16) T2D Flashcards

1
Q

What is MODY?

A

Maturity onset diabetes of the young

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2
Q

What is T2D?

A

chronic hyperglycaemia sufficient to cause tissue damage (insulin resistance leading to insulin deficiency)

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3
Q

What is the fasting glucose threshold for diabetes diagnosis?

A

7+

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4
Q

Is T1D or T2D affected more by genetics?

A

T2D

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5
Q

Factors that increase risk of developing T1D:

A

Low birth weight
intrauterine environment
microbiota
diet/excercise

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6
Q

What happens to insulin secretion and resistance with age?

A

Insulin secretion decreases
Insulin resistance increases

Eventually reach an age where insulin secretion is too low to match insulin resistance

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7
Q

What is T2D a complex interaction between and what is eventually required?

A

Complex interaction between lack of insulin and insulin not working properly

Eventually become insulin deficient (insulin req)

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8
Q

What 2 things make up hepatic glucose output?

A

glycogenolysis + gluconeogenesis

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9
Q

What type of obesity is most relevant to T2D?

A

Centropetal - omental adipocytes are most active

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10
Q

4 ways T2D may present:

A

Osmotic symptoms
Infection
screening
complications

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11
Q

What are 3 possible microvascular vs macrovascular complications of T2D?

A

Microvascular:

  • retinopathy
  • neuropathy
  • nephropathy

Macrovascular: (bigger vessels)

  • IHD
  • stenosis
  • PVD
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12
Q

What is the incretin effect?

A

More insulin is secreted when glucose is given orally rather than IV (due to gut hormones-GLP-1)

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13
Q

How is T2D managed?

A

Education
Diet/excercise
Drugs
screening

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14
Q

How do Beta cells work?

A

Glucose enters + is metabolised to ATP

ATP blocks ATP sensitive K+ channels so K+ builds up=depolarisation–>Ca2+ influx–>insulin secreted

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