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Finals > Opthalmology Online And SDL > Flashcards

Opthalmology Online And SDL Flashcards

1
Q

Lecture 1/4: Cell struc and innervation of eye

what part of eye described by:
epithelium, stroma, accessory lacrimal glands?

A

conjuctiva (outer skin of eye)

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2
Q

what is the role of accessory lacrimal glands in conjuctiva?

A

secrete aq component of tears alongside lacrimal gland

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3
Q

The conjunctival epithelium has 2-5 layers of keratinised or non keratinised epithelium?

A

non keratinised

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4
Q

what are the two cell types that compose the non keratinised epithelial layers of the conjunctival epithelium of the eye?

A

stratified squamous and stratified columnar

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5
Q

are stratified squamous or stratified columnar cells known as palpebral/limbal?

A

stratified squamous

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6
Q

true or false, the term bulbar is associated with stratified columnar cells?

A

true

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7
Q

What is the role of microvilli in the conjunctival epithelium?

A

secrete glycoproteins, forms glycocalyx which stabilises tear film

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8
Q

what cell type is responsible for producing the mucin layer of tear film?

A

goblet

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9
Q

what is the main type of collagen that is found on the basement membrane of the conjunctival epithelium which anchors fibrils and hemidesmosomes?

A

4

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10
Q

what are the two layers of the conjunctival stroma?

A

superficial lymphoid and deeper fibrous

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11
Q

the superficial lymphoid layer of the conjunctival stroma contains lymphoid tissue, what is its purpose?

A

attaches to epithelium via basement membrane

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12
Q

which layer of the conjunctival stroma attaches to the episclera aka tenons layer?

A

deeper fibrous

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13
Q

what are the 2 different types of tissue that make up the deeper fibrous layer of the conjunctival stroma?

A

collagenous elastic and neurovascular

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14
Q

what are the functions of the tear film

A

protect, lubricate, reduces infection risk, washes away foreign particles

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15
Q

why does tear film reduce infection risk?

A

has antimicrobial protective substances

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16
Q

what are the 3 layers of the tear film going in order of proximity to the cornea

A

mucin, aqueous and phospholipid

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17
Q

The mucin layer of the tear film is made of goblet cells, why does it stabilise aq substances against the hydrophobic corneal epithelium?

A

hydrophilic surface

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18
Q

what different things would you expect to find in the aq layer of the tear film?

A

lacrimal and accessory lacrimal glands
water
growth factors
lactoferrin
lysozyme
immunoglobulins
cytokines

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19
Q

what is the name of the sebaceous glands on the eyelids that are present in and secrete the phospholipid layer of the tear film?

A

meibomian

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20
Q

what is the role of the phospholipid layer of the tear film?

A

reduces evaporation of aq layer, increases surface tension of tear film, makes it more stable

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21
Q

what is the maximal volume of the conj sac/ tear volume in microlitres?

A

7-30

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22
Q

what is the volume of an eye drop in microlitres

A

25-70

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23
Q

how many drops can the conj sac of the eye roughly support?

A

1

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24
Q

list some of the different factors that can affect the rate and extent of ocular absorption of eye drops ?

A

tear volume
tear turnover time
spontaneous blink rate
corneal thickness
lipophilic hydrophilic lipophilic nature of cornea

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25
Q

tear turnover time is 0.5-2.2 microlitres/min roughly, what effect would an irritating drug have on tear turnover time potentially?

A

increase

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26
Q

how long does a drug remain in the conj sac on average?

A

3-5 mins

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27
Q

do ointments have better or worse penetration than drops and why

A

better because they stay longer in the sac

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28
Q

what is the rate of ocular absorption?

A

1 to 7%

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29
Q

what is the function of the cornea?

A

clear view and protection from infection, trauma

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30
Q

how many layers does the cornea have ?

A

5

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31
Q

describe the epithelial layer of the cornea

A

5-7 layers of non keratinised squamous cells
hemidesmosomes to basement membrane
flatter wing cells superficially
microvilli
limbus junction between cornea and sclera

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32
Q

describe the cellular structure of the bowmans layer of the cornea

A

superficial strong layer of stromal collagen
beneath epithelial basement membrane
avascular unable to regenerate
heals by scarring

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33
Q

describe the cellular structure of the stroma layer of cornea

A

75% water
collagen type 1,2,3 and 4
fibres arranged in regular way to confer transparency and allow light through
proteoglycan around substance
made of modified fibroblasts called keratocytes - remodelling after injury

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34
Q

describe the cellular structure of the descements membrane of the cornea

A

basement membrane of endothelium
produced and repaired by endothelial cells

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35
Q

cornea endothelium cornea is made from monolayer of hexagonal cells but cant regenerate due to damage/ cell loss, how does it compensate for this?

