CFB OPHTH02 Ocular Manifestations Of Systemic Disease
Ocular manifestations of systemic disease refer to the eye findings—such as retinopathy, uveitis, optic neuropathy, or vascular changes—that arise as complications of underlying systemic conditions including diabetes, hypertension, autoimmune disorders, and infections.
Ocular Manifestations of Systemic Disease
This lecture, delivered by Dr. Kendrick Shih, centres on one crucial concept: the retina is the only place in the body where we can non-invasively visualize microvasculature, making fundoscopy a window into systemic vascular health. The lecture focuses on three retinal manifestations:
- Diabetic Retinopathy — the most frequent cause of preventable blindness in working-aged adults
- Hypertensive Retinopathy — a grading system for hypertension control, not a standalone disease
- Retinal Vein Occlusion — a common complication of hypertension-induced arteriosclerosis
The exam loves this lecture because it bridges medicine and ophthalmology: you must understand the systemic disease (DM, HTN) to interpret the fundoscopic signs, and you must recognize the fundoscopic signs to diagnose/stage the systemic disease. Past papers have tested diabetic retinopathy classification, hypertensive retinopathy grading, hydroxychloroquine maculopathy (SLE context), and Graves' ophthalmopathy — all fall under "ocular manifestations of systemic disease."
1. The Retina: Anatomy You Must Know for Fundoscopy
"The retina is the sensory portion of the eye and contains layers of photoreceptors, nerves, and supporting cells. The layer containing the ganglion cells, bipolar cells, and rod and cone photoreceptors is known as the neurosensory retina." [1]
"The retina is the only place where we can non-invasively visualize the micro-vessels in our body, thus allowing us to better understand systemic vascular health." [1]
Why this matters: When an examiner asks you to perform fundoscopy on a hypertensive or diabetic patient, they're testing whether you understand that you're looking at a live microvascular bed — the same vessels that are being damaged in the kidneys, brain, and heart.
| Structure | What to Look For | Clinical Significance |
|---|---|---|
| Optic disc | Margins (sharp vs blurred), colour (yellow-pink vs pale), cup-to-disc ratio | Papilloedema (blurred margins = ↑ICP); optic atrophy (pale disc) |
| Retinal vasculature | Arteries vs veins, AV crossings, calibre, tortuosity | HTN changes (silver wiring, AV nipping); diabetic changes |
| Macula lutea | Pigmented area, contains xanthophyll pigment (lutein + zeaxanthin = antioxidants) | Central vision; diabetic macular oedema threatens this area |
| Fovea centralis | Thin pit within the macula; derives nutrition ENTIRELY from underlying choroid | Susceptible to injury in retinal detachment (no retinal blood supply here) |
"The macula is the pigmented area of the retina responsible for central vision. The yellow tone is due to the presence of xanthophyll pigment (lutein and zeaxanthin), which serve as anti-oxidants." [1]
"The fovea is very thin and derives its nutrition entirely from the underlying choroid, making it susceptible to injury during retinal detachments." [1]
Why the fovea is special: Because it has no overlying retinal vessels (to avoid scattering light), it is entirely dependent on choroidal blood supply. This is why a retinal detachment that reaches the macula causes severe, often irreversible, central vision loss.
This is a classic exam question: "Why do haemorrhages look different in different conditions?"
