Glaucoma Flashcards
What are the parts of the ciliary body?
Pars plicata anteriorly
pars plana posteriorly
Where is aqueous humour produced?
by the ciliary processes of the pars plicata
What are the methods of secretion of the aqueous humour?
- Diffusion: due to a concentration gradient
- ultrafiltration: pressure gradient between oncotic and hydrostatic pressures (capillary verses intraocular pressures)
- Active (account for approx 80% of secretion): active transport is mediated by transmembrane aquaporin activated by Na+ / K+ ATPase enzye and carbonic anhydrase enzyme
how is aqueous humour secretion controlled?
by sympathetic (adrenergic innervation) system
B2 receptor stimulation = increases aqueous secretion and A2 receptor = decreased secretion
What is the composition of aqueous humour?
Water >99% of normal humour
Lower concentration of protein and glucose than plasma
higher concentration of ascorbic acid, chloride and lactate than plasma
similar concentration of sodium to plasma
Describe the different aqueous outflow routes
posterior –> Anterior
- trabecular out flow approx 70-90%%:
TM –> Schelmm’s Canal –> episcleral veins
-Uveoscleral outflow: ciliary muscle –> suprachoroidal space –> eventually drained by choroidal veins, emissary canal of sclera (vortex veins) or veins of ciliary body
What is the trabecular meshwork made up of?
inner –> outer
- uveal meshwork (innermost): contains relatively large holes
- corneosclera meshwork: contains smaller holes, accounting for greater resistance
Juxtacanalicular meshwork - connects the trabecular meshwork with Schlemm canals, contains narrow intercellular spaces supplies major part of the normal outflow resistance
What is Schlemm’s canal?
endothelial lined oval canal
situated circumferentially in the sclera sulcus
contains holes for collector channels which terminate in the episclera veins
What are the two parts of the optic nerve?
Neuroretinal Rim and Cup to Disc Ratio
What is the neuroretinal rim?
area of the optic disc
between margins of central cup and disc
contains retinal neuronal cells
Describe the neuroretinal rim
RIM IS THICKEST INFERIORLY, FOLLOWED BY SUPERIORLY, NASALLY AND THEN TEMPORALLY (‘ISNT’ RULE)
What happens to the neuroretinal rim during glaucoma?
it thins
What is the cup to disc ratio?
DEFINED AS THE VERTICAL DIAMETER OF THE OPTIC CUP DIVIDED BY THE VERTICAL DIAMETER OF THE OPTIC DISC
What is the normal cup to disc ratio?
NORMAL CD RATIO IS 0.3, SOME INDIVIDUALS MAY HAVE PHYSIOLOGICAL CUPPING OF 0.6 OR 0.7 WITHOUT GLAUCOMATOUS CHANGES
What is a trabeculectomy?
TRABECULECTOMY IS AN IOP-LOWERING SURGICAL TECHNIQUE
INVOLVES THE CREATION OF A FISTULA FOR AQUEOUS OUTFLOW FROM THE ANTERIOR CHAMBER TO THE SUB-TENON SPACE, CREATING A BLEB
What can be used to prevent bleb failure in a trabeculectomy?
ADJUNCTIVE USE OF ANTI METABOLITES MAY BE USED TO SLOW THE HEALING PROCESS IN ORDER TO PREVENT BLEB FAILURE
What are some examples of anti metabolites used?
F-FLUOROURACIL (5-FU): A PYRIMIDINE ANALOGUE WHICH INHIBITS FIBROBLASTS BY BLOCKING DNA SYNTHESIS
MITOMYCIN C: AN ALKYLATING AGENT WHICH ALSO INHIBITS FIBROBLASTS
What is ocular hypertension?
IOP > 21MMhG WITHOUT GLAUCOMATOUS DAMAGE
What percentage of people with OHT were found to then develop open angle glaucoma?
9.5%
What are the risk factors for conversion of OHTN to Open angle glaucoma?