A

enlargement and migration

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36
Q

the cornea gets nutrition from aq, limbus (+ tera film), transparency is dependant on what? 2

A

correct water amount in stroma
regular orientation and spacing of collagen fibres

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37
Q

water amount in stroma is dependant/ derived from the water + nutrients flowing passively from aq –> stroma.
how does the endothelium control water vol and prevent overhydration?

A

actively pumps Na+ back into aq (Na/K ATPase), water follows Na passively

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38
Q

what is the episclera?

A

loose connective tissue overlying the sclera
that provides the nutrition to sclera
also providing low friction to allow free movement of the eye

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39
Q

what is the episclera composed of? 3 layers

A

inner layer
intermediate loose connective tissue
outer layer - muscle sheaths fused & conjuctiva at limbus

and heavily vascularised
- anterior and posterior plexus

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40
Q

what are the main functions of the sclera?

A

protect
maintain shape
tolerance of intraocular pressure fluctuations
blocking of light

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41
Q

name of the tough outer coat of the eye?

A

sclera
continuous w cornea and optic nerve

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42
Q

T/F sclera has own blood vessels

A

false
avascular but pierced by vessels

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43
Q

what does the sclera consist of?

A

collagen (1,2,5, also 4,6,8)
proteoglycans
glycoproteins
elastin

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44
Q

2 main layers of the sclera?

A

outer stroma: criss cross of collagen
inner lamina fusca: blends w uveal tract, separated by suprachoroidal space

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45
Q

what are the three components of the uveal tract?

A

iris
choroid
ciliary body

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46
Q

what is the iris composed of?

A

Anterior surface - Connective tissue, incomplete border layer overlying
stroma

Stroma
Contains vessels, nerves Sphincter pupillae(circular)
Smooth muscle (short ciliary nerves – CNIII – parasympathetic)
Dilator pupillae (radial)
Smooth muscle (sympathetic supply, carried by long ciliary
nerves (Va))

Posterior epithelium
Cuboidal, pigmented

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47
Q

what is the function of the iris?

A

control pupil size to regulate light, depth of focus, minimising optical aberrations

blood-aqueous barrier due to tight junctions between iris and endothelium cells

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48
Q

what is the ciliary body composed of?

A
  1. Ciliary epithelium
    * Cuboidal bilayer, apex to apex, gap junctions
    - Inner layer – nonpigmented, high metabolic activity
    - Outer layer – pigmented
  2. Ciliary muscle
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49
Q

whats the function of the ciliary body?

A
  • Blood aqueous barrier (tight junctions between inner nonpigmented cells)
  • Aqueous humour production (both epithelial layers)
  • Accommodation (ciliary muscle)
    *Contracts => zonules relax => lens fattens =>
    enables focus on near objects
    *Parasympathetic (short ciliary nerves CNIII)
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50
Q

whats the structure of the choroid? in order

A

bruchs membrane
choriocapillaries
stroma - larger blood vessels

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51
Q

most vascular layer of eye?

A

choroid

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52
Q

choroid functions?

A

Vascular supply:
1. Nutrition
2. Waste removal
3. Heat dissipation
4. Ocular immunity

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53
Q

what structure of the eye is:
80% ocular volume
99% water
Transparent “gel”
Hyaluronic acid
Collagen (II, IX, V/XI hybrid)

A

vitreous

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54
Q

4 parts of the lens?

A

capsule (BM)
epithelium
fibres
zonules

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55
Q

what % refractive power of eye from lens and cornea?

A

30% lens
70% cornea

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56
Q

what is the epithelium of the lens like
a) centrally
b) peripherally

A

a) cuboidal and non-mitotic
b) columnar and mitotic

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57
Q

stretch

what do lens cells lose when they become FIBRES?

A

elongate and lose organelles

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58
Q

in the lens, where are the a) older fibres
b) newer formed fibres found?

A

nucleus
cortex

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59
Q

in lens, name for sheets of suspensory fibres, made of fibrililin, and attach ciliary body to lens at and around equator?

A

zonules

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60
Q

what strutcure helps hold lens in place?

A

zonules

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61
Q

what % of lens is water andprotein?

A

low water 65%
high protein 35%

relatively hypoxic

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62
Q

the clarity of lens maintained by what?

A

narrow lens fibre membs
small interfibre spaces
tightly packed contents (crystallin)
no blood cells
loss of organelles from cells when they -> fibres

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63
Q

what is the structure of RPE (pigment epithelium) like in retina?

A
  • Hexagonal monolayer epithelial cells
  • Microvilli – envelop photoreceptor outer segments
  • Tight juncs – outer blood-retinal barrier
  • Rich in mitochondria
  • BM – forms part of Bruchs membrane
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64
Q

4 cell types as integrators in retina?

A

bipolar cells
horizontal cells
amacrine …
ganglion …

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65
Q

what cells support retina?

A

muller cells

(R also is neural and photoreceptors: rods and cones involved)

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66
Q

the X in the retina is area of highest acuity, multilayered ganglion cell layer and has Fovea struct in centre of it.

