Ant Seg Exam 2 Study Guide PDF

Allergic diseases antibody Type I Hypersensitivity: involves IgE which bind to mast cells → histamine ○ Vasodilation, erythema, ↑ vascular permeability (edema), neural stimulation (itching) atti.EE Type IV Hypersensitivity: mediated by T-cells, NOT a...

Allergic diseases antibody Type I Hypersensitivity: involves IgE which bind to mast cells → histamine ○ Vasodilation, erythema, ↑ vascular permeability (edema), neural stimulation (itching) atti.EE Type IV Hypersensitivity: mediated by T-cells, NOT antibody mediated Delayed Ocular Allergy Pharmacological Agents ○ Oral Antihistamines: Zerter H1 receptors: found in conj, cause drowsiness and dry eyes/mouth (not good for ocular allergies) ○ Mast Cell Stabilizers: prevent mast cell degranulation/release of mediators Good choice for chronic presentation, need to start weeks before allergy season/sx → not good for acute presentation Topical OTC: Alomide, Crolom ○ Antihistamines: block histamine receptors but don’t block other inflammatory mediators, don’t prevent mast cell degranulation, may actually cause it Pheniramine: old, causes mydriasis (alpha agonist) so caution with narrow angles Cetirizine (Zerviate): ocular Zyrtec, relieves itching w/in 3 min, BID dosing, $$ ○ Combo Dual: preferred for ocular allergies, act fast and long lasting Olopatadine (Pataday), Ketotifen (Zaditor, Alaway BID), Alcaftadine qd, Azelastine (generic Optivar) BID ○ Steroids: I Alrex (loteprednol): same as lotemax but lower concentration, soft so safe for long term use (>12mo) FML, Pred Acetate (low dose): reserve for severe, non-responsive cases Dextenza (ophthalmic insert): lasts for 30 days, FDA approved for itching Triamcinolone: cream for contact dermatitis, eczema, rash, short term use ○ NSAIDs: inhibit production of COX enzyme and blocks PGE formation, ↓ itching Topical NSAIDs all Rx, caution w/chronic conditions → corneal melt, delayed wound healing (abrasions, infiltrates, ulcers) Ketorolac (Acular): onset of relief within 1 hour Seasonal Allergic Conjunctivitis (SAC) ○ Caused by outdoor allergens puring peak allergy season (spring and fall) ○ Signs/Sx: itching, allergic shiner (discolored skin under eyes), papillae (not pathognomonic sign), stringy mucus Perennial Allergic Conjunctivitis (PAC) ○ Constant year round exposure to indoor allergens (animals, food, dust, mites) SAC/PAC Management (same for both) ○ Supportive Care: avoidance, pet/dust control (nighttime showers), minimize eye ween rubbing, cool compresses, ATs refrigerated, sterile eye washes ○ Dual mechanism agents are best (can also use soft steroids, antihistamine, MCS) Giant Papillary Conjunctivitis (GPC) ○ Inflammation associated with mechanical etiology (NOT rxn to airborne antigen) So not really an allergy, no ↑histamine, immune response to released components of cellular trauma, caused primarily by CLs i iimmn Iiiiit  ○Key symptoms: FBS, CL intolerance, itching, blurry vision ○Signs: superior tarsal plate papillae ≥ 0.3 mm(know #), excess mucus production ○Management: address the cause (d/c CL use, remove suture etc) Initially: dual mechanism, topical steroids or oral AH, then MCS for maintenance (if problem continues) Vernal Keratoconjunctivitis (VKC) ○ Mixed type I and IV, chronic, recurrent, bilateral but often asymmetric ○ Children-young adults, M>F, h/o systemic allergy (asthma) ○ Increased prevalence in warmer climates/warmer months ○ Key symptoms: intense itching (more than others) ○ Key signs: cobblestone papillae superior palp conj, trantas dots at limbus, corneal shield ulcer (non-infectious) ○ Management: Topical cyclosporine (Verkazia approved QID), steroids (soft if mild/moderate, strong