weeks 1) Systemic (Still disease): <5 yo, systemic sx w/ minimal joint inflammation initially, rarely assoc w/ uveitis 2) Polyarticular: > 4 joints involved, 7-14% get uveitis, if +RF --> no uveitis 3) Pauciarticular: < 4 joints, account for 80-90% of JIA pts w/ uveitis, type 1 (females, <5yo, ANA +), type 2 (males, older, 75% HLA-B27+) |
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AUTOIMMUNE: Anterior uveitis
-What is the correlation b/w joint and ocular inflammation in JIA? -What is the average age of onset of uveitis in JIA? -What are major risk factors for development of uveitis in JIA? |
Anterior uveitis
-No correlation b/w ocular & joint inflammation in JIA-uveitis -Risk factors: female, pauciarticular, ANA+, RF negative -Average age of onset of uveitis = 6 yo |
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AUTOIMMUNE: Anterior uveitis
-What is the recommended screening schedule for uveitis in JIA pts? (i.e., screening schedule for <7 yo and >7yo) -When should steroids be initiated? -What is the most commonly used steroid-sparing agent? |
Anterior uveitis - JIA-associated
-Screening for <7 yo: q3-4 mo (if ANA+), q6 mo (if ANA neg) -Screening for >7yo: q6 months for all except Still's disease -Still disease: q12 months -Indications for steroids: active cellular reaction (do not use in pts w/ chronic flare but no cell) -MTX (weekly, low dose): most commonly used steroid-sparing drug |
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AUTOIMMUNE: Anterior uveitis
-What are complications of cataract surgery in pts w/ JIA uveitis who develop cataract? -What are some guidelines to follow in considering cataract surgery in JIA pts? |
Anterior uveitis - JIA-associated
-Cataract surgery in JIA pts complicated by aggressive post-op inflammation -Guidelines for cataract surgery: inflamm should be well controlled for at least 3 months, use only acrylic lenses, low threshold for explantation of IOL, close follow up, long term immunomodulatory tx before and after surgery |
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AUTOIMMUNE: Anterior uveitis
-What is the clinical presentation of Fuch's heterochromic iridocyclitis? -When does the lighter colored iris indicate the involved eye? -What are characteristics of abnormal vessels within the angle in this disease? -What is a major cause of visual disability? -Prognosis? |
Anterior uveitis - Fuch's heterochromic iridocyclitis
-Presentation: unilateral, diffuse iris stromal atrophy, diffuse stellate KPs, AC and vitreous cells -Typically DO NOT see synechiae, fundus lesions -Complicated by glaucoma, cataract -AC angle shows abnormal vessels bridging the angle --> can bleed during surgery --> postop hyphema -Visual disability may result from vitreous opacification, even after uncomplicated CE/IOL -Good prognosis, but inflamm may persist for decades |
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AUTOIMMUNE: Intermediate uveitis
-Int uveitis accounts for what % of all cases of uveitis? -What is the most common form of intermediate uveitis? |
Intermediate uveitis
-Accounts for 15% of all cases of uveitis -Pars planitis = snowbanks, snowballs w/o associated infection/systemic disease --> most common form of intermediate uveitis |
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AUTOIMMUNE: Intermediate uveitis - Pars planitis
-Age distribution? -HLA associations? -Laterality? -What % of cases develop CME, neovasc, RD? |
Intermediate uveitis - Pars planitis
-Bimodal age distribution (5-15 yo, 20-40 yo) -HLA-DR15 & DR51 (DR15 also assoc w/ MS) -80% bilateral -CME, neovasc & RD develop in 10% of pts |
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AUTOIMMUNE: Intermediate uveitis - Pars planitis
-What other causes of intermediate uveitis must be ruled out before dx of pars planitis is made? -What dx should be considered in presence of vitritis w/o any other ocular features? -Histology? |
Intermediate uveitis - Pars planitis
-Other causes of intermediate uveitis: syphilis, Lyme, Tb, toxocariasis, MS, sarcoid -Consider primary CNS lymphoma if vitritis seen w/o other ocular disease features -Histology: vitreous condensation & cellular infiltration at vitreous base --> macrophages, lymphoctes, plasma cells |
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AUTOIMMUNE: Intermediate uveitis - Pars planitis
-Prognosis? -Indications for treatment? -Steps 1, 2, 3 & 4 of treatment approach? |
Intermediate uveitis - Pars planitis
-Prognosis: 10% self-limited, 30% smoldering, 60% prolonged course w/o exacerbations (disease may burn out after 5-15 yrs) -Indications for treatment: VA affected, symptoms present, CME/retinal vasculitis present (may not need tx if mild cases w/ no CME) -Step 1: periocular steroids (1st line) --> systemic steroids --> intravitreal steroids -Step 2: laser/cryo to peripheral retina (do not directly treat snowbanks) -Step 3: PPV, peripheral laser (use if systemic immunomodulatory tx is contraindicated) -Step 4: systemic immunomodulation (if all else fails) --> MTX and cyclosporine preferred |
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AUTOIMMUNE: Intermediate uveitis - Pars planitis
-What are the most common complications and their incidence? |
Intermediate uveitis - Pars planitis
-Complications: cataract (15-60%), glaucoma (10%), CME (50% --> hallmark of pars planitis), neovasc (5-15%) |
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AUTOIMMUNE: Intermediate uveitis - MS
-What is the incidence of uveitis in MS? -Laterality? -HLA association? -Severity of illness compared to pars planitis? |
Intermediate uveitis - MS
-1% incidence of uveitis in MS (10x more common in MS pts than in general population) -95% of cases bilateral -HLA-DR15 association -Tends to be milder disease than in pars planitis |
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AUTOIMMUNE: Posterior uveitis
-What are the most common races affected by SLE? -Pathophysiology? -Antibodies associated? -What % of cases have ocular involvement? |
Posterior uveitis - SLE
-African Americans & Hispanics most commonly affected -Pathophys: polyclonal B cell activation --> hypergammaglobulinemia, autoantibodies, immune complex deposition -Antibodies: Anti-ssdNA/dsDNA, anti-Sm/Ro/La, antiphospholipid, ANA -Ocular manifestations in 50% of pts |
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AUTOIMMUNE: Posterior uveitis
-Which ocular manifestation of SLE is considered an important marker of systemic disease activity? -How does this ocular disease present? |
Posterior uveitis - SLE
-Lupus retinopathy = important marker of systemic disease activity -Manifestations: cotton wool spots +/- retinal hemorrhages, retinal vascular occlusive disease (arterial/venous thrombosis --> ischemia, neovasc, hemorrhage --> seen w/ antiphospholipid Ab), choroidopathy (ischemia, CNV) |
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AUTOIMMUNE: Posterior uveitis
-What is polyarteritis nodosa (PAN)? -Pathogenesis? -Associations (gender, systemic disease)? -Antibody? |
Posterior uveitis - PAN
-Definition: focal, episodic, necrotizing vasculitis of small/medium sized muscular arteries -Assoc w/ men, Hep B positivity -Pathogenesis: immune complex deposition -p-ANCA positive suggestive of diagnosis |
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AUTOIMMUNE: Posterior uveitis - PAN
-What is the most common symptom? -What % of pts have ocular involvement? -Name some manifestations of ocular disease in PAN |
Posterior uveitis - PAN
-Most common symptom: mononeuritis multiplex -Suspect PAN in any pt w/ retinal vasculitis + multiple systemic complaints concerning for necrotizing vasculitis -Ocular disease: choroidal infarction, Elschnig spots, neuro-oph disease, PUK, scleritis |
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AUTOIMMUNE: Posterior scleritis - Wegener's
-Classic triad? -Most characteristic clinical feature? -What % of pts have ocular/orbital involvement? -What % of pts have uveitis? -Antibody? |
Posterior scleritis - Wegener's
