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PHSL231 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

define the circadian rhythm

A

environmental rhythm determined by light

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2
Q

where is melatonin secreted

A

pineal gland, located at the base of the hypothalamus

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3
Q

what do the ant and pit gland regulate in the body

A

water balance
metabolism
body growth
milk secretion and reproduction

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4
Q

describe the hypothalamic control of the anterior pituitary

A

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

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5
Q

media eminence

A

window to to the brain, interface between blood and CSF where many regulatory hormones are released.

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6
Q

describe the basis of the hypothalamic-pit axes

A

hypothalamus releases hormones which act on the ant pituitary which releases more hormones into the peripheral target tissue to produce a cascade of events.

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7
Q

describe the HPA axes of gonads

A

gonadotropin releasing hormone (GnRH) acts on follicular stimulating hormone (FSH) and luteinzing hormone (LH) which acts on the gonads to stimulate a response

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8
Q

describe the HPA axes of the adrenal gland

A

corticotropin releasing hormone acts on adrenocorticotropic hormone which acts on the adrenal glands.

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9
Q

describe the HPA axes of somatostatin

A

somatostatin negatively feeds back on GH

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10
Q

describe the HPA axes acting on the thyroid gland

A

thyroid releasing hormone acts on thyroid stimulation hormone which acts to produce a response from the thyroid gland.

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11
Q

describe the HPA axes on the liver

A

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

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12
Q

how is the GHRH axes stimulated

A

exercise, sleep, fasting and stress

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13
Q

describe the release of GH

A

diurnal pulsatile release however not a true circadian rhythm

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14
Q

control of GH secretion

A

IGF-1 negatively feedback on growth hormone to inhibit secretion

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15
Q

describe the cascade of events that occurs when GH binds to the GHRH receptor/ G protein

A

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.

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16
Q

how does somatostatin affect the GH G protein cascade

A

SS acts on AC to inhibit the ATP-cAMP dephosphorylation preventing the release of GH

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17
Q

what are the indirect growth effects of GH in the body

A

stimulates bone growth, by the stimulation of mitogenesis via IGF-1

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18
Q

what are the indirect growth effects of GH in the body

A

stimulates protein synthesis which directly acts on muscle growth

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19
Q

what are both of the direct metabolic effects of GH

A

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

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20
Q

what two hormones does the posterior pit produce

A

vasopressin and oxytocin

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21
Q

why is vasopressin released

A

secreted in response to increased plasma osmotic pressure or decreased blood pressure

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22
Q

one word to describe vasopressin

A

anti-diuretic

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23
Q

what are the effects of vasopressin

A

inhibits urine production and vasoconstriction

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24
Q

what is the main function of oxytocin

A

acts on kidney to increase sodium excretion

25
Q

oxytocin (babies)

A

contracts mammary ducts for milk let down during suckling, also causes uterine contractions during delivery

26
Q

anatomy of the adrenal gland

A

cortex 80% - cortisol

medulla - 20% - adrenaline and noradrenaline

27
Q

what is the rate limiting step in the synthesis of adrenal cortex hormones

A

the enzyme P450scc cleavage of cholesterol into progenolone

28
Q

progenolone goes to what hormones in the adrenal cortex

A

glucocorticoids- cortisol
mineralocorticoids- aldosterone
sex steroid precursors - androsterone

29
Q

what is the function of mineralocorticoids - aldosterone

A

acts to maintain fluid volume in the kidneys

30
Q

how does aldosterone maintain fluid volume in the body

A

increases reabsorption of sodium and water

increases secretion of potassium

31
Q

how is aldosterone release controlled indirectly

A

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

32
Q

how is aldosterone release controlled directly

A

increase potassium load - increase potassium in plasma which increases aldosterone production in the adrenal gland

33
Q

what is the role of the cerebellum

A

integrates sensory feedback from the brain etc and regulates motor movements, controls voluntary movements such as posture and speech

34
Q

control of cortisol release

A

vasopressin can increase the release of ACTH which acts on the p450scc enzyme increasing the level of cortisol in the body

35
Q

adrenaline and noradrenaline cause what changes

A

vascular changes

36
Q

cortisol cause wht changes

A

energy mobilisation

37
Q

describe the absorptive state

A

anabolic, high insulin

38
Q

describe the post-absorptive state

A

catabolic, high glucagon

39
Q

ghrelin main function

A

stimulates hinger and food intake

40
Q

where us ghrelin secreted

A

fundus of the stomach

41
Q

when are ghrelin levels at their highest

A

highest levels before meals as it stimulates hunger

42
Q

describe the feedback of leptin and ghrelin on the need to eat in the hypothalamus

A

ghrelin acts on NPY neurons to stimulate the need to eat

leptin acts on POMC neurons to inhibit the drive to eat

43
Q

where is leptin secreted

A

adipose tissue

44
Q

describe the g-alpha s cascade

A

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

45
Q

what is the effect of g alpha i on adenylyl cyclase and cAMP

A

alpha i inhibits AC which causes a decrease in cAMP, PKA is inactive therefore cannot stimulate target cells.

46
Q

G alpha q

A

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

47
Q

G alpha t

A

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

48
Q

what binds to tyrosine kinase receptors

A

ligands such as NGF and insulin

49
Q

describe the events of tyrosine kinase receptors

A

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

50
Q

synthesis of aCH

A

acetyl CoA + choline -choline transferase- Ach

51
Q

breakdown of Ach

A

ach - acetylcholine esterase- acetic acid + choline

52
Q

how are muscarinic aCH channels opened

A

metabotropic therefore are activated indirectly not by a receptor

53
Q

how are nicotinic ach receptors activated

A

when two aCH molecules bind causing the pore to open and for na+ entry

54
Q

myasthenia gravis definition

A

auto immune disease of the NMJ caused by antibodies to the Ach receptor

55
Q

what helps MG

A

ache blockers as it allows for ach to build up and make it more likely for some transmission to occur

56
Q

malignant hypothermia

A

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

57
Q

what G protein does cholera toxin effect and how

A

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

58
Q

how does pertussis toxin effect the body

A

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

PHSL231 (3 decks)

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