GC042 Deterioration Of Eyesight In A Diabetic Patient Diabetic Complications
Progressive visual impairment in a diabetic patient resulting from complications such as diabetic retinopathy, macular edema, or accelerated cataract formation due to chronic hyperglycemia-induced microvascular and lens damage.
Deterioration of Eyesight in a Diabetic Patient: Diabetic Complications
Lecture Map
This lecture is a comprehensive walk-through of all chronic diabetic complications — not just the eye — and the pharmacological arsenal used to prevent and treat them. It starts with the eye as the entry point (because diabetic retinopathy is the archetypal microvascular complication), then expands to cover nephropathy, neuropathy, macrovascular disease, and the full management framework including diet, oral hypoglycaemic agents, incretins, SGLT2 inhibitors, and insulin. The lecture is co-taught by Endocrinology (Prof Karen Lam) and Ophthalmology (Prof Christopher Leung), reflecting the multidisciplinary nature of diabetic care. [1]
- Diabetic complications are among the most heavily examined topics in the Fourth Summative, appearing in MCQ, SAQ, and minicase formats.
- Questions commonly test: classification of retinopathy findings on fundus photo, which drugs have cardio-renal benefits, side effects of oral agents, indications for insulin, and management principles for the subclinical/overt stages of microvascular complications.
- Past papers have directly asked about: DKA management (Q4, 2019 SAQ), fundus photo diagnosis of diabetic retinopathy (Q15, 2024 MCQ; Q11, 2025 MCQ), contraindication of pioglitazone in heart failure (Q28, 2024 MCQ), and diabetic macular oedema as cause of vision loss (Q11, 2025 MCQ). [2][3][4][5]
- List ocular complications of diabetes mellitus
- Classify diabetic retinopathy (NPDR vs. PDR) and describe fundoscopic findings
- Explain the pathogenesis of chronic diabetic complications
- Outline the principles of treating chronic complications at subclinical and overt stages
- Describe the pharmacology of all major anti-diabetic drug classes
- Know the side effects of every anti-diabetic drug (high yield)
- Understand insulin types, their kinetics, and indications for insulin therapy
- Describe the comprehensive management approach to T2DM (ADA framework)
Part 1: Ocular Complications of Diabetes Mellitus
"Important ocular complications of diabetes mellitus: Diabetic retinopathy (non-proliferative vs. proliferative), Diabetic macular edema, Neovascular glaucoma, III/IV/VI nerve palsies, and Cataract" — HIGH YIELD [1]
1.1 Diabetic Retinopathy (DR)
Diabetic retinopathy is the leading cause of preventable blindness in working-age adults. It occurs because chronic hyperglycaemia damages retinal microvasculature through several pathways: non-enzymatic glycation, polyol (sorbitol) pathway activation, formation of advanced glycation end-products (AGEs), and PKC activation. These lead to capillary basement membrane thickening, pericyte loss, increased vascular permeability, and eventual ischaemia. [1][6]
Pathophysiology Chain
Chronic hyperglycaemia → retinal microangiopathy → microaneurysms + haemorrhages (NPDR) → progressive ischaemia → VEGF release → neovascularisation (PDR) → vitreous haemorrhage / tractional retinal detachment
| Feature | Non-Proliferative DR (NPDR) | Proliferative DR (PDR) |
|---|---|---|
| Microaneurysms | ✓ (earliest clinical sign) | Present |
| Dot & blot haemorrhages | ✓ (deeper retinal layers) | Present |
| Soft exudates (cotton wool spots) | ✓ — swollen/infarcted nerve fibre layer; whitish fluffy lesions | Present |
| Hard exudates | ✓ — lipid & proteinaceous leak from chronic vascular damage; yellowish discrete lesions | Present |
| Venous beading | In severe NPDR | Present |
| IRMA | In severe NPDR | Present |
| Retinal neovascularisation | ✗ | ✓ — hallmark of PDR |
| Vitreous haemorrhage | ✗ | ✓ |
| Tractional retinal detachment | ✗ | ✓ |
"Soft exudates – swollen nerve fiber (whitish fluffy lesions). Hard exudates – lipid and proteinaceous materials from chronic vascular leakage (yellowish discrete lesions)." — Know this definition for fundus photo interpretation. [1]
Exam Trap: Soft vs Hard Exudates
Students frequently confuse soft and hard exudates. Soft exudates = cotton wool spots = nerve fibre infarction = white/fluffy. Hard exudates = lipid deposits = yellow/discrete/waxy borders. Hard exudates near the macula (especially arranged in a circinate pattern) suggest diabetic macular oedema.
