Diabetes Flashcards

1
Q

What is diabetes

A

 A metabolic disorder characterized by the presence of hyperglycemia due to:

  • defective insulin secretion and/or
  • Defective insulin action
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2
Q

what are the longterm complication of diabetes

A
  • kidney, eye, nerves, heart, and blood vessels
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3
Q

what % of the population has diabetes

how many people will have it in 2019?

what % is undiagnosed

A

 Prevalence is ~6.3% of the population (all ages and males/females grouped together).
 This is expected to be 3.7 million by 2019.
 Estimated that up to 20% of diabetes cases are undiagnosed.

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4
Q

Type 1 is also increasing but why is type 2 more?

A

due to:

  • Population is again
  • Obesity rate are rising
  • Sedentary lifestyle
  • Aboriginal people are 3-5x more likely to develop type 2 diabtes
  • 77% of new Canadians come from pepulations at increased risk for type 2 diabetes. Eg. Hispanics, asina, south Asian, African descent.
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5
Q

what is type 1

A

primarily a result of pancreatic beta cell destruction and is prone to ketoacidosis.

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6
Q

what is type 2

A

may range from predominant insulin resistance with relative insulin deficiency to a predominant secretory defect with insulin resistance.

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7
Q

What is GESTATIONAL DIABETES MELLITUS (GDM)

A

) refers to glucose intolerance with onset or first recognition during pregnancy.

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8
Q

there are other uncommon forms of diabetes- what do they consist of

A

specific genetically defined forms of diabetes – NOT common (eg. Single gene defect)

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9
Q

diabetes can also stem from other diseases:

A

Pancreatitis
Pancreatic cancer and surgical removal of pancrease
Cystic fibrosis
Excess glucocorticoids
- chronic administration as a drug eg. Prednisone
- excess endogenous production (cushing’s syndrome- overactivity of adrenal cortex)

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10
Q

Type 1:
what % of all diabetes
who does it affect

A

 ~5-10% of cases of diabetes
 Usually but not always < 30 years of age
 Occurs more commonly in people of European descent. Marked geographic variation in annual incidence.
 Insulin deficient (production).

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11
Q

what are other characteristics of type 1: how much is it increasing per year
how does it appear

A

 Prone to development of ketosis.(excess production of ketones- can progress to ketoacidosis- (low blood ph due to excessive ketones)
 Typical Type 1 patient is a child or adolescent at onset
 Disease appears more suddenly with severe symptoms.
 Less common in pre-school age children but incidence is ing.
 Incidence overall is ing at a rate of 3%/year
- Dupports the role of environment etiology.

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12
Q

What causes type 1: etiology

A

idiopathic (unknown)
 Genetic defects plus environmental factors necessary.(they interact) (polygenic)
 Genetic pattern transmits (many genes involved) transmit predisposition to diabetes.
 # of susceptibility genes under study.|(already have the susceptibility but what triggers it) e.g. candidate =
 Environmental factors that have been studied: eg. Vitamin D
 viruses – e.g. enteroviruses, rotavirus, rubella but evidence is mostly against
 dietary factors. e.g. exposure to cows’ milk protein
 vitamin D intake

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13
Q

what is TEDDY

A

The Environmental Determinants of Diabetes in the Young
 large international study to follow high risk infants from birth to adolescence to try to establish the importance of specific environmental factors.

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14
Q

Pathogenesis of type 1

A

 Autoimmune destruction of insulin-producing beta cells in the pancreas by CD4+ and CD8+ T cells and macrophages infiltrating the islets.
 When fully developed  little or no insulin is produced

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15
Q

what is the treatment for type 1

A

diet insulin and exercise

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16
Q
Type 2:
who does it affect,
who prevalent compared all diabetes
clinical symptoms
what happenes
A

 Usually middle aged or elderly at onset
 ….But recent alarming  incidence in childhood
- Predominimantly adolecents
- Especially in aboriginal population

 Most are not ketosis prone (a small proportion are). (but a small proportion is)
 Clinical symptoms often subtle and unnoticed by the patient
 Accounts for majority of DM (~ 90% )
 Patient has a combination of:
- Insulin resistance: diminished tissue response to insulin ( impaired insulin signaling arising from postreceptor defects) AND
- An insulin secretion defect (metabolic defect) (different than type 1)- the dgree of these two in people varies-

 Relative importance of insulin resistance versus secretion defect varies among patients
 Thus, a heterogenous group of disorders with the common endpoint of hyperglycemia.

17
Q

Etiology and pathogenesis

A

Etiology and Pathogenesis
 Genetic predisposition (polygenic) PLUS environmental factors.(interacting)
 Recall basic endocrine physiology.
 How does an endocrine hormone such as insulin exert its action? – it’s a protein- it needs to bind to a receptor on the surface of the cell.
 How is it determined which are the target tissues or cells? – the cells with the insulin receptors.

18
Q

normal glucose tolerance

A

ability to remove a specified glucose load from the blood and within a defined period of time. Means that their body put out insulin to keep their glucose normal

19
Q

what is  Fasting hyperglycemia

A

caused by abnormally high hepatic glucose output due to hepatic resistance to insulin action.

20
Q

what are the pathways in the liver

A

gluconeogenesis and glycogenolysis