Mircovascular complication of Diabetes Flashcards
What are the three most important microvascular complication of DM? Why do these occur?
Diabetic retinopathy
Diabetic nephropathy
Diabetic neuropathy
Retinal vessels, Glomeruli vessels and Vasa Nervorum are small and abundant and are therefore highly vulnerable
What are the causes of vessel damage in diabetes?
Possible mechanisms for vascular damage include sorbitol, which is thought to be produced in excess in individuals with high plasma glucose because glucose is reduced to sorbitol by the enzyme aldol reductase.
Another possible mechanism is the production of advanced glycation end products (AGE). Glycation is the term used for nonenzymatic addition of hexoses to protein and glycosylation is the term used when the process is enzymatic. Glycation of haemoglobin to form HbA1c is well recognised. A similar process is known to affect other proteins, in particular the lens protein (causing cataracts), fibrin and collagen. The latter might be responsible for microangiopathy. Fructosamine is another example of a glycated protein. We can use both HbA1c and fructosamine to get an idea of long term glucose control.
AGE receptors are thought to trigger inflammation signalling cascades along with hypoxia and oxidative stress - the pro-inflammatory cytokines produces lead to inflammation which leads to vascular damage.
How are the different types of retinopathy treated?
Prevention always important - frequently check the eyes of diabetics, control blood glucose and blood pressure. If background retinopathy spotted, inform patient.
In case of pre-proliferative and proliferative retinopathy use pan retinal photocoagulant
In case of Maculopathy use GRID retinal photocoagulant
How often in diabetics does nephropathy occur? After how long?
In 30-40% of T1DM patients after about 30-40, presumed that prevalence in T2DM patient’s is same.
What are the histological features of diabetic nephropathy?
Glomerular Changes
Vascular Changes
Tubulointerstitial changes
How is diabetic nephropathy clinical investigated? What can be used to predict risk?
Progressive proteinuria
Increased BP
Deranged renal function
Microalbuminuria can be used to predict patient’s likely to develop nephropathy and intervene quickly
What is a common outcome of nephropathy? How can this be prevented?
Patients with Clinical Nephropathy usually go on to end stage renal failure within a period of 2 to 7 years of the appearance of significant proteinuria. Interventions which can slow this down include:
Diabetic control
Blood pressure control
Inhibition of the renin-angiotensin system
Stopping smoking
What are the types of neuropathy?
Peripheral polyneuropathy Mononeuropathy Mononeuritis multiplex Radiculopathy Autonomic neuropathy Diabetic amyotrophy
What is the presentation of Peripheral polyneuropathy?
Usually bilateral and symmetrical. Loss of sensation is common. Occurs more commonly in tall people and those with poor glucose control. Can be painful.
Signs: absent ankle jerks and loss of vibration sense (using a tuning fork).
X-ray might show multiple fractures and Charcot’s joints.
What is the presentation of Mononeuropathy?
Single nerve loss. Usually noted motor loss since a single nerve with sensory loss is rarely symptomatic. 3rd, 4th or 6th nerve palsy.
Signs of a diabetic (pupil sparing) 3rd nerve palsy: Eyelid function and Ocular Motor function of CN III lost
Pupil function of CN III retained
Signs of a space occupying lesion causing a third nerve palsy: Eyelid, Ocular motor and Pupil function of CN III impaired
What is the presentation of Mononeuritis multiplex?
This is a random combination of peripheral nerve lesions.
Hard to predict effects
What is the presentation of Radiculopathy?
Pain over spinal nerves, usually affecting chest or abdomen.
What is the presentation of Autonomic neuropathy?
Impairment of autonomic nervous system functions e.g sweating and bladder emptying
What is the presentation of Diabetic amyotrophy?
Weakness followed by wasting of pelvifemoral muscles, either unilaterally or bilaterally, with associated pain. Sensory impairment is minimal in the cutaneous distribution sharing the same root or peripheral nerve as affected musculature.
Reflexes in lower extremity may be absent