A

macula

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67
Q

where is maximal density of cones in retina?

A

in fovea (centre of macula)

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68
Q

where does blood supply of retina come from?

A

retinal circ (supplies inner 2/3)
from: central retinal artery

choroidal circ (supplies outer 1/3)
from: post ciliary arteries

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69
Q

what struc maintains outer blood-retina barrier
stores metabolites and Vit A
supply nutrition for photorecs
absorb scattered light
make and recycle photopigments
phagocytosis of photorec discs

A

RPE

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70
Q

rods and cones are the 2 parts of photoreceptors, describe each

A

rods - low light and peripheral vision
cones - bright/normal, colour

Light perception by outer segments of photoreceptors
- G proteins – “opsins”
- Vitamin A derived molecules (chromophores)

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71
Q

role of chromophores in photoreceptors?

A

vit a derived molecules
they alter light signal -> electrical, to brain

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72
Q

rods and cones synapse with what cells?

A

bipolar, which synapse w ganglion

negative feedback, moderation
horizontal between photorecs
amacrine between bipolar and ganglion

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73
Q

describe the ganglion cells (2)

A

Optic nerve - produced a Light signal => brain

  1. Parvocellular - Fine vision, colour,
    Mainly in fovea
  2. Magnocellular - Motion, coarse vision,
    Peripheral
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74
Q

what nerves are important to the eye?

A

optic 2
oculomotor trochlear adbucent 3,4,6
trigeminal 5
facial 7
parasymps 3,7
symps T1 pupil dilation

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75
Q

optic nerve and visual pathways, learn detail?

A

?

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76
Q

extraocular muscles, covered in prev CN lec.. inferior oblique, medial rectus, eye movement

A
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77
Q

nerve supply of extraocular muscles?

A

slide 46

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78
Q

autonomic innervation?

A
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79
Q

A

A
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80
Q

A

A
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81
Q

A

A
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82
Q

Lecture 2/3: Retinopathy

what is meant by retinopathy

A

disease of retina that -> vision impairment or loss

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83
Q

list some different causes of retinopathies

A

diabetes
htn
radiation
trauma
retinal vasc disease
…

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84
Q

diabetic retinopathy causes microangiopathy, what does this mean

A

affects small vessels

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85
Q

what small vessels are affected in diabetic retinopathy due to microangiopathy

A

precapillary arteries
capillaries
post capillary venules

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86
Q

pathology of diabetic retinopathy

A

thickening of basement membranes, capillary non-perfusion and ischaemia

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87
Q

what are microaneurysms in the context of diabetic retinopathy

A

weakening and bulging of vessel wall

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88
Q

what are the 3 different types of haemorrhage that can occur in the retina

A

dot
blot
flame

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89
Q

which type of retinal haemorrhage is due to a rupture of capillaries in outer plexiform layer

A

dot

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90
Q

how are blot haemorrhages different to dot haemorrhages

A

larger
bleeding from capillaries
tracks between photoreceptors and RPE

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91
Q

in flame haemorrhages you get a rupture of the small arterioles which leads to leakage into the

A

nerve fibre layer

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92
Q

hard exudates in the retina are caused by endothelial damage which lead to plasma leakage into the

A

outer plexiform layer

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93
Q

what is the term given to the swollen ends of interrupted axons in nerve fibre layer due to microinfarction

A

cotton wool spots

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94
Q

in venous beading veins have a beaded appearance in the retina, this reflects

A

retinal ischaemia

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95
Q

intraretinal microvascular abnormalities (IRMA) are vascular abnormalities in the venous side of the capillary bed and do not leak. What are they precursors of

A

neovascularisation

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96
Q

what is neovascularisation

A

new vessels grow from venous side of capillary bed in area of non perfusion

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97
Q

what releases vasoproliferative factors that can cause neovascularisation

A

ischaemic retina

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98
Q

new vessels can bleed into vitreous and cause retinal detachment leading to what condition

A

glaucoma

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99
Q

how many disease severity levels are there for retinopathy

A

4

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100
Q

what is meant by diabetic macular oedema DMO

A

leakage into macula often with exudates and surrounding a microaneurysm

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101
Q

what is the criteria for macular laser

A

clinically significant macular oedema CSMO
involves
- retinal thickening 500 microm of mac centre
- hard exudates
- retinal thickening of >1 disc area

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102
Q

how might a diabetic retinopathic retina differ from an image of a normal retina

A

cotton wool spots
microaneurysms
oedema
exudates
neovascularisation

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103
Q

what systemic management is involved in the management for retinopathy

A

glycaemic control
bp control
cholesterol control (statins, fibrates)
support renal function
smoking cessation
weight control
exercise

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104
Q

what is the bp aim for someone with diabetic retinopathy

A

130/80

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105
Q

for diabetic patients with no retinopathy or background/mild non proliferative diabetic retinopathy how often should patients be monitored for screening