OLDER AGE
HIGHER IOP
LARGE CUP/DISC RAITO
THINNER CCT: PATIENTS WITH A RELATIVELY THIN CENTRAL CORNEAL THICKNESS HAD 3.4 TIMES HIGHER RISK OF CONVERSION THAN PATIENTS WITH CCT > 558 UM
OTHER RISK FACTORS:
- AFRICAN AMERICAN ORIGIN
- MALES
- HEART DISEASE
What is the management for ocular hypertension?
REGULAR MONITORING
MEDICAL TREATMENT IS INDICATED IN CASES WITH PERSISTENT IOP> 30 OR WITH HIGH-RISK PROFILE PATIENTS
What is primary open angle glaucoma?
CHRONIC DISORDER CHARACTERISED BY GLAUCOMATOUS VISUAL FIELD DEFECTS DUE TO OPTIC NERVE DAMAGE
What genes have the potential to cause POAG?
MYOC AND OPTN GENE MUTATIONS
What are the features of POAG? (4)
OPEN ANTERIOR CHAMBER ANGLE
HIGH C/D RATIO AND THINNING OF THE NEURORETINAL RIM
RAISED IOP > 21mmHg
GLAUCOMATOUS VF DEFECTS
What Ix are used in POAG?
FUNDOSCOPY: EVALULATE OPTIC DISC
GONIOSCOPY: ASSESSMENT OF ANGLE
PACHYMETRY: MEASURE CCT
PERIMETRY: VISUAL FIELD TESTING
What is the management for POAG?
TOPIC IOP-LOWERING AGENTS SUCH AS PRSOTAGLANDIN ANALOGUES OR BETA BLOCKER
LASER TRABECULOPLASTY
TRABECULECTOMY IF FAILURE OF OTHER TREATMENTS
What is normal tension glaucoma?
A FORM OF POAG WITH A PERSISTENLY NORMAL IOP <21mmHg
What did the collaborative normal-tension glaucoma study group find?
reducing IOP by 30% reduced the risk of progression of NTG (12% risk of progression in treated group vs 35% in the untreated group)
What are some risk factors for normal tension glaucoma?
AGE, COMMONLY OLDER PATIENTS WITH POAG
RACE: EAST ASIAN E.G
CCT: COMMONLY LOWER THAN PATIENTS WITH POAG
SYSTEMIC VASCULAR DISEASE: CONDITIONS SUCH AS RAYNAUD PHENOMENON, MIGRAINES AND SYSTEMIC HYPOTENSION ARE MORE ASSOCIATED WITH NTG RATHER THAN POAG
What are some features of normal tension glaucoma?
SIMILAR TO POAG
NOTABLE DIFFERENCES:
- OPTIC NERVE HEAD CAN BE LARGER IN PATIENTS WITH NTG
- FLAME SHAPED HAEMORRHAGES ON OPTIC NERVE RIM ARE MORE COMMON IN NTG
What is primary angle closure glaucoma?
OCCLUSION OF THE TM, CAUSING OBSTRUCTION OF AQUEOUS OUTFLOW WITH THE POTENTIAL OF CAUSING A RISE IN IOP AND OPTIC NERVE DAMAGE
What are some differences between primary angle-closure suspect, primary angle closure and primary angle closure glaucoma?
- PRIMARY ANGLE CLOSURE SUSPECT: A NARROW ANGLE IN WHICH THE PERIPERHAL IRIS IS ALMOST TOUCHING THE TM
NO PERIPERHAL ANTERIOR SYNCHIAE (PAS) PRESENT
(PAS REFERS TO THE ADHERENCE OF THE PERIPHERAL IRIS ANTERIORLY IN THE ANTERIOR CHAMBER) - PRIMARY ANGLE CLOSURE (PAC): PAS+ ELEVATED IOP
HOWEVER, NO GLAUCOMATOUS OPTIC NERVE CHANGES - PRIMARY ANGLE CLOSURE GLAUCOMA: PACG: PAS + ELEVATED IOP + GLAUCOMATOUS CHANGES AND VF DEFECTS
What are some risk factors for primary angle closure glaucoma?
