Week 4: Diabetes Flashcards

1
Q

What random plasma glucose level defines diabetes

A

> 11.1 mmol/L

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2
Q

What fasting plasma glucose level defines diabetes

A

> 7 mmol/L

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3
Q

What 2h (after oral glucose tolerance test) plasma glucose level defines diabetes

A

> 11.1 mmol/L

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4
Q

What HbA1c level defines diabetes

A

> 48 mmol/mol

should repeat and get similar result within 2 weeks

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5
Q

What type of inheritance is MODY

A

Autosomal dominant

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6
Q

Explain the pathophysiology of MODY

A

Single gene mutation in gene that creates glucose channels for beta cells

  • > more glucose has to enter cell before insulin is secreted
  • > insulin secretion remains regulated
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7
Q

Clinical features and complications of MODY

A
  • May be asymptomatic or present like T2DM (hyperglycaemia, polyuria, polydipsia)
  • No microvascular complications
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8
Q

What treatment is used for glucokinase MODY

A

No need treatment for glucokinase MODY

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9
Q

What treatment is used for transcription factor MODY

A

Sulfonylureas for HNF-1a and HNF-4a MODY

Insulin for HNF-1b MODY

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10
Q

At what age can T1DM be diagnosed

A

Any age above 6 months old

possible to be diagnosed even after 50yo

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11
Q

What gene is associated with familial risk of developing T1DM

A

HLA on chromosome 6

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12
Q

What 2 blood markers are used in T1DM? What are they markers for?

A

C peptide (marker of insulin levels. Cleaved with insulin from proinsulin)

Islet antibodies (marker of B cell response)

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13
Q

Risk factors for developing T2DM

A
  • Family history, obesity, race
  • Fat accumulation in liver & pancreas
  • Number of hours of being sedentary a day (in spite of activity at other times)
  • Previous gestational diabetes
  • PCOS
  • Socio-economic factors: higher risk in urban areas
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14
Q

Plasma glucose criteria for diagnosis of gestational diabetes

A

o Fasting glucose 5.6mmol/L OR

o 2h plasma glucose 7.8mmol/L

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15
Q

Who should be screened for gestational diabetes

A
  • BMI >30
  • Previous macrosomic baby >4.5kg
  • Previous gestational diabetes
  • Family history of diabetes
  • High risk ethnicities
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16
Q

Clinical features/ complications of neonatal diabetes

A
  • High glucose levels/ DKA
  • Low birth weight
  • Very low C peptide (low insulin release)
  • May lead to transient or permanent diabetes
17
Q

Pathophysiology of neonatal diabetes

A

Mutated K-ATPase channel in B cell

B cell cannot depolarised, insulin not released

18
Q

How might Cushing’s syndrome lead to diabetes

A
  • Cortisol blocks effects of insulin
  • Reduced insulin sensitivity in liver and muscle
  • Stimulates gluconeogenesis
19
Q

How might hyperthyroidism lead to diabetes

A

-T3/T4 stimulates gluconeogenesis and glycolysis

20
Q

How might acromegaly lead to diabetes

A
  • Growth hormone blocks effects of insulin
  • Reduced insulin sensitivity in liver and muscle
  • Growth hormone stimulates gluconeogenesis
21
Q

How might phaeochromocytoma lead to diabetes

A
  • Catecholamines inhibit insulin secretion

- Catecholamines stimulate gluconeogenesis

22
Q

How might glucagonoma (tumour resulting in overproduction of glucagon) lead to diabetes

A

-Glucagon stimulates gluconeogenesis

23
Q

What drugs are commonly associated with higher risk of developing diabetes

A
  • HIV drugs (protease inhibitors and NRTIs)
  • steroids
  • antipsychotics
24
Q

Why do HIV drugs (protease inhibitors and NRTIs) cause increased blood sugar

A

Block uptake of glucose,

Stimulate gluconeogenesis

25
Why do steroids cause increased blood sugar
Reduce sensitivity of liver to insulin, stimulates gluconeogenesis Reduces muscle/fat uptake of glucose, more glucose circulating in bloodstream
26
Why do antipsychotics cause increased blood sugar
Blocks pancreatic receptors, beta cells unable to take up glucose
27
What are the 3 criteria for diagnosing Diabetic Ketoacidosis
1. Capillary BM >11 2. Capillary ketones >3mmol/L or urine ketones ++ or more 3. Venous pH less than 7.3 or HCO3 <15mmol/L
28
Describe the pathophysiology of why DKA occurs
Under stress (eg illness), body cannot produce enough insulin Too little insulin -> glucose not taken up by cells -> body breaks down fatty acids to ketones for energy
29
Why do thirst and dehydration occur in DKA
Too much glucose in blood, pass glucose out in urine, water follows glucose in urine
30
What electrolyte disturbance is associated with DKA? Why?
Hyperkalemia Excess H+ in blood, so H+ is pumped into cells, K+ is pumped out of cells into blood