At annual review - Digital retinal screening - Foot risk assessment - ACR (albumin creatinine ratio)

Diabetes: Complications Flashcards by Isla Carter

Chronic complications

Macrovascular

IHD
Stroke

Microvascular
- Neuropathy
-Retinopathy
-Nephropathy 
(Strong relationship of HbA1c to risk of microvascular complications)

Cognitive dysfunction dementia

Erectile dysfunction

Psychiatric

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Screening

At annual review

Digital retinal screening
Foot risk assessment
ACR (albumin creatinine ratio)

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Glucose Metabolism (Pathophysiology)

Normally, glucose is completely oxidised via both glycolysis and mitochondrial metabolism via TCA

Glycolysis is inefficient but high throughput
Mitochondrial metabolism is efficient but low throughput

When faced with excess glucose, glycolic flux is high but mitochondria can’t keep up
–> Alternative pathways are used

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Consequences of hyperglycaemia

Inflammation
Fibrosis
Osmotic Damage
Release of reactive oxygen species

Excess glucose exposure (and impaired mitochondrial metabolism) results in increased flux of glucose via alternative pathways, many of which precipitate inflammation and increased ROS.

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Diabetic Retinopathy

Disorder of the retina resulting in impairment or loss of vision

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Diabetic Retinopathy Aetiology

Long-standing diabetes with poor glycemic control

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Pathology

Damage to the blood-retina barrier

Damage causes occlusion or leakage in the retinal circulation

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Classification of diabetic retinopathy

Background Retinopathy
Pre-proliferative Retinopathy
Proliferative Retinopathy
Advanced retinopathy

Mild, moderate and severe non-proliferative
Proliferative

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Background retinopathy

(HOME)

Haemorrhage

leakage of blood into retina
dot, blot, flame-shaped

Oedema

leakage of fluid (transudate)
diabetic macular oedema can occur even in background disease

Microaneurysms

out pouching of venous end of capillaries
earliest sign of retinopathy, found in central macula

Exudates

leakage of lipid
yellowish deposits, usually in macula

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Pre-proliferative Retinopathy

Cotton Wool Spot
- Blockage of fine retinal capillaries flow is slowed, producing a feathery whitish area- represents focal infarct

Vein Abnormalities

characterize an ischaemic retina
venous looping, beading and engorgement

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Intra-retinal microvascular abnormalities(IRMA)

Areas of capillary dilatation and intraretinal new vessel formation

Arise within retinal ischaemia

Present in numbers: Pre-proliferative

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Retinal detachment

As new vessel mature, connective tissue and fibrosis (gloss) occurs allow vitreous to exert traction which may cause detachment

If detachment extends across fovea - vision loss

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Retinopathy treatment

Laser

Pan retinal photo coagulation
reduces oxygen retirement of retina. Reduces ischaemia that is driving retinopathy

Vitrectomy
- if virtual haemorrhage

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Diabetic macular oedema treatment

Optical coherence tomography
- Assess oedema

Intraviteal Anti-VEGF
- mainstay of treatment

Grid laser to macula may be required

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Nephropathy

Progressive kidney disease caused by damage to the capillaries in kidneys glomeruli

Diabetes commonest cause of kidney failure and dialysis in the UK

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Nephropathy Characteristics

Proteinuria
Diffuse scarring of glomeruli
Nodular glomerulosclerosis

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Consequences of nephropathy

Development of hypertension

Relentless decline in renal function
- reduction of GFR of 1ml/min/month if untreated

Accelerated vascular disease

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Screening for nephropathy

Urinary albumin concentration and serum creatinine measure at diagnosis and at regular intervals

Urinary albumin conc
- Random urine sample

Urinary albumin: creatinine ratio
- laboratory method

Abnormal result requires to be confirmed by a further 1st pass sample without delay

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Urine Protein Measures

Microalbuminuria

Dipstick -ve
PCR > 15
ACR >2.5/3.5 (M/F)
Need to repeat test and have ⅔ +ve due to variation and false positives

