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2 ENDOCRINE > Insulin > Flashcards

Insulin Flashcards

1
Q

what kind of hormone is insulin

A

peptide hormone

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2
Q

why is insulin used as a murder weapon

A

causes hypoglycaemic coma and death

very difficult to prove as cause of death

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3
Q

what cell makes insulin

A

beta cell in the pancreas - only cells that can make insulin - sense blood glucose

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4
Q

what cells make glucagon

A

alpha cells

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5
Q

what cells make somatostatin

A

delta cells

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6
Q

what does somatostatin do

A

controls the release of glucagon and insulin

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7
Q

what do PP cells secrete

A

pancreatic polypeptide

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8
Q

where is insulin synthesised

A

in the rough endoplasmic reticulum of pancreatic B cells as larger chain peptide - cleaved to form insulin

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9
Q

what is the chemical structure of insulin

A

two polypeptide chains linked by disulfide bones

connecting C peptide has no use - bi product of cleaving

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10
Q

how do you make lispro insulin

A

swap two amino acids - PRO and LYS

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11
Q

characteristics of lispro

A

short acting- ultra fast
injected within 15 mins of beginning meal

compbination with longer acting preparation for type 1 diabetes

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12
Q

how to make insulin glargine

A

swap GLY for ARG ARG amino acids

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13
Q

characteristics of glargine

A

ultra long acting

given as single bedtime dose

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14
Q

how does glucose enter B cells

A

via GLUT2 transporter

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15
Q

what enzyme phosphorylises glucose in B cells

A

glucokinase

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16
Q

why is glucokinase used to sense glucose levels

A

small change in glucose conc causes a dramatic change in glucokinase activity

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17
Q

what causes depolarisation of the B cell membrane

A

ATP inhibiting the K+ channel

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18
Q

what causes the opening of Ca++ channels in the B cells

A

depolarisation of the cell

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19
Q

what happens then the level of Ca++ in the cell increases

A

fusion of secretory vesicles with the cell membrane and release of insulin

20
Q

what level of blood glucose triggers insulin release

A

5mM

21
Q

those with T1DM have B cells true/false

A

true but they’re mostly lost

22
Q

those with T2DM have B cells true/false

A

true

they’re just not sensitive anymore due to hyperglycaemia taking glucose conc outwit the km of glucokinase

23
Q

what are there two waves of insulin release

A

a reserve pool of secondary preparations is there and available for release in case the first one isnt enough

24
Q

pharmacological treatment options for T2DM

A

restoring physiological glucose to enhance insulin secretion

pharmacological regulation os the secretion process - drugs mimic ATP to depolarise B cells

25
Q

what class of drugs target the Katp channel

A

sulphonylurea drugs (SURs)

allow depolarisation of B cells stimulating insulin release

26
Q

what stimulates Katp channels to inhibit insulin secretion

A

diazoxide

27
Q

why are SURs only second line in T2DM

A

the B cells are already working v hard and are v stressed so making the work harder can be counter intuitive

28
Q

what mutations can lead to neonatal diabetes

A

Kir6.2

give contritiutively activated Katp channels

29
Q

what is maturity-onset diabetes of the young

A

monogenic diabetes with genetic defect in B cell function

famillial form of early onset T2DM

mutations in at least 6 different genes can cause this

30
Q

what happens to glucokinase in maturity-onset diabetes of the young

A

glucokinase activity impaired

glucose secreting defect - blood glucose threshold for insulin increased

31
Q

what is type 1 diabetes

A

loss of insulin secreting B cells

32
Q

what is MODY

A

maturity onset diabetes of the young

defective glucose sensing in the pancreas and/or loss of insulin secretion

33
Q

what is t2dm

A

initial hyperglycaemia with hyperinsulinemia so primary problem is desensitisation of B cells

34
Q

what happens when insulin is being released (anabolic hormone)

A 
amino acid uptake in muscle 
DNA synthesis 
protein synthesis 
growth responses 
glucose uptake in muscle and adipose tissu e
lipogenesis in adipose tissue and liver 
glycogen syntehsis
35
Q

what happens when insulin binds to an insulin receptor

A

receptor tyrosine kinase activity - autophosphylates leading to binding of proteins to the receptor starting a cascade

36
Q

what are the 2 major pathways insulin uses for its dozen of pathways

A

PI3K (PI3 kinase)

Ras

37
Q

what causes insulin resistance

A

reduces insulin sensing and/or signalling

causes by obesity or near complete absence of adipose tissue

38
Q

best treatment for obesity linked T2DM

A

WEIGHT LOSS

39
Q

what is leprechaunism

A

rare autosomal recessive genetic treat

mutations in the gene for the insulin receptor causing severe insulin resistance

developmental abnormalities - absence of subcutaneous fat, decreases muscle mass, growth retardation

40
Q

what is rabson Mendenhall syndrome

A

rare autosomal recessive genetic trait

severe insulin resistance, hyperglycaemia and hyperinsulinemia

diabetic ketoacidosis

linked to mutations in insulin receptor

41
Q

symptoms of diabetic ketoacidosis

A

vomiting
dehydration
increased heart rate
distinctive smell on breath

42
Q

where are ketone bodies formed

A

in the liver in the mitochondria

43
Q

what do Ketone bodies do

A

molecules of energy metabolism for heart muscle and renal cortex

44
Q

how do low levels of insulin prevent ketone body overload

A

by inhibiting lipolysis

45
Q

consequences of accumulation of ketone bodies

A

coma and death

46
Q

when are ketone bodies formed

A

when glucose is not available fatty acids are oxidised to provide energy this doesn’t need acetyl co-A involvement

excess acetyl co-A is converted to ketone bodies

2 ENDOCRINE (32 decks)

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