What is Diabetes Mellitus? Flashcards

1
Q

Diabetes Mellitus

A

“a group of metabolic diseases of multiple aetiologies characterised by hyperglycaemia together with disturbances of carbohydrate, fat and protein metabolism resulting from defects in insulin secretion, insulin action, or both”

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2
Q

What are the symptoms of hyperglycaemia?

A
  • Polydipsia
  • Polyuria
  • Blurred vision
  • Weight loss
  • Infections
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3
Q

What are the possible long term complications of hyperglycaemia?

A

Microvascular

  • Retinopathy
  • neuropathy
  • Nephropathy

Macrovascular

  • Stroke
  • MI
  • PVD
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4
Q

What metabolic decompensation can occur with hyperglycaemia?

A

DKA

HHS

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5
Q

How is diabetes diagnosed?

A
  • Diagnostic glucose levels (venous plasma) fasting >7.0 mmol/l, random >11.1 mmol/l
  • OGTT 2h after 75g CHO >11.1 mmol/l
  • Diagnostic HbA1c ≥ 48 mmol/mol.
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6
Q

What is considered intermediate hyperglycaemia?

A
  • Impaired fasting glucose 6.1-7 mmol/l
  • Impaired glucose tolerance 2h glucose ≥7.8 and <11mmol/l
  • HbA1c 42-47mmol/mol
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7
Q

What do diabetes diagnostic criteria identify?

A

A group with significantly increased premature mortality and increased risk of microvascular and cardiovascular complications

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8
Q

What does intermediate hyperglycaemia identify?

A

Identifies a group at higher risk of future diabetes and adverse outcomes such as cardiovascular disease

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9
Q

Normoglycaemia

A

Glucose levels associated with low risk of developing diabetes or cardiovascular disease

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10
Q

What is required for a definitive diagnosis of diabetes?

A
  • ONE diagnostic lab glucose plus symptoms

- TWO diagnostic lab glucose or HbA1c levels without symptoms.

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11
Q

What is HbA1c?

A

Glycated haemoglobin

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12
Q

What does HbA1c give an indication of?

A

Blood glucose levels over last 8-12 weeks

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13
Q

When can HbA1c not be used for diagnosis?

A

-Children and young people.
-Pregnancy—current or recent (< 2 months).
-Short duration of diabetes symptoms.
-Patients at high risk of diabetes who are acutely ill
(HbA1c ‡ 48 mmol⁄ mol confirms pre-existing diabetes, but a value < 48 mmol ⁄ mol does not exclude it and such patients must be retested once the acute episode has resolved).
-Patients taking medication that may cause rapid glucose rise; for example, corticosteroids, antipsychotic drugs (2 months or less).
-Acute pancreatic damage or pancreatic surgery.
-Renal failure.
-HIV

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14
Q

How can diabetes be classified?

A
  • T1DM
  • T2DM
  • Other types
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15
Q

What is normal metabolism?

A

Levels of glucose and other nutrients entering the blood vary markedly during the day but, between a complete carbohydrate blow-out and NO food ingested, [BG] is maintained over a fairly tight range

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16
Q

What dominates the absorptive state?

A

Insulin

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17
Q

What is the only hormone which lowers [BG]?

A

Insulin

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18
Q

What role do a-cells play in [BG] control?

A
  • a-cells secret glucagon

- Stimulation of the liver (glycogenolysis and gluconeogenesis)

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19
Q

What role do B-cells play in the[BG] control?

A
  • B-cells secrete insulin

- Insulin involved in glucose uptake in adipose, liver and skeletal muscle

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20
Q

What are the genetic linked risks of developing T1DM?

A
  • Monozygotic twins 30-50% concordance
  • If father has Type 1: 6% risk
  • If mother has Type 1: 1% risk
  • If sibling has Type 1: 8% risk
  • If non-identical twin has Type 1: 10% risk
  • If both parents have Type 1: 30% risk
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21
Q

What does development of T1DM require?