A

annually

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106
Q

pre proliferative to moderate to severe NPDR should be monitored in

A

hospital

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107
Q

what can be used for the management of proliferative retinopathy

A

laser - panretinal photocoagulation

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108
Q

what anti VEGF drug can be used off licence for the treatment of proliferative diabetic retinopathy

A

bevacizumab

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109
Q

what can be used for the management of non central macular oedema

A

macular laser

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110
Q

what 2 drug classes can be used for the management of centre involving macula oedema

A

intravitreal therapy

anti vegf and corticosteroids

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111
Q

what laser is used for panretinal photocoagulation PRP

A

argon green 514nm laser

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112
Q

how does PRP (panretinal photocoagulation) help treat retinopathy

A

laser absorbed by rpe pigment
converted to thermal energy -> outer retinal cell death + coagulative necrosis
reduces stimulus for neovascularisation

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113
Q

list some different complications/ risks of PRP

A

pain
loss of peripheral field
decreased acuity
retinal detachment
haemorrhage

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114
Q

macular laser is similar to PRP but is used to treat macular oedema, how does it work

A

gentle burns to macula
release of anti angiogenic factors
inhibition of angiogenic factors

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115
Q

how can hyperglycaemia lead to DME (diabetic macula edema)

A

hyperglycaemia -> retinal capillary damage
release of inflammatory cytokines and vegf
disrupts blood retinal barrier
vascular leakage
dme

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116
Q

what 2 drugs are licensed as intravitreal anti vegf therapies to treat diabetic macular oedema

A

afilbercept
ranibizumab

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117
Q

what procedure uses infrared light to capture images of layers of the retina to investigate for things like DMO/AMD

A

optical coherence tomography

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118
Q

true or false, optical coherence tomography cannot measure central retinal thickness

A

false
in DMO >400 at any point in centre = NICE Tx recomm

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119
Q

in DMO afilbercept is given every month for x consecutive months

A

5

120
Q

after 5 consecutive months of afilbercept therapy for DMO patients are given 1 injection every x months

A

2

121
Q

after the first 12 months of aflibercept therapy for DMO the treatment interval may be extended based on what 2 things

A

visual and anatomic outcomes

122
Q

true or false, aflibercept should be discontinued if the patient is not benefitting from continued treatment

A

true

123
Q

what drug is recommended as an option for treating visual impairment due to diabetic macula oedema if the eye has a central retinal thickness of 400 micrometers or more at the start of treatment

A

ranibizumab

124
Q

ranibizumab should be given monthly and continued until maximum visual acuity has been reached, how would you know when to determine this

A

visual acuity has been stable for 3 consecutive months

125
Q

after visual acuity has stabilised following treatment with ranibizumab visual acuity should be monitored at what intervals

A

monthly

126
Q

treatment with ranibizumab may have to continue if monitoring indicates a loss of visual acuity caused by diabetic macular oedema until 3 consecutive months of stable visual acuity. However, the interval between doses should not be shorter than x month

A

1

127
Q

intravitreal corticosteroids suppress inflammation to reduce oedema, give some examples of preparations for this use

A

triamcinolone acetate
dexamethasone implant
flucinolone acetonide implant

128
Q

how long does a dexamethasone implant last

A

6 months

129
Q

how long does a flucinolone implant last

A

3 years

130
Q

list some different risks of intravitreal corticosteroids

A

endophthalmitis
haemorrhage
retinal detachment
increased IOP
cataract

131
Q

true or false steroid drugs themselves can increase IOP

A

true

132
Q

true or false steroid drugs can themselves cause cataract

A

true

133
Q

dexamethasone implants should be used as second line treatments if what other methods have failed

A

anti vegf or macular laser

134
Q

intravitreal implants deliver dexamethasone for 6 months and may be repeated after 6 months if the patient experiences decreased vision or increase in retinal thickness with recurrent or worsening diabetic macular oedema

how much drug is delivered by the implant in this 6 month period

A

700 micrograms

135
Q

give one important side effect it is important to check for with intravitreal dexamethasone implants

A

increased IOP

136
Q

hypertensive retinopathy also exists, what is the best and only treatment option

A

bp control

137
Q

what are the different treatment options for retinal vein occlusion

A

risk factor modification
treat underlying condition
PRP
control iop
intravitreal therapy

138
Q

would you treat retinal vein occlusion with PRP if associated with ischaemia or oedema

A

ischaemia

139
Q

would you treat retinal vein occlusion with PRP or intravitreal therapies like corticosteroids or anti vegf if associated with ischaemia or oedema

A

oedema

140
Q

list some different treatment options for retinal artery occlusion

A

modify risk factors
treat underlying cause
lower iop

141
Q

give 3 ways that iop may be lowered

A

iv acetazolamide
ocular massage
rebreathing into paper bag(?)

