Diabetes Introduction Lecture Flashcards
What is diabetes?
Metabolic disorder characterised by chronic hyperglycaemia due to defects in insulin secretion and/or action
Normal fasting and 2h OGTT
Fasting <6.1 mmol/mol
OGTT <7.8 mmol/mol
Diabetes fasting glucose value
Value >7 mmol/mol
D
Diabetes OGTT 2hr value
Value ``>11.1 mmol/mol
Impaired glucose tolerance values
- Impaired Fasting glycaemia - 6.1 - 6.9
- Impaired glucose tolerance - 7.8 - 11
Impaired fasting glucose value
5.5 - 6.9 mmol/mol
Different types of classifications of Diabetes
- Type 1 (beta cell destruction, 5-10%)
- Type 2 (insulin secretion defect, 90%)
- Genetic defects of beta cell function - mitochondiral or neonatal diabetes
- Genetic defects in insulin action
- Disease of exocrine pancreas
- Endocrinology problems
- Infections - CMV, congenital rubella
- Drugs
- Syndrome - downs, klinefelter, turners
Genetic defects of insulin secretion
- Lipodystrophy
- Type 1 insulin resistance
- anti-insulin receptor antibodies
- Insulin signalling defects
Gold standard for diagnosing diabetes
- 2hr OGTT
- HbA1C
Value of HbA1C suggesting diabetes
48mmol/mol. (6.5%)
Causes of secondary diabetes
- Pancreas problems - pancreatitis, cancer of pancreas
- Medication - eg steroids, antipsychotics
- Cushings
Type 1 diabetes vs type 2 age of onset
Type 1: 12 years old
Type 2: 60
Presentation of Type 1 diabetes vs type 2
Type 1 - osmotic symptoms eg polyuria, polydipsia, weight loss, DKA
Type 2 - Diabetic complications, or found on routine testing, hyperglycaemia symptoms
Cause of type 1 vs type 2
Type 1 - beta cell autoimmune destruction
Type 2 - beta cell dysfunction and insulin resistance
Type 1 vs type 2 treatment
Type 1 - insulin as insulin dependent
Type 2 - diet (obesity is often co-existing), oral hypoglycaemic agentsm insulin last
Complications of diabetes - macrovascular
- TIA
- Stroke
- Angina
- MI
- Heart failure
- Peripheral vascular disease
Complications of diabetes - microvascular
- Retinopathy - non-proliferative, proliferative, macular oedema
- Nephropathy - microalbuminuria, macroalbuminuria, end stage renal disease
- Neuropathy - autonomic, peripheral
- Osteomyelitis
- Amputation
- Erectile dysfunction
Non-proliferative retinopathy vs proliferative on fundoscopy
Non-proliferative - haemorrhageem aneurysm and hard exudate on fundoscopy
Proliferative - growrth of abnormal blood vessels
Classification of diabetic retinopathy
- Background retinopathy - R1 - microaneurysms, dot haemorrhages, cottton wool spots and hard exudate
- Pre-proliferative - R2 - multiple blots, venous bleeding, intraretinal microvascular abnormalities
- Proliferative - R3 - retinal neovasculariation, retinal detachment, vitreous haemorrhage
- M1 - maculopathy
- O - other diabetic lesion
- P - previous laser therapy/photocoagulation
- U - unclassified often due to cataract
When do immediate refer to opthalmologist?
- Neovascular glaucoma/ rubeosis iridis (new vessels causing glaucoma or new vessels on iris)
- Vitreous haemorrhage
- Retinal detachment
When to urgent refer to ophthalmologist (<2 weeks)?
R3 - proliferative retinopathy
When to routine refer to opthalmologist (<13 weeks)?
R2 - preproliferative retinopathy
M1 changes
Treatment for diabetic retinopathy - medical
- Gllycaemic control
- BP control
- Lipid control
- Antiplatelets
- Smoking cessation
Treatment for diabetic retinopathy - surgical
- Laser therapy
- Vitrectomy
- Intravitreal VEGF
What is diabetic nephropathy?
Presence of proteinuria +ve on dipstick (albumin conc of 300mg/g over 24hrs or 200 mcg/min)
Microalbuminuria value
30-300mg/g
CKD classification values using eGFR
- G1 (normal or high) - 90 or more
- G2 (mild decrease) - 60-89
- G3a (mild-moderate decrease) - 45-59
- G3b (moderate to severe decrease) - 30-44
- G4 - ( severe decrease) - 15-29
- G5 (kidney failure) - <15
CKD albuminuria values
- A1 (normal-mild increase) - <30mg/g or <3mg/mmol
- A2 (moderate increase) - 30-300mg/g or 3-30 mg/mmol
- A3 (severely increased) - >300mg/g or >30mg/mmol
What are the changes seen in microscopic kidney during nephropathy?
