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Week 9 - Phase 3 > Treatments T1DM > Flashcards

Treatments T1DM Flashcards

1
Q

What % of the islets do B cells occupy?

A

75%

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2
Q

Which vessel is insulin and C-peptide released to to get to the blood stream?

A

Portal vein to the liver.

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3
Q

What is the principle stimulant of insulin secretion?

A

glucose.

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4
Q

What is the basal secretion rate of insulin under fasting conditions?

A

40 micrograms/hour.

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5
Q

Describe insulin secretion?

A

Glucose is taken up by the B cells via the glut 2 receptor.
It becomes glucokinase and is dephosphorylated.
It undergoes glycolysis and respiration to make ATP.
Increased ATP causes blocking of the ATP-sesnsitive potassium channel so there is high K+ in the cell.
High K+ causes depolarization to the cell.
Depolarisation causes opening of the voltage-gated calcium channel.
Calcium influx causes storage granules to release insulin via exocytosis.

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6
Q

When does the liver secrete glucose to the blood?

A

All the time.

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7
Q

How is T1DM treated?

A

Insulin given via subcutaneous injection.

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8
Q

What is the insulin regimen mainly used in T1DM?

A

Basal-bolus.

  • long acting insulin once or twice a day as ‘background cover’
  • short acting insulin as bolus for meal times.
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9
Q

When would you need an insulin injection when snacking?

A

If snack is over 10g carbs.

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10
Q

Give 2 examples of long-acting insulin and how long they act?

A

Glargine (Lantus): 20h

Detemir (Levemir): 16h

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11
Q

Give examples of short-acting insulins?

A

Novorapid
Humalog
Apidra

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12
Q

What is Humalog mix 25 50?

A

A mixed insulin made of 25% short acting and 50% intermediate acting insulin.

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13
Q

What are the benefits of an insulin pen than a syringe?

A
  • Easy to transport
  • More accurate doses
  • Easier for those with visual impairments and problems with fine motor skills to use
  • Less injection pain as needles are not dulled by insertion to a vial and then second insertion to the skin
  • Can be used without being noticed.
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14
Q

What are the possible complications of Continuous Subcutaneous Insulin Infusion (CSII)?

A
  • May have reactions or infections at the cannula site.
  • Tube blockage.
  • Pump malfunction.
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15
Q

What are the disadvantages of CSII?

A
  • Costly: Batteries, reservoirs, infusion sets, glucometers.
  • Need to also carry back up insulin pen incase pump malfunctions.
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16
Q

What are the advantage of CSII?

A
  • Push a button to deliver bolus for meals.
  • Changes the way basal insulin is delivered in that it is dripped throughout the day.
  • Can match circadian rhythm.
  • Can preprogramme to an individuals blood glucose patterns.
  • Can reduce insulin if going to exercise.
  • Can change the release in different conditions e.g. week vs. weekend.
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17
Q

List ‘curative’ treatments for T1DM patients?

A
  • Islet cell transplant: New donor cells injected to the portal vein. Downside is immunosuppression.
  • Pancreas transplant.
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18
Q

What is Whipple’s triad of hypoglycemia?

A
  1. symptoms of low blood glucose: autonomic or neuroglycopaenic.
  2. Measured plasma glucose <2.8mmol (normal) or <4mmol in insulin treated DM.
  3. They are better after glucose.
19
Q

At what blood glucose level is insulin release inhibited?

What symptoms occur here

A

4.6mmol/L

General malaise, headache, nausea.

20
Q

At what blood glucose concentration are counter regulatory hormones glucagon and adrenaline released?
What are the symptoms?

A

3.8mmol/L

Onset of autonomic symptoms such as sweating, palpitations, shaking, nausea, anxiety, hunger.

21
Q

At what level of blood glucose is cognitive function impaired?
What are the symptoms?

A

2.5mmol/L
Impairment of cognition and concentration, confusion, drowsy, odd behavior, speech difficulty, incoordination, weakness, visual change, dizzy, tired.

22
Q

At what blood glucose concentration would you get EEC changes and seizures?

A

<2mmol/L

23
Q

At what level of blood glucose would you get convulsions and a coma?

A

<1.5mmol/L

24
Q

Outline the hypoglycemia severity scale?

A

Mild: autonomic symptoms.
Moderate: autonomic and neuroglycopaenic.
Severe: autonomic and neuroglycopaenic.

25
Q

What should a DM patients blood glucose be before driving?

A

> 5mmol/L

26
Q

What would you do if blood glucose was between 4-5mmol before driving?

A

Eat before driving

27
Q

What you do if blood glucose was <4mmol before driving?

A

Eat and wait an hour

28
Q

When must you inform the DVLA about hypoglycemic episodes?

A

If you’ve had >1 severe hypo while awake in the last 12 months or more recently in <3 months when filling in form.

29
Q

What is defined as a severe hypoglycemic episode?

A

Requiring help from another person due to hypoglycemia.

30
Q

What are the 3 features of DKA?

A

Metabolic acidosis
High plasma glucose
Urinary/plasma ketones.

31
Q

Outline the pathophysiology of DKA?

A

Absolute insulin deficiency + Increase in stress level hormones.

Results in…

  1. Lipolysis: FFA’s result in ketogenesis.
  2. Gluconeogensis: Severe hyperglycaemia.
  3. Osmotic diuresis + acidosis: Dehydration.
32
Q

What are the clinical features of DKA?

A 
Osmotic symptoms 
Weight loss 
SOB and Kussmaul breathing (due to metabolic acidosis with respiratory compensation) 
Abdominal pain (especially in kids) 
Leg cramps 
Nausea and vomiting 
Confusion
33
Q

List some precipitating factors of DKA?

A

Insulin omission - depression, eating disorder, to avoid hypo’s
Infections
New onset DM
Acute Illness - MI, trauma, pancreatitis.
Steroids
CSII pump failure Substance abuse

34
Q

List typical key loses of water, sodium, chloride and potassium in DKA?

A

6-8L of water
500-1000mmol of sodium
350 mmol of chloride
300-1000mm of potassium

35
Q

How is DKA treated?

A

Consider/treat the precipitant

  • Fluids: Restore circulating volume with crystalloids. Clear ketone with 10% dextrose.
  • Potassium
  • Insulin
36
Q

Why do we worry about hypokalemia?

A

Associated with cardiac problems such as arrhythmias and MI.

37
Q

What is Hyperglycaemic Hyposmolar State (HHS)?

A

Hypovolaemia and very high blood glucose

38
Q

What are precipitating factors of HHS?

A

Infection
Poor compliance
Drugs

39
Q

How is HHS treated?

A

Treat precipitant

  • Fluids: saline. Restore slowly as HHS has an insidious onset.
  • Insulin: only if glucose doesn’t fall with fluid alone
  • Other: LMWH, foot protection.
40
Q

How is retinopathy risk reduced in DM patients?

A

Annual photographic retinal screening with triggers for ophthalmology referral.

41
Q

How is nephropathy risk reduced in DM patients?

A

Annual monitoring or renal function and urinary albumin excretion.
Referral to renal team if nephropathy progresses.

CDK4: Macroalbuminuria.

42
Q

How is neuropathy risk reduced in DM patients?

A

Annual foot screening (minimum) with risk stratification and referral to podiatry/vascaular as appropriate e.g. progressive neuropathy, structural change, ischemia.

43
Q

How is CV risk reduced in DM patients?

A

Aim for BP <130/80, lower if they have nerphropathy.

Statin therapy is T2DM and age >40. Consider in T1DM especially if complications.

Week 9 - Phase 3 (8 decks)

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