Diabetes complications Flashcards
Outline what metabolic syndrome is
Clustering of risk factors for CVD
- visceral adiposity/central obesity
- Impaired glucose metabolism
- Dyslipidaemia: increased triglycerides, decreased HDL-cholesterol
- Hypertension
- visceral/central obesity and insulin resistance are central in pathogenesis of metabolic syndrome
What are the aims of therapy eg insulin therapy in diabetes?
- ) remove symptoms of uncontrolled diabetes
- improve glycaemic control - )Reduce risk of complications of diabetes
- Multiple risk factor modification: Glycaemic control,BP,Lipids, lifestyle - ) Prevent disability ( related to diabetes or its treatment); acute-chronic complications
- ) Early detection of complications
- screening
Outline the microvascular complications of diabetes
- Diabetic retinopathy(&cataracts, glaucoma)
- Diabetic neuropathy(& sensory impairment i.e peripheral neuropathy)
- Diabetic nephropathy
- Limb amputation
Outline the macrovascular complications of diabetes
- CHD
- stroke
- congestive heart failure (&atherosclerosis & poor blood supply to lower limbs-peripheral vascular disease)
Outline the non-vascular complications of diabetes
- Cancer
- Infections(bacterial & fungal infections of the skin)
- Degenerative diseases
- Depression
- Congenitive disorders
- sexual dysfunction
- gangrene
- Ulceration
- Necrobiosis lipidoica (rare granulomatous skin disorder which can affect the shin of T1DM pts)
How can the lifestyle of a diabetic pt be modified to prevent diabetes emergencies
- ) Diet: normal healthy diet
- avoid ‘diabetic foods’
- portion size - ) Weight control
- ) exercise
- )stop smoking
How do we decide which treatment to use for glycaemic control
- Evidence of effectiveness (surrogate/hard endpoints)
- Other effects (eg weight/hypoglycaemia)
- Other considerations: route of administration,co-morbidities
Outline the different mechanisms of actions for gylcaemic control treatments
- Insulin sensitivity
- Insulin secretion
- Slow glucose absorption
How can we cause weight gain in a diabetic pt
- Incretin therapies
- Increase glucose excretion
What are incretins
A group of metabolic hormones that stimulate a decrease in blood glucose level
-They are released after eating & augment the secretion of insulin released from the pancreatic beta cells of the islets of Langerhans by a blood glucose-dependent mechanism
Explain the idea of ‘glycaemic legacy’ in T2DM
- If you generate a ‘bad glycaemic legacy’ it drives your risk of complications
- Idea of metabolic memory
- Better prognosis with early glycaemic control in the course of the disease
Outline the multiple defects that contribute to the progression of T2DM
The following all lead to hyperglycaemia:
- Decreased incretin effect
- Increased lipolysis
- Increased glucose reabsorption
- Decreased glucose uptake from skeletal muscles
- Neurotransmitter dysfunction
- Increased hepatic glucose production
- Increased glucagon secretion from alpha cells of the pancreas
- Decreased insulin secretion from the pancreas
Outline the neurogenic symptoms of hypoglycaemia
- ) Adrenergic:
- palpitations
- tremor
- anxiety/arousal - )Cholinergic
- sweating
- hunger
- paresthaesia
Outline the neyroglycopenic symptoms of hypoglycaemia
- Cognitive impairments
- Behavioural changes
- Psychomotor abnormalities
- Seizure
- Coma
Outline the complications & effects of severe hypoglycaemia
- ) Increased risk of cardiac arrhythmia
- Abnormal prolonged cardiac repolarisation; increased QTc and QTd
- Sudden death - ) Progressive neuroglycopenia
- cognitive impairement
- Unusual behaviour
- Seizure
- Coma
- Brain death
