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Endocrine: Basic Science > Biochemistry > Flashcards

Biochemistry Flashcards

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1
Q

what have the physiological processes in the body evolved to ensure surrounding the function of glucose?

A
  • accurate sensing of blood glucose changes
  • correct amount of insulin is released to maintain euglycaemia
  • counterregulatory mechanisms to protect against hypoglycaemia
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2
Q

what is the pancreas made up of?

A

islets of Langerhans including alpha (glucagon), beta (insulin), delta (somatostatin) and PP cells (polypeptide)

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3
Q

formation of insulin

A
  • synthesised in the RER of beta cells as a single chain preprohormone (preproinsulin)
  • cleaved to form insulin which contains two polypeptide chains linked by disulfide bonds
  • connecting C peptide is a by-product of cleavage
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4
Q

two types of insulin

A

ultrafast/short acting: insulin lispro (lysine and proline)

ultra-long acting: insulin glargine

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5
Q

describe the use of ultrafast/short-acting insulin

A

this is injected within 15 minutes of beginning a meal
short duration of action
monomeric
combined with longer preparations in T1DM

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6
Q

describe ultra-long acting insulin

A

recombinant insulin analogue that precipitates in a neutral environment of subcutaenous tissue
single bedtime dose

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7
Q

what blood glucose concentration do beta cells respond to?

A

release insulin in response to blood glucose rising above 5nM

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8
Q

what happens to beta cells in T2DM

A

they lose their ability to sense glucose changes due to hyperglycaemia taking it outside the Km of glucokinase

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9
Q

describe insulin release

A

it is biphasic as only 5% of insulin granules are immediately available for release (RRP)
the reserve pool undergoes preparatory reactions

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10
Q

two proteins in the KATP channel

A

inward rectifier unit (KIR)- Kir6

SU receptor- SUR1

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11
Q

how does the KATP channel exist structurally?

A

octomeric

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12
Q

what inhibits the KATP channel?

A

SUs

diazoxide

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13
Q

what does a mutation in Kir6.2 of the KATP channel lead to

A

neonatal diabetes

manage with SUs

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14
Q

what do some Kir6.2 and SUR1 mutations lead to?

A

congenital hyperinsulinaemia

manage with diazoxide

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15
Q

define MODY (maturity-onset diabetes of the young)

A

genetic defect resulting in early onset T2DM

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16
Q

examples of mutations in MODY

A
  • MODY2= glucokinase impaired (sensing defeat) so blood glucose threshold for insulin secretion is increased
  • HNF transcription factors and MODY1/3= pancreatic foetal development and neogenesis
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17
Q

what does genetic screening allow for MODY?

A

differentiates MODY from T1DM so SUs can be used rather than insulin as MODY still have beta cell function

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18
Q

insulins functions as an anabolic hormone

A
  • amino acid and glucose uptake in muscle, DNA and protein synthesis
  • growth responses
  • lipogenesis in adipose tissue and liver
  • glycogenesis in liver and muscle
  • switches off lipolysis and gluconeogenesis
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19
Q

what does insulin bind to?

A

tyrosine kinase alpha subunit causes the beta subunit to dimerise and autophosphorylation activates the receptor

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20
Q

two insulin pathways

A

PI3K

Ras

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21
Q

what receptor does GH bind to?

A

cytokine receptor

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22
Q

what receptor does calcium bind to?

A

GPCR

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23
Q

what is a key mediator in insulin sensitivity?

A

adipose tissue

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24
Q

what causes monogenic insulin resistance?

A

mutations in the signalling pathway (AKT2)

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25
Q

is T2DM polygenic

A

yes

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26
Q

describe how Leprechaunism (Donohue Syndrome) has insulin resistance

A

AR mutation in gene for insulin receptor

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27
Q

describe how Rabson Mendenhall syndrome has insulin resistance?