INCREASING AGE
EAST ASIAN RACE
HYPERMETROPIA
FAMILY HISTORY
SHORT AXIAL LENGTH OF THE EYE
What is the pathophysiology of Primary angle closure glaucoma?
RELATIVE PUPILLARY BLOCK:
- REPRESENTS THE MAJORITY OF ANGLE CLOSURE
CASES - FAILURE OF THE NORMAL AQUEOUS FLOW THROUGH PUPIL –> INCREASE IN PRESSURE DIFFERENCE BETWEEN THE POSTERIOR AND ANTERIOR CHAMBERS
RESULTS IN ANTERIOR BOWING OF THE PERIPHERAL IRIS LEADING TO ANGLE CLOSURE
RISK IS HIGHEST IN A MID-DILATED PUPIL DUE TO MAXIMUM CONTACT BETWEEN IRIS AND LENS AT THIS LEVEL
IRIS CONFIGURATION (NON-PUPILLARY BLOCK):
IMPORTANT PATHOPHYSIOLOGICAL MECHANISM IN THE EAST ASIAN DESCENTS
CHARACTERIZED BY A FLAT IRIS, NORMAL ANTERIOR CHAMBER DEPTH AND ANTERIORLY POSITIONED CILIARY PROCESSES WHICH DISPLACES THE IRIS BASE LEADING TOA NARROW / CLOSED ANGLE
What are the features of primary angle closure glaucoma?
SUDDEN ONSET HEADACHE, VOMITING, HALOES AND BLURRING OR TRANSIENT VISUAL LOSS
SYMPTOMS ARE EXACERBATED BY WATCHING TV IN A DARK ROOM, PAHRMACOLOGICAL MYDRIASIS OR READING
FIXED MID-DILATED PUPIL,
CORNEAL OEDEMA,
CONJUNCTIVAL HYPERAEMIA AND
HIGHLY RAISED IOP
RESOLVED ACUTE ATTACK, DESCEMET MEMBRANE FOLDS, LOW IOP AND GLAUKOMOFLECKEN
What is the management of primary angle closure glaucoma?
ACUTE: SUPINE POSITION, SYSTEMIC ACETAZOLAMIDE, TOPICAL BETA-BLOCKERS +/- ALPHA-2 AGONISTS +/- TOPICAL PREDNISOLONE
BILATERAL PERIPHERAL Nd: YAG LASER IRIDOTOMIES TO BE PERFORMED AFTER RESOLUTION OF ACUTE ATTACK
CATARACT EXTRACTION HAS SHOWN TO BE EFFECTIVE IN LOWERING IOP IN BOTH ACUTE AND CHRONIC STAGES OF THE DISEASE
What is neovascular glaucoma?
CAUSE OF EITHER SECONDARY OPEN OR CLOSED-ANGLE GLAUCMA
NVG OCCURS DUE TO PROLIFERATION OF FIBROVASCULAR TISSUE IN THE ANTERIOR ANGLE AND RESULTS FROM REBEOSUS IRIDIS
What are some causes of neovascularisation glaucoma?
ISCHAEMIC CENTRAL RETINAL VEIN OCCLUSION (CRVO) (NVG USUALLY OCCURS ABOUT 3 MONTHS AFTER ONSET OF CRVO ‘100-DAY GLAUCOMA’)
CENTRAL RETINAL ARTERY OCCLUSION
DIABETES MELLITUS
OCULAR ISCHAEMIC SYNDROME
RETINAL DETACHMENT
Describe the pathophysiology of neovascular glaucomoa
RETINAL ISCHAEMIA
HYPOXIA TO THE RETINA CELLS
RELEASE OF ANGIOGENIC FACTORS (VEGF AND IL-6)
THE RESULTS IS NEOVASCULARISATION OF THE ANTERIOR SEGMENT (IRIS AND IRIDOCORNEAL ANGLE) WITH SUBSEQUENT OVERLYING FIBROVASCULAR MEMBRANE FORMATION
What are the features of neovascular glaucoma?
