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CPT + Prescribing > Diabetes: Insulins and oral hypoglycaemic agents > Flashcards

Diabetes: Insulins and oral hypoglycaemic agents Flashcards

1
Q

Give a brief outline of insulin

A

Protein secreted by B cells in pancreas

STIMULATED BY:

Secreted in response to raised glucose levels

Increased by incretins (glucagon like peptide 1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP)

Parasympathetic activity (M3 receptors)

INHIBITED BY:

Low glucose levels

Cortisol (stress hormone thus don’t want to decrease glucose levels)

Sympathetic activity (alpha-2)- increase glucose availability thus inhibit insulin release

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2
Q

Briefly describe the role of insulin

A
  • Decreases hepatic glucose output via inhibition of gluconeogenesis
  • Inhibits glycogenolysis
  • Promotes uptake of fats
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3
Q

Describe the normal daily profile of plasma insulin levels

A
  • Normally maintained at a basal level
  • Spikes around meal times

Treatment of diabetes involves replicating these typical insulin spikes alongside a basal level of activity

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4
Q

Provide a definition for diabetes and list some common symptoms experienced by patients

A

Hyperglycaemia; random plasma glucose > or equal to 11 mmol/L

Single raised plasma glucose without symptoms not sufficient for diagnosis

Symptoms present due to alterations in palsma glucose levels and hence osmolarity

​

  • Polyuria
  • Polydipsia
  • Weight loss
  • Fatigue/lethargy
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5
Q

List some risk factors for developing diabetes

A
  • Obesity (more fat leads to insulin resistance)
  • Family Hx
  • Ethnicity
  • Diet
  • DRUGS; thiazide/thiazide-like diuretics, glucocorticoids, B-blockers – all increase glucose levels (pt in pre-diabetic state whilst on these meds)
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6
Q

What does the HbA1C show?

A

Glycated haemoglobin

% of RBCs with sugar coating

Reflects average blood sugar over the last 10-12 wks; mmol/mol (or %)

(IMMEDIATE MEASURE OF BLOOD GLUCOSE LEVELS- mmol/L)

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7
Q

Why must insulin be given parenterally?

A

It is a protein, thus must be given parenterally to avoid digestion in the gut

Hence, given as subcutaneous injections daily/IM/IV infusion (emergency)

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8
Q

Give the standard insulin dosing and formulation

A

Usually formulated in 100 U/mL – UNITS PER ML

Larger doses available to reduce volume; 300 and 500 U/mL; (in obesity, insulin resistance where higher doses of insulin are required)

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9
Q

Give some modes of delivery of insulin

A
  • Routine delivery by SC injection into upper arms/thighs/buttocks/abdomen
  • IV infusion- emergency treatment
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10
Q

Why is a dose of insulin taken 15-30 mins prior to a meal?

A

As the greatest plasma concentration of insulin is after 2-3 hrs of dosing

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11
Q

How would you describe the structure of insulin?

A

Hexamer

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12
Q

Why are protamine and/or zinc sometimes given with insulin?

A

To modify insulin absorption

As protamine/ zinc can increase or decrease breakdown rate of the insulin hexamer

Alllows for short or long acting effects of insulin

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13
Q

What is lipodystrophy?

A

Atrophy/hypertrophy of adipose tissue at insulin injection sites

Thus, is important to rotate the sites of administration

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14
Q

List the main insulin analogues and their class (ie rapid, short, intermediate or long acting)

A
  • Insulin aspart - RAPID
  • Soluble insulin; Humulin S, Actrapid - SHORT
  • Isophane insulin (NPH) - INTERMEDIATE
  • Insulin glargine - LONG
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15
Q

Which insulin analogue is given in an emergency (eg ketoacidotic crisis)?

A

IV soluble insulin

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16
Q

List some insulin prescriptions

A
  • Syringes
  • Pens
  • Pumps
  • (inhalers)
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17
Q

Give some warnings/contraindications of taking insulin

A
  • Hypoglycaemia
  • Lipohypertrophy, lipoatrophy (at injection site)
  • Renal impairment - risk of hypoglycaemia (as renal clearance of insulin)
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18
Q

Give some important interactions/considerations of insulin

A
  • Other hypoglycaemic agents- caution
  • Increased dose with steroids
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19
Q

Describe basal-bolus dosing

A
  • Rapid acting bolus - aspart (at meal times)
  • Long acting basal - glargine (maintenance throughout the day)

Tailored to patients

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20
Q

Define diabetic ketoacidosis (DKA)

A
  • Hyperglycaemia
  • Acidosis
  • Ketonaemia

Pear drops fruity breath smell

DKA may present with low blood ketones

Hyperglycaemia may not always be present (in some pt’s)

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21
Q

When should you suspect DKA?