"The morphology of the retinal hemorrhage is determined by the retinal layer." [1]
| Haemorrhage Type | Location | Morphology | Why This Shape? | Think Of... |
|---|---|---|---|---|
| Pre-retinal haemorrhage | Between vitreous and retina | Boat-shaped / retrohyaloid | Sits in the potential space between vitreous and retina; gravity causes blood to pool with a flat upper level; no nerve fibres to restrict horizontal spread | Proliferative diabetic retinopathy |
| Flame-shaped haemorrhage | Superficial nerve fibre layer (intra-retinal) | Flame/splinter | Nerve fibres in superficial layer run horizontally → blood tracks along them | Hypertensive retinopathy, retinal vein occlusion |
| Dot and blot haemorrhage | Deep retinal layers (intra-retinal) | Dot or blot | Deep layers have vertical arrangement of cells → blood pools in small round pockets | Diabetic retinopathy |
Exam Trap: Haemorrhage Morphology
Flame-shaped haemorrhages are superficial (nerve fibre layer) and suggest hypertension or vein occlusion. Dot-and-blot haemorrhages are deep and suggest diabetic retinopathy. Pre-retinal/boat-shaped haemorrhages suggest proliferative diabetic retinopathy with new fragile vessels. The shape tells you the layer, and the layer tells you the disease.
2. Diabetic Retinopathy (DR)
"Most frequent cause of preventable blindness in working-aged adults." [1]
| Fact | Detail |
|---|---|
| Prevalence in Type 1 DM | ~80% |
| Prevalence in Type 2 DM | ~40% |
| Overall lifetime risk | ~80% amongst all diabetics |
| Trend | Increasing prevalence in recent decades |
Why "preventable"? Because regular screening fundoscopy + tight glycaemic/BP control can catch DR before it threatens sight, and early treatment (laser, anti-VEGF) can prevent blindness. This is a public health question as well as a clinical one.
From both the lecture and supporting notes [1][2]:
- Duration of DM — 80% have DR after 20 years of disease
- Poor glycaemic control (HbA1c)
- Vascular comorbidities — especially hypertension, smoking
- Pregnancy — can accelerate DR progression
- Rapid implementation of tight glycaemic control — paradoxically can worsen DR transiently
The lecture explicitly states: "You won't be tested on this in MBBS IV" for the detailed pathway, but you MUST understand the broad concept because it explains every clinical sign.
Hyperglycaemia
→ Oxidative stress, AGEs, PKC activation, inflammation, sorbitol accumulation
→ Vascular endothelial dysfunction
→ Two consequences:
1. ↑Vascular permeability → leakage → oedema, hard exudates
→ DIABETIC MACULAR OEDEMA
2. Retinal ischaemia → VEGF/IGF release
→ Retinal neovascularization
→ PROLIFERATIVE DRFirst principles explanation:
- Chronic hyperglycaemia damages the endothelial cells lining retinal capillaries through multiple biochemical pathways (oxidative stress, advanced glycation end-products, protein kinase C activation, sorbitol accumulation via the polyol pathway)
- This endothelial damage causes two problems simultaneously:
- Leaky vessels (↑vascular permeability) → fluid and lipoproteins leak into the retina → retinal oedema and hard exudates
- Blocked vessels (microthrombosis, capillary occlusion) → retinal ischaemia → the ischaemic retina screams for help by releasing VEGF → new (but fragile, abnormal) blood vessels grow = neovascularization
"Intraretinal hemorrhages — usually visually insignificant" [1] "Hard exudates — lipoproteins following partial/complete resorption of retinal edema" [1] "Cotton wool spots — focal areas of ischemic infarcts" [1] "Intraretinal microvascular abnormalities (IRMA) — pre-neovascularization retinal vascular abnormalities" [1]
| Sign | What It Is | Why It Happens | Layer/Significance |
|---|---|---|---|
| Microaneurysms | Tiny outpouchings of capillary walls | Pericyte loss → weakened capillary wall | Earliest clinical sign of DR |
| Dot-and-blot haemorrhages | Small round intraretinal haemorrhages | Microaneurysm rupture in deep retinal layers | Deep layer → round shape |
| Hard exudates | Yellow, waxy deposits with sharp margins | Lipoprotein residue after retinal oedema partially resorbs | Indicate vascular leakage; concerning if near macula |
| Cotton wool spots | White, fluffy patches | Focal ischaemic infarcts of retinal nerve fibre layer → axoplasmic flow stasis → swollen axon tips | Indicate retinal ischaemia |
| IRMA | Abnormal shunt vessels within the retina | Represent pre-neovascularization changes; dilated capillary channels | Indicate severe NPDR → about to tip into PDR |
| Venous beading | Irregular calibre of retinal veins | Retinal ischaemia affecting venous wall | Predictor of progression to PDR |
2.5 The Two Sight-Threatening Conditions
"Two major sight-threatening conditions in diabetic retinopathy: (1) Diabetic macular oedema, (2) Proliferative diabetic retinopathy." [1]
This is the critical clinical distinction: DMO can occur at ANY stage of DR (even mild NPDR), while PDR represents advanced ischaemia-driven neovascularization.
