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Metabolism > Pituitary and adrenal disorders > Flashcards

Pituitary and adrenal disorders Flashcards

0
Q

What is the function of TSH?

A

-Activates follicular cells to produce and secrete T3 and T4

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1
Q

What are the 5 hormones produced in the pituitary?

A
  • Thyroid Stimulating Hormone (TSH)
  • Adrenocorticotropic Hormome (ACTH)
  • Growth Hormone (GH)
  • Leutinizing Hormone (LH)/ Folicular Stimulating hormone (FSH)
  • Prolactin
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2
Q

What stimulates TSH release?

A

-Thyrotropin Releasing Hormone is released into the HPA portal and stimulates the thyrotrophic cells in the pituitary to secrete TSH

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3
Q

What is the function of ACTH?

A

-Stimulates production and release of cortisol from the adrenal cortex

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4
Q

What controls ACTH release?

A

-Corticotropin releasing hormone from the hypothalamus released into the HPA portal and stimulates corticotrophic cells of the pituitary

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5
Q

What is the function of GH?

A
  • Important in growth and metabolism

- Acts on all tissues

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6
Q

What stimulates GH release?

A

-GH releasing hormone from the hypothalamus released into the HPA portal stimulates somatotrophs in the pituitary

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7
Q

What type of rhythm is GH release?

A

-Pulsatile-> most during sleep

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8
Q

What are the functions of LH and FSH?

A
  • LH in men drives testosterone secretion
  • FSH in men drives sperm production
  • LH in women causes oestrogen release and ooctye release
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9
Q

What controls the release of LH and FSH?

A

-Gonadotropin releasing hormone from the hypothalamus into HPA portal stimulates gonadotrophin cells in pituitary

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10
Q

What is the function of prolactin?

A

-Initiates and maintains lactation

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11
Q

How is prolactin secretion controlled?

A

-Through dopamine release from the hypothalamus into the HPA portal by inhibitory control (increase in dopamine=decrease in prolactin)

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12
Q

What can high levels of prolactin cause in women?

A

-Disturbances in lactation and the menstrual cycle

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13
Q

What is the HPA portal?

A

-A vessel connecting two capillary beds located in the hypothalamus and the pituitary

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14
Q

What is the purpose of the HPA portal?

A
  • Allows decreased release of hormones as they are not diluted by the whole circulation
  • Larger effect with smaller secretions
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15
Q

What are the adrenal glands?

A

-A pair of multifunctional endocrine glands which cap the upper poles of the kidneys and lie against the diaphragm

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16
Q

What are the two main regions of the adrenal glands?

A
  • Cortex

- Medulla

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17
Q

What three zones is the adrenal cortex split into?

A
  • Zona glomerulosa
  • Zona Fasciculata
  • Zona Reticularis
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18
Q

What is the function of the Zona glomerulosa? Give an example of secretion

A
  • To secrete mineralocorticoids to regulate Na+ and K+ levels
  • Aldosterone
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19
Q

What does the zona fasciculata produce?

A
  • Glucocorticoids

- eg Cortisol

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20
Q

What does the Zona reticularis secrete?

A

-Sex hormones (and some glucocorticoids)

eg Androgens

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21
Q

What does the adrenal medulla secrete?

A

-Adrenaline

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22
Q

What is adrenaline synthesised from?

A

-Tyrosine

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23
Q

What are the two general functions of adrenaline?

A

-Acts as a hormone and neurotransmitter

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24
Q

What are the general effects of adrenaline?

Hint: think fight or flight

A
  • Increase heart rate
  • Increase respiratory rate
  • Vasoconstriction
  • Stimulates glycogenolysis in liver and muscle
  • Triggers lipolysis in adipose tissue
  • Increases blood supply to muscle
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25
Q

What receptors does adrenaline act through?

A

-Adrenergic receptors

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26
Q

What are the comorbidities associated with overproduction of adrenaline?

A
  • Hypertension
  • Anxiety
  • Palpitations
  • Pallor
  • Sweating
  • Glucose intolerance
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27
Q

What are the 5 classes of steroid hormones?

A
  • Glucocorticoids
  • Mineralocorticoids
  • Androgens
  • Oestrogens
  • Progestogens
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28
Q

Where are steroid hormones produced?

A
  • Adrenal glands

- Gonads

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29
Q

What is the precursor of steroid hormones?

A

-Cholesterol

30
Q

What type of solubility are steroid hormones and what does this allow?

A
  • Lipid-soluble

- Passage through cell membranes

31
Q

How are steroid hormones transported?

A

-Bound to specific carrier proteins in the blood to increase solubility

32
Q

Why can cross-talk occur between steroid hormones?

