EENT Clinical Medicine & High-Yield Disorders

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Comprehensive vocabulary practice flashcards covering eye, ear, nose, throat, oral, dental, and neuro-ophthalmologic disorders, their pathophysiology, clinical presentations, diagnostic findings, and emergency treatments.

81 Terms

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Blepharitis

Chronic inflammation of the eyelid margins caused by bacterial overgrowth (commonly staphylococcal) and/or meibomian gland dysfunction, leading to abnormal lipid secretions, tear-film instability, and ocular surface irritation. Manifests with burning, gritty irritation, eyelid margin erythema, and scales or flaking/crusting around eyelash bases. Managed with warm compresses, lid hygiene, artificial tears, and addressing associated rosacea or seborrheic dermatitis.

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Chalazion

A chronic, sterile lipogranulomatous inflammation caused by obstruction of a meibomian gland leading to retained lipid secretions. Presents as a firm, gradually developing, non-tender, painless eyelid nodule (which may follow an acute focal lid infection). Managed with warm compresses and lid massage; persistent, atypical, or recurrent lesions in the same location require ophthalmology referral for biopsy to exclude sebaceous gland carcinoma.

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Hordeolum (Stye)

An acute, localized staphylococcal infection or abscess of an eyelid gland (external involving glands of Zeis or Moll; internal involving meibomian glands). Presents as an acute, tender, erythematous, focal eyelid nodule. Managed with warm compresses; patients should be advised not to squeeze the lesion.

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Ectropion

Outward rotation of the eyelid margin, leading to displacement of the punctum away from the tear lake. Etiologies include involutional changes, facial nerve palsy, cicatrix, or mechanical forces. Presents with epiphora (excess tearing), corneal exposure, irritation, and dryness. Managed with ocular lubricants for surface protection and referral for definitive surgical correction.

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Entropion

Inward rotation of the eyelid margin, usually affecting the lower lid, causing eyelashes to rub against the corneal surface. Typically caused by involutional laxity, chronic inflammation, or cicatricial scarring. Presents with foreign-body sensation, tearing, conjunctival injection, and risk of corneal abrasions. Managed with ocular lubrication and definitive surgical repair.

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Dacryoadenitis

Infection or immune-mediated inflammation of the lacrimal gland located in the superolateral orbit. Manifests with acute pain, tenderness, erythema, and swelling over the superolateral eyelid/orbit, S-shaped ptosis, and possible pain with extraocular movements. Managed with supportive care for viral causes or systemic antibiotics for bacterial infection.

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Dacryocystitis

Infection and inflammation of the lacrimal sac, usually caused by tear duct obstruction resulting in tear stasis and secondary bacterial overgrowth. Presents with painful, erythematous swelling over the medial canthus and tear drainage area, tearing, and reflux of purulent material from the punctum upon pressure. Managed with systemic antimicrobial therapy and eventual definitive correction of the ductal obstruction.

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Dacryostenosis

Narrowing or blockage of the nasolacrimal passage, most commonly caused by congenital delayed canalization (typically at the valve of Hasner). Characterized by persistent tearing, tear overflow, and mucoid discharge in infants without marked conjunctival injection or acute erythema. Most congenital obstructions resolve spontaneously with observation and gentle massage.

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Keratoconjunctivitis Sicca

Disorder of the ocular surface driven by tear film instability and hyperosmolarity resulting from aqueous deficiency or increased evaporation (associated with Sjogren disease, meibomian dysfunction, aging, or antihistamines). Manifests as burning, dryness, gritty foreign-body sensation, fluctuating blurry vision, and paradoxical tearing. Slit-lamp exam shows diffuse punctate epithelial defects and a shortened tear break-up time; managed with artificial tears and environmental modification.

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Corneal Abrasion

Superficial epithelial defect of the clear front ocular surface that exposes underlying sensory nerve endings. Manifests with acute severe eye pain, foreign-body sensation, photophobia, tearing, and conjunctival injection. Fluorescein staining reveals a discrete, bright green epithelial defect under cobalt-blue light without a stromal infiltrate. Managed with removal of foreign bodies, topical antibiotics (covering Pseudomonas in contact lens wearers), oral analgesics, and avoiding eye patching or topical corticosteroids.

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Seidel Sign

A bedside diagnostic test using fluorescein and cobalt-blue illumination where leaking aqueous humor streams through and dilutes the concentrated dye on the ocular surface. A positive test indicates a full-thickness corneal or scleral perforation and open globe rupture; testing should not be provoked if an open globe is already obvious.

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Orbital Blowout Fracture

Fracture of the thin bony eye socket floor (maxillary bone) or medial wall caused by blunt facial trauma from hydraulic or buckling forces. Presents with periorbital swelling, ecchymosis, enophthalmos, diplopia (especially on upward gaze due to inferior rectus muscle entrapment), and infraorbital nerve (CN V2\text{CN}\,V_2) numbness. Diagnosed via non-contrast maxillofacial/orbital CT (bone windows); initial care includes ice, protecting the eye, and avoiding nose blowing.