-Classic triad: necrotizing granulomatous inflammation of upper and lower respiratory tracts, focal segmental glomerulonephritis, necrotizing vasculitis of small arteries/veins -Characteristic clinical feature: involvement of paranasal sinuses -15% have eye involvement at presentation (29% during course of illness) -10% have uveitis -c-ANCA positive |
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AUTOIMMUNE: White dot syndromes - Birdshot
-Epidemiology? -HLA association? -Distribution of lesions? -Mgmt and clinical course? -ICG? |
White dot syndromes - Birdshot retinochoroidopathy
-Epi: Caucasian females, northern European, 4th decade -HLA-A29+ in 90% -Lesions concentrated nasally, spread radially (follow underlying choroidal vessels) -ICG: multiple hypofluorescent spots (more numerous than seen on exam) -Mgmt: multiple exacerbations/remissions --> give systemic steroids f/b early initaition of steroid-sparing tx |
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AUTOIMMUNE: White dot syndromes - APMPPE
-Laterality? -Clinical features? -IVFA? -HLA association? -ICG? -Mgmt/prognosis? |
White dot syndromes - APMPPE
-Bilateral (one eye first --> then other eye) -50% w/ flulike prodrome -50% have vitritis -Large lesions (1-2 disc areas in size) -IVFA: block early --> stain late in area w/ lesions -ICG: hypofluorescence of lesions -HLA-B7 & DR2 -Good prognosis (resolves over weeks, no recurrence); no treatment (steroids do not benefit) |
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AUTOIMMUNE: White dot syndromes - Serpiginous choroidopathy
-Pathophysiology? -Genetic/Ag associations? -Clinical features? -Laterality? -IVFA? ICG? -Mgmt? |
White dot syndromes - Serpiginous choroidopathy
-Immune-mediated occlusive vasculitis -HLA-B7 & retinal S-Ag associations -Clinical: no vitritis, pseudopodial/geographic lesions starting at disc -Bilateral -IVFA: Block early --> late staining of active edge of lesion -ICG: early hypofluorescence --> late stain -Recurrent, progressive --> unclear optimal mgmt (steroids alone = ineffective) |
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AUTOIMMUNE: White dot syndromes - MCP
-Epidemiology? -Clinical? -Complications & frequencies of each? -IVFA? ICG? -Prognosis/mgmt? |
White dot syndromes - MCP
-Epi: young, myopic females -Clinical: punched-out, white-yellow spots (like PIC & OHS), +vitritis in all cases (unlike PIC & OHS) --> dots evolve to atrophic scars -Complications: CNV (33%), macular edema (14-41%) -IVFA: block early --> stain late -ICG: multiple hypofluorescent spots in mid-phase -Prognosis: dx of exclusion, poor prognosis --> chronic, recurrent -Steroids/immunosuppressive therapy |
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AUTOIMMUNE: White dot syndromes - PIC
-Epidemiology? -Clinical? -IVFA? -ICG? -Mgmt? |
White dot syndromes - PIC
-Epi: young, myopic females -Clinical: lesions rarely extend to midperiphery (unlike MCP), no vitritis, progress to atrophic scars, CNV is common -IVFA: early HYPERfluorescence w/ late staining (unlike MCP) -ICG: midphase hypofluorescence in peripapillary distribution (same as MCP) -Favorable prognosis if CNV does not occur; mgmt includes periocular/systemic steroids |
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AUTOIMMUNE: White dot syndromes - SFU
-Epidemiology? -Clinical? -IVFA? |
White dot syndromes - Subretinal fibrosis & uveitis syndrome
-Epi: young, myopic females -Clinical: vitritis is present -Chronic, recurrent -IVFA: blocked areas & hyperfluorescence early --> late staining w/o leakage |
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AUTOIMMUNE: White dot syndromes - MEWDS
-Epidemiology? -Clinical? -VF defect? -IVFA? -ERG? -Mgmt? |
White dot syndromes - MEWDS
-Epi: young, myopic females -Clinical: 80% unilateral, flulike prodrome, transitory lesions --> leave granular pigment changes (pathognomonic) -VF: enlarged blind spot -IVFA: wreath-like configuration of lesions around fovea, stain late -ERG: decreased A wave and ERP amplitudes -No treatment --> good prognosis |
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AUTOIMMUNE: White dot syndromes - ARPE
-Epidemiology? -Clinical? -IVFA? -VF? -ERG/EOG? -Prognosis? |
White dot syndromes - Acute retinal pigment epitheliitis (Krill disease)
-Epi: Healthy young adults -Clinical: unilateral, small hyperpigmented lesions with yellow halo in posterior pole -Central scotoma -IVFA: early hyperfluorescence of dots and surrounding hyperfluorescent halo w/ late staining -Normal ERG, abnormal EOG -Prognosis: benign, self limited |
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AUTOIMMUNE: White dot syndromes - AZOOR
-Epidemiology? -Clinical? -ERG/EOG? -Differential diagnosis? |
White dot syndromes - Acute zonal occult outer retinopathy (AZOOR)
-Epi: young, myopic females -Clinical: initial subtle RPE changes w/ depigmentation in areas of visual loss --> later, vessel attenuation, pigment migration, focal perivenous sheathing -Bilatearl, recurrent in 1/3 of cases -50% have vitritis -ERG: delayed 30-Hz flicker -EOG: reduced light rise -DDx: CAR, RP |
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AUTOIMMUNE: Panuveitis
-What % of pts w/ sarcoidosis have eye involvement? -What is the most frequent ocular manifestation? -Epidemiology? -HLA association? |
Panuveitis - Sarcoidosis
-15-50% of pts have eye involvement -Uveitis = most frequent ocular manifestation (occurs in 2/3 of pts w/ ocular sarcoidosis) -Epi: African Americans, F>M, pediatric disease rare -HLA-DRB1 association |
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AUTOIMMUNE: Panuveitis
-What does a sarcoid tubercle contain (histologically)? -What are Schaumann/lamellar bodies & asteroid bodies? |
Panuveitis - Sarcoid
-Sarcoid tubercle: noncaseating granuloma --> epitheliod cells, multinucleated giant cells, thin rim of lymphocytes -Schaumann/lamellar bodies: ovoid, basophilic, calcific bodies containing iron in cytoplasm of giant cells -Asteroid bodies: star-shaped acidophilic bodies within cytoplasm of giant cells |
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AUTOIMMUNE: Panuveitis
-What is Lofgren syndrome? -What is Heerfoldt syndrome? |
Panuveitis - Sarcoidosis
-Lofgren syndrome: erythema nodosum, febrile arthropathy, hilar adenopathy, acute iritis -Heerfordt syndrome: parotiditis, fever, facial nerve palsy, uveitis |
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AUTOIMMUNE: Panuveitis
-Name some ocular manifestations of sarcoidosis |
Panuveitis - Sarcoidosis
-Granulomas (orbid, lids, etc) -KCS -Anterior uveitis -Cornea, posterior disease |
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AUTOIMMUNE: Panuveitis
-What is the best screening test? -What is the most sensitive imaging test? -What combo of tests is most specific for the diagnosis in pts w/ active disease? -Whihc lab tests reflect total body granuloma content? -Definitive dx? |
Panuveitis - Sarcoidosis
-CXR = best screening test -Spiral CT = most sensitive screening test -ACE + gallium scan = specific for dx in pts w/ active disease -ACE, lysozyme = not diagnostic or specific, reflects total body granuloma content -Histopathologic = definitive method of dx |
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AUTOIMMUNE: Panuveitis
-What is the most common precipitating event for sympathetic opththalmia? -Clinical presentation? -IVFA during acute stage? -ICG? |
Panuveitis - SO
-Ocular surgery (esp vitreoretinal) = most common precipitating factor for SO -Clinical: bilateral diffuse granulomatous non-necrotizing uveitis; worse in exciting eye; Dalen-Fuchs nodules -IVFA: multiple hyperfluorescent sites of leakage at RPE --> persists in late phase; dye pooling beneath exudative RD -Dalen-Fuchs nodules appear hypofluorescent early (or have block early --> stain late pattern like APMPPE) -ICG: numerous h ypofluorescent foci |
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AUTOIMMUNE: Panuveitis
-What does B scan show in sympathetic ophthalmia? -What areas of the retina are involved in SO? -What is the significance of Dalen-Fuchs nodules in SO? -Are the immunogenetics of SO and VKH similar or different? How to distinguish b/w SO and VKH? |
Panuveitis - SO
