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Stage 4: CSIM 2 > Week 4: Diabetes > Flashcards

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
Q

Why do steroids cause increased blood sugar

A

Reduce sensitivity of liver to insulin, stimulates gluconeogenesis

Reduces muscle/fat uptake of glucose, more glucose circulating in bloodstream

26
Q

Why do antipsychotics cause increased blood sugar

A

Blocks pancreatic receptors, beta cells unable to take up glucose

27
Q

What are the 3 criteria for diagnosing Diabetic Ketoacidosis

A
  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
Q

Describe the pathophysiology of why DKA occurs

A

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
Q

Why do thirst and dehydration occur in DKA

A

Too much glucose in blood, pass glucose out in urine, water follows glucose in urine

30
Q

What electrolyte disturbance is associated with DKA?

Why?

A

Hyperkalemia

Excess H+ in blood, so H+ is pumped into cells, K+ is pumped out of cells into blood

Stage 4: CSIM 2 (47 decks)

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