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Endocrinology > Diabetes Pharmacology > Flashcards

Diabetes Pharmacology Flashcards

1
Q

Which drugs have an insulin dependent action

A 
Sulphonylurea 
Incretin mimetics 
Glinides 
DPP-4 inhibitors 
Biguanides - metformin 
Thiazolidinedione
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2
Q

Which drugs have an insulin independent action

A

a glucosidase inhibitors SGLT2 inhibitors

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3
Q

How do insulin dependent drugs work

A

Can increase secretion of insulin - so need some residual B cell function
OR
Decrease insulin resiatnce and reduce hepatic glucose output

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4
Q

How do insulin independent drugs work

A

Slow glucose absorption from GI tract (α-glucosidase inhibitors)
OR
Enhancing glucose excretion by the kidney (SGLT2 inhibitors)

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5
Q

Describe how insulin is secreted from B cells in the pancreas

A

Elevated blood glucose
More glucose is moved into B cell by GLUT-2 facilitated transporter
Undergoes glycolysis etc to produce more ATP
Increased ATP closes the KATP channel causing membrane depolarisation
This opens Ca channels which moves Ca into the cell and triggers insulin release by exocytosis

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6
Q

What subunits make up the KATP channel

A

4 potassium inward rectifier Kir6.2 subunits

4 sulphonylurea receptor 1 subunits (SUR1)

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7
Q

What closes the KATP channel

A

ATP binding to the Kir6.2 subunits
Occurs when glucose is high - leads to more ATP
Triggers insulin release

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8
Q

What opens the KATP channel

A

ADP binding to the SUR1 subunits
Occurs when glucose is low
It maintains resting potential of B cell and inhibits insulin secretion

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9
Q

List examples of sulphonylureas

A

Tolbutamide
Glibeclamide
Glicazide
Glipizide

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10
Q

How do sulphonylureas work

A

Displace ADP from SUR1 subunit of KATP channel so close the channel
This stimulates insulin release by causing depolarisation and Ca influx
Requires some B cells to be effective

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11
Q

When would you use sulphonylurea

A

First-line in patients intolerant of metformin, or with weight loss
Second-line in conjunction with metformin
Third line in conjunction with metformin and thiazolidinediones, or other drugs
Only in T2DM

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12
Q

What are some negative effects of sulphonylureas

A

May cause hypoglycaemia by excessive secretion of insulin - more common with longer acting agents, in those with reduced liver/renal function and in the elderly
Cause undesirable weight gain
Avoid the long acting ones in CKD, elderly and pregnancy
Effectiveness can be reduced in late stage disease as it needs functioning B cells

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13
Q

How do glinides work

A

Similar to sulphonylureas - bind to SUR1 and close KATP channel
Also their action is related to plasma glucose level

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14
Q

How do you use glinides

A

Given orally

Use in conjunction with metformin and thiazolidinediones

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15
Q

Which is safer, glinides or sulphonylureas

A

Glinides
Less likely to cause hypoglycaemia - shorter acting
Are subject mainly to hepatic metabolism

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16
Q

When should glinides be avoided

A

In severe hepatic impairment, pregnancy and breast feeding

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17
Q

Describe the incretin effect

A

Ingestion of food stimulates released of GLP-1 and GIP from enteroendocrine cells in the small intestine
These peptides enhance insulin release from B cells and GLP-1 decreases glucagon release
This enhances glucose uptake and utilisation and also decreases new glucose production
Overall decreases blood sugar

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18
Q

Insulin response to oral glucose is greater than the response to IV glucose - true or false

A

TRUE

this is part of the incretin effect

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19
Q

How does the DPP-4 enzyme usually work

A

Rapidly terminates the actions of GLP-1 and GIP - inhibits them
Reduces the incretin effect and therefore insulin release

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20
Q

How do Gliptins work

A

Competitively inhibit DPP-4
Prolongs the actions of endogenous GLP-1 and GIP and increases plasma insulin
Overall lowers blood sugar