Pathophysiology: ↑vascular permeability pathway → fluid accumulation in the macular area → thickened retina → reduced central visual acuity.
Clinical examination findings:
- Hard exudates near or at the macula
- Retinal oedema (thickened retina, best seen on OCT)
Why DMO matters most for vision: The macula is responsible for central vision (reading, driving, recognizing faces). Even mild oedema here causes disproportionate visual impairment compared to peripheral retinal changes.
Investigation: Optical Coherence Tomography (OCT) — cross-sectional imaging of retinal layers showing increased macular thickness and fluid pockets (the lecture notes "you won't be tested on this" but understand the concept) [1].
Treatment (marked as not testable in MBBS IV, but know the principles):
- Macular laser photocoagulation
- Intravitreal anti-VEGF agents injection
- Intravitreal steroid injection
"Diabetic macular oedema is the commonest cause of vision loss in DM patients." [2]
Pathophysiology: Retinal ischaemia → VEGF/IGF release → growth of new vessels (neovascularization).
"Characterized by the presence of new vessels — thin (hair-like), pre-retinal, blind-ending." [1]
Why new vessels are dangerous: These new vessels are:
- Fragile — they lack the structural integrity of normal vessels
- Pre-retinal — they grow on the retinal surface into the vitreous cavity
- Leaky — they allow fluid/blood to escape (fluorescein angiography shows leakage = hallmark of unstable new vessels)
Complications of PDR (cascade of worsening):
| Complication | Mechanism | Visual Impact |
|---|---|---|
| 1. Pre-retinal haemorrhage | Fragile new vessels bleed between retina and vitreous | Boat-shaped haemorrhage, may obscure vision |
| 2. Vitreous haemorrhage | Blood fills the vitreous cavity | Sudden painless loss of vision ("red out") |
| 3. Fibrovascular proliferation | Fibrous tissue grows along with new vessels | Creates tractional membranes on retinal surface |
| 4. Tractional retinal detachment | Fibrovascular membranes contract, pulling retina off | Severe, often irreversible vision loss |
| 5. Neovascular glaucoma | Neovascularization of iris (rubeosis iridis) → new vessels + fibrous tissue block aqueous drainage angle | Painful eye with very high IOP → optic nerve damage |
High Yield: Why Rubeosis Iridis Causes Glaucoma
When the ENTIRE retina is ischaemic, massive VEGF is released. VEGF has nowhere to go posteriorly, so it diffuses anteriorly to the iris and anterior chamber angle. New vessels grow on the iris surface (rubeosis iridis) and in the drainage angle. The ensuing fibrosis blocks aqueous outflow → acute angle closure → neovascular glaucoma. This is why PDR can cause both posterior segment (vitreous haemorrhage, retinal detachment) AND anterior segment (glaucoma) complications. [1][2]
Treatment of PDR (marked as not testable in MBBS IV, but important concepts):
- Panretinal photocoagulation (PRP) — destroys peripheral ischaemic retina → reduces VEGF production → regression of new vessels
- Anti-VEGF injection — if no traction (because anti-VEGF can accelerate traction by causing fibrosis of new vessels)
- Vitrectomy — for non-resolving vitreous haemorrhage, tractional retinal detachment, tractional-rhegmatogenous retinal detachment
| Complication | Mechanism |
|---|---|
| Cataract | Activation of polyol/pentose pathway → sorbitol accumulation within lens → osmotic swelling → opacification |
| CN III, IV, VI palsies | Mononeuritis multiplex from vasa nervorum ischaemia |
| Neovascular glaucoma | Rubeosis iridis (see above) |
| Fluctuating refractive errors | Osmotic lens swelling with glucose fluctuations |
| ↓ Tear production | Autonomic neuropathy |
3. Hypertensive Retinopathy
"Not a disease, just a grading system for hypertension control." [1]
This framing is critical for exams. The lecture explicitly states this is an arteriosclerotic grading system, not a separate diagnosis. It tells you about the chronicity and severity of hypertension.