<p>Fracture of the thin bony eye socket floor (maxillary bone) or medial wall caused by blunt facial trauma from hydraulic or buckling forces. Presents with periorbital swelling, ecchymosis, enophthalmos, diplopia (especially on upward gaze due to inferior rectus muscle entrapment), and infraorbital nerve ($$\text{CN}\,V_2$$) numbness. Diagnosed via non-contrast maxillofacial/orbital CT (bone windows); initial care includes ice, protecting the eye, and avoiding nose blowing.</p>
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Globe Rupture

A full-thickness traumatic wound of the cornea and/or sclera leading to loss of intraocular integrity, hypotony, and prolapse of intraocular contents. Signs include severe pain, markedly decreased vision, peaked or irregular pupil, hyphema, large subconjunctival hemorrhage, shallow anterior chamber, and visible uveal prolapse. Requires an emergent rigid eye shield, systemic antibiotics, tetanus update, antiemetics, and urgent surgical repair; tonometry and ocular manipulation are contraindicated.

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Hyphema

Accumulation of blood layering in the anterior chamber of the eye, most commonly caused by blunt ocular trauma, which can obstruct the Canal of Schlemm and elevate intraocular pressure (IOP). Graded: Grade 1 (<33%< 33\% filling), Grade 2 (33–50%33\text{--}50\%), Grade 3 (50–99%50\text{--}99\%), and Grade 4/8-ball (100%100\% completely filled). Managed with head elevation, an eye shield, avoidance of NSAIDs and antiplatelets, cycloplegics, and close ophthalmology follow-up to monitor for ghost cell glaucoma.

<p>Accumulation of blood layering in the anterior chamber of the eye, most commonly caused by blunt ocular trauma, which can obstruct the Canal of Schlemm and elevate intraocular pressure (IOP). Graded: Grade 1 ($$< 33\%$$ filling), Grade 2 ($$33\text{--}50\%$$), Grade 3 ($$50\text{--}99\%$$), and Grade 4/8-ball ($$100\%$$ completely filled). Managed with head elevation, an eye shield, avoidance of NSAIDs and antiplatelets, cycloplegics, and close ophthalmology follow-up to monitor for ghost cell glaucoma.</p>
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Orbital Compartment Syndrome

A vision-threatening emergency resulting from rapid accumulation of a retrobulbar hematoma following trauma, which decreases circulation to the optic nerve. Signs include severe pain, decreased visual acuity, proptosis, resistance to retropulsion, and significantly elevated intraocular pressure. Treated emergently with lateral canthotomy with cantholysis to decompress the orbit.

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Corneal Ulcer

A focal epithelial defect of the clear front surface of the eye accompanied by underlying stromal infiltration and inflammation, most commonly bacterial (Pseudomonas in contact lens wearers, which can cause perforation within 24 hours24\,\text{hours}), viral (HSV), fungal, or parasitic (Acanthamoeba). Manifests with pain, redness, photophobia, tearing, decreased vision, and a visible white opacity/infiltrate; managed with urgent ophthalmology referral, cultures, and intensive topical antibiotics while strictly avoiding corticosteroids.

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Herpetic Keratitis

Ocular surface infection caused by reactivation of herpes simplex virus (HSV) latent in the trigeminal ganglion. Hallmark presentation includes unilateral eye pain, photophobia, redness, and a classic branching dendritic epithelial ulcer with terminal bulbs seen on fluorescein staining under cobalt-blue illumination. Treated with topical (ganciclovir, trifluridine) or oral (acyclovir, valacyclovir) antivirals; topical corticosteroids are strictly contraindicated during active epithelial disease.

<p>Ocular surface infection caused by reactivation of herpes simplex virus (HSV) latent in the trigeminal ganglion. Hallmark presentation includes unilateral eye pain, photophobia, redness, and a classic branching dendritic epithelial ulcer with terminal bulbs seen on fluorescein staining under cobalt-blue illumination. Treated with topical (ganciclovir, trifluridine) or oral (acyclovir, valacyclovir) antivirals; topical corticosteroids are strictly contraindicated during active epithelial disease.</p>
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Anterior Uveitis (Iritis)

Inflammation of the iris and/or ciliary body disrupting the blood-aqueous barrier, often idiopathic or associated with HLA-B27, systemic autoimmune conditions, or infections. Characterized by unilateral eye pain, consensual photophobia, blurred vision, ciliary flush (perilimbal injection), a small/irregular pupil from posterior synechiae, and anterior chamber cells and flare on slit-lamp exam. Managed urgently with cycloplegic drops and topical corticosteroids.

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Scleritis

Immune-mediated, potentially necrotizing inflammation of the deep fibrous outer tunic of the eye, frequently associated with systemic autoimmune diseases such as rheumatoid arthritis or granulomatosis with polyangiitis. Manifests as severe, deep, boring ocular pain that radiates to the forehead or jaw and worsens with eye movements, accompanied by deep violaceous vascular injection that does not blanch with topical phenylephrine. Managed with systemic NSAIDs, systemic corticosteroids, or immunomodulatory therapy.

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Pterygium

A benign, triangular fibrovascular proliferation of conjunctival tissue that advances across the limbus onto the cornea, driven by chronic exposure to UV radiation, wind, dust, and dry conditions. Presents as an asymptomatic or irritating fleshy growth on the nasal side of the eye that can induce astigmatism or obstruct the visual axis. Managed with UV protection, lubrication, and surgical excision if vision-limiting.

