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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
Q

What IOP might you expect to see in angle closure glaucoma?

A

40-80mmHg

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26
Q

List 5 characteristics of POAG

A

Often bilateral but asymmetric
Open anterior chamber angle
IOP often mildly elevated (over 21mmHg)
Drainage system clogged or dysfunctional
Typical aysmptomatic until advanced signs

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27
Q

How might the drainage system be clogged or dysfucntional in POAG?

A

loss of trabecular endothelial cells
closure of schlemm’s canal

28
Q

Is NTG (normal tension glaucoma) symptomatic?

A

typically asymptomatic until advancd stages

29
Q

True/False: people with NTG typically experience large diurnal fluctuations in their IOP?

A

true

30
Q

How does ONH damage occur in glaucoma? (2)

A

Elevated IOP can cause mechanical damage to lamina cribrosa
Mechanosensitive astrocytes in the ONH become activated

31
Q

What does activation of mechanosensitive astrocytes in the ONH lead to?

A

can cause abnormal deposition of elastin, forming irregularities and deformation

32
Q

What is the mechanism behind NTG?

A

unknown

33
Q

What are the mechanisms behind optic neuropathy in NTG? (3)

A

Due to enhanced sensitivity to physiologically normal IOPs:
- structural changes to lamina cribrosa
- vascular dysregulation

34
Q

What can vascular dyregulation in NTG patients consist of? (2)

A

Reduced ocular perfusion pressure: (causing reduced blood flow to ONH and subsequent ON damage)
Vasospastic disorder: increased frequency of Raynaud’s phenomenon

35
Q

List 6 risk factors for NTG progression

A

IOP with blood pressure and other factors
Age
Gender (females>males)
Race (african> caucasion > asian)
Migraines
Presence of dischaemoorhage

36
Q

What is the diagnosis for this seminar’s patient?

A

Normal Tension Glaucoma

37
Q

What relevant screening tests are we using on this seminar’s patient and why? (4)

A

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
Q

True/False: Uneven glaucomatous progression can induce RAPD

A

true

39
Q

How might a patient with RAPD in NTG compare to a patient with RAPD in POAG?

A

Might see lesser RAPD magnitude in NTG

40
Q

List 5 clinical features of NTG on Dilated Fundus Exam

A

Progressive optic nerve “cupping”
Narrower neuroretinal rim thinning
Optic disc haemorrhage (flame shape)
Halo or crescent peripapillary atrophy
RNFL defects

41
Q

How do NTG patients generally perform in visual field testing?

A

often greater damage in superior or inferior retina about horizontal meridian

42
Q

Name 8 typical glaucomatous visual field defects

A
  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
Q

Where do points of loss tend to cluster in NTG vs POAG in visual field testing?

A

NTG: points clustering in central superior subfield
POAG: points clustering in superior arcuate subfield

44
Q

What can you expect to see in OCT of NTG patients? (1)

A

RNFL thinning corresponds with disc cupping or disc haemorrhage location

45
Q

When does diurnal IOP peak (2) and trough (1)?

A

Peak in AM and early PM
trough during PM

46
Q

How can we assess diurnal blood pressure variation in NTG patients? (1)

A

Monitor BP of NTG patients over 24 hours

47
Q

How does diurnal blood pressure variation differ in NTG compared to normal?

A

Greater nocturnal BP drop

48
Q

What is the role of ocular perfusion pressure?

A

regulate blood flow to optic nerve

49
Q

What is the formula used for calculating ocular perfusion pressure?

A

opp = 2/3MAPbrachial - IOP

50
Q

How does blood pressure correlate with glaucoma incidence?

A

Extreme blood pressure (either high or low) has a significant correlation with glaucoma risk

51
Q

How does high blood pressure affect autoregulation?

A

systemic hypertension alters autoregulation in systemic circulation

52
Q

How should we manage this patient? (NTG) (4)

A

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
Q

When should treatment be started in a NTG patient?

A

when a diagnosis is made or if at high risk for OAG progression

54
Q

Why do we want to lower IOP in this patient?

A

slow down progression –> preserve ON health and visual field staus

55
Q

What is our initial target for reducing IOP in NTG patients?

A

reduce IOP by >/= 30%

56
Q

What is the ideal IOP for a treated NTG patient?

A

IOP at which deterioration ceases

57
Q

If first choice medication for NTG patient doesn’t work: What should you do?

A

If unresponsive, trial different drug treatments

58
Q

True/False: many treatments for POAG and NTG are the same

A

true

59
Q

What should you consider in long term management of NTG patients? (5)

A

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
Q

When can management plan for NTG patient be altered? (5)

A

If:
- target IOP not reached
- progression despite target IOP reached
- poor adherence
- stable IOP and optic nerve status

61
Q

When should you review when a new medication is started to tx NTG? (3)

A

In 2 weeks: to determine IOP response
In 1 month, followed by 3 months
After 12 months, review every 6 months

62
Q

What should you consider if an NTG patient is unresponsive to any topical medication?

A

Laser therapy or surgery

63
Q

When can laser trabeculoplasty be considered? (1)

A

if fail to maintain target IOP with topical medication

64
Q

What does laser trabeculoplasty achieve? (1)

A

reduces resistance of TM to aqueous outflow

65
Q

What does trabeculectomy achieve? (1)

A

surgery that aids aqueous humour drainage

OD2 S2 (63 decks)

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