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Endocrinology > Biochemistry > Flashcards

Biochemistry Flashcards

1
Q

Beta cells are the only cells in the body capable of making insulin true or false

A

True

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2
Q

What do PP cells of the pancreatic islet secrete

A

Pancreatic polypeptide

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3
Q

Describe how insulin is synthesized

A

Made in RER of beta cells as large single chain preproinsulin
Cleaved to form mature insulin

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4
Q

Describe the structure of insulin

A

Two polypeptide chains linked by disulphide bonds

Has a connecting C peptide - no known function

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5
Q

What is the main difference between the different insulin preparations used clinically

A

How long acting they are in the body

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6
Q

Give an example of ultra-short acting insulin

A

Insulin lispro
Position of Lys and Pro are switched in chain
Usually taken when eating

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7
Q

Give an example of ultra-long acting insulin

A

Insulin glargine
Asp at end of A chain is switched to Gly
2 Arg are added to end of B

Given at night to prevent hypoglycemia at night

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8
Q

What effect does increased glucose metabolism have on ATP

A

Leads to an increase in intracellular ATP concentration

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9
Q

How many ATP molecules are produced per glucose

A

36

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10
Q

Which channel does ATP inhibit

A

The ATP-sensitive K+ channel KATP

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11
Q

What does inhibition of the KATP channel cause

A

Depolarisation of cell membrane
Opening of voltage-gated Ca2+ channels
Increase of internal Ca2+ causes insulin release from vesicles

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12
Q

What happens to beta cells in T1DM

A

Mostly lost

Autoimmune process

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13
Q

Insulin release is biphasic - true or false

A

True

2nd phase is dependent on how well the 1st phase has dealt with glucose increase

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14
Q

What forms the 2 phases of insulin release

A

1st phase - immediate release insulin (5% total)

2nd phase - reserve pool that must undergo preparation reactions before release

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15
Q

Which class of drugs directly inhibits the KATP channel

A

Suphonylurea

Second line in T2DM

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16
Q

Which drug stimulates the KATP channel

A

Diazoxide

Inhibits insulin secretion

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17
Q

What can mutations in Kir6.2 r SUR1 lead to

A

neonatal diabetes
usually responds to SURs

Hyperinsulinism
Can be helped by diazoxide

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18
Q

How do you differentiate between MODY and T1DM

A

Robust genetic screening

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19
Q

How does treatment differ between MODY and T1DM

A

MODY - treated with sulphonylurea

T1DM - treated with insulin

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20
Q

What is the effect of insulin on DNA and protein synthesis

A

Switches these processes on

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21
Q

What is the effect of insulin on gluconeogenesis in the liver

A

Switches it off

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22
Q

Which type of receptor is the insulin receptor

A

Receptor tyrosine kinase

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23
Q

Through which pathways can insulin stimulation cell growth

A

PI3K

Ras

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24
Q

What can cause insulin resistance

A

Reduced insulin sensing and/or signalling

Associated with obesity - most common
Also seen in complete lack of adipose tissue

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25
Q

Describe the cause of T2DM

A

Polygenic with large environmental input

Associated with obesity

26
Q

What is Donohue syndrome

A

Rare autosomal recessive disorder
Mutation is in the gene for insulin receptor
Severe insulin resistance
Also cause leprechaunism
Patients have elfin facial features, growth retardation and absence of fat

27
Q

What is Rabson Mendenhall syndrome

A

Rare autosomal recessive condition
Severe insulin resistance - hyperglycaemic and high insulin
Get hypoglycemic attacks and ketoacidosis

28
Q

What are the symptoms of diabetic ketoacidosis

A

Vomiting
Dehydration
Increased heart rate
Distinctive smell on breath

29
Q

Where are ketone bodies formed

A

Liver mitochondria

30
Q

What is the physiological use for ketone bodies

A

Travel through blood to peripheral tissue where the are used for energy metabolism in the heart muscle and renal cortex

