Treatments T1DM Flashcards

(43 cards)

1
Q

What % of the islets do B cells occupy?

A

75%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A

Portal vein to the liver.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the principle stimulant of insulin secretion?

A

glucose.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A

40 micrograms/hour.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

When does the liver secrete glucose to the blood?

A

All the time.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How is T1DM treated?

A

Insulin given via subcutaneous injection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

When would you need an insulin injection when snacking?

A

If snack is over 10g carbs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

Glargine (Lantus): 20h

Detemir (Levemir): 16h

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Give examples of short-acting insulins?

A

Novorapid
Humalog
Apidra

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is Humalog mix 25 50?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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?

23
Q

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

24
Q

Outline the hypoglycemia severity scale?

A

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

25
What should a DM patients blood glucose be before driving?
>5mmol/L
26
What would you do if blood glucose was between 4-5mmol before driving?
Eat before driving
27
What you do if blood glucose was <4mmol before driving?
Eat and wait an hour
28
When must you inform the DVLA about hypoglycemic episodes?
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
What is defined as a severe hypoglycemic episode?
Requiring help from another person due to hypoglycemia.
30
What are the 3 features of DKA?
Metabolic acidosis High plasma glucose Urinary/plasma ketones.
31
Outline the pathophysiology of DKA?
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
What are the clinical features of DKA?
``` 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
List some precipitating factors of DKA?
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
List typical key loses of water, sodium, chloride and potassium in DKA?
6-8L of water 500-1000mmol of sodium 350 mmol of chloride 300-1000mm of potassium
35
How is DKA treated?
Consider/treat the precipitant - Fluids: Restore circulating volume with crystalloids. Clear ketone with 10% dextrose. - Potassium - Insulin
36
Why do we worry about hypokalemia?
Associated with cardiac problems such as arrhythmias and MI.
37
What is Hyperglycaemic Hyposmolar State (HHS)?
Hypovolaemia and very high blood glucose
38
What are precipitating factors of HHS?
Infection Poor compliance Drugs
39
How is HHS treated?
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
How is retinopathy risk reduced in DM patients?
Annual photographic retinal screening with triggers for ophthalmology referral.
41
How is nephropathy risk reduced in DM patients?
Annual monitoring or renal function and urinary albumin excretion. Referral to renal team if nephropathy progresses. CDK4: Macroalbuminuria.
42
How is neuropathy risk reduced in DM patients?
Annual foot screening (minimum) with risk stratification and referral to podiatry/vascaular as appropriate e.g. progressive neuropathy, structural change, ischemia.
43
How is CV risk reduced in DM patients?
Aim for BP <130/80, lower if they have nerphropathy. | Statin therapy is T2DM and age >40. Consider in T1DM especially if complications.