Diabetes mellitus Flashcards
When blood glucose is too high (hyperglycaemia) for long periods of times (years)
over the years leads to damage of the small and large blood vessels causing premature death from cardiovascular disease
DM and kidney disease
1/4 diabetics develop kidney disease
how much of NHS budget spent on diabetes
around 10%
DM is the leading cause of
blindness in working age
DM is the most common cause of
traumatic lower limb amputation
(15% life time risk of amputation)
70% of DM patients die due to
CVD
life expectancy reduced on average by
5 to 15 years in T1 DM and 5 to 10 in T2DM
When you eat, your body breaks food down into glucose. Glucose is a type if sugar that is your body’s main energy source.
As blood glucose rises……
signals to the pancreas beta cells to release insulin
insulin has its affect on which cells
skeletal muscle, liver and fat
how does insulin decrease blood glucose
binds to insulin receptors which triggers the transcription and translocation of GLUT4 to the surface of the cell allowing glucose to enter
pancreatic islet cells
In Dm why does glucose rise
- Inability to produce insulin due to beta cell failure
- Insulin production adequate but insulin resistance prevents insulin working effectively and invariably linked to obesity
type 1 diabetes
Due to autoimmune beta cell destruction
- Beta cells- secrete insulin
- Autoantibodies made are directed against the beta cells and insulin producing cells destroyed
- Mostly genetic predisposition
in T1DM the pancrease does not produce enough insulin this is called an
absolute insulin deficiency (immune destruction of beta cells)
Type 2 DM
Pancreas may not produce enough insulin or cells do not use insulin properly (resistance)
- relative insulin deficiency
how does DM present
hyperglycaemia
inadequare energy utilisation
hyperglycaemia will cause
- polyuria
- polydipsia
- blurry vision
- urogenital infections- thrush
Symptoms of inadequate energy utilisation
- tiredness
- weakness
- lethargy
- weight loss
severity of DM symptoms will depend on
the rate of rise of blood glucose as well as the absolute levels of glucose achieved
tests use to diagnose diabetes
- Fasting glucose
- Oral glucose tolerance test
- HbA1c
HbA1c
measure of glucose control over the last few months (number of glucose molecules attached to HbA1C – over 3 months because glucose have a lifespan of 120 days)
- best measure doesnt need fasting and not reactive to recent changes in diet
if asymptomatic
need two abnormal blood tests
(probably first discovered during routine screening)
if symptomatic
1 abnormal test adequate for diagnosis
prevalence of T1DM is
on the rise
- Prevalence doubled every 20 years since 1945
90% of T1 diabetics are
aetiology of T1DM
- Aetiology not fully understood
- Twin studies
- Hygiene hypothesis
Presentation of T1DM
- Rapid onset (usually weeks)
- Weight loss
- Polyuria
- Polydipsia (excessive thirst)
- Late presentation- may be vomiting due to ketoacidosis
T1DM patient
- Young usually under 30
- Elevated venous plasma glucose
- Presence of ketones
treatment of T!DM
- Exogenous insulin
- Giving by subcutaneous injections several times per day
ketone production is suppressed by
insulin
- except in starvation
- trace or + ketone in healthy starved people (serum or urien)
ketones and T1DM
in the absence of insulin ketone production is activated
*presenc eof ketones is indication for immediate insulin therapy- should not wait*
ketoacidosis signs
- Hyperglycaemia
- Ketonemia
- Acidosis
- Absolute or relative deficiency of insulin
what leads to uncontroleld ketosis
enhanced lipolysis
types of ketone bodies formed
- 3- beta hydroxybutyrates
- acetoacetic acid
- acetone
prevalence of T2DM
- 4.6 million
- Prevalence increasing dramatically
- Many asymptomatic
- Most over 40
- Increasingly seen in younger people and children
What cases insulin resistance to develop
- Obesity- in particular central obesity (accounts for 85%)
- Muscle and liver fat deposition
- Elevated free fatty acids
- Physical inactivity
- Genetic influences
T2DM is due to a
relative insulin deficiency
- Pancreas may not produce enough insulin
- or your cells do not use insulin properly
how should we manage T2DM
- Lifestyle
- Non-insulin therapies
- Insulin
- Patient education and ability to monitor results of therapy
- Look for other vascular risk – BP, lipids, smoking exercise, diet
- Surveillance for chronic complications
lifestyle changes
weight loss and diet
Lessons from bariatric surgery and very low calorie diets
Restrictive low calorie diets seem to help reduce liver fat and help revert diabetes
MRI scan of the liver showing high levels of fat in green (left) and a sharp decrease in liver fat achieved using a low-calorie diet (right)
non-insulin therapies
- Biguanides
- Sulphonylureas
- GLP1 analogues
biguanides
these drugs work by reducing the production of glucose from digestion. Metformin is the only biguanide currently available in most countries for diabetes treatment.
sulphonylureas
work by causing the body to secrete insulin
GLP1 analogues
works by increasing the levels of hormones called ‘incretins’. These hormones help the body produce more insulin only when needed and reduce the amount of glucose being produced by the liver when it’s not needed
acute complications of hyperglycameia
- Diabetic ketoacidosis in type 1
- Hyperosmolar non-ketotic syndrome in type 2
acute complications of hypoglycaemia
- Coma
- Brain
- Needs glucose
- Caused by hypoglycaemic therapy
chronic macrovascular complications of
- Cerebrovascular
- Cardiovascular e.g. coronary A
- Peripheral vascular disease (stroke, heart attack, intermittent claudication, gangrene)
chronic microvascular or capillary complications
- Retinopathy
- Nephropathy
- Neuropathy
retinopathy
blindness
nephropathy
need for renal replacement therapy
Thickened basement membrane of the glomerulus- filtering function of tissue is damaged – loss of protein (albumin) in urine
neuropathy
erectile dysfunction, foot ulceration, diarrhoea, constipation, painful peripheral neuropathy
Ulceration and peripheral neuropathy
probs cant feel this
Metabolic syndrome
- Cluster of the most dangerous risk factors associated with:
- CVD
- Diabetes and raised fasting plasma glucose
- Abdominal obesity
- High cholesterol and BP
- Together they confer a marked increase in CVD risk
requirments for person to have the metabolic syndrome:
- Waist measurement >94cm for men and >80 for women
- Plus any 2 of the following
- Raised TAG >1.7 mmol/l
- Reduced HDL cholesterol <1.0 for men and 1.2 mmol/l for women
- Raised blood pressure >135/85
- Or raised fasting blood glucose >5.6 mmol/l
causes of metabolic syndrome
