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Diabetic drugs Flashcards

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1
Q

What stimulates the release of insulin?

A
  • Secreted by B cells in response to:
    1. Increase in glucose
    2. Incretins
    3. Parasympathetic activity
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2
Q

What is the half life of insulin?

A
  • ~5 minutes in plasma
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3
Q

What inhibits the release of insulin?

A
  • Decreased glucose concentration
  • Cortisol
  • Sympathetic activity
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4
Q

What is the role of insulin?

A
  • Decreases hepatic glucose output via inhibition of gluconeogenesis and glycogenolysis
  • Increases glycogen stores
  • Promote uptake of glucose into tissues - muscle and adipose especially
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5
Q

How is insulin in the body regulated?

A
  • Secreted into blood even during fasting - prevents receptor downregulation
  • Rate and extent of glucose concentration change leads to biphasic pattern of insulin release
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6
Q

What are the symptoms of type 1 diabetes mellitus?

A
  • Typically present in children and young adults
  • Polyuria
  • Polydipsia
  • Weight loss
  • Fatigue/lethargy
  • Generalised weakness
  • Blurred vision
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7
Q

How is type 1 diabetes diagnosed?

A
  • Hyperglycaemia
  • Fasting glucose >6.9 mmol/L
  • Or random plasma glucose >11 mmol/L
  • Plasma or urine ketones in presence of hyperglycaemia
  • HbA1c >48 mmol/mol (>6.5%)
  • Single raised plasma glucose without symptoms not sufficient for diagnosis
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8
Q

Compare plasma glucose with HbA1c

A
  • Glucose - immediate measure of glucose levels in blood mmol/L
  • HbA1c - measures percentage of red blood cells with a sugar coating (glycated haemoglobin)
  • HbA1c reflects average blood sugar over last 10-12 weeks
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9
Q

What is the biochemical triad of diabetic ketoacidosis?

A
  • Hyperglycaemia
  • Ketonaemia
  • Acidosis
  • Predominantly in type 1 diabetes mellitus
  • Particularly common in children on diagnosis
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10
Q

When do we suspect diabetic ketoacidosis?

A
  • Blood glucose >11 mmol/L
  • Polydipsia
  • Polyuria
  • Abdominal pain
  • Vomiting and diarrhoea
  • Lethargy
  • Confusion
  • Visual disturbance
  • Acetonic breath
  • Symptoms of shock
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11
Q

What do we test for when we suspect diabetic ketoacidosis?

A
  • Ketones
  • Urine or blood
  • Venous pH <7.3
  • Or HCO3- <15 mmol/L
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12
Q

What are the precipitating factors for diabetic ketoacidosis?

A
  • Infection
  • Trauma
  • Non adherence to insulin treatment
  • DDIs
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13
Q

How must insulin treatment be given?

A
  • Parenterally to avoid digestion in the gut
  • Because insulin is a protein
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14
Q

How is insulin formulated?

A
  • In 100 units/mL
  • 300 and 500 units/mL available to reduce volume
  • Be careful when measuring dose
  • Ensure you’re using correct vial so that you don’t prescribe an overdose
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15
Q

What is the routine delivery of insulin?

A
  • Subcutaneous injection
  • Upper arms, thighs, buttocks, abdomen
  • I.V.I used for emergency treatment
  • Rotate site of administration to limit lipodystrophy
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16
Q

How do we slow insulin absorption?

A
  • Protamine and/or zinc complexes added to natural insulins (used less now)
  • Causes soluble insulin to form hexamers - delays absorption from site of injection
  • [plasma] is greatest after 2-3hours
  • Dosing 15-30 minutes prior to meals
  • Insulin analogues also used - a few amino acid changes
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17
Q

Which insulin types are fast acting?

A
  • Insulin aspart - rapid acting
  • Soluble insulin (Humulin S, Actrapid) - short acting
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18
Q

Which insulin types are longer acting?

A
  • Isophane insulin (NPH) - intermediate
  • Insulin glargine - long
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19
Q

What things do we need to consider when prescribing insulin?

A
  • Combinations often prescribed - by brand name
  • Short and long-acting mixtures
  • May take them separately
  • Basal-bolus dosing is common
  • Other dosing regimens can be used - patient centred
  • Syringes, pens, pumps, inhalers
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20
Q

What are the adverse side effects of insulin treatment?

A
  • Hypoglycaemia
  • Lipodystrophy
  • Lipohypertrophy or lipoatrophy
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21
Q

What are the contraindications for insulin treatment?

A
  • Renal impairment
  • Hypoglycaemia risk
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22
Q

What are the DDIs for insulin treatment?

A
  • Dose needs increasing with systemic steroids
  • Caution with other hypoglycaemic agents
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23
Q

What is basal-bolus dosing?

A
  • Given rapid acting insulin - bolus e.g. aspart
  • Patient generally takes this before a meal
  • Given long acting insulin - basal e.g. glargine
  • Commonly used for young active T1DM patients
  • Allows flexibility if adherence is good
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24
Q

What is diabulimia?

