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GERR > Pharmacology of diabetes 2 > Flashcards

Pharmacology of diabetes 2 Flashcards

1
Q

Name two other types of diabetes outside type 1 & 2

A

Latent Autoimmune diabetes (adults)
Maturity Onset diabetes (young)
Gestational Diabetes (during pregnancy)
Steroid Induced diabetes (glucocorticoids elevate glucose)

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2
Q

What is LADA?

A
  • autoimmune disease affecting beta cells
  • onset adulthood
  • don’t have to have elevated BMI which see in most type 2
  • will lose weight and be non-responsive to medications
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3
Q

What is MODY?

A
  • Rare genetic diabetes

- may not need insulin

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4
Q

What are the diagnostic criteria for Type 1?

A
  • rapid weight loss
  • BMI <25
  • possibly DKA
  • no autoimmune disease present
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5
Q

What are the diagnostic criteria for Type 2?

A
  • HbA1c > 48 mmol/mol must be taken at least twice (3 month apart)
  • Fasting glucose > 7 mmol/L
  • Random plasma glucose >11.1 mmol/L
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6
Q

What is HbA1c?

A
  • glycosylated Haemoglobin
  • Testing for the sugar present on the surface of the haemoglobin molecules
  • if in sugary blood will have higher levels
  • Higher the HbA1c the greater the risk of complications
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7
Q

When can HbA1c not be used?

A
  • Not used in type 1
  • Can also be less sensitive then fasting blood glucose levels even in Type 2
  • If anaemic or pregnant where high RBC turnover can’t be used
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8
Q

What should the target HbA1c be?

A
  • changes between individuals usually between (48-53 mmol/mol and 6.5%)
  • may end up being above the 48 mmol/mol used in diagnosis
  • advice that the lower they get there HbA1c the lower there risk for complications (any reduction will help)
  • Avoid suggesting highly intensive management levels try and bring it down gradually (otherwise may cause hypoglycaemia)
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9
Q

What are the different treatments used in control of type 2 diabetes?

A
  • Education
  • Lifestyle (stop smoking + drinking)
  • Control BP
  • Metformin (control glucose)
  • Statin (lower lipids)
  • Aspirin (anti-platelet to reduce macro/microvascular disease)
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10
Q

What are the non-pharmacological managements of diabetes?

A
  • Education (educational groups online)
  • Diet (dietician, diet sheets)
  • Lifestyle (increase exercise and weight loss)
  • Foot care (diabetic neuropathy)
  • Retinal photography (prevent diabetic retinopathy)
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11
Q

What diabetes complications should be looked out for?

A 
Kidneys
Neuropathy
Infections
Vascular
Eyes
Skin
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12
Q

What are the different drug treatments in diabetes?

A
  • Biguanide
  • Sulfonylureas
  • Glucagon like peptide
  • Dipeptidylpeptidase IV inhibitors
  • Na/Glucose Co-transport 2-inhibitors
  • Thiazolidinesdiones
  • Meglitinides
  • aGlucosidase inhibitors
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13
Q

Example of Biguanides?

A

Metformin (only one in the class)

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14
Q

Example of Sulfonylureas?

A

Gliclazide

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15
Q

Example of Glucagon like peptides?

A

Liraglutide

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16
Q

Example of Dipeptidylpeptidase IV inhibitors?

A

sitagliptin

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17
Q

Example of sodium glucose co-transport 2-inhibitors?

A

dapagliflozin

18
Q

Example of Thiazolidinedione?

A

pioglitazone

19
Q

Example of Meglitinides?

A

repaglinide

20
Q

Example of alpha glucose inhibitors?

A

Acarbose

21
Q

What is the first treatment tried to get HbA1c down?

A

1) Lifestyle mesures

22
Q

What is the first line drug treatment for type 2 diabetes?

A

Monotherapy Metformin

23
Q

What is currently second line treatment for diabetes?

A
  • SGLT2 inhibitors (sodium glucose transport proteins)
    OR
  • GLP-1RA (glucagon-like peptide-1 receptor agonist)
24
Q

When should SGLT2 inhibitors or GLP-1RA be preferentially used?

