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Metabolism > Pituitary and Adrenal Glands > Flashcards

Pituitary and Adrenal Glands Flashcards

1
Q

what does ADH stand for and what does it do?

A

antidiuretic hormone

stimulates H2O retention, raises BP by contracting arterioles

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2
Q

why does oxytocin do?

A

stimulates contractions in labour

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3
Q

what is the difference between the anterior and posterior pituitary?

A

posterior had direct neurological release whereas the anterior is controlled by hormones therefore the reaction is much slower

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4
Q

where does GH have its affect and what is it via?

A

direct affect on all tissues

via insulin growth factor 1 produced by the liver

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5
Q

what stimulates and what inhibits GH release?

A

growth hormone releasing hormone stimulates

somatostatin inhibits

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6
Q

what kind of release does GH have over the day? when is most GH secreted?

A

pulsatile

during sleep

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7
Q

what are the functions of GH?

A

Skeletal growth and bone density
metabolism (works against insulin)
muscle strength

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8
Q

what is the difference in presentation of excessive GH in adults and children?

A

in adults it is more subtle as your bones cant grow anymore.

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9
Q

what stimulates TSH?

A

thyroxin releasing hormone (TRH)

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10
Q

what does TSH do?

A

activates follicular cells in thyroid to produce T3 + T4

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11
Q

what kind of feedback does TSH undergo?

A

negative

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12
Q

what does ACTH stand for and what is its release stimulated by?

A

adrenocorticotrophic hormone

stimulated by corticotrophin releasing hormone (CRH)

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13
Q

how are ACTH and CRH secreted?

A

in a pulsatile fashion

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14
Q

What else can cause ACTH release?

A

stress

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15
Q

When is activity of ACTH increased and decreased? When is it at its lowest?

A

Increased in am, decreased activity in pm, lowest at midnight

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16
Q

what stimulates FHS and LH production?

A

gonadotrophin releasing hormone

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17
Q

what happens when LH and FSH production is stimulated in men?

A

LH drives testosterone secretion.

FSH drives sperm production

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18
Q

what happens when LH and FSH production is stimulated in women?

A

follicular phase, LH pulses cause oestrogen release.

mid-late luteal phase LH pulses cause progesterone release

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19
Q

what type of feedback occurs on LH and FSH in women mid cycle surge of these hormones? what is it called?

A

+ve feedback, ovulation

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20
Q

what does prolactin do?

A

initiates and maintains lactation

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21
Q

what does prolactin act on?

A

peripheral tissues with no target gland

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22
Q

what is prolactin inhibited by?

A

dopamine

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23
Q

what affect does oestrogen have on prolactin?

A

increases secretion

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24
Q

what are the 5 p’s that cause high prolactin levels?

A

pregnancy
physiological (stress)
pharmacological (drugs that block dopamine, antipsychotics)
pituitary (prolactinomas, secreting excess prolactin)
polycystic ovaries

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25
Q

what do prolactinomas cause?

A

galactorrhoea, cause milk to be secreted outside of pregnancy
infertility in men/women

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26
Q

what is diabetes insipidus caused by?

A

ADH deficiency/resistance so water is not reabsorbed by the kidney causing polydipsia and polyuria. This causes high serum osmolality and low urine osmolality (lots of water, not very concentrated)

27
Q

What is acromegaly caused by and what are the symptoms?

A

GH secreting pituitary tumour.

growth of hands and feet, coarse features, sweating, headaches, hypertension, diabetes

28
Q

when does gigantism occur?

A

if you get a pituitary tumour (acromegaly) before puberty

29
Q

what are the three zones of the adrenal cortex and what tyoe of hormones do they secrete? example of each

A

zona glomerulosa - mineralocorticoids, aldosterone
zona fasciculata - glucocorticoids, cortisol
zona reticularis - androgens, testosterone

30
Q

what makes up the adrenal gland?

A

the adrenal cortex and the medulla (secretes adrenaline)

31
Q

what is the action/mechanism of ACTH?

A

is hydrophilic and interacts with high affinity receptors on the cell surface of the zona fasciculata and zona reticularis. This leads to activation of cholesterol esterase increasing conversion of cholesterol esters to free cholesterol (stimulating the synthesis of cortisol from the free cholesterol)

32
Q

What is the receptor on the cell surface of the zona fasciculata and zona reticularis that the ACTH binds to?

A

type of melanocortin receptor or corticotrophin receptor

33
Q

what affect does cortisol have on metabolism?

A

Decrease aa uptake, decrease protein synthesis, increase proteolysis (not in liver) to release more aas.
Increase hepatic gluconeogenesis and glycogenolysis to release more glucose.
increase lipolysis in adipose to release more FAs.
Decrease peripheral uptake of glucose

34
Q

what does aldosterone do?

A

stimulates Na+ reabsorption in the kidney in exchange for K+ (increased retention of Na+)

35
Q

what happens in over/under secretion of aldosterone?

A

over secretion increases Na+ and water retention and loss of K+ causing muscle weakness and hypertension.
under secretion does the opposite and causes hypotension

36
Q

What do androgens do in men?

A

stimulate the growth and development of male genital tract and male secondary sexual characteristics.
Also have anabolic actions especially on muscle protein.

37
Q

what does oestrogen do in women?

A

Stimulate growth and development of female genital tract, breasts and female secondary characteristics.
decrease circulating cholesterol levels

38
Q

what is the structure of cortisol?