A
  • When a type 1 diabetic stops or reduces their insulin to control their weight
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25
Give an overview of type 2 diabetes mellitus?
- Slow progression of disease over many years - Many people are asymptomatic early on - Vast majority of T2DM patients are overweight or obese - Age profile of T2DM has decreased - Insulin into cells reduced due to cellular resistance associated with obesity
26
Outline the pathophysiology of insulin resistance
- Insulin resistance initially overcome by increased pancreatic insulin secretion - Decreased insulin receptors - Decreased GLP 1 secretion in response to oral glucose - Response reduced at B cells - Eventually insulin production reduced
27
Why is type 2 diabetes mellitus diagnosed later in life?
- Blood sugar rise typically slower than type 1 DM - Symptoms are variable - Often diagnosed through midlife MOT
28
How is type 2 diabetes managed?
- Lifestyle - Education - Weight loss (surgery in more and more instances) - Initially non-insulin therapies - Adherence is challenging in many patients - Insulin forms part of treatment plan in poorly managed or later stage disease - Treat co-morbidities
29
What are the different classes of hypoglycaemic agents?
- Sulphonylureas - Biguanides - Thiazolidinediones (glitazones) - Dipeptidyl peptidase 4 inhibitors (gliptins) - SGLT-2 inhibitors (gliflozins) - GLP-1 receptor agonists
30
Give an example of a biguanide
- Metformin
31
What is the mechanism of action of biguanides?
- Decrease hepatic glucose production by inhibiting gluconeogenesis - Some gluconeogenic activity remains so hypoglycaemia risk is reduced - Supresses appetite so weight gain is limited - Typically first drug offered - Can be taken concomitantly with other hypoglycaemic agents
32
What are the adverse side effects of metformin?
- GI upset - Nausea - Vomiting - Diarrhoea
33
What are the contraindications for metformin?
- Stop if eGFR ,30 mL/min - Alcohol intoxication
34
What are the DDIs of metformin?
- Drugs that may impair renal function e.g. ACEi, diuretics, NSAIDs - Drugs that increase glucose levels e.g. loop and thiazide like diuretics
35
Give an example of a sulfonylurea
- Gliclazide
36
What is the mechanism of action of sulfonylureas?
- Stimulate B cell pancreatic insulin secretion - Blocks ATP-dependant K+ channels - Need residual pancreatic function to work - Weight gain through anabolic effects of insulin - Typically taken in combination with other agents
37
What are the adverse side effects of sulfonylureas?
- Mild GI upset - Nausea - Vomiting - Diarrhoea - Hypoglycaemia
38
What are the contraindications of sulfonylureas?
- Hepatic and renal disease
39
What are the DDIs of sulfonylureas?
- Other hypoglycaemic agents - Loop and thiazide like diuretics - increase glucose so reduce action of sulfonylureas
40
Give some examples of glitazones
- Pioglitazone - Rosiglitazone
41
Outline the mechanism of action of glitazones
- Insulin sensitisation in muscle and adipose - Decrease hepatic glucose output by activation of PPAR-g - Gene transcription - Weight gain because of fat cell differentiation - Used much less frequently than other agents
42
What are the adverse side effects of glitazones?
- GI upset - Fluid retention - Fracture risk - Bladder cancer
43
What are the contraindications of glitazones?
- Heart failure because of fluid retention
44
What are the DDIs of glitazones?
- Other hypoglycaemic agents
45
Give some examples of gliflozins
- dapagliflozin - canagliflozin
46
What is the mechanism of action of gliflozins?
- Decreased glucose absorption from tubular filtrate - Increased urinary glucose excretion - Competitive reversible inhibition of SGLT-2 in PCT - Modest weight loss, hypoglycaemic risk is low - Add on therapy in T2DM - Treats HFrEF
47
What are the adverse side effects of gliflozins?
- UTI - Genital infection - Thirst - Polyuria - Pancreatitis?
48
What are the contraindications of gliflozins?
- Hypovolaemia - possible hypotension
49
What are the DDIs of gliflozins?
- Antihypertensive and other hypoglycaemic agents
50
Diabetic drugs are GLP-1 agonists. What are the physiological effects of GLP-1?
- Increases insulin secretion and biosynthesis - Decreases glucagon secretion - Decreases food intake by increasing satiety - Decrease glucose production by the liver - Increase glucose uptake by muscles - Decrease gastric emptying
51
Give some examples of DPP-4 inhibitors (gliptins)
- Sitagliptin - Saxagliptin
52
Outline the mechanism of action of gliptins
- Prevent incretin degradation - increase incretin plasma concentration - Glucose dependant so acts after patient eats - Does not stimulate insulin secretion at normal blood glucose - Lower hypoglycaemic risk - Suppress appetite so they are weight neutral
53
What are the adverse side effects of gliptins?
- GI upset - Small pancreatitis risk
54
What are the contraindications of gliptins?
- Avoid in pregnancy - History of pancreatitis
55
What are the DDIs of gliptins?
- Other hypoglycaemics - Drugs that increase glucose can oppose gliptin action e.g. loop and thiazide like diuretics
56
Give some examples of GLP-1 receptor agonists
- Exenatide - Liraglutide - Semaglutide
57
What is the mechanism of action of GLP-1 receptor agonists?
- Increase glucose dependant synthesis of insulin and secretion from B cells - Activate GLP-1 receptor - Resistant to degradation by DPP-4 - Given by subcutaneous injection - Promote satiety
58
What are the adverse side effects of GLP-1 receptor agonists?
- GI upset - Decreased appetite with weight loss
59
What are the contraindications of GLP-1 receptor agonists?
- Renal impairment
60
What are the DDIs of GLP-1 receptor agonists?
- Other hypoglycaemic agents
61
Which type 2 diabetes drugs are modified/extended release?
- Metformin - Incretin mimetics
62
What are the advantages of modified/extended release preparation diabetic drugs?
- Overcome GI upset - Less frequent dosing - Slower release changes PK properties - Improved adherence - But more difficult to modify dose
63
Why swallow an extended release tablet whole?
- Modified release preparation coats tablet - Crushing up tablets overrides effects

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