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Duke Elder 2020 > Glaucoma > Flashcards

Glaucoma Flashcards

1
Q

What are the parts of the ciliary body?

A

Pars plicata anteriorly

pars plana posteriorly

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2
Q

Where is aqueous humour produced?

A

by the ciliary processes of the pars plicata

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3
Q

What are the methods of secretion of the aqueous humour?

A
  1. Diffusion: due to a concentration gradient
  2. ultrafiltration: pressure gradient between oncotic and hydrostatic pressures (capillary verses intraocular pressures)
  3. Active (account for approx 80% of secretion): active transport is mediated by transmembrane aquaporin activated by Na+ / K+ ATPase enzye and carbonic anhydrase enzyme
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4
Q

how is aqueous humour secretion controlled?

A

by sympathetic (adrenergic innervation) system

B2 receptor stimulation = increases aqueous secretion and A2 receptor = decreased secretion

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5
Q

What is the composition of aqueous humour?

A

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

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6
Q

Describe the different aqueous outflow routes

A

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

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7
Q

What is the trabecular meshwork made up of?

A

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

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8
Q

What is Schlemm’s canal?

A

endothelial lined oval canal

situated circumferentially in the sclera sulcus

contains holes for collector channels which terminate in the episclera veins

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9
Q

What are the two parts of the optic nerve?

A

Neuroretinal Rim and Cup to Disc Ratio

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10
Q

What is the neuroretinal rim?

A

area of the optic disc

between margins of central cup and disc

contains retinal neuronal cells

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11
Q

Describe the neuroretinal rim

A

RIM IS THICKEST INFERIORLY, FOLLOWED BY SUPERIORLY, NASALLY AND THEN TEMPORALLY (‘ISNT’ RULE)

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12
Q

What happens to the neuroretinal rim during glaucoma?

A

it thins

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13
Q

What is the cup to disc ratio?

A

DEFINED AS THE VERTICAL DIAMETER OF THE OPTIC CUP DIVIDED BY THE VERTICAL DIAMETER OF THE OPTIC DISC

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14
Q

What is the normal cup to disc ratio?

A

NORMAL CD RATIO IS 0.3, SOME INDIVIDUALS MAY HAVE PHYSIOLOGICAL CUPPING OF 0.6 OR 0.7 WITHOUT GLAUCOMATOUS CHANGES

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15
Q

What is a trabeculectomy?

A

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

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16
Q

What can be used to prevent bleb failure in a trabeculectomy?

A

ADJUNCTIVE USE OF ANTI METABOLITES MAY BE USED TO SLOW THE HEALING PROCESS IN ORDER TO PREVENT BLEB FAILURE

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17
Q

What are some examples of anti metabolites used?

A

F-FLUOROURACIL (5-FU): A PYRIMIDINE ANALOGUE WHICH INHIBITS FIBROBLASTS BY BLOCKING DNA SYNTHESIS

MITOMYCIN C: AN ALKYLATING AGENT WHICH ALSO INHIBITS FIBROBLASTS

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18
Q

What is ocular hypertension?

A

IOP > 21MMhG WITHOUT GLAUCOMATOUS DAMAGE

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19
Q

What percentage of people with OHT were found to then develop open angle glaucoma?

A

9.5%

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20
Q

What are the risk factors for conversion of OHTN to Open angle glaucoma?

A

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
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21
Q

What is the management for ocular hypertension?

A

REGULAR MONITORING

MEDICAL TREATMENT IS INDICATED IN CASES WITH PERSISTENT IOP> 30 OR WITH HIGH-RISK PROFILE PATIENTS

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22
Q

What is primary open angle glaucoma?

A

CHRONIC DISORDER CHARACTERISED BY GLAUCOMATOUS VISUAL FIELD DEFECTS DUE TO OPTIC NERVE DAMAGE

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23
Q

What genes have the potential to cause POAG?

A

MYOC AND OPTN GENE MUTATIONS

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24
Q

What are the features of POAG? (4)

A

OPEN ANTERIOR CHAMBER ANGLE

HIGH C/D RATIO AND THINNING OF THE NEURORETINAL RIM

RAISED IOP > 21mmHg

GLAUCOMATOUS VF DEFECTS

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25
Q

What Ix are used in POAG?

A

FUNDOSCOPY: EVALULATE OPTIC DISC

GONIOSCOPY: ASSESSMENT OF ANGLE

PACHYMETRY: MEASURE CCT

PERIMETRY: VISUAL FIELD TESTING

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26
Q

What is the management for POAG?

A

TOPIC IOP-LOWERING AGENTS SUCH AS PRSOTAGLANDIN ANALOGUES OR BETA BLOCKER

LASER TRABECULOPLASTY

TRABECULECTOMY IF FAILURE OF OTHER TREATMENTS

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27
Q

What is normal tension glaucoma?

A

A FORM OF POAG WITH A PERSISTENLY NORMAL IOP <21mmHg

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28
Q

What did the collaborative normal-tension glaucoma study group find?

