Diabetes Management Flashcards

(34 cards)

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
Package of care for people with T2DM [11]
* 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
Targets HBA1C depend on management: Lifestyle AND/OR metformin only Already on one drug, but HbA1c has risen to 58 mmol/mol (7.5%)
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
Fluid replacement regime in DKA admission with systolic BP >90 mmHg (for 19 hours)
``` 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
``` Main complication of treating DKA in young people Specific age range Symptoms Onset Mx ```
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
Goals of management of HHS | What NOT to do...
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
Fluid replacement in HHS [2] Aim? What is a safe rate of fall of plasma glucose? [2]
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
Complications of HHS treatment When can you expect total normalization? What target blood glucose is used?
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
Why can insulin treatment cause cardiovascular collapse?
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
When would insulin be indicated in HHS? | What ROA and dose of insulin would be recommended?
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
Potassium in HHS
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