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After the MSA > Treatment of diabetes > Flashcards

Treatment of diabetes Flashcards

1
Q

What is the natural progression of diabetes due to?

A

A disruption of an individual’s ability to metabolise glucose, progressive beta cell failure, low/falling insulin and low insulin sensitivity

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2
Q

What is the NICE guideline for measuring blood glucose?

A

Measure blood glucose at least 4 times a day (before and after each meal and at bedtime)

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3
Q

What measurements are indicative of diabetes?

A
  • Fasting levels above 7mM
  • Random glucose measurement over 11.1mM
  • HbA1c - levels above 7%
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4
Q

At which level of glucose does the renal system get overloaded?

A

Blood glucose levels >10mM

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5
Q

What glucose levels should be maintained in those with type 1 diabetes on insulin replacement therapy?

A
  • 4-7mM

* <7.8mM

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6
Q

How is insulin administered and why?

A
  • Parentally/ subcutaneously/ IV

* It is a protein that would be digested/destroyed by the gut if taken orally

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7
Q

What are the rapid acting soluble insulins?

A
  • Insulin lispro
  • Insulin aspart
  • Insulin Glulisine
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8
Q

What are the different insulin regimes?

A
  • Fixed does= amount of insulin taken at each meal doesn’t vary day to day
  • Flexible insulin therapy: gives patients more control of what they eat and how they balance their blood glucose levels
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9
Q

What are the pros/ cons of fixed dose insulin therapy?

A
  • can help to simplify a patient’s understanding of glucose metabolism
  • doesn’t offer flexibility of how much carbohydrates a patient may chose to consume at each meal - must be fixed
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10
Q

What are the pros/cons of flexible insulin therapy?

A
  • Allows doses to be varied in response to different carbohydrate quantities in meals
  • Requires a good understanding of glucose metabolism - requires time and commitment
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11
Q

what is the main adverse effect of insulin therapy?

A

Hypoglycaemia

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12
Q

What type of drug is metformin?

A
  • Biguanide

* Oral hypoglycaemic agent

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13
Q

How does metformin work?

A
  • Increases insulin sensitivity
  • Reduces gluconeogenesis in the liver and opposes the action of glucagon
  • Increases glucose uptake and utilisation in skeletal muscle
  • Slightly delays carbohydrate absorption in the gut
  • Increases fatty acid oxidation - reducing circulating LDL and VLDL (can help in obesity related diabetes and with atherosclerosis)
  • Suppresses apetite
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14
Q

What are incretins?

A
  • Stimulate insulin biosynthesis/secretion, inhibit glucagon secretion in the pancreas, delay gastric emptying, increase cardiac output and increase Brain satiety signals
  • Indirectly increases insulin sensitivity in muscle and decreases gluconeogenesis in the liver
  • Glucagon like peptide- 1 and Gastric inhibitory peptide
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15
Q

What secretes glucagon like peptide 1?

A

L cells in the gut

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16
Q

What secretes gastric inhibitory peptide?

A

K cells in the gut

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17
Q

What are incretins rapidly degraded by?

A

Dipeptidyl peptidase 4 (DPP-4)

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18
Q

name 3 incretin mimetics

A
  • Exenatide
  • Exenatide LAR
  • Liraglutide
19
Q

How do incretin analogues work to treat diabetes?

A
  • Lower blood glucose after a meal by increasing insulin secretion
  • Suppresses glucagon secretion
20
Q

How are incretin analogues administrated?

A

Subcutaneously

21
Q

What are gliptins?

A
  • DPP-4 inhibitors
  • Enhances endogenous incretin effects
  • Lowers blood glucose by increasing first phase of insulin response after meals
22
Q

Name 2 gliptins

A
  • Sitagliptin

* Vildagliptin

23
Q

What are the insulin secretagogues?