31
Q

What happens if there is an excess of ketones in the blood

A

Leads to acidosis

32
Q

Where is ADH released from

A

The posterior pituitary

33
Q

What is the function ADH

A

Control of water balance
Makes you pee less by causing water reabsorption in the renal tubules
Urine will be more concentrated

34
Q

How is urine concentration measured

A

Measured in urine osmolality

Concentrated urine has a high osmolality

35
Q

What can cause ADH to stop functioning

A

Can stop being produced after head trauma etc
Kidneys can be resistant
Will start peeing out huge volumes

36
Q

What controls sodium balance

A

Steroids released from adrenals

Their effect is known as mineralocorticoid activity

37
Q

Which steroids have mineralocorticoid activity

A

Mainly aldosterone

Others such as cortisol also have the effect

38
Q

What does too much mineralocorticoid activity cause

A

sodium gain

occurs with hormone excess such as Cushing’s

39
Q

What does too little mineralocorticoid activity cause

A

Sodium loss

40
Q

What balance can cause low sodium

A

too little sodium itself (lost from ECF)
OR
too much water – dilutes every body compartment

41
Q

What balance can cause high sodium

A

too much sodium (gained exclusively in ECF)
OR
too little water (lost from all compartments)

42
Q

Which body compartment has the greatest volume of water

A

Intracellular

Has twice as much

43
Q

Which compartment is water found in

A

It’s present in all compartments
Can move between them all as well
Therefore loss/gain of water occurs from the whole body

44
Q

Which compartment is sodium found in

A

Confined to the extracellular fluid

Loss or gain of sodium occurs solely from ECF

45
Q

How is the movement of water and sodium linked

A

Water follows solute by osmosis
As Na is the most abundant solute it pretty much always follows Na
if you lose/gain Na+ from the ECF, you lose/gain water with it.

46
Q

What are the symptoms of sodium loss

A

Very symptomatic
Dehydrated - dryness, low urine output
Hypotensive
Tachycardia

47
Q

What are the symptoms of sodium gain

A

Symptoms of fluid overload
Swelling of abdomen, legs
Pulmonary oedema etc

48
Q

What are the symptoms of water gain/loss

A

Often mostly asymptomatic

This is because effect on individual compartments is minor

49
Q

What can cause low sodium

A

Diarrhoea and vomiting
Loss of fluid through skin in burn victims
Loss of Na through kidneys – due to steroid hormones not working
Can be fatal
Decreased sodium intake (rare)

50
Q

What can cause high water content (therefore lower sodium)

A

Decreased water excretion - SIADH (very common)

Increased water intake is rare

51
Q

What can cause increased sodium

A 
Increased sodium intake 
Near drowning in salt-water
Malicious 
Some iV meds 
Deceased sodium loss 
All very rare
52
Q

What can cause low water levels (therefore high sodium)

A

Increased water loss - diabetes insipidus etc

Decreased water intake - common

53
Q

How do you treat low sodium levels

A

If due to too little Na - gove sodium

If due to too much water - fluid restrict

54
Q

How do you treat high sodium

A

Too much Na- remove sodium

Too little water - give water in form of dextrose

55
Q

What is SIADH

A

Syndrome of inappropriate ADH
Non-osmotic stimuli can cause release when it’s not needed
E.g. hypovolaemia/hypotension, pain, nausea/vomiting

56
Q

What is the cause of oedema and how do we treat it

A

Too much water and sodium

Treat with loop diuretics

57
Q

What is pseudohyponatremia

A

Low sodium result when patient is actually fien
Caused by excess protein in blood (sample) as it causes sodium to be lower due to lower volume its distributed in
Actual relative conc of Na is fine

58
Q

What is Addison’s disease

A

Adrenal insufficiency - don’t make enough steroids
Low mineralocorticoid activity
Lose Na and water through kidneys
Become clinically dehydrated

59
Q

What are the common symptoms of Addison’s disease

A

Dizziness
Hypotension
Hyperpigmentation - caused by excess ACTH which is broken down to MSH (melanocyte stimulating hormone)

60
Q

What is a T1 weighted MRI

A

where you see cs fluid as dark

Posterior pituitary will show up as white

Endocrinology (13 decks)

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