-B scan: choroidal thickening -In SO, choroid primarily involved (no inflammation of choriocapillaris or retina) -Dalen Fuchs nodules: present in 1/3 of pts w/ SO, not pathognomonic -Immunogenetics of VKH & SO are identical (same associations found in both) -How to distinguish: no history of trauma and presence of systemic sx in VKH |
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AUTOIMMUNE: Panuveitis
-Epidemiology of VKH? -Pathophysiology? -HLA assoc in Japanese? |
Panuveitis - VKH
-Epi: darkly pigmented ethnic groups (but rare among African Americans); F>M in Japanese population -Pathophys: T-cells directed against self-Ags assoc w/ melanocytes -Target Ags on melanocytes: Tyrosinase/tyrosinase-related proteins, S-100 protein -HLA-DR4 assoc in Japanese |
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AUTOIMMUNE: Panuveitis
-Describe the 4 stages of VKH 1) prodromal (systemic sx)? 2) acute (eye findings)? 3) convalescent (eye and systemic findings)? 4) chronic/recurrent |
Panuveitis - VKH
-Prodromal stage: flulike sx, auditory problems (75%), meningismus, CSF lymphocytosis (80%) -Acute uveitic stage: 1-2 days after CNS signs, cloverleaf shaped serous RD, nonnecrotizing granulomatous inflammation concentrated in peripapillary choroid, Dalen Fuchs nodules -Convalescent stage: resolution of exudative RD, depigmentation of fundus (sunset glow fundus), depigmented Dalen Fuchs nodules, perilimbal vitiligo (Sugiura sign) in 85% of Japanese, alopecia, poliosis -Chronic recurrent stage: if inadequately treated in stages 2 and 3 |
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AUTOIMMUNE: Panuveitis
-What are essential features for diagnosis of VKH (to differentiate from SO)? -IVFA? -ICG? -B-scan? |
Panuveitis - VKH
-Essential for diagnosis: bilateral disease, no hx of trauma, no other ocular/systemic disease -IVFA (acute): punctate hyperfluorescent lesionsat RPE --> pooling of dye in areas of exudative RD -IVFA (chronic): multiple window defects 2/2 RPE loss/atrophy -ICG: delay in choriocapillaris/choroidal vessel perfusion, multiple hypofluorescent spots -Ultrasound: thickening of posterior choroid, most in peripapillary area --> extends to equator |
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AUTOIMMUNE: Panuveitis
-What is the management of acute and chronic VKH, respectively? |
Panuveitis - VKH
-Acute: early, aggressive topical/periocular/systemic steroids & cycloplegia -Chronic: recurrent episodes increasingly steroid resistant --> need immunomodulatory drugs |
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AUTOIMMUNE: Panuveitis
-Epidemiology of Bechet's? -Pathophysiology? -4 major diagnostic criteria? |
Panuveitis - Bechet's
-Epi: eastern Mediterranean, eastern Asia; M>F -Pathophys: lack of T-cell hypofunction, hyperactive B cells, no HLA association (sporadic), chronic relapsing occlusive vascuilitis -4 diagnostic criteria: recurrent oral aphthous ulcers, skin lesions (i.e., erythema nodosum), recurrent genital ulcers, uveitis |
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AUTOIMMUNE: Panuveitis
-Describe the nature of uveitis in Bechet's disease |
Panuveitis - Bechet's
-Explosive onset anterior uveitis (develops over hours) -Posterior uveitis: essential retinal finding is an obliterative, necrotizing retinal vasculitis -Optic nerve affected in 25% |
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AUTOIMMUNE: Panuveitis
-What are principles of mgmt of Bechet's disease? (i.e., meds used) -Which immunomodulatory agent is most effective? |
Panuveitis - Bechet's
-Steroids used initially, but most pts become resistant to corticosteroids --> eventually need immunomodulatory drugs -Azthioprine, cyclophosphamide & chlorambucil used in Bechet's disease -Chlorambucil may be the most effective of all immunomodulatory agents |
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INFECTIONS: Herpesvirus uveitis
-What organism should be considered in Ddx of chronic unilateral anterior uveitis? -What conditions cause stellate KPs? -What condition is a frequent complication and diagnostic hallmark of herpesvirus uveitis? -What is the mechanism of this condition? |
Herpesvirus uveitis
-Consider VZV in Ddx of chronic unilateral ant uveitis -Stellate KP: seen in herpesvirus uveitis & Fuch's heterochromic iridocyclitis -Glaucoma = frequent complication of herpetic uveitis & diagnostic hallmark (as uveitis usually causes low IOP) -Mechanisms of glaucoma: trabeculiitis, TM obstruction by inflammatory cells |
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INFECTIONS: Herpesvirus uveitis
-What is varicella zoster sine herpete? -What is the umbrella aterm for ARN/PORN type disease? -What is the constellation of findings diagnostic of ARN? |
Herpesvirus uveitis
-Varicella zoster sine herpete: development of ocular VZV disease w/o cutaneous component -Necrotizing herpetic retinopathy: umbrella term for ARN, PORN -Clinical findings for ARN: 1) occlusive retinal arteriolitis, 2) multifocal yellow-white peripheral retinitis, 3) vitritis, 4) significant AC reaction |
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INFECTIONS: Herpesvirus uveitis
-What is the mechanism of RD in pts w/ ARN? -What etiologic agent of ARN is assoc w/ encephalitis? -Name 2 diagnostic tests for ARN |
Herpesvirus uveitis
-RD in ARN: 2/2 multiple retinal breaks, PVR --> can do prophylactic laser to uninvolved areas -HSV-1 ARN assoc w/ HSV encephalitis -Diagnosis of ARN: goldmann-witmer coefficient (if >4 indicates high intraocular Ab production, diagnostic); PCR (most sensitive, specific & rapid) |
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INFECTIONS: Herpesvirus uveitis
-What is the most common etiologic agent for ARN? -What is the mgmt of ARN? -What is PORN (pt population, most common organism, how to differentiate from ARN, prognosis, mgmt)? |
Herpesvirus uveitis
-VZV = most common etiology of ARN -Mgmt of ARN: IV acyclovir, f/b long term PO antivirals -PORN (progressive outer retinal necrosis): advanced AIDS, immunosuppressed pts -VZV = most common cause of PORN -In contrast to ARN: post pole involved early, NO vitritis, minimal initial vasculitis -Poor prognosis -Mgmt: combo IV & intravitreal antivirals |
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INFECTIONS: Herpesvirus uveitis
-What are featues of non-necrotizing herpetic retinitis? (laterality, mgmt, clinical findings) |
Herpesvirus uveitis
-Non-necrotizing herpetic retinitis: bilateral, systemic antivirals used for tx, can cause CME & birdshot-like appearance |
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INFECTIONS: Herpesvirus uveitis
-What is the most common congenital viral infection? -Is it nessary to follow pts w/ presumed congenital infection even without ocular disease? -What are the 3 forms of congenital infection? |
Herpesvirus uveitis
-CMV = most common congenital viral infection -Must follow pts w/ congenital CMV even w/o eye findings --> can develop later -3 forms: fulminant (prominent hemorrhage, necrosis, post pole, assoc w/ vessels), granular (peripheral, minimal edema/heme/vascualr sheathing), perivascular (frosted branch angiitis) |
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INFECTIONS: Herpesvirus uveitis
-What is the most common ophthalmic manifestation of congenital CMV & HIV/AIDS-assoc CMV? -How does CMV spread to the eye? -What is the association b/w CMV retinitis and mortality in HIV/AIDS? |
Herpesvirus uveitis
-CMV retinitis = most common ophthalmic manifestation of congen CMV & HIV/AIDS-assoc CMV -Spreads hematogenously to eye --> infects retinal vascular endothelial cells -CMV retinitis assoc w/ 1.6x increased mortality in HIV/AIDS --> treatment of CMV retinitis is assoc w/ decreased mortality (independent of other factors) |
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INFECTIONS: Herpesvirus uveitis
-What are histologic features of CMV retinitis? |
Herpesvirus uveitis
-Histology of CMV retinitis: full thickness coagulative necrosis of retina w/ secondary diffuse choroiditis -Eosinophilic intranclear inclusions -Basophilic cytoplasmic inclusions |
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INFECTIONS: Herpesvirus uveitis