if severe), BCL or AMT Cyclosporines are used for type IV hypersensitivity (Restasis, Cequa) Tacrolimus ointment: nonsteroidal immunomodulator, similar to cyclosporine but higher potency, inhibits T-cell activation/calcineurin Atopic Keratoconjunctivitis (AKC) ○ Mixed type I and IV, rare genetic but sight threatening, M>F, peaks at 30-50 you ○ Chronic, not season dependent like VKC, no cobblestone papillae ○ Key symptoms: severe itching, copious mucus discharge, inferior areas first ○ Key signs: lid scaling, papillary rxn (bulbar, palpebral, limbal), shield ulcer, atopic cataracts, corneal neo, periocular eczema, bleph (hypersensitivity to staph) Chronic inflammatory changes: cicatricial, ectropion, madarosis ○ Management: requires long term therapy and more aggressive than VKC, topical II as cyclosporine, topical NSAIDs, topical steroids, tacrolimus ointment Comanage with allergist and/or dermatologist Contact Dermatitis (Eyelid Allergic Dermatitis) ○ Type IV, 24-72 hours post exposure, F>M, caused by ophthalmic solutions, preservatives, cosmetics, metals, hair dye, nickel (glasses frames) ○ Management: oral antihistamine, tacrolimus ointment, steroid ointment Mucus Fishing Syndrome (MFS) ○ Initial inflammatory event → ↑mucus uncomfy/gross → pt goes digging into eyes to remove mucus →mechanical trauma causes ↑inflammation→ ↑mucus (repeat) ○ Management: topical mucolytic agent (↓viscosity) = Mucomyst QID, then taper Stop Eating Viral Conditions For each of the following conditions, be able to diagnose and manage each condition, what medications are MOST indicated, what medications should be AVOIDED, what if any laboratory testing is needed Viral Conjunctivitis in general papillae Classp eye not ○ Characterized by acute follicular conjunctivitis, monocular but quickly → binocular, (+) preauricular lymphadenopathy, systemic signs of viral infection ieUpperRespiratorytractInfection ○ Usually self limiting and benign, may last for 2-4 weeks  Adenoviral Conjunctivitis (3 types) dsDNA, nonenveloped Most common cause of viral conjunctivitis, extremely contagious Transmission: close contact with ocular/respiratory secretions, fomites (towels, pillow cases), contaminated swimming pools, close living quarters (schools, nursing homes etc) Non-Specific Viral Conjunctivitis (serotypes 1-11, 19) ○ Most common, self limited, transmitted by upper respiratory droplets or direct contact with secretions (rubbing eye then touching something), ↑risk when stressed ○ Signs/sx: FBS, burning, serous discharge (watery), moderate follicular response, diffuse pink bulbar injection (pink eye), mild chemosis Eta li ○ Management: antivirals are not effective → supportive therapy (ATs, cold compresses), hygiene: don’t touch eyes, shake hands, share towels, no CLs or makeup until resolved, don’t go to school or work So NOT initiating any treatment ○ Systemic Sickness: no sickness but exposed to someone w/conjunctivitis Pharyngoconjunctival Fever (PCF) (serotypes 3, 4, 7) 3 4 7 ○ Most common in children, transmission by UR droplets and swimming pools aka (swimming pool conjunctivitis), self limited 10-14 days ○ Ocular Signs/Sx: FBS, serous discharge, acute follicular conjunctivitis (sometimes hemorrhagic), lid edema t ○ Systemic Signs/Sx: pharyngitis (sore throat?), fever (probably goes to pediatrician before you), GI infection, preauricular lymphadenopathy ibeprofin worksing No ○ Management: VERY contagious, antivirals not effective, use analgesics for fever probes Epidemic Keratoconjunctivitis (EKC) (serotypes 8, 19, 37, D) fromtono ○ Common in developed countries, transmission in workplace, eye care facilities, close personal contact, contralateral