142
Q

Lecture 3/4: Glaucoma

what is glaucoma

A

progressive optic neuropathy

143
Q

glaucoma is characterised by optic nerve head (disc) changes and corresponds with loss of

A

visual field

144
Q

what is the most important treatable risk factor

A

raised intraocular pressure (glaucoma)

145
Q

what is the name of angle between the cornea and iris known as

A

anterior chamber angle

146
Q

what is contained within the anterior chamber angle

A

trabecular meshwork

147
Q

the ciliary body produces aqueous, how does it get to the anterior chamber of the eye

A

goes into post chamber behind the iris and then through the pupil

148
Q

what structure in the eye is a circumferential structure that drains aqueous into collector channels

A

schlemms canal

149
Q

from the collector channels where does the aqueous drain into

A

episcleral veins

150
Q

name of the fibrocellular structure through which aqueous drains into schlemms canal

A

trabecular meshwork

151
Q

what are the 2 aqueous humour outflows in the eyes

A

uvoscleral and trabecular

152
Q

if the aqueous humour is drained via uveoscleral outflow where does it drain into

A

choroidal circulation

153
Q

when the aqueous humours drains via trabecular outflow, where does it drain into

A

episcleral circulation

154
Q

what is the term given to the inflow and outflow of aqueous in the eye

A

IOP

155
Q

true or false, the range for IOP in the general population is 11-21 mmHg with values over 21 associated with increased risk of glaucoma

A

true

156
Q

true or false, you cannot get glaucoma with an IOP value below 21 mmhg

A

false

157
Q

IOP can fluctuate between individuals, list some different causative factors

A

time of day
heartbeat
blood pressure
respiration

158
Q

what are the 4 different types of glaucoma

A

primary open angle
primary angle closure
secondary open angle
secondary angle closure

159
Q

which type of glaucoma is most common

A

primary open angle

160
Q

what is the cause of primary open angle glaucoma

A

abnormal resistance to outflow of aqueous mainly in trabecular meshwork

161
Q

primary open angle glaucoma causes pressure induced ischaemia of the x

A

optic nerve capillary bed

162
Q

in primary open angle glaucoma there is mechanical pressure on the optic nerve head, what does this lead to

A

reduced axoplasmic flow

163
Q

different risk factors for developing primary open angle glaucoma

A

smoking
diabetes
htn
high cholesterol
myopia

164
Q

primary angle closure glaucoma may be acute in nature i.e. sudden rise in IOP or

A

chronic

165
Q

what is the cause of primary angle closure glaucoma

A

drainage angle becomes narrow
fluid cannot exit through trabecular meshwork/ schlemms canal

166
Q

secondary open angle glaucoma is caused by blockage of the trabecular meshwork, list some different things that can cause this

A

cells
proteins
blood
tumour cells
drugs

167
Q

give a type of drug that could cause secondary open angle glaucoma

A

steroids

168
Q

what might be the cause of cells/protein in the trabecular meshwork that eventually block it and give rise to secondary open angle glaucoma

A

inflammation

169
Q

what is the cause of secondary closed angle glaucoma

A

narrowing of angle

170
Q

list some different factors that can cause angle narrowing in secondary closed angle glaucoma

A

tumours pushing iris or lens forward
iris sticking to angle
new blood vessels

171
Q

how can diagrams of visual fields show defects that would be indicative of glaucoma and its progression

A

dark spots represent areas missed by patients on testing

172
Q

3 Tx options for glaucoma/ visual field defect

A
  • medical: drops, systemic
  • laser: iridotomy/ trabech/ cyclophotocoag
  • surgery
173
Q

topical medical therapy for glaucoma commonly involves eye drops, list some different drug classes that would be used to treat this disease

A

prostaglandin analogues
beta blockers
carbonic anhydrase inhibitors
alpha 2 agonists
miotics

174
Q

alpha 2 agonists aka

A

sympathomimetics

175
Q

miotics aka

A

parasympathomimetics

176
Q

what classes of drug can be used for systemic medical therapy for the treatment of glaucoma

A

carbonic anhydrase inhibitors
osmotics

177
Q

what drug class is often used as first line in the treatment of glaucoma

A

prostaglandin inhibitors

178
Q

what is the moa of prostaglandin inhibitors in the treatment of glaucoma

A

increase uveoscleral outflow

179
Q

side effects of prostaglandin inhibitors

A

red eye
pigmentation
inflammation
bronchospasm

180
Q

list some areas where pigmentation can occur as a side effect of prostaglandin inhibitor use

A

iris
skin
lash

181
Q

true or false, prostaglandin inhibitors can cause eyelash thickening and lengthening

A

true

182
Q

give some examples of prostaglandin inhibitors which may be used in the treatment of glaucoma