This table is directly from the lecture slides and is extremely high yield. [1]
| Grade | Findings | What's Happening |
|---|---|---|
| Grade 0 | No changes | Normal |
| Grade 1 | Barely detectable arterial narrowing (silver wiring) | Arteriosclerosis → thickened arterial wall becomes more light-reflective |
| Grade 2 | Obvious arterial narrowing with focal irregularities (arterio-venous nipping) | Thickened artery at AV crossing compresses the vein (they share a common adventitial sheath) |
| Grade 3 | Grade 2 + retinal haemorrhages and/or exudates | Venous obstruction → flame-shaped haemorrhages + cotton wool spots (ischaemia) |
| Grade 4 | Grade 3 + disc swelling (papilloedema) | Raised intracranial pressure or severe malignant hypertension |
Critical Definition: Malignant Hypertension
"Hypertensive emergency is the coexistence of very high BP values ( > 180/120 mmHg) with evidence of end-organ damage. A diagnosis of malignant hypertension requires evidence of end-organ damage. Retinal findings of end-organ damage require at least Grade 3 hypertensive retinopathy." [1]
This means: You CANNOT diagnose malignant hypertension without at least Grade 3 retinopathy (haemorrhages/exudates). Silver wiring and AV nipping alone (Grades 1-2) indicate chronic arteriosclerosis but NOT acute end-organ damage.
3.2 Individual Signs Explained
"Due to arteriosclerosis, the muscle wall of the arteries become thicker and more light-reflective." [1]
Normal retinal arteries have a thin, transparent wall so you see the blood column through them. With chronic HTN, the media hypertrophies and becomes sclerotic → the wall reflects light → the artery looks like a "silver wire."
"At areas where the artery and vein cross, and also within the optic nerve canal, the retinal arteries and veins share a common adventitial sheath. Therefore within a finite space, the increasingly thickened artery may compress the vein." [1]
Why this matters clinically: AV nipping is the anatomical basis for branch retinal vein occlusion — the thickened artery physically compresses the vein at the crossing point, causing venous stasis → thrombosis → occlusion. This directly links Section 3 to Section 4 of this lecture.
"Prolonged/severe venous obstruction, leading to hemorrhage and retinal ischemia." [1]
These indicate acute/active damage — the hypertension is causing real-time harm to the retinal vasculature.
"Signifies presence of raised intracranial pressure." [1]
In hypertensive context, papilloedema reflects either:
- Severely elevated BP causing cerebral oedema → ↑ICP → disc swelling
- OR it can indicate hypertensive encephalopathy — a true emergency
From the supporting HTN lecture [4], hypertension causes end-organ damage to 5 regions:
| Organ | History | Examination/Investigation |
|---|---|---|
| Brain | Headache, vertigo, TIAs, sensory/motor deficit | Carotid bruit, neurological deficits |
| Eyes | Impaired vision → ischaemic retinopathy | Fundoscopic abnormalities, retinal artery narrowing |
| Heart | Palpitations, chest pain, SOB, ankle swelling | LVH, S3, rales, oedema |
| Kidney | Thirst, polyuria, nocturia | ↑Creatinine, proteinuria |
| Peripheral vessels | Claudication | Absent pulses, bruits |
4. Retinal Vein Occlusion (RVO)
| Type | Proportion | Presentation |
|---|---|---|
| Branch RVO (BRVO) | 69.5% | Visual field loss or may be asymptomatic |
| Central RVO (CRVO) | 30.5% | Presents with vision loss |
Why BRVO may be asymptomatic: If the occluded branch supplies peripheral retina, the patient may not notice the visual field defect. CRVO blocks the entire venous outflow → diffuse retinal ischaemia/haemorrhage → central vision affected.