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Endophthalmitis

Severe, sight-threatening intraocular infection and inflammation involving the vitreous and aqueous humors, typically developing after intraocular surgery (e.g., cataract extraction), penetrating trauma, or via hematogenous spread. Manifests with rapidly worsening ocular pain, marked vision loss, hypopyon (white blood cell layering in the anterior chamber), and vitritis with a loss of red reflex. Managed emergently with intravitreal antibiotics (vancomycin and ceftazidime) and vitrectomy.

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Preseptal (Periorbital) Cellulitis

Infection of the eyelid and periocular soft tissues located anterior to the orbital septum, commonly arising from superficial skin trauma, insect bites, or hordeolum, predominantly in children <10 years< 10\,\text{years} old. Characterized by eyelid erythema and edema without proptosis, pain with extraocular movements, or visual impairment. Treated with oral antibiotics (e.g., amoxicillin-clavulanate) or IV antibiotics if severe.

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Postseptal (Orbital) Cellulitis

Serious suppurative infection involving the structures posterior to the fibrous boundary separating the superficial lid from the deeper eye socket, most commonly arising via direct extension from adjacent paranasal (especially ethmoid) sinusitis. Signs include fever, proptosis, external ophthalmoplegia, pain with extraocular movements, and vision changes. Diagnosed via CT with IV contrast and treated with inpatient admission, broad-spectrum IV antibiotics (e.g., vancomycin plus ceftriaxone), and emergency ophthalmology consult.

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Papilledema

Bilateral swelling of the optic nerve head (optic disc edema) resulting from elevated intracranial pressure. Presents with headache, nausea, vomiting, pulsatile tinnitus, and transient visual obscurations, while central visual acuity remains preserved early on. Fundoscopy demonstrates bilateral swollen optic discs with blurred margins and venous engorgement; mandates urgent neuroimaging prior to lumbar puncture.

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Nystagmus

Rhythmic, involuntary oscillation of the eyes that may be classified as horizontal, vertical, or torsional. Can stem from congenital visual disruption or acquired vestibular, cerebellar, toxic, or medication-related dysfunction. A new onset in adults mandates neuroimaging and vestibular workup.

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Strabismus

Misalignment of the visual axes caused by extraocular muscle, cranial nerve, or developmental disruption, categorized as esotropia (inward deviation), exotropia (outward deviation), hypertropia (upward deviation), or hypotropia (downward deviation). Evaluated using the corneal light reflex and cover-uncover tests; persistent ocular misalignment in childhood requires correction of refractive error, patching, or surgery to prevent irreversible amblyopia.

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Amblyopia

Functional reduction in best-corrected visual acuity in one or both eyes due to chronic disruption of normal binocular visual stimulation during childhood, commonly caused by strabismus, anisometropia (refractive asymmetry), or visual deprivation (e.g., cataract, ptosis). Treated during the sensitive developmental window with optical correction and patching or atropine penalization of the sound eye.

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Presbyopia

Normal age-related physiological loss of crystalline lens elasticity and ciliary muscle accommodative power, leading to difficulty focusing on near objects. Patients hold reading materials farther away and require near-vision correction such as reading glasses, bifocals, or progressives.

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Cataract

Opacification and fiber degeneration of the crystalline lens that impairs light transmission onto the retina. Risk factors include aging, diabetes mellitus, prolonged systemic corticosteroid use, UV radiation, and ocular trauma. Manifests with gradually progressive, painless blurry vision, glare, halos around lights at night, and a diminished red reflex; treated definitively with surgical phacoemulsification and intraocular lens implantation.

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Dry Age-Related Macular Degeneration (DAMD)

Gradual deterioration of central vision characterized by retinal pigment epithelium (RPE) dysfunction, geographic atrophy, and the accumulation of soft drusen in the central fundus. Manifests with difficulty reading, central blurring, and preserved peripheral vision; managed with lifestyle modifications (smoking cessation), regular monitoring, and AREDS antioxidant/vitamin formulations.

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Wet Age-Related Macular Degeneration (WAMD)

Advanced retinal condition driven by choroidal neovascularization (CNV) originating beneath the neurosensory layer, causing rapid leakage of subretinal fluid, hemorrhages, and scarring. Presents with acute or rapidly progressive central vision loss and metamorphopsia (straight lines appearing wavy). Managed promptly with intravitreal anti-VEGF injections (e.g., ranibizumab, bevacizumab, aflibercept, brolucizumab).

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Drusen

Extracellular waste deposits located between the retinal pigment epithelium and Bruch's membrane, serving as the hallmark of age-related maculopathy.

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Acute Angle-Closure Glaucoma

An ophthalmologic emergency caused by sudden obstruction of the anterior chamber drainage angle (frequently by pupillary block pushing the peripheral iris against the trabecular meshwork), producing a rapid elevation in intraocular pressure. Presents with sudden severe unilateral eye pain, headache, nausea/vomiting, blurry vision, rainbow halos around lights, a hazy/edematous cornea, and a mid-dilated, nonreactive pupil. Treated emergently with topical beta-blockers, alpha-2 agonists, systemic acetazolamide, IV mannitol, and definitive laser peripheral iridotomy.

