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A13THP @ UoN > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

(48 cards)

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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?

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A

Obesity
Hypertension
Hyperlipidaemia

21
Q

What is the management of mild DMT2?

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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?

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A

After 3 months of dietary changes alone

23
Q

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

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A

Sulphonylureas
Meglitinide analogues
Biguanides
Thiazoldinediones (glitazones)

24
Q

How do Sulphonylureas work?

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A

Increase insulin secretion

Inhibit ATP-sensitive K channels

25
What are the three clinically common Sulphonylureas?
Glibenclamide Gliclazide Tolbutamide
26
What are the main side effects of Sulphonylureas?
Weight gain + increased insulin resistance w/ beta-blockers mask signs of hypo Cause hypos
27
How do Meglitinde analogues work?
Act on beta-cells | Closure of KATP channels - insulin release
28
What are the two clinically common Meglitinide analogues?
Nateglinide | Repaglinide
29
What are the advantages of Meglitinide analogues?
Rapid rate of onset | Given at meal times, stimulate post-prandial insulin secretion
30
By what other name are Meglitinide analogues known?
Prandial glucose regulators
31
How do Biguanides work?
MoA unclear | -may activate AMP-kinase?
32
What is the main Biguanide used clinically?
Metformin
33
When is Biguanide use indicated?
Obese patient's | Doesn't cause weight gain/hypos
34
When is Biguanide use contrindicated?
Should not be used in renal impairment
35
How do Thiazolidinediones (glitazones) work?
Activate nuclear peroxisome proliferator-activated receptors gamma (PPAR-y) Alters gene expression, results in insulin-like effects
36
What is the main Thiazoldinedione (glitazone) used clinically?
Pioglitazone
37
What are the cellular effects of treatment with Thiazoldinediones (glitazones)?
Reduced hepatic glucose output Increased GLUTs in skm. Increased peripheral glucose utilisation Increased fatty acid uptake into adipose cells
38
What is the guidance regarding treatment with Thiazoldinediones (glitazones)?
Liver function monitored Used alone Not as 2nd line therapy (unless met+sulph not tolerated)
39
What is the first stage of treatment for DMT2?
3 months of diet control
40
What is the second stage of treatment for DMT2?
Normal renal function - Metformin | Renally impaired - Sulphonylurea
41
What is the third stage of treatment for DMT2?
2 from Met/Sulph/Glitazone | Add Insulin?
42
What is the main complication of DM?
Increased risk of IHD/stroke
43
What is the target BP for sufferers of DM?
<140/80mmHg
44
What is the first choice BP medication in DM sufferers?
ACEIs - reduce diabetic complications
45
What is diabetic nephropathy?
Damage to capillaries in the kidney glomeruli | Progressive
46
What should all patients with DMT1 and Microalbuminuria receive?
ACEI
47
In what patients is diabetic nephropathy likely?
Patients w/: Albumin in urine Increased plasma creatinine levels
48
What are the targets for patients w/ albumin in the urine or increased plasma creatinine levels?
HbA1c <47.5-53.0mmol/mol | BP <135/75mmHg

A13THP @ UoN (19 decks)

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