The pathogenesis follows directly from the hypertensive retinopathy discussion:
- Hypertension → arteriosclerosis → thickened retinal artery
- At AV crossing points (shared adventitial sheath), the artery compresses the vein
- Venous compression → stasis → thrombosis → vein occlusion
- Upstream: venous congestion → haemorrhages, oedema
- Downstream: ischaemia → VEGF release → potential neovascularization
"Hypertension (95% of all cases)" [1]
| Risk Factor | Mechanism |
|---|---|
| Hypertension (95%) | Arteriosclerosis → AV compression → venous stasis |
| Diabetes | Endothelial dysfunction, hyperviscosity |
| Acute glaucoma | ↑IOP compresses central retinal vein at lamina cribrosa |
| Hypercoagulable state | ↑Tendency for thrombosis (e.g. APLS, malignancy) |
| Cardiovascular disease | Generalized atherosclerosis |
Exam Pearl: HTN is the #1 Risk Factor for RVO
If an exam question presents a patient with sudden visual field loss or vision loss + dilated tortuous veins + flame-shaped haemorrhages on fundoscopy, the diagnosis is retinal vein occlusion. The FIRST thing to look for and manage is hypertension (present in 95% of cases). Always check BP and cardiovascular risk factors. [1]
"Dilated and tortuous veins, flame-shaped hemorrhages, cotton wool spots, hard exudates." [1]
The fundoscopic picture of RVO is dramatic — sometimes described as "blood and thunder" fundus in CRVO:
- Dilated, tortuous veins — because outflow is blocked
- Flame-shaped haemorrhages — blood leaks in the nerve fibre layer (superficial)
- Cotton wool spots — ischaemic infarcts
- Hard exudates — lipoprotein leakage from damaged vessels
"May improve spontaneously." [1]
- Development of collaterals — bypass vessels may form
- Recanalization of thrombus — the clot may resolve
- 50% develop optociliary shunt vessels [1]
- Progression with ischaemic complications — if collaterals are insufficient:
- Neovascular glaucoma (same mechanism as PDR: ischaemia → VEGF → rubeosis iridis)
- Retinal neovascularization
"Identify & treat risk factors. Treat complications (if visual impairment present). Intravitreal anti-VEGF agents injection. Pan-retinal or sectoral laser photocoagulation." [1]
| Step | Action | Why |
|---|---|---|
| 1 | Identify and treat risk factors | BP control is paramount (95% have HTN); manage DM, lipids |
| 2 | Treat complications if visual impairment present | Macular oedema → anti-VEGF; neovascularization → laser |
| 3 | Intravitreal anti-VEGF injection | Reduces macular oedema and inhibits neovascularization |
| 4 | Pan-retinal or sectoral laser photocoagulation | Destroys ischaemic retina to reduce VEGF drive |
5. Beyond the Retina: Other Ocular Manifestations of Systemic Disease
While the lecture focuses on retinal manifestations, the broader topic of "ocular manifestations of systemic disease" is frequently tested. Integrating from supporting sources:
| Feature | Detail |
|---|---|
| Pathogenesis | Anti-TSHr antibodies → bind TSHr on orbital fibroblasts → cytokine release → adipogenesis + GAG accumulation → ↑retroocular tissue volume |