A
  • Blood glucose greater than 11 mmol/L
  • Infection
  • Stress/trauma
  • Poor insulin adherence
  • Adverse drug reactions
  • Ketosis
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22
Q

Outline the treatment for DKA

A
  1. Fluids priority, then insulin
  2. Glucose
  3. K+ (as stat dose of insulin)

Fluids - due to diuresis from raised glucose levels

Insulin - IV (or IM dose of insulin)

Glucose - due to hypoglycaemic state from insulin

K+ - due to hypokalaemia (masked)

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23
Q

Why do you need to give K+ in DKA despite a high measured blood K+ level?

A

Due to a large dose of insulin given, the patient has hypokalaemia - thus the total blood K+ levels are low in DKA

However, K+ levels in the blood may be high due to the acidosis that is also present

Thus, the total blood K+ levels are low, but are measured as being high due to the acidosis (reciprocal cation shifts)

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24
Q

What sort of treatment are patients with T2DM initially offered?

A

Non-insulin therapies (eg metformin)

Lifestyle modification, education

Bariatric surgery

25
Q

Describe the pathophysiology of T2DM

A
  • Insulin into cells reduced due to cellular resistance associated with obesity
  • 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

Glucotoxicity (due to raised glucose levels) from fatty acids + ROS leads to B-cell dysfunction

26
Q

Provide an outline of the NICE guidelines for T2DM glucose lowering therapy and give some examples of drugs used in the dual therapy approach

A

Metformin (biguanide) first line for most pt’s

Dual therapy:

  • Metformin + DPP-4 inhibitor
  • Metformin + pioglitazone
  • Metformin + sulphonylurea
  • Metformin + SGLT-2 inhibitor
27
Q

Describe the mechanism of action of biguanides

A
  • Reduce hepatic glucose output (gluconeogenesis + glycogenolysis) - action at hepatocytes
  • Increase glucose utilisation in skeletal muscle
  • Suppress appetite, thus limit weight gain
28
Q

Give an example of a biguanide

A

Metformin

Typically 1st drug offered (unless contraindicated)

Can be taken with other options

29
Q

Give some warnings/contraindications for metformin

A
  • GI upset; N&V, diarrhoea, lactic acidosis (rare)
  • Excreted unchanged by kidneys, thus stop if eGFR< 30ml/min (low renal function)
30
Q

Give some inportant interactions/considerations of metformin

A
  • ACEi’s, diuretics, NSAIDS; drugs impairing renal function
  • Thiazide- like diuretics; increase glucose, thus reduce action of metformin
31
Q

Describe the mechanism of action of sulphonylureas (SU)

A
  • Stimulate B-cell pancreatic insulin secretion by blocking ATP-dependent K+ channels
  • Depolarisation mechanism leads to increased Ca2+ and insulin secretion (Ca2+ influx leads to insulin secretion)
  • Need a residual pancreatic function for SU’s to be effective

Sulfonylureas bind to and close ATP-sensitive K+(KATP) channels on the cell membrane of pancreatic beta cells, which depolarizes the cell by preventing potassium from exiting. This depolarization opens voltage-gated Ca2+ channels.

32
Q

Give an example of a sulphonylurea

A

Gliclazide

33
Q

Do sulphonylureas cause weight loss or weight gain? Explain why

A

Weight gain

Due to anabolic effects of insulin

34
Q

How are sulphonylureas usually given?

A

In combination with other agents, or 1st line if metformin contraindicated

35
Q

Give some warnings/contraindications for sulphonylureas

A
  • Mild GI upset; N+V, diarrhoea (esp gliclazide)
  • Hypoglycaemia (with other agents)
  • Rare hypersensitivity reactions
36
Q

Give some important interactions/considerations for sulphonylureas eg gliclazide

A
  • Other hypoglycaemic agents
  • Hepatic + renal impairment (excretion of drug)
  • Thiazide-like diuretics; increase glucose this can reduce action of SU’s (opposing actions)
37
Q

Describe the mechanism of action of thiazolidinediones (glitazones)

A
  • Increase insulin sensitisation in muscle and adipose
  • Decrease hepatic glucose output
  • Activation of PPAR-gamma - GENE TRANSCRIPTION; leads to increased insulin sensitivity in muscle + adipose cells
38
Q

Give 2 examples of thiazolidinediones (glitazones)

A

Poiglitazone

Rosiglitazone

39
Q

Do thiazolidinediones (glitazones) cause weight loss or weight gain? Explain why

A

Weight gain

Due to fat cell (lipid) differentiation

40
Q

How are thiazolidinediones (glitazones) used?

