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Pharmacology - Year 2 AC > Week 9 - Insulin And Hypoglycaemics > Flashcards

Week 9 - Insulin And Hypoglycaemics Flashcards

1
Q

What do a-cells release?

A

Glucagon

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2
Q

What do delta-cells release?

A

Somatostatin

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3
Q

What do e-cells (epsilon cells) release?

A

Ghrelin (hunger hormone)

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4
Q

What do PP-cells release?

A

Pancreatic polypeptide

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5
Q

How do pancreatic B-cells sense glucose and how do they respond?

A
  1. Food intake
  2. Digestion
  3. Glucose uptake by B-cells
  4. Inhibition of Katp channels
  5. Depolarisation of the cell
  6. Ca2+ influx
  7. Insulin release
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6
Q

What are the incretin hormones?

A

Glucagon-like peptide-1

Gastric inhibitory peptide

(Incretin hormones stimulate insulin secretion in response to meals)

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7
Q

What are the functional effects of insulin?

A
  • increases glucose uptake, storage and utilisation
  • increases protein synthesis and decreases proteolysis
  • increases gene expression and growth
  • increases triglyceride synthesis and decreases lipolysis and lipid oxidation
  • increases conversion of glucose to glycogen (liver and skeletal muscle), glucose to fat (adipose tissue), AA’s to protein (muscle and increases glucose and AA transport into cells
  • decreases glycogen breakdown and glucose formation
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8
Q

How does insulin flower blood sugar?

A
  • absorbs glucose from outside of cell to inside of cell
  • glucose goes into cells
  • blood sugar falls as a result
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9
Q

How does the body protect against hypoglycaemia?

A

Glucagon gets released

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10
Q

What are most cases of type 1 DM caused by?

A

Destruction/damage to B-cells

Autoimmune disease

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11
Q

What are most cases of type 2 DM caused by?

A

Insulin producing cells are “failing”

Tissues are insensitive to insulin

Or both

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12
Q

What is used to treat people with type 1 diabetes?

A

Insulin therapy

Because B-cells are either damaged/destroyed so can’t produce insulin

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13
Q

Name the different insulin therapies

A

-short duration; rapid onset of action
(Soluble insulin and rapid acting human insulin analogues, insulin aspart, insulin glulisine, insulin lispro)

-intermediate action
(Isophane insulin, can be porcine, go an or bovine)

-longer lasting: slower in onset and lasts for long periods
(Protamine zinc insulin - porcine, human, bovine/ insulin determir - insulin glargine - recombinant human)

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14
Q

What is parentaral insulin?

A

Insulin given by injection/infusion

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15
Q

What insulins are short acting?

A

Insulin aspart

Insulin glulisine

Insulin lispro

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16
Q

How long do short duration insulins last and when are they administered?

A
  • rapid onset - 30-60 minutes
  • peak action 2-4 hours
  • duration - 8 hours

Injected just before, with or after food and only lasts long enough for the meal at which it is taken

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17
Q

Name the intermediate action insulins

A

Isophane insulin

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18
Q

Name the longer lasting insulins

A

Insulin detemir

Insulin glargine

Insulin zinc suspension

Protamine zinc insulin

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19
Q

How long do the intermediate and longer duration insulins last?

A

Onset: 1-2 hours

Peak action: 4-12hours

Duration: 16-35 hours

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20
Q

What are biphasic insulin preparations and can you name some?

A

mixture of intermediate and fast acting
(Rapid onset, long-lasting actions)

Biphasic insulin aspart
Biphasic insulin lispro
Biphasic isophane insulin

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21
Q

How can insulin be administered?

A

Injection:
-subcutaneous often 3-4 times daily

Device:

  • syringe and needle pens
  • portable infusion pump (short acting insulins by continuous subcut infusions, pumps deliver a continuous basal insulin and patient-activated bonus doses at meal times, closed loop system)
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22
Q

What is used to treat hypoglycaemia?

A

Glucagon therapy (hyperglycaemia inducing)

  • first aid treatment for severe hypoglycaemia when oral glucose is not possible or desired
  • route: i.m, i.v, sc
  • acutely raises plasma glucose levels

Glucagon promotes - glycogenolysis (glycogen to glucose), gluconeogenesis, lipolysis (fat to FA’s)

23
Q

What are the common side effects of glucagon therapy?

A

Headache

Nausea

24
Q

What medications are used to treat people with type 2 DM?

A

Insulin secretagogues (GLP-1 receptor antagonists, DPP4 inhibitors, Katp channel inhibitors)

Insulin sensitisers (thiazolidinediones, biguanides)

Delay glucose absorption (a-glucosidase inhibitors)

Promotes glucose loss (SGLT2 inhibitors)

25
Q

What drugs are prandial glucose regulators, what is their mechanism of action?

A
  • secretagogues
  • meglitinides (neteglinide)

-inhibit Katp channels/small molecule antagonists of the Katp channel

26
Q

What class of drugs are meglitinides in, how are they administered and what effect do they have?

A
  • prandial glucose regulators/ secretagogues
  • small molecule antagonists of the Katp channel
  • boost insulin release, enhance the normal physiology of glucose-stimulated insulin secretion
  • oral agents: once or twice daily with or shortly before a meal
  • short acting - repaglinide, nateglinide
  • may have a decreased risk of hypoglycaemia compared to sulphonylureas, particularly in the elderly
27
Q

What drugs are sulphonureas, what is their mechanism of action and how are they administered?

A
  • insulin secretagogues
  • small molecule antagonists of the Katp channel
  • boost insulin release; enhance the normal physiology of glucose stimulated insulin secretion
  • oral agents - once or twice daily or shortly before a meal
  • short lasting formulations (gliclazide, tolbutamide)
  • long lasting formulations (chlorpropamide, glibenclamide, glipizide, glimepiride)
  • combined with other therapies
28
Q

What is there a risk of when taking sulphonylureas?