A
  • Sulphonylureas

* Meglitinides

24
Q

Describe sulphonylureas

A
  • Interfere with beta cell ion channels to potentiate insulin secretion
  • Increase appetite so can lead to weight gain
  • Requires functional beta cells
25
Q

Name 4 sulphonylureas

A
  • Tolbutamide
  • Chloropropamide
  • Glibenclamide
  • Glipizide
26
Q

Describe meglitinides

A
  • Block K-ATP channel to increase insulin release

* short duration of activity leads to lower risk of hypoglycaemia

27
Q

Name 2 meglitinides

A
  • Repaglinide

* Nateglinide

28
Q

Why must you monitor patients of sulphonylureas closely?

A

Can interact with other drugs to produce severe hypoglycaemia due to competition for metabolising enzymes, plasma binding proteins and excretory pathways

29
Q

What is the mechanism of action of Sulphonylureas?

A
  • High affinity receptors present in beta cell membranes
  • Block ATP sensitive potassium channels in the beta cells
  • Causes beta cell depolarisation which leads to insulin secretion
30
Q

Name 3 selective sodium glucose cotransporter 2 (SGLT2) inhibitors

A
  • Canagliflozin
  • Dapagliflozen
  • Empagliflozin
31
Q

What is the mechanism of action of SGLT 2 inhibitors?

A

•Block glucose reabsorption in the proximal tubules leading to therapeutic glycosuria

32
Q

When are SGLT 2 inhibitors used?

A

mono-therapy in type 2 diabetics when exercise or diet alone is not adequate and for whom metformin is contraindicated or inappropriate

33
Q

What are the risks of SGLT 2 inhibitors?

A

They increase the chance of getting an urinary tract infection

34
Q

What are thiazolidinediones?

A
  • Also called glitazones
  • Peroxisome proliferator activated receptor - gamma agonist
  • Increase insulin sensitivity, lowers blood glucose and promotes esterification/storage of free fatty acids in the adipose tissue
35
Q

Describe physiological effects of thiazolidinediones

A
  • Reduces amount of exogenous insulin needed by 30%
  • Promotes the transcription of several genes that increase the storage of fatty acids in adipocytes, decreasing the amount of circulating FFAs
  • cells become more dependent on the oxidation of carbohydrates, reducing blood glucose levels
  • Can cause weight gain and fluid retention
36
Q

What have thiazolidinediones been linked to?

A
  • bladder cancer
  • Heart failure
  • Osteoporotic fractures
37
Q

Describe the mechanism of pioglitazone

A

•PPAR- gamma ligands promote transcription of genes important in insulin signalling: lipoprotein lipase, fatty acid transporters, Glut 4 and others

38
Q

What are alpha glucosidase inhibitors?

A
  • competitive inhibitors of intestinal alpha-glucosidase

* Delay carbohydrate absorption in the small intestine reducing postprandial spike in glucose

39
Q

what are the side effects of alpha glucosidases?

A
  • Flatulence

* Diarrhoea

40
Q

What are the risk factors for gestational diabetes?

A
  • Family history of diabetes
  • History of glucose intolerance
  • Ethnicity
  • Previous pregnancy where baby weights >4.5 kg
  • BMI > 30
  • Age
41
Q

What are complications for babies whose mothers have diabetes?

A
  • Stillbirth
  • Congential malformation
  • macrosomia
  • Birth injury
  • Perinatal mortality
42
Q

How does the WHO define prediabetes?

A
  • Impaired fasting glucose: 6.1-6.9mmol

* Impaired glucose tolerance: 7.8-11.0mmol after ingestion fo 75g of glucose

43
Q

What causes impaired fasting glycaemia?

A
  • Reduced hepatic insulin sensitivity
  • Low beta cell mass
  • Inappropriately elevated glucagon secretion
44
Q

What causes impaired glucose tolerance?

A
  • Reduced peripheral insulin sensitivity
  • Loss of beta cell function
  • Reduced incretin secretion

After the MSA (22 decks)

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