- Duration of DM (most important — 80% have DR after 20 years)
- Poor glycaemic control (HbA1c)
- Hypertension
- Renal impairment
- Smoking
- Pregnancy (can accelerate DR)
- Rapid implementation of tight glycaemic control (paradoxical short-term worsening)
- "Usually none in early stages!" — This is why annual fundus screening is critical
- Later: gradual blurring (macular oedema), sudden deterioration (vitreous haemorrhage, retinal detachment)
DMO can occur at ANY stage of DR and is the commonest cause of vision loss in DM patients. [6]
DMO occurs when there is breakdown of the blood-retinal barrier near the macula, leading to fluid and lipid accumulation (hard exudates) in the macular region. The fovea is the centre of the macula responsible for fine central vision, so even mild oedema here dramatically reduces visual acuity.
2025 MCQ Q11 tested this directly: a patient with dot/blot haemorrhages + hard exudates at the macula (especially fovea), no new vessels → answer = Diabetic macular oedema (not vitreous haemorrhage, not neovascular glaucoma, not tractional retinal detachment). [4]
"Growth of new vessels on iris extending to the angle of the anterior chamber, leading to high intraocular pressure and optic nerve degeneration" [1]
Why does this happen? When the entire retina becomes severely ischaemic, massive VEGF production occurs. This VEGF diffuses anteriorly because there is "nowhere else to go" — it reaches the iris, causing rubeosis iridis (new vessels on the iris). These new vessels and associated fibrous tissue obstruct the trabecular meshwork (drainage angle), causing secondary angle-closure glaucoma with very high IOP. [8]
Diabetic mononeuropathy can affect any of the extraocular muscle nerves. CN III palsy is the most classic: the patient presents with sudden-onset ptosis, "down and out" eye. Crucially, in diabetic CN III palsy, the pupil is typically spared (because the ischaemia affects the central nerve fibres while the parasympathetic pupillary fibres run on the outer surface and are supplied by the vasa nervorum of the sheath). This differentiates it from a compressive CN III palsy (e.g., posterior communicating artery aneurysm) where the pupil is involved. [1]
"Activation of pentose (polyol) pathway leads to accumulation of sorbitol within the lens" [8]
Aldose reductase converts glucose to sorbitol in the lens. Sorbitol cannot easily diffuse out, causing osmotic water influx into the lens → lens swelling → opacification. Diabetic cataracts tend to occur at a younger age and progress faster than age-related cataracts.
"PREVENTION IS ALWAYS THE BEST CURE!!!" [1]
| Condition | Treatment |
|---|---|
| PDR — new blood vessels | Panretinal photocoagulation (PRP); anti-VEGF monoclonal antibody |
| PDR — vitreous haemorrhage / retinal detachment | Vitrectomy and laser |
| Clinically significant macular oedema | Focal or grid laser; increasing use of anti-VEGF — very effective |
| NPDR mild/moderate without macular oedema | Observation; optimise glycaemic/BP/lipid control |
| Severe NPDR | Consider PRP to prevent progression to PDR |
Panretinal photocoagulation (PRP) works by deliberately destroying peripheral ischaemic retina. This reduces the total retinal oxygen demand, decreases VEGF production, and causes regression of new vessels. Side effects include loss of peripheral vision, poor night vision (dark adaptation), and mild reduction in visual acuity. [9]
Anti-VEGF agents (bevacizumab, ranibizumab, aflibercept) are given as intravitreal injections. They directly block VEGF, shrinking neovascularisation and reducing macular oedema. [9]
Part 2: Classification of All Chronic Diabetic Complications
"Diabetes is associated with increased mortality & morbidity due to its microvascular & macrovascular complications" [1]
| Category | Complications |
|---|---|
| Microvascular (small vessel disease; more HbA1c-dependent) | Retinopathy — see above |
| Nephropathy — microalbuminuria → albuminuria → ↑creatinine → ESRF | |
| Neuropathy — peripheral, autonomic, acute mononeuropathy, diabetic amyotrophy | |
| Macrovascular (large vessel disease; less HbA1c-dependent) | Stroke, Coronary artery disease, Peripheral artery disease |
Screening Timing
T1DM: Screen 5 years after diagnosis (or at puberty if diagnosed in childhood). T2DM: Screen at diagnosis — because T2DM may have been present subclinically for years before detection. Annual microvascular screen includes: dilated fundus exam, UACR (urine albumin:creatinine ratio), foot examination (monofilament test). [10]
The natural history: normal → hyperfiltration → microalbuminuria (UACR 3–30 mg/mmol) → macroalbuminuria (overt proteinuria) → declining GFR → ESRF.
