Endocrine Flashcards
define the circadian rhythm
environmental rhythm determined by light
where is melatonin secreted
pineal gland, located at the base of the hypothalamus
what do the ant and pit gland regulate in the body
water balance
metabolism
body growth
milk secretion and reproduction
describe the hypothalamic control of the anterior pituitary
cell bodies located in the hypothalamus secret a hormone which acts on the ant pit which produces a hormone which acts on target cells in the body
media eminence
window to to the brain, interface between blood and CSF where many regulatory hormones are released.
describe the basis of the hypothalamic-pit axes
hypothalamus releases hormones which act on the ant pituitary which releases more hormones into the peripheral target tissue to produce a cascade of events.
describe the HPA axes of gonads
gonadotropin releasing hormone (GnRH) acts on follicular stimulating hormone (FSH) and luteinzing hormone (LH) which acts on the gonads to stimulate a response
describe the HPA axes of the adrenal gland
corticotropin releasing hormone acts on adrenocorticotropic hormone which acts on the adrenal glands.
describe the HPA axes of somatostatin
somatostatin negatively feeds back on GH
describe the HPA axes acting on the thyroid gland
thyroid releasing hormone acts on thyroid stimulation hormone which acts to produce a response from the thyroid gland.
describe the HPA axes on the liver
growth hormone releasing hormone acts on growth hormone which acts on the liver to produce IGF-1 which has metabolic and growth effects which are both direct and indirect
how is the GHRH axes stimulated
exercise, sleep, fasting and stress
describe the release of GH
diurnal pulsatile release however not a true circadian rhythm
control of GH secretion
IGF-1 negatively feedback on growth hormone to inhibit secretion
describe the cascade of events that occurs when GH binds to the GHRH receptor/ G protein
AC is bound to the receptor which causes ATP-cAMP this energy released is used to activate PKA, PKA then acts on Ca2+ channel causing an influx of ions into the cell which causes GH to be released.
how does somatostatin affect the GH G protein cascade
SS acts on AC to inhibit the ATP-cAMP dephosphorylation preventing the release of GH
what are the indirect growth effects of GH in the body
stimulates bone growth, by the stimulation of mitogenesis via IGF-1
what are the indirect growth effects of GH in the body
stimulates protein synthesis which directly acts on muscle growth
what are both of the direct metabolic effects of GH
increase in blood glucose by stimulating glucose synthesis in liver an inhibiting cellular glucose uptake
increase in TAG breakdown and ffa mobilisation in adipose tissue
what two hormones does the posterior pit produce
vasopressin and oxytocin
why is vasopressin released
secreted in response to increased plasma osmotic pressure or decreased blood pressure
one word to describe vasopressin
anti-diuretic
what are the effects of vasopressin
inhibits urine production and vasoconstriction
what is the main function of oxytocin
acts on kidney to increase sodium excretion
oxytocin (babies)
contracts mammary ducts for milk let down during suckling, also causes uterine contractions during delivery
anatomy of the adrenal gland
cortex 80% - cortisol
medulla - 20% - adrenaline and noradrenaline
what is the rate limiting step in the synthesis of adrenal cortex hormones
the enzyme P450scc cleavage of cholesterol into progenolone
progenolone goes to what hormones in the adrenal cortex
glucocorticoids- cortisol
mineralocorticoids- aldosterone
sex steroid precursors - androsterone
what is the function of mineralocorticoids - aldosterone
acts to maintain fluid volume in the kidneys
how does aldosterone maintain fluid volume in the body
increases reabsorption of sodium and water
increases secretion of potassium
how is aldosterone release controlled indirectly
Na+ deprivation causes renin release in the kidney which converts angiotensiongen to angiotensin one, the liver then produces the angiotensiongen, the angiotensin one is then converted into angiotensin two by a enzyme from the lungs which then acts on the adrenal gland to produce aldosterone
how is aldosterone release controlled directly
increase potassium load - increase potassium in plasma which increases aldosterone production in the adrenal gland
what is the role of the cerebellum
integrates sensory feedback from the brain etc and regulates motor movements, controls voluntary movements such as posture and speech
control of cortisol release
vasopressin can increase the release of ACTH which acts on the p450scc enzyme increasing the level of cortisol in the body
adrenaline and noradrenaline cause what changes
vascular changes
cortisol cause wht changes
energy mobilisation
describe the absorptive state
anabolic, high insulin
describe the post-absorptive state
catabolic, high glucagon
ghrelin main function
stimulates hinger and food intake
where us ghrelin secreted
fundus of the stomach
when are ghrelin levels at their highest
highest levels before meals as it stimulates hunger
describe the feedback of leptin and ghrelin on the need to eat in the hypothalamus
ghrelin acts on NPY neurons to stimulate the need to eat
leptin acts on POMC neurons to inhibit the drive to eat
where is leptin secreted
adipose tissue
describe the g-alpha s cascade
g alpha s stimulates adenylyl cyclase which generates the second messenger cAMP by attaching to the effector AC ATP is converted to cAMP which then acts to stimulate PKA which phosphorylates target proteins
what is the effect of g alpha i on adenylyl cyclase and cAMP
alpha i inhibits AC which causes a decrease in cAMP, PKA is inactive therefore cannot stimulate target cells.
G alpha q
stimulates the effector PLC which causes a signalling cascade causing the release of calcium from the ER which allows the activation of calmodulin and calmodulin dependent kinases
G alpha t
light activates the cell receptor, stimulates the effector phosphodiesterase which causes cGMP-GMP causing a change in membrane potential which helps the retina detect light
what binds to tyrosine kinase receptors
ligands such as NGF and insulin
describe the events of tyrosine kinase receptors
when ligand activates the receptor it causes a conformational change which activates the kinase
the kinase binds to effector proteins and catalyses the addition of phosphate groups onto tyr aa
synthesis of aCH
acetyl CoA + choline -choline transferase- Ach
breakdown of Ach
ach - acetylcholine esterase- acetic acid + choline
how are muscarinic aCH channels opened
metabotropic therefore are activated indirectly not by a receptor
how are nicotinic ach receptors activated
when two aCH molecules bind causing the pore to open and for na+ entry
myasthenia gravis definition
auto immune disease of the NMJ caused by antibodies to the Ach receptor
what helps MG
ache blockers as it allows for ach to build up and make it more likely for some transmission to occur
malignant hypothermia
caused by volatile anaesthetics, happens due to mutations in the rhyanodene receptors which cause continuos calcium release which the over uptake into the ER caused heat energy
what G protein does cholera toxin effect and how
G alpha S as it inhibits GTPase activity of G alpha s causing g alpha s to be continuously active causing a continuos rise in cAMP and activation of chloride and water secretion into the GI tract
how does pertussis toxin effect the body
inhibits the action of g alpha i, and inhibits the exchange of GDP-GTP therefore g alpha i is continuously produces and because it normally inhibits production of cAMP its inhibition causes a rise in cAMP and downstream activation of downstream pathways which leads to inflammation