-Which herpesvirus has a tropism for B cells and is assoc w/ Burkitt lymphoma? -What is the most common ocular manifestation of this condition? -What is the name of the systemic infection associated with this virus? |
Herpesvirus uveitis
-EBV has tropism for B cells, assoc w/ Burkitt lymphoma -Follicular conjunctivitis (self limited) = most common ocular manifestation -Infecious mononucleosis = systemic condition caused by EBV |
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INFECTIONS: Herpesvirus uveitis
-What are the antibodies that appear during acute mononucleosis? -What antibody titers rise with the onset of clinical disease? -Which antibody rises slowly and then persists for life? -What antibodies are associated with chronic infection? |
Herpesvirus uveitis
-IM: acute infection --> IgM and then IgG to viral capsid antigen appear -Early antibody (EA) rises with onset of clinical disease (becomes undetectable 6-12 mo after resolution) -Nuclear antibody (NA) rises slowly, persists for life -Chronic disease: IgM for VCA and EA chronically elevated |
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INFECTIONS: Rubella
-What are the most common clinical findings assoc w/ congenital rubella syndrome? -What are some systemic manifestations? -DIagnostic criteria? -Mgmt? |
Rubella - Congenital
-Salt-and-pepper pigmentary retinopathy is most common ocular manifestation (25-50% of pts) --> assoc w/ nl vision, vessels & optic nerve -Other findings: cataracts (15%), glaucoma (10%) -Systemic: cardiac disease, deafness -Diagnosis: need to see 4x increased IgG and new IgM Ab -Supportive treatment |
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INFECTIONS: Rubella
-What are the most common ocular manifestations of acquired rubella infection? -What are systemic features? -Mgmt? |
Rubella - Acquired
-Conjunctivitis is most common ocular manifestation (70%) -Other eye disease: epithelial kerititis, multifocal chorioretinitis -Systemic: rash spreading from face --> trunk; prodromal constitutional sx -Supportive mgmt (can give steroids for retinitis) |
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INFECTIONS: Lymphocytic choriomeningitis virus
-What animal is the reservoir for this virus? -What is the genetic material of this virus? -Clinical findings? How to differentiate from congenital toxoplasmosis? |
LCMV
-RNA virus -Rodents = reservoir -Similar findings to congenital toxo (chorioretinal scars, intracranial calcifications) --> note that in toxo, calcifications are diffuse; in LCMV, calcifications are periventricular |
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INFECTIONS: Measles
-What are the most common ocular complications of measles? -Is measles retinopathy more common in congenital or acquired disease? -What are ERG findings in measles retinopathy? -Mgmt of systemic and ocular measles? -Mgmt of measles retinopathy? |
Measles
-Keratitis & mild papillary nonpurulent conjunctivitis = most common ocular manifestations -Measles retinopathy: more common in acquired measles; ERG extinguished -Mgmt of ocular and systemic measles: symptomatic (self limited disease) -Steroids can be used for measles retinopathy |
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INFECTIONS: Measles
-What % of patients with subacute sclerosing panencephalitis have ocular findings? -What is the most consistent ocular finding? -Diagnosis of SSPE? |
Measles
-10-50% of pts w/ SSPE have ocular findings -Maculopathy (focal retinitis, RPE changes) = most consistent eye finding -Dx of SSPE: clinical sx, periodic EEG discharges, IgG measles titer |
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INFECTIONS: West Nile Virus
-What are presenting ocular symptoms/signs of west nile virus? -Mgmt? -Diagnosis? -IVFA? |
West Nile Virus
-Eye findings: pain, photophobia, conj injection, blurry vision, multifocal chorioretinitis, nongranulomatous inflammation --> follows course of choroidal vessels -Mgmt: self-limited in majority of pts --> VA returns to baseline in months (no proven treatment) -Dx: IgM Ab to virus -IVFA: central hypofluorescent & peripheral hyperfluorescence of lesions |
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INFECTIONS: Ocular histoplasmosis
-Clinical findings? -Pathogenesis? -What is the 3 yr risk of maculopathy if macular histo spots present? if no macular histo spots present? |
Ocular histoplasmosis
-Clinical: 1) histo spots; 2) peripapillary pigment changes; 3) no vitritis; 4) CNV -Pathogenesis: focal choroidal inflammation at time of initial systemic infection --> may resolve w/ atrophy OR cause Bruch's disruption & CNV -Macular histo spots --> 25% risk of maculopathy in 3 yrs -If no macular histo spots --> 2% risk of retinopathy |
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INFECTIONS: Ocular histoplasmosis
-IVFA of active disease vs CNV? -Definition of clinically significant CNV? Mgmt of each type? -Why is submacular surgery not advocated for mgmt of CNV? |
Ocular histoplasmosis
-IVFA (active disease lesion): block early --> hyperfluorescence late -IVFA (CNV): hyperfluorescence early --> leakage late -Clinically significant CNV: 1) extrafoveal - 20-200 um from center; 2) juxtafoveal - 1-199 um from center; 3) subfoveal -Mgmt of extrafoveal/juxtafoveal: thermal laser (Macular Photocoagulation Study) -Mgmt of subfoveal: PDT (Visudyne in OHS study), intravitreal VEGF/steroids -Submacular surgery trials (SST) showed high rate of recurrent CNV s/p submacular surgery --> not useful treatment |
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INFECTIONS: Measles
-What % of patients with subacute sclerosing panencephalitis have ocular findings? -What is the most consistent ocular finding? -Diagnosis of SSPE? |
Measles
-10-50% of pts w/ SSPE have ocular findings -Maculopathy (focal retinitis, RPE changes) = most consistent eye finding -Dx of SSPE: clinical sx, periodic EEG discharges, IgG measles titer |
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INFECTIONS: West Nile Virus
-What are presenting ocular symptoms/signs of west nile virus? -Mgmt? -Diagnosis? -IVFA? |
West Nile Virus
-Eye findings: pain, photophobia, conj injection, blurry vision, multifocal chorioretinitis, nongranulomatous inflammation --> follows course of choroidal vessels -Mgmt: self-limited in majority of pts --> VA returns to baseline in months (no proven treatment) -Dx: IgM Ab to virus -IVFA: central hypofluorescent & peripheral hyperfluorescence of lesions |
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INFECTIONS: Ocular histoplasmosis
-Clinical findings? -Pathogenesis? -What is the 3 yr risk of maculopathy if macular histo spots present? if no macular histo spots present? |
Ocular histoplasmosis
-Clinical: 1) histo spots; 2) peripapillary pigment changes; 3) no vitritis; 4) CNV -Pathogenesis: focal choroidal inflammation at time of initial systemic infection --> may resolve w/ atrophy OR cause Bruch's disruption & CNV -Macular histo spots --> 25% risk of maculopathy in 3 yrs -If no macular histo spots --> 2% risk of retinopathy |
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INFECTIONS: Ocular histoplasmosis
-IVFA of active disease vs CNV? -Definition of clinically significant CNV? Mgmt of each type? -Why is submacular surgery not advocated for mgmt of CNV? |
Ocular histoplasmosis
-IVFA (active disease lesion): block early --> hyperfluorescence late -IVFA (CNV): hyperfluorescence early --> leakage late -Clinically significant CNV: 1) extrafoveal - 20-200 um from center; 2) juxtafoveal - 1-199 um from center; 3) subfoveal -Mgmt of extrafoveal/juxtafoveal: thermal laser (Macular Photocoagulation Study) -Mgmt of subfoveal: PDT (Visudyne in OHS study), intravitreal VEGF/steroids -Submacular surgery trials (SST) showed high rate of recurrent CNV s/p submacular surgery --> not useful treatment |
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INFECTIONS: Candidiasis
-Predisposing conditions? -Clinical appearance? -Pathophysiology? -Follow up? |
Candidiasis
