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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

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
mechanism of andrenocorticoids | the slow release
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
26
HRE
H response element | GC RE - AGAACAnnnTGTTCT - palindromic - work as dimer
27
nnn
any nucleotide
28
RE
restriction enzyme
29
decrease in free H
cortisol bind to CrP (few hrs) - won't get high peak (buffering) stop being broken down
30
steroid H receptor has 3 functional domain
ligand binding DNA binding Ligand dependent transcription activating
31
1 - ligand binding domain
dependent nuclear translocation signal | chaperone bind to steroid
32
2 - DNA binding domain
contain2 Zn finger motif
33
3 - ligand dependent transcription activating domain
recruit transcriptional co-activator | bind to chaperone - masks
34
steroid binds to ligand binding domain - process
``` conformational change (CC) - lose chaperone = CC - COOH of ligand binding domain open = nuclear localisation ```
35
nuclear localisation occurs - process (1)
complex carried into nucleus with co activator protein - sits over 3 and 1 with receptor binding element = transcription regulating complex for target genes
36
change in expression of target genes
modification of receptor binding sequence - allows interactions when bind to it e.g. GC RE
37
HRE short - function
acting sequences located within promoter/ enhancer of target genes - receptor interact with
38
receptor activation causes
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
specification of system
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
GC - glucocorticoids function
drive catabolism | breakdown molecules and release energy
41
carbohydrate in metabolic pathway - GC cortisol (corticosterone)
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
protein in metabolic pathway - GC cortisol (corticosterone)
increase breakdown of protein in liver - gluconeogenesis especially from muscles and collagen in bone and skin decrease protein content of all tissues
43
lipids in metabolic pathway - GC cortisol (corticosterone)
increases use for fuel and a.a. change lipid deposition lose lipid being laid down in chest and lower neck
44
GC characteristic
v. potent anti flammatory effects hydro cortisone | increase if modified
45
decrease in inflammation
stabilises capillary membrane decrease WBC activity and release lysosomal E and migration decrease lymphocyte division or lysis
46
steroids used in disease
e.g. hydrocortisones - skin inflammation
47
Cushing's disease
excessive GC - active tumour in hypo/pit/adrenal cortex tumour in hypo/pit - secondary causes in adrenal cortex - primary cause
48
giving high levels of steroid / give tumour
form GC - high blood glucose - can't reabsorb | in filtration in kidney = increase urination and drinking
49
if tumour is caused of GC
produce more ACTH - make more androstenedione - androgen | increase in androgen production - precursor virilization
50
MC - aldosterone secretion
need ACTH but not regulated by it from glomerulus angiotensin 2 regulate level
51
MC-aldosterone - important for regulation NaCl and water reabsorption
increase absorption of EC fluid - increase arterial pressure and release aldosterone - reduce excretion of Na - increase reabsorption in kidney
52
aldosterone function in reabsorption
regulate NaCl and water reabsorption and loss of K+ - high ECK+
53
JG cells
juxtaglomerular cells
54
how aldosterone release is regulated - location
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
regulation of aldosterone - Renin-angiotensin system - decrease in BP - process
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
regulation of aldosterone - inhibitory pathway - ANF | increase in BP
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
ANF
atrial natriuretic factor
58
ANP
atrial natriuretic peptide
59
DCT
distal convoluted tubule
60
regulation of aldosterone - minor direct effect
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
aldosterone function
has no carrier protein - effects are shorter drives Na+ and water absorption = loss of K+ relatively slow regulate metabolism
62
aldosterone - no carrier causes
produce Na+ channels - got into Apex of DCT cells | = Na+/K+ pump - increase metabolism
63
aldosterone - relatively slow means
does not make more aquaporin - through transcription pathway
64
aldosterone - change in metabolism - process
aldosterone diffuse into cell and bind to receptor and carried into nucleus transcription = new protein and increase mitochondrial activity - metabolism increases
65
role of CRH/ACTH
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
action potential becoming excitable
resting membrane potential - closer to threshold then drives it into having action potential
67
failure in production of both corticoids - decrease in aldosterone = decrease in BP
increase EC K+ - excitable cells become more excitable | drive cardia arrhythmia - increase K+ - in EC fluid loss = muscle weakness
68
decrease in GC
can't respond to stress - decrease blood system unnoticeable - until stress - go into Addisonian crisis increase ACTH lost (more POMc - ACTH precursor formed )
69
level of ACTH and POMC increases
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
-ve loop in aldosterone function depend on 3 parts of body
keep regulated heart, kidney, Pit.

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

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