Diabetes: Complications Flashcards
Chronic complications
Macrovascular
- IHD
- Stroke
Microvascular - Neuropathy -Retinopathy -Nephropathy (Strong relationship of HbA1c to risk of microvascular complications)
Cognitive dysfunction dementia
Erectile dysfunction
Psychiatric
Screening
At annual review
- Digital retinal screening
- Foot risk assessment
- ACR (albumin creatinine ratio)
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
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.
Diabetic Retinopathy
Disorder of the retina resulting in impairment or loss of vision
Diabetic Retinopathy Aetiology
Long-standing diabetes with poor glycemic control
Pathology
Damage to the blood-retina barrier
Damage causes occlusion or leakage in the retinal circulation
Classification of diabetic retinopathy
Background Retinopathy
Pre-proliferative Retinopathy
Proliferative Retinopathy
Advanced retinopathy
Mild, moderate and severe non-proliferative
Proliferative
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
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
Intra-retinal microvascular abnormalities(IRMA)
Areas of capillary dilatation and intraretinal new vessel formation
Arise within retinal ischaemia
Present in numbers: Pre-proliferative
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
Retinopathy treatment
Laser
- Pan retinal photo coagulation
- reduces oxygen retirement of retina. Reduces ischaemia that is driving retinopathy
Vitrectomy
- if virtual haemorrhage
Diabetic macular oedema treatment
Optical coherence tomography
- Assess oedema
Intraviteal Anti-VEGF
- mainstay of treatment
Grid laser to macula may be required
Nephropathy
Progressive kidney disease caused by damage to the capillaries in kidneys glomeruli
Diabetes commonest cause of kidney failure and dialysis in the UK
Nephropathy Characteristics
Proteinuria
Diffuse scarring of glomeruli
Nodular glomerulosclerosis
Consequences of nephropathy
Development of hypertension
Relentless decline in renal function
- reduction of GFR of 1ml/min/month if untreated
Accelerated vascular disease
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
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