Pathology: diabetic glomerulosclerosis — diffuse mesangial expansion, nodular glomerulosclerosis (Kimmelstiel-Wilson nodules), arteriolar hyalinosis (afferent and efferent). [11]
Red flags for non-diabetic nephropathy in a diabetic (i.e., don't just blame diabetes — think about biopsy): [12]
- Gross haematuria / active urine sediment
- Rapid decline in GFR
- Short duration of diabetes (< 5 years in T1DM)
- Absence of diabetic retinopathy — since microvascular complications tend to occur together, no retinopathy suggests the kidney disease is NOT from diabetes
- Nephrotic-range proteinuria with preserved GFR
| Type | Features |
|---|---|
| Peripheral neuropathy (most common) | Distal symmetric polyneuropathy — "glove and stocking" sensory loss, starts with feet; pain, numbness, tingling; loss of vibration/proprioception/ankle jerks. Leads to foot ulcers due to loss of protective sensation |
| Autonomic neuropathy | Gastroparesis (delayed gastric emptying), postural hypotension, resting tachycardia, erectile dysfunction, bladder dysfunction, gustatory sweating |
| Acute mononeuropathy | CN III palsy (pupil-sparing), CN VI palsy, carpal tunnel, femoral neuropathy |
| Diabetic amyotrophy (acute/subacute) | Painful proximal muscle wasting of thigh/hip (femoral neuropathy variant); asymmetric; may improve with glycaemic control |
- IHD: 3–5× higher risk of MI; leading cause of death in T2DM [6]
- Stroke: 2.5× higher risk
- Peripheral artery disease: 15× higher risk of lower limb amputation
These are driven not only by hyperglycaemia but also by the clustering of risk factors in metabolic syndrome: hypertension, dyslipidaemia (↑TG, ↓HDL), obesity, insulin resistance, and pro-inflammatory/pro-thrombotic state.
Part 3: Pathogenesis of Chronic Diabetic Complications
"Genetic predisposition + Prolonged hyperglycaemia + Accelerating factors (↑BP, etc) → Chronic diabetic complications" [1]
- Non-enzymatic glycation of proteins → formation of AGEs (advanced glycation end-products) → cross-linking of collagen, endothelial dysfunction, pro-inflammatory signalling
- Polyol (sorbitol) pathway activation → aldose reductase converts glucose to sorbitol → osmotic stress → damage in lens (cataract), Schwann cells (neuropathy), pericytes (retinopathy)
- PKC activation → altered vascular permeability, abnormal angiogenesis
- Hexosamine pathway → altered gene expression in endothelial cells
Understanding pathogenesis explains why strict glycaemic control prevents microvascular complications (DCCT/UKPDS trials), why hypertension accelerates all complications, and why certain drugs (ACEI, ARB, SGLT2i, GLP-1RA, finerenone) have specific protective effects beyond glucose lowering.