A

AR mutation of insulin receptor that reduces sensitivity

28
Q

presentation of Leprechaunism

A 
severe insulin resistance
elfin facial appearance
growth retardation
absence of subcutaneous fat
decreased muscle mass
29
Q

presentation of Rabson Mendenhall syndrome

A

developmental abnormalities
acanthosis nigricans
fasting hypoglycaemia can lead to DKA

30
Q

presentation of DKA

A

vomiting
dehydration
increased HR
distinctive smell on breath

31
Q

how are ketone bodies produced

A

liver mitochondria derived from acetyl-CoA from beta oxidation of fats
diffuse into blood stream and peripheral tissues
accumulation leads to acidosis
high glucose excretion causes dehydration, exacerbating acidosis leading to coma and death

32
Q

management of DKA

A

insulin

rehydration

33
Q

what hormone controls water balance?

A

ADH which causes water to be reabsorbed from renal tubules

34
Q

what does increased ADH cause?

A

small volume of concentrated urine

35
Q

how is urine concentration measured?

A

urine osmolality

36
Q

what is sodium balance controlled by?

A

steroids e.g. aldosterone and cortisol from adrenals

37
Q

describe mineralocorticoid activity surrounding sodium balance

A

MR activity causes Na+ to be reabsorbed in exchange for K+/H+
excess MR activity gains sodium

38
Q

two fluid compartments in the body

A
  1. extracellular 33.3% (Na+= 140mmol/L)

2. intracellular 66.6% Na+= 4mmol/L

39
Q

what does the extracellular fluid compartment consist of?

A

plasma

interstitial fluid

40
Q

can water move between all body compartments?

A

yes

41
Q

where can sodium move in terms of body compartments

A

it is confined to the extracellular fluid ECF

  • interstitial fluid
  • plasma fluid
42
Q

process by which water follows solutes?

A

osmosis

43
Q

two causes of hyponatraemia

A
  1. too little Na+

2. too much water

44
Q

how does too little Na+ lead to hyponatraemia and dehydration?

A

there is a reduction in fluid in the ECF leading to dehydration

45
Q

presentation of hyponatraemia caused by too little Na+

A

dry mucous membrane
tachycardia
decreased consciousness
low BP

46
Q

causes of too little sodium

A

losses from the gut e.g. vomiting/diarrhoea
losses from adrenal/kidneys
losses from the skin
low intake (rare)

47
Q

management of hyponatraemia due to too little Na+

A

give sodium

48
Q

how does too much water cause hyponatraemia

A

less of an effect as water can spread through all compartments

49
Q

causes of hyponatraemia due to too much water

A 
low H2O excretion (SIADH)
increased intake (compulsive water drinking)
50
Q

management of hyponatraemia due to too much water

A

fluid restriction

51
Q

two reasons hypernatraemia can occur?

A

too much Na+

too little water

52
Q

describe the impact of too much Na+

A

causes fluid overload in the ECF

53
Q

presentation of too much Na+

A 
pulmonary oedema
pitting oedema
reduced CO
SOB
ascites
54
Q

causes of too much Na+

A

increased intake e.g. IV meds, near drowning or low Na+ loss

55
Q

management of too much Na+

A

remove sodium

56
Q

role of too little water in hypernatraemia

A

little significance as water can move through all body comparments

57
Q

causes of too little water leading to hypernatraemia

A

excess water loss e.g. DI

low intake in young/elderly

58
Q

management of too little water causing hypernatraemia

A

dextrose

59
Q

fluid management options

A
  • plasma/blood fills plasma compartment
  • 0.9% saline fills plasma and interstitial fluid (ECF)
  • dextrose fills all compartments
60
Q

what is oedema a sign of?

A

fluid overload

61
Q

describe how oedema occurs

A
  • reduced blood volume increases aldosterone and ADH secretion
  • sodium and water retention and hypernatraemia
  • body is acting dehydrated so too much water is retained in the interstitial fluid compartment
62
Q

management of oedema

A

loops diuretics as they cause loss of sodium (and water)

63
Q

define Addison’s disease

A

lack of mineralocorticoid activity

64
Q

what does addison’s disease cause

A

sodium cannot be retained so there is loss (along with water)
leads to dehydration
pigmentation due to high ACTH

65
Q

define DI

A

disruption of the pituitary or pituitary stalk so there is an inability to secrete ADH
no action of the kidneys so no water is reabsorbed and excess is lost in urine

66
Q

management of DI

A

desmopressin

Endocrine: Basic Science (7 decks)

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