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Diabetes Mellitus 2 (Macrovascular Complications (Stroke is 2x more common…
Diabetes Mellitus 2
Macrovascular Complications
Stroke is 2x more common in patients with DM
MI is 4x more common in patients with DM
Atherosclerosis results in stroke, IHD and peripheral vascular disease
Peripheral vascular disease: decreased perfusion due to atherosclerosis.
Diabetes is a risk factor for atherosclerosis, this risk is worsened with smoking, hypertension + hyperlipidaemia
Women are at a high risk of macrovascular complications as DM removes the vascular advantage conferred by female sex
Risk is reduced by control of blood pressure - target <130/80 mmHg
Patient must stop smoking
Prescribe statin e.g. simvastatin and ACE inhibitor e.g. ramipril
Other Types of Diabetes
Maturity Onset Diabetes of the Young (MODY)
HNF4A mutation (MODY 1) - young age of onset, macrosomia (heavy baby >4.4 kg at birth), neonatal hypoglycaemia
Diagnosis is made <25 years
HNF1A mutation (MODY 3)
Glucokinase is the glucose-sensor of beta cells and controls the release of insulin.
There is a single gene defect altering beta cell function - either in hepatic nuclear factor or glucokinase gene
GCK mutation means there is a higher glucose level in the blood (a higher set point) before insulin is released. As insulin is still ultimately released, this type of diabetes is mild and requires no treatment.
Most common type of monogenic diabetes - autosomal dominant inheritance
Non-insulin dependent
Parents will have diabetes
Absence of islet autoantibodies and still has measurable c-peptide
Patients are sensitive to sulphonylurea treatment
Permanent Neonatal Diabetes
Mutations prevent the closure of the channel so insulin is not secreted
Treatment is sulphonylureas to close the channel
Normally, rising levels of ATP due to hyperglycaemia close the channel, depolarising the membrane and causing insulin to be secreted
Signs: small babies, epilepsy, muscle weakness
There is a mutation in the genes that encode Kir6.2 and SUR1 subunits of the beta cell ATP sensitive potassium channel
Diagnosed <6 months
Maternally Inherited Diabetes and Deafness
Loss of beta cell mass
Similar presentation to type 2
Mutation in mitochondrial DNA
Lipodystrophy
Very insulin resistant so very hyperglycaemic
Very high cholesterol levels and fatty liver
Selective loss of adipose tissue and no production of adipose tissue
Pancreatic Disease
Chronic inflammatory pancreatic disease breaks down the pancreas, impairing insulin secretion
Hereditary hemochromatosis is an autosomal recessive condition where excess iron is deposited in the liver, pancreas, pituitary - causes cirrhosis and diabetes
Acute inflammatory pancreatic disease can cause increased glucagon secretion. Inflamed pancreas may not produce insulin due to shock
Patients with pancreatic cancer may have to have their pancreas removed, resulting in diabetes
Diabetes can be caused from disease to the exocrine pancreas
Endocrine Causes of Diabetes
Cushing's Syndrome
- excessive glucocorticoids which increases insulin resistance and gluconeogenesis
Pheochromocytoma
- uncontrolled release of adrenaline which increases gluconeogenesis and decreases glucose uptake
Acromegaly
- excessive secretion of GH which stimulates glucose production and resistance to insulin
Drug Induced Diabetes
Glucocorticoids increase insulin resistance
Thiazide diuretics, antipsychotics and protease inhibitors increase risk of diabetes
Hypoglycaemia
Presents as sweating, anxiety, hunger, tremor, palpitations, dizziness, confusion, coma, drowsiness, seizures
Can be caused by alcohol or Addison's - in this case, low insulin, increased ketones
Caused by insulin/sulphonylurea treatment via accidental dose, missed meal or increased activity
Give oral sugar + long acting starch
Plasma glucose <3 mmol/L
Insulin Types
Short Acting Analogues
Faster onset and shorter duration than soluble short acting insulin
Reduced carry-over effect so are used at evening meal for patients prone to nocturnal hypoglycaemia
E.g. insulin aspart, insulin lispro
Long Acting
Intermediate 12-24 hours, long acting >24 hours
Insulin is mixed with retarding agents e.g. zinc
Short Acting Soluble
Given 15-30 minutes before meals
Given to patients on multiple dose regimens, patients in labour, during medical emergencies, surgery and on those using insulin pumps
Last 4-6 hours
Complications of Insulin Treatment
Lipohypertrophy at injection site
Insulin resistance
Hypoglycaemia
Weight gain - insulin makes you feel hungry
Microvascular Complications
Diabetic Retinopathy
Pre-proliferative Retinopathy
: Infarcts, haemorrhage. Retinal ischaemia
Proliferative Retinopathy
: New vessels form. Ischaemia results in the release of vascular growth factors which causes new blood vessels to grow in the retina.
Background Retinopathy
: Microaneurysms, haemorrhages + hard exudates (lipid deposits). Form due to metabolic consequences of poorly controlled diabetes causing pericyte death. Haemorrhage occurs after a breach of microaneursyms.
Maculopathy
: Damage to macula which provides central vision. Fluid from leaking vessels causes macula oedema. This distorts and thickens the retina
Greatest risk in patients who are pregnant, hypertensive, have poor glycaemic control or who have had DM for a long time
Capillary endothelial change > Vascular leak > Microaneurysms > Capillary occlusion > Local hypoxia > Ishchaemia > New vessel formation
Hyperglycaemia causes high retinal blood flow, damaging capillary pericytes
Eye screening via retinal photography detects retinopathy early
Blindess can occur from sugar deposits
Treat with laser eye surgery - does not improve sight but prevents deterioration
Diabetic Nephropathy
Patients will have a raised ESR
Patients will have normochromic normocytic anaemia
Microalbuminuria occurs - urine dipstick is negative for albumin but albumin:creatinine ratio >3
Treatment
Use angiotensin receptor blocker e.g. candesartan to reduce disease progression
Metformin should be avoided
Use ACE inhibitor to control blood pressure
Those with end stage kidney disease will need dialysis or transplant
Basement membrane thickens due to glomerular damage caused by poor glycaemic control
Nephropathy is secondary to glomerular disease
Diabetic Neuropathy
Risk factors: hypertension, smoking, high BMI, long diabetes duration
Limb symptoms: pain, paraesthesia (pins and needles), burning
Accumulation of fructose and sorbitol disrupts the structure and function of the nerve
Autonomic presentation: Postural hypotension, gastroparesis, diarrhoea, constipation, incontinence, erectile dysfunction
Isolated mononeuropathies are thought to result from occlusion of the vasa nervorum (these provide blood to the peripheral nerves)
Sensory loss in the foot can result in ischaemia, foot ulceration, infection, amputation and falls
Most common form is distal symmetrical neuropathy
Treatment
Opioids
Capsaicin - activates nerve cells by heat
Good glycaemic control
Acupuncture
Avoid weight bearing
Affects 30-35% of patients
Foot screening is essential. Patients must be educated on complications and check feet daily for ulcers.
Screening
Test vibration perception using a tuning fork
Test ankle reflexes
Test sensation using microfilament (10g)
Take a Doppler ultrasound to evaluate peripheral vascular disease
Infections + Skin
Infection is particularly prone in urinary tract and skin
Lipohypertrophy occurs at injection site
Poorly controlled diabetes impairs function of polymorphonuclear leucocytes, leading to increased susceptibility to infections
Candidiasis and UTIs are common infections