Glaucoma Flashcards

1
Q

Aqueous secretion

A
By the ciliary epithelium of the ciliary body pars plicata
1. Sympathetic nervous system
     ➕beta 2 receptors
     ➖alpha 2 receptors
2. Enzymatic action: Carbonic anhydrase
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2
Q

Aqueous outflow

A

PC➡️pupil➡️AC➡️

 1. Trabecular outflow (%90)➡️Schlemm➡️episcleral veins
 2. Uveoscleral drainage (%10)➡️suprachoroidal space➡️venous circulation
 3. Iris
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3
Q

Applanation tonometry-sources of error

A
  1. Inappropriate fluorescein pattern
  2. Pressure on the globe
  3. CCT
  4. Corneal oedema
  5. Astigmatism
  6. Incorrect calibration
  7. Wide pulse pressure
  8. Repetead readings over a short period
  9. Tight collar, breath-holding
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4
Q

Angle structures

A
  1. Schwalbe line
  2. Corneal wedge
  3. Trabeculum
    • anterior: non-functional, whitish
    • posterior: functional, pigmented
  4. Schlemm canal
  5. Scleral spur
  6. Ciliary body
  7. Iris processes
  8. Blood vessels
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5
Q

Grading of angle width

A
Schaffer system - Grade: 
4⃣ (35-45): ciliary body
     -myopia, PF
3⃣ (25-35): scleral spur
2⃣ (20): trabeculum
1⃣ (10): only Schwalbe
Slit angle: no angle structures+no iridocorneal contact
0⃣ (0): closed due to iridocorneal contact
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6
Q

Pathological findings-PAS

A
  1. Primary angle-closure glaucoma
  2. Anterior uveitis
  3. Iridocorneal endothelial (ICE) syndrome
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7
Q

Pathological findings-NV

A
  1. NV glaucoma
  2. Fuchs heterochromic cyclitis
  3. Chronic anterior uveitis
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8
Q

Pathological findings-Hyperpigmentation

A
  1. Physiological variant
  2. Pigment dispersion syndrome
  3. Pseudophakic pigment dispersion
  4. Pex syndrome
  5. Blunt ocular trauma
  6. Anterior uveitis
  7. Following acute angle-closure glaucoma
  8. Following YAG laser iridotomy
  9. Iris or angle melanoma or naevus
  10. Iris pigment epithelial cysts
  11. Naevus of Ota
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9
Q

Pathological findings-Trauma

A
  1. Angle recession
  2. Trabecular dialysis
  3. Cyclodialysis
  4. Foreign bodies
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10
Q

Pathological findings-Blood in the Schlemm canal

A
  1. Physiological variant
  2. Carotid-cavernous fistula and dural shunt
  3. Sturge-Weber syndrome
  4. Obstruction of the VCS
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11
Q

OD size

A

1.5-1.7 mm

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12
Q

Subtypes of glaucomatous damage

A
  1. Focal ischemic discs
    • localized field defects
  2. Myopic disc with galucoma
    • dense superior and inferior scotomas
    • younger, male patients
  3. Sclerotic discs
    • peripheral visual field loss
    • older patients
  4. Concetrically enlarging discs
    • diffuse visual field loss
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13
Q

Non-specific signs of glaucomatous damage

A
  1. Disc haemorrhages
    • most: inferotemporal
  2. Baring of circumlinear blood vessels
    • early sign
  3. Bayoneting
  4. Collaterals btw two veins at the disc
    • uncommon
  5. Loss of nasal NRR
    • moderately advanced
  6. The laminar dot sign
    • advancing
  7. Sharpened edge / sharpened rim
    • advancing
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14
Q

Peripapillary changes in glaucoma

A
  1. Alpha(outer) zone
  2. Beta(inner) zone
    • its location seems to indicate the orientation of likely visual field loss
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15
Q

RNFL defects in glaucoma

A
  1. Localized wedge-shaped defects
  2. Diffuse defects with indistinct borders
  • use red-free(green) light
  • not specific (can be seen in neurological diseases/normal people)
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16
Q

The visual field

A
50
            ⬆️
(T)90⬅️    ➡️60(N)
            ⬇️
            70
-blind spot: temporal btw 10-20 and slightly below the horizontal
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17
Q

Apostilbs (asb)

A

The intensity or brightness of a light stimulus

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18
Q

Decibels (dB)

A

Sensitivity of retina

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19
Q

False positives in perimetry

A

-The printout appears;
abnormally pale
-SITA➡️>%15
Full-threshold➡️>%33 is highly significant

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20
Q

False negatives in perimetry

A

-the printout has a
clover leaf shape🍀
-SITA➡️>%15
Full-threshold➡️>%33 is highly significant

