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

Diabetes: Insulins and oral hypoglycaemic agents Flashcards

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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?

Study These Flashcards
A

Non-insulin therapies (eg metformin)

Lifestyle modification, education

Bariatric surgery

25
Describe the pathophysiology of T2DM
* Insulin into cells reduced due to **c****ellular 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
Provide an outline of the NICE guidelines for T2DM glucose lowering therapy and give some examples of drugs used in the dual therapy approach
**Metformin (biguanide) first line** for most pt's Dual therapy: * Metformin + DPP-4 inhibitor * Metformin + pioglitazone * Metformin + sulphonylurea * Metformin + SGLT-2 inhibitor
27
Describe the mechanism of action of biguanides
* **Reduce hepatic glucose output** (gluconeogenesis + glycogenolysis) - action at hepatocytes * **Increase glucose utilisation in skeletal muscle** * **Suppress appetite, thus limit weight gain**
28
Give an example of a biguanide
**Metformin** Typically 1st drug offered (unless contraindicated) Can be taken with other options
29
Give some warnings/contraindications for metformin
* **GI upset; N&V, diarrhoea, _lactic acidosis (rare)_** * Excreted unchanged by kidneys, thus stop if eGFR\< 30ml/min (low renal function)
30
Give some inportant interactions/considerations of metformin
* **ACEi's, diuretics, NSAIDS**; drugs impairing renal function * **Thiazide- like diuretics;** increase glucose, thus reduce action of metformin
31
Describe the mechanism of action of sulphonylureas (SU)
* **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
Give an example of a sulphonylurea
## Footnote **Gliclazide**
33
Do sulphonylureas cause weight loss or weight gain? Explain why
**Weight gain** Due to anabolic effects of insulin
34
How are sulphonylureas usually given?
**In combination** with other agents, or **1st line if metformin contraindicated**
35
Give some warnings/contraindications for sulphonylureas
* Mild GI upset; N+V, diarrhoea (esp gliclazide) * Hypoglycaemia (with other agents) * Rare hypersensitivity reactions
36
Give some important interactions/considerations for sulphonylureas eg gliclazide
* Other hypoglycaemic agents * **Hepatic + renal impairment** (excretion of drug) * **Thiazide-like diuretics**; increase glucose this can reduce action of SU's (opposing actions)
37
Describe the mechanism of action of thiazolidinediones (glitazones)
* **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
Give 2 examples of thiazolidinediones (glitazones)
## Footnote **Poiglitazone** **Rosiglitazone**
39
Do thiazolidinediones (glitazones) cause weight loss or weight gain? Explain why
Weight gain Due to fat cell (lipid) differentiation
40
How are thiazolidinediones (glitazones) used?
2nd line/ add on in T2DM Used much less frequently
41
Give some warnings/contraindications of thiazolidinediones (glitazones)
* GI upset * **Fluid retention** * **Fracture risk** * **CVD concerns** * **Bladder cancer**
42
Give an important interaction/consideration of thiazolidinediones (glitazones)
* Other hypoglycaemic agents
43
Describe the mechanism of action of SGLT-2 inhibitors (gliflozins)
* **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
Give 2 examples of SGLT-2 inhibitors (gliflozins)
**Dapagliflozin** **Canagliflozin** **Used in T1DM (DKA risk) and T2DM as _add on therapy_**
45
Give some warnings/contraindications for SGLT-2 inhibitors (gliflozins)
* **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
Give some important interactions/considerations for SGLT-2 inhibitors (gliflozins)
* Antihypertensives (as reducing Na+ reabsorption in PCT as well) * Other hypoglycaemic agents
47
Describe the physiological effects of glucagon-like peptide 1 (GLP-1)
* 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
Describe the mechanism of action of dipeptidyl peptidase-4 (DPP-4) inhibitors (gliptins)
* 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
Give 2 examples of DPP-4 inhibitors and explain how they are used
**Sitagliptin** **Saxagliptin** Used in combination with other agents, or **1st line option if metformin contraindicated**
50
Give some warnings/contraindications for DPP-4 inhibitors (gliptins)
* GI upset * **Pacreatitis** risk * Avoid in pregnancy
51
Give some important interactions/considerations for DPP-4 inhibitors (gliptins)
* Other hypoglycaemic agents * Drugs that increase glucose and oppose action of gliptins; **thiazide-like, loop diuretics**
52
Describe the mechanism of action of glucagon-like peptide-1 (GLP-1) receptor agonists (incretin mimetics) (GLP-1 ANALOGUES)
* **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
What is the route of administration of GLP-1 receptor agonists (incretin minetics)
## Footnote **Subcutaneous injection**
54
Give 2 examples of GLP-1 receptor agonists (incretin mimetics) and explain how they are used
**Exenatide** **Liraglutide** Promote satiety; weight loss Add-on if triple therapy ineffective
55
Give some warnings/contraindications of GLP-1 receptor agonists (incretin mimetics) Give an important interaction/consideration for incretin mimetics
* GI upset * GORD * Stop if eGFR \< 30 ml/min * Other hypoglycaemic agents
56
Describe the effect of using a GLP-1 analoge (incretin mimetic) alongside a standard treatment
**Use exanatide as adjunct to maintain lowered HbA1C levels**
57
Describe the advantages of using different drug preparations and combinations and list some potential disadvantages
58
What is diabulimia?
Eating disorder When someone with T1DM deliberately doesn't take their insulin to control their weight (ie for the purpose of weight loss)
59
Provide an outline for the hypoglycaemic agents used in the management of T2DM, and give their primary mechanisms of action

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