NEW RADIALLY ORIENTATED VESSELS ON IRIS SURFACE AND PUPILLARY MARGINS
PAS AND POSTERIOR SYNECHIAE CAN FORM
CORNEAL OEDEMA
ELEVATED IOP WITH OPEN ANGLE AT BEGINNING –> FIBROVASCULAR TISSUE PROLIFERATION LEADING TO PAS FORMATION AND ANGLE CLOSURE
What Investigations are used for neovascular glaucoma?
ESTABLISH THE CAUSE OF RETINAL ISCHAEMIA
How is neovascular glaucoma managed?
PRP +/- INTRAVITREAL ANTI-VEGF INJECTIONS TO REDUCE NEOVASCULARISATION
MEDICAL TREATMENT
SIMILAR TO POAG
AVOID MIOTIC AGENTS, AS THEY CAN WORSEN
SYNECHIAL ANGLE CLOSURE
USE PROSTAGLANDIN ANALOGUES CAREFULLY AS
THEY MAY EXACERBATE OCULAR INFLAMMATION
OSMOTIC AGENTS CAN BE USED FOR CORNEAL
OEDEMA
What are the surgical options for neovascular glaucoma?
IF GOOD VISUAL PROGNOSIS = GLAUCOMA DRAINAGE DEVICE
IF BAD VISUAL PROGNOSIS = CYCLODIODE LASER (DESTRUCTION OF THE CILIARY BODY EPITHLEIUM LEADING TO REDUCTION OF AQUEOUS HUMOUR SECRETION)
TRABECULECTOMY CAN OFTEN RESULT IN BLEB FAILURE DUE TO SCARRING
What is pigment dispersion syndrome?
AN auto dominant
CAUSE OF SECONDARY OPEN ANGLE GLAUCOMA,
CHARACTERIZED BY EXCESSIVE SHEDDING OF PIGMENTED MATERIAL OF THE IRIS DEPOSITED THORUGH THE ANTERIOR SEGMENT
What population is pigment dispersion syndrome common in?
myopic males
What are the features of pigment dispersion syndrome?
BLURRED VISION AND HALOES ON EXERTION
FOLLOWING SIGNS MAY BE SEEN:
MID PERIPHERAL SPOKE LIKE DEFECT OF THE IRIS ON
TRANSILLUMINATION
INCREASED IOP AND GLAUCOMATOUS DRAINAGE
VERTICAL OVAL-SHAPED PIGMENTS ON THE
CORNEAL ENDOTHELIUM
TM PIGMENTATION
SAMPAOLESI LINE MAY BE PRESENT (A BAND OF
PIGMENTED ANTERIOR TO THE SCHWALBE LINE ON
GONIOSCOPY)
CONCAVE PERIPHERAL IRIS
What is the management of pigment dispersion syndrome?
AVOID EXTRANEOUS EXERCISE
MEDICAL TREATMENT IS SIMILAR TO POAG
PROSTAGLANDIN ANALOGUES ARE GENERALLY preferred
PILOCARPINE HAS SHOWN TO BE A PROPHYLACTIC MEASURE TO PREVENT EXERCISE INDUCED ELEVATION OF IOP
LASER TRABECULOPLASTY
TRABECULECTOMY
What are the risks of pilocarpine?
myopia and retinal detachment
What is pseudoexfoliation syndrome?
CAUSE OF SECONDARY OPEN ANGLE GLAUCOMA IN WHICH GREY-WHITE FIBRILLAR DEPOSITS BLOCK THE ANTERIOR CHAMBER ANGLE
What gene mutation is pseudoexfoliation syndrome associated with?
ASSOCIATED WITH MUTATION IN THE LOXL1 (ENZYME THAT CONTRIBUTES TO ELASTIC FORMATION)
which populations is pseudoexfoliation syndrome more common in?
MORE LIKELY TO PRESENT IN SCANDINAVIANS, FEMALES AGED >50
What are the Ix and Tx for pseudoexfoliation syndrome?
similar to POAG
What are the features of pseudoexfoliation syndrome?
