Diabetes Management Flashcards

1
Q

What is the mainstay and first line options of Type 1 treatment? [2]

A

Lifestyle changes and Insulin!

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2
Q

How is insulin delivered? [2]

Why is it delivered any other route

A

By SC or IV

Because its a polypeptide inactivated by the GI tract so it doesnt work orally

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3
Q

What are the types of insulin? [5]

A
  • Rapid acting
  • Short Acting
  • Intermediate Acting
  • Long acting
  • Continuous SC insulin infusion (CSII)
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4
Q

What changes the time insulin takes to take effect? [2]

A

Soluble insulin associates into hexamers in SC fat.

  • It needs to dissociate into monomers in order to diffuse into capillaries.
  • Altering the structure/solubility of insulin affects how long it takes to dissociate
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5
Q

Describe a twice daily insulin regime [1]

Timings [2]

A
Mix of rapid and intermediate acting insulin 
Before breakfest (BB) & before tea (BT)
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6
Q

Describe a thrice daily insulin regime? [1]

Timings [2]

A

Mix of rapid and intermediate BB

Rapid BT

Intermediate Bbed

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7
Q

Describe a 4x daily insulin regime? [2]

A

Mix of: Short acting insulin BB, BL & BT

Then Intermediate Bbed or long acting insulin at a fixed time once per day

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8
Q

How is Type 2 Diabetes treated?

Name drugs from 1st to 3rd line

A

Lifestyle modifications
1st line - Metformin (OHG)
2nd line - A Sulphonyurea (E.g. glimepiride)
3rd line - A thiazolidinedione (e.g. pioglitazone) (aka Glitazones)

Further 3rd line meds include:
DPP-IV inhibitors - SGLT-2 inhibitors - GLP-1 agonist - Insulin

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9
Q

What does metformin do? [1]

A

It increases insulin sensitivity

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10
Q

What aspects of hypoglycemia is it important to educate patients on? [4]

A
  • How to test their blood sugar
  • How to recognise the signs of a hypo
  • How to treat it
  • How to avoid it
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11
Q

Treatment of hypoglycaemia
Give 3 options for non-hospital and hospital settings
Follow up [1]

A

Rapid acting carb e.g. 200ml of fruit juice
OR 1mg IM glucagon
OR if in hospital then 80ml 20% glucose

Follow up with a long acting carbohydrate

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12
Q

How do patients avoid based on causes of hypoglycemia? [4]

A
  • Blood glucose monitoring
  • Rotate & check injection sites
  • Review diet (carb counting)
  • Maybe change the insulin regime
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13
Q

What are the rules for driving and Hypos?

What are the contraindications for driving that the DVLA impose on diabetics [2]

A

Diabetics have to check their glucose within 2 hours of driving [1] and repeat on long journeys [1]
They should carry short acting carbs in the car
If they can’t recognise a hypo [1] or have >1 severe hypo a year they can’t drive [1]

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14
Q

How would we advise a patient to deal with DKA at home? [6]

A

1) They think they’re getting symptoms
2) Test their ketones
3) +ve? Test Blood Glc
4) Elevated? Take an extra insulin dose
5) still high after 4 hours? Take another dose
6) Call diabetes team, notify them of possible DKA

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15
Q

How do we treat DKA? [7]

A

Fluid replacement 0.9% NaCl 1L for 1st hour
- Once BM <15 mmol/l start 5% dextrose infusion
Insulin:
- IV infusion 0.1 unit/kg/hour
- Continue long acting insulin usual dose
- Stop short acting insulin
Correct hypokalaemia

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16
Q

Management of DM complications

How do we manage diabetic nephropathy? [4]

A
  • Glycaemic control
  • BP control
  • ACE inhibitor slows progression & treats BP
  • CVD risk factor control
17
Q

Diarrhoea is a potential diabetic autonomic neuropathy, how do you treat it? [1]

A

Loperamide (i.e. imodium)

18
Q

Gastric stasis and vomiting is a potential diabetic autonomic neuropathy, how do you treat it?

A

Domperidone.

