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RE > Long term complications of diabetes > Flashcards

Long term complications of diabetes Flashcards

1
Q

Which cells are able to reduce glucose transport in response to extracellular hyperglycaemia?

A

Retinal endothelial cells
Mesangial cells of glomerulus
Schwann cells and peripheral nerve cells

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2
Q

What is diabetic retinopathy?

A

A progressive ophthalmic microvascular complication of diabetes.

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3
Q

When does diabetic retinopathy present in T1 and T2 diabetics?

A

T1DM - after 3-5 years of diagnosis
T2DM - may already be present but 50-80% have it at 20 years post diagnosis.

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4
Q

What is the pathophysiology of retinopathy?

A

Glucose is metabolised to sorbitol within retinal cells by aldose reductase.
Increase in glucose = increase in sorbitol.
Accumulation of sorbitol in retinal cells causes oxidative stress and hypoxia. This alters PKC leading to increased Vascular Endothelial Growth Factor activity and dysregulation of permeability.
Neovascularisation –> Proliferative retinopathy (R)
Increased permeability –> Macula oedema (M)

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5
Q

What are the clinical features of diabetic retinopathy?

A

Floaters
Blurred vision
Reduced visual acuity
Loss of vision

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6
Q

What tests are used to determine diabetic retinopathy?

A

Visual acuity - Snellen chart
Fundoscopy

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7
Q

What are cotton wool spots?

A

Chronic ischaemia

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8
Q
A
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9
Q

How is diabetic retinopathy graded?

A

R = neovascularisation
R0, R1, R2, R3
M = Maculopathy
M1, M1, P

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10
Q

What Is R0?

A

No neovascularisation

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11
Q

What is R1?

A

Background neovascularisation e.g. Microaneurysm, retinal haemorrhages, hard exudates

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12
Q

What is R2?

A

Preproliferative neovascularisation
e.g. cotton wool spots, venous bleeding, loops, reduplication, intraretinal microvascular anomalies, multiple deep round or blot haemorrhages.

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13
Q

What is R3?

A

Proliferative neovascularisation
NVD - New vessel in disc
NVE - New vessel elsewhere
Preretinal or vitreous haemorrhage
Preretinal fibrosis +/- retinal detachment

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14
Q

What is M0?

A

No maculopathy

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15
Q

What is M1?

A

Maculopathy
Exudates within one disc diameter of centre of fovea, micro aneurysm, or haemorrhage within one disc diameter of centre of fovea associated with visual acuity <6/12.

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16
Q

What is P in the diabetic retinopathy grading scale?

A

Previous photocoagulation (laser therapy)

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17
Q

For those with R0 + R1, how often are they screened?

A

Annually.

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18
Q

For those with R3, how quickly should they be seen by an ophthalmologist?

A

Immediately.

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19
Q

For R2/MI, how quickly should they be seen by an ophthalmologist?

A

Within 4 weeks.

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20
Q

What treatment is given to those with diabetic retinopathy to prevent further deterioration/development?

A

Glycaemic control
BP control - Lisinopril
Fibrates (reduces risk of laser treatment in T2DM)

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21
Q

What specific treatments are given to those with diabetic retinopathy?

A

Photocoagulation
Intravitreal steroids - to reduce macular oedema + improve visual acuity
Vitrectomy - removal of opaque vitreous humour
Growth factor inhibitors - intravitreal bevacizumab. This reduces new vessel formation in retina.

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22
Q

What condition is this?

A

Rubeosis Iridis
End stage retinopathy - neovascularisation of the iris.

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23
Q

At what age do patients start diabetic eye screening?

A

From aged 12.

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24
Q

What is diabetic nephropathy?

A

Kidney damage caused by diabetes.

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25
Q

How is diabetic nephropathy defined?

A

Microalbuminuria - 30-300mg albumin in urine/day
Proteinuria >300mg/day - then there is a steady decline in eGFR

26
Q

20-30% of diabetics will have developed diabetic nephropathy after how many years of their diabetic diagnosis?

A

10 years

27
Q

In which ethnicities is the risk of diabetic nephropathy increased in?

A

African-Caribbean, Mexican and Pima Indians

28
Q

What is the pathophysiology of nephropathy?

A

Increase in advanced glycation end products and growth factors leads to;
-Glomerular hyperfiltration
-Altered glomerular composition
-Renal hypertrophy
-Glomerular hypertension
These all lead to albuminuria and deposition of ECM –> Glomerulosclerosis and interstitial fibrosis.

29
Q

Which histological changes are seen in diabetic nephropthy?

A

Expansion of mesangium
Glomerular BM thickening
Glomerular sclerosis
Fusion of foot processes
Loss of podocytes

30
Q
A
31
Q

What is the legacy affect?