INCREASED IOP AND GLAUCOMATOUS DAMAGE
FLAKY WHITE DEPOSITS ON THE ANTERIOR LENS CAPSULE
SAMPAOLESI LINE
PERIPUPILLARY DEFECT ON TRANSILLUMINATION SLIT LAMP
What is posner-schlossman syndrome?
DISORDER CHARACTERISED BY RECURRENT UNILATERAL ACUTE ATTACKS OF IOP ELEVATION
MAY CAUSE SECONDARY OPEN-ANGLE GLAUCOMA (UNCOMMON, ONLY IF REPEATED ATTACKS)
In which patients is posner-schlossman syndrome more common?
middle aged patients
What is posner-schlossman syndrome associated with? (microrganisms and antigens)
CMV
H. pylori
HLA-BW5
What are the features of posner-schlossman syndrome?
DISCOMFORT, HALOES AND BLURRED VISION
ANTERIOR CHAMBER INFLAMMATION
MYDRIASIS
What is the treatment for posner-schlossman syndrome?
TOPICAL STEROIDS AND IOP LOWERING AGENTS
What is phacolytic glaucoma?
A SECONDARY OPEN ANGLE GLAUCOMA
hypermature cataract –> leakage of lens protein –> trabecular obstruction
What are the features of phacolytic glaucoma?
PAINFUL RED EYE WITH PHOTOPHOBIA AND DECREASED VISION
CORNEAL OEDEMA, MATURE CATARACT AND WHITE PARTCILES MAY BE SEEN IN THE ANTERIOR CHAMBER
What is the treatment for phacolytic glaucoma?
TOPICAL OR SYSTEMIC: IOP-LOWERING AGENTS
DEFINITIVE TREATMENT: CATARACT EXTRACTION
WHAT IS PHACOMORPHIC GLAUCOMA?
AN ACUTE SECONDARY ANGLE-CLOSURE GLAUCOMA DUE TO A SWELLING OF A CATARACTOUS LENS POTENTIATING A PUPILLARY BLOCK
How does phacomorphic glaucoma present?
SIMILAR TO ACUTE PACG
What is the treatment for phacomorphic glaucoma?
IOP REDUCTION: SAME AS ACUTE PACG (AVOID MIOTICS, CAN POTENTIATE PUPILLARY BLOCK)
DEFINITIVE TREATMENT: CATARACT EXTRACTION
What is red cell glaucoma?
A HYPHEMA (COLLECTION OF BLOOD INSIDE THE ANTERIOR CHAMBER CAN FORM, USUALLY FOLLOWING BLUNT TRAUMA TO THE EYE, WHICH LEADS TO BLOCKAGE OF THE TM LEADING T ORAISED IOP AND SECONDARY OPEN ANGLE GLAUCOMA
A SECONDARY BLEED MAY OCCUR 3-7 DAYS POST INITIAL INJURY
What is ghost cell glaucoma?
A TYPE OF SECONDARY OPEN ANGLE GLAUCOMA OCCURRING 2-4 WEEKS AFTER A VITREOUS HAEMORRHAGE DUE TO TM OBSTRUCTION WITH RED BLOOD CELLS
What is angle recessions glaucoma?
A CHAUSE OF CHRONIC SECONDARY OPEN ANGLE GLAUCOMA DUE TO CILIARY BODY RUPTURE CAUSED BY BLUNT TRAUMA
What does gonioscopy show in angle recession glaucoma?
GONIOSCOPY SHOWS IRREGULAR WIDENING OF THE CILIARY BODY FACE
What is the risk of glaucoma occuring after the traumatic accident in angle recession glaucoma?
10%
What is sturge-weber syndrome?
A CONGENITAL NEURO-OCULOCUTANEOUS DISORDER THAT CAN CAUSE SECONDARY OPEN ANGLE GLAUCOMA
Describe the pathophysiology of glaucoma in sturge-weber syndrome
ANTERIOR CHAMBER ANGLE MALFORMATION (CAUSES EARLY ONSET GLAUCOMA DURING THE FIRST YEAR OF LIFE) OR INCREASE VENOUS PRESSURE (CAUSES LATER ONSET GLAUCOMA)
What are the features of sturge-weber syndrome?
