Outer layer: fiber layer

Middle layer: uvea

Inner layer: retina

Aqueous humor

lens

Vitreous body

Anterior chamber

back room

vitreous cavity

palpebral conjunctiva

bulbar conjunctiva

fornix conjunctiva

lacrimal gland

duct of tears

artery

vein

Innervates extraocular muscles

Nasociliary nerve

ciliary ganglion

retinitis pigmentosa

Late stage glaucoma

Retrobulbar optic neuritis

peripheral retinochoroiditis

homonymous hemianopia

Temporal hemianopia

Sector-shaped visual field defect

dark spot

Fluorescein fundus angiography FFA

Indocyanine green angiography ICGA

External blepharitis

Internal blepharitis

Early stage: local hot compress, oral antibiotics if systemic symptoms occur

Abscess formation, incision and drainage of pus

It has not become an abscess and should not be incised.

seborrhea

Eyelashes can be regenerated

Staphylococcus aureus infection

Eyelashes cannot regenerate and can lead to bald eyelashes

Common hair: outer canthus

Treatment: zinc sulfate eye drops, proper intake of vitamin B2

Herpes simplex virus type I

Varicella-zoster virus

Acute phase: saline or boric acid wet compress

Systemic antihistamines

Histological classification

Can occur in patients with high blood lipids

Prevalent: upper eyelid near canthus

Commonly occurs in the medial canthus of the lower eyelid

Most likely to occur on the upper eyelids

Commonly occurs at the skin and mucosal transition of the eyelid margin

Degenerative

Scarring

paralytic

Facial nerve palsy

(Often) Hypoplasia of the oculomotor nucleus or levator palpebrae superioris muscle

Oculomotor nerve palsy

Levator palpebrae superioris muscle injury

Sympathetic nerve damage

myasthenia gravis

Mechanical eyelid opening dysfunction

reflective

watery layer

Basic (main components of tear film)

include

Lipids (meibomian glands and Zeiss glands)

Mucin

"S" shape of upper eyelid

Treatment: Antibiotics or antivirals

proliferative inflammation

Mostly immune factors

Rarely tearing or popping eyes

Treatment: Immunosuppression, anti-inflammatory

lacrimal gland pleomorphic adenoma

Adenoid cystic carcinoma of the lacrimal gland (common)

Lacrimal gland pleomorphic adenocarcinoma

congenital

Acquired nature

"Crocodile Tears"

Do not perform lacrimal probing or lacrimal duct flushing

Surgical treatment of choice

It is more common in middle-aged and older women (the nasolacrimal ducts are narrower in women)

conjunctival hyperemia

conjunctival secretions

Nipple hyperplasia

follicle formation

True membrane and fake membrane

bulbar conjunctival edema

subconjunctival hemorrhage

conjunctival granuloma

conjunctival scarring

pseudoptosis

swollen lymph nodes before ear

clinical examination

Pathological examination

Cytological examination

Do not bandage the affected eye in the acute stage

hyperacute bacterial conjunctivitis

Acute or subacute bacterial conjunctivitis/acute catarrhal conjunctivitis

chronic bacterial conjunctivitis

epidemic keratoconjunctivitis

Pharyngeal conjunctivitis

enterovirus type 70

Incubation period: 18~48h

acute follicular conjunctivitis

subconjunctival hemorrhage

swollen lymph nodes before ear

Type A, B, C or Ba

Treatment duration: 3 to 8 weeks

identify

D～K type

Both humoral and cellular immunity are involved

Itchy eyes, worsened at night

Paving stone hyperplasia of palpebral conjunctiva

corneal shield ulcer

Horner-Trantas nodule

Wearing contact lenses or prosthetic eyes

Solid nodular vesicles at the limbus or bulbar conjunctiva

treat

Sjogren's syndrome

Stevens-Johnson syndrome

cicatricial pemphigoid

Infectious: bacteria, viruses, fungi, parasites

Endogenous: autoimmune

local spread

Causative factors ➡️Congestion of limbal vascular network

Corneal infiltration (localized gray-white opacities)

Ulcerative stage: corneal ulcer

ulcer resolution period

healing period

Eye pain, photophobia, tearing, blepharospasm

Clinical manifestations ➕Medical history (infectious? non-infectious?) ➕Laboratory diagnosis

Principle: remove the cause, control infection, promote scar healing, and reduce scar formation

Glucocorticoids (generally only used for non-ulcerative stromal keratitis)

pathogenic bacteria

clinical manifestations

treat

Cause

clinical manifestations

Primary herpes simplex virus infection

Recurrent herpes simplex virus infection

Cause

Point-like shedding ➡️ into flaky epithelial defects ➡️ ulcers ➡️ secondary infection, purulent corneal ulcer

Cause

autoimmune disease

The ulcer develops in a circular shape along the corneal limbus and infiltrates into the central area.