| Clinical: Lid signs | Lid retraction, lid lag, lagophthalmos |
| Clinical: Orbital signs | Proptosis/exophthalmos, ophthalmoplegia (IR > MR > SR > LR) |
| Sight-threatening | Compressive optic neuropathy (papilloedema, ↓colour vision, VF defects) |
| Risk factors | Smoking (2.22× risk), RAI treatment, higher TRAb titres |
From past paper [7] — Bull's eye maculopathy:
- HCQ accumulates in retinal pigment epithelium → toxic maculopathy
- Presents as bilateral progressive blurring of vision
- Bull's eye appearance on fundoscopy: ring of depigmentation around the fovea
- Irreversible once established
- Screening: annual eye check after 5 years of HCQ use [8]
- Corneal deposits from HCQ are reversible (distinguish from maculopathy)
| Disease | Ocular Manifestations |
|---|---|
| Rheumatoid Arthritis | 2° Sjögren's, peripheral ulcerative keratitis (PUK), episcleritis, scleritis, uveitis [10] |
| Seronegative SpA (e.g. AS) | Anterior uveitis (most classic), conjunctivitis (Reiter's syndrome triad) [10] |
| Behçet's Disease | Anterior/posterior/panuveitis, retinal vasculitis [10] |
| Giant Cell Arteritis | Anterior ischaemic optic neuropathy (AAION), central retinal artery occlusion (CRAO) [10] |
| IBD | Uveitis (usually anterior), episcleritis, scleritis, iritis [11] |
| Sarcoidosis | Uveitis (anterior > posterior), lacrimal gland involvement [12] |
- Roth's spots: yellow-centred haemorrhages (septic emboli to retina) [14]
Exam Intelligence
- Fundoscopy image → identify signs → classify DR stage / HTN grade
- "A 55-year-old diabetic presents with sudden painless loss of vision" → vitreous haemorrhage from PDR
- "Describe the retinal findings in this patient with poorly controlled hypertension" → Modified Scheie grading
- "What is the most common risk factor for retinal vein occlusion?" → Hypertension (95%)
- "Name two sight-threatening conditions in diabetic retinopathy" → DMO + PDR
- "A patient on HCQ for 8 years develops bilateral progressive blurring of vision" → Bull's eye maculopathy [7]
| Trap | Correct Answer |
|---|---|
| Confusing flame-shaped (superficial/HTN) with dot-blot (deep/DM) haemorrhages | Layer determines morphology |
| Thinking HTN retinopathy is a standalone disease | It's a grading system for HTN control |
| Assuming DMO only occurs in advanced DR | DMO can occur at any stage |
| Grade 1-2 HTN retinopathy = malignant HTN | Need at least Grade 3 for end-organ damage |
| Calling all disc swelling "papilloedema" | Papilloedema specifically = disc swelling due to ↑ICP; papillitis = inflammatory disc swelling with vision loss |
- "Diabetic retinopathy is the most frequent cause of preventable blindness in working-aged adults."
- "The two sight-threatening conditions in DR are: (1) diabetic macular oedema, (2) proliferative diabetic retinopathy."
- "Modified Scheie Grade 3: arterial narrowing with AV nipping PLUS retinal haemorrhages and/or exudates. This grade or above constitutes end-organ damage required for diagnosing malignant hypertension."
- "Hypertension is the most important risk factor for retinal vein occlusion, present in 95% of all cases."