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Chronic Primary Open-Angle Glaucoma

Progressive optic neuropathy characterized by loss of retinal ganglion cells and optic nerve cupping resulting from chronically increased resistance to aqueous humor outflow through an anatomically open trabecular meshwork. Usually asymptomatic early, gradually progressing to peripheral visual field loss ('tunnel vision'). Managed with IOP-lowering topical drops (first-line prostaglandin analogs like latanoprost), laser trabeculoplasty, or filtration surgery.

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Retinal Detachment

Separation of the neurosensory retina from the underlying pigmented epithelium, occurring via three mechanisms: rhegmatogenous (full-thickness break allowing fluid ingress), tractional (fibrous proliferation pulling inward, as in advanced diabetic eye disease), or exudative (fluid accumulation without tears). Presents with a sudden increase in floaters, photopsias (flashes of light), and a progressive dark curtain/shadow descending over the visual field without pain; repaired using laser photocoagulation, cryotherapy, vitrectomy, or pneumatic retinopexy.

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Central Retinal Artery Occlusion (CRAO)

Acute ischemic infarction of the inner retina caused by embolic or thrombotic blockage of its primary arterial supply. Manifests as sudden, profound, painless monocular vision loss with a relative afferent pupillary defect (RAPD). Fundoscopy reveals a pale, milky-white ischemic fundus with an accentuated foveal 'cherry-red spot' and attenuated vessels. Evaluated and managed emergently as an acute stroke equivalent.

<p>Acute ischemic infarction of the inner retina caused by embolic or thrombotic blockage of its primary arterial supply. Manifests as sudden, profound, painless monocular vision loss with a relative afferent pupillary defect (RAPD). Fundoscopy reveals a pale, milky-white ischemic fundus with an accentuated foveal 'cherry-red spot' and attenuated vessels. Evaluated and managed emergently as an acute stroke equivalent.</p>
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Central Retinal Vein Occlusion (CRVO)

Obstruction of major ocular venous outflow leading to high intravascular pressure, vascular congestion, ischemia, and widespread hemorrhage. Presents with sudden painless monocular vision loss or blurring; fundoscopy classically reveals extensive flame-shaped and dot-blot hemorrhages, tortuous engorged veins, cotton-wool spots, and optic disc edema ('blood-and-thunder' appearance). Managed with urgent ophthalmology evaluation, intravitreal anti-VEGF or steroid injections for macular edema, and panretinal photocoagulation for neovascularization.

<p>Obstruction of major ocular venous outflow leading to high intravascular pressure, vascular congestion, ischemia, and widespread hemorrhage. Presents with sudden painless monocular vision loss or blurring; fundoscopy classically reveals extensive flame-shaped and dot-blot hemorrhages, tortuous engorged veins, cotton-wool spots, and optic disc edema ('blood-and-thunder' appearance). Managed with urgent ophthalmology evaluation, intravitreal anti-VEGF or steroid injections for macular edema, and panretinal photocoagulation for neovascularization.</p>
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Amaurosis Fugax

Transient monocular vision loss caused by temporary ocular ischemia, typically resulting from atherosclerotic microemboli originating in the ipsilateral internal carotid artery or heart. Classically described as a painless 'curtain' or 'shade' passing vertically over the eye that resolves completely within seconds to minutes; acts as a retinal transient ischemic attack (TIA) requiring urgent vascular, carotid duplex, and cardiac evaluation.

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Giant Cell Arteritis (Temporal Arteritis)

A systemic granulomatous large-vessel vasculitis of extracranial carotid branches occurring in individuals ≥50 years\ge 50\,\text{years} old. Characterized by new headache, scalp tenderness, jaw claudication, fever, polymyalgia rheumatica symptoms, and acute ischemic optic neuropathy. Diagnosed by elevated ESR/CRP and confirmed by cranial arterial biopsy or duplex ultrasound; mandates immediate high-dose systemic corticosteroid therapy without waiting for biopsy to prevent irreversible bilateral blindness.

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Optic Neuritis

Acute inflammatory demyelinating injury of the second cranial nerve, strongly linked to multiple sclerosis. Classic presentation is a young adult woman with subacute unilateral vision loss, dyschromatopsia (reduced color vision), pain exacerbated by extraocular movements, and a relative afferent pupillary defect (RAPD); the disc may initially appear normal. Diagnosed via brain/orbital MRI and treated with IV methylprednisolone.

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Viral Conjunctivitis

Infection of the transparent membrane covering the sclera and inner lids most commonly caused by adenovirus, highly contagious via direct contact. Presents with acute unilateral redness that often spreads to the other eye, copious watery discharge, a gritty foreign-body sensation, lymphoid follicles on the tarsal surface, and tender preauricular lymphadenopathy. Managed supportively with cold compresses and hygiene counseling.

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Bacterial Conjunctivitis

Superficial pyogenic infection of the ocular mucosal lining caused by organisms including Staphylococcus aureus, Streptococcus pneumoniae, Haemophilus, or Moraxella. Characterized by thick purulent or mucopurulent discharge, morning eyelid matting/crusting, and tarsal papillae. Treated with topical antimicrobial eye drops (e.g., polymyxin/trimethoprim, fluoroquinolones).

