Notes on Sensory Pathophysiology: Eye and Ear Disorders

Glaucoma

• Definition and significance- Glaucoma is a group of eye diseases driven by intraocular hypertension (IOP) that damages the optic nerve.

  • Key consequences: progressive peripheral visual field loss; leading cause of irreversible blindness worldwide.

  • Prevalence: affects more than 70,000,000 people globally; about 0.10 (10%) of cases are bilaterally blind.

  • Often asymptomatic until late stages.

• Pathophysiology- Aqueous humour drainage pathway becomes partially/completely blocked, hindering drainage.

  • Fluid accumulation increases intraocular pressure (IOP).

  • Elevated IOP leads to optic nerve changes: atrophy of the optic nerve rim and loss of peripheral vision; nerve cell loss causes visual field loss.

• Types- Open angle glaucoma (most common)

  • Closed angle (angle-closure) glaucoma

• Open-angle glaucoma (OA-Glaucoma)- Angle between cornea and iris remains open.

  • Pathogenesis: aqueous humour flow impairment through the trabecular network -> increased IOP.

  • Epidemiology: most common form; typically presents in the 6th decade of life; develops gradually and is often asymptomatic.

  • Consequences: can lead to permanent vision damage if not screened and treated.

  • Screening: regular intraocular pressure screening is key.

• Closed-angle glaucoma (CA-Glaucoma)- Anatomical narrowing/closure of the anterior chamber angle -> reduced drainage of aqueous humour -> increased IOP -> optic nerve damage.

  • Medical emergency: vision loss can occur within 24 hours of symptom onset.

  • Pupil dynamics: dilation can worsen IOP; dark environments, stress, excitement, and certain meds can precipitate dilation.

• Primary vs Secondary glaucoma- Primary: no definitive cause; no pre-existing eye disease that caused the glaucoma.

  • Secondary: due to another condition or factor (e.g., ocular trauma, prolonged steroid use, tumors, inflammatory eye processes).

• Open-angle glaucoma – clinical features- Impairment of aqueous humor flow through the trabecular network -> higher IOP.

  • Common age range: around the 60s.

  • Clinical course: insidious progression with few or no symptoms in early stages; gradual vision loss.

  • Management focus: regular screening and treatment to reduce IOP and prevent progression.

• Closed-angle glaucoma – clinical features and emergency management- Acute presentation with severe symptoms: sudden eye pain, headache, blurred vision, halos around lights, nausea/vomiting.

  • Pupil typically mid-dilated and non-reactive to light.

  • Immediate medical attention required to prevent rapid vision loss.

• Signs, symptoms, and risk factors by glaucoma type- Open-angle: gradual peripheral vision loss; tunnel vision in advanced stages; signs include elevated IOP and optic nerve damage visible on exam.

  • Angle-closure: sudden, severe eye pain; headaches; vision changes; halos around lights; nausea/vomiting; reddened eye; corneal edema; mid-dilated pupil.

  • Secondary glaucoma: signs depend on underlying cause.

• Risk factors- Intraocular pressure (IOP) elevation is the most significant risk factor.

  • Age: risk increases with age, especially >60 years.

  • Family history: higher risk with family history.

  • Ethnicity: higher incidence in African Americans, Hispanics, and Asians.

  • Eye conditions: myopia (nearsightedness) and prior eye injuries contribute.

  • Medical conditions: diabetes, hypertension, autoimmune diseases.

  • Medications: long-term corticosteroid use can raise IOP.

  • Ocular anatomy: thinner corneas and shallow anterior chamber increase risk.

  • Previous eye surgery can elevate risk for secondary glaucoma.

  • Other factors: high myopia, low refractive errors, etc.

• Cataracts

• Definition and progression- Cataracts involve clouding of the eye’s lens due to protein clumping within the lens fibers.

  • Age-related: natural changes in the lens protein over time lead to cloudiness.

  • Pathophysiology: cloudiness reduces transmission of light through the lens.

• Lens changes and vision effects- Lens becomes harder with age, reducing flexibility.

  • Light scatter increases, leading to blurred vision and difficulty focusing light on the retina.

  • Color discrimination may decline.

• Causes of cataracts- Aging (most common)

  • Genetic factors (family history)

  • Medical conditions: diabetes, hypertension, obesity, etc.

