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Diabetic agents Flashcards

(49 cards)

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1
Q

What is the first line action given to t2 prediabetic patients

A

Lifestyle modification

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2
Q

What is the first line drugs offered to patients with t2dm?

A

Metformin or DDP4 if contraindicated

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3
Q

What blood glucose level is considered high and requiring treatment?

A

> 48 mmol

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4
Q

T1DM require insulin, how is this produced?

A

Plasmid vector in bacteria carrying the human insulin gene (recombinant DNA) or enzyme modification of porcine insulin.
There is no C chain produced in artificial insulin.

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5
Q

What features are needed to diagnose T1DM?

A

Random plasma glucose >11mmol/L

  • polydipsia
  • polyuria
  • lethargy
  • weight loss

A raised glucose without symptoms is insufficient

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6
Q

How does metformin work?

A

It decreases gluconeogenesis and glycogenolysis in the liver, decreasing the circulating glucose.
It increases the use of glycogen stored within the muscles.

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7
Q

What is meant by a basal bolus regime?

A

Using two formulations of insulin which have different lengths of half life, typically use a long acting insulin once a day and a short acting insulin after meals

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8
Q

How do sulfonylureas work? Why can’t they be prescribed in T1DM?

A

They work by inhibiting the K ATP channel, causing the release of insulin.
Patients must have a pancreas which is still functionally able to produce and secrete insulin

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9
Q

If metformin is contraindicated, what is the first line drug of choice?
What is the HB1AC to initiate ?

A

DPP4 inhibitors or sulfonylureas

48mmol/mol

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10
Q

How do SGLT2 blockers act?

A

They prevent reabsorption of glucose in the PCT, as a competitive reversible inhibitor, resulting in loss within the urine.

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11
Q

What are the likely issues with taking a SGLT2 inhibitor?

A

Increased likelihood of UTI

Thirst and polyurea

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12
Q

Insulin is a hormone of which class and what is it secreted in response to?

A

It is a protein hormone

Secreted in response to:

  • glucose concentration increase
  • incretins concentration increase (GLP-1 & GIP)
  • glucagon
  • parasympathetic activity (M2)
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13
Q

What inhibits insulin?

A
  • decreased plasma glucose
  • cortisol
  • sympathetic activity (alpha2)
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14
Q

What is the role of insulin?

A

Promote fat uptake

Inhibit glycogenolysis and gluconeogenesis

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15
Q

Why must insulin be given parentally?

A

To avoid digestion

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16
Q

What are the signs of diabetic ketoacidosis?

A

Hyperglycaemia, acidosis and ketonaemia

Can present with low blood ketones and hyperglycaemia may not always be present

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17
Q

What is the main treatment of diabetic ketoacidosis?

A

Fluids and then insulin, with glucose and potassium.

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18
Q

What are the contraindications of biguanides?

A

GI upset- Nausea, vomiting, diarrhoea, lactic acidosis

Not used if eGFR <30ml/min (unchanged)

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19
Q

What drugs interact with biguanides?

A

ACEi
Diuretics
NSAIDs
- any drugs which may impair renal function

Thiazide like diuretics increase glucose so can reduce action.

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20
Q

What are the contraindications of sulfonylureas?

Study These Flashcards
A

Mild GI upset - vomiting, diarrhoea, hypoglycaemia

21
Q

What drugs interact with sulfonylureas?

Study These Flashcards
A

Hypoglycaemic agents
Thiazide like diuretics
Hepatic or renal impairment.

22
Q

Name a sulfonylurea

23
Q

How do Thiazolidinediones work?

Study These Flashcards
A

Increased insulin sensitivity in muscle and adipose, decreasing hepatic glucose production.
Activate PPAR-gamma; takes 6-8 weeks to have an effect and causes increased storage of fatty acids in adipocytes.

24
Q

What are the side effects of glitazones?

Study These Flashcards
A 
GI upset
Fluid retention
Weight gain
Fracture risk 
CVD concerns 
Bladder cancer
25
Name a Thiazolidinedione (glitazone)
Pioglitazone or rosiglitazone
26
what drug interactions should be considered when prescribing a SGLT2 inhibitor?
Antihypertensive and hypoglycaemic drugs already being taken
27
Name a SGLT-2 inhibitor
Dapaglifozin | Canagliflozin
28
What are the physiological effects of GLP-1?
``` Increase insulin secretion and decrease glucagon secretion Increase satiety Decrease liver glucose production Decrease gastric emptying Increase muscle glucose uptake ```
29
Name a DPP-4 inhibitor
Sitagliptin | Saxagliptin
30
How do DDP-4 inhibitors work?
Prevent incretin degradation and therefore increase plasma level. This inhibits glucagon release. Causes insulin secretion and delay gastric emptying, reducing blood glucose.
31
Why do DDP-4 inhibitors have a lower risk of hypoglycaemia?
They do not stimulate insulin secretion at a normal blood glucose
32
What are the contraindications for DPP-4 inhibitors?
GI upset Pancreatitis Avoid in pregnancy
33
What drug interactions should you be aware of with use of DPP-4 inhibitors?
Hypoglycaemic agents | Thiazide like and loop diuretics - drugs increasing glucose can oppose action
34
How do GLP-1 receptors agonists work?
Increased glucose dependant synthesis of insulin, activation of GLP-1 receptors.
35
Name a GLP-1 receptor agonist
Exenatide | Liraglutide
36
How is GLP-1 administered?
Subcutaneous injection
37
What are GLP-1 contraindications?
GI upset GORD Stop below <30ml/min
38
What is the half life of insulin and it’s metabolism?
5 mins in plasma Renal and hepatic metabolism
39
When is plasma glucose highest after meals?
2-3 hours
40
What two things modify absorption of insulin ?
Protamine and zinc
41
Name a rapid insulin and it’s features
Insulin aspart 10-20mins onset Peak @ 40-50 mins 3-5 hr duration
42
Name a short acting insulin and it’s features
Soluble insulin ; humulin S or actrapid 30-60 min onset Peak at 2-5hrs 5-8hr duration
43
Name a intermediate acting insulin and it’s features
Isophane insulin Onset at 60-120 mins Peak @ 4-12 hrs 18-24hr duration
44
Name a long acting insulin and it’s features
Insulin glargine Onset 60-90 mins Peak between 2-20hrs (plateau) 20-24 hr duration
45
What are the warnings for insulin’s?
Hypoglycaemia Lipohypertrophy Lipoatrophy Renal impairment increasing hypo risk
46
What are the interaction problems with insulin?
Increase dose with steroids | Caution with other agents
47
What would make you suspect DKA?
``` BM > 11mmol/l and ... Infection Trauma\ stress Poor adherence ADR Ketosis ```
48
For first intensification what is considered treatment and optimal HB1AC?
Dual therapy Rise to 58 mmol/mol Aim for 53 mmol/mol
49
If second intensification, what is the management and HB1AC aim?
Triple therapy or insulin (if metformin contraindicated) | Aim for 53 mmol/mol

Pharmacology (22 decks)

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