- Early - kidney enlarged due to tubular hypertrophy and hyperplasia
- 5 years - increased GBM and matrix accumulation
- Glomerulosclerosis - diffuse
- Nodular glomeruloscelrosis - Kimmelstiel-Wilson nodules
- Tubulointersititial changes - nephron loss and direct disease
Treatment for diabetic nephropathy
- Glycaemic control
- BP control - ACEi, ARBs for BP <130/80
- Lipid control
- Diet - protein <0.8g/kg
- Manage anaemia, hyperPO4, hyperkalaemia, Vit D deficiency
When to refer nephropathy to nephrologist?
- CKD stage 4 or worse (15-29 eGFR)
- Rapid decline eGFR (>5ml/min/1/73m2/year)
- Microscopic/macroscopic haematuria
- Systemic distease - SLE, Sjogrens syndrome
- Uncontrolled BP despite 4 drugs
- Proteinuria >1g/day or ACR >70mg/mmol
- Suspected renal artery stenosis
- FH of genetic disorder eg PCKD
Cause of diabetic neuropathy
- Distal axonal loss with focal demyelination and attempts at nerve regeneration
- Changes to vasa nervorum - nutrients to nerve
- = partial/complete loss of nerve function
Classifications of neuropathy
- Sensory-motor - acute/chronic, large fibre or small fibre, distal to proximal loss
- Autonomic neuropathy - erectile dysfunction, gastroparesis, postural hypotension
- Proximal motor neuropathy - loss of proximal, AKA diabetic amyotrophy, often in quads
- Mononeuropathy and entrapment neuropathy eg carpal tunnel syndrome/ulnar nerve/lat popliteal
Treatment for neuropathy
Treat the pain - start on SNRI eg duloxetine and then maybe add opioids/anticonvulsant like pregabalin
Cau use:
* Anticonvulsant - eg pregabalin
* SNRI - eg duloxetine
* TCA - eg amitryptyline
* Opioid - eg morphine
Treatment for autonomic neuropathies
- Treat symptom eg postural hypotension - steroid like fludrocortisone
- Sildenafil for ED
Consequences of gastroparesis and treatment
- Vomitting
- Flatulence
- Constipation
- Bloating
Due to not enough force
Treat with metoclopramide/stomach pacemaker
Diabetic foot examination steps
- Inspect - colour, ulcers, hair loss
- Between toes - inspect for small ulcers
- Palpate - assess each side comparing temp
- Capillary refill and pulses (dorsalis pedis and posterior tibial, popliteal fossa if possible)
- Sensation - test on clavicle, then to crude touch (cotton), fine touch (monofilament needs to BEND), pain (sharp), vibration and proprioception
- If loss vibration on toe, move to malleolus, tibia and then anerior spine of hip
- Ankle reflex
- Gait
- Assess shoes
Two types of diabetic foot
- Neuropathic feet
- Ischaemic feet
Features of neuropathic diabetic foot
- Warm
- Dry skin
- Palpable pulses
- Not painful
- Callus present
Features of ischaemic diabetic foot
- Cold/cool
- Atrophic/hairless
- No palpable pulses
- Tender/painful
- Claudication/rest pain
- Skin blanches on elevation and reddens on dependency
Grading system used for diabetic foot
Wangers classfication
0 - high risk, no ulcers
1- superficial ulcer, no infection
2 - deep ulcer, no abscess/bone involved
3 - deep ulcer, abscess or bone involved
4 - localised gangrene
5 - gangrene of whole foot
What causes Charcot foot?
- Increased blood flow due to loss of sympathetic nerves
- Osteoclast activty then increases and increased bone turnover
X-ray signs Charcot foot
- Osteolysis and joint subluxation/dislocation
- Consider MRI/bone scan
Treatment for Charcot foot
Immobilise 2-3 months
Appearance of charcto foot
Tarsal-metatarsal region or MTP joints involved
Warm/hot, swollen and often painful
If untreated - ‘rocker bottom’ deformity or medical convexity
UK prevalance of type 1 vs type 2
Type 1 - 0.25%
Type 2 - 5-7%