A

Hypoglycaemia

29
Q

Why cant GLP-1 be used?

A

Has a very short half-life and is rapidly broken down by the endogenous enzyme dipeptydylpeptidase (DPP-4)

30
Q

What are parental incretin mimetics, what is the mechanism of action?

A
  • secretagogues that have a different mode of action
  • boost insulin release by enhancing the normal physiology of incretin-mediated insulin secretion
  • peptide agonists of the GLP-1 receptor and NOT broken down by DDP-4 - promote insulin release from B-cells

-exenatide, liraglutide

31
Q

How are parenteral incretin mimetics administered?

A
  • injectable agents - s.c.
  • combined with other therapies

-much reduced risk of hypoglycaemia compared to sulphonylureas

32
Q

What are the side effects of parenteral incretin mimetics?

A

Exenatide, liraglutide

  • GI disturbances (N+V, diarrhoea, dyspepsia (indigestion), abdo pain and distension, gastro-oesophageal reflux disease, decreased appetite)
  • headache, dizziness
  • agitation
  • asthenia (abnormal phys weakness or lack of energy)
  • increased sweating
  • injection site reactions
  • antibody formation
33
Q

What are gliptins and what is their mechanism of action?

A
  • secretagogues - DPP-4 inhibitors
  • incretin mimetic - boost insulin release by enhancing the normal physiology of incretin-mediated insulin secretion
  • inhibitors of DPP-4, raised the half life of serum GLP-1
  • sitagliptin, vildagliptin
34
Q

How are gliptins administered?

A
  • tablet - oral

- can be combined with other medications (e.g. Gliptins and metformin)

35
Q

What are the side effects of gliptins?

A
  • vomiting, dyspepsia, gastritis
  • peripheral oedema
  • headache, dizziness, fatigue
  • upper respiratory tract infection, gastroenteritis, sinusitis, nasopharyngitis
  • hypoglycaemia
  • myalgia (muscle pain)

Less common - dislipidaemia, hypertriglyceridaemia, erectile dysfunction , rash

36
Q

Name a hyperglycaemic therapy, what it is used to treat and its mechanism of action

A

Diazoxide

  • used to treat congenital hyperinsulinsim in infancy, insulinomas, severe cases of transient hypoglycaemia
  • small molecule agonist of Katp channel
37
Q

How is diazoxide administered?

A
  • orally, given its chlorothiazide

- small molecule agonist of the Katp channel (stops insulin release)

38
Q

What are the side effects of diazoxide?

A
  • anorexia, N+V, hyperuricaemia
  • hypotension, oedema, tachycardia, arrhythmias
  • extrapyramidal effects - hypertrichosis on prolonged treatment (excessive hair growth)
39
Q

In which different ways do insulin sensitisers act?

A

Overall, they improve the sensitivity of target organs to insulin

  • activating enzymes - biguanides
  • modifying the transcription of genes - thiazolidinediones
40
Q

What are biguanides and what is their mechanism of action?

A

Insulin sensitisers
-agonist of AMP-activated protein kinase (AMPK) - enzyme activator

-metformin

  1. Receptor activation
  2. Signal transduction
  3. Signalling cascades - mediated by IRS2
  4. Functional effects
41
Q

What are the two modes of action of biguanides?

A
  • prevents hepatic production of glucose
  • overcomes insulin resistance by improving insulin sensitivity

-metformin

42
Q

How are biguanides administered?

A
  • metformin

- up to 3 times a day with or immediately after a meal

43
Q

What patients is it safe to give biguanides to and why?

A

-doesn’t cause weight gain and best choice for patients who also have heart failure

44
Q

What combination therapies of metformin are available?

A

Pioglitazone, glipizide, glibenclamide, sitagliptin, repaglinide

45
Q

What are thiazolidinediones/glitazones and what is their mechanism of action?

A
  • insulin sensitisers
  • activate PPARy, a regulatory protein involved in the transcription of insulin-sensitive genes which regulate glucose and fat metabolism
  • pioglitazone
  • rosiglitazone (also combined with metformin or glimepiride)
46
Q

How are thiazolidinediones administered?

A

Oral

-one/two times daily

47
Q

What is the principle target of thiazolidinediones?

A

Adipocytes

48
Q

What concerns are raised with the thiazolidinedione drug rosiglitizone?

A

History of concerns in patients with diabetes and ischaemic heart disease, or peripheral arterial disease

49
Q

What is the mechanism of action of a-glucosidase inhibitors?

A

-e.g. Acarbose

  • A-glucosidase converts oligosaccharides to glucose
  • acarbose inhibits this enzyme
  • absorption of starchy foods is slowed, thereby slowing down rises in blood glucose following a meal
  • in patients this means a closer alignment of (impaired) insulin output with hyperglycaemia
50
Q

What are the side effects of a-glucosidase inhibitors?

A
  • acarbose
  • flatulence, diarrhoea, abdo pain, N+V, indigestion, liver function problems, oedema, blood disorders, allergic skin reactions, intestinal problems
51
Q

What is SGLT2 inhibitors mechanism of action?

A
  • dapagliflozin, canagliflozin, empagliflozin
  • SGLT2 - sodium-coupled glucose transporter (causes glucose reabsorption)

SGLT2 inhibitors cause excess glucose to be eliminated in the urine; reducing hyperglycaemia

52
Q

What are the potential advantages of SGLT2 inhibitors?

A

-weight loss, insulin dependant, low risk of hypoglycaemia, osmotic diuresis reduces hypertension

53
Q

What do B-cells release?

A

Insulin

Pharmacology - Year 2 AC (14 decks)

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