  • Trauma or eye injuries

  • Medications: long-term corticosteroids and some other drugs

  • Environmental exposures: prolonged UV exposure and tobacco use

  • Radiation exposure

  • Alcohol consumption

  • Previous eye conditions (e.g., glaucoma) and obesity may contribute; poor nutrition can influence risk.

• Signs and symptoms- Blurry vision; particularly worsened at night.

  • Difficulty with night vision; increased sensitivity to light and halos around lights.

  • Yellowing or fading of colors.

  • Double vision in one eye; frequent changes in prescription glasses.

  • Overall deterioration in vision.

• Risk factors- Age: primary risk factor; more common with advancing age.

  • Family history.

  • Diabetes and systemic conditions; smoking and alcohol use.

  • Prolonged exposure to UV light.

  • Obesity and hypertension.

  • Long-term corticosteroid use and certain medications.

  • Previous eye conditions or surgeries.

  • Poor nutrition; low antioxidant intake.

• Macular Degeneration (AMD)

• Overview and epidemiology- AMD is a leading cause of vision loss in older adults.

  • Global burden: accounts for 8.7% of all blindness worldwide.

  • In Australia: approximately 1/7 of Australians over age 50 have some evidence of AMD.

  • Central vision is affected due to macular deterioration; can cause a central blind spot (scotoma).

  • Typical progression is gradual but can advance rapidly, causing severe vision loss in one or both eyes; damage is irreversible, but early detection and treatment may reduce the extent of loss.

• Pathophysiology- Complex interplay of genetic, environmental, and biochemical factors affecting the retinal pigment epithelium (RPE), photoreceptors, and other retinal components.

  • The macula (central retina) provides normal central vision; cones dominate central vision while rods support night vision.

  • RPE dysfunction disrupts nutrient/waste exchange between retina and choroid, leading to waste accumulation and impaired signaling to the brain, causing blurred vision.

• Causes and risk factors- Age: risk increases significantly after age 50.

  • Genetics: family history; CFH gene variants increase risk.

  • Environment: smoking increases oxidative stress and reduces retinal blood flow; UV exposure; diet low in antioxidants (vitamins C/E, lutein, zeaxanthin); high saturated fat intake.

  • Obesity and cardiovascular disease: higher BMI and vascular factors contribute.

  • Ocular history: prior eye diseases or surgeries; chronic inflammation within the eye.

  • Hormonal factors: possible influence (e.g., menopause effects).

  • Ethnicity: Caucasians at higher risk.

• Signs and symptoms- Distorted or blurred central vision; difficulty recognizing faces or reading fine print.

  • Central scotoma (central blind spot).

  • Night vision difficulties; colors appear faded.

  • Metamorphopsia: straight lines appear wavy or bent.

  • Peripheral vision changes may occur as AMD progresses; glare sensitivity.

• Outward appearance (context)- Visual aids (illustrations) show differences: normal retina, cataracts, glaucoma, AMD as observed in the back of the eye.

• Otitis Media (OM)

• Overview and epidemiology- OM is an infection/inflammation of the middle

• ear, typically starting from Eustachian tube dysfunction leading to fluid accumulation and infection.

  • Prevalence: about 80% of children experience OM at least once.

  • In Australia, OM accounts for about 0.10 of primary care consultations in children.

  • Recurrent OM reduces quality of life for children and parents and has long-term burden due to potential hearing loss.

  • In adults, OM is less common; smoking increases risk.

• Pathophysiology and mechanisms- Eustachian Tube Dysfunction: Eustachian tube connects middle ear to nasopharynx, equalizes pressure, allows drainage; dysfunction leads to negative middle-ear pressure and fluid accumulation.

  • Microbial infection: AOM often follows URI; common pathogens include Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis.

  • Otitis Media with Effusion (OME): fluid accumulation without active infection, may follow AOM or result from persistent Eustachian tube dysfunction.

  • Immune response: presence of pathogens/fluids triggers proinflammatory cytokines, swelling of middle ear mucosa, worsened Eustachian tube dysfunction, creating a cycle of fluid retention and infection.

• Complications and chronic changes- Acute complications: spread to surrounding structures (e.g., mastoiditis, rare meningitis).

