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A13THP @ UoN > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

1
Q

At what age does DMT1 usually first present?

A

<40 years

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2
Q

What causes DMT1?

A

Destruction of beta-cells

Following viral infection/autoimmune process

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3
Q

What is the defining feature of DMT1

A

Inability of the beta-cells to produce insulin

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4
Q

How is DMT1 managed pharmacologically?

A

Insulin replaced to return BG to normal

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5
Q

What are the three insulin preparations used clinically?

A

Human insulin analogues
Short acting analogues
Intermediate/long acting analogues

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6
Q

Describe human insulin analogues

A

Modified insulin peptides (lispro/apart)
Rapid onset, short duration
Useful around meals

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7
Q

Describe short acting insulins

A

Effects of 6-8 hours (peak at 2-5)

Given 15-30 mins before meals

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8
Q

Describe intermediate/long acting insulins

A

Intermediate - Combination of insulin w/ protamine
Intermediate/LA - Combination of insulin w/ zinc
LA - Combination of insulin w/ protamine + zinc
Can have biphasic preparations

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9
Q

What are the three main type of insulin dosing regiments?

A

Twice daily
Multiple dosing
Single daily

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10
Q

Describe twice daily insulin dosing

A

2 daily injections
30 mins before breakfast/evening meals
Mix of SA/LA

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11
Q

Describe multiple dose insulin dosing

A

Single dose of intermediate acting insulin at bedtime
Doses of SA 30 mins before meals
BASAL-BOLUS

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12
Q

Describe single daily insulin dosing

A

Single injection of intermediate acting insulin before breakfast/bedtime
Generally DMT2 w/ poor control

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13
Q

What factors can increase insulin requirement?

A 
Stress
Infection
Trauma
Puberty
Pregnancy (T2/3)
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14
Q

What factors can reduce insulin requirement?

A

Coeliac disease
Renal/hepatic impairment
Endocrine disorders

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15
Q

What are the three main routes of insulin administration?

A

Intravenous injection
Subcutaneous injection
Insulin pumps

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16
Q

Why should patients rotate the site of subcutaneous injection?

A

Repeated infections leads to lipohypertrophy - unpredictable insulin absorption

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17
Q

At what age does DMT2 usually present?

A

> 40 years

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18
Q

What causes DMT2?

A

Strong family association

Loss of beta-cells/reduced glucose sensitivity

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19
Q

What is the defining feature of DMT2?

A

Increased insulin resistance

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20
Q

What diseases are commonly associated with DMT2?

A

Obesity
Hypertension
Hyperlipidaemia

21
Q

What is the management of mild DMT2?

A

Dietary modification

  • replace simple with complex carbs (50-55%)
  • limit intake of mono/disaccharides
  • reduce intake of fat (30-55%)
  • weight loss/exercise
22
Q

At what point does management of DMT2 progress from dietary modification to antidiabetic drugs?

A

After 3 months of dietary changes alone

23
Q

What are the four classes of drugs available to treat DMT2?

A

Sulphonylureas
Meglitinide analogues
Biguanides
Thiazoldinediones (glitazones)

24
Q

How do Sulphonylureas work?

A

Increase insulin secretion

Inhibit ATP-sensitive K channels

25
Q

What are the three clinically common Sulphonylureas?

A

Glibenclamide
Gliclazide
Tolbutamide

26
Q

What are the main side effects of Sulphonylureas?

A

Weight gain + increased insulin resistance
w/ beta-blockers mask signs of hypo
Cause hypos

27
Q

How do Meglitinde analogues work?

A

Act on beta-cells

Closure of KATP channels - insulin release

28
Q

What are the two clinically common Meglitinide analogues?

A

Nateglinide

Repaglinide

29
Q

What are the advantages of Meglitinide analogues?

A

Rapid rate of onset

Given at meal times, stimulate post-prandial insulin secretion

30
Q

By what other name are Meglitinide analogues known?

A

Prandial glucose regulators

31
Q

How do Biguanides work?

A

MoA unclear

-may activate AMP-kinase?

32
Q

What is the main Biguanide used clinically?

A

Metformin

33
Q

When is Biguanide use indicated?

A

Obese patient’s

Doesn’t cause weight gain/hypos

34
Q

When is Biguanide use contrindicated?

A

Should not be used in renal impairment

35
Q

How do Thiazolidinediones (glitazones) work?

A

Activate nuclear peroxisome proliferator-activated receptors gamma (PPAR-y)
Alters gene expression, results in insulin-like effects

36
Q

What is the main Thiazoldinedione (glitazone) used clinically?

A

Pioglitazone

37
Q

What are the cellular effects of treatment with Thiazoldinediones (glitazones)?

A

Reduced hepatic glucose output
Increased GLUTs in skm.
Increased peripheral glucose utilisation
Increased fatty acid uptake into adipose cells

38
Q

What is the guidance regarding treatment with Thiazoldinediones (glitazones)?

A

Liver function monitored
Used alone
Not as 2nd line therapy (unless met+sulph not tolerated)

39
Q

What is the first stage of treatment for DMT2?

A

3 months of diet control

40
Q

What is the second stage of treatment for DMT2?

A

Normal renal function - Metformin

Renally impaired - Sulphonylurea

41
Q

What is the third stage of treatment for DMT2?

A

2 from Met/Sulph/Glitazone

Add Insulin?

42
Q

What is the main complication of DM?

A

Increased risk of IHD/stroke

43
Q

What is the target BP for sufferers of DM?

A

<140/80mmHg

44
Q

What is the first choice BP medication in DM sufferers?

A

ACEIs - reduce diabetic complications

45
Q

What is diabetic nephropathy?

A

Damage to capillaries in the kidney glomeruli

Progressive

46
Q

What should all patients with DMT1 and Microalbuminuria receive?

A

ACEI

47
Q

In what patients is diabetic nephropathy likely?

A

Patients w/:
Albumin in urine
Increased plasma creatinine levels

48
Q

What are the targets for patients w/ albumin in the urine or increased plasma creatinine levels?

A

HbA1c <47.5-53.0mmol/mol

BP <135/75mmHg

A13THP @ UoN (19 decks)

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