T2DM- Presentation and complications Flashcards
True or False?
Over 25% of the patients with diabetes in the UK do not know they have it
True
Type 2 diabetes has an insidious onset
• T : True • F : False
True
What is meant by an insidious onset
Compared to type 1 diabetes that always presents acutely with ketosis, type 2 diabetes patients spend months to years not knowing they have diabetes at all: insidious.
Patients don’t often know that they have T2DM- slowly rising glucose
T1DM- will present more acutely with acidosis and hyperglycaemia.
What are the symptoms of a slowly rising blood glucose in T2DM
– Tiredness, lethargy
– Polyuria and polydipsia
– Often drink Lucozade (or coke) because of thirst
– Glucose SLOWLY rises further
– With other co-morbidities it become difficult to drink enough
– Osmotic diuresis causes loss of water and a rise in sodium
– EVENTUALLY the glucose is VERY high, as is the sodium
Hyperosmolar and rising Na+ because of polyuria.
Water leaves the brain- can result in confusion
Blood is like treacle- increasing risk of strokes
How do we calculate osmolality
Osmolality = cations + anions + glucose + urea
Na + K Cl + bicarb
= 2(cations) + glucose + urea
= 2(Na + K ) + glucose + urea Glucose rises to 90mM
Na rises to 160mM Osmolality=430mM
Normal osmolality=296
Neutral charge of body is why we just double the cations by 2 (a lot more anions to measure)
Describe the issue with the insidious onset of T2DM
- Patients may have type 2 diabetes for many months or years before they know they have diabetes
- They have hyperglycaemia but no acidosis
- Intermittent polyuria and polydipsia
- Assumed to be “prostate trouble” or “water work infections”
- Half of patients with diabetes do NOT know they have it.
Describe the consequences of the insidious onset of T2DM
- Months to years of hyperglycaemia
- Slow damage to the endothelium
- Micro and Macrovascular damage
- If the patients ignore the polyuria, the first time they present might be with a complication …
What are the microvascular complications
Microvascular – Aetiology: Glycosylation of basement membrane proteins -> “leaky” capillaries – Retinopathy – Nephropathy – Neuropathy
What are the macrovascular complications
– Aetiology: Dyslipidaemia, hypertension, hypercholesterolaemia – IHD – CVA – Peripheral gangrene
Old infarcts will be white
What’s important to remember about the treatment of HHS in older patients
Can’t suddenly normalise their numbers- they don’t cope well with a. rapid ‘flux’ of fluid from different compartments.
What are the bigger vessels in retinopathy
Veins
What can be seen in background diabetic retinopathy
- Hard exudates (cholesterol) • Microaneurysms (“dots”)
* Blot haemorrhages
What treatment should we use for background diabetic retinopathy
Improve blood glucose control
Purpose of regular screening
What can be seen in pre-proliferative retinopathy
Cotton wool spots- these are due to ischaemia
Why is ischaemia in the eye a problem
Ischaemia — hypoxia — (same as intermittent claudication in legs)- will stimulate new vessel growth (proliferative stage)
these vessels are thin-walled- bleed easily (probably also hypertensive)- blood in vitreous is bad- blindness
We aim to stop it getting to the proliferative stage
How do we manage diabetic retinopathy
Background:
–improve control of blood glucose
–warn patient that warning signs are present
- Pre-proliferative (cotton wool spot) • Suggests general ischaemia
- If left alone, new vessels WILL grow
- Needs: Pan retinal photocoagulation
• Proliferative (visible new vessels)
• Also needs:
–Pan retinal photocoagulation
Where on the eye is pan-retinal photocoagulation performed
Periphery- can lose up to 1/3rd of the peripheral vision without noticing- same cannot be said for the macula!
Aim to protect macula- can still see normally without periphery- other parts of periphery help you detect motion
• Is there real evidence that good glucose control prevents complications?
YES
UKPDS study (1977-1997) Cumulative risk reduction of 25% with intensive vs conventional Reduction in any diabetes related end-point (12%) Micro-vascular complications (25%) Retinopathy progression (21%) Micro-albuminiaria (34%) MI (16%) Diabetes-related death (10%) All-cause related death (6%)\
• But only after about 15 years in NEWLY
diagnosed type 2 diabetes
Describe the follow up from 1998 to 2008
- Of 5102 patients with newly diagnosed type 2 diabetes, 4209 were randomly assigned to receive either conventional therapy (dietary restriction) or intensive therapy (either sulfonylurea or insulin or, in overweight patients, metformin) for glucose control.
- In post-trial monitoring, 3277 patients were asked to attend annual UKPDS clinics for 5 years, but no attempts were made to maintain their previously assigned therapies.
- What happened to glucose control?\
- The glucose control became the same as the control group (they gave up trying).
- What happened to the patients mortality when they stopped having “good control”?\
Mortality stayed better
Describe the legacy effect of intensive blood glucose control
- With more than 66,000 person-years of follow up, this large post-trial study showed that benefits of an intensive strategy to control blood glucose levels in patients with type 2 diabetes were sustained for up to 10 years after the cessation of randomized interventions.
- Benefits persisted despite the early loss of within-trial differences in glycated hemoglobin levels between the intensive-therapy group and the conventional- therapy group — a so-called legacy effect.
- The trial showed the extended effects of improved glycemic control in patients with newly diagnosed type 2 diabetes, some of whom were followed for up to 30 years.