A

SGLT2 inhibitors = CKD
GLP-1RA = high risk CVD
SGLT2 inhibitors cautioned in those with neuropathic feet problems as increased risk of amputation so use GLP-1RA

25
Q

What is the MoA of Metformin?

A
  • activates liver AMP-kinase reducing glucose output from the liver
  • increases liver, muscle and fat cell sensitivity to insulin
  • enhances glucose peripheral uptake and utilisation
26
Q

What are side effects of metformin/biguanide?

A
  • Causes weight loss (may be useful)
  • GI adverse effects e.g. nausea, diarrhoea and flatulence
  • Unlikely to cause hypoglycaemia as enhances natural insulin signal
  • Lactic acidosis (very rare) only seen in whose with CKD already
27
Q

How can side effects be prevented?

A
  • Start on low dose then increase over period of weeks
  • Take with meals
  • If struggling to take pill give modified release preparation
  • Can damage kidneys so use with caution in those with renal damage check U&Es
28
Q

Why should Metformin be stopped?

A

If serum creatinine above 150 micro mol/L or eGFR < 30mL/min/1.73m(squared)

29
Q

What is the MoA of sulfonylureas?

A
  • sulfonylurea binds to sulfonylurea receptor of pancreatic Beta cell
  • this closes ATP-K channels
  • less potassium leaves the cell
  • increase in calcium influx
  • beta cell depolarises and insulin is released
30
Q

When is sulfonylurea used/not used?

A
  • used less now used to be second line treatment
  • patients need to have functioning beta cells
  • antagonised by corticosteroids and thiazide-like diuretics
31
Q

Side effects of Sulfonylurea?

A
  • prolonged hypoglycaemia (bypass natural negative feedback loop so insulin constantly secreted)
  • weight gain
  • hyponatraemia
  • oedema
  • Hepatotoxicity
  • photosensitivity
  • allergy/rash
32
Q

How do incretin effects differ in healthy and diabetic patients?

A

Diabetes: incretin signal reduced so less insulin secreted
healthy: after meal get activity of incretin group which promotes insulin signal

33
Q

What are the incretin hormones?

A

1) GLP-1 (Glucagon like peptide)

34
Q

Where is GLP-1 released from and what stimulates release?

A
  • L-cells in small intestines

- Stimulated by lipids and carbohydrates

35
Q

What is MoA of GLP-1?

A
  • Binds to G-protein coupled receptors on beta cells which stimulates insulin secretion
  • also stimulates B cell growth
  • insulin synthesis
  • inhibits glucagon secretion
  • decreases hepatic glucose output and gastric emptying
  • promotes satiety
36
Q

What enzyme degrades GLP-1?

A

Dipeptidyl peptidase IV

37
Q

What are the two drug types acting on the GLP-1 mechanism?

A

1) incretin mimetics Glucagon like peptides (analogues of GLP-1 which take longer to breakdown)
2) Incretin Enhancers (inhibitors of dipeptidyl Peptidase IV, keep natural GLP-1 levels larger for longer)

38
Q

Why can GLP-1 analogues be disliked?

A
  • Injection whereas tablets would be more convenient
  • causes GI disturbance (nausea and vomiting)
  • slight increase in pancreatitis risk and pancreatic cancer
39
Q

Side effects of GLP-1 analogues?

A
  • causes GI disturbance (nausea and vomiting)
  • causes weight loss
  • can cause Hypoglycaemia
  • slight increase in pancreatitis risk and pancreatic cancer
  • caution in renal disease
  • Delays gastric emptying so contraindicated in people with gastroparesis
40
Q

What are the advantages and disadvantages of using DPPIV inhibitors over GLP-1 analogues?

A
  • Tablet form
  • slight increased risk of hypoglycaemia
  • don’t help in weight loss
41
Q

Adverse effects of DPPIV inhibitors?

A
  • nasopharyngitis
  • headache, nausea
  • possible risk of heart failure
42
Q

What should be checked after 6 months of use of either incretin hormones?

A

HbA1c checked
In GLP-1 if not decreased by 1% than stopped or If weight not decreased by more than 3% than stopped
In DPPIV if not degreased by more than 0.5% stopped

GERR (49 decks)

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