Cumulative superficial corneal calcific degeneration of Descemet's membrane

Good hair: youth

Bilateral peripheral corneal ectasia

Symmetrical corneal edge thinning and dilation (most common in the superior nasal quadrant)

Generally no pain or photophobia

Grayish white dots or patches

Chang Xian

Menopausal woman, both eyes

Progressive damage to corneal endothelium

Corneal droplets appear in the Descemet's membrane of the cornea

progressive loss of vision

Triad: Fleischer’s ring (siderosis) ➕ Vogt’s lines (increased stromal lamellar folds) ➕ Munson’s sign (cone compressing the lower eyelid margin)

Early, corneal topography

Early and mid-term vision correction

cornea transplant

visual impairment

Diplopia

cortical cataract

nuclear cataract

Posterior subcapsular cataract

medical treatement

Surgical treatment

genetics

environment

Vossius Ring

Diet therapy

Glass factory, steel factory

eyelid contusion

corneal contusion

Iris ciliary body contusion

lens contusion

Vitreous hemorrhage

Choroidal and retinal contusion

ruptured eyeball

corneal penetrating injury

Corneoscleral transmission injury

scleral transmission injury

Traumatic infectious endophthalmitis

Sympathetic ophthalmia

Traumatic proliferative vitreoretinopathy

Early stage

Post-traumatic inflammation and infection prevention and treatment

Second stage surgery

Determine whether strabismus or strabismus is apparent

Is there a tendency for the eyes to tilt?

Determine the degree of strabismus

Eye movements in the same direction

heterodirectional movement of eyes

Identify the authenticity of external rotation movement restrictions

In vertical strabismus, identify whether the primary paralyzed muscle is the superior oblique muscle or the superior rectus muscle of the other eye

Worth four-point light inspection

Bago linear microscopy

Red filter plus prism method

Measure paralyzed muscles

Precise glasses

Covering the dominant eye of monocular amblyopia

glasses

prism

Mydriatic and miotic agents

Botulinum toxin type A

Within 6 months

refractive accommodative esotropia

partial accommodative esotropia

High AC/A type accommodative esotropia

mixed accommodative esotropia

According to the relationship between the principal meridians

discitis

Retrobulbar optic neuritis

Demyelination (multiple)

Infect

autoimmune disease

Pain when moving the eyeballs

Uhthoff's sign

Multiple eyes in children

Visual field: central scotoma or concentric reduction of visual field

Relative afferent pupillary disorder RAPD (must and objective)

pseudooptic disc edema

Anterior ischemic optic neuropathy AION

Leber hereditary optic neuropathy LHON

Toxic or metabolic optic neuropathy

Combined intravenous corticosteroids

Downward

Upward

glioma

Optic nerve sheath meningioma

retinal edema

Retinal exudation

retinal hemorrhage

Exudative (serous) retinal detachment

PRE damaged

central retinal artery occlusion CRAO

branch retinal artery occlusion BRAO

Ciliary retinal artery occlusion

Retinal precapillary arteriolar occlusion—cotton wool spots

venous tortuosity

Retinal hemorrhage is flame-shaped and distributed along retinal veins

cystoid macular edema

Main reason: hardened arteries compression

More common in superior temporal branch obstruction

Classification

macular edema

Retinal neovascular hemorrhage

Non-value-added (simple) NPDR

Value-added PDR

control blood sugar

Severe NPDR and PDR, panretinal photocoagulation

Macular edema, macular grid photocoagulation

decreased vision

Vision becomes darker, deformed, or smaller

macular drusen

Pigmentary disorders and geographic atrophy

Treatment: Intravitreal injection of anti-VEGF drugs

Two major elements

The most common degeneration: lattice degeneration

Principle: seal the hole

diabetes, lipid particles

Iritis, iridocyclitis, anterior cyclitis

symptom

physical signs

Complicated cataract

secondary glaucoma

Low intraocular pressure and eye atrophy

acute conjunctivitis

acute angle closure glaucoma

panuveitis that can cause anterior uveitis

Principle: Dilate pupils immediately

Mostly caused by non-infectious factors and do not require antibiotics

The eyes change like sunset

Prodromal stage (within 1 to 2 weeks before the onset of grape inflammation)

Post-uveitis stage (within 2 weeks after uveitis occurs)

Anterior uveal involvement stage (about 2 weeks to 2 months after onset)

Recurrent period of anterior uveitis (2 months after onset)

First onset, glucocorticoids for more than one year

Relapse, immunosuppressants

Goldmann tonometer (gold standard)

Pupil block type (main)

Non pupillary block type

Multiple mechanisms coexist

acute angle closure glaucoma

chronic angle closure glaucoma

Unclear, related to the trabecular meshwork-Schlemm canal system

Paracentral scotoma and nasal step

Parasympathomimetic drugs (miotics): Pilocarpine (pilocarpine)

beta-blockers: timolol/timolidine

Carbonic anhydrase inhibitor: Acetazolamide

alpha2 agonist

Reduce aqueous humor production

Prostaglandin derivatives: latanoprost (Xalida)

hypertonic agent

medical treatement

hemolytic glaucoma

Characteristic expression

Enlarged cornea and deepened anterior chamber

Haab stripes