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BIOL1025 - Fundamentals of cell biology and physiology > Endocrinology (3) - metabolic response to longer term stress > Flashcards

Endocrinology (3) - metabolic response to longer term stress Flashcards

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1
Q

thyroxine

A

axis running from hypo and Ant Pit

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2
Q

3 main axis and entire function

A

maintain metabolism

thyroid, adrenal cortex and growth H

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3
Q

adrenal gland H location

A

above kidney and v small

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4
Q

adrenal gland H - medulla

A

inner (neuronal) part - make catecholamines
produce adrenaline from deamination and modification
has huge BV - heavily vascularised of a.a

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5
Q

adrenal gland H - cortex

A

outer epithelium - make series of steroids

has 3 region

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6
Q

3 regions of cortex

A

outer - glomerulosa - produce aldosterone
middle - fascicular - bundle
largest - reticular - network both produce cortisol and androgens

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7
Q

cholesterol

A

branch and OH group - removed and changed
highly lipophilic - can’t be stored
oestrogen, progesterone, androgens, glucocorticoids and mineralocorticoids, vit D

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8
Q

hypothalamus function

A

release into small portal vessels
release H-G cortitropic
carried to Pit gland - bind to corticotropes - receptor for CRH = corticotrope release ACTH into blood supply carried to adrenal gland - bind to cortex cells

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9
Q

ACTH function

A

drives levels of cortisol made - only needed to produce amount of aldosterone and levels of being made

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10
Q

fascicular and reticular layer function for cholesterol and ACTH

A

more cholesterol brought into call and more released
E. cholesterol desmolase - activated cleaves cholesterol = intermediate
pregnenolone has 17 alpha hydroxylase
used to produce corisol

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11
Q

glomerulosa layer function for ACTH

A

activates desmolase and release cholesterol into cell
E hydroxylase not active
pushes to produce corticosterone
modification of aldosterone driven by aldosterone synthase which is regulated by angiotensin II

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12
Q

E produced and regulated causes

A

different steroid H secretion rates

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13
Q

cortisol

A

small MC effect (U.I) unlike aldosterone

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14
Q

MC

A

mineralocorticoids

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15
Q

GC

A

glucocorticoids

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16
Q

artificial - other steroids toles

A

modify immune system - anti flammatory

modifies - produce cortisone and dexamethasone

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17
Q

cortisone

A

weak GC and MC effect - strong inflammatory effect

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18
Q

synthetic - dexamethasone

A

high anti inflammatory effect compared to cortisol as dexamethasone - 0 - GC and 2.0 - MC effect

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19
Q

secretion of CRH - ACTH - cortisol pathway - cortisol released

A

1- circadian rhythm caused by feedback loop (long/short) - GC increases in morning
2- stress - increase cortisol level

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20
Q

secretion of CRH - ACTH - cortisol pathway - process as hypo responds to stress

A

release CRH binds to corticotropes in Pit

= POMC - cleaved by PC1 = ACTH - secreted and released to bind to receptors at adrenal cortex - release cortisol

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21
Q

POMC

A

pro-opiomelanocortin

prehormone

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22
Q

PC1

A

prohormone convertase 1

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23
Q

ACTH and other parts of POM cursor cuntion

A

cleaves in different ways = products

e.g. MSH - melanocytes stimulating H

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24
Q

controls for GC secretion

A

hypo responds to circadian/stress = CRH release to Ant
release ACTH to adrenal gland
release cortisol - -ve feedback

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25
Q

mechanism of andrenocorticoids

the slow release

A

cortisol carried by transcortin in blood
slow release - cross membrane and binds to receptor - carried into nucleus and bind to transcription factor into areas closes to promoter of specific gene/repressor/enhancer regions

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26
Q

HRE

A

H response element

GC RE - AGAACAnnnTGTTCT - palindromic - work as dimer

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27
Q

nnn

A

any nucleotide

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28
Q

RE

A

restriction enzyme

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29
Q

decrease in free H

A

cortisol bind to CrP (few hrs) - won’t get high peak (buffering)
stop being broken down

30
Q

steroid H receptor has 3 functional domain

A

ligand binding
DNA binding
Ligand dependent transcription activating

31
Q

1 - ligand binding domain

A

dependent nuclear translocation signal

chaperone bind to steroid

32
Q

2 - DNA binding domain

A

contain2 Zn finger motif

33
Q

3 - ligand dependent transcription activating domain

A

recruit transcriptional co-activator

bind to chaperone - masks

34
Q

steroid binds to ligand binding domain - process

A 
conformational change (CC) - lose chaperone
= CC - COOH of ligand binding domain open = nuclear localisation
35
Q

nuclear localisation occurs - process (1)

A

complex carried into nucleus with co activator protein - sits over 3 and 1 with receptor binding element = transcription regulating complex for target genes

36
Q

change in expression of target genes

A

modification of receptor binding sequence - allows interactions when bind to it
e.g. GC RE

37
Q

HRE short - function

A

acting sequences located within promoter/ enhancer of target genes - receptor interact with

38
Q

receptor activation causes

A

induce modulation of transcription of specific gene with HRE
made of inverted repeats - specific to gene - acts upon
e.g. oestrogen and GC receptor