Part 4: Principles of Treating Chronic Complications
This is the framework the lecture gives — learn it as a hierarchy. [1]
"Good glycaemic control" [1]
"e.g. microalbuminuria — improve glycaemic control, treat other risk factors (BP, smoking), pharmacological intervention: ACEI, ARB, SGLT2i/GLP-1RA, Finerenone" [1]
| Intervention | Why It Helps |
|---|---|
| ACEI / ARB | Reduce intraglomerular pressure by dilating efferent arteriole → reduce proteinuria → slow nephropathy progression; also lower systemic BP |
| SGLT2 inhibitors | Reduce glucose reabsorption → lower blood glucose; also reduce tubuloglomerular feedback → lower intraglomerular pressure; cardio-renal protective effects independent of glucose lowering |
| GLP-1 receptor agonists | Cardio-renal protection; anti-inflammatory effects on endothelium; weight loss |
| Finerenone (non-steroidal MRA) | Blocks aldosterone → reduces kidney fibrosis and inflammation; less hyperkalaemia than spironolactone due to molecular selectivity [12] |
"Progression slowed by: ↑glycaemic control, risk factor management (hypertension, hyperlipidaemia, smoking). Specific: nephropathy — renin-angiotensin blockade, SGLT2i, GLP-1RA, finerenone. Symptomatic — dialysis/transplant, pain relief. Prevention of drastic consequences — laser therapy, foot care" [1]
Part 5: Achieving Glycaemic Control — Diet
"Dietary management: integral part of therapy for all patients with diabetes" [1]
| Parameter | Target |
|---|---|
| Energy | ~30 kcal/kg ideal body weight/day (adjust for lifestyle, body weight) |
| Carbohydrate | 40–50% |
| Fat | 30% ( < 7% saturated fat) |
| Protein | 20–30% |
| Fibre | 20–35 g/day |
| Goal | Achieve normal body weight |
- Personalised — according to individual preference and culture
- Consistency of meal timings and quantity — especially if on insulin (to prevent hypo/hyperglycaemia)
- Healthy foods consistent with population-wide recommendations
- Emphasise high fibre (vegetables, fruits, wholegrains, legumes), low-fat dairy, fresh fish
- Minimise high-energy foods (high saturated fats, sweet desserts, snacks)
- Hypocaloric diet for obese T2DM patients
Part 6: Oral Hypoglycaemic Agents — Mechanisms and Targets
Gut → α-glucosidase inhibitors (↓glucose absorption)
Liver → Biguanides (metformin) (↓hepatic glucose output, ↓insulin resistance)
→ Thiazolidinediones (↓hepatic insulin resistance)
Pancreas → Sulphonylureas, Meglitinides (↑insulin secretion)
→ DPP-4 inhibitors (↑endogenous incretins → ↑insulin, ↓glucagon)
Muscle/Fat → Thiazolidinediones (↓peripheral insulin resistance)
→ Biguanides
Kidney → SGLT2 inhibitors (↓glucose reabsorption)"Incretins physiologically regulate insulin and glucagon in a glucose-dependent manner"
GLP-1 and GIP are gut hormones released after food ingestion. They:
- ↑ Insulin secretion from β-cells (glucose-dependent → no hypoglycaemia when glucose is normal)
- ↓ Glucagon secretion from α-cells (GLP-1)
- Slow gastric emptying (GLP-1)
- Promote satiety
In T2DM, the incretin effect is diminished — partly because GIP's effect on β-cells is reduced, and both GLP-1 and GIP are rapidly degraded by DPP-4. [1]
6.3 Incretin-Based Therapies [1]
"No hypoglycaemia if monotherapy" [1]
| Feature | Details |
|---|---|
| Route | Injectable peptides (except oral semaglutide); resistant to DPP-4 degradation |
| Mechanism | ↑ post-prandial insulin, ↓ glucagon, delay gastric emptying, ↓ appetite |
| Weight effect | ↓ Body weight |
| Frequency | Twice daily (exenatide), Daily (lixisenatide, liraglutide), Weekly (exenatide LAR, dulaglutide, semaglutide SC/oral) |
| Cardio-renal benefits | Liraglutide, dulaglutide, semaglutide |
| Combinations | Can use with insulin and other ADMs except DPP-4i |
| Renal caution | Exenatide: avoid if eGFR < 30 |
"Tirzepatide — even higher efficacy" [1]
| Feature | Details |
|---|---|
| Route | Oral |
| Mechanism | Inhibit DPP-4 → ↑ endogenous active GLP-1 and GIP |
| Weight effect | Weight neutral |
| Examples | Sitagliptin, Vildagliptin, Saxagliptin, Linagliptin, Alogliptin |
| Renal dosing | Renal dose adjustment for all EXCEPT linagliptin |
| Fixed-dose combos | Available with metformin, pioglitazone, SGLT2i |