eye affected in 70% of cases2 eyenotassevere ○ Very fast onset, happens to a lot of people, occurs in 2 phases ○ Acute Phase: begins unilateral, then less severe in fellow eye (7-16 day course) Preceded by URTI, sudden onset of profuse serous discharge, periorbital pain, severe follicular conjunctivitis, chemosis, petechial hemes on palp conj (from eye rubbing), A LOT of eyelid edema Preauricular lymphadenopathy, Pseudomembranes, cornea involved ○ K Sequelae Phase: more severe corneal involvement → subepithelial infiltrates or KeratoCornea w/in 7-14 days after onset of ocular sx, delayed hypersensitivity rxn to viral antigen on overlying epithelium ○ Only adenoviral syndrome with significant corneal involvement photophobia ○ Key symptom: photophobia in cases with corneal involvement ○ Potential complications due to conjunctival membranes: subepithelial conj scarring, symblepharon formation, dry eye ○ Management: everything you’d do for nonspecific plus Peeling off pseudomembrane membrane 1Removepseudo Topical steroid/abx combo QID then taper: Tobradex, Maxitrol Betadine Sterile Ophthalmic Prep Soln (off label) in Reduces viral load, don’t use past 5 days after onset 0.1% dexamethasone / 0.4% povidone-iodine to Iovineallergy RTC 4 5days  Topical immunosuppressants (Cyclosporine) ○ Adenoplus: 10 minute in office lab, detects viral antigens in tears for EKC/nonspecific Test positive: study shows they are unsure if you in fact have it or not Test negative: confident that you do NOT have adenovirus ○ Systemic Sickness: URTI in recent past 5% Betadine Ophthalmic Prep Solution Process ○ Used for ophthalmic surgery, kills everything on surface (↓ viral load), reduce chance of corneal infiltrate in EKC, quicker recovery time ○ Process: 2 drops of proparacaine OU → 4-6 Betadine drops OU → close and roll eyes for minimum 60 seconds → lavage out Betadine w/irrigating soln → optional lotemax QID x 4 days for inflammation → RTC 4-5 days ○ Contraindication: iodine allergy, hyperthyroid issue (Hashimoto, Graves) Molluscum Foxvirus Common in children, direct contact or infected swimming pools, incubation 1-3 weeks Infection produces 1 or more umbilicated nodules on the skin/eyelid margin Clinical Manifestation: Chronic Follicular Conjunctivitis, multiple lesions may be present in immunocompromised pts (HIV+) ○ Translucent painless cutaneous nodules: umbilicated centers, erythematous base Diagnosis: detection of umbilicated nodules on eyelids + follicular conjunctivitis Management: spontaneous recovery may occur (months-years), surgical removal of E central core of lesion, cryotherapy How can you differentiate this from other eyelid bumps? Erin T Acute Hemorrhagic Conjunctivitis (RNA) ciznr.EE Short incubation period giving rapid spread as soon as you’re touched (maybe 1 day) Signs/Sx: sudden onset, rapid spread to fellow eye, follicular conjunctivitis, seromucus iii discharge, conjunctival hemorrhage, petechial hemorrhages (spread and become total EE a subconj heme), common to have 2º bacterial infection (mucopurulent conj, gonorrhea) Resolution in 5-10 days on itsownbutrarelycancauseparalysis Neurologic Sequelae: polio-like paralysis (1-8 weeks after conj), begins with fever, malaise, pain along a nerve root → paralysis Management: avoid corticosteroids!! (worsen condition, promote 2º infection, prolong recover), use prophylactic antibiotics Viral Follow-ups Non-specific Follicular: they’re very contagious and you're not initiating any Tx, if you wait until they’re not contagious, chances are they’re totally fine by then ○ Exception: if you did a Betadine wash (RTC after 4 days) or gave a steroid/abx combo (5-7 days for IOP check/sx