Treatment of Type 1 Diabetes

Question 1

What is the main treatment for type 1 diabetes?

Answer 1

Insulin - peptide administered by subcutaneous injections into the venous systemic circulation

Question 2

What are the different types of insulin regimes?

Answer 2

Once daily basal injection
- not optimal
- used for those with mental illnesses or eating disorders
Twice daily mix insulin
- a mix of long and short acting insulin is given twice a day
- best if they can’t inject themselves and they need a nurse to come and do it
Basal-bolus therapy
- best mimics natural endogenous insulin release
- short acting given at meals
- long acting given at the start of the day

Question 3

What are the names of the different types of insulin?

Answer 3

Rapid acting 
Ragular (short acting)
NPH (1 or 2 day a day)
- good for night or control between meals 
Detemir and Glargine
- long acting
- less peaked and lasts longer
- less likely to hypo
- used in basal-bolus regimes

Question 4

What are the benefits of insulin pens?

Answer 4

Easy to transport
Accurate dosages
Easier to use for those with visual or fine motor impairment
Minimised injection pain (polished, coated needles)
Subtle

Question 5

What is continuous subcutaneous insulin infection (CSII)?

Answer 5

‘Pump therapy’

• small needle continously under the skin administering insulin steadily
• can be adjusted depending on glycameic control by the wearer

Question 6

What are the pros and cons of CSII?

Answer 6

Pros
- easier glucose control
- reduced risk of hypoglycaemia 
Cons
- reactions
- infections at the cannula site
- tube blockage 
- pump malfunction
- expensive

Question 7

What are the curative treatment options for type 1 diabetes?

Answer 7

Islet cell transplant
- cells infused into the patient’s portal vein
- attach to blood vessels and begin release insulin
Pancreatic transplant

Question 8

What is Whipples Triad?

Answer 8

Symptoms of low blood glucose (autonomic or neuroglyceopaenic)
Measured plasma is <2.8mmol/l (<4mmol/l is diabetic)
Better after glucose

Question 9

What is the hierarchy of hypoglycaemia?

Answer 9

4.6mmol/l - inhibition of insulin secretion
3.8mmol/l - release of counter-regulatory hormones (glucoagon and adrenaline) and onset of autonomic symptoms
2.8mmol/l - impairment of cognitive function, inability to perform complex tasks
<1.5mmol/l - coma and convulsions

Question 10

What are the symptoms of hypoglycaemia?

Answer 10

3.0mmol/l
- autonomic, sweating, palpitations, shaking and hunger
2.5mmol/l - neuroglucopaenic: confusion, drowsiness, odd behaviours, speech difficulty and inco-ordination
General malaise, headache and nausea

Question 11

What are the DVLA rules about Group 1 entitlement and hypoglycaemia (cars/motorbikes)?

Answer 11

Adequate hypo awareness
No more than one severe hypo in 12 months 
BM monitoring evidence 
Not a danger to the public 
Acuity and visual fields are ok

Question 12

What are the DVLA rules about Group 2 entitlement and hypoglycaemia (lorrys/buses)?

Answer 12

Full hypo awareness and understanding of the risks 
No severe hypos in the last 12 months 
BM monitoring evidence (3 months)
Not a danger to the public 
Acuity and visual fields are OK

Question 13

How high must blood glucose be before driving?

Answer 13

> 5mmol/l, with carbohydrates and identifiers

• if 4-5mmol/l, eat before driving
• stop for BM every 2 hours

Question 14

How low a blood sugar is too low to drive?

Answer 14

<4mmol/l
- eat and wait 45 minutes to an hour before driving again
Don’t drive if feeling hypo, even if BM is OK

Question 15

What is the pathophysiology of HHS?

Answer 15

Hyperglycaemic hyperosmolar state
Relative insulin deficiency releases amino acid from muscles
These enter the liver where they undergo glycogenolysis and gluconeogensis
This causes hyperglycaemia and dehydration

Question 16

What is the pathophysiology of DKA?

Answer 16

Diabetic ketoacidosis
Absolute insulin deficiency causes release of free fatty acids from adipose tissue (lipolysis)
These enter the liver where ketone bodies are produced (acetate)
This causes hyperketonemia and acidosis

Question 17

What are the diagnostic criteria for DKA?

Answer 17

Metabolic acidosis
- venous bicarbonate <18mmol
- hydrogen ions >45mEq/l
- pH <7.3
Plasma glucose >13.9mmol/l
Urinary/plasma ketones >3mmol/l (or > 2mmol/l and ketouria)

Question 18

Describe the physiologic cascade in DKA

Answer 18

Decrease insulin and increased counter-regulatory hormones

• ketoacidosis (causes renal function, CNS function and CV changes)
• hyperglycaemia (causes osmotic diresis and therefore dehydration, electrolyte depletion and hyperosmolality)

Question 19

What are the biggest causes of mortality in childhood and adult DKA?

Answer 19

Young
- cerebral oedema (hyperglycaemia forces water out the blood vessels and into the brain)
Adults
- hypokalaemia 
- ARDS
- illness causing decompensation

Question 20

What are the most common causes of DKA?

Answer 20

Infections
New onset T1DM
Insulin omission
Acute illness (MI, trauma)

Question 21

What is the treatment for DKA?

Answer 21

Consider and treat the precipitant
Fluid - restore circulatory volume (crystalloid) and clearance of ketones (10% dextrose)
Potassium
Insulin (IV intially)
Glucose (when blood glucose falls below 14mmol/l)

Question 22

What biochemistry would you expect to find with HHS?

Answer 22

Hypovolaemia
Very high blood glucose >30mmol/l
Serum osmolality >320mOsmol/l
- very high sodium
Bicarbonate >15mmol/l
Absence of ketones

Question 23

What are the precipitating factors of HHS?

Answer 23

Infection (60%)
Poor compliance (30%)
Drugs

Question 24

How is HHS treated?

Answer 24

Precipitant
Fluid
- 0.9% sodium chloride (0.45% if fluid balance reaches, but osmolality is still falling)
- positive fluid balance of 3-6 litres by 12 hours
- rate of sodium fall should not be more than 10mmol in 24 hours (risk of demyelination syndrome)
Insulin
- fall no more than 5mmol/l/hr
- only start if glucose doesn’t fall with fluid alone
- 0.05units/kg/hr
Other
- LMWH
-Foot protection