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21
Q

Most important defects in glaucoma occur…

A

Centrally-within a 30 radius from the fixation point

22
Q

Prostaglandin derivatives

A

-‘uveoscleral’ aqueous outflow⬆️
-IOP lowering effect is greater than alternatives:
🏆1⃣st-line treatment in glaucoma (1x1 at bedtime)
✔️latanoprost (XALATAN)
🔺fewer ocular adverse effects
✔️travoprost (TRAVOPROST)
✔️bimatoprost (LUMIGAN)
🔺greater IOP-lowering effect, more conjunctival hyperemia
🔺periorbital fat loss
✔️tafluprost

23
Q

Side effects (ocular) - prostaglandin derivatives

A

OCULAR
-conjunctival hyperaemia-common
☑️more with bimatoprost, less with tafluprost
-eyelash lengthening, thickening, hyperpigmentation
-iris hyperpigmentation-in 1/4 patients after 6 months, irreversibl
-hyperpigmentation of periocular skin-reversibl
-periorbital fat loss
☑️common with bimatoprost
-increased risk of CMO following cataract surgery when used preoperatively⚠️
-anterior uveitis, promotion of herpetic keratitis
⚠️use with caution in those patients!

24
Q

Side effects (systemic) - prostaglandin derivatives

A

SYSTEMIC

  • headache
  • precipitation of migraine
  • malaise
  • myalgia
  • skin rash
  • mild upper respiratory system symptoms
25
Q

Beta-blockers

A

-aqueous production⬇️ (mediated by an effect on the ciliary epithelium)
-tachyphylaxis in %10
-2x1
-should not be instilled on bedtime⚠️ (BP⬇️)
-preferred when: Monoocular treatment, ocular inflammation, CMO, history of HSV keratitis (❌PG❌)
✔️timolol (TIMOPTIC) - usually used in combinations
🔺non-selective➡️❌asthma, bradycardia, AV block❌
✔️betaxolol (BETOPTIC)
🔺lower hypotensive effect
🔺Ca channel blocking effect➡️optic nerve blood flow⬆️ ➡️ visual field preservation may be superior
🔺relatively cardioselective(B1)➡️less bronchoconstriction️️➡️ advantage in asthma
✔️levobunolol
✔️carteolol (CARTEOL)
🔺intrinsic sympathomimetic activity
🔺more selective on 👀 than on the cardiopulmonary system➡️less systemic side effect, advantage in bradycardia, AV block
✔️metipranolol
🔺granılomatosis anterior uveitis

26
Q

Side effects (ocular) - beta blockers

A
OCULAR
-allergy
-punctat keratitis
-granulomatous uveitis
     ☑️metipranolol
27
Q

Side effects (systemic) - beta blockers

A
SYSTEMIC
-bronchospasm
     ⚠️critical to exclude asthma before prescribing
-cardiovascular: heart block, bradycardia, worsening of heart failure, hypotension
     ⚠️pulse should be assessed before prescription
     ⚠️caution in patients with peripheral vascular disease(Reynaud)
-sleep disorders
-reduced exercise tolerance
-hallucinations
-confusion
-depression
-fatigue
-headache
-nausea, dizziness
-decreases libido
-dyslipidemia
28
Q

Combined preparations

A
timolol ➕ ...
     dorzolamide ➡️ COSOPT, OFTOMIX, DORZOTIM -2x1
     brinzolamide ➡️ AZARGA -2x1
     brimonidine ➡️ COMBIGAN -2x1
     latanoprost ➡️ XALACOM -1x1
     travoprost ➡️ DUOTRAV -1x1
     bimatoprost ➡️ GANFORT -1x1
     pilocarpine ➡️ TIMPILO -2x1

brimonidine ➕ brinzolamide ➡️ SIMBRINZA -2x1

29
Q

Alpha-2 agonists

A

-aqueous production⬇️ (via an effect on the ciliary epithelium) and ‘uveoscleral’ outflow⬆️
-probably neuroprotective
-cross the blood-brain barrier➡️severe CNS depression and hypotension in young children
⚠️contraindicated

30
Q

Topical carbonic anhydrase inhibitors

A

-aqueous secretion⬇️
-3x1 (monotherapy) or 2x1 (adjunction)
-slightly less effective than beta-blockers
-probably neuroprotective
-may precipitate corneal decompensation in patients with corneal endothelial disfunction⚠️
-some benefits in the treatment of CMO
-idiosyncratic bone marrow supression
-chemically related to sulfanomide antibiotics
⚠️relatively contrandicated in patients allergic to sulfanomides
✔️dorzolamide (TRUSOPT✖️)
✔️brinzolomide (AZOPT)

31
Q

Side effects - topical carbonic anhydrase inhibitors

A
  • stinging
  • transient bitter taste following administration
  • allergic blepharoconjunctivitis☑️more with dorzolamide