Dopamine antagonist that acts as an antiemetic and progastrokinetic

19
Q

Postural Hypotension is a potential diabetic autonomic neuropathy, how do you treat it? [3]

A

Advice: avoid getting up to quickly

NSAIDS or Fludrocortisone

20
Q

Erectile dysfunction is a potential diabetic autonomic neuropathy, how do you treat it? [1]

A

Phosphodiesterase inhibitors e.g. Viagra

21
Q

Management of peripheral neuropathy

  • Rx [2]
  • Non pharmacological [3]
A

Pain relief:

  • Capsaicin cream
  • Amitriptyline

Protection of feet from ulceration:

  • Fitted footwear
  • Regular podiatry visits
  • Foot screening and risk assessment
22
Q

How do we treat maculopathy? [3]

A

Grid laser therapy
Glc Control
BP control

23
Q

Treatment: proliferative retinopathy [2]
Describe rationale for each [4]
Natural progression if untreated [2]

A

We can do a vitrectomy if theres a vitreous haemorrhage

Laser photocoagulation destroys ischaemic retina [1] , reducing Endothelial Growth Factors [1] causing the new vessels to regress [1]

If untreated, scarring can occur which can lead to retinal detachment.

24
Q

CV risk reduction is an example of primary prevention [4]

A

Lifestyle mods
Control BP to <130/80
Smoking cessation services
Statin therapy - simvastatin for over 40 and in younger patients with significant complications

25
Q

Package of care for people with T2DM [11]

A
  • Blood glucose levels (annually)
  • Blood Pressure (annually)
  • Blood Lipids (annually)
  • Eyes Screened (annually)
  • Feet checked (annually)
  • Kidney function (annually)
  • Weight
  • Smoking Cessation Support
  • Individual Care plan
  • Education Course
  • Emotional and psychological support
26
Q

Targets HBA1C depend on management:
Lifestyle AND/OR metformin only
Already on one drug, but HbA1c has risen to 58 mmol/mol (7.5%)

A

Lifestyle AND/OR metformin only:
- Target for 48

Already on one drug, but HbA1c has risen to 58 mmol/mol (7.5%)
- Target for 53

27
Q

Fluid replacement regime in DKA admission with systolic BP >90 mmHg (for 19 hours)

A
1L over 1st hour 0.9% NaCl
1L over next 2h 0.9% NaCl with KCl
- Another 1L over next 2h
- Another 1L over next 4h
- Another 1L over next 4h
- Another 1L over next 6h
28
Q
Main complication of treating DKA in young people
Specific age range
Symptoms
Onset
Mx
A

Fluid therapy can cause cerebral edema so slower infusion is needed

  • 18-25yo
  • need 1:1 nursing to monitor neuro-observations, headache, irritability, visual disturbance, focal neurology etc
  • Usually occur 4-12h after commencement of treatment
  • CT head and senior review
29
Q

Goals of management of HHS

What NOT to do…

A
  1. Normalise the osmolality (gradually)
  2. Replace fluid and electrolyte losses
  3. Normalise blood glucose (gradually)

Don’t use insulin in first instance, fluid replacement alone can facilitate a gradual decline in BM and plasma osmolarity. Because most patients with HHS are insulin sensitive (e.g. it usually occurs in T2DM), administration of insulin can result in a rapid decline of serum glucose and thus osmolarity.

30
Q

Fluid replacement in HHS [2]
Aim?
What is a safe rate of fall of plasma glucose? [2]

A

Intravenous (IV) 0.9% sodium chloride solution is the first line fluid for restoring total body fluid.
2nd line if unresponsive: 0.45% NaCl

Aim: achieve positive balance of 3-6L by 12h, replace remaining losses within next 12h

A safe rate of fall of plasma glucose of between 4 and 6 mmol/hr is recommended. The rate of fall of plasma sodium should not exceed 10 mmol/L in 24 hours.

31
Q

Complications of HHS treatment
When can you expect total normalization?
What target blood glucose is used?

A

Cardiovascular collapse
Central pontine myelinolysis

Complete normalisation of electrolytes and osmolality may take up to 72 hours.

A target blood glucose of between 10 and 15 mmol/L is a reasonable goal.

32
Q

Why can insulin treatment cause cardiovascular collapse?

A

Insulin treatment prior to adequate fluid replacement may result in cardiovascular collapse as the water moves out of the intravascular space, with a resulting decline in intravascular volume.

33
Q

When would insulin be indicated in HHS?

What ROA and dose of insulin would be recommended?

A

If significant ketonaemia is present (3β-hydroxy butyrate is more than 1 mmol/L) this indicates relative hypoinsulinaemia and insulin should be started at time zero (e.g. mixed DKA / HHS picture).

The recommended insulin dose is a fixed rate intravenous insulin infusion given at 0.05 units per kg per hour.

34
Q

Potassium in HHS

A

Patients with HHS are potassium deplete but less acidotic than those with DKA so potassium shifts are less pronounced
Hyperkalaemia can be present with acute kidney injury
Replace as required