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Year 1 > Endocrine homeostasis and interventions > Flashcards

Endocrine homeostasis and interventions Flashcards

1
Q

Define exocrine

A

Released into the lumen or externally out of the cell

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2
Q

Define endocrine

A

Released internally

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3
Q

What are examples of lipid soluble hormones?

A

Glycolipids and steroid hormones, Adrenal cortical hormones and gonadal hormones. They require a transport protein to travel in the blood and receptors are located intracellularly.

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4
Q

What are examples of water soluble?

A

Insulin and anterior pituitary hormones such as FSH and LH. Do not require a transport protein to move in the bloodstream and receptors are located extracellularly on the membrane

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5
Q

What is the categories of hormone?

A

Steroid hormones, amino acid derivatives and polypeptides.

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6
Q

What is the action of polypeptide hromones?

A

They are not lipid soluble and act on the surface receptors.

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7
Q

What is the structure of amino acid derivative hormones?

A

Mostly not lipid soluble and act on surface receptors.

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8
Q

What is the structure of steroid hormones?

A

Lipid soluble and receptors are located intracellularly

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9
Q

How do cholesterol derived hormones travel in the body?

A

Via globulin transport proteins. These are higher molecular weight proteins produced in the liver, similar to albumin.

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10
Q

How is hormone release controlled?

A

Neuronal stimulation, hormonal stimulation and humoural stimulation

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11
Q

What is humoural stimulation?

A

Changes in ions or nutrients stimualtes hormone release.

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12
Q

What is the optic chiasma?

A

Crossover of multiple optic nerves which is above the pituitary gland.

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13
Q

What is the sella turcica?

A

Depression in the sphenoid bone where the pituitary gland is located.

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14
Q

What is the diaphragm sellae?

A

Fold of dura mater separating the optic chiasmata from the adrenohypophysis.

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15
Q

Which portion of the pituitary gland is separated from the optic chiasma?

A

Adrenohypophysis.

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16
Q

What is the neurohypohpysis?

A

Neural tissue exxtension of the hypothalamus which only stores hormones and releases them via neural stimulation from the hypothalamus. It does not synthesise hormones.

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17
Q

Which hormones does the neurohypophysis release?

A

ADH/vasopression and oxytocin.

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18
Q

Where is ADH synthesised?

A

From the supraoptic nucleus of the hypothalamus

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19
Q

Where is oxytocin synthesised?

A

From the paraventricular nucleus of the hypothalamus.

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20
Q

What is the adrenohypophysis?

A

Endocrine gland which communicates with the hypothalamus via the hypophyseal portal system to synthesise and release hormones.

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21
Q

Hypothalamo-pituitary axis

A

Communication between the hypothalamus and the anterior or posterior portion of the pituitary gland

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22
Q

Hypothalamo-adrenohypophysis axis

A

Release of GnRH, GRH (Growth releasing hormone), PRH (Pro-lactin releasing hormone), PIF (Prolactin inhibiting factor) and (TRH) Thyroid releasing hormone.

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23
Q

What is the function of the hypothalamus?

A

Endocrine and hormonal regulation, autonomic nervous system regulation, temperature, feeding.

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24
Q

What is the role of the anterior pituitary?

A

Synthesise and release thyroid stimulating hormone, FSH, LH, growth hormone and prolactin.

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25
Q

What reduces the release of growth hormone?

A

Somatostatin produced by the hypothalamus which acts on adrenohypophysis.

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26
Q

What reduces the release of prolactin?

A

Prolactin Inhibitng factor which is dopamine.

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27
Q

What is adrenal insufficency?

A

Adrenal galnd does not produce enough of either or all mineralcorticoid aldosterone, glucocorticoid cortisol or androgens. Causes hypotension (low aldosterone), low libido (low androgen), weight loss (low cortisol), acidosis and metabolic acidosis and hyperkalemia (low alosterone)

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28
Q

What is adrenal insufficency?

A

Adrenal galnd does not produce enough of either or all mineralcorticoid aldosterone, glucocorticoid cortisol or androgens. Causes hypotension (low aldosterone), low libido (low androgen), weight loss (low cortisol), acidosis and metabolic acidosis and hyperkalemia (low alosterone)

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29
Q

What is the effect of aldosterone?

A

Regulates Na+ and K+ levels by causing efflux of excess K+ into the tubal lumen and increasing Na+ retention for H+ excretion into the urine and water reabsorption. When it is low, hyperkalemia, metabolic acidosis due to high H+ and hypotension occur.

30
Q

What is primary adrenal insufficeincy?

A

Also known as Addison’s disease. Autoimmune disease where there is destruction of the adrenal gland. It results in hyperpigmentation due to levels of ACTH increasing from the pituitary gland to stimulate the poor secretion of the adrenal cortex.

31
Q

What is proopiomelanocortin?

A

A molecule derived from ACTH along with melanocyte stimulating hormone. When ACTH levels rise in Addision’s disease, due to adrenal gland destruction, it increases production of these pigmenting molecules.

32
Q

What is secondary adrenal insufficeincy?
.

A

Low levels of ACTH is released from the pituitary gland due to tumour which reduces production of adrenal cortex hromones

33
Q

What is tertiary adrenal insufficeincy?

A

Low levels of CRH is released from the hypothalamus due to damage/tumour to the hypothalamus.

34
Q

What is dynamic function testing?

A

Testing the hormonal response in the body through injection with a hormone.

35
Q

What is the synacthen stimulation test?

A

Injection with synthetic ACTH to assess cortisol production in Addison’s disease.

36
Q

What is hypercortisolemia?

