Diabetes mellitus Flashcards

1
Q

When blood glucose is too high (hyperglycaemia) for long periods of times (years)

A

over the years leads to damage of the small and large blood vessels causing premature death from cardiovascular disease

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2
Q

DM and kidney disease

A

1/4 diabetics develop kidney disease

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3
Q

how much of NHS budget spent on diabetes

A

around 10%

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4
Q

DM is the leading cause of

A

blindness in working age

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5
Q

DM is the most common cause of

A

traumatic lower limb amputation

(15% life time risk of amputation)

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6
Q

70% of DM patients die due to

A

CVD

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7
Q

life expectancy reduced on average by

A

5 to 15 years in T1 DM and 5 to 10 in T2DM

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8
Q

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……

A

signals to the pancreas beta cells to release insulin

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9
Q

insulin has its affect on which cells

A

skeletal muscle, liver and fat

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10
Q

how does insulin decrease blood glucose

A

binds to insulin receptors which triggers the transcription and translocation of GLUT4 to the surface of the cell allowing glucose to enter

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11
Q

pancreatic islet cells

A
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12
Q

In Dm why does glucose rise

A
  1. Inability to produce insulin due to beta cell failure
  2. Insulin production adequate but insulin resistance prevents insulin working effectively and invariably linked to obesity
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13
Q

type 1 diabetes

A

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
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14
Q

in T1DM the pancrease does not produce enough insulin this is called an

A

absolute insulin deficiency (immune destruction of beta cells)

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15
Q

Type 2 DM

A

Pancreas may not produce enough insulin or cells do not use insulin properly (resistance)

  • relative insulin deficiency
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16
Q

how does DM present

A

hyperglycaemia

inadequare energy utilisation

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17
Q

hyperglycaemia will cause

A
  • polyuria
  • polydipsia
  • blurry vision
  • urogenital infections- thrush
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18
Q

Symptoms of inadequate energy utilisation

A
  • tiredness
  • weakness
  • lethargy
  • weight loss
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19
Q

severity of DM symptoms will depend on

A

the rate of rise of blood glucose as well as the absolute levels of glucose achieved

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20
Q

tests use to diagnose diabetes

A
  • Fasting glucose
  • Oral glucose tolerance test
  • HbA1c
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21
Q

HbA1c

A

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
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22
Q

if asymptomatic

A

need two abnormal blood tests

(probably first discovered during routine screening)

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23
Q

if symptomatic

A

1 abnormal test adequate for diagnosis

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24
Q

prevalence of T1DM is

A

on the rise

  • Prevalence doubled every 20 years since 1945
25
Q

90% of T1 diabetics are

A
26
Q

aetiology of T1DM

A
  • Aetiology not fully understood
    • Twin studies
    • Hygiene hypothesis
27
Q

Presentation of T1DM

A
  • Rapid onset (usually weeks)
  • Weight loss
  • Polyuria
  • Polydipsia (excessive thirst)
  • Late presentation- may be vomiting due to ketoacidosis
28
Q

T1DM patient

A
  • Young usually under 30
  • Elevated venous plasma glucose
  • Presence of ketones
29
Q

treatment of T!DM

A
  • Exogenous insulin
  • Giving by subcutaneous injections several times per day
30
Q

ketone production is suppressed by

A

insulin

  • except in starvation
  • trace or + ketone in healthy starved people (serum or urien)
31
Q

ketones and T1DM

A

in the absence of insulin ketone production is activated

*presenc eof ketones is indication for immediate insulin therapy- should not wait*

32
Q

ketoacidosis signs

A
  • Hyperglycaemia
  • Ketonemia
  • Acidosis
    • Absolute or relative deficiency of insulin
33
Q

what leads to uncontroleld ketosis

A

enhanced lipolysis

34
Q

types of ketone bodies formed

A
  1. 3- beta hydroxybutyrates
  2. acetoacetic acid
  3. acetone
35
Q
A
36
Q

prevalence of T2DM

A
  • 4.6 million
  • Prevalence increasing dramatically
  • Many asymptomatic
  • Most over 40
  • Increasingly seen in younger people and children
37
Q

What cases insulin resistance to develop

A
  • Obesity- in particular central obesity (accounts for 85%)
  • Muscle and liver fat deposition
  • Elevated free fatty acids
  • Physical inactivity
  • Genetic influences
38
Q

T2DM is due to a

A

relative insulin deficiency

  • Pancreas may not produce enough insulin
  • or your cells do not use insulin properly
39
Q

how should we manage T2DM

A
  • 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
40
Q

lifestyle changes

A

weight loss and diet

41
Q

Lessons from bariatric surgery and very low calorie diets

A

Restrictive low calorie diets seem to help reduce liver fat and help revert diabetes

42
Q

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)

A
43
Q

non-insulin therapies

A
  • Biguanides
  • Sulphonylureas
  • GLP1 analogues
44
Q

biguanides

A

these drugs work by reducing the production of glucose from digestion. Metformin is the only biguanide currently available in most countries for diabetes treatment.

45
Q

sulphonylureas

A

work by causing the body to secrete insulin

46
Q

GLP1 analogues

A

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

47
Q
A
48
Q

acute complications of hyperglycameia

A
  • Diabetic ketoacidosis in type 1
  • Hyperosmolar non-ketotic syndrome in type 2
49
Q

acute complications of hypoglycaemia

A
  • Coma
  • Brain
  • Needs glucose
  • Caused by hypoglycaemic therapy
50
Q

chronic macrovascular complications of

A
  • Cerebrovascular
  • Cardiovascular e.g. coronary A
  • Peripheral vascular disease (stroke, heart attack, intermittent claudication, gangrene)
51
Q

chronic microvascular or capillary complications

A
  • Retinopathy
  • Nephropathy
  • Neuropathy
52
Q

retinopathy

A

blindness

53
Q

nephropathy

A

need for renal replacement therapy

Thickened basement membrane of the glomerulus- filtering function of tissue is damaged – loss of protein (albumin) in urine

54
Q

neuropathy

A

erectile dysfunction, foot ulceration, diarrhoea, constipation, painful peripheral neuropathy

55
Q

Ulceration and peripheral neuropathy

A

probs cant feel this

56
Q

Metabolic syndrome

A
  • 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
57
Q

requirments for person to have the metabolic syndrome:

A
  • 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
58
Q

causes of metabolic syndrome

A