A

Genetic pre-disposition plus

  • Trigger e.g.? Viral infection
  • Auto immunity
22
Q

What effect does insulin have on adipose tissue?

A

Reduced lipolysis

23
Q

What effect does insulin have on the liver?

A

Reduced glucose production

24
Q

What effect does insulin have on muscle?

A

Increased glucose uptake

25
How does insulin cause stimulation?
It binds to receptors on cell surfaces and controls a range of intracellular processes
26
What is T1DM characterised by?
Insulin deficiency
27
What can hyperglycaemia lead to in T1DM?
- Ketoaemia | - DKA
28
In T1DM presentation, what may there be a short history of?
- Thirst - Tiredness - Polyuria / nocturia - Weight loss - Blurred vision - Abdominal pain
29
What might be found on examination of T1DM?
- Ketones on breath - Dehydration - May have increased respiratory rate, tachycardia, hypotension. - Low grade infections, thrush / balanitis
30
What are the genetic linked risks of developing T2DM?
- Identical twin: 90-100% risk - One parent: 15% - Both parents: 75% - Sibling: 10% - Non-identical twin: 10%
31
What is the pathophysiology of T2DM?
- May initially have hyperinsulinaemia but there is a progressive decrease in insulin production - Increased cellular insulin resistance - Altered lipolysis - Increased glucose production - Reduced glucose uptake
32
What are the symptoms of T2DM?
- May have no symptoms - Thirst - Tiredness - Polyuria / nocturia - Sometimes weight loss - Blurred vision - Symptoms of complications e.g. CVD
33
What are the signs of T2DM?
- Not ketotic - Usually overweight but not always - Low grade infections, thrush / balanitis - In type 2 DM may have micro vascular or macrovascular complications at Dx
34
When screening for T2 diabetes in asymptomatic populations what risk factors are loked at?
Risk factors—any two present • Overweight • Family history • Over age 30 years if Maori ⁄ Asian (Indian subcontinent) ⁄ Pacific Island descent • Over age 40 years if European • Previous history of diabetes in pregnancy (Gestational Diabetes) Had a big baby (more than 4 kg)—not in immediate post-natal period • Inactive lifestyle, lack of exercise • Previous high blood glucose ⁄ impaired glucose tolerance
35
What 'other' types of diabetes are there?
- Recognised genetic syndromes :MODY - Gestational diabetes - Secondary diabetes
36
What is MODY?
Maturity Onset Diabetes in the Young which is an autosomal dominant condition which leads to impaired beta cell function
37
What causes MODY?
Single gene defect
38
How proportion of diabetes cases does MODY account for?
5%
39
What is it important to do when someone is diagnosed with diabetes?
Take a family history
40
Describe MODY due to glucokinase mutations.
- Onset at birth - Stable hyperglycaemia - Diet treatment - Complications rare
41
Describe MODY due to transcription factor mutations.
- Adolescence/young adult onset - Progressive hyperglycaemia - 1/3 diet, 1/3 OHA, 1/3 Insulin - Complications frequent
42
How is secondary DM treated?
Drug therapy such as corticosteroids
43
What can cause pancreatic destruction in secondary diabetes?
- Haemochromatosis- excess iron deposition - Cystic fibrosis - Chronic pancreatitis - Pacreatectomy
44
What can cause secondary diabetes?
- Pancreatic destruction - Recognised genetic syndromes= DIDMOAD - Rare endocrine disorders (Cushing's syndrome, acromegaly, pheochromocytoma)
45
What is gestational diabetes?
Hyperglycaemia of pregnancy
46
What is gestational diabetes associated with?
-Family history of T2DM
47
When does gestational diabetes develop?
2nd or 3rd trimester
48
What does gestational diabetes increase the mothers risk of?
Increased risk of T2DM later in life
49
When is gestational diabetes more common?
When the mother is overweight and inactive
50
What problems can gestational diabetes cause in the neonate?
- Macrosomia - Respiratory distress - Neonatal hypoglycaemia