Proteinuria

Dipstick +ve
PCR >50
ACR >30

Nephrotic Range Proteinuria

Dipstick +++
PCR >300
ACR > 250

Nephropathy Treatment

First Line
- ACEi/ ARB

BP should be maintained <140/80mmHg (target is 130/70)

SGLT2i

T2Dm started on SGLT2i irrespective of HbA1c
Reduce filtration pressure by decreasing renal afferent dilatation

Good glycemic control

Role of ACEi/ ARBs in diabetic nephropathy

Dilation of renal arteries
Decrease filtration pressure
Decrease proteinuria
–> Decrease GFR

(Allow up to 20% deterioration of eGFR)

Neuropathy

Disease of peripheral nerves

Types of neuropathy (4)

Peripheral Neuropathy
Proximal neuropathy
Autonomic neuropathy
Focal neuropathy

Peripheral neuropathy

Pain/ loss of feeling in feet +/- hands

Proximal neuropathy

Pain in thighs, hips or buttock leading to weakness in legs

Autonomic neuropathy

changes in - bowel function - bladder function - sexual response - Sweating - HR - BP

Focal neuropathy

sudden weakness in one nerve or a group of nerves causing muscle weakness or pain

Neuropathy Risk factors

``` Increased length of diabetes Poor glycemic control T1DM>T2DM (related to length of disease) High cholesterol/ lipids Smoking Alcohol Genetics Mechanical Injury ```

Peripheral neuropathy

Distal symmetric or sensorimotor neuropathy 'glove and stocking distribution'

Peripheral neuropathy symptoms

``` Numbness/ insensitivity Tingling/ burning Sharp pain or cramps Sensitivity to touch Loss of balance and co-ordination ```

Peripheral neuropathy consequences

Charcot foot Painless trauma Foot ulcer - may require hospitalisation

Diabetic foot aetiology

Peripheral neuropathy - neuropathic ulcer - clawing of toes Peripheral vascular disease - proximal arterial occlusion - digital gangrene - Charcot foot

Charcot Arthropathy

Destructive inflammatory process Fractures/ bony destruction Deformity of the foot

Charcot Arthropathy Presentation

Hot swollen foot in someone with neuropathy

Charcot Arthropathy Investigations

MRI can help to differentiate from infection

Charcot Arthropathy Natural History

Active destruction ~3months Healing Phase- 4 to 8 months Chronic Phase 8+ months

Charcot Arthropathy treatment

Non-weight bearing | - total contact cast or air cast boot

Painful neurp[athy treatment

Amitryptylline Duloxetine Gabapentin Pregablin Localised Pain - Topical capasaicin cream

proximal neuropathy

Diabetic amyotrophy Typically more common in elderly T2DM

Proximal neuropathy presentation

Starts with pain in thigh, hips, buttocks or legs. Usually on one side of the body Proximal muscle weakness often associated with marked weight loss

Autonomic Neuropathy

Affects nerves regulating HR and BP as well as internal organs Impacts digestive system, sweat glands, heart and blood vessels

Autonomic Neuropathy: Digestive System

Gastric slowing/ frequency Gastroparesis - slow stomach emptying - Nausea and vomiting, bloating, loss of appetite - Blood glucose levels can fluctuate due to abnormal food digestion oesophagus nerve damage

Autonomic Neuropathy; Gastroparesis Treatment

``` Improved glycemic control Dietary Promotility drugs (metoclopramide) Anti-nausea Pain relief Gastric pacemaker ```

Autonomic Neuropathy: Sweat Glands

Prevents sweat glands from working properly Body unable to properly regulate temperature - nerve damage can cause profuse sweating at night/ while eating Treatment --> Topical glycopyrrolate

Autonomic Neuropathy: Heart & Blood vessels

Nerve damage interferes with body's ability to adjust blood pressure and heart rate BP may drop sharply after sitting or standing --> feeling faint HR may stay high

Mononeuropathy

Can increase risk of - carpal tunnel syndrome - VI cranial nerve palsy