relief) ○ Tell them to come back if vision gets blurry → may indicate EKC EKC: corneal involvement + you started a steroid (caution, still very contagious) AHC: more of a peace of mind for them, still caution because very contagious HSV Ocular Conditions HSV Epidemiology ○ Most common manifestation: orofacial lesion aka cold sore ○ Leading infectious cause of blindness in the US (2nd most for corneal blindness) HSV ISVType I I Ingijinglion body re I upper ○ Transmission: direct contact, open lesions, contaminated secretions Reactivation: lies dormant in the autonomic ganglia (trigeminal) or in corneal stroma re I Logi ○ Tendency to recur at certain sites (lips, cornea, genitals), cannot eradicate in latent state over2 to tango ○ Trigger mechanisms: emotional upset, fever, menstruation, sun, trauma, IC, med ○ Reactivation risks: Most never reactivate 1 reactivation = 40% chance for 2nd Episodes closer together or severity of 1st episode = ↑risk HSV Blepharoconjunctivitis (Classic and Erosive) →1º HSV ○ Signs/Sx: 1º usually in kids, key sign of vesicles on skin/eyelid margin (don’t scar) in viiiiii ○ Classic: pinhead vesicles along base of lashes/periocular skin, lid edema, lid dermatitis, resolve without scarring ○ Erosive-Ulcerative: erosions of mucocutaneous junction of lid → L AKA9 Also usually resolve without scarring, madarosis in ulcer HSV Bleph Management ○ Steroids contraindicated (good at suppressing inflammatory response of HSV but prolong virus by ↑viral shedding) ○ Skin lesions resolve w/in 2 weeks, restrain children from itching, warm compress r im ○ Antibiotic ointment if secondary infection (especially if ulcerative): Erythromycin or Ciloxan BID ○ Topical Antivirals useless, oral Famciclovir 250 mg TID, Acyclovir 400 mg 5x, Valacyclovir 500 mg TID → caution in kidney disease/IC patients Immunosupressed Infectious Epithelial (Dendritic) Keratitis → 1º HSV ○ Presentation of both primary and recurrent HSV infection (looks same, same tx) ○ Key Sx: ↓ corneal sensitivity (especially if recurrent), intense ciliary injection ○ Key Signs: Early punctate staining (w/more pain and photophobia than DES) that later take on dendritic pattern, dendrite bed stains w/NaFl, edges w/LG or RB ○ HSV = DECREASED CORNEAL SENSITIVITY Dueto ganglionloss ○ Lab Eval: in all cases of suspected neonatal herpes infection (↑ meningitis) Tests: Culture, ELISA, Elvis, HerpCheck, SureCell cyclopagi At ○ Management: Homatropine/scopolamine (dilate for pain), topical antivirals not OralFAV great, avoid steroids, oral antivirals FAV Follow up: HSV Bleph w/o corneal involvement: 3-5 days, with: 1-3 days Follow up for Dendritic Keratitis: 1-3 days an metamerret Post-infectious Keratitis (Geographic ulcer) → Recurrent Deoritickeratitis ○ Breakdown of epithelium during/after recovery from Dendritic-K, non-infectious ○ Dendriform area of epithelial erosion, with elevated heaped up borders thatwontstain ○ Management: lubrication, Muro 128 (hypotonic to draw water out of cornea, pulls layers of epi together to heal), prophylactic Abx (broad), BCL, topical antivirals not indicated b/c not infectious (use orals to treat HSV) → use orals instead x2 Famvir 500 BID, Acyclovir 800 5x, Valacyclovir 1000 TID → 14-21 days ○ “Tears every hour, amniotic membrane, oral antiviral, topical Abx (FQN)” ○ Conj white most likely neurotrophic and can’t feel anything/not irritated Stromal (non-necrotizing) → Recurrent ○ Non-necrotizing: inflammatory process (immune mediated) → not active infection  ○ Interstitial Keratitis: unifocal or multifocal interstitial haze/whitening of stroma Inferior corneal haze = stromal involvement → corneal neovascularization (kinda hard to