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Allergic Conjunctivitis

An IgE-mediated type I hypersensitivity reaction of the ocular mucosal surface triggered by environmental allergens. Characterized by intense bilateral ocular pruritus, chemosis (edema), watery or stringy discharge, and tarsal papillae ('cobblestoning'), often accompanied by upper airway seasonal symptoms. Treated with topical antihistamine/mast-cell stabilizer drops and oral antihistamines.

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Nonproliferative Diabetic Retinopathy (NPDR)

Early to intermediate retinal microvascular disease driven by chronic hyperglycemia without abnormal vascular proliferation. Characterized on fundoscopy by microaneurysms, dot-blot hemorrhages, lipid-rich hard exudates, cotton-wool spots (nerve fiber layer infarcts), and venous abnormalities. Managed by optimizing glycemic, blood pressure, and lipid control, alongside regular ophthalmology surveillance.

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Proliferative Diabetic Retinopathy (PDR)

Advanced retinal microvascular complication driven by chronic hyperglycemia and ischemia-induced upregulation of VEGF, stimulating pathological abnormal vessel growth on the retina or optic disc. The fragile new vessels lead to severe complications including vitreous hemorrhage, fibrous proliferation, and tractional retinal detachment; treated with panretinal photocoagulation (PRP) and intravitreal anti-VEGF therapy.

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Diabetic Macular Edema

Accumulation of extracellular fluid within the central retina resulting from microvascular breakdown and hyperpermeability in individuals with chronic hyperglycemia, representing a leading cause of central vision loss in this population. Identified via optical coherence tomography (OCT) and treated with intravitreal anti-VEGF therapy or focal laser photocoagulation.

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Hypertensive Retinopathy

Retinal vascular damage produced by chronic or acute elevation of systemic blood pressure. Chronic findings include diffuse arteriolar narrowing, copper or silver wiring (vessel wall sclerosis), and arteriovenous (AV) nicking. Malignant blood pressure spikes produce flame-shaped hemorrhages, cotton-wool spots, hard exudates (macular star), and optic disc edema.

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Acoustic Neuroma (Vestibular Schwannoma)

A benign, slow-growing neoplasm arising from the myelin sheath of the balance branch of cranial nerve VIII. Classic presentation includes progressive unilateral sensorineural hearing loss, unilateral tinnitus, gait unsteadiness, and trigeminal (CN V\text{CN}\,V) facial numbness due to cerebellopontine angle compression. Screened with audiometry showing asymmetric sensorineural loss and confirmed by contrast-enhanced MRI.

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Meniere Disease

An inner ear disorder characterized by endolymphatic hydrops (excess fluid and pressure within the endolymphatic system). Diagnosed by episodic peripheral vertigo lasting 20 minutes to 24 hours20\,\text{minutes}\text{ to }24\,\text{hours}, fluctuating low-to-high frequency sensorineural hearing loss, tinnitus, and aural fullness. Managed with low-salt diet, avoidance of caffeine, alcohol, and nicotine, and diuretics (e.g., hydrochlorothiazide-triamterene).

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Benign Paroxysmal Positional Vertigo (BPPV)

The most common cause of peripheral vestibular illusion of motion, caused by canalithiasis (displaced otoconia freely floating in the semicircular canals, typically posterior). Characterized by sudden, brief spinning episodes lasting <60 seconds< 60\,\text{seconds} provoked by specific head position changes, without associated hearing loss. Diagnosed with the Dix-Hallpike maneuver (inducing vertigo and torsional/rotary nystagmus) and treated with the Epley canalith repositioning maneuver.

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Labyrinthitis

Inflammation involving both the cochlea and semicircular canals along with CN VIII, frequently following a viral upper respiratory infection. Manifests with acute, rapid onset of continuous peripheral vertigo, severe nausea/vomiting, and gait instability, accompanied by unilateral sensorineural hearing loss and tinnitus. Treated with systemic corticosteroids (prednisone) and short-term vestibular suppressants.

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Vestibular Neuritis

Acute, unilateral inflammation limited strictly to the balance branch of cranial nerve VIII, typically post-viral. Presents with abrupt, continuous, severe peripheral vertigo lasting >24 hours> 24\,\text{hours}, nausea, oscillopsia, gait instability, and spontaneous unidirectional horizontal-torsional nystagmus beating away from the affected side, without hearing loss or tinnitus; managed with short-term antiemetics and early rehabilitation.

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Conductive Hearing Loss

Auditory deficit resulting from mechanical obstruction or impaired sound transmission through the external auditory canal or middle ear (e.g., cerumen impaction, otitis media, tympanic membrane perforation, otosclerosis). On tuning fork examination, the Weber test lateralizes to the affected (impaired) ear, and the Rinne test demonstrates bone conduction greater than or equal to air conduction (BC≥ACBC \ge AC) in the affected ear.

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Sensorineural Hearing Loss

Auditory deficit caused by damage to the cochlea (hair cells), auditory nerve (CN VIII\text{CN}\,VIII), or central processing pathways, driven by aging (presbycusis), loud noise exposure, or ototoxic drugs. On tuning fork evaluation, the Weber test lateralizes to the unaffected (better) ear, and the Rinne test exhibits a normal pattern where air conduction exceeds bone conduction (AC>BCAC > BC).