"↓hyperglycaemia by increasing urine glucose loss; ↓weight, fat mass, BP; no hypoglycaemia if monotherapy; Cardio-renal protection; reduces heart failure even in patients without diabetes" [1]
| Feature | Details |
|---|---|
| Mechanism | Block SGLT2 in proximal tubule → ↓ glucose reabsorption → glycosuria |
| Non-glycaemic benefits | Interaction with renal Na/H exchanger, improved renal haemodynamics, natriuresis, ↓weight, ↓BP |
| Approved agents | Dapagliflozin, Canagliflozin, Empagliflozin, Ertugliflozin |
| Drug | Side Effects / Cautions |
|---|---|
| Metformin | Dyspepsia, diarrhoea; Lactic acidosis (rare — risk with renal/hepatic/cardiac failure, alcoholism, MI, sepsis); B12 deficiency with long-term high doses; Do NOT use if eGFR < 30; Withhold before and 48h after contrast if eGFR < 60, liver disease, HF, alcoholism, or intra-arterial contrast |
| Sulphonylureas / Meglitinides | Weight gain; Hypoglycaemia; Prefer insulin if renal insufficiency |
| α-glucosidase inhibitor (Acarbose) | Flatulence, diarrhoea; Must use glucose (not sucrose) to treat hypoglycaemia (acarbose blocks sucrose digestion) |
| Thiazolidinediones (TZD, pioglitazone) | Fluid retention → CONTRA-INDICATED in heart failure; Weight gain++; ↑fractures; Anaemia; ?↑bladder cancer |
| DPP-4 inhibitors | Pancreatitis (very uncommon); rarely joint pain |
| SGLT2 inhibitors | Genital fungal infections; UTI; Osmotic diuresis → postural hypotension; Rare euglycaemic DKA (risk: longstanding DM, low carb diet, fasting, dehydration, alcohol); Stop 3 days before surgery/endoscopy; Dapagliflozin: avoid in active bladder cancer; Canagliflozin: ↓bone mass, ↑fracture risk |
2024 MCQ Q28 — Pioglitazone Contraindicated in HF
A patient with T2DM, exertional dyspnoea, and ankle oedema (i.e., heart failure features) — which drug is contraindicated? Pioglitazone (TZD) — causes fluid retention, worsens HF. SGLT2i is actually beneficial in HF. Also avoid saxagliptin in HF. [3]
SGLT2i and Euglycaemic DKA
SGLT2 inhibitors can cause DKA with NORMAL or only mildly elevated blood glucose. This is because glycosuria keeps glucose low, but the shift to fatty acid metabolism and ketogenesis still occurs (especially in insulin-deficient states, starvation, or dehydration). Risk factors: longstanding DM, low carb intake, prolonged fasting, dehydration, alcoholism. Action: stop SGLT2i 3 days before surgery/endoscopy. [1]
Part 7: Insulin Therapy
- Subcutaneous injection (1–4 times/day; pen or syringe): maintenance
- IV infusion or IM injection: acute/temporary hyperglycaemia (e.g., DKA, perioperative)
- Continuous SC insulin infusion (CSII): insulin pump
- Inhaled insulin: high cost, low acceptance, not used in HK
This slide is extremely high yield for pharmacology MCQs.
| Category | Examples | Onset | Duration | Notes |
|---|---|---|---|---|
| Rapid-acting analogues | Aspart (NovoRapid), Lispro (Humalog), Glulisine | 10–15 min | 4–6 h | Less self-association after SC injection → faster onset, shorter duration, more physiological → less premeal hypoglycaemia |
| Ultra-rapid acting | Lispro-aabc, Fast-acting insulin aspart (Fiasp) | Even faster | ~4 h | |
| Short-acting | Regular human: Actrapid, Humulin R | 30 min | 6–9 h | Prandial insulin |
| Intermediate-acting | Protaphane, Humulin N (protamine as retardant) | 1–2 h | 12–18 h | |
| Premixed | Mixtard 30, NovoMix 30, Humulin 70/30, Humalog Mix | — | — | Fixed ratio of short + intermediate |
| Long-acting analogues | Glargine (Lantus) | 1–2 h | 20–24 h | Precipitates in SC tissue (isoelectric point shift) → slow-releasing depot → less nocturnal hypoglycaemia |
| Ultra-long acting | Glargine 300 (T½ 19h), Degludec (T½ 25.4h) | 1–2 h | > 24 h | Basal insulin |
| Weekly insulin | Icodec (Awiqli), Efsitora alfa | — | ~7 days | New; for simplifying basal regimens |
"Short-acting analogues: less self-association than human insulin after SC injection"
Normal human insulin forms hexamers in SC tissue, which must dissociate into monomers before absorption. Lispro has a swap of proline and lysine at B28–B29; Aspart has an aspartate substitution at B28. These changes reduce hexamer formation → faster monomer absorption → quicker onset, shorter duration → more closely mimics physiological prandial insulin secretion.