CUTANEOUS: PORT WINE STAIN, TYPICALLY ALONG CNV1 AND CNV2 (choroidal nerovascularisation distribution, non blanching on pressure and does not cross midline)
NEUROLOGICAL: SEIZURES AND LEARNING DISABILITY
OCULAR: CHOROIDAL HAEMANGIOMAS AND GLAUCOMA IPSILATERAL TO THE CUTANEOUS LESIONS
How is glaucoma in sturge-weber syndrome treated?
EARLY-ONSET GLAUCOMA: GONIOTOMY OR TRABECULOTOMY OR COMBINED TRABECULOTOMY-TRABECULECTOMY
LATER ONSET GLAUCOMA: MEDICAL THERAPY FIRST, THEN TRABECULAR IF MEDICAL THERAPY FAILS
What is primary congenital glaucoma?
RARE BILATERAL (IN TWO THIRDS OF PATIENTS) CONDITION DUE TO MALFORMATION OF THE ANTERIOR CHAMBER ANGLE THAT OCCURS IN THE FIRST YEAR OF LIFE
Describe the epidemiology of primary congenital glaucoma
MORE COMMON IN BOYS
MOSTLY SPORADIC BUT CAN BE AR
PREVALENCE HIGHER IN PATIENTS WITH CYP1B1 GENE
Describe the features of primary congenital glaucoma (signs)
PHOTOPHOBIA, EPIPHORA AND BLPHAROSPASM
CORNEAL OEDEMA
LARGE CORNEAL DIAMETER (>12MM)
BUPHTHALMOS: LARGE EYE DUE TO ELEVATE IOP
HAAB STRIAE: HEALED BREAKS IN DESCEMENT’S MEMBRANE DUE TO CORNEAL OEDEMA, BEST SEEN ON RETROILLUMINATION
What investigations are used for primary congenital glaucoma?
IOP MEASUREMENT (NORMAL IOP IN NEWBORNS IS 10-12mmH)
OPTIC DISC EVALUATION FOR CUPPING: LOOK FOR ASYMMETERY OR A RATIO OF >0.3
CORNEAL DIAMETER MEASUREMENT (NORMAL RANGE IS 9.5-10.5 MM IN NEWBORNS)
What is the management for primary congenital glaucoma?
ANGLE SURGERY IF CORNEA IS CLEAR
IF CORNEA IS CLOUDY THEN TRABECULOTOMY CAN BE TRIED
What are some side effects of beta blockers?
DECREASED CORNEAL SENSATION
DRY EYE
TACHYPHYLAXIS
BRADYCARDIA
BRONCHOSPASM
NOCTURNAL HYPOTENSION
What are some side effects of prostaglandin analogues?
CONJUNCTIVAL HYPERAEMIA
IRIS HYPERPIGMENTATION
INCREASED EYELASH LENGTH
CYSTOID MACULAR OEDEMA
What are some side effects of alpha-2-agonists?
FOLLICULAR CONJUNCTIVITIS
CONTACT DERMATITIS
TACHYPHYLAXIS
DRY MOUTH
SEDATION
CAUTION IN INFANTS AS IT CAN CROSS BLOOD BRAIN BARRIER
What are some side effects of topical carbonic anhydrase inhibitors?
OCULAR STINGING
BITTER TASTE
PUNCTATE KERATITIS
CONTRAINDICATED IN PATIENTS WITH SULPHONAMIDE ALLERGIES
What are some side effects of systemic carbonic anhydrase inhibitors?
PARATHESIA
URINE FREQUENCY (DIURETIC EFFECT)
HYPOKALAEMIA
STEVEN JOHNSON SYNDROME
METABOLIC ACIDOSIS
What are some side effects of osmotic agents?
CARDIOVASCULAR OVERLOAD