A

latanoprost
bimatoprost
travoprost

183
Q

what is the moa of bb in the treatment of glaucoma

A

reduce aq production the ciliary body

184
Q

list 2 respiratory Contra Indications for the use of bb to treat glaucoma

A

asthma, COPD

185
Q

list 3 cardiac CI for the use of bb to treat glaucoma

A

heart failure
heart block
bradycardia

186
Q

list some different side effects of beta blockers when used in the treatment of glaucoma

A

allergic conjunctivitis
bronchospasm
bradycardia
hypotension
lethargy
glucose intolerance
impotence

187
Q

most common bb used for topical eye drops to treat glaucoma

A

timolol,

levobunolol and cartelol also used

188
Q

what is the moa of carbonic anhydrase inhibitors when used in the treatment of glaucoma

A

decrease aq production in ciliary body

189
Q

list some CI for carbonic anhydrase inhibitors

A

sulphonamide sensitivity
renal failure
liver failure

190
Q

true or false, the use of acetazolamide is only contraindicated in liver/renal failure when the drug is given systemically

A

true

191
Q

carbonic anhydrase inhibitors topical/ local SEs

A

burning
watery eyes
metallic taste
allergic conjunctivitis

192
Q

list some different systemic side effects that are associated with the use of carbonic anhydrase inhibitors

A

lethargy
depression
metallic taste
hypokalemia

193
Q

dorzolamide and brinzolamide are examples of what class of drugs that are used to treat glaucoma

A

carbonic anhydrase inhibitors

194
Q

are dorzolamide/brinzolamide used topically or systemically

A

topically

195
Q

acetazolamide is a drug that is used systemically in the treatment of glaucoma either PO or IV, list some different side effects

A

lethargy
depression
metallic taste
hypokalemia
renal calculi
blood dyscrasia

196
Q

what class of drugs does acetazolamide interact with to cause profound hypokalemia

A

thiazide diuretics

197
Q

alpha 2 agonists have a dual mechanism when used in the treatment of glaucoma, what is this

A

decrease aq production
increase uveoscleral outflow

198
Q

what ocular side effect could occur as a result of alpha 2 agonist use

A

allergic conjunctivitis

199
Q

what systemic side effects could occur due to use of alpha 2 agonists

A

bradycardia
hypotension
insomnia
irritability
GI disturbance

200
Q

name 2 alpha 2 agonists that may be used in the treatment of glaucoma

A

brimonidine
apraclonidine

201
Q

how do miotics work to treat glaucoma

A

muscarinic agonists
ciliary muscle contraction
opens trabecular meshwork
increases trabecular outflow

202
Q

why are miotics commonly used in angle closed glaucoma

A

iris constriction may pull iris away from angle

203
Q

list some different side effects of miotics

A

sweating
salivation
nausea
headache
bradycardia

204
Q

name one example of a miotic drug

A

pilocarpine

205
Q

give an example of an osmotic agent that is used iv

A

mannitol

206
Q

under what circumstances would you give IV mannitol to patients with glaucoma

A

acute angle closure where temporary drop in IOP is required that cannot be achieved by other means

207
Q

moa of mannitol when used in the treatment of glaucoma

A

water drawn out of vitreous into blood
by osmotic gradient
decrease in vitreous volume
so IOP decreases

208
Q

list 2 side effects of mannitol when used in this way

A

urinary retention and fluid overload

209
Q

CI for the use of mannitol in the treatment of glaucoma

A

cardiac disease /
heart failure

210
Q

Lecture 4/4: age related macular degeneration ARMD

what is ARMD

A

age related deterioration in the macula

211
Q

what effect does armd have on central vision

A

reduction

212
Q

list some different risk factors for developing armd

A

age
smoking
female
white
dietary
cv risk
hypermetropia

213
Q

is hypermetropia more of a risk factor for glaucoma or armd

A

armd

214
Q

is myopia more of a risk factor for glaucoma or armd

A

glaucoma

215
Q

2 types of ARMD?

A

dry (non-neovascular)
wet (neovascular)

216
Q

what is meant by dry armd

A

non neovascular age related macular degradation

217
Q

there are 4 categories of armd and they are ranked by severity, what ARED classification does no amd fall under

A

1

218
Q

what category is advanced/late amd

A

4

219
Q

is the majority of amd dry or wet

A

dry

220
Q

true or false, dry AMD is associated with a gradual but potentially significant reduction in central vision

A

true

221
Q

list 4 different features of dry amd

A

drusen
rpe changes
geographic atrophy
basement membrane deposit

222
Q

in dry amd what is meant by drusen and where does it occur

A

PAS positive amorphous deposit between RPE basement membrane and inner collagenous layer of bruchs membrane

223
Q

what RPE changes can be observed in dry amd

A

focal hyperpigmentation seen as clumps of pigment cells

224
Q

geographic atrophy occurs in the later stages of dry amd and results in the loss of what 2 things

