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2 Endocrine > Insulin Production, Secretion and Action > Flashcards

Insulin Production, Secretion and Action Flashcards

1
Q

what level are blood glucose levels kept at in normal people?

A

5mmol

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2
Q

what does glucagon do?

A

increases endogenous glucose levels in the blood

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3
Q

what blood glucose level is indicative of diabetes?

A

> 7mmol

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4
Q

most common type of cell present in the pancreatic islets?

A

beta cells

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5
Q

what do beta cells do?

A

secrete insulin

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6
Q

what do alpha cells do?

A

secrete glucagon

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7
Q

what do delta cells do?

A

secrete somatostatin

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8
Q

what do PP cells in the pancreatic islets do?

A

secrete pancreatic polypeptide

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9
Q

what structure in the B cell is insulin’s preprohormone synthesised?

A

RER

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10
Q

what is insulin’s preprohormone called?

A

preproinsulin

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11
Q

what is C peptide?

A

a by product of preproinsulin’s synthesis into insulin

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12
Q

name an ultra short acting insulin preparation?

A

lispro

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13
Q

what is the name given to an insulin preparation that is short acting?

A

regular

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14
Q

name an intermediate acting insulin preparation?

A

NPH

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15
Q

what are the names given to long acting insulin preparations?

A

lente

ultralente

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16
Q

what is the name given to an ultra long acting insulin preparation?

A

glargine

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17
Q

when should insulin lispro be injected?

A

within 15 minutes of beginning of a meal

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18
Q

what should insulin lispro be combined with in T1DM?

A

a longer acting preparation

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19
Q

how can you indicate level of insulin in blood and why?

A

C peptide as it is in 1:1 ratio with insulin in blood

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20
Q

when should you give ultra long acting insulin?

A

before bedtime

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21
Q

when does the body make insulin?

A

when blood glucose levels are rising

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22
Q

how is insulin secreted?

A

glucose enters beta cells via GLUT 2 transporter
phosphorylated by glucokinase to g6p which initiates glycolysis
ATP made which inhibits potassium ATP channels
get depol which causes voltage Ca channels to open
increased Ca in cell = release of insulin

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23
Q

what effect does extremely high blood sugar have on glucokinase?

A

glucokinases KM only works within normal blood glucose ranges so in diabetes glucokinase can’t work and no insulin can be made

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24
Q

when is the only time insulin should be made

A

when blood glucose levels exceed 5mmol

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25
Q

what happens to the beta cells in T1DM?

A

beta cells are lost

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26
Q

what happens to beta cells in T2DM?

A

unable to sense changes in glucose

27
Q

how many ATP are made per glucose in glycolysis?

A

36ATP

28
Q

how many phases of insulin release is there?

A

2

29
Q

why are there 2 phases of insulin release?

A

5% of insulin is readily available after release

the rest needs to become mobilised for release

30
Q

what do sulfonurea drugs do?

A

mimic the action of ATP on the sulfonurea receptors of kATP channels (blocking them) to depolarise beta cells

31
Q

what type of diabetes are sulfonurea drugs effective in?

A

type 2

32
Q

what does diazoxide do?

A

inhibits insulin secretion by stimulating kATP channels

33
Q

2nd line therapy for T2DM?

A

sulfonurea drugs

34
Q

who are sulfonurea drugs best for?

A

those who have trouble injecting insulin or when they have improved glucose control

35
Q

what mutation can lead to neonatal diabetes?

A

kir6.2

36
Q

what happens when you have a kir 6.2 mutation?

A

increase in kATP numbers or they are constantly activated

37
Q

what does MODY stand for?

A

monogenic diabetes of the young

38
Q

what actually is MODY?

A

monogenic diabetes with genetic defect in beta cell function; usually a form of early type 2

39
Q

most common mutation for MODY?

A

glucokinase aka MODY 2

40
Q

should MODY patients be treated with insulin or sulfonurea?

A

sulfonurea

41
Q

what is type 2 diabetes?

A

initially hyperglycaemia with hyperinsulinaemia so get reduced insulin sensitivity

42
Q

how does insulin get into the cell?

A

via signal transduction by binding to an insulin receptor

43
Q

what kind of receptor is an insulin receptor?

A

tyrosine kinase receptor

44
Q

does insulin bind to the alpha or beta subunit first?

A

alpha

45
Q

what does insulin binding to the alpha subunit cause?

A

B units will dimerise and phosphorylate themselves

46
Q

what is the correlation between BMI and insulin resistance?

A

if BMI goes up, insulin resistance goes down

47
Q

what is donohue syndrome?

A

leprauchanism

48
Q

symptoms of diabetic ketoacidosis

A

vomiting
dehydration
increased heart rate
distinctive smell on breath

49
Q

where are ketone bodies formed?

A

liver mitochondria

50
Q

when would a T1DM patient be at risk of DKA?

A

if insulin supplementation is missed

51
Q

what effect do low levels of insulin do?

A

inhibit lipolysis

prevent ketone body overload

52
Q

when will acetyl coA be converted into ketones?

A

limited oxaloacetate supply

53
Q

why do ketone bodies increase when glucose is not available?

A

fatty acids are oxidised to provide energy and acetyl coA is converted to ketone bodies

54
Q

which quick acting insulin drug is actually quite slow acting?

A

actrapid

55
Q

how long are long acting drugs SUPPOSED to act?

A

lantus

levemir

56
Q

how many times should you take long acting insulin?

A

1 or 2x pd

57
Q

when would you use U500 insulin?

A

insulin resistant people eg obese

58
Q

what should you look at before starting insulin?

A

BMI
age
ability to self manage
lifestyle

59
Q

when should you take humulin M3 in relation to meals?

A

30 mins before

60
Q

when should you take intermediate mixed analogues other than humulin M3 in relation to meals?

A

same time

61
Q

can site change cause hypos?

A

yes

62
Q

why do renal problems cause hypo?

A

body can’t clear insulin at the rate they should so insulin stays in the body

63
Q

how can you check for renal function in diabetes?

A

Us + Es

64
Q

causes of hyperglycaemia?

A

steroids
not enough insulin
compliance
infection

2 Endocrine (35 decks)

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