L8 - Diabetes Flashcards

1
Q

What stimulates glucose release?

A

Increased blood glucose
Incretins (GLP-1, GIP)
Glucagon
Parasympathetic activity (M3)

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

What inhibits insulin release?

A

Low blood glucose
Cortisol
Sympathetic activity (alpha 2)

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

Role of insulin

A

Decreased hepatic glucose output by inhibiting gluconeogenesis and glycogenolysis

Promotes the uptake of fat

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

Symptoms of diabetes

A
Polyuria 
Polydipsia 
Weight loss 
Lethargy 
Fatigue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Random plasma glucose hyperglycaemia

A

Above 11mmol/L

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

Risk factors for type 2 diabetes

A
Obesity 
Family history 
Ethnicity 
Diet - high carbohydrate and sugar 
Drugs - thiazides/ thiazide like diuretics/ glucocorticoids/ Beta blockers 
Low birth weight
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

HbA1c

A

Percentage of glycated haemoglobin over 3 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How is insulin given?

A

Subcutaneous injection in:

  • upper arms
  • thighs
  • buttocks
  • abdomen

Can be given via syringe, pen, pump or inhaler

IV insulin - emergency treatment

Insulin is a protein therefore if given as a pill orally, will be digested

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

Types of insulin

A

Bovine (cow) - 3 amino acid difference
Porcine (pig) - 1 amino acid difference
Human insulin - recombinant DNA or enzymatic modification of porcine insulin

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

Normal formula of insulin

A

100 U/ml

If obese or insulin resistant, higher doses of 300 - 500 U/ml are given

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

Half life on insulin

A

5 mins in plasma

- renal and hepatic metabolism and elimination

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

When should insulin be given?

A

15-30 mins prior to meals as has the greatest effect 2-3hr after dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Protamine

A

Change hexomer formation

Fast acting insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Zinc

A

Delays absorption

Slow acting insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Why is the site of insulin administration rotated

A

Prevent lipodystrophy:

- atrophy or hypertrophy of lipids around the injection site

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Insulin aspart

A

Onset of action - 10- 20 min
Peak - 40-50 min
Duration - 3- 5 hours

  • rapid action
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Soluble insulin - humulin S, actrapid

A

Onset of action: 30 -60 mins
Peak - 2-5 hours
Duration - 5-8 hours

  • short acting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Isophane insulin

A

Onset of action: 1-2 hours
Peak - 4-12 hours
Duration - 18-24hours

  • Intermediate acting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Insulin glargine

A

Onset of action: 60-90 mins
Peak: plateau between 2 - 20 hours
Duration: 20-24 hours

Long acting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Contraindications and interactions of insulin

A

Contraindications:

  • hypoglycaemia
  • lipohypertrophy
  • lipoatrophy
  • renal impairment (hypoglycaemia if not cleared)

Interactions:

  • increased dose with steroids
  • other hypoglycaemic agents
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Basal bolus dosing

A

Bolus dose

  • insulin aspart
  • mimic spike in insulin after eating food

Basal dose

  • insulin glargine
  • mimics baseline insulin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Diabetic ketoacidosis

A

Causes:
Hyperglycaemia
Metabolic acidosis
Ketoneamia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What can cause diabetic ketoacidosis?

A

Blood glucose 11 + mmol/L and:

  • infection
  • trauma
  • poor insulin adherence
  • ADR
  • ketosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How to treat diabetic ketoacidosis

A

FLUIDS - 1st
Insulin
K+
Glucose

25
Q

K+ concentration in diabetic ketoacidosis

A

K+ in blood may be high due to acidosis
But overall K+ in body is low due to diuresis and osmolality
Therefore when giving fluids - K+ fluctuates

26
Q

Type 2 diabetes mellitus

A
  1. Cellular resistance to insulin due to obesity
  2. Resistance overcome by increased insulin production by pancreas
  3. Overtime:
    - insulin receptors decrease
    - GLP-1 decreases due to decrease in beta cells and oral glucose
  4. Glucotoxicty from FA and ROS - beta cell dysfunction
27
Q

Treatment of T2DM

A

Lifestyle modifications:

  • increased exercise
  • decreased carb diet
  • weight reduction

Bariatric surgery
Education

28
Q

Treatment when HbA1c rises above 48mmol (6.5%)

A

Standard releases metformin

Aim for 48 mmol

29
Q

HbA1c above 58mmol (7.5%)

A

Metformin + adjunct

30
Q

Biguanides

A

Decreases hepatic glucose output
Decreases gluconeogenesis and glycogenolysis
Increases glucose utilisation in skeletal muscle
Suppress appetite - limit weight gain

31
Q

Example of biguanides

A

Metformin

32
Q

Contraindications and interactions of metformin

A

Contraindications:

  • GI upset
  • nausea
  • vomiting
  • diarrhoea
  • lactic acidosis (rare)
  • eGFR below 39 ml/min

Interactions:

  • ACEi (impair renal function)
  • NSAIDs (impair renal function)
  • thiazide like diuretics- increases glucose
33
Q

Sulfonylureas mechanism of action

A

Stimulates beta cell pancreatic insulin secretion
Decreases insulin resistance
1. Inhibits ATP - dependent K+ channels
2. Decreased efflux of K+
3. Membrane depolarisation
4. Ca2+ influx
5. Insulin exocytosis - increasing insulin

Needs residual pancreatic function

34
Q

Contraindications and interactions of sulfonylureas

A

Contraindications

  • mild GI upset
  • nausea
  • vomiting
  • diarrhoea
  • hypoglycaemia
  • rare hypersensitivity reactions

Interactions:

  • other hypoglycaemic agents
  • hepatic impairment
  • renal impairment
  • thiazide like diuretics
35
Q

Name of a sulfonylurea

A

Gliclazide

36
Q

When is gliclazide used?

A

Commonly used with metformin when metformin is not enough

Can be used alone if patient has a intolerance to metformin

37
Q

Thiazolidinediones (glitazones)

A

Increases insulin sensitivity in muscle and adipose
Decreased hepatic glucose output

  • activates PPAR - gamma
  • causes gene transcription
  • increased storage of FAs therefore less circulation
  • increased need for glucose uptake by cells
38
Q

Gliclazide affect on weight

A

Increased weight gain as has anabolic effects of insulin

39
Q

Glitazones affect on weight

A

Weight gain - fatty acid storage

40
Q

Contraindications and interactions of glitazones

A
Contraindications:
GI upset 
Fluid retention 
Fracture risk 
CVD concerns 
Bladder cancer 

Interactions:
Other hypoglycaemic agents

41
Q

Name of glitazones

A

Pioglitazone

Rosiglitazone

42
Q

Sodium glucose co-transporter inhibitors SGLT2 (gliflozins)

A

Inhibition of sodium- glucose cotransporter in PCT
Therefore less glucose reabsorption

  • modest weight loss
  • hypoglycaemia risk is low
43
Q

SGLT 2 inhibitor use

A

T1DM - dka risk

T2DM - adjunct

44
Q

Contraindications and interactions of SGLT 2inhibitors

A

Contraindications:

  • UTI
  • Genital infection
  • thirst
  • polyuria

Interactions:

  • antihypertensives
  • other hypoglycaemic agents
45
Q

GLP-1 effects

A

Pancreas:

  • increased insulin secretion
  • decreased glucagon secretion
  • increased insulin biosynthesis

Brain:
- increased satiety therefore decreases food intake

Liver:
- indirect decreases in glucose production

Muscle:
- increased glucose uptake

Stomach:
- decreased gastric emptying

46
Q

Where is GLP - 1 secreted from

A

Intestines

47
Q

Name of SGLT2 inhibitors

A

Dapagliflozin

Canagliflozin

48
Q

Dipeptidyl peptidase - 4 inhibitors (DPP-4) - gliptins

A

Prevent incretin degradation
Increased plasma GLP-1

  • glucose dependent on postprandial action
  • works after eating therefore decreased risk of hypoglycaemia
  • suppresses appetite - weight neutral
49
Q

When is DPP-4 inhibitors used

A

If metformin is contraindicated (first line)

As adjunct

50
Q

Contraindications and interactions of gliptins

A

Contraindications:

  • GI upset
  • small risk of pancreatitis
  • pregnancy

Interactions:

  • other hypoglycaemic agents
  • thiazides and loop diuretics- increase glucose
51
Q

Examples of DPP-4 inhibitors

A

Sitagliptin

Saxagliptin

52
Q

GLP-1 receptor agonist - incretin mimetics

A

Increase glucose dependent synthesis of insulin from Beta cells
Activate GLP-1 receptors
Not degraded by DPP-4

53
Q

How are incretin mimetics given

A

Subcutaneous injection

54
Q

GLP-1 receptor agonist effect on weight

A

Increase satiety - weight loss

55
Q

When is GLP -1 receptor agonist given

A

Add on if Triple therapy is not effective

56
Q

Contraindications and interactions of GLP-1 receptor agonists

A

Contraindications:
GI upset
GORD
Stop if eGFR below 30ml/min

Interactions:
- other hypoglycaemic agents

57
Q

Combined hypoglycaemic pill

A

Increased adherence
Less frequent dosing
Taken whole as slowly absorbed and dissolved in stomach

Harder to change individual drug doses

58
Q

Diabulimia

A

Not taking insulin appropriately in order to lose weight