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endocrine system 1 > What is Diabetes Mellitus? > Flashcards

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
Q

How does insulin cause stimulation?

A

It binds to receptors on cell surfaces and controls a range of intracellular processes

26
Q

What is T1DM characterised by?

A

Insulin deficiency

27
Q

What can hyperglycaemia lead to in T1DM?

A
  • Ketoaemia

- DKA

28
Q

In T1DM presentation, what may there be a short history of?

A
  • Thirst
  • Tiredness
  • Polyuria / nocturia
  • Weight loss
  • Blurred vision
  • Abdominal pain
29
Q

What might be found on examination of T1DM?

A
  • Ketones on breath
  • Dehydration
  • May have increased respiratory rate, tachycardia, hypotension.
  • Low grade infections, thrush / balanitis
30
Q

What are the genetic linked risks of developing T2DM?

A
  • Identical twin: 90-100% risk
  • One parent: 15%
  • Both parents: 75%
  • Sibling: 10%
  • Non-identical twin: 10%
31
Q

What is the pathophysiology of T2DM?

A
  • 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
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
33
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
34
Q

When screening for T2 diabetes in asymptomatic populations what risk factors are loked at?

A

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
Q

What ‘other’ types of diabetes are there?

A
  • Recognised genetic syndromes :MODY
  • Gestational diabetes
  • Secondary diabetes
36
Q

What is MODY?

A

Maturity Onset Diabetes in the Young which is an autosomal dominant condition which leads to impaired beta cell function

37
Q

What causes MODY?

A

Single gene defect

38
Q

How proportion of diabetes cases does MODY account for?

A

5%

39
Q

What is it important to do when someone is diagnosed with diabetes?

A

Take a family history

40
Q

Describe MODY due to glucokinase mutations.

A
  • Onset at birth
  • Stable hyperglycaemia
  • Diet treatment
  • Complications rare
41
Q

Describe MODY due to transcription factor mutations.

A
  • Adolescence/young adult onset
  • Progressive hyperglycaemia
  • 1/3 diet, 1/3 OHA, 1/3 Insulin
  • Complications frequent
42
Q

How is secondary DM treated?

A

Drug therapy such as corticosteroids

43
Q

What can cause pancreatic destruction in secondary diabetes?

A
  • Haemochromatosis- excess iron deposition
  • Cystic fibrosis
  • Chronic pancreatitis
  • Pacreatectomy
44
Q

What can cause secondary diabetes?

A
  • Pancreatic destruction
  • Recognised genetic syndromes= DIDMOAD
  • Rare endocrine disorders (Cushing’s syndrome, acromegaly, pheochromocytoma)
45
Q

What is gestational diabetes?

A

Hyperglycaemia of pregnancy

46
Q

What is gestational diabetes associated with?

A

-Family history of T2DM

47
Q

When does gestational diabetes develop?

A

2nd or 3rd trimester

48
Q

What does gestational diabetes increase the mothers risk of?

A

Increased risk of T2DM later in life

49
Q

When is gestational diabetes more common?

A

When the mother is overweight and inactive

50
Q

What problems can gestational diabetes cause in the neonate?

A
  • Macrosomia
  • Respiratory distress
  • Neonatal hypoglycaemia

endocrine system 1 (25 decks)

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