A

2nd line/ add on in T2DM

Used much less frequently

41
Q

Give some warnings/contraindications of thiazolidinediones (glitazones)

A
  • GI upset
  • Fluid retention
  • Fracture risk
  • CVD concerns
  • Bladder cancer
42
Q

Give an important interaction/consideration of thiazolidinediones (glitazones)

A
  • Other hypoglycaemic agents
43
Q

Describe the mechanism of action of SGLT-2 inhibitors (gliflozins)

A
  • Reduce glucose absorption from tubular filtrate thus increased urinary glucose excretion
  • Competitive reversible inhibition of SGLT-2 in PCT

Modest weight loss, hypoglycaemic risk is low

44
Q

Give 2 examples of SGLT-2 inhibitors (gliflozins)

A

Dapagliflozin

Canagliflozin

Used in T1DM (DKA risk) and T2DM as add on therapy

45
Q

Give some warnings/contraindications for SGLT-2 inhibitors (gliflozins)

A
  • UTI + genital infection (due to increased glucose excretion in urine)
  • Thirst (secondary to polyuria)
  • Polyuria (diuretic effect due to inhibition of glucose reabsorption thus increased glucose remaining within tubular filtrate)
46
Q

Give some important interactions/considerations for SGLT-2 inhibitors (gliflozins)

A
  • Antihypertensives (as reducing Na+ reabsorption in PCT as well)
  • Other hypoglycaemic agents
47
Q

Describe the physiological effects of glucagon-like peptide 1 (GLP-1)

A
  • Increases insulin secretion from pancreas
  • Decreases foot intake through increased satiety
  • Decreases glucose production by liver
  • Increases glucose uptake by muscles

GLP-1 = secreted from the intestines

48
Q

Describe the mechanism of action of dipeptidyl peptidase-4 (DPP-4) inhibitors (gliptins)

A
  • DPP-4 normally degrades GLP-1 (incretin)
  • DPP-4 inhibitors prevent incretin degeneration thus increased plasma incretin levels
  • Incretins are glucose dependent so postprandial action (ONLY AT HIGH GLUCOSE LEVELS)
  • Thus, do not stimulate insulin secretion at normal blood glucose – lower hypoglycaemic risk
  • Suppress appetite (weight neutral)
49
Q

Give 2 examples of DPP-4 inhibitors and explain how they are used

A

Sitagliptin

Saxagliptin

Used in combination with other agents, or 1st line option if metformin contraindicated

50
Q

Give some warnings/contraindications for DPP-4 inhibitors (gliptins)

A
  • GI upset
  • Pacreatitis risk
  • Avoid in pregnancy
51
Q

Give some important interactions/considerations for DPP-4 inhibitors (gliptins)

A
  • Other hypoglycaemic agents
  • Drugs that increase glucose and oppose action of gliptins; thiazide-like, loop diuretics
52
Q

Describe the mechanism of action of glucagon-like peptide-1 (GLP-1) receptor agonists (incretin mimetics)

(GLP-1 ANALOGUES)

A
  • Increase glucose dependent synthesis of insulin secretion from B-cells
  • Activate GLP-1 receptor
  • Incretin mimetics are not degraded by DPP-4, thus no need to give DPP-4 inhibitors alongside
53
Q

What is the route of administration of GLP-1 receptor agonists (incretin minetics)

A

Subcutaneous injection

54
Q

Give 2 examples of GLP-1 receptor agonists (incretin mimetics) and explain how they are used

A

Exenatide

Liraglutide

Promote satiety; weight loss

Add-on if triple therapy ineffective

55
Q

Give some warnings/contraindications of GLP-1 receptor agonists (incretin mimetics)

Give an important interaction/consideration for incretin mimetics

A
  • GI upset
  • GORD
  • Stop if eGFR < 30 ml/min
  • Other hypoglycaemic agents
56
Q

Describe the effect of using a GLP-1 analoge (incretin mimetic) alongside a standard treatment

A

Use exanatide as adjunct to maintain lowered HbA1C levels

57
Q

Describe the advantages of using different drug preparations and combinations and list some potential disadvantages

58
Q

What is diabulimia?

A

Eating disorder

When someone with T1DM deliberately doesn’t take their insulin to control their weight (ie for the purpose of weight loss)

59
Q

Provide an outline for the hypoglycaemic agents used in the management of T2DM, and give their primary mechanisms of action

CPT + Prescribing (7 decks)

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