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Endocrine: Basic Science > Biochemistry > Flashcards

Biochemistry Flashcards

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
is T2DM polygenic
yes
26
describe how Leprechaunism (Donohue Syndrome) has insulin resistance
AR mutation in gene for insulin receptor
27
describe how Rabson Mendenhall syndrome has insulin resistance?
AR mutation of insulin receptor that reduces sensitivity
28
presentation of Leprechaunism
``` severe insulin resistance elfin facial appearance growth retardation absence of subcutaneous fat decreased muscle mass ```
29
presentation of Rabson Mendenhall syndrome
developmental abnormalities acanthosis nigricans fasting hypoglycaemia can lead to DKA
30
presentation of DKA
vomiting dehydration increased HR distinctive smell on breath
31
how are ketone bodies produced
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
management of DKA
insulin | rehydration
33
what hormone controls water balance?
ADH which causes water to be reabsorbed from renal tubules
34
what does increased ADH cause?
small volume of concentrated urine
35
how is urine concentration measured?
urine osmolality
36
what is sodium balance controlled by?
steroids e.g. aldosterone and cortisol from adrenals
37
describe mineralocorticoid activity surrounding sodium balance
MR activity causes Na+ to be reabsorbed in exchange for K+/H+ excess MR activity gains sodium
38
two fluid compartments in the body
1. extracellular 33.3% (Na+= 140mmol/L) | 2. intracellular 66.6% Na+= 4mmol/L
39
what does the extracellular fluid compartment consist of?
plasma | interstitial fluid
40
can water move between all body compartments?
yes
41
where can sodium move in terms of body compartments
it is confined to the extracellular fluid ECF - interstitial fluid - plasma fluid
42
process by which water follows solutes?
osmosis
43
two causes of hyponatraemia
1. too little Na+ | 2. too much water
44
how does too little Na+ lead to hyponatraemia and dehydration?
there is a reduction in fluid in the ECF leading to dehydration
45
presentation of hyponatraemia caused by too little Na+
dry mucous membrane tachycardia decreased consciousness low BP
46
causes of too little sodium
losses from the gut e.g. vomiting/diarrhoea losses from adrenal/kidneys losses from the skin low intake (rare)
47
management of hyponatraemia due to too little Na+
give sodium
48
how does too much water cause hyponatraemia
less of an effect as water can spread through all compartments
49
causes of hyponatraemia due to too much water
``` low H2O excretion (SIADH) increased intake (compulsive water drinking) ```
50
management of hyponatraemia due to too much water
fluid restriction
51
two reasons hypernatraemia can occur?
too much Na+ | too little water
52
describe the impact of too much Na+
causes fluid overload in the ECF
53
presentation of too much Na+
``` pulmonary oedema pitting oedema reduced CO SOB ascites ```
54
causes of too much Na+
increased intake e.g. IV meds, near drowning or low Na+ loss
55
management of too much Na+
remove sodium
56
role of too little water in hypernatraemia
little significance as water can move through all body comparments
57
causes of too little water leading to hypernatraemia
excess water loss e.g. DI | low intake in young/elderly
58
management of too little water causing hypernatraemia
dextrose
59
fluid management options
- plasma/blood fills plasma compartment - 0.9% saline fills plasma and interstitial fluid (ECF) - dextrose fills all compartments
60
what is oedema a sign of?
fluid overload
61
describe how oedema occurs
- 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
management of oedema
loops diuretics as they cause loss of sodium (and water)
63
define Addison's disease
lack of mineralocorticoid activity
64
what does addison's disease cause
sodium cannot be retained so there is loss (along with water) leads to dehydration pigmentation due to high ACTH
65
define DI
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
management of DI
desmopressin

Endocrine: Basic Science (7 decks)

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