Diabetes Mellitus Flashcards

1
Q

What is the definition of DM?

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 six symptoms of hyperaemia?

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

What are two metabolic decompensation of hyperglycaemia?

A

Diabetic ketoacidosis and Hyperosmolar hyperglycemic state

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4
Q

Name some long term complications of hyperglycaemia

A
  • Microvascular (retinopathy, neuropathy, nephropathy),

* Macrovascular (stroke, MI, PVD)

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5
Q

How is diabetes diagnosed?

A

Measuring blood glucose of HbA1c

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6
Q

What are the BG results diagsnotic of DM?

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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7
Q

What are the BG results diagnostic of 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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8
Q

Why is it important to determine intermediate hyperglycaemia?

A

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

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9
Q

What is OGTT?

A

Oral glucose tolerance test

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10
Q

What is CHO?

A

Carbohydrate

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11
Q

What is the diagnostic criteria of DM?

A
  • FBG ≥7
  • 2h BG ≥ 11.1
  • HbA1c ≥ 48
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12
Q

What is normoglycemia?

A

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

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13
Q

What is it important to see if a patient fits in with the diagnostic criteria of DM?

A

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

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14
Q

How many samples are required for diagnostic criteria of DM?

A
  • ONE diagnostic lab Glc plus symptoms

* TWO diagnostic lab Glc or HbA1c levels without symptoms

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15
Q

Why measure HbA1c to diagnose DM?

A

When blood glucose levels are high, glucose molecules attach to the hemoglobin in red blood cells. The longer hyperglycemia occurs in blood, the more glucose binds to hemoglobin in the red blood cells and the higher the glycated hemoglobin.

Gives indication of BG levels over last 8-12 weeks

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16
Q

When can HbA1c not be used for diagnosis?

A
  • Children and young people
  • Pregnancy (or recently < 2 months)
  • Short duration of DM symptoms
  • Acutely ill
  • On meds cause rapid Glc rise (corticosteroids, antipsychotic drugs)
  • Acute pancreatic damage or surgery
  • Renal failure
  • HIV
17
Q

What is the effect of insulin on different types of tissue?

A
  • Adipose tissue -> reduced lipolysis
  • Liver -> reduced glucose production
  • Muscle -> increased glucose uptake
18
Q

What is the aetiology of Type 1 DM?

A
  • Positive autoantibodies i.e. anti-GAD

* FH of Type 1

19
Q

What is required for Type 1 DM to develop?

A

Genetic pre-disposition, plus:
• Trigger i.e. viral infection, change in environment or immune system response to environment
• Auto immunity (destruction of Islet and thus B cells)

20
Q

How is the incidence of Type 1 diabetes changing?

A

Although proportion of diabetic population with IDDM is decreasing, total numbers of IDDM increasing.

21
Q

What are the effects in different tissue types of decrease in insulin

A
  • Adipose tissue -> increase lipolysis
  • Liver -> raised Glc production
  • Muscle -> reduced Glc uptake
  • Hyperglycaemia, ketoaemia -> diabetic ketoacidosis
22
Q

What are the symptoms of IDDM?

A
Short duration of:
• Thirst 
• Tiredness
• Polyuria / nocturia 
• Weight loss
• Blurred vision 
• Abdominal pain
23
Q

What are the signs of IDDM?

A
  • Ketones on breath
  • Dehydration
  • May have increased respiratory rate, tachycardia, hypotension
  • Low grade infections, thrush / balanitis
24
Q

Describe the evolution of Type 2 DM

A

Blood glucose levels increase as β-cell function declines.

As the β-cells become damaged by lipotoxicity and glucotoxicity as a result of insulin resistance, they can eventually no longer compensate, resulting in hyperglycaemia.

Type 2 diabetes is therefore a result of underlying insulin resistance and subsequent β-cell dysfunction.

25
Q

How has the prevalence of NIDDM in Scotland changed?

A

Increasing - approx 5% of population in Scotland

26
Q

Is IDDM or NIDDM more prevalent?

A

T2DM (NIDDM)

27
Q

What occurs to insulin effects in T2DM?

A
  • Adipose tissue -> altered lipolysis
  • Liver -> increased Glc production
  • Muscle -> Reduced Glc uptake
28
Q

What are the symptoms of T2DM?

A
  • May have no symptoms
  • Thirst
  • Tiredness
  • Polyuria / nocturia
  • Sometimes weight loss
  • Blurred vision
  • Symptoms of complications e.g. CVD
29
Q

What are the signs of T2DM?

A
  • 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
30
Q

Name risk factors for T2DM

A
Any two:
• Overweight 
• FH 
• Over 30yrs if Maori/Asian
• Over 40yrs if European 
• History of diabetes in pregnancy 
• Inactive lifestyle 
• Previous high blood glucose / impaired Glc tolerance
31
Q

Name three other types diabetes

A
  • Recognised genetic syndromes : MODY
  • Gestational diabetes
  • Secondary diabetes
32
Q

Describe MODY: maturity onset diabetes in the young

A
  • Autosomal dominant
  • Impaired beta-cell function
  • Single gene defect
  • Important to take FH in patient with new onset diabetes
33
Q

What are the two categories of stations that can occur in MODY?

A

Glucokinase mutations and transcription factor mutations

34
Q

What are the features of glucokinase mutations in MODY?

A
  • Onset at birth

  • Stable hyperglycaemia

  • Diet treatment

  • Complications rare
35
Q

What are the features of transcription factor mutations?

A

• Adolescence/young adult onset
• 
Progressive hyperglycaemia

• 1/3 diet, 1/3 OHA, 1/3 Insulin

• Complications frequent

36
Q

Describe secondary diabetes mellitus

A
• Pancreatic destruction
   - Haemochromatosis- excess iron deposition
   - Cystic fibrosis 
   - Chronic pancreatitis
pacreatectomy
• Recognised genetic syndromes-DIDMOAD
• Rare endocrine disorders e.g. Cushings syndrome, Acromegaly, Pheochromocytoma
• Drug therapy i.e. corticosteroids
37
Q

Describe gestational diabetes (hyperglycaemia of pregnancy)

A

• Increasing insulin resistance in pregnancy
• Associated with FH of Type 2 diabetes
• Increased risk of Type 2 diabetes later in life
• Develops 2nd / 3rd trimester
• More common if overweight and inactive
• Neonatal problems:
macrosomia / respiratory distress / neonatal hypoglycaemia