A

High levels of cortisol causing protein depletin that results in muscle wasting and poor wound healing alongisde immune suppression, inhibition of osteoblasts so bone resoprtion and osteoporosism, weight gain, hyperlipidemia and hyperglycemia.

37
Q

What is Cushing’s syndrome?

A

Collection of symptoms caused by hypercortisolemia due to pituitary gland tumour, ACTH secreting tumour, adrenal tumour or long term glucocorticoid use.

38
Q

What is Cushing’s disease?

A

Endogenous-High levels of ACTH is released from the pituitary gland which drives hypercortisolemia due to pituitary gland tumour or ACTH secreting tumour.

39
Q

What are causes of Cushing’s syndrome?

A

Caused by high cortisol levels. Adrenal or pituitary tumour or exogenous cause via long term use of glucocorticoid medications for immune suppression.

40
Q

What is dynamic pituitary testing?

A

Injection with exogenous steroid dexametasone. This should cause cortisol to increase to suppress the steroid. If there is dysfunction with cortisol production, the levels of dexamethasone will not be suppressed.

41
Q

Hypothalamo-pituitary thyroid axis?

A

Hypothalamus releases TRH to cause pituitary to release TSH and act on TSH receptors thyroid gland follicular cells via capillary blood supply. This causes Iodine trapping and synthesis of thyroglobulin protein. Both together forms T3 and T4 hormones which bind to thyroxin globulin protein to act on the body’s receptors.

42
Q

What is the funcitonal unit of the thyroid gland?

A

Follicular cell with internal cavity of colloid.

43
Q

What are the sympotms of hyperthyroidism?

A

Weight loss, tremor, heat intolerance, increased appetite.

44
Q

What are the signs of hyperthyroidism?

A

Tremor, tacycharida, goitre and examphalmos.

45
Q

What is exophthalmos?

A

Bulging eyes due to hyperparathyroidism

46
Q

What is goitre?

A

Swelling of thyroid gland due to hyperparathyroidism.

47
Q

What is hypothyroidism?

A

Low production of T3 and T4 which causes periorbital oedema, coarse, sparse hair and eyebrows, puffy face and dry skin.

48
Q

What is primary hypothyroidism?

A

Issue with the thyroid gland due to autoimmune disease. Low levels of thyroid hormones but high levels of TSH and TRH.

49
Q

What is secondary hypothyroidism?

A

Issue with the pituitary gland that means there is low release of TSH and therefore T4. TRH is high.

50
Q

What is pituitary hyperthyroidism?

A

Excess production of TSH that causes high production of T4 due to pituitary tumour or TSH secreting tumour. Low production of TRH.

51
Q

What is the hypothalamo-pituituary gonadal axis?

A

Responisble for body development and maintenance of reproductive organs via production of LH and FSH from the anterior pituitary gland.

52
Q

What is primary hypogonadism?

A

Autoimmune disease or tumour affecting the ovaries or testes which decreases oestrogen/testosterone production.

53
Q

What is secondary hypogonadism?

A

Autoimmune disease or tumour affecting the pituitary gland resulting in decreased production of LH, FSH and oestrogen/testosterone.

54
Q

What is the effect of anabolic steroids on sex hormones?

A

Suppresses release of FSH and LH from the pituitary gland so it decreases. Levels of oestrogen/testosterone remain high.

55
Q

What is the effect of pulsatile infusion of GnRH on sex hormones?

A

Increases levels of FSH, LH and oestrogen/testosterone.

56
Q

What is the effect of continuous infusion of GnRH on sex hormones?

A

Decreases levels of FSH, LH and oestrogen/testosterone due to desensitisation of the HPG axis.

57
Q

How does dopaine act on prolactin release?

A

It is a prolactin inhibitnig factor produced by the hypothalamus which reduces prolactin release from the pituitary gland.

58
Q

How can prolactin be increased?

A

Via metoclopromide which is a dopamine antagonist

59
Q

How can prolactin be inhibited?

A

Bromocriptine which is a dopamine agonist.

60
Q

How is growth hromone released?

A

GHRH is released by the hypothalamus to act on the pituitary gland to release GH (Growth hormone). It travels in the bloodstream and acts on the liver to produce Insulin-growth factor/IGF-1 which will cause protein synthesis and utilisation of free fatty acids and bone growth.

61
Q

What is the effect of growth hormone?

A

Increases levels of insulin and glucose.

62
Q

What is the effect of IGF-1?

A

Protein synthesis, FFA use and decreases insulin release at high levels of IGF-1 and increases insulin sensitivity.

63
Q

What is gigantism?

A

Tumour in the pituitary gland leads to excess production of growth hormone.

64
Q

What is somatostatin’s role?

A

Suppress release of growth homrone from the pituitary gland. Somatostatin is released from hypothalamus.

65
Q

What is ocreotide?

A

Somatostatin mimetic to reduce growth hormone release for those with gigantism.

66
Q

What hormones are released from the posterior pituitary gland?

A

Vasopressin/ADH and oxytocin.

67
Q

What is diabetes insipidus?

A

Diabetes symptoms with excessive thirst due to issues with ADH release that leads to excess water loss in the urine.

68
Q

What is hypertonicity?

A

High osmotic pressure acts on osmoreceptors on the hypothalamus to increase thirst and ADH releasefrom the neurophysis.

69
Q

What is hypervolemia?

A

High volume of extracellular fluid activates baroreceptors and increases angiotesin II production which acts on the hypothalamus to increase thirst and ADH release from the neurophysis pituitary gland.

70
Q

Where is oxytocin released from?

A

The hypothalamus and acts on smooth muscle to induce uterine contractions and release of milk present in the breast already.

Year 1 (191 decks)

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