see in pic) ○ Disciform Keratitis: a primary endotheliitis leading to a stromal issue Leads to disc-shaped stromal edema and epithelial edema with A/C rxn May also present with iridocyclitis, neo, Wessley immune ring, keratic precipitates on underlying endothelium (←see pic) ○ Management: If steroid (inflammatory so steroid ok), must use with an oral antiviral Must use strong steroid: Pred Acetate(QID - q2hr then taper every 1-2 weeks) for minimum 10 weeks + antiviral endotheliitis dosing then prophylactic dosing after 7-10 days (see table below) Disciform more sensitive to steroid than interstitial Cycloplegic BID for pain Stromal (necrotizing)→ Recurrent ○ Necrotizing = active virus/infection eating away at the cornea ○ Least common, cheese-like appearance, deep neovascularization, severe and progresses rapidly, overlying epithelial defect/ulceration (thinning/perforation) ○ Desmetocele: corneal perforation, only descemet’s showing ○ Management: oral antiviral (same dosage as geographic ulcers), reduce to prophylactic dose after 7-10 days + Pred acetate BID-QID + cyclo BID HSV Iridocyclitis ○ Often very mild (faint flare, few cells) but grossly elevated IOP!!! (40-70 mmHg) ○ Can also present with focal iris atrophy (illumination defects) ○ Management: oral acyclovir 400mg 5x daily, topical steroid + cyclo IOP responds well with beta-blockers HEDS Study ○ 1. Do topical steroids treat stromal keratitis? Yes, significantly ↓ stromal inflammation Pred 1 every 2his ○ 2. Is oral Acyclovir (+ steroids) helpful for stromal k? No (but we do it anyways) aday ○ 3. Is it useful for HSV Iritis? Not enough patients to determine Acyclovir yoong ○ 4. Does oral acyclovir prevent pts w/epithelial keratitis from developing stromal? No ○ 5. Does acyclovir prophylaxis minimize HSV recurrence? Yes by 50% Most useful for prophylaxis in cases of stromal-k to prevent recurrence, corneal scarring, and loss of vision SO RECAP of Non-Necrotizing Interstitial Keratitis: ○ “HEDS Algorithm”: Prednisolone q2hr, oral acyclovir 400 mg BID (or others), pred tapered every 1-2 weeks, continued for a minimum of 10 weeks Recurrent HSV Follow Ups Dadritinatitis ○ Geographic Ulcer: initially 24 hours, then 1-3 days ○ Interstitial and Disciform Keratitis: 1-3 days, then weekly ○ Necrotizing Keratitis: initially 24 hours, then 1-3 days, then weekly HSV Complications: diffuse PEE, Persistent Bullous Keratopathy (painful, lesions rupturing), irregular astigmatism, neo, neurotrophic keratitis (most common cause of NK, treat aggressively) iii was  Respects midline Herpes Zoster Ophthalmicus Primary Infection (Chicken Pox) Itinyrush posture ○ Ocular involvement is uncommon, eyelid vesicles (crust over) ○ Vesicle scrapings: Cytology, PCR, culture HZO differential: ○ HSV: presents with cluster of vesicles close together, recurrence not uncommon ○ Orbital Cellulitis (bacterial), contact dermatitis (doesn’t respect midline) Pathogenesis: adulthood (60-90), M=F ○ Risk factors: elderly, immunosuppressed, systemic malignancy, HIV, sx/trauma ○ HZO infects branches of CN V1: Lacrimal N., Frontal (upper lid, forehead, superior conj), Nasociliary N. (sclera, cornea, iris, CB, choroid, side/tip of nose) ○ Hutchinson’s sign: herpes rash on the side, root, or tip of the nose → ocular inv. Clinical manifestation: headache, malaise fever, chills → neuralgic pain, hyperesthesia/edema of dermatome → clear vesicle eruption followed by yellowing/scarring Ocular Manifestations of HZO Lid Involvement ○ Mechanical ptosis, edema, bleph, trichiasis/madarosis, entropion/ectropion (from scarring), full-thickness lid loss Conjunctival involvement: mucopurulent conjunctivitis UsPh hinter Episcleritis