POAG Flashcards
Definition of Glaucoma
A group of conditions that have in common
a chronic progressive optic neuropathy
characterised by morphological changes at the ONH& in the RNFL.
Progressive GCL death & VF loss are associated.
IOP is a key modifiable factor.
Symptoms of POAG
- Asymptomatic
- Gradual dim inution of distant vision or peripheral vision
- coloured haloes, frequent change of glasses, early mousing/ afternoon buoned vision (IOP spike) w/ wo heaviness of eyes
Important points in old records for POAG
- Baseline IOP, baseline VF(HVF)
- CCT
- How many AGM, if IOP & VF loss controlled
- Others: GOCT, GDX, Disc photo
Important points in systemic illness in POAG
- DM/ HTN/ Thyroid
- Cardiovascular- if on Beta blockers
- vaso spastic- Migraine, Raynaud’s
- Hemodynamic crisis -Acute blood loss (post partum hge, ruptured AAA, severe trauma, stroke).→CausesSEVERE SYST.HYPOTN→reduces blood flow to ONH.
5.Endocrine- DM /They/ Cushing’s→ endogenous steroid release
6.H/o cardiovasc/ renal ds/ Bronchial asthma - before starting AGM - Neurofibromatosis/sturge Weber/CCF/Thyrotoxicosis- to rule out secondary OAG
Drug history in POAG
- Systemic beta blockers
- HSTreactionto any ocular/ syst drug- esp SULFA
- Local/ocular/ Systemic intolerance to any drugs
- OCP intake (blocking of protective effect of estrogen)
- Long term steroid use- to rule out steroid induced glaucoma
Ocular- VKC, post keratoplasty, uveitis, self medicated
Nasal spray
Systemic- skin ds
post major transplantation surgery- kidney, liver
6.Topiramate (enquire nero/psych)- to rule out PACG (uveal effusion)
Family history in POAG
Offspring: 2 times the risk
siblings: 4 times the risk
( O2, S4)
Ocular exam in POAG
- VA
- Pupils- RAPD in advanced cases
- Lids -Hyperpigmentation & long lashes in PG analog use
- Conjunctiva -May be congested (AGM toxicity)esp inf quad
- Cornea-CCT grossly,toxic effects of AGM (honeycomb epithelial edema in RhoK inhibitors)
- AC & Iris-AC depth,angle narrowing (VH grade), pX f material,signs of PDS,NVI,Ac cells/flare
- IOP-Before gonio & pupil dilated, time of day to be noted, if it is > 21
- Gonio- AR,PDS,PAS,NVA
- Disc-Early:Cup enlargement, deepening; NRR thinning/saucerisation, disc hage, ppa(beta); VCDR >0.7/ asymmetry 0.2; laminar dot sign
Disc changes in POAG (5Rs)
- Ring- observe scleral ring → OD LIMIT& SIZE
- Rim - size
- RNFL
- Region of para papillary atrophy
- Retinal & disc hges
Vascular changes at disc in POAG
(These are non-specific sighs of glaucoma damage)
1. Disc hges (more comm in NTG)
2. Baring of circumlinear bld vessels: Space b/W NRR & a sf. bld vess
3. Bayonetting: NRR loss → vessel entering disc wr angle sharply backwards into disc
4. Collaterals b/w 2 veins at disc
4 morphological glaucomatous disc types
- Focal ischemic: sup &/or inf notching; local field defects w. early threat to fixation
- Myopic disc w ith glancoma: tilted shallow disc with temporal crescent of ppa+ features of glauc damage; douse sup /inf Scotoma threat fixatn
- Sclerotic disc: shallow saucerised up with gently sloping NRR t variable ppa; peripheral Vf loss
- Concentrically enlarging disc: uniform NRR thinning; diffuse VF loss
ISNT rule & significance
Normally thickmen of Inf rim> Sup> Nasal> Temp
Hence, normally inf t nicdkent, Temp thinnest
Any i’m thinking not following this rule → suspect glauc
Importance of DVT in glancoma
DVT ( Diurnal Variation Test)
1. Diagnosis: Basline IOP, magnitude of fluctuation, timing of peak
2. Management: AGM to maintain IOP below target with fluctuation<5,& prescribe AGM to cover peak times
Target IOP definition
Target IOP may be defined as a pressure, rather a range of intraocular pressure levels within which the progression of glaucoma and visual field loss will be delayed or halted. It is calculated depending on severity of glaucomatous optic damage
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