-a white residue may be left on the eyelids after instillation
☑️brinzolamide

32
Q

Systemic carbonic anhydrase inhibitors

A

-aqueous secretion⬇️
-used for short-term treatment
-chemically related to sulfanomide antibiotics
⚠️relatively contrandicated in patients allergic to sulfanomides
✔️acetazolamide (DIAZOMID) -2/4x1
✔️dichlorphenamide
✔️methaxolamide

33
Q

Side effects - systemic carbonic anhydrase inhibitors

A
OCULAR
-choroidal effusion, particularly after cataract surgery
-angle closure
SYSTEMIC
-paraesthesia
-hypokalemia
-malaise and lowered mood
-GIS symptoms
-renal stones
-Stevens-Johnson syndrome (very rare)
-dose-related bone marrow suppression
-idiosyncratic aplastic anaemia
34
Q

Miotics

A

-cholinergic agonists
-used in angle-closure
-opens the angle (by pulling the iris away from trabeculum) ➕ ‘trabecular’ outflow⬆️ (by contraction of the ciliary muscle)
✔️pilocarpine -4x1
🔺equal effect to beta-blockers
✔️carbachol

35
Q

Side effects - miotics

A
LOCAL
-miosis
-brow ache
-myopic shift
-exacervation of symptoms of cataract
SYSTEMIC (rare)
-confusion
-bradycardia
-bronchospasm
-GIS symptoms
-urinary frequency
36
Q

Osmotic agents

A

-creates an osmotic gradient so that water is ‘drawn out’ from the vitreous into the blood
-when a short-term reduction in IOP is required
-of limited value in inflammatory glaucoma, in which the integrity of the blood-aqueous barrier is compromised⚠️
✔️mannitol
🔺peak action occurs within 30 minutes
✔️glycerol
🔺metabolized to glucose➡️be careful in diabetics⚠️
✔️isosorbide

37
Q

Side effects - osmotic agents

A
-CVS overload
     ⚠️caution in patients with cardiac or renal disease
-urinary retention
-headache
-backache
-nausea
-confusion
38
Q

Lens-related glaucoma

A
PHACOLYTIC:
Open angle, deep AC, intact capsule
PHACOGENIC/PHACOANAPHYLACTIC:
Compromised lens capsule
PHACOMORPHIC:
Angle closure, shallow AC
39
Q

BAIT - BADI

A

Moxifloxacine

BAIT: iris pigment epithelium
BADI:iris stroma

40
Q

Secondary-open angle-pre trabecular

A

Neovascular glaucoma
ICE syndrome
Epithelial ingrowth

41
Q

Ocular HT-risk factors

A
Age
IOP
CCT
C/D ratio
PSD
—————
African-American race
Gender
Heart disease

⚠️increased risk of RVO

42
Q

POAG and NTG-risk factors

A
Age
Race
IOP
Family history of POAG
OD area
Ocular perfusion pressure
Translaminar pressure gradient
Vascular disease(HT,CVD,migraine vb)
DM
Myopia
Contraceptive pill
FOR NTG:
\+Gender
\+CCT
\+Systemic hypotension
\+OSAS
\+Autoantibody levels
\+Thyroid disease
43
Q

PACG-risk factors

A
Age
Gender
Race
Family history
Refraction
AL
44
Q

TRAB-high risk for failure

A
NVG➡️➡️➡️➡️AGV
Inflammatory glaucoma
POS-traumatic angle recession
ICE
Previous failure

✳️USE MMC

45
Q

NF

A

NF1➡️glaucoma, retinal astrocytoma

NF2➡️cataract

46
Q

Wilms tumor

A

Aniridia (sporadic) ⚠️ ⚠️%75 risk of glaucoma

47
Q

Peters anomaly

A

Bilateral
⚠️%50 risk of glaucoma

Central corneal opacity
Posterior corneal defect-iridocorneal or lenticulocorneal adhesions

48
Q

Axenfeld Rieger syndrome

A

Bilateral
⚠️%50 risk of glaucoma

Axenfeld anomaly: posterior embryotoxon, attached strands of peripheral iris
Rieger anomaly: posterior embryotoxon, iris stromal hypoplasia, ectropion uveae, corectopia, full-thickness iris defects
Rieger syndrome: dental anomalies, facial anomalies, redundant paraumblical skin, hypospadias

49
Q

Malignant glaucoma

A

High IOP, shallow AC, absent bleb, negative Seidel

Treatment: Atropine

50
Q

Pupillary block

A

High IOP, shallow AC, flat bleb, negative Seidel, iris bombe

Treatment: LPI

51
Q

Inflammatory glaucomas

A
FUS-%60
JIA
Herpes Zoster-Simplex
Toxoplasma
Posner-Schlossman

Ciliary body shutdown, steroid responders, CLOSE: angle closure with/without pupillary block, OPEN: trabecular obstruction, acute trabeculitis, trabecular scarring