  • Chronic OM: persistent middle-ear effusion, potential long-term hearing loss or speech delay in children.

  • Structural changes: tympanic membrane perforation; cholesteatoma development.

• Signs and symptoms- Severe ear pain due to pressure from fluid and inflammation.

  • Hearing loss (often temporary) during OM/OME.

  • Persistent middle-ear effusion reduces hearing, impacting speech and language development in children.

  • Irritability, sleep disturbances from pain.

  • Tugging at the ear in children due to discomfort.

  • Fever and inflammation;

  • Fluid drainage from the ear when tympanic membrane perforates.

  • Balance issues due to fluid affecting the inner ear (cochlea/balance organs).

• Risk factors- Age: highest risk in children under 2 years.

  • Eustachian tube dysfunction.

  • Recurrent upper respiratory infections.

  • Allergies causing nasal congestion that blocks Eustachian tubes.

  • Exposure to tobacco smoke.

  • Daycare attendance (higher exposure to URIs).

  • Family history of OM.

  • Cleft palate/anatomical abnormalities affecting Eustachian tube function.

  • Immune system deficiency.

  • Crowded living conditions.

• Ménière's Disease

• Overview and epidemiology- Inner-ear disorder causing severe vertigo, tinnitus, and hearing loss.

  • Prevalence is not precisely known in Australia, but an estimate is around 40,000 Australians affected.

  • Onset typically in the 3rd decade of life; symptoms are rare to begin after age 60.

  • Not life-threatening, but significantly affects quality of life; no cure, but symptoms can be managed.

• Pathophysiology- Central mechanism: abnormal accumulation of endolymph fluid in the inner ear (cochlea and vestibular system).

  • Endolymphatic hydrops increases fluid pressure in the endolymphatic space, causing dilation of inner-ear structures.

  • This disrupts hair cell function in the cochlea (hearing) and vestibular system (balance).

  • Over time, structural changes damage hair cells, contributing to tinnitus, fluctuating hearing loss, and balance problems.

• Causes- Swelling of the endolymphatic sac disrupts filtration/excretion of inner-ear fluid.

  • Otitis media, head injury, viral illnesses (respiratory infections).

  • Use of certain medications such as aspirin.

• Signs and symptoms- Vertigo (episodic spinning sensation), dizziness, and imbalance.

  • Tinnitus and headaches; abdominal discomfort and diarrhea can accompany.

  • Hearing may recover between attacks but tends to worsen with time.

  • Nystagmus (involuntary eye movements) can occur during vertigo.

  • Low-frequency hearing loss tends to be affected first.

• Hearing loss

• Overview and types- Hearing loss is impairment of auditory function and can be categorized as conductive, sensorineural, or mixed.

• Conductive hearing loss- Pathophysiology: impairment of sound transmission through the outer canal, tympanic membrane, or middle-ear ossicles.

  • Common causes/risk factors:

  • Earwax impaction blocks sound transmission.

  • Eustachian tube dysfunction causing middle-ear fluid and impaired vibration of the tympanic membrane/ossicles.

  • Middle-ear infections (OM) disrupt ossicle movement.

  • Ossicular chain disruption (otosclerosis, dislocation).

  • Outer-ear abnormalities affecting sound entry.

• Sensorineural hearing loss- Pathophysiology: damage to inner ear (cochlea) or auditory nerve pathways.

  • Causes/risk factors:

  • Aging (presbycusis): degeneration of sensory hair cells and spiral ganglion cells.

  • Noise-induced hearing loss: prolonged exposure to loud sounds damaging hair cells.

  • Ototoxic medications: aminoglycoside antibiotics, some chemotherapy agents harming hair cells.

  • Infections: viral/bacterial inner-ear infections (labyrinthitis, meningitis potential involvement).

  • Genetic factors: hereditary inner-ear abnormalities.

• Mixed hearing loss- Involves a combination of conductive and sensorineural components.

  • Examples include concomitant earwax obstruction with age-related cochlear changes; other combinations as applicable.

• Practical considerations and implications- Understanding the type of hearing loss guides treatment (e.g., address conductive components with wax removal or tubes; manage sensorineural loss with amplification, cochlear implants, or rehab).

  • Early detection and management of AMD, glaucoma, and OM can preserve quality of life and communication abilities.