A

-They are all structurally similar allowing low affinity activation of each others receptors

33
Q

What is the function of aldosterone?

A

-Stimulates Na+ reabsorption from kidney tubules in exchange for K+

34
Q

WHat are the consequences of overproduction of aldosterone?

A
  • Increased Na+ causing water retention

- Increased loss of K+ causing hypertension and muscle weakness

35
Q

What is the consequence of undersecretion of aldosterone?

A

-Hypotension

36
Q

What are the functions of androgens in males?

A
  • Development of male genital tract
  • Development of male secondary characteristics including height, body shape, facial and body hair and lower voice pitch
  • Anabolic effects on muscle protein
37
Q

What does oversecretion of androgens cause in women?

A

-Hair growth, acne and menstrual problems

38
Q

What does oestrogen do in women?

A
  • Stimulates growth of female genital tract and breasts
  • Stimulates secondary characteristics including broad hips, accumulation of fat in breast and buttocks and body hair distribution
39
Q

What is the mechanism of control of cortisol secretion by CRH and ACTH?

A
  • Negative feedback
  • Hyothalamus secretes CRH in response to physical, chemical or emotional stressors
  • Induces ACTH release from pituitary
  • Stimulates cortisol production and release which negatively feedsback on both the pituitary and hypothalamus
40
Q

What type of hormone is ACTH?

A

-Single chain polypeptide

41
Q

What is the precursor to ACTH?

A

-Pre-opiomelanocortin (POMC)

42
Q

How is ACTH produced from POMC?

A

-Post-translational processing by enzymatic cleavage produces ACTH, a-melanocyte stimulating hormones and endorphins

43
Q

What type of rhythm is ACTH release?

A

-Pulses which follow a circadian rhythm

44
Q

How does ACTH exert its action on the adrenal gland?

A
  • ACTH is hydrophilic so cannot cross the PM and interacts with high affinity receptors located on the cells surface at the zona fasciculata and zona reticularis
  • This activates secondary messanger cAMP which leads to a cascade resulting in increased cortisol production
45
Q

Why can oversecretion of ACTH lead to increased pigmentation in areas of the body?

A
  • Overproduction of ACTH also leads to an overproduction of a-melanocyte stimulating hormone due to the two hormones sharing a common precursor
  • Increased a-msh stimulates melanocytes resulting in a rise in melanin leading to hyperpigmentation
46
Q

How is cortisol transported in the body?

A
  • Lipid-soluble steroid hormone so must be bound to a specific protein carrier
  • Major binding protein is corticosteroid-binding globulin
  • Carries 90% of plasma cortisol
  • Remaining 10% is free and biologically active
47
Q

What is the mechanism of action of cortisol?

A

-Lipid soluble so can cross pm
-Binds to cytosolic receptor (bound to hsp for stabilty)
-Dissociation and translocation to nucleus
or
-Binds to cortisol receptor in nucleus
-Receptor:Hormone complex binds to DNA and initiates transcription changing cellular activity

48
Q

-When is cortisol secreted?

A

-When the body is in a catabolic, starvation and stressed state

49
Q

What are cortisol’s major effects on metabolism?

A
  • Decrease a’a uptake and protein synthesis and increase proteolysis
  • Increase glycogenolysis and gluconeogenesis
  • Increase lipolysis in adipose tissue
  • Decrease peripheral uptake of glucose
50
Q

What are the three main causes of oversecretion of cortsol?

A
  • Increased adrenal cortex activity due to tumour in the adrenal gland (adenoma)
  • Increased ACTH production due to pituitary adenoma resulting in increased cortisol stimulation
  • Increased secretion of ACTH by an ectopic tumour (lung tumour most common)
51
Q

What is the clinical name for oversecretion of cortisol?

A
  • Cushing’s Disease

- Cushing’s syndrome

52
Q

What is the difference between cushing’s disease and suching’s syndrome?

A

-Cushings disease is a disorder of the pituitary (pituitary adenoma)
-Cushing’s syndrome is disorder at the level of the adrenal gland
(adrenal adenoma)

53
Q

What are the signs and symptoms of cushing’s

A
  • Increased muscle proteolysis leading to wastage of proximal muscles
  • Increased hepatic gluconeogenesis which may lead to hyperglycaemia, polydipsia and polyuria (steroid diabetes)
  • Increased lipogenesis in central adipose tissue causing deposition of fat in the abdomen, neck (buffalo hump) and face (moon face)
  • Purple striae on lower abdomen, upper arms and thighs
  • Increased susceptibility to bacterial infections and acne
  • Back pain and collapse of ribs
  • Hypertension
54
Q

Why do purple striae appear in cushings?

