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GERR > Pharmacology of diabetes 1 > Flashcards

Pharmacology of diabetes 1 Flashcards

1
Q

Define diabetes

A

Metabolic disorder characterised by chronic hyperglycaemia with disturbances in carbohydrate, fat and protein metabolism resulting from defects in insulin secretion or action

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2
Q

What are the three types of diabetic complications?

A

Microvascular (retinopathy, nephropathy)
Macrovascular (atherosclerosis)
Neuropathy

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3
Q

What is the difference between type 1 and 2 Diabetes Mellitus?

A

1) Insulin-dependant
- pancreatic beta cells destroyed and no insulin made
2) non-insulin dependant
- insulin stops working at target tissue
- insulin resistant or insufficient insulin

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4
Q

What is the age of onset for type one and two?

A

1) childhood/puberty

2) middle age > 35

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5
Q

What is the nutritional status of type one and two diabetes?

A

1) Frequently malnourished

2) usually obese

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6
Q

What is the prevalence of type 1 and 2 diabetes?

A

1) 10-20% of all cases

2) 80-90% of cases

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7
Q

What is the genetic predisposition to type 1 and 2?

A

1) moderate

2) very strong

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8
Q

When is insulin prescribed?

A
  • All patients with type 1 diabetes
  • Emergency treatment of ketoacidosis
  • In type 2 for improving control of diabetes and for intercurrent events
  • during pregnancy
  • emergency treatment of hyperkalaemia to lower extracellular potassium
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9
Q

What test is used to measure insulin?

A

C-peptide ELISA

  • measures C-chain peptide released in the final step of insulin synthesis proinsulin > insulin
  • means test only measures active form insulin
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10
Q

What are the phases in insulin release?

A

Phase 1) rapid, triggered by increase glucose levels

Phase 2) Slow, sustained, newly formed vesicles triggered independently of glucose

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11
Q

What is the half life of insulin?

A

5-6 mins, most removed through liver by first pass

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12
Q

Which transporters take up Glucose?

A

GLUT 2

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13
Q

What are the steps of insulin secretion within the beta cells?

A
  • Glucose in cell metabolised to form ATP
  • ATP inhibits ATP-sensitive potassium channels preventing potassium from leaving the cell
  • causes cell depolarisation
  • results in voltage gated calcium channels to open and calcium enters
  • calcium required to release insulin from storage granules
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14
Q

What enzyme is needed to metabolise glucose?

A

Glucokinase phosphorylises glucose into glucose-6-phosphate

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15
Q

What times would you measure fasting and peak glucose?

A

Fasting: 5 am
Peak: 8-9 am (breakfast)
peak after every meal

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16
Q

How does insulin stimulate glucose uptake?

A
  • insulin binds to insulin receptor
  • signal transducer by activated receptor
  • triggers glucose uptake by GLUT4 (found in liver, muscle and fat)
17
Q

Why do glucose transporters in brain and heart differ from the liver, muscles and fat?

A

Don’t want insulin to affect glucose uptake in brain and heart as want to always keep uptake high as very metabolically active

18
Q

What is the insulin receptor on cells called?

A

Insulin receptor tyrosine kinase

19
Q

What four organs does insulin affect?

A

Liver
Muscle
Adipose tissue
Brain (stimulates hunger in the brain)

20
Q

What are effects of insulin in the liver?

A
  • increase glucose uptake
  • increased glycolysis (conversion of glucose > energy)
  • increased glycogenesis
  • decreased gluconeogenesis
  • decreased glycogenolysis (doesn’t need the energy)
21
Q

What are effects of insulin in the Muscles?

A
  • increase glucose uptake
  • increase glycogenesis
  • increased glycolysis (muscle want the energy)
  • increased amino acid uptake and protein synthesis (to build muscle)
22
Q

What are effects of insulin in the Fat?

A
  • increase glucose uptake
  • increase triglyceride formation
  • overall increased fat deposition (create storage of fat in form of glycogen)
23
Q

How do we manufacture insulin?

A

Recombinant human protein in bacteria

24
Q

Why can we not use oral insulin and what do we do instead?

A

Broken down by GI so injected subcutaneously

25
Q

what machine is used to check blood glucose?

A
  • Glucometer is manual machine to check where need to take finger prick blood
  • Can also use transdermal sensor for glucose which is attached to the arm
26
Q

What types of insulin can be injected?

A

1) Short acting (Insulin Pen)
- before every meal
- e.g. Novorapid
2) Intermediate acting
- insulin zinc suspension which extends half life
- twice daily
3) Long-acting
- insulin zinc suspension
- once/twice daily

27
Q

Give an example of long-acting insulin?

A

Insulin Glargine (Lantus = brand)

  • provides constant basal insulin supply and prolonged absorption from injection site
  • useful in preventing hypoglycaemia at night
28
Q

What is the best form of insulin to be taking as treatment for type 1 diabetes?

A

Short acting before meals and long acting via insulin pump

29
Q

Where on the body can insulin be injected?

A

abdomen, arm, buttock and thighs

30
Q

What factors affect the absorption of the insulin after injection?

A
  • site of injection
  • exercise
  • depth of injection
  • concentration of dose
  • insulin degrading activity in subcutaneous tissue
31
Q

What are the side effects of injection too much insulin?

A

1) hypoglycaemia - sweating, shaky, irritable and dizzy (treat by drinking sugary drink)
2) allergic reactions
3) lipodystrophy (excessive fat breakdown)
4) lipohypertrophy (fat accumulation at site of infection)

32
Q

How does insulin affect serum potassium?

A
  • Insulin decreases serum potassium
  • stimulates potassium uptake into cells via activation of Na/K ATPase pump
  • potassium leaves blood all intracellular
33
Q

How is hypoglycaemia treated?

A

1) If patient is conscious given sugary drink or quick acting carb
2) If conscious but not cooperating give oral glucose gel or glucagon
3) if unconscious give IV glucose or IM glucagon

34
Q

Why are there insulin specific syringes?

A

Use micro litres unlike millilitres in the syringes

35
Q

What are the symptoms of ketoacidosis?

A
  • unconscious
  • alcoholic breath
  • dehydrated
  • blood glucose + ketones high
  • vomiting
  • excessive thirst
  • fruity smelling breath
36
Q

What is ketoacidosis?

A
  • Type 1 patient doesn’t take their insulin
  • body compensates by starting to breakdown fat as energy source
  • fat breakdown generates ketones (acids)
  • Lowers PH of blood and patient goes into diabetic ketoacidosis
37
Q

How is DKA (diabetic ketoacidosis) treated?

A
  • Need to get blood glucose down and resolve venous ketones
  • Give saline
  • and IV infusion of insulin
  • Need to check serum potassium to ensure no hypokalaemia

GERR (49 decks)

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