"Shift in isoelectric point → precipitates in subcutaneous tissue → forms a slow-releasing depot"
Glargine has two arginine residues added at the C-terminus of the B chain and a glycine substitution at A21. This shifts the isoelectric point to pH 4 (the formulation pH). After injection into neutral pH subcutaneous tissue, it precipitates into microcrystals, creating a slow-release depot. This gives a peakless, flat profile — ideal basal insulin.
- Continuous SC insulin infusion + continuous glucose monitoring system
- Artificial pancreas = closed-loop system where pump and sensor communicate directly; patient inputs carb intake via smartphone. FDA approved.
Insulin-requiring patients:
- Marked recent weight loss
- Marked ketosis
- Underweight; clinically ill (dehydrated, infection, infarction)
- Severe hyperglycaemia at diagnosis: HbA1c > 10%, fasting glucose > 16.7 mmol/L
- Pregnancy
- Failed oral therapy (GLP-1RA preferred alternative if HbA1c < 11%, especially if obese, CVD, or CKD)
Part 8: ADA Framework — Management of Hyperglycaemia in T2DM [1]
"Healthy lifestyle + medication choice according to treatment goals"
I. Reduction of CV and renal risk (if high risk or established CVD/CKD):
- SGLT2i (especially if HF+), GLP-1RA, or both preferred
- Avoid TZD and saxagliptin if heart failure
II. Achievement of weight and glycaemic goals:
- Metformin: superior glycaemic and weight effects vs. DPP-4i and sulphonylurea
- Increasing emphasis on weight as treatment goal: SGLT2i / GLP-1RA / tirzepatide
- Minimise hypoglycaemia: assess need/dosage of SU, meglitinides, insulin
- Initial combination therapy if HbA1c 1.5–2.0% above target
- Consider accessibility and cost
"Patient education + diet/drugs/insulin + treat risk factors (HT, lipids, smoking, obesity) + individualised targets + regular complication assessment"
| Domain | Target |
|---|---|
| HbA1c | ≤ 7% (HK standard); individualise (looser for elderly/high hypo risk, tighter for young/newly diagnosed) |
| BP | ≤ 130/80 mmHg (for diabetics with end-organ damage) |
| LDL | ≤ 1.8 mmol/L (DM = high CVD risk → statin indicated) |
| Smoking | Cessation |
| Weight | BMI target; prioritise weight-reducing agents |
Part 9: Other Important Complications (Integrating Related Material)
Combination of neuropathy (loss of protective sensation) + peripheral artery disease (poor healing) + immunocompromise (infection risk) → foot ulcers → osteomyelitis → amputation. Annual foot examination with 10g monofilament is mandatory screening. [10]
- UTI (glycosuria promotes bacterial growth)
- Candidiasis (oral, genital — also SGLT2i side effect)
- Pulmonary TB
- Mucormycosis (rhinocerebral — classic in DKA)
- Osteomyelitis of foot
Autonomic neuropathy destroys interstitial cells of Cajal (ICC) → delayed gastric emptying → early satiety, nausea, vomiting, postprandial fullness. Exacerbates glucose variability.
Likely Exam Questions
-
Fundus photo showing dot/blot haemorrhages, hard exudates at macula, no new vessels → Diagnosis?
- Answer: Diabetic macular oedema (with background NPDR)
-
T2DM with HF symptoms — which drug contraindicated?
- Answer: Pioglitazone (fluid retention; worsens HF)
-
Which DPP-4 inhibitor does NOT need renal dose adjustment?
- Answer: Linagliptin (hepatically cleared)
-
Patient on SGLT2i develops ketoacidosis with BG 14 mmol/L — what is this called?
