ENDO - Diabetes assessment & Mx Flashcards

1
Q

What are the types of diabetes?

A

Definition base on etiologic differences

Type 1: Autoimmune, idiopathic, absolute insulin deficiency 2o beta cell destruction

Type 2: spectrum with insulin resistance and varying degrees of insulin secretion
•In developed countries, 90% overweight ± metabolic syndrome

Other – 5% cases
•Gestational (Pregnancy related)
•Terms like insulin dependent, non insulin dependent, juvenile onset, maturity onset etc. no longer used

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2
Q

How do you diagnose diabetes?

  • RBG
  • FPG (fasting plasma glucose)
  • HbA1C
  • 2 hour value in OGTT (oral glucose tolerance test with 75g)
A

–Symptoms + RBG >11.1mmol/L or
–FPG > 7.0mmol/L* or
–HbA1C > 48 mmol/mol (6.5%)*†
–2 hour value >11.1mmol/l in the OGTT

*In absence of unequivocal hyperglycaemia with acute metabolic decompensation, criteria should be confirmed by repeat testing

† HbA1C became available as a Medicare funded test for the diagnosis of diabetes in November 2014.

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3
Q

What is the FPG (fasting plasma glucose) of normal person?

A

Less than 6.1mM

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4
Q

What is the FPG (fasting plasma glucose) of an impaired fasting glucose person?

A

FPG 6.1-6.9mM

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5
Q

What is the FPG (fasting plasma glucose) of a diabetic?

A

> 7.0mM

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6
Q

Describe (3) characterisations of type 1 diabetes

A
  • Characterised by autoimmune destruction, of the pancreatic beta cells
  • Absolute insulin deficiency
  • Insulin required to prevent death
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7
Q

Pathophysiology of T1D

  • genetic susceptibility
  • environmental susceptibility
  • prediabetic stage
  • when diabetic
A
  • Genetic susceptibility (MZ concordance less than 50%)
  • Environmental event triggers process susceptible people
  • Prediabetic stage: mulitple antibodies (eg. Anti GAD, anti islet cell) detected in blood. Variable duration
  • Diabetes – occurs when insufficient insulin is produced to maintain normal blood glucose (by this stage most beta cells have been destroyed)
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8
Q

What is the (5 steps) natural history of T1D?

A
  1. Genetically at risk (genetic predisposition)
  2. Environmental triggers (insulitis; beta cell damage)
  3. Islet antibody positive (insulitis; beta cell damage)
  4. First phase insulin response impaired (pre-diabetes)
  5. Diabetes
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9
Q

(3) characterisations of T2D

A
  • Most common type of diabetes
  • Variable degrees of insulin deficiency and resistance
  • Often part of the metabolic syndrome
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10
Q

Pathophysiology of T2D

  • genetic susceptibility
  • environmental susceptibility
A
  • Both beta cell defects and insulin resistance are present
  • Major environmental factor is obesity
  • GENETICS (MZ twin concordance up to 80%; higher than T1D)
  • Likely polygenic, > 250 candidate genes examined
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11
Q

When you’re doubtful of T1D or T2D as diagnosis, what (2) tests can you do?

A
  • measure C-peptide (good indicator of endogenous insulin production). There will be none in T1D
  • Anti GAD & anti islet cell antibodies: likely to be positive in T1D
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12
Q

Above what glucose level consistently would cause tiredness & susceptibility to infection?

A

> 13-14mM

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13
Q

What (5) factors determine risk for long term complications of T2D?

A

–Duration of diabetes: in Type 2, complications present in 50% at time of diagnosis because diagnosis is often very late
–Degree of glucose control: HbA1C
–Degree of BP control
–Control of other CV risk factors: Lipids, Smoking
–Individual (genetic) susceptibility

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14
Q

What are the principals of T2D Mx?

A
  • Healthy eating / weight loss if overweight (refer to dietitian. Low GI, reduced fats)
  • Exercise
  • Oral anti-diabetic agents
  • Self blood glucose monitoring for some patients*.
  • Regular surveillance for microvascular complications (eyes, kidneys, nerves)
  • Risk reduction macrovascular complications (blood pressure, lipids, smoking)
  • Useful particularly of patients treated with insulin or sulphonylureas where hypoglycaemia may occur.
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15
Q

Discuss the relationship between BGL & exercise in diabetes

A
  • Increases glucose uptake into muscle
  • Can stimulate release of stress hormones leading to short term glucose increase. However this is variable depending on intensity and duration.
  • In the longer term, BGL’s usually decrease.
  • Hypoglycaemia following exercise can occur up to 24 hours later (if treated with insulin or SU).
  • Improved sensitisation of muscle to exercise can last 2-3 days
  • Best to exercise consistently and regularly.
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16
Q

What correlates with complications development in T1D?

A

HbA1C

17
Q

For each 1% fall in HbA1C, how much % reduction is there in T2D microvascular complications?

A

25% reduction

18
Q

What is the hierarchical approach of current Mx of T2D?

A
  1. Diet & exercise
  2. Oral monotherapy
  3. Oral dual combination
  4. Oral triple combination
  5. Oral + insulin
  6. Insulin