-
SAQ: "Name the two sight-threatening conditions in diabetic retinopathy. Briefly describe the pathophysiology of each." (4 marks)
- DMO: ↑vascular permeability → fluid leakage into macular area → reduced central VA
- PDR: Retinal ischaemia → VEGF release → neovascularization with fragile pre-retinal vessels → risk of vitreous haemorrhage, tractional RD, neovascular glaucoma
-
MCQ: Patient with HTN, fundoscopy shows silver wiring and AV nipping. What grade? → Grade 2
-
SAQ: "List 4 complications of proliferative diabetic retinopathy." (4 marks)
- Pre-retinal haemorrhage, vitreous haemorrhage, fibrovascular proliferation, tractional retinal detachment, neovascular glaucoma (any 4)
-
MCQ: "Most common risk factor for retinal vein occlusion?" → Hypertension
-
SAQ: "A 60-year-old hypertensive patient presents with sudden visual field loss in one eye. Fundoscopy shows dilated tortuous veins, flame-shaped haemorrhages, cotton wool spots in one sector. What is the diagnosis? What is the management?" → BRVO; identify and treat risk factors (HTN!), anti-VEGF if macular oedema, laser if neovascularization
-
MCQ (past paper style): "A 54-year-old SLE patient on HCQ for 8 years develops bilateral progressive blurring of vision. Most likely cause?" → Bull's eye maculopathy [7]
High Yield Summary
-
The retina is the only non-invasive window to systemic microvasculature — fundoscopy is essential in DM and HTN assessment.
-
Haemorrhage morphology = retinal layer: Flame-shaped (superficial/NFLayer → HTN/vein occlusion); Dot-blot (deep → DM); Boat-shaped/pre-retinal (→ PDR).
-
DR is the #1 cause of preventable blindness in working-aged adults. Two sight-threatening conditions: (1) Diabetic macular oedema (can occur at any DR stage; commonest cause of vision loss in DM), (2) Proliferative DR (neovascularization → vitreous haemorrhage, tractional RD, neovascular glaucoma).
-
Hypertensive retinopathy = grading system (Modified Scheie 0–4), NOT a disease. Malignant HTN requires ≥ Grade 3 (haemorrhages/exudates ± disc swelling). Silver wiring = arteriosclerosis; AV nipping = shared adventitial sheath compression → predisposes to RVO.
-
Retinal vein occlusion: 2nd most common sight-threatening vascular disorder. HTN in 95% of cases. BRVO (69.5%) > CRVO (30.5%). Management: treat risk factors + anti-VEGF/laser for complications.
-
Other high-yield ocular manifestations: HCQ → Bull's eye maculopathy (irreversible, screen after 5 years); Graves' → proptosis, lid retraction, ophthalmoplegia (IR > MR > SR > LR); RA/SpA → episcleritis/scleritis/uveitis; GCA → AAION/CRAO; Wilson's → Kayser-Fleischer rings + sunflower cataract.
Active Recall - Ocular Manifestations of Systemic Disease
[1] Lecture slides: CFB (OPHTH02) Ocular Manifestations of Systemic Disease.pdf [2] Senior notes: Ryan Ho Endocrine.pdf (Section: Diabetic Retinopathy and Eye Complications) [3] Senior notes: Block A - Deterioration of eyesight in a diabetic patient_ diabetic complications.pdf [4] Senior notes: Block A - High blood pressure_ hypertension.pdf (Target organ damage section) [5] Senior notes: Ryan Ho Opthalmology.pdf (Section 7.1: Dysthyroid Eye Disease) [6] Senior notes: MBBS Final MB (Surgery) (Felix PY Lai).pdf (Graves' ophthalmopathy) [7] Past papers: 2021 Fourth Summative Assessment MCQ.pdf (Question 13) [8] Senior notes: Maksim Medicine Notes.pdf (SLE section, HCQ monitoring) [9] Senior notes: Block A - Facial rash and painful fingers_ SLE.pdf [10] Senior notes: Ryan Ho Opthalmology.pdf (Section 7.2: Rheumatological Disease and the Eye) [11] Senior notes: Block A - Chronic diarrhoea_ irritable bowel syndrome and inflammatory bowel disease.pdf (Extraintestinal manifestations) [12] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (Sarcoidosis section) [13] Senior notes: Ryan Ho GI.pdf (Wilson's disease section) [14] Senior notes: Ryan Ho Fundamentals.pdf (Fundoscopy section)
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