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21
Q

List examples of gliptins

A

Sitagliptin

Vildagliptin

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22
Q

How are glitptins normally used

A

Usually in combination with a SU or metformin
Can be employed as monotherapy
Weight neutral

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23
Q

List examples of incretin analogues

A

Extenatide

Liraglutide

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24
Q

How do incretin analogues work

A

Mimic the action of GLP-1 but are much longer lasting as they resist breakdown by DPP-4
Stimulate insulin release from B cells by binding to the GLP-1 receptors

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25
Q

How are incretin analogues administered

A

Subcutaneously

Can be 2x daily, daily or weekly

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26
Q

As well as stimulating insulin secretion, what other effects do incretin analogues have

A 
Supress glucagon secretion 
Slow gastric emptying 
Decrease appetie 
Modest weight loss 
Reduce hepatic fat accumulation
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27
Q

What are some side effects of incretin analogues

A

Nausea

Rarely pancreatitis

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28
Q

How does the a-Glucosidase enzyme normally work

A

Brush border enzyme in small intestine

Breaks down starch and disaccharides into absorbable glucose

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29
Q

How do a-Glucosidase inhibitors work

A

Prevent breakdown of carbs etc into glucose by inhibiting enzyme
Delays glucose absorption after a meal so reduces the normal post-prandial increase

30
Q

List examples of a-glucosidase inhibitors

A

Acarbose
Miglitol
Voglibose

31
Q

When are a-glucosidase inhibitors used

A

in 2TDM patients inadequately controlled by life style measures or other drugs
Infrequently used in UK

32
Q

What are the adverse effects of a-glucosidase inhibitors

A

GI tract symptoms due to undigested carbs leaving small intestine:
flatulence, loose stools, diarrhoea, abdominal pain, bloating

33
Q

Which drug is the only one in the biguanide class

A

Metformin

34
Q

When is metformin used

A

First line agent in the treatment of T2DM patients irrespective of obesity

35
Q

How does metformin work

A

Reduces hepatic gluconeogenesis
Increases glucose uptake and utilisation by skeletal muscle
Reduced carb absorption
Increases fatty acid oxidation
Prevents hyperglycaemia but doesn’t cause hypo

36
Q

What are the benefits of using metformin

A 
Reduces microvascular complications 
Can be given orally 
Prevents hyperglycaemia 
Doesn't cause hypo 
Causes weight loss 
Can be combined with other agents
37
Q

What are the adverse effects of metformin

A

GI upset - diarrhoea, nausea and anorexia
Lactic acidosis - more common with excess alcohol intake
- potentially fatal
Shouldn’t be given to those with impaired renal and hepatic function

38
Q

How do Thiazolidinediones work

A

Enhance the action of insulin at target tissues
Act as agonist of a nuclear receptor PPARy which acts as a transcription factor when activated
Increase the expression of several proteins involved in insulin signalling and lipid metabolism

39
Q

What are the desirable effects of thiazolidnediones

A

Promote fatty acid uptake and storage in adipocytes, rather than in skeletal muscle and liver
Reduce hepatic glucose output
Enhance peripheral glucose uptake
Do not cause hypoglycaemia

40
Q

What are some of the adverse effects of thiazolidnediones

A

Weight gain
Fluid retention - promotes Na reabsorption
Severe hepatotoxicity
Increased incidence of bone fractures - doubles risk
Don’t use in heart failure

41
Q

List examples of thiazolidnediones

A

Pioglitazone

42
Q

How do SGLT2 inhibitors work

A

They selectively block the reabsorption of glucose by SGLT2 in the proximal tubule
Causes more glucose to be excreted in urine