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Otosclerosis

An abnormal bony remodeling condition of the otic capsule resulting in progressive fixation of the stapes footplate against the oval window. Manifests in young to middle adulthood as progressive conductive or mixed hearing loss and tinnitus, with a normal-appearing eardrum on otoscopy. Managed with amplification (hearing aids) or surgical stapedectomy with prosthesis replacement.

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Otitis Externa

Infection and inflammation of the external auditory canal skin ('swimmer's ear'), commonly caused by Pseudomonas aeruginosa or Staphylococcus aureus. Manifests with intense canal pain, erythema, edema, purulent exudate, and exquisite pain on manipulation of the auricle, pinna, or tragus. Managed with canal debridement, topical acidifying solutions (mild), or topical ciprofloxacin with hydrocortisone (moderate-to-severe).

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Eustachian Tube Dysfunction (ETD)

Failure of the pharyngotympanic conduit to periodically dilate and regulate pressure between the nasopharynx and middle ear, leading to negative middle ear pressure. Presents with aural fullness, popping sensations, muffled hearing, and discomfort with atmospheric pressure changes; otoscopy may reveal eardrum retraction. Managed with intranasal corticosteroids, oral or topical decongestants, and autoinflation maneuvers.

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Acute Otitis Media (AOM)

Acute suppurative infection of the middle ear space with purulent effusion, predominantly affecting young children (6–24 months6\text{--}24\,\text{months} old) and caused by Streptococcus pneumoniae, Haemophilus influenzae, or Moraxella catarrhalis. Manifests with otalgia, ear tugging, fever, and a distinctively bulging, opaque, erythematous eardrum with decreased mobility. First-line therapy is high-dose amoxicillin, switching to amoxicillin-clavulanate if antibiotics were received in the prior 30 days30\,\text{days}.

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Chronic Otitis Media (COM)

Persistent or recurrent middle ear inflammation lasting >2–6 weeks> 2\text{--}6\,\text{weeks} in the presence of an eardrum perforation. Typically painless, it presents with chronic purulent otorrhea and conductive hearing loss, often involving Pseudomonas aeruginosa, Proteus, or Staph species; managed with careful aural toilet, topical fluoroquinolone drops, water precautions, and surgical tympanoplasty.

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Cholesteatoma

An abnormal, destructive accumulation of keratinizing squamous epithelium forming an expanding sac within the middle ear and mastoid, typically developing from a deep superior retraction pocket of the eardrum. Manifests with painless malodorous otorrhea, progressive conductive hearing loss, and vertigo; otoscopy classically reveals a pearly white keratin mass or crust in the attic/epitympanum. Treated definitively with surgical excision/mastoidectomy to prevent bony erosion and intracranial spread.

<p>An abnormal, destructive accumulation of keratinizing squamous epithelium forming an expanding sac within the middle ear and mastoid, typically developing from a deep superior retraction pocket of the eardrum. Manifests with painless malodorous otorrhea, progressive conductive hearing loss, and vertigo; otoscopy classically reveals a pearly white keratin mass or crust in the attic/epitympanum. Treated definitively with surgical excision/mastoidectomy to prevent bony erosion and intracranial spread.</p>
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Mastoiditis

Suppurative bacterial infection and bony erosion of the temporal air cells behind the pinna, occurring as a direct complication of acute otitis media. Signs include fever, persistent otalgia, postauricular erythema, tenderness, fluctuance, and downward/outward protrusion of the auricle. Diagnosed via temporal bone CT showing coalescence and loss of bony septae; treated with IV broad-spectrum antibiotics and surgical intervention if unresponsive.

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Tympanic Membrane Perforation

A tear or hole in the eardrum caused by infection (AOM), acoustic or mechanical trauma (e.g., cotton swabs), or otic barotrauma. Manifests with sudden relief of ear pain followed by hearing loss, bloody or purulent otorrhea, and tinnitus. Most small defects heal spontaneously; managed by keeping the ear dry, avoiding ototoxic topical aminoglycoside drops, and performing surgical myringoplasty if persistent.

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Auricular Hematoma

Subperichondrial accumulation of blood between the cartilage and overlying perichondrium of the pinna resulting from direct shearing trauma (wrestling, boxing, rugby). Deprives the underlying avascular tissue of perfusion, leading to ischemic necrosis and fibrocartilaginous remodeling known as 'cauliflower ear'. Managed with immediate evacuation (I&D) and application of a compressive bolster dressing to prevent reaccumulation.

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Nasal Polyps

Benign, pale, teardrop-shaped edematous mucosal overgrowths originating within the paranasal sinuses and nasal cavity due to chronic eosinophilic inflammation. Frequently associated with asthma, allergic rhinitis, and aspirin intolerance (Samter's triad). Presents with bilateral nasal obstruction, anosmia, rhinorrhea, and facial fullness; treated with intranasal corticosteroids and surgical excision for refractory cases.

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Allergic Rhinitis

An IgE-mediated type I hypersensitivity inflammatory reaction of the nasal mucous membranes provoked by inhaled aeroallergens. Characterized by paroxysmal sneezing, clear watery rhinorrhea, nasal pruritus, pale or violaceous boggy turbinates, infraorbital shiners, and a transverse nasal crease. Managed primarily with allergen avoidance and intranasal corticosteroid sprays.