- Answer: Euglycaemic DKA
-
Earliest clinical sign of diabetic retinopathy on fundoscopy?
- Answer: Microaneurysms
-
A 55-year-old man with T2DM for 15 years presents with sudden painless loss of vision in one eye. Fundoscopy shows extensive new vessels and blood in the vitreous cavity.
- (a) What is the diagnosis? → Proliferative diabetic retinopathy with vitreous haemorrhage
- (b) What is the definitive treatment? → Vitrectomy + endolaser; also PRP and/or anti-VEGF for new vessels
- (c) What systemic interventions reduce progression? → Strict glycaemic control (HbA1c ≤ 7%), BP control (ACEI/ARB), lipid control, smoking cessation
-
List 4 side effects of SGLT2 inhibitors. → Genital fungal infection, UTI, osmotic diuresis/postural hypotension, euglycaemic DKA, (canagliflozin: fracture risk)
-
A patient with T1DM omits 2 insulin doses because of vomiting — what acute complication? Name 3 physical signs, 4 investigations. (cf. 2019 SAQ Q4)
- Complication: DKA
- Signs: Kussmaul breathing, acetone breath, dehydration/dry mucous membranes, tachycardia, hypotension, altered consciousness
- Investigations: Blood glucose, ABG (pH, bicarbonate), serum ketones (β-hydroxybutyrate), U&E (K+), serum osmolality, urine ketones
High Yield Summary
Ocular complications of DM: Retinopathy (NPDR → PDR), macular oedema, neovascular glaucoma, CN III/IV/VI palsies, cataract.
NPDR features: Microaneurysms, dot/blot haemorrhages, soft exudates (cotton wool spots = nerve infarcts), hard exudates (lipid leak).
PDR features: Neovascularisation, vitreous haemorrhage, tractional retinal detachment.
Treatment: PDR → PRP + anti-VEGF; DMO → anti-VEGF + focal laser; vitreous haemorrhage → vitrectomy.
Chronic complications framework: Prevention → Subclinical (reversible with ACEI/ARB, SGLT2i, GLP-1RA, finerenone) → Overt (slow progression + symptomatic Rx).
Drug side effects to know cold: Metformin (lactic acidosis, B12 def, stop if eGFR < 30), SU (hypo, weight gain), TZD (fluid retention — CI in HF), SGLT2i (genital infection, euglycaemic DKA — stop 3 days pre-op), DPP-4i (renal dose except linagliptin).
Insulin: Rapid (Aspart/Lispro) for prandial, Long (Glargine/Degludec) for basal. Glargine forms SC depot via isoelectric precipitation. Weekly insulin now available (Icodec).
ADA T2DM management: CVD/CKD → SGLT2i/GLP-1RA first. Weight/glycaemia → Metformin first line. Avoid TZD/saxagliptin in HF. Individualise targets.
Active Recall - Lecture Notes
[1] Lecture slides: GC 042. Deterioration of eyesight in a diabetic patient diabetic complications [Update 2025].pdf (all pages) [2] Past papers: 2019 Fourth Summative SAQ.pdf (Q4) [3] Past papers: 2024 Fourth Summative MCQ.pdf (Q15, Q28) [4] Past papers: 2025 Fourth Summative MCQ.pdf (Q11, Q40) [5] Past papers: 2024 Fourth Summative MCQ.pdf (Q29) [6] Senior notes: Maksim Medicine Notes.pdf (Endocrinology section — Complications of DM) [7] Lecture slides: GC 122. Chronic Visual Loss.pdf (p37 — Diabetic retinopathy) [8] Senior notes: Block A - Deterioration of eyesight in a diabetic patient_ diabetic complications.pdf (p1) [9] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (p1518–1520 — Treatment of DR) [10] Senior notes: Adrian Lui Pediatrics Notes.pdf (p303 — Chronic Diabetic Complications screening) [11] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (p1522 — Diabetic nephropathy pathology) [12] Senior notes: Block A - Nephrology Interactive Tutorial.pdf (p4 — Red flags, finerenone) [13] Senior notes: Block A - Indigestion and heartburn_ nausea and vomiting; gastric motility problems; benign esophageal lesions.pdf (p25 — Gastroparesis)
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