is common (topical phenyl will vasoconstrict episcleritis) Corneal Epithelium Involvement Rainononoblbsonlystairsw RB ○ Coarse SPK, multiple pseudodendrites, nummular keratitis w/anterior stromal infiltrates, mucus plaque keratitis, disciform & interstitial keratitis ○ HSV vs. HZV Dendrites HSV: branching, flat, terminal end bulbs, stain well centrally with NaFl, peripheral cells/end bulbs stain with RB/LG (top pic ←) HZV: grayish, raised, “painted on appearance”, no end bulbs, stain poorly w/ NaFl, stain well with RB (bottom pic ←) Stromal Involvement ○ Nummular Keratitis: coin shape in superficial stroma below area of previous epithelial keratitis (anterior stromal infiltrates) ○ Disciform Keratitis: similar to HSV ○ Interstitial Keratitis: neovascularization with “leash of vessels” to area of scarring (pic →) ⇒ exude lots of lipid → opacification Uveal Involvement ○ Chronic uveitis: most common presentation of ocular involvement ○ Fine KPs, faint flare and moderate cells (similar to HSV) ○ Iris atrophy w/permanent sphincter damage, often associated ↑IOP (trabeculitis) HZV uveitis: more chronic (lasts more than 2 months) HSV uveitis: more recurrent (gets better faster, happens again frequently) ○ Oral antiviral and topical steroids are effective Retinal Involvement: Acute Retinal Necrosis (ARN), more in immunocompromised Management  Iiii ○ Famciclovir 500 TID, Acyclovir 800 5x daily, Valacyclovir 1000 TID ○ Ideally start Tx w/in 72 hours from first lesion to ↓ postherpetic neuralgia risk ○ Lesions: Acyclovir cream TID, Antibiotic/steroid cream TID (erythromycin) ○ Topical steroids for uveitis (+ cyclo) and stromal involvement iiiiiii iii ○ Oral steroids for patients >60 y/o, ↓ pain, controversial (may prolong virus) Vaccination ○ Zostavax: live attenuated, same strain in Varivax (chicken pox vaccine), not available in usa ○ Shingrex: 2017 FDA approved for prevention of shingles, inactivated virus (50+) Patient Education Questions ○ Am I contagious? Yes, spread via contact and airborne, can cause a 1º infection ○ For how long? Until the lesions crust, approximately 14 days Complications of HZO Systemic: PHN, meningoencephalitis, CN VII palsy, Ramsay Hunt Syndrome (ear vesicles) Ocular: glaucoma (2º to uveitis), CN III palsy, optic neuritis, chorioretinitis, ARN/PORN Post-Herpetic Neuralgia (PHN): painful abnormal persistent sensations, ↓ QOL of pts ○ Ex: Chronic fatigue, anorexia, weight loss, depression/anxiety → suicide in elderly ○ Treatment: Topical: cold compresses, capsaicin, Lidocaine TCAs: amitriptyline; Anticonvulsants: LyricaAKAPregabalin mono Epstein-Barr Virus Pathogenesis: transmission via salive, subclinical infection in 1st decade of life, may be acquired later in life → infectious mono, lies latent in B-cells and pharyngeal mucosal epi Clinical Manifestation: most common vial anamnatin cause of acute dacryoadenitis (lac gland virus) ○ Also acute follicular conjunctivitis, bulbar conj nodules, Stromal Keratitis: ○ Type I: subepithelial infiltrates, similar to adenovirus keratitis ○ Type II: blotchy infiltrates, active inflammation, ring shaped opacities ○ Type III: deep/full thickness peripheral infiltrates, +/- vascularization (like syphilis) Management ○ Acyclovir is not effective for mono, don’t know if help corneal issues ○ Topical steroid for EBV stromal keratitis + prophylactic antiviral Oral Antiviral Uses Drug: HSV (7-10 days) HSV (Prophylactic) Endotheliitis Necrotizing/Geographic Iridocyclitis HZO (7-14 days) Famvir 250 TID 250 BID 250 BID 500 BID 500 TID Acyclovir 400 5x daily 400 BID 400 5x daily 800 5x daily 400 5x daily 800 5x daily Valacyclovir 500 TID 500 qday 500 BID 1000 TID 1000 TID