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OD2 S2 > wk7: Fusion Group 2-4 > Flashcards

wk7: Fusion Group 2-4 Flashcards

1
Q

Define Hypertension

A

blood pressure >/= 140/90mmHg

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2
Q

List 3 ocular complications of hypertension

A

choroidopathy
retinopathy
optic neuropathy

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3
Q

Name the 3 phases of Hypertensive Retinopathy

A
  1. vasoconstictive
  2. sclerotic
  3. exudative
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4
Q

What occurs in vasoconstrictive phase of hypertensive retinopathy? (2)

A

Acute rise in B.P
Arteriolar narrowing (A/V ratio around 1/3rd)

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5
Q

What occurs in sclerotic phase of hypertensive retinopathy? (4)

A

chronic HTN
pronounced arteriolar narrowing
av crossing
copper wiring

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6
Q

What occurs in exudative phase of hypertensive retinopathy (3)

A

persistent uncontrolled HTN
BRB disrupted
retinal haemorrhage

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7
Q

What percentage of diabetics are type 2?

A

90%

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8
Q

What proportion of type 1 diabetics are affected by diabetic retinopathy in some way within the first 2 decades of diabetes?

A

Almost all

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9
Q

What proportion of type 2 diabetics are affected by diabetic retinopathy within the first 2 decades of diabetes?

A

Over 60% affected

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10
Q

Describe the clinical characteristics/mechanism of Diabetic retinopathy (5)

A

(Earliest changes =) Reduced retinal perfusion
Weakening of retinal blood vessels
Nerve fibre swelling
Adverse metabolic reactions degrade retinal endothelial cells
Ultimately retinal ischaemia

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11
Q

Define non-proliferative DR

A

microaneurysms form in the blood vesselsof the eye, which can burst to leak blood

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12
Q

Define proliferative retinopathy

A

new blood vessels and scar tissue form on the retina causing loss of vision

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13
Q

Can non proliferative diabetic retinopathy lead to diabetic macular oedema?

A

yes

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14
Q

What happens in diabetic macular oedema?

A

vascular leakage and accumulation of plasma constituents in the macula

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15
Q

Does fish oil help treat diabetes?

A

No effect on prevention and treatment of type 2 diabetes

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16
Q

Types of primary glaucoma? (2)

A

Angle closure
Primary open angle

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17
Q

How can you classify angle closure glaucoma? (2)

A

acute or chronic

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18
Q

Name 3 different secondary glaucomas

A

traumatic glaucoma
neovascular (rueotic) glaucoma
pigmentary glaucoma

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19
Q

Describe the mechanism behind angle closure glaucoma (4)

A

Drainage angle obstructed –> increased IOP –> ONH damage –> VF loss

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20
Q

What IOP is considered an emergency?

A

over 30mmHg

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21
Q

Why does primary angle closure glaucoma occur?

A

due to pupillary block

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22
Q

Why does secondary angle closure glaucoma occur?

A

due to another identifiable pathology (e.g. neovascularisation)

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23
Q

List the symptoms of acute angle closure glaucoma (7)

A

rapid IOP elevation
sudden onset of pain
headache
nausea
vomiting
transient vision loss
halos

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24
Q

Can chronic angle closure glaucoma be asymptomatic?

