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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
What drugs are prandial glucose regulators, what is their mechanism of action?
- secretagogues - meglitinides (neteglinide) -inhibit Katp channels/small molecule antagonists of the Katp channel
26
What class of drugs are meglitinides in, how are they administered and what effect do they have?
- 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
What drugs are sulphonureas, what is their mechanism of action and how are they administered?
- 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
What is there a risk of when taking sulphonylureas?
Hypoglycaemia
29
Why cant GLP-1 be used?
Has a very short half-life and is rapidly broken down by the endogenous enzyme dipeptydylpeptidase (DPP-4)
30
What are parental incretin mimetics, what is the mechanism of action?
- 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
How are parenteral incretin mimetics administered?
- injectable agents - s.c. - combined with other therapies -much reduced risk of hypoglycaemia compared to sulphonylureas
32
What are the side effects of parenteral incretin mimetics?
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
What are gliptins and what is their mechanism of action?
- 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
How are gliptins administered?
- tablet - oral | - can be combined with other medications (e.g. Gliptins and metformin)
35
What are the side effects of gliptins?
- 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
Name a hyperglycaemic therapy, what it is used to treat and its mechanism of action
Diazoxide - used to treat congenital hyperinsulinsim in infancy, insulinomas, severe cases of transient hypoglycaemia - small molecule agonist of Katp channel
37
How is diazoxide administered?
- orally, given its chlorothiazide | - small molecule agonist of the Katp channel (stops insulin release)
38
What are the side effects of diazoxide?
- anorexia, N+V, hyperuricaemia - hypotension, oedema, tachycardia, arrhythmias - extrapyramidal effects - hypertrichosis on prolonged treatment (excessive hair growth)
39
In which different ways do insulin sensitisers act?
Overall, they improve the sensitivity of target organs to insulin - activating enzymes - biguanides - modifying the transcription of genes - thiazolidinediones
40
What are biguanides and what is their mechanism of action?
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
What are the two modes of action of biguanides?
- prevents hepatic production of glucose - overcomes insulin resistance by improving insulin sensitivity -metformin
42
How are biguanides administered?
- metformin | - up to 3 times a day with or immediately after a meal
43
What patients is it safe to give biguanides to and why?
-doesn't cause weight gain and best choice for patients who also have heart failure
44
What combination therapies of metformin are available?
Pioglitazone, glipizide, glibenclamide, sitagliptin, repaglinide
45
What are thiazolidinediones/glitazones and what is their mechanism of action?
- 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
How are thiazolidinediones administered?
Oral -one/two times daily
47
What is the principle target of thiazolidinediones?
Adipocytes
48
What concerns are raised with the thiazolidinedione drug rosiglitizone?
History of concerns in patients with diabetes and ischaemic heart disease, or peripheral arterial disease
49
What is the mechanism of action of a-glucosidase inhibitors?
-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
What are the side effects of a-glucosidase inhibitors?
- acarbose - flatulence, diarrhoea, abdo pain, N+V, indigestion, liver function problems, oedema, blood disorders, allergic skin reactions, intestinal problems
51
What is SGLT2 inhibitors mechanism of action?
- 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
What are the potential advantages of SGLT2 inhibitors?
-weight loss, insulin dependant, low risk of hypoglycaemia, osmotic diuresis reduces hypertension
53
What do B-cells release?
Insulin

Pharmacology - Year 2 AC (14 decks)

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