-most common fungus causing endogenous retinal, choroid and vitreous infection -Predisposing factors: recent major GI surgery, bacterial sepsis, hyperalimentation, systemic abx, indwelling catheters, prolonged neutropenia, organ transplantation, debilitating disease (i.e., diabetes) -Clinical: multifocal, bilateral, white lesions < 1 mm diameter assoc w/ overyling vitritis -Pathophys: budding yeast w/ pseudohyphae, hematogenous dissemination to choroid --> breaks through Bruch's & infects retina -Follow up: all pts w/ candidemia have baseline DFE, followed for at least 2 weeks for development of ocular candidiasis |
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INFECTIONS: Candidiasis
-What is the mgmt of candidal lesions not yet involving vitreous vs those involving vitreous? |
Candidiasis
-Lesions not yet involving vitreous: PO fluconazole or voriconazole -Lesions involving vitreous: intravitreal ampho/voriconazole w/ PPV |
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INFECTIONS: Aspergillosis
-Risk factors? -Clinical appearance? -Histologic appearance of fungus? -Mgmt? |
Aspergillosis
-Risk factors: IVDA, cancer, chronic pulmonary infection, endocarditis -Clinical: bilateral vitritis, fluffy exudates (similar to candida) often in post pole/macula, hemorrhagic, broad areas of infarction, rapid progression -Histo: septate, dichotomously branching hyphae in vitreous fluid; difficult to culture from blood -Mgmt: systemic + intraocular antifungals, PPV |
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INFECTIONS: Cryptococcosis
-What organ system does this have a predilection for? -What disease entity is this the most common cause of? -Clinical? -Definitive dx? -Mgmt? |
Cryptococcosis
-Most common cause of fungal meningitis & most frequent fungal eye infection in HIV/AIDS -Predilection for CNS -Found in pidgeon feces -Clinical: multifocal chorioretinitis w/ yellow-white lesions in post pole -Definitive dx: demonstration of organism w/ India Ink staining or CSF culture -Mgmt: IV ampho B & PO flucytosine |
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INFECTIONS: Coccidiomycosis
-Endemic areas? -How common is ocular involvement? -Stain used to identify fungus? -What type of inflammation is present within the eye? -Mgmt? |
Coccidiomycosis
-Endemic areas: Southwestern US, central/south America, San Joaquin Valley in CA -Ocular involvement is uncommon even w/ disseminated disease --> various forms of eye disease including granulomatous iritis, granuloma formation -Papanicolaou stain used to identify fungus -Granulomatous inflammation --> consider in DDx of any pt w/ idiopathic granulomatous iritis who has lived/traveled through endemic areas -Mgmt: Ampho B = most effective for active infection (can also use PO azoles) |
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INFECTIONS: Toxoplasmosis
-How common is this condition? -Definitive hosts? -3 major forms? -Which population of pts gets Type I strain & which gets Type II strain? |
Toxoplasmosis
-Most common cause of infectious retinochoroiditis in both adults & children! -Cats = definitive host -3 forms: 1) oocyst (soil); 2) tachyzoite (infectious); 3) tissue cyst (latent) -Type I strains: immunocompetent pts -Type II strains: HIV/AIDS pts, congenital infections |
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INFECTIONS: Toxoplasmosis
-Principle modes of transmission? -When during pregnancy is the risk of congenital infection the highest? -Presentation of congenital toxo? -Standard of care for congenital toxo? |
Toxoplasmosis
-Transmission: undercooked, infected meat; cat feces exposure; unpasteurized goat milk or contaminated fruit/veg; contact w/ infected blood (transfusion, organ transplant), transplacental -40% of primary maternal infections result in congenital infection (highest rate of transmission in 3rd trimester) -Presentation: chorioretinitis, hydrocephalus, intracranial califications -Newborns w/ toxo should be treated for at least 1 year to prevent ocular involvement |
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INFECTIONS: Toxoplasmosis
-Ocular presentation? -What is Kyrieleis arteriolitis? -What is PORT? |
Toxoplasmosis
-Ocular presentation: focal white retinal lesion w/ overlying vitritis ("headlight in fog") adjacent to old chorioretinal scar --> usually in posterior pole -Kyrieleis arteriolitis: perivasculitis in vicinity of active lesion (sheathing of vessels) -PORT (punctate outer retinal toxo): small multifocal deep retinal lesions assoc w/ scant overlying vitritis |
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INFECTIONS: Toxoplasmosis
-What are patterns of antibody titers in toxo? -Indications for treatment? |
Toxoplasmosis
-Antibodies: IgG remain positive for life, appear 2 weeks after infection; IgM start early in acute phase, positive for < 1 yr, do not cross placenta -Presence of IgM in newborns confirms congenital infection -Indications for tx: lesions near optic nerve/fovea, dec VA, mod to severe vitritis, lesions > 1 DD size, persistence > 1 month, multiple active lesions |
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INFECTIONS: Toxoplasmosis
-Disease course in immunocompetent vs immunocompromised pts? -What drugs should NOT be used? -Classic tx regimen? -What drug can be used if sulfa allergic? -What labs should be monitored? -Are steroids useful? -What is an alternative treatment to the classic regimen? |
Toxoplasmosis
-Disease may be self limited in immunocompetent; always treat in immunocompromised -Classic triple therapy: pyrimethamine, sulfadiazine & folinic acid -Clindamycin used if sulfa allergic -Monitor WBC & plts weekly -Use systemic steroids at time of tx or within 48 hrs in immunocompetent pts --> DO NOT use long acting periocular or intraocular steroids! -Alternative tx: Bactrim (same efficacy as triple tx) |
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INFECTIONS: Toxoplasmosis
-What is the mgmt of toxoplasmosis in pregnant pts? -How are newborns w/ congenital toxo treated? -What has long term intermittent bactrim shown to be useful for? |
Toxoplasmosis
-Pregnant pts: use spiramycin; alternatives: azithromycin, clinda & atovaquone -Newborns: pyrimethamine & sulfonamides x 1 yr (w/ peds ID specialist) -HIV/AIDS - extended systemic tx needed -Long term intermittent Bactrim decreases risk of reactivation in recurrent toxo chorioretinitis |
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INFECTIONS: Toxocariasis
-What type of worm is toxocara canis? -Name of systemic disease? -Pt population? |
Toxocariasis
-Roundworm -Caucasians most commonly affected -Visceral larvae migrans = systemic disease |
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INFECTIONS: Toxocariasis
-What are the 3 recognizable posterior ocular syndromes? -Symptoms? -Laterality? |
Toxocariasis
-Usually unilateral (bilateral disease rare) -Posterior segment: 1) luekocoria 2/2 vitritis mimicking endophthalmitis (25%); 2) localized macular granuloma (25%); 3) peripheral granuloma (50%) |
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INFECTIONS: Toxocariasis
-Laboratory testing? -Most important consideration for differential diagnosis? How to differentiate b/w this condition and toxocariasis? -Mgmt? |
Toxocariasis
-Labs: serum ELISA 1:8 (90% sensitive & specific for prior exposure) --> but if negative, does not rule out diagnosis! -Retinoblastoma: most important DDx consideration --> B scan & CT will NOT show calcification in toxocariasis (will see in Rb) -No uniformly satisfactory tx -Can use systemic/periocular steroids |
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INFECTIONS: Cysticercosis
-Type of worm? -Risk factors for infection? -Most common intraocular location for infection? -First sign of cerebral cysticercosis? |
Cysticercosis
-Tapeworm -Risk factors: poor hygeine (acquired via ingestion of eggs/worm) -Most common intraocular location: subretinal space --> eye is more commonly affected than any other organ in this disease -Neurocysticercosis: epileptiform seizures = first sign |
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INFECTIONS: Cysticercosis
-Clinical findings? -Pathognomonic finding? -What % of pts have +Abs? -Mgmt? |
Cysticercosis
