physiology of the HPA axis (see notes!) Flashcards
what 2 hormones are released by the posterior pituitary gland
- anti-diuretic hormone (ADH)
- oxytocin
is the posterior pituitary gland an endocrine gland
no, not a true endocrine gland -> doesn’t produce its own hormones, it just stores and releases them
what kind of connection does the hypothalamus and posterior pit gland have
neural - the posterior pituitary is and extension of the hypothalamus and they communicate via nerves
what area of the hypothalamus is responsible for oxytocin release
paraventricular nuclues
what area of the hypothal is responsible for ADH release
supraoptic nucleus
what is the “neck” of the pituitary gland called
infundibulum
what kind of organ is the anterior pituitary gland
endocrine organ -> hypothal sends hormonal signals via the hypophyseal portal system to the pituitary gland
what 5 hormones does the hypothalamus release
- thyroid releasing hormone (TRH)
- prolactin releasing hormone (PRH)
- gonadotropin releasing hormone (GnRH)
- corticotropin releasing hormone (CRH)
- growth hormone releasing hormone (GHRH)
6 hormones released by the anterior pituitary gland
- Thyroid stimulating hormone (TSH)
- prolactin
- FSH
- LH
- adrenocorticotropin hormone (ACTH)
- growth hormone (GH)
HP-gonadal axis
GnRH -> LH -> ovaries/testes -> stimulates oestrogen/testosterone synthesis
HP-Thyroid axis
TRH -> TSH -> thyroid gland -> stimulate thyroxine synthesis
HP-adrenal axis
CRH -> ACTH -> adrenal cortex -> stimulates corticosteroid synthesis
what is the role of the HPA axis
to modulate stress responses leading to the release of cortisol
what kind of cells secrete CRH
small bodied neurones
what area of the hypothalamus is CRH secreted from
paraventricular nucleus
what is the short -ve feedback loop in the HPA axis
CRH-> anterior pit gland -> ACTH release -> ACTH inhibitsCRH release
what cells are responsible for ACTH release
corticotrophs
ACTH release cellular mechanism (draw out)
CRH binds to CRHR -> g protein coupled receptor causes ATP -> cAMP -> activates PKA -> PKA binds to Ca2+ receptors -> Ca2+ influx -> causes exocytosis of ACTH vesicles
HPA axis long -ve feedback loop
CRH -> ant pituitary gland -> ACTH release -> adrenal glands -> cortisol synthesis -> cotrisol downregulates both CRH and ACTH release
ACTH action on adrenal gland cells mechanism (intracellularly)
ACTH binds to melanocortin-2 receptor -> g coupled protein receptor causes ATP -> cAMP -> activates PKA -> increases activity of P450scc and increases enzyme synthesis
when is cortisol secreted (2)
- throughout the day in a pulsitile manner
- in response to stress
how does cortisol prepare the body for flight or flight response (2)
- provided adequate nutrients for ATP synthesis
- glucose sparing for the brain
what are the 4 zones to the adrenal gland and what does each produce
- medulla -> adrenaline, NA
cortex: - zona Glomerulosa -> aldosterone (RAAS system)
- zona fasiculata -> glucocorticoids (e.g. cortisol), allows energy to be provided to vital tissues
- zona reticularis -> androstenedione -> androgens (sex hormones)
how do hormones work (3)
- enters cell and binds to the receptor in the cytoplasm
- hormone-receptor complex enter nucleus
- acts as a transcription factor can causes transcription/inhibition of certain genes from the DNA
why must glucose be spared for the brain in stress response
the brain will pretty much only metabolise glucose and so it must be reserved for the brain as other tissues can use other metabolites e.g. fatty acids
what is the action of cortisol on adipose tissue, the liver and extra-hepatic tissue (e.g. skeletal muscle)
- adipose tissue - increased lipolysis => more free fatty acids in the blood that can be metabolised
- liver - gluconeogenesis and glycogenolysis => increased glucose in the blood
- extra-hepatic tissue - decreased protein synthesis, increased proteolysis => more free amino acids in the blood, these can be used for ATP release instead of glucose; increased fat oxidation (for ATP release); decreased glucose metabolism (more glucose for brain) -> i.e. shifting the metabolism of these tissues away from glucose
what is the preferred metabolite for skeletal muscle in stress
fat