A

rpe and photoreceptors

225
Q

in dry amd where does basement membrane deposit/ basal linear deposit occur

A

between RPE basement membrane and RPE cells

226
Q

give 2 symptoms of dry amd

A

Dec vision
Distortion

227
Q

what supportive treatment exists for dry amd

A

counselling
support groups
visual aids

228
Q

what does refraction involve when used as a treatment method for dry amd

A

best spectacle correction
magnification

229
Q

what grid allows for the self monitoring of distortion in dry amd

A

Amsler

230
Q

what lifestyle changes can you recommend to patient with dry amd

A

smoking cessation and dietary changes

231
Q

true or false, vitamin supplementation may help in the treatment of dry amd

A

true

232
Q

supplements are shown to reduce the progression of dry AMD, what is the current recommended daily amount of vitamin c

A

500mg

233
Q

how many international units of vitamin E are recommended for dry amd

A

400

234
Q

is wet or dry amd associated with rapid and severe loss of vision

A

wet

235
Q

give 3 features of wet amd

A

new capillary growth
proliferation
sequelae

236
Q

in wet amd new capillaries grown from x through bruchs membrane and is known as choroidal neovascularisation

A

choriocapillaris

237
Q

where does proliferation occur in wet amd

A

beneath rpe or retina

238
Q

give 3 causes of sequelae as seen in wet amd

A

haemorrhage
leakage
scarring

239
Q

what might cause scarring and fibrosis in the eye

A

activation of macrophages and endothelial cells

240
Q

list some different clinical features of amd

A

decreased vision
distortion
scotoma
grey haemorrhage
fluid
subretinal fibrosis

241
Q

what does scotoma mean

A

missing patches

242
Q

what imaging technique is important in investigating and monitoring the following features:

subretinal fluid
intraretinal fluid
cystoid macular oedema
pigment epithelial detachment
fibrosis/ scarring

A

OCT

243
Q

what is injected iv to allow for fundus fluorescein angiograms

A

fluorescein

244
Q

fluorescein absorbs blue light in what wavelength

A

465-490nm

245
Q

fluorescein emits light with a longer wavelength at 520-530nm which corresponds to what colour in the spectrum

A

yellow-green

246
Q

for fundus fluorescein angiogram a camera used with a filter, which only lets x through to take images of circulation

A

light of wavelength emitted by fluorescein

247
Q

as well as supportive therapies for wet amd what 2 other therapies exist

A

intravitreal anti vegf and photodynamic

248
Q

rationale behind using intravitreal therapy to inhibit vegf-a

A

induces angiogenesis
increases vascular permeability
induces inflammation

249
Q

4 anti vegf therapies that may be used for the treatment of wet amd

A

ranibizumab
afilbercept
pegaptinib
bevacizumab

250
Q

name the anti vegf therapy

humanised mab fragment
binds to all vegf isoforms
prevents binding to its receptors vegfr1 and vegfr2

A

ranibizumab

251
Q

name the anti vegf therapy

fusion protein
binds to vegf a

A

afilbercept

252
Q

name the anti vegf therapy

oligonucleotide with polyethylene glycol attached
binds to vegf-165
not recommended by nice

A

pegaptinib

253
Q

name an anti vegf therapy that is derived from the same antibody as ranibizumab

A

bevacizumab

254
Q

name the 2 licensed anti veg f therapies

A

ranibizumab
aflibercept

255
Q

list some different risks/ complications of anti vegf therapy in the treatment of wet amd

A

endophthalmitis (infection)
retinal detachment
lens damage
cataract
raised iop
haemorrhage
inflammation
pain
visual loss
floaters

256
Q

why do most centres advise caution with anti vegf therapies in patients who have had a stroke/mi/heart failure in the last 3 months

A

possible risk of stroke/ MI

257
Q

what is the recommended dose of ranibizumab

A

0.5mg

258
Q

what is the treatment regimen of ranibizumab in the loading phase

A

1 injection per month for 3 consecutive months

259
Q

during the maintenance phase of ranibizumab what are patients monitored for monthly

A

visual acuity

260
Q

during the maintenance phase if patients experience a loss greater then x letters on a snellen chart or one snellen line equivalent a further dose of ranibizumab should be administered

A

5

261
Q

the interval between doses of ranibizumab should not be shorter than x months

A

1

262
Q

what is the recommended dose of afilbercept

A

2mg
wet armd

263
Q

when starting afilbercept treatment should be given monthly for x consecutive months

A

3

264
Q

after the initial 3 month period on afilbercept, 1 injection should be given every x months

A

2

265
Q

true or false, afilbercept solution for injection must only be admin by a qualified doctor experienced in admin intravitreal injections

A

true

266
Q

is there a need for monitoring in between injections of aflibercept yes or no

A

no

267
Q

after the first 12 months of aflibercept treatment the treatment interval may be extended based on what 2 outcomes

A

visual and anatomic

268
Q

if treatment on aflibercept is prolonged monitoring schedules should be determined by who

A

treating doctor

269
Q

photodynamic therapy or PDT is no longer widely used since the introduction of anti vegf therapies, however what drug does it use