43
Q

As well as lowering blood glucose, what other effect do SGLT2 inhibitors have

A

Calorie loss which contributes to weight gain

Also helps diabetes

44
Q

List examples of SGLT2 inhibitors

A

dapagliflozin, canagliflozin and empagliflozin

45
Q

List the devices available to administer insulin

A

Syringe
Disposable pen
Reusable cartridge pen
Insulin pumps

46
Q

What are the aims of treatment in T1DM

A

Prevent hyperglycaemia
Avoid hypoglycaemia
Reduce chronic complication - micro and macrovascular disease

47
Q

Describe the usual secretion/level of insulin in the body

A

Secreted at low basal rate throughout day - 50% of insulin used this way
More is secreted after eating to cope with additional glucose intake

48
Q

List some rapid acting insulins

A

Humalog

NovoRapid

49
Q

List some long acting insulins

A

Lantus

Levemir

50
Q

Describe the basal bolus insulin regime

A

seen as the “best” regime to mimic physiological insulin production
take long acting insulin to act as basal level then take rapid acting with meals
Much more flexible

51
Q

Describe the twice daily insulin regime

A

Insulin is taken 2x per day - usually morning/evening
Less flexible than basal-bolus
Use intermediate insulin or a mixture of rapid and intermediate

52
Q

What level of insulin do you normally start someone on

A

0.3 units/kg of body weight
Adjust over time if needed
Divide between 50% basal and 50% post-prandial

53
Q

Describe advanced carbohydrate counting

A

This is where you synchronise the amount of insulin taken to amount of carbohydrate consumed
Good for those on daily injections and insulin pumps

54
Q

What are the benefits and limitations of finger prick blood glucose measuring

A

Allows for day-tday management and insulin adjustment

Only provides a snap-shot

55
Q

What are the limitations of currently available insulin treatments

A

Injections or pumps put insulin into SC tissue
Peak too slow to stop post-meal spike
Slow clearance
Can be affected by temperature (absorbs faster when warm)

56
Q

What pathology can occur at injection sites

A

Lipohypertrophy

More likely if you don’t rotate your injection sites

57
Q

What are the approximate blood glucose targets

A

Pre-prandial - 4-7 mmol
Post meal <10 mmol

Though are individualised

58
Q

When might you use IV insulin

A

DKA
HHS
Acute illness
Fasting patients

59
Q

How must you monitor someone on IV insulin

A

Hourly blood glucose monitoring
Check ketones if BG>12
Check U&Es daily

60
Q

What is the major limitation of oral insulin

A

Variable absorption so not reliable

61
Q

What type of transplants may be able to treat T1DM

A

Pancreas

Pancreatic islet cell

62
Q

Which diabetes drugs are known to cause weight gain

A

Insulin

TZD - pioglitazone

63
Q

What are the criteria for diabetic ketoacidosis

A

elevated plasma or urinary ketones

Venous bicarbonate <15 mmol/L

64
Q

When should you suspect DKA

A

Anyone with type 1 DM with high blood sugar and feeling unwell

65
Q

What is the most common cause of mortality in DKA

A

cerebral oedema

fluid on the brain

66
Q

What effect does insulin have on hexokinase activity

A

Increases the activity of it

This increases glucose breakdown

67
Q

What is diabetic ketoacidosis

A

An acute metabolic complication of diabetes characterized by hyperglycaemia, hyperketonaemia and metabolic acidosis

68
Q

What are the symptoms of DKA

A 
Nausea and vomiting 
Abdominal pain 
Tiredness 
Coma 
Polydipsia 
Polyuria 
Kussamaul breathing 
cerebral oedema 
death
69
Q

What signs of diabetic ketoacidosis would show up in urinalysis

A

Low pH
High glucose
High ketones

70
Q

List risk factors for DKA

A 
Sepsis - underlying infection 
Poor control 
Pregnancy 
Vascular events - MI 
Alcohol abuse 
Trauma 
Iatrogenic - some drugs 
Acute pancreatitis
71
Q

Name 3 ketone bodies

A

Acetone
Beta-hydroxybutyrate
Acetoacetate

Endocrinology (13 decks)

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