-Clinical: white cyst w/ head/scolex that undulates in response to examining light within vitreous/subretinal space --> motile anterior chamber, intravitreal or subretinal worm is pathognomonic -Abs+ in 80% w/ neural cysticercosis & 50% w/ ocular cysticercosis -Mgmt: antihelminthic drugs not effective for eye disease --> need systemic steroids also & surgical removal of larva from vitreous |
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INFECTIONS: DUSN
-Pt population? -Causative organisms? -Workup & Mgmt? |
Diffuse Unilateral Subacute Neuroretinitis
-Healthy, young pts -Organisms: ancylostoma canium (smaller), Baylisascaris procyonis (larger) -Systemic/lab workup usually negative -Mgmt: direct laser of subretinal worm, albendazole |
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INFECTIONS: DUSN
-Clinical presentation and findings? |
Diffuse Unilateral Subacute Neuroretinitis
-Unilateral vision loss 2/2 recurrent inflammation of retina/RPE/nerve -Multiple, focal, gray white lesions that are evanescent --> looks like white dot syndrome -Later: abnl EEG, RPE atrophy, optic atrophy |
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INFECTIONS: Onchocerciasis
-Endemic areas? -Transmitting insect? -Name for eye disease? -How do the microfilariae reach the eye? (3 routes) |
Onchocerciasis: "River blindness"
-Endemic areas: Sub-Saharan Africa, Central/South America -Transmitted by blackfly -3 routes of spread to eye: direct invasion of cornea from conj; scleral penetration (direct or thru vessels), hematogenous spread |
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INFECTIONS: Onchocerciasis
-Manifestations of eye disease? -Treatment of choice & dosing? -What is a Mazzotti reaction? |
Onchocerciasis
-Eye disease: severe anterior uveitis, chorioretinal changes, optic atrophy --> confirm dx by seeing organism in eye or skin bx -Mgmt: Ivermectin (kills microfilariae but does not kill adult worm) ---> singly monthly dose for 10 yrs needed -Slows progression of vision loss & optic atrophy -Mazzotti reaction: caused by massive worm kill when treatment was diethylcarbamazine --> no longer used now |
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INFECTION: Syphilis
-What are the systemic findings of early and late congenital syphilis? -What are the most common ocular findings in early and late congenital syphilis? |
Syphilis - congenital
-Early systemic: long bone changes, skin rash, hepatosplenomegaly -Late systemic: Hutchinson teeth, mulberry molars, CN VIII deafness, saber shins, abnl facies -Early ocular: salt-and-pepper pigmentary retinopathy (nonprogressive, nl vision --> like rubella); retinal vasculitis & chorioretinitis may precede the pigmentary retinopathy -Late ocular: Nonulcerative stromal interstitial keratitis + anterior uveitis |
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INFECTIONS: Syphilis
-What is the Hutchinson Triad? |
Syphilis - congenital
-Hutchinson triad: interstitial keratitis + CN VIII deafness + Hutchinson teeth |
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INFECTIONS: Syphilis
-Describe clinical maniefstations of primary, secondary and tertiary syphilis -During which stage does syphilis uveitis occur? -What is the most common posterior segment manifestation? |
Syphilis - acquired
-Primary: painless chancre at site of inoculation -Secondary: lymphadenopathy, generalized rash -Tertiary: gummas, cardiovascular syphilis, neurosyphilis -Uveitis can occur in ANY stage of syphilis -Posterior segment: focal, multifocal chorioretinitis assoc w/ vitritis; neuroretinitis also possible |
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INFECTIONS: Syphilis
-What are the nontreponemal antigen tests for syphilis? -What are the treponemal antigen tests? -When do treponemal antigen tests become positive and how are they useful? -Which tests should be used in the setting of uveitis? |
Syphilis
-Nontreponemal tests: RPR, VDRL -Treponemal tests: FTA-ABS, MHA-TP -Treponemal tests correlate w/ disease activity, used for monitoring tx for systemic & ocular disease -FTA-ABS becomes positive during secondary stage, remains positive for life -In uveitis: need BOTH treponemal & nontreponemal tests (do not skip treponemal test if nontreponemal tests negative) --> treponemal tests have higher predictive value in uveitis! |
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INFECTIONS: Syphilis
-What test is warranted in all cases of syphilitic uveitis? -What other disease should be tested for in pts w/ syphilis? -What diagnostic tests are always positive in congenital syphilis? -What is the most important test for serodiagnosis of congenital syphilis? |
Syphilis
-All syphilis pts should be tested for HIV -All pts w/ syphilis uveitis should have LP for neurosyphilis -Congenital syphilis: all newborns are + VDRL & FTA-ABS (due to passive transfer of maternal IgG across placenta) -Need IgM FTA-ABS for serodiagnosis of congenital syphilis --> presence indicates that infection originated within infant (as IgM does not cross placenta) |
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INFECTIONS: Syphilis
-What is the preferred tx for all stages of syphilis? -What dosing regimen should be used for syphilitic uveitis? -What is the mgmt of congenital syphilis? |
Syphilis
-IV PCN G is preferred for all stages of disease -Syphilitic uveitis should be considered a form of neurosyphilis --> use neuro dosing (18-24 mil units aqueous crystalline PCN G/day x 10-14 days) -Congenital syphilis: crystalline PCN G x 10 days |
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INFECTIONS: Syphilis
-What alternatives are available for PCN-allergic pts? -What is the Jarisch-Herxheimer reaction? -What other disease is assoc w/ Jarsich-Herxheimer reaction? |
Syphilis
-If PCN allergic --> need desensitization and then tx w/ PCN *no other alternatives available) -Jarisch-Herxheimer reaction: host hypersensitivity response to treponemal Ags released in large numbers are spirochetes killed --> occurs in 1st 24 hrs --> concomitant increase in ocular inflamamtion (may need steroids) -Lyme can also cause Jarisch-Herxheimer reaction when treated |
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INFECTIONS: Lyme
-Epidemiology? -Describe systemic features of stage 1, 2 and 3 disease? |
Lyme
-Epi: M>F (53%), May-August -Stage 1: erythema migrans (target rash at site of inoculation) & constitutional sx -Stage 2: disseminated disease --> erythema chronicum (sites remote from inoculation), joint disease, neurologic disease -Stage 3: episodic arthritis, acrodermatitis chronica atrophicans (bluish red lesion on extremities), fibrous bands/nodules |
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INFECTIONS: Lyme
-Most common ocular manifestations of stage 1, 2 and 3 disease (respectively)? -2 step protocol for diagnosis? -Mgmt of eye disease? |
Lyme
-Stage 1: follicular conjunctivitis -Stage 2: intermediate uveitis -Stage 3: immune stromal keratitis (responds to steroids) -2 step protocol for diagnosis: 1) IFA or ELISA for IgM & IgG; 2) confirmatory Western blot -Mgmt: route/duration of abx not established; need LP for neuro eval if eye disease present; give steroids for anterior segment inflammation after abx started |
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INFECTIONS: Leptospirosis
-Epi? -Systemic features? -What is Weil disease? |
Leptospirosis
-Tropical/subtropical regions, water sports -Systemic features: constitutional and GI sx (abrupt onset) --> 85-90% of pts have self limited anicteric illness; 10-15% develop severe septicemia/Weil disease -Weil disease: renal and hepatocellular dysfunction --> 15-30% mortality rate |
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INFECTIONS: Leptospirosis
-Ocular findings? --> which is pathognomonic? -Visual prognosis? -Diagnostic testing? -Mgmt? |
Leptospirosis
-Ocular findings: circumcorneal conjunctival hyperemia (pathognomonic), anterior/diffuse uveitis --> more vision threatening -Good prognosis for vision despite severe panuveal inflammation -Diagnosis: MAT (microagglutination test) = gold standard; can also do ELISA, complement-fixation for IgM detection -May see false + FTA-ABS or RPR w/ this disease -Mgmt: IV PCN G x 1 week or PO doxy for 1 week (if milder disease) |