A

Good control of blood sugars/HTN over a number of years reduces the risk of developing diabetic nephropathy.

32
Q

How is diabetic nephropathy treated?

A

ACE or ARB for BP control
Glycaemia control
Lipid management
Protein restricted diet

33
Q

What is diabetic neuropathy?

A

Where myelinated and unmyelinated nerve fibres are lost. More common in T1DM.

34
Q

What are the metabolic risk factors for diabetic neuropathy?

A

Advanced glycosylation end-products (AGE’s)
Sorbitol –> Reduced Na-K-ATPase –> Slows conduction velocity
Oxidative stress

35
Q

What are the vascular risk factors of diabetic neuropathy?

A

Morphological abnormalities and vasa nervorum
Thrombomodulin and tissue plasminogen activator levels reduced

36
Q

Why are advanced glycosylated end products a risk factor for developing diabetic neuropathy?

A

Can lead to ROS + inflammation
Macrophages, chemokine and cytokines can signal further inflammation.
These lead to damage in Schwann cells.

37
Q

Why does a poor production of growth stimulating factors such as nerve growth factor and neurotrophin 3 lead to diabetic neuropathy?

A

They are required for nerve growth and repair.

38
Q

What is distal symmetrical polyneuropathy?

A

Glove and stocking distribution.
Loss of pinprick, temp, vibration and joint position with reduced ankle reflexes.

39
Q

Which common deficiency can cause distal symmetrical polyneuropathy?

A

B12

40
Q

What is polyradiculopathy?

A

Severe pain in 1+ nerve root distribution.
Usually resolves over 6-12 months.

41
Q

What is mononeuropathy?

A

Affects a single cranial or peripheral nerve.

42
Q

What is autonomic neuropathy?

A

Damage to nerves controlling involuntary functions.

43
Q

What are the common presentations of autonomic neuropathy?

A

Cardiovascular - Resting tachycardia + postural hypotension
GI - Delayed gastric emptying
Genitourinary - Bladder dysfunction
Hypoglycaemic unawareness
Hyperhidrosis

44
Q

What are the differential diagnoses for diabetic neuropathy?

A

Uraemia
B12 deficiency
Hypothyroidism
Amyloidosis
Toxins/Alcohol/Heavy nmetals
Inflammation
Infection - HIV, leprosy
Paraneoplastic syndromes

45
Q

What analgesics are used to treated diabetic neuropathy?

A

Duloxetine
TCA’s
Gabapentin

46
Q

What is peripheral vascular disease?

A

Arterial narrowing due to atheroma deposition.
A microvascular complication of diabetes.

47
Q

What conditions is PVD associated with?

A

IHD
CVD

48
Q

Hows do arteries get damaged in PVD?

A

Vasoconstriction - from HTN + vascular SMC growth
Inflammation - from chemokine and cytokine release
Thrombosis - increased viscosity

49
Q

What are the clinical features of PVD?

A

Can be asymptomatic
Cramp on exertion
Reduced circulation
Leg discolouration
Ulcers
Hair loss to extremities

50
Q

How test is used to identify PVD and what are the normal parameters?

A

ABPI (Ankle Brachial Pressure Index)
Normal 1.0 - 1.3
<0.9 - PVD
>1.3 - Calcification of vessels

51
Q

What are the clinical features of diabetic foot ulcers?

A

Neuropathy
Ischaemia
Bony deformity
Callus
Swelling
Skin breakdown
Infection
Necrosis

52
Q

What is osteomyelitis?

A

Inflammation of bone/bone marrow.

53
Q

What factors increase the likelihood of osteomyelitis?

A

Visible bone
Bigger ulcer (>2cm x 2cm)
Bigger depth (>3mm)
Longer duration (>1-2 weeks)
ESR >70 per hour (Erythrocyte Sedimentation Rate)

54
Q

How are diabetic foot ulcer treated?

A

Mechanical offloading
Debridement
Abx
Amputation

55
Q

What is Charcot arthropathy?

A

Sudden onset unilateral warmth, redness and oedema over foot/ankle, usually with a hx of minor trauma.
Slowly progressive over months/years, results in collapse of the arch and bony deformities.

56
Q

How is Charcot arthropathy treated?

A

Avoid weight bearing
PO/IV Bisphosphonates

57
Q

What condition is this?

A

Acanthosis nigricans

58
Q

What condition is this?

A

Diabetic dermopathy

59
Q

What condition is this?

A

Necrobiosis lipoidica diabeticorum

60
Q

Is there a risk of IHD with a low HbA1C?

A

Yes - due to hypoglycaemia.
also increases the risk of CVD.

RE (18 decks)

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