A

-Due to the catabolic effects of protein structures in the skin which leads to easy bruising due to thinning of skin and subcutaneous tissue

55
Q

Why are people with cushings susceptible to bacterial infection and acne?

A

-Cortisol has immunosuppressive, anti-inflammatory and anti-allergc effects

56
Q

Why can cushings cause back pain and collapse of the ribs?

A

-Cortisol can lead to osteoporosis due to disturbances in Ca2+ metabolism and loss of bone matrix protein

57
Q

Why can cushings lead to hypertension?

A

-Cross talk leads to mineralocorticoid effects causing Na+ and fluid retention

58
Q

What is another cause of the signs and symptoms of cushings?

A

-Long-term glucocorticoid treatment for chronic inflammatory conditions

59
Q

What are the two main causes of undersecretion of cortisol?

A
  • Hypoactivity of the adrenal cortex due to:
  • > diseases of the adrenal cortex causing a reduction in glucocorticoid production
  • > Disorders of the pituitary/hypothalamus that leads to a decreased production of ACTH
60
Q

What is addisons disease?

A

-Chronic autoimmune destruction of the adrenal gland

61
Q

How is addisons disease characterised?

A
  • Insidious onset with initial non-specific symptoms of tiredness, extreme muscular weakness, anorexia and weightloss, abdominal pain
  • Dehydration
  • Hyperpigmentation
  • Hypotension
  • Hypoglycaemic episodes
62
Q

What is the cause of dehydration in addisons disease?

A

-Mineralocorticoid disruption due to destruction of adrenal cortex

63
Q

What causes hyperpigmentation in addisons disease?

A
  • Decreased cortisol production due to destruction of adrenal cortex results in a high increased in ACTH production to try and stimulate cortisol production and a simultaneous increase of a-msh due to them sharing the common precursor POMC
  • a-msh stimulated melanocytes to produce melanin resulting in hyperpigmentation
64
Q

Why does addisons disease result in hypotension?

A
  • Decreased aldosterone secretion means that Na+ is not reabsorbed meaning that water remains in the kidney tubules due to the change in osmotic pressure
  • More water is excreted causing a depleted plasma volume causing hypotension
65
Q

Why does addisons cause hypoglycaemic episodes, especially during fasting?

A

-Decrease in cortisol means that glycogenolysis and gluconeogenesis are not stimulated in the liver leading to hypoglycaemia

66
Q

What can precipitate an addisonian crisis?

A

-Trauma or stess

67
Q

What are the further symptoms of addisonian crisis?

A
  • Nausea
  • Vomiting
  • Confusion
  • Dehydration
  • Hypotension
  • Fever
  • Coma
68
Q

How is an addisonian crisis treated?

A

-Intravenous cortisol and fluid replacement

69
Q

Name the adrenal cortisol function tests

A
  • Measurement of plasma cortisol/ACTH levels
  • 24hr urinary excretion of cortisol breakdown products and cortisol itself
  • Dexamethasome supression test
  • ACTH stimulatory tests
70
Q

What is a dexamethasone suppression test?

A
  • Dexamethasone is a potent synthetic steroid
  • Oral ingestion should suppress the secretion of ACTH and thus cortisol as it will suppress pituitary secretion of ACTH through negative feedback
71
Q

How does dexamethasone distinguish between cushings disease and cushings syndrome/ectopic tumour?

A
  • Dexamethasone suppression of cortisol by >50% is characteristic of cushing’s disease as although the disease pituitary is insensitive to cortisol negative feedback, it remains sensitive to the potent synthetic steroid
  • If suppression of cortisol does not occur then there is a problem at the level of the adrenal gland or ectopic ATCH as neither of these mechanisms are under control of negative feedback so levels of cortisol will not be decreased by an increase in glucocorticoid
72
Q

How do ACTH stimulatory tests exclude addisons disease from the diagnosis?

A
  • Administration of synacthen (synthetic analougue of ATCH) intramuscularly would normally increase cortisol by >200nm/L
  • A normal response to synacthen would exclude addisons disease due to the fact that synacthen would be ineffective on the destroyed adrenal gland
73
Q

How can cortisol have weak mineralocorticoid and androgen effects?

A

-Steroid hormone and steroid receptor homology -> steroid hormone receptors share sequence homology in the hormone binding region. The sequence homology between the hormones allows cortisol to bind to the hormone binding region of mineralocorticoid and androgen receptors with low affinity resulting in mineralocorticoid and androgen effects

Metabolism (14 decks)

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