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Epistaxis

Bleeding originating from nasal mucosal blood vessels, divided anatomically into anterior bleeds (most common, arising from Kiesselbach's plexus in Little's area) and posterior bleeds (more severe, arising from Woodruff's plexus/sphenopalatine artery branches, often associated with hypertension). First-line treatment is continuous direct compression of the lower soft third of the nose while leaning forward, followed by topical vasoconstrictors, silver nitrate cautery, or nasal packing (e.g., Rhino Rocket).

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Acute Rhinosinusitis (ARS)

Inflammation of the mucosal lining of the nasal cavity and paranasal sinuses lasting <4 weeks< 4\,\text{weeks}. Differentiated into viral etiology, which resolves within 7–10 days7\text{--}10\,\text{days} and is managed supportively, and bacterial etiology, characterized by symptoms persisting ≥10 days\ge 10\,\text{days} without improvement, severe onset (fever ≥39∘C\ge 39^\circ\text{C} with purulent discharge for 3–4 days3\text{--}4\,\text{days}), or a biphasic 'double-sickening' worsening; managed with amoxicillin-clavulanate when bacterial.

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Peritonsillar Abscess

Suppurative collection of pus tracking between the palatine tonsillar capsule and the superior pharyngeal constrictor muscle, typically complicating acute tonsillitis in adolescents and young adults. Manifests with severe unilateral sore throat, high fever, trismus, a muffled 'hot potato' voice, drooling, and extensive unilateral tonsillar bulge with contralateral displacement of the uvula. Treated with needle aspiration or incision and drainage, combined with systemic antibiotics covering GAS and oral anaerobes.

<p>Suppurative collection of pus tracking between the palatine tonsillar capsule and the superior pharyngeal constrictor muscle, typically complicating acute tonsillitis in adolescents and young adults. Manifests with severe unilateral sore throat, high fever, trismus, a muffled 'hot potato' voice, drooling, and extensive unilateral tonsillar bulge with contralateral displacement of the uvula. Treated with needle aspiration or incision and drainage, combined with systemic antibiotics covering GAS and oral anaerobes.</p>
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Ludwig Angina

A rapidly spreading, potentially fatal gangrenous cellulitis of the floor of the mouth involving the bilateral submandibular, sublingual, and submental fascial spaces, typically originating from an infected second or third mandibular molar. Characterized by woody brawny induration of the submandibular region, elevation and backward displacement of the tongue, trismus, fever, and stridor indicating impending airway compromise. Managed with emergent airway protection, broad-spectrum IV antibiotics (e.g., ampicillin-sulbactam or vancomycin plus Zosyn), and surgical decompression.

<p>A rapidly spreading, potentially fatal gangrenous cellulitis of the floor of the mouth involving the bilateral submandibular, sublingual, and submental fascial spaces, typically originating from an infected second or third mandibular molar. Characterized by woody brawny induration of the submandibular region, elevation and backward displacement of the tongue, trismus, fever, and stridor indicating impending airway compromise. Managed with emergent airway protection, broad-spectrum IV antibiotics (e.g., ampicillin-sulbactam or vancomycin plus Zosyn), and surgical decompression.</p>
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Epiglottitis

A rapidly progressive, life-threatening inflammation and edema of the supraglottic cartilaginous fold and aryepiglottic tissues that can cause acute airway obstruction, historically caused by Haemophilus influenzae type b (Hib). Classic presentation includes sudden high fever, sore throat, inspiratory stridor, and the '3 Ds': Dysphagia, Drooling, and Distress with forward tripod posturing. Soft-tissue lateral neck radiography shows an enlarged, swollen outline known as the 'thumb sign'; immediate management mandates securing the airway in a controlled setting.

<p>A rapidly progressive, life-threatening inflammation and edema of the supraglottic cartilaginous fold and aryepiglottic tissues that can cause acute airway obstruction, historically caused by Haemophilus influenzae type b (Hib). Classic presentation includes sudden high fever, sore throat, inspiratory stridor, and the '3 Ds': Dysphagia, Drooling, and Distress with forward tripod posturing. Soft-tissue lateral neck radiography shows an enlarged, swollen outline known as the 'thumb sign'; immediate management mandates securing the airway in a controlled setting.</p>
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Infectious Mononucleosis (EBV)

Infection caused by HHV-4 (a gammaherpesvirus) transmitted via saliva, infecting B lymphocytes and oropharyngeal epithelial cells. Presents with the classic triad of fever, posterior/diffuse cervical lymphadenopathy, and exudative pharyngitis, accompanied by profound fatigue and splenomegaly. Administration of ampicillin or amoxicillin classically induces a maculopapular rash; peripheral smear reveals atypical reactive lymphocytes; patients must avoid contact sports due to the risk of splenic rupture.

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Diphtheria

Infection caused by a toxigenic Gram-positive club-shaped bacillus that produces a potent exotoxin causing respiratory and cutaneous disease. Characterized by pharyngitis, low-grade fever, massive cervical lymphadenopathy giving a 'bull neck' appearance, and a tough, gray, adherent fibrinous pseudomembrane on the tonsils and posterior pharynx that bleeds on dislodgement. Managed with neutralizing antitoxin, antibiotics (erythromycin or penicillin), and airway monitoring.