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INFECTIONS: Nocardiosis
-Systemic disease features? -Ocular findings? -Mgmt? |
Nocardiosis
-Systemic disease: pneumonia, disseminated abscesses -Ocular: choroidal abscesses (spreads hematogenously to eye) -Mgmt: systemic sulfonamide x 6 weeks (immunocompetent) or 1 yr (immunosuppressed) |
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INFECTIONS: Tuberculosis
-Features of the organism? -Most common organs infected? -What % of pts develop pulmonary and extrapulmonary Tb (respectively)? -What is primary ocular Tb and its manifestations? |
Tuberculosis
-Organism: acid-fast, obligate aerobe --> found most commonly in apices of lung and choroid (highest blood flow rate in body) -Pulmonary Tb occursi n 80% of pts (extrapulmonary Tb occurs in 20% --> half of these pts have normal CXR) -Primary ocular Tb = eye is primary port of entry --> conj, corneal & scleral disease |
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INFECTIONS: Tuberculosis
-What is secondary ocular Tb and its manifestations? -Characteristic lesions of choroiditis? -IVFA findings? |
Tuberculosis
-Secondary ocular Tb: uveitis (disseminated choroiditis) is most common presentation --> granulomatous disease -Choroiditis --> classic lesions are tubercles or tuberculoma (single large elevated choroidal mass) -IVFA: active lesions show early hyperfluorescence & late leakage; cicatrical lesions show early blocekd fluorescence w/ late staining |
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INFECTIONS: Tuberculosis
-What is Eales disease? -When should PPD testing be used for diagnosis? -Mgmt of eye disease? |
Tuberculosis
-Eales disease: peripheral retinal perivasculitis w/ recurrent unilateral vitreous/retinal heme --> subsequently involves other eye, healthy young men -PPD: use selectively for pts w/ high index of suspicion for disease (not for routine screening) -Mgmt: systemic tx of uveitis --> 4 drug therapy; can use steroids in conjunction |
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INFECTIONS: Ocular Bartonellosis
-Epidemiology? -Systemic manifestations? -Ocular disease features? -Most well known posterior segment manifestation of disease? |
Ocular Bartonellosis
-Epi: fall and winter; southern states (CA, Hawaii) -Systemic features: flu-like illness, regional adenopathy, erythematous papule at primary site -Ocular disease (5-10% of pts): Parinaud oculoglandular syndrome --> unilateral granulomatous conjunctivitis & regional adenopathy -Neuroretinitis = most common posterior segment manifestation of B. henslae infection (caused by B. henslae in 2/3 of cases) -Clinical features of neuroretinitis: abrupt vision loss, unilateral disc swelling, macular star |
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INFECTIONS: Ocular Bartonellosis
-Diagnostic testing? -Prognosis? -Mgmt? |
Ocular Bartonellosis
-Diagnosis: single positive IFA or EIA (enzyme immunoassay) titer for IgG or IgM is sufficient to confirm dx -Prognosis: self-limited, good systemic & visual prognosis -Mgmt: doxy 100 bid x 2-4 weeks (in peds pts, azithromycin can be used) - |
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INFECTIONS: Whipple disease
-Organism? -Clinical syndrome? -Eye disease? -Gold standard for diagnosis? -Mgmt? |
Whipple disease
-Tropheryma whippelii -Syndrome: middle-aged Caucasian males w/ diarrhea, weight loss, migratory arthritis (protein loss causes pitting edema) -Eye disease is rare --> bilateral panuveitis & retinal vasculitis; granular deposits on iris, capsule and IOL -Gold standard for dx: duodenal biopsy --> PAS+ macrophages within intestinal villa -Mgmt: systemic Bactrim x 1-3 months (relapses occur in 30% of cases) |
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ENDOPHTHALMITIS: Exogenous
-What are the 3 types of exogenous endophthalmitis? -Are clear corneal incisions associated with lower or higher risk of endophthalmitis? -What is the rate of endophthalmitis after PPV? -What are the primary sources of infection in postoperative endophthalmitis? What organisms? |
Exogenous
-3 types of exogenous endophthalmitis: postoperative, post-traumatic and bleb-associated -CCI associated w/ higher risk of endophthalmitis -PPV: has low (0.05%) rate of endophthalmitis -Eyelids & conjunctiva = primary infection source in postop endophthalmitis |
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ENDOPHTHALMITIS: Exogenous
-What are specific sources of contamination in postoperative endophthalmitis? -Which IOL material is associated w/ positive bacterial cultures? |
Exogenous
-Sources contamination in postop endophthalmitis: secondary infection (i.e., from lacrimal system), blepharitis, contaminated gtts, breach in sterility, contaminated fluids -IOL material assoc w/ positive bacterial cultures: polypropylene (in haptics) |
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ENDOPHTHALMITIS: Acute postoperative
-Timeline? -Difference b/w mild and severe cases (causative organism, VA, time of onset)? |
Acute postoperative endophthalmitis
-Up to 6 weeks after surgery -Mild: VA > 20/400, less painful, 3-14 days postop, coag negative staph -Severe: VA < 20/400, severe pain and vitritis, 1-4 days postop, S. aureus, Strep spp., gram negative bugs |
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ENDOPHTHALMITIS: Chronic postoperative
-Timeline? -Name a characteristic organism and type of infection -What is the most important fungal cause of chronic postop endophthalmitis? |
Chronic postoperative endophthalmitis
-Timeline: 6 wks - years after surgery -P. acnes: granulomatous KP, white plaque in capsular bag (contains residual lens material, bacteria) -Candida = most important fungal cause of chronic postop endophthalmitis |
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ENDOPHTHALMITIS: Post-traumatic
-What factors are related to increased incidence? -Organism responsible for most fulminant infection? |
Post-traumatic
-Highest incidence in rural settings and when intraocular foreign body present -Bacillus = most fulminant cause of endophthalmitis |
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ENDOPHTHALMITIS: Bleb-associated
-Risk factors? -Does this occur in intact or leaking blebs? |
Bleb-associated endophthalmitis
-Risk factors: diabetes, use of antimetabolites, inferior bleb, h/o previous resolved blebitis -Can occur in intact OR leaking blebs |
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ENDOPHTHALMITIS: Endogenous
-Risk factors? -Most common bacterial organisms? |
Endogenous
-Risk factors: chronic illness (DM, renal failure), immunosuppression, IVDA, indwelling catheters, immediate postop or postpartum -Bacteria: strep (endocarditis), staph (cutaneous), bacillus (IVDA), gram negatives (i.e., klebsiella - klebsiella endophthalmitis is most common type of endogenous infection in Asia, due to liver abscesses) |
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ENDOPHTHALMITIS: Endogenous fungal
-Which part of the eye is initially affected? -Most common organisms? |
Endogenous fungal endophthalmitis
-Choroid initially affected --> overlying vitritis -Candida (most common) & aspergillus (second most common) |
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ENDOPHTHALMITIS: Endogenous fungal - Candida
-Risk factors? -% of pts w/ endophthalmitis who are on tx vs those not on tx? -Diagnosis? -Follow up? -Mgmt? |
Endogenous fungal - Candida
-Risk factors: immunosuppression, hyperalimentation, IVDA -Occurs in 10-37% of those not on antifungals; occurs in 3% of those on antifungals -Diagnosis: blood cultures, intraocular fluid PCR -Newly diagnosed cases of candidemia should have DFE initially and again 1-2 weeks apart -Mgmt: voriconazole, caspofungin, ampho B, ketoconazole |
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ENDOPHTHALMITIS: Endogenous fungal - Aspergillus
-Risk factors? -Clinical findings? |
Endogenous fungal - Aspergillus
-Risk factors: severe chronic pulmonary disease, severe immunocompromise, IVDA, orthotopic liver transplant -Clinical: subretinal/subhyaloid hypopyon, hemorrhage in all layers, vitreous abscesses, angiocentric inflammation |