A

yes

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25
What IOP might you expect to see in angle closure glaucoma?
40-80mmHg
26
List 5 characteristics of POAG
Often bilateral but asymmetric Open anterior chamber angle IOP often mildly elevated (over 21mmHg) Drainage system clogged or dysfunctional Typical aysmptomatic until advanced signs
27
How might the drainage system be clogged or dysfucntional in POAG?
loss of trabecular endothelial cells closure of schlemm's canal
28
Is NTG (normal tension glaucoma) symptomatic?
typically asymptomatic until advancd stages
29
True/False: people with NTG typically experience large diurnal fluctuations in their IOP?
true
30
How does ONH damage occur in glaucoma? (2)
Elevated IOP can cause mechanical damage to lamina cribrosa Mechanosensitive astrocytes in the ONH become activated
31
What does activation of mechanosensitive astrocytes in the ONH lead to?
can cause abnormal deposition of elastin, forming irregularities and deformation
32
What is the mechanism behind NTG?
unknown
33
What are the mechanisms behind optic neuropathy in NTG? (3)
Due to enhanced sensitivity to physiologically normal IOPs: - structural changes to lamina cribrosa - vascular dysregulation
34
What can vascular dyregulation in NTG patients consist of? (2)
Reduced ocular perfusion pressure: (causing reduced blood flow to ONH and subsequent ON damage) Vasospastic disorder: increased frequency of Raynaud's phenomenon
35
List 6 risk factors for NTG progression
IOP with blood pressure and other factors Age Gender (females>males) Race (african> caucasion > asian) Migraines Presence of dischaemoorhage
36
What is the diagnosis for this seminar's patient?
Normal Tension Glaucoma
37
What relevant screening tests are we using on this seminar's patient and why? (4)
V.A: distance + near, for baseline reading Oc. Motility: to rule out severe headaches potentially caused by multiple sclerosis, but unlikely due to age Confrontation: to identify any neglects or extinction, need further visual field testing Pupil size: smaller for patients above 60. Can be affected by medications such as IOP lowering drop
38
True/False: Uneven glaucomatous progression can induce RAPD
true
39
How might a patient with RAPD in NTG compare to a patient with RAPD in POAG?
Might see lesser RAPD magnitude in NTG
40
List 5 clinical features of NTG on Dilated Fundus Exam
Progressive optic nerve "cupping" Narrower neuroretinal rim thinning Optic disc haemorrhage (flame shape) Halo or crescent peripapillary atrophy RNFL defects
41
How do NTG patients generally perform in visual field testing?
often greater damage in superior or inferior retina about horizontal meridian
42
Name 8 typical glaucomatous visual field defects
1. nasal step 2. temporal wedge 3. established superior arcuate defect 4. early superior paracentral defect at 10 deg 5. superior, fixation threatening paracentral defect 6. superior arcuate with peripheral breakthrough and early inferior defect 7. tunnel vision defect with temporal crescent sparing 8. end stage, complete field loss
43
Where do points of loss tend to cluster in NTG vs POAG in visual field testing?
NTG: points clustering in central superior subfield POAG: points clustering in superior arcuate subfield
44
What can you expect to see in OCT of NTG patients? (1)
RNFL thinning corresponds with disc cupping or disc haemorrhage location
45
When does diurnal IOP peak (2) and trough (1)?
Peak in AM and early PM trough during PM
46
How can we assess diurnal blood pressure variation in NTG patients? (1)
Monitor BP of NTG patients over 24 hours
47
How does diurnal blood pressure variation differ in NTG compared to normal?
Greater nocturnal BP drop
48
What is the role of ocular perfusion pressure?
regulate blood flow to optic nerve
49
What is the formula used for calculating ocular perfusion pressure?
opp = 2/3MAPbrachial - IOP
50
How does blood pressure correlate with glaucoma incidence?
Extreme blood pressure (either high or low) has a significant correlation with glaucoma risk
51
How does high blood pressure affect autoregulation?
systemic hypertension alters autoregulation in systemic circulation
52
How should we manage this patient? (NTG) (4)
Start tx after dx or if at high risk for OAG progression (aim to lower IOP to target IOP) Trial first choice medication and monitor Long term monitoring to evaluate tx effectiveness If unresponsive to topical medication, consider laser therapy or surgery
53
When should treatment be started in a NTG patient?
when a diagnosis is made or if at high risk for OAG progression
54
Why do we want to lower IOP in this patient?
slow down progression --> preserve ON health and visual field staus
55
What is our initial target for reducing IOP in NTG patients?
reduce IOP by >/= 30%
56
What is the ideal IOP for a treated NTG patient?
IOP at which deterioration ceases
57
If first choice medication for NTG patient doesn't work: What should you do?
If unresponsive, trial different drug treatments
58
True/False: many treatments for POAG and NTG are the same
true
59
What should you consider in long term management of NTG patients? (5)
Detect progression and reassess risk factors for progression Evaluate effectiveness of treatemnet Ongoing communication with GP about tx Provide counselling As this is progressive in advanced stages, vision rehabilitation may be required in addition to tx plan
60
When can management plan for NTG patient be altered? (5)
If: - target IOP not reached - progression despite target IOP reached - poor adherence - stable IOP and optic nerve status
61
When should you review when a new medication is started to tx NTG? (3)
In 2 weeks: to determine IOP response In 1 month, followed by 3 months After 12 months, review every 6 months
62
What should you consider if an NTG patient is unresponsive to any topical medication?
Laser therapy or surgery
63
When can laser trabeculoplasty be considered? (1)
if fail to maintain target IOP with topical medication
64
What does laser trabeculoplasty achieve? (1)
reduces resistance of TM to aqueous outflow
65
What does trabeculectomy achieve? (1)
surgery that aids aqueous humour drainage

OD2 S2 (63 decks)

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