<p>Infection caused by a toxigenic Gram-positive club-shaped bacillus that produces a potent exotoxin causing respiratory and cutaneous disease. Characterized by pharyngitis, low-grade fever, massive cervical lymphadenopathy giving a 'bull neck' appearance, and a tough, gray, adherent fibrinous pseudomembrane on the tonsils and posterior pharynx that bleeds on dislodgement. Managed with neutralizing antitoxin, antibiotics (erythromycin or penicillin), and airway monitoring.</p>
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Cytomegalovirus (CMV) Infection

A double-stranded DNA herpesvirus infection that establishes lifelong latency and reactivates during periods of immunosuppression (e.g., transplant recipients, HIV/AIDS, ICU patients). Congenital infection is a major TORCH pathogen causing sensorineural hearing loss; severe reactivated disease causes retinitis, esophagitis, pneumonitis, and colitis. Histopathology demonstrates pathognomonic large basophilic intranuclear inclusion bodies surrounded by a clear halo, known as 'owl's eye' inclusions; treated with ganciclovir.

<p>A double-stranded DNA herpesvirus infection that establishes lifelong latency and reactivates during periods of immunosuppression (e.g., transplant recipients, HIV/AIDS, ICU patients). Congenital infection is a major TORCH pathogen causing sensorineural hearing loss; severe reactivated disease causes retinitis, esophagitis, pneumonitis, and colitis. Histopathology demonstrates pathognomonic large basophilic intranuclear inclusion bodies surrounded by a clear halo, known as 'owl's eye' inclusions; treated with ganciclovir.</p>
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Sialadenitis

Bacterial inflammation and infection of a salivary gland (most commonly the parotid or submandibular gland), usually caused by Staphylococcus aureus in the setting of dehydration, ductal obstruction, or salivary stasis. Manifests as painful, tender, indurated glandular swelling that intensifies with meals, with purulent discharge expressible from Stensen's or Wharton's duct. Managed with hydration, warm compresses, gland massage, sialogogues, and antistaphylococcal antibiotics.

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Mumps

A highly contagious viral infection caused by a paramyxovirus, transmitted via respiratory droplets and saliva. Characterized by fever, malaise, headache, and acute, tender, painful parotitis (unilateral or bilateral). Unvaccinated patients are at risk for complications including orchitis (often unilateral with risk of testicular atrophy), pancreatitis, aseptic meningitis, and sensorineural hearing loss; prevented by the MMR vaccine.

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Aphthous Ulcers

Common, self-limiting, painful lesions of the non-keratinized oral mucosa (e.g., buccal and labial mucosa, floor of mouth) driven by local cell-mediated immune responses. Present as discrete, shallow, round-to-oval erosions with a necrotic yellow-gray fibropurulent base surrounded by a prominent erythematous halo; managed symptomatically with topical corticosteroids (e.g., triamcinolone dental paste) and topical analgesics.

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Oral Candidiasis (Thrush)

Opportunistic fungal infection of the oral mucosa caused by an opportunistic diploid yeast species, common in infants, denture wearers, patients on inhaled corticosteroids, and immunocompromised hosts. Characterized by white, curd-like plaques on the tongue, palate, and buccal mucosa that can be scraped off with a tongue depressor, leaving an underlying erythematous, raw, bleeding mucosal base. Diagnosed with KOH prep showing pseudohyphae; treated with topical nystatin oral suspension or oral fluconazole.

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Dental Caries

Infectious demineralization and breakdown of the calcified tooth structure (enamel and dentin) caused by organic acids produced when acidogenic plaque bacteria (predominantly Streptococcus mutans) metabolize dietary fermentable carbohydrates. Manifests as tooth pain, sensitivity to hot, cold, or sweets, and visible white-spot or cavitated brown/black enamel lesions; treated with topical fluoride, restorative fillings, or endodontic root canal therapy.

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Permanent Tooth Avulsion

The complete traumatic displacement of a secondary adult dentition unit from its alveolar bone socket, disrupting the periodontal ligament and neurovascular bundle. Represents a true dental emergency requiring immediate reimplantation within 60 minutes60\,\text{minutes} for optimal periodontal cell survival; the tooth must be handled solely by the crown without touching the root, and if immediate reimplantation is not possible, it should be stored in cold milk, Hank's Balanced Salt Solution, or saliva while seeking emergency dental care (primary teeth must never be reimplanted).

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Leukoplakia

A firmly adherent, keratotic white plaque or patch on the oral mucous membranes that cannot be rubbed or scraped off and cannot be characterized pathologically as any other specific disease. Strongly associated with chronic tobacco use, heavy alcohol consumption, and chronic mucosal irritation; considered a potentially premalignant lesion requiring biopsy to evaluate for oral epithelial dysplasia or squamous cell carcinoma.

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Oral Squamous Cell Carcinoma

The most common malignant neoplasm of the mouth and oropharynx, strongly linked to tobacco use, heavy alcohol consumption, and high-risk human papillomavirus (HPV). Classically presents in older adults as a persistent, non-healing, painless or painful ulcer with indurated borders, an exophytic mass, or non-scrapable red (erythroplakia) or white plaques, frequently on the lateral border of the tongue or floor of the mouth; diagnosed by tissue biopsy.