A

reducing IOP by 30% reduced the risk of progression of NTG (12% risk of progression in treated group vs 35% in the untreated group)

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29
Q

What are some risk factors for normal tension glaucoma?

A

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

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30
Q

What are some features of normal tension glaucoma?

A

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
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31
Q

What is primary angle closure glaucoma?

A

OCCLUSION OF THE TM, CAUSING OBSTRUCTION OF AQUEOUS OUTFLOW WITH THE POTENTIAL OF CAUSING A RISE IN IOP AND OPTIC NERVE DAMAGE

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32
Q

What are some differences between primary angle-closure suspect, primary angle closure and primary angle closure glaucoma?

A
  • 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
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33
Q

What are some risk factors for primary angle closure glaucoma?

A

INCREASING AGE

EAST ASIAN RACE

HYPERMETROPIA

FAMILY HISTORY

SHORT AXIAL LENGTH OF THE EYE

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34
Q

What is the pathophysiology of Primary angle closure glaucoma?

A

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

35
Q

What are the features of primary angle closure glaucoma?

A

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

36
Q

What is the management of primary angle closure glaucoma?

A

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

37
Q

What is neovascular glaucoma?

A

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

38
Q

What are some causes of neovascularisation glaucoma?

A

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

39
Q

Describe the pathophysiology of neovascular glaucomoa

A

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

40
Q

What are the features of neovascular glaucoma?

A

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

41
Q

What Investigations are used for neovascular glaucoma?

A

ESTABLISH THE CAUSE OF RETINAL ISCHAEMIA

42
Q

How is neovascular glaucoma managed?

A

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

43
Q

What are the surgical options for neovascular glaucoma?

A

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

44
Q

What is pigment dispersion syndrome?

A

AN auto dominant

CAUSE OF SECONDARY OPEN ANGLE GLAUCOMA,

CHARACTERIZED BY EXCESSIVE SHEDDING OF PIGMENTED MATERIAL OF THE IRIS DEPOSITED THORUGH THE ANTERIOR SEGMENT

45
Q

What population is pigment dispersion syndrome common in?

A

myopic males

46
Q

What are the features of pigment dispersion syndrome?

A

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

47
Q

What is the management of pigment dispersion syndrome?

A

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

48
Q

What are the risks of pilocarpine?

A

myopia and retinal detachment

49
Q

What is pseudoexfoliation syndrome?

A

CAUSE OF SECONDARY OPEN ANGLE GLAUCOMA IN WHICH GREY-WHITE FIBRILLAR DEPOSITS BLOCK THE ANTERIOR CHAMBER ANGLE

50
Q

What gene mutation is pseudoexfoliation syndrome associated with?

A

ASSOCIATED WITH MUTATION IN THE LOXL1 (ENZYME THAT CONTRIBUTES TO ELASTIC FORMATION)

51
Q

which populations is pseudoexfoliation syndrome more common in?

A

MORE LIKELY TO PRESENT IN SCANDINAVIANS, FEMALES AGED >50

52
Q

What are the Ix and Tx for pseudoexfoliation syndrome?

A

similar to POAG

53
Q

What are the features of pseudoexfoliation syndrome?

A

INCREASED IOP AND GLAUCOMATOUS DAMAGE

FLAKY WHITE DEPOSITS ON THE ANTERIOR LENS CAPSULE

SAMPAOLESI LINE

PERIPUPILLARY DEFECT ON TRANSILLUMINATION SLIT LAMP

54
Q

What is posner-schlossman syndrome?

A

DISORDER CHARACTERISED BY RECURRENT UNILATERAL ACUTE ATTACKS OF IOP ELEVATION

MAY CAUSE SECONDARY OPEN-ANGLE GLAUCOMA (UNCOMMON, ONLY IF REPEATED ATTACKS)

55
Q

In which patients is posner-schlossman syndrome more common?

A

middle aged patients

56
Q

What is posner-schlossman syndrome associated with? (microrganisms and antigens)

A

CMV

H. pylori

HLA-BW5

57
Q

What are the features of posner-schlossman syndrome?

A

DISCOMFORT, HALOES AND BLURRED VISION

ANTERIOR CHAMBER INFLAMMATION

MYDRIASIS

58
Q

What is the treatment for posner-schlossman syndrome?

A

TOPICAL STEROIDS AND IOP LOWERING AGENTS

59
Q

What is phacolytic glaucoma?

A

A SECONDARY OPEN ANGLE GLAUCOMA

hypermature cataract –> leakage of lens protein –> trabecular obstruction

60
Q

What are the features of phacolytic glaucoma?

A

PAINFUL RED EYE WITH PHOTOPHOBIA AND DECREASED VISION

CORNEAL OEDEMA, MATURE CATARACT AND WHITE PARTCILES MAY BE SEEN IN THE ANTERIOR CHAMBER

61
Q

What is the treatment for phacolytic glaucoma?

A

TOPICAL OR SYSTEMIC: IOP-LOWERING AGENTS

DEFINITIVE TREATMENT: CATARACT EXTRACTION

62
Q

WHAT IS PHACOMORPHIC GLAUCOMA?