A

member of C21 steroid family. Differ from others in:
number of C’s
presence of functional groups
distribution of C=C
lipophilic so must be transported bound to membrane plasma proteins

39
Q

How is cortisol synthesised?

A

synthesised from cholesterol via progesterone

40
Q

what is the mechanism of action of cortisol?

A

can cross the plasma membrane (lipophilic) of target cells and bind to intracellular receptors. The hormone-receptor complex enters the nucleus to interact with specific regions of DNA. This changes the rate of transcription

41
Q

what is the mechanism of action of adrenaline?

A

doesnt cross cell membranes, instead binds to adrenoreceptor on the outside of the cell. a secondary messenger then affects cell activity.

42
Q

How is cortisol secretion controlled by ACTH and CRH?

A

ACTH secreted from the corticotrophs in the anterior pituitary is the main factor affecting the release of cortisol. The secretion of ACTH is under the control of CRH, a peptide produced in the hypothalamus.

43
Q

when is CRH secreted?

A

in response to physical, chemical or emotional stressors

44
Q

How is the secretion of CRH and ACTH regulated?

A

by negative feedback by glucocorticoids on the hypothalamus and pituitary

45
Q

how is adrenaline formed?

A

tyrosine to dopa to dopamine to noradrenaline to adrenaline

46
Q

what are the actions of adrenaline?

A

increases cardiac output, increased blood supply to muscles, increases mental alertness, increases glycogenolysis in muscles and liver, increases lipolysis in adipose.

47
Q

what are the clinical consequences of overproduction of adrenaline?

A 
hypertension
palpitations
sweating
anxiety
pallor
glucose intolerance
48
Q

how can pituitary tumours affect vision?

A

growing upwards can put strain on eye nerves and cause tunnel vision (cant see laterally)
bleed from this (pituitary apoplexy) can cause sudden lateral expansion of vision and acute headache.

49
Q

how can ACTH lead to increased pigmentation?

A

ACTH’s precursor is a large protein called POMC. post translational processing of POMC produces biologically active peptides including ACTH and MSH (melanocyte stimulating hormone). The MSH sequence is contained within the ACTH sequence in POMC giving ACTH some MSH activity when present in excess.

50
Q

what 4 things may cushings be caused by? which are ACTH independent/dependent?

A

pituitary tumour - ACTH dependent
adrenal tumour - ACTH independent
ectopic tumour - ACTH independent
taking steroids

51
Q

what do you diagnose first with cushings and when would you change this diagnosis?

A

syndrome

if it is not just down to taking steroids, it would be due to a tumour and would be cushings disease

52
Q

what are some signs and symptoms of cushings?

A

increased muscle proteolysis and hepatic gluconeogenesis, may lead to hyperglycaemia associated with polydipsia/uria.
Leads to thin arms and legs and increased glucose levels.
increased lipogenesis and redistribution of fat to abdomen, face and back of neck, producing characteristic moonshaped face.
mineralcorticoid effects of excess cortisol may produce hypertension due to sodium and fluid retention.
easy bruising due to effects of protein structures in the skin (thinning)

53
Q

what may Addison’s disease be due to?

A

diseases of the adrenal cortex, autoimmune destruction, reduce glucocorticoids and mineralcorticoids
disorders in pituitary or hypothalamus that lead to decreased secretion of ATCH or CRH, only affects glucocorticoids

54
Q

what are some of the non specific symptoms of Addison’s disease?

A

tiredness, extreme muscular weakness, anorexia, vague abdominal pain, weight loss and occasional decreased blood pressure due to Na and fluid depletion, postural hypotension (dizziness when standing) due to fluid depletion, hypoglycaemia.

55
Q

what is a more specific sign of Addison’s disease?

A

increased pigmentation

56
Q

why may you get hypoglycaemia in Addison’s disease?

A

decreased cortisol which decreases catabolic stimulation

57
Q

what can exacerbate symptoms and cause an Addisonian crisis? what can it lead to?

A

stress such as trauma or severe infection.

nausea, vomiting, extreme dehydration, hypotension, confusion, fever and even coma

58
Q

How do you treat an Addisonian crisis?

A

intra-venous cortisol and fluid replacement (dextrose in normal saline) to avoid death.

59
Q

What should you do in a test if you think a hormone is in excess/depleted?

A

excess - try and inhibit it

depleted - try and stimulate it

60
Q

What tests can you do to measure cortisol/ACTH levels?

A

Measure the 24hr urinary excretion for cortisol and ACTH levels
Dexamethasone suppression test - synthetic steroid that would normally suppress the secretion of ACTH therefore cortisol.
synACTHen test - synthetic analogue of ACTH given intramuscularly would normally increase plasma cortisol.

61
Q

In a dexamethasone suppression test, what would the results indicate?

A

High levels of cortisol (no suppression) - adrenal or ectopic tumour
normal levels of cortisol (no suppression but not very high levels implying some response) - pituitary tumour.

62
Q

what does a normal response to synACTHen exclude?

A

Addison’s

63
Q

Which hormones are secreted by each part of the pituitary gland and where are they produced?

A

posterior - oxytocin and ADH
anterior - FSH/LH (gonadotrophs), Prolactin (lactotrophs), Growth hormone (somatotrophs), ACTH (corticotrophs), TSH (thryotrophs)

Metabolism (3 decks)

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