39
Q

specification of system

A

dependent on receptor expressed by cell and co activator being made in cell
- steroids can go into every single cell type
receptor-binding element is present in all cells

40
Q

GC - glucocorticoids function

A

drive catabolism

breakdown molecules and release energy

41
Q

carbohydrate in metabolic pathway - GC cortisol (corticosterone)

A

save glucose - decrease its general use
gluconeogenesis in liver - breakdown protein and convert a.a. to glucose
make more glycogen - decrease use
increase blood glucose level - used for tissues needed
excess cortisol - adrenal diabetes - glucose can’t be absorbed

42
Q

protein in metabolic pathway - GC cortisol (corticosterone)

A

increase breakdown of protein in liver - gluconeogenesis especially from muscles and collagen in bone and skin
decrease protein content of all tissues

43
Q

lipids in metabolic pathway - GC cortisol (corticosterone)

A

increases use for fuel and a.a.
change lipid deposition
lose lipid being laid down in chest and lower neck

44
Q

GC characteristic

A

v. potent anti flammatory effects hydro cortisone

increase if modified

45
Q

decrease in inflammation

A

stabilises capillary membrane
decrease WBC activity and release lysosomal E and migration
decrease lymphocyte division or lysis

46
Q

steroids used in disease

A

e.g. hydrocortisones - skin inflammation

47
Q

Cushing’s disease

A

excessive GC - active tumour in hypo/pit/adrenal cortex
tumour in hypo/pit - secondary causes
in adrenal cortex - primary cause

48
Q

giving high levels of steroid / give tumour

A

form GC - high blood glucose - can’t reabsorb

in filtration in kidney = increase urination and drinking

49
Q

if tumour is caused of GC

A

produce more ACTH - make more androstenedione - androgen

increase in androgen production - precursor virilization

50
Q

MC - aldosterone secretion

A

need ACTH but not regulated by it
from glomerulus
angiotensin 2 regulate level

51
Q

MC-aldosterone - important for regulation NaCl and water reabsorption

A

increase absorption of EC fluid - increase arterial pressure and release aldosterone - reduce excretion of Na - increase reabsorption in kidney

52
Q

aldosterone function in reabsorption

A

regulate NaCl and water reabsorption and loss of K+ - high ECK+

53
Q

JG cells

A

juxtaglomerular cells

54
Q

how aldosterone release is regulated - location

A

at the kidney - next to glomerulus - cell lining close to JG cells
smooth muscle cell sit around BV going into glomerulus and macular densa cell in walls of DCT of nephron

55
Q

regulation of aldosterone - Renin-angiotensin system - decrease in BP - process

A

JG cells detect change - sit around BV - decrease pressure - sensed and get excited
decrease Na+/ increase K+
macular densa cells get excited stimulated JG cell - increase renin cleave angiotensin = angiotensin 1 and cleaved by ACE
= angiotensin 2 = adrenal zona glomerulosa = aldosterone

56
Q

regulation of aldosterone - inhibitory pathway - ANF

increase in BP

A

produced by muscle cells in heart - atrium
stretch releases ANF - blocks formation of renin by JG cells
decrease Na+/ water reabsorption and hence BP

57
Q

ANF

A

atrial natriuretic factor

58
Q

ANP

A

atrial natriuretic peptide

59
Q

DCT

A

distal convoluted tubule

60
Q

regulation of aldosterone - minor direct effect

A

monitor [Na+] and [K+] in plasma by adrenal gland
Ant. Pit. gland - increase K+/ decrease Na+
release renin = angiotensin 2
direct effect overcome increase in BP = ANP factor
inhibitory = regulation of aldosterone

61
Q

aldosterone function

A

has no carrier protein - effects are shorter
drives Na+ and water absorption = loss of K+
relatively slow
regulate metabolism

62
Q

aldosterone - no carrier causes

A

produce Na+ channels - got into Apex of DCT cells

= Na+/K+ pump - increase metabolism

63
Q

aldosterone - relatively slow means

A

does not make more aquaporin - through transcription pathway

64
Q

aldosterone - change in metabolism - process

A

aldosterone diffuse into cell and bind to receptor and carried into nucleus
transcription = new protein and increase mitochondrial activity - metabolism increases

65
Q

role of CRH/ACTH

A

AI - Addison’s disease - more antibodies against cells in adrenal cortex
make less GC and MC - survive longer without GC
without MC - can’t regulate EC K+ levels

66
Q

action potential becoming excitable

A

resting membrane potential - closer to threshold then drives it into having action potential

67
Q

failure in production of both corticoids - decrease in aldosterone = decrease in BP

A

increase EC K+ - excitable cells become more excitable

drive cardia arrhythmia - increase K+ - in EC fluid loss = muscle weakness

68
Q

decrease in GC

A

can’t respond to stress - decrease blood system
unnoticeable - until stress - go into Addisonian crisis
increase ACTH lost (more POMc - ACTH precursor formed )

69
Q

level of ACTH and POMC increases

A

feedback loop don’t work and try to compensate - CRH will increase as -ve feedback control don’t work - produce by byproduct by cleavage of POMC = MSH
more made - effect skin pigment

70
Q

-ve loop in aldosterone function depend on 3 parts of body

A

keep regulated heart, kidney, Pit.

BIOL1025 - Fundamentals of cell biology and physiology (21 decks)

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