A

AN ACUTE SECONDARY ANGLE-CLOSURE GLAUCOMA DUE TO A SWELLING OF A CATARACTOUS LENS POTENTIATING A PUPILLARY BLOCK

63
Q

How does phacomorphic glaucoma present?

A

SIMILAR TO ACUTE PACG

64
Q

What is the treatment for phacomorphic glaucoma?

A

IOP REDUCTION: SAME AS ACUTE PACG (AVOID MIOTICS, CAN POTENTIATE PUPILLARY BLOCK)

DEFINITIVE TREATMENT: CATARACT EXTRACTION

65
Q

What is red cell glaucoma?

A

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

66
Q

What is ghost cell glaucoma?

A

A TYPE OF SECONDARY OPEN ANGLE GLAUCOMA OCCURRING 2-4 WEEKS AFTER A VITREOUS HAEMORRHAGE DUE TO TM OBSTRUCTION WITH RED BLOOD CELLS

67
Q

What is angle recessions glaucoma?

A

A CHAUSE OF CHRONIC SECONDARY OPEN ANGLE GLAUCOMA DUE TO CILIARY BODY RUPTURE CAUSED BY BLUNT TRAUMA

68
Q

What does gonioscopy show in angle recession glaucoma?

A

GONIOSCOPY SHOWS IRREGULAR WIDENING OF THE CILIARY BODY FACE

69
Q

What is the risk of glaucoma occuring after the traumatic accident in angle recession glaucoma?

A

10%

70
Q

What is sturge-weber syndrome?

A

A CONGENITAL NEURO-OCULOCUTANEOUS DISORDER THAT CAN CAUSE SECONDARY OPEN ANGLE GLAUCOMA

71
Q

Describe the pathophysiology of glaucoma in sturge-weber syndrome

A

ANTERIOR CHAMBER ANGLE MALFORMATION (CAUSES EARLY ONSET GLAUCOMA DURING THE FIRST YEAR OF LIFE) OR INCREASE VENOUS PRESSURE (CAUSES LATER ONSET GLAUCOMA)

72
Q

What are the features of sturge-weber syndrome?

A

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

73
Q

How is glaucoma in sturge-weber syndrome treated?

A

EARLY-ONSET GLAUCOMA: GONIOTOMY OR TRABECULOTOMY OR COMBINED TRABECULOTOMY-TRABECULECTOMY

LATER ONSET GLAUCOMA: MEDICAL THERAPY FIRST, THEN TRABECULAR IF MEDICAL THERAPY FAILS

74
Q

What is primary congenital glaucoma?

A

RARE BILATERAL (IN TWO THIRDS OF PATIENTS) CONDITION DUE TO MALFORMATION OF THE ANTERIOR CHAMBER ANGLE THAT OCCURS IN THE FIRST YEAR OF LIFE

75
Q

Describe the epidemiology of primary congenital glaucoma

A

MORE COMMON IN BOYS

MOSTLY SPORADIC BUT CAN BE AR

PREVALENCE HIGHER IN PATIENTS WITH CYP1B1 GENE

76
Q

Describe the features of primary congenital glaucoma (signs)

A

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

77
Q

What investigations are used for primary congenital glaucoma?

A

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)

78
Q

What is the management for primary congenital glaucoma?

A

ANGLE SURGERY IF CORNEA IS CLEAR

IF CORNEA IS CLOUDY THEN TRABECULOTOMY CAN BE TRIED

79
Q

What are some side effects of beta blockers?

A

DECREASED CORNEAL SENSATION

DRY EYE

TACHYPHYLAXIS

BRADYCARDIA

BRONCHOSPASM

NOCTURNAL HYPOTENSION

80
Q

What are some side effects of prostaglandin analogues?

A

CONJUNCTIVAL HYPERAEMIA

IRIS HYPERPIGMENTATION

INCREASED EYELASH LENGTH

CYSTOID MACULAR OEDEMA

81
Q

What are some side effects of alpha-2-agonists?

A

FOLLICULAR CONJUNCTIVITIS

CONTACT DERMATITIS

TACHYPHYLAXIS

DRY MOUTH

SEDATION

CAUTION IN INFANTS AS IT CAN CROSS BLOOD BRAIN BARRIER

82
Q

What are some side effects of topical carbonic anhydrase inhibitors?

A

OCULAR STINGING

BITTER TASTE

PUNCTATE KERATITIS

CONTRAINDICATED IN PATIENTS WITH SULPHONAMIDE ALLERGIES

83
Q

What are some side effects of systemic carbonic anhydrase inhibitors?

A

PARATHESIA

URINE FREQUENCY (DIURETIC EFFECT)

HYPOKALAEMIA

STEVEN JOHNSON SYNDROME

METABOLIC ACIDOSIS

84
Q

What are some side effects of osmotic agents?

A

CARDIOVASCULAR OVERLOAD

Duke Elder 2020 (9 decks)

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