A

verteporfin

270
Q

verteporfin is given at a dose of 6mg/m2 of BSA over 10 mins via what route

A

IV

271
Q

15 mins after the start of the verteporfin infusion what is applied over a circular area slightly larger than the lesion

A

low powered laser at 689nm

272
Q

how does PDT help to manage wet amd

A

laser light absorbed by drug
becomes activated
forms cytotoxic free radicals
damage new blood vessels
leading to closure

273
Q

recommendation of PDT depends on the type of wet PDT and this is determined by the

A

appearance on fundus fluorescein angiogram

274
Q

name 3 different types of wet amd

A

classic cnv
occult cnv
mixed picture

275
Q

which type of wet amd
well demarcated lacy hyperfluorescence and progressive leakage

A

classic cnv

276
Q

which type of wet amd

fibrovascular PED, irregular elevation, stippled hyperfluorescence

A

occult cnv

277
Q

PDT is recommended for people with a confirmed diagnosis of

A

classic with no occult subfoveal choroidal neovascularisation

278
Q

Opthalmology SDL

What are the four main types of conjunctivitis?

A
  • Allergic
  • Bacterial
  • Adenoviral
  • Chlamydial
279
Q

What questions should you ask a px with suspected conjunctivitis?

A

Check if need referral

Onset and duration.
Pain in or around the eye?
Photophobia?
Any associates systemic symptoms - headaches, sickness
Discharge from eyes - colour, how much
Itching
Changes in vision such as blurring
Eyelid changes such as swelling, flaking and vesicles

280
Q

what are the red flags for suspected conjuctivitis?

A

Severe pain in eye
Swelling/ pain around
Visual acuity.
Red sticky eye in neonates.
Lots of discharge.
Upper resp infections.
Enlarged tender lymph nodes.
Contact lens.
Recurrent infections.
Ophthalmic surgery.
Drug Hx - anticholinergics and anticoagulants.

281
Q

How should you manage complaints of conjunctivitis in patients who wear contact lenses?

A

Refer to specialist.

Advise to stop wearing contact lenses immediately.

282
Q

advice for contact lens wearers when using chloramphenicol/ conjuctivitis Tx?

A
  • Do not wear contacts during treatment
  • Avoid contacts until 24 hours after treatment stopped
  • Do not reuse old contact lenses  reinfection
283
Q

restrictions on prescribing ranibizumab for diabetic macular oedema (DMO) in the NHS?

A

Recommended for treating visual impairment due to DMO if:
Eye has central retinal thickness of 400 microM or more at start of treatment

… and manufacturer provides drug with discount agreed in px access scheme revised in context of this appraisal

284
Q

Mechanism of action of ranibizumab?

A

When a patient has DMO, the body produced too much VEGF which causes blood vessel to grow too thickly and too quickly.

Ranibizumab is a human recombinant monoclonal antibody and it inhibits VEGF. Therefore it reduces oedema and improves vision.

285
Q

What are barriers to drug like ranibizumab being administered systemically?

A

Drug delivery to the back of the eye by systemic administration is restricted by the tight junctions of the blood brain barrier.

286
Q

Why is ranibizumab administered as an injection and not a topical eye drop solution?

A

site of action: post segment of eye

bypass ocular barriers

o high tier turnover, the nasal drainage, reflex blinking
o or things like poor interocular penetration.
direction of penetration opposite to direction of intraocular liquid circ

287
Q

How can drug delivery to the posterior segment of the eye be improved?

A

prodrugs and nanoparticles

288
Q

why us aflibercept better than bevacizumab

A

binds VEGf A with higher affinity

289
Q

complications of intravitreal therapy

A

cataract, inflammation, pain, raised IOP, visual loss, floaters

290
Q

do the DVLA need to be notified of a diagnosis of diabetic macular oedema

A

yes

291
Q

What is Sjogren’s syndrome?

A

systemic autoimmune disease that affects exocrine galnds - causes a deficiency in saliva, tears, skin lubrication, and other exocrine secretions -

292
Q

What types of medications cause dryness? Make symptoms of dryness worse? E.g.dry mouth

A

anticholinergics

293
Q

what meds also exacerbate dryness symptoms?

A

o Antihistamines
o Some antidepressants: tricyclics, amitriptyline
o Some antipsychotics
o Antimuscarinics: hyoscine butylbromide/ hydrobromide

294
Q

Sjogren’s syndrome treatnent

A

Good eyelid hygiene
eye ointments more effective at adhering to eye for long time

  • Immunosuppressive meds hydroxychloroquine
  • Lozenges/ gels (saliva substitutes)
  • Pain relief
295
Q

why may the parotid gland be swollen in SJS?

A

B lymphocytes overactive, cause inflammation.
build up in salivary glands etc, damage
B cell lymphoma likely. Must exclude - ultrasound

Finals (29 decks)

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