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ENDOPHTHALMITIS: Endogenous fungal - Aspergillus
-How to differentiate Candidal and Aspergillus endophthalmitis? -Mgmt of aspergillus endophthalmitis? Prognosis? |
Endogenous fungal - Aspergillus
-Candida vs aspergillus: primary focus of inflammation is vitreous in Candida but retinal/choroidal vessels and subretinal space in Aspergillus -Mgmt of aspergillus: PPV + intravitreal ampho B/voriconazole + intravitreal steroids -Poor prognosis (often involves macula) |
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ENDOPHTHALMITIS: Prophylaxis
-What measures are proven to reduce endophthalmitis after cataract surgery? -What is the utility of PO moxifloxacin in prophylaxis of postop endophthalmitis? |
Prophylaxis
-Preventative measures for cataract surgery: 1) preop 5% iodine antisepsis (including prep of lids/conj); 2) preop topical, broad spectrum abx; 3) careful isolation of lids/lashes from surgical field -PO moxi does reach inhibitory concentrations in aqueous & vitreous but is not used routinely for postop prophylaxis |
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ENDOPHTHALMITIS: DIagnosis
-What is TASS? -Why is it important to obtain vitreous cultures in addition to aqueous cultures? -Which method is better to obtain positive culture results: needle tap of intraocular fluid vs mechanized biopsy? |
Diagnosis
-Toxic anterior segment syndrome: caused by introduction of unknown toxic substances by surgery via instruments, fluids, IOLs -Important to obtain vitreous in addition to aqueous cultures because may have + vitreous culture even when aqueous culture is negative -Equivalent utility of needle tap and mechanized biopsy in obtaining + cultures and in terms of complication rates |
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ENDOPHTHALMITIS: Treatment
-Criteria for surgical mgmt (PPV) -Most effective antimicrobial agents? -What is the utility of systemic abx? -What is the utility of subconj, topical abx? -What % of traumatic endophthalmitis cases have VA 20/400 or better after treatment? |
Treatment
-If VA is HM or better, do tap/inject instead of PPV (per endophthalmitis vitrectomy study) -Most effective drugs: vanco (gram positives), aminoglycosides (gram negatives), ceftazidime (not as complete gram negative rod coverage) -Systemic abx are controversial --> good ocular penetration and broad coverage w/ PO fluoroquinolones -Subconj/topical abx have little benefit after intravitreal abx given -Only 10% of pts w/ posttraumatic endophthalmitis have VA > 20/400 after treatment |
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MASQUERADES: Non-neoplastic
-What is a masquerade syndrome? -What are some non-neoplastic masquerade syndromes? -What is Schwartz syndrome? |
Non-neoplastic
-Masquerade syndrome: cells in AC but not of immune origin -RP: nyctalopia, ERG depression, bilateral, +FHx, pigmentary fundus changes w/ vascular attenuation and optic atrophy -Ocular ischemic syndrome: hypoperfusion 2/2 carotid artery obstruction (>75%); neovascularization, flare>cell, clear vitreous, tortuous vessels and heme -Chronic peripheral RRD -Schwartz syndrome: RRD liberates photoreceptor outer segments --> phagocytosed by TM endothelial cells --> secondary open angle glaucoma -IOFB -Pigment dispersion |
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MASQUERADES: Neoplastic
-What is the most common non-neoplastic masquerade syndrome? -How does it manifest? |
Neoplastic
-Primary CNS lymphoma: most common neoplastic masquerade syndrome -Non-Hodgkin B cell lymphoma, 5-7th decades -25% of PCNSL have ocular disease; 15% have only ocular disease -Clinical: decreased vision, floaters, vitritis w/ spillover AC cells, creamy subretinal infiltrates |
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MASQUERADES: Neoplastic
-Mgmt of primary CNS lymphoma? -CNS manifestations? -what is GUN syndrome? -IVFA? |
Neoplastic
-Mgmt: becomes resistant to steroid tx --> PPV to diagnose, chemo, radiation -CNS: behavioral changes, periventricular lesions on imaging -GUN syndrome: uveitis, glaucoma & neurologic sx -IVFA: hypofluorescence due to blockage from subretinal tumor; hyperfluorescence due to window defect from RPE atrophy |
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MASQUERADES: Non-neoplastic
-What is the best method of diagnosis of primary CNS lymphoma? -What does cytokine analysis show? -Prognosis? |
Non-neoplastic
-Best method of diagnosis: tissue diagnosis w/ vitreous bx -Consider vitreous bx if vitreous cells of unidentifiable cause present in pt over 65 yo -Cytokine analysis: IL-10 elevated in lymphoma (produced by malignant B cells); IL-6 elevated in pts w/ inflammatory uveitis (therefore, increased ratio of IL-10:IL-6 suggests lymphoma) -Poor overall prognosis |
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MASQUERADES: Metastatic tumors
-What are the most common primary tumors that metastasize to the eye? -What % of pts w/ uveal melanoma present w/ uveal melanoma? |
Metastatic tumors
-Most common metastatic tumors to eye: breast, lung, cutaneous melanoma -5% of uveal melanomas present w/ ocular inflammation |
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COMPLICATIONS: Cataracts
-What type of IOL should be avoided in uveitic eyes? -Where should IOLs not be placed in uveitic eyes? |
Cataracts
-Avoid foldable silicone IOLs --> associated w/ greater post op inflammation and because future vitreoretinal surgery may be necessary -Do not place IOL in ciliary sulcus and anterior chamber! |
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COMPLICATIONS: Glaucoma
-What is uveitic glaucoma vs uveitic ocular HTN? -What IOP elevation increases the risk of glaucoma? -When does steroid-induced ocular HTN occur? |
Glaucoma
-Uveitic ocular HTN: IOP >/= 10 mm Hg above baseline without glaucomatous cupping -Uveitic glaucoma: elevated IOP w/ progression of cupping and glaucomatous VF defects -IOP elevation to >24 mm Hg increases risk of glaucoma -Steroid-induced OHTN rarely occurs before 3 weeks of tx |
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COMPLICATIONS: Glaucoma
-Describe the types of secondary angle closure uveitic glaucoma (mechanisms, most common causes) |
Glaucoma
-Acute secondary angle closure: choroidal inflammation --> forward movement of lens-iris diaphragm (SO, VKH) --> need aggressive steroids to control inflammation; PI doesn't help as underlying cause is choroidal inflammation -Subacute secondary angle closure: posterior synechiae, pupillary block, iris bombe (sarcoid, VKH) --> need multiple, large PI (laser if light iris, surgical if dark iris) -Chronic secondary angle closure: PAS formation; may also be due to chronic steroids --> may need surgery |
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COMPLICATIONS: Glaucoma
-Name types of secondary open angle uveitic glaucoma (mechanisms, most common causes) |
Glaucoma
-Acute secondary open angle: blockage of TM by inflammatory cells/debris (toxoplasmosis, ARN, herpetic uveitis) -Chronic secondary open angle: PAS, direct injury to TM --> need CAIs, beta blockers, alpha agonists (AVOID parasympathomimetics and prostaglandins) --> often also need surgery (tubes better than trabs) |
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COMPLICATIONS: Hypotony
-Mechanisms of hypotony? -Mgmt of hypotony early in course of disease? -Mgmt of chronic hypotony? |
Hypotony
-Mechanisms: decreased aqueous production due to acute CB inflammation or chronic CB damage -Early: intensive steroids, cycloplegics -Late: topical ibopamine (nonselective dopaminergic agonist, not in US --> increases aqueous production 3-4x) |
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COMPLICATIONS: Others
-Most common diseases assoc w/ CME? -Permanent vitreous opacification? -Retinal/choroidal neovasc? |
Others
-CME: assoc w/ pars planitis, birdshot, retinal vasculitis -Permanent vitreous opacification: toxoplasmosis, pars planitis -Retinal/choroidal neovasc: pars planitis, sarcoid, retinal vasculitis (does not always require PRP - may resolve w/ resolution of disease) |