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ENDOCRINE > A. ADRENAL GLAND AND HORMONES > Flashcards

A. ADRENAL GLAND AND HORMONES Flashcards

1
Q

how many adrenal glands do we have

A

2 - sit on top of kidneys

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2
Q

2 main parts of adrenal gland

A
  • outer cortex
  • inner medulla
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3
Q

where are catecholamines released from

A

adrenal medulla

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4
Q

examples of catecholamines

A
  • adrenaline (fight or flight - speed up heart rate)
  • noradrenaline
  • dopamine
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5
Q

where are adrenal steroid hormones released from

A

adrenal cortex

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6
Q

examples of adrenal steroid hormones

A
  • glucocorticoids (gluco = involved in glucose metabolism, corticoids = cortex) eg - cortisol
  • mineralocorticoids (mineral = electrolytes) eg - aldosterone
  • weak androgens (like male sex hormones but weaker) eg - dehydroepiandrosterone and androstenedione
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7
Q

what is the name of the endocrine axis relating to adrenal gland

A

hypothalamus-pituitary-adrenal axis

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8
Q

what hormone is the central regulator of the hypothalamic-pituitary-adrenal axis

A

CRH = corticotropin-releasing hormone released by hypothalamus (+ve)

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9
Q

what hormone is the released by anterior pituitary in HPA axis

A

ACTH = Adrenocorticotropic hormone (+ve)

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10
Q

what activates the feedback loop in the HPA axis and reduce cortisol production

A

exogenous glucocorticoids

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11
Q

what is the only adrenal steroid hormone involved in feedback control

A

glucocorticoids ie - cortisol

(androgens and aldosterone regulated by ACTH (and other unknown factors), but no feedback on CRH/ACTH)

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12
Q

what is aldosterone secretion stimulated by

A
  • increased plasma potassium levels and angiotensin II (largely independent of ACTH)
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13
Q

what is the renin-angiotensin-aldosterone system (RAAs)

A
  • critical regulator of blood volume, electrolyte balance and systemic vascular resistance
  • aldosterone is a part of the RAAs
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14
Q

what effects does aldosterone have on the kidney

A
  • stimulates reabsorption of sodium and water into blood from filtrate causing an increase in blood volume
  • causes increased secretion (excretion) of potassium during formation of urine (lost in urine)
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15
Q

what effect does angiotensin II have on blood vessels

A

vasoconstriction

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16
Q

main effects of activation of RAAs

A
  • increases vascular resistance
  • increased blood volume
    = increased BP
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17
Q

where does aldosterone principally act

A
  • DCT and collecting duct of kidney
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18
Q

what is Conn’s syndrome

A
  • excess aldosterone causing hypokalaemia and hypertension
  • due to adrenal tumour or primary hyperaldosteronism
  • accounts for 1% of all causes of hypertension
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19
Q

treatment of Conn’s syndrome

A
  • surgery to remove tumour
  • aldosterone receptor antagonists (eg - spironolactone)
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20
Q

what % of all androgenic activity does DHEA and androstenedione account for in a woman’s body

A
  • 50% (other 50% from testosterone)
  • axillary/pubic hair growth and libido
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21
Q

what % of all androgenic activity does DHEA and androstenedione account for in a man’s body

A
  • 10%: insignificant contribution due to more potent testosterone
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22
Q

what type of corticoid is cortisol

A

glucocorticoid AND mineralocorticoid

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23
Q

what stimulates increased cortisol production

A

stress:
emotional - anxiety, fear
physiological - pain, fever, hypoglycaemia, injury, surgery etc

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24
Q

what causes endogenous circadian rhythms

A

suprachiasmatic nucleus in the hypothalamus

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25
Q

how does cortisol plasma levels vary with typical diurnal rhythm

A
  • peak in early morning
  • trough in late evening (tired)
  • associated with sleep-wake cycle
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26
Q

what do exogenous steroids do

A
  • we need to limit suppressive action of steroids on cortisol secretion by mimicking normal cortisol hormone levels:

as a single dose in morning as this is when levels are high (eg - oral in asthma)

high dose AM, low dose PM (Addison’s disease)

27
Q

what are the 3 main actions of cortisol

A
  1. metabolic effects
  2. anti-inflammatory/immunosuppressive effects
  3. role in adaptation to stress
28
Q

what metabolic effect does cortisol have

A
  • counter-regulatory to insulin
  • build up of glycogen stores which is a readily source of glucose due to increased amino acids and FFA and glycerol
29
Q

effects of cortisol on muscle

A
  • decreases glucose uptake (via insulin-mediated GLUT-4)
  • increases protein breakdown
  • decreases protein synthesis
30
Q

effects of cortisol on adipose tissue

A
  • decreases glucose uptake (via insulin-mediated GLUT-4)
  • increases lipolysis
  • decreases lipogenesis
31
Q

effects of cortisol on liver

A
  • increases gluconeogenesis
  • increases glycogen synthesis (easily broken down to glucose ie if stress lasts longer)
32
Q

when does cortisol have anti-inflammatory/immunosuppressive effects

A
  • at high physiological levels of natural glucocorticoids cortisol
33
Q

how does cortisol have anti-inflammatory effects

A
  • stimulates production of annexin 1 (lipocortin 1)
  • this inhibits PLA₂ which is an enzyme that generates arachidonic acid - the precursor for prostanoids and leukotrienes (therefore decreased inflammatory mediators)
  • decrease number and activation of T-lymphocytes
  • decrease production of cytokines (interleukins, TNF-alpha)
  • stabilises lysosomes
  • decrease NO production
    etc…
34
Q

when would glucocorticoid analogues (prednisolone, dexamethasone) be used

A
  • anti-inflammatory: asthma, UC, rheumatoid arthritis, skin conditions, rhinitis etc
  • immunosuppression: organ transplantation
  • replacement therapy: Addison’s disease
  • pre-term labour to enhance foetal lung maturation
35
Q

what is stress

A
  • a state of threatened homeostasis or disharmony
  • body responds by a complex repertoire of physiological and behavioural mechanisms to re-establish homeostasis
36
Q

what is a stressor

A
  • a stimulus that induces state of stress
  • psychological/emotional - anxiety, fear
  • physiological - pain, fever, hypoglycaemia, injury, heavy exercise etc
37
Q

physiological mechanisms to re-establish homeostasis

A

re-direction of energy
- increased CV tone, ventilation
- increased glucose availability
- decreased energy-consuming activities like digestion and reproduction as you are dealing with stress

38
Q

behavioural mechanisms to re-establish homeostasis

A
  • increased arousal, alertness, vigilance
39
Q

what hormones are involved in the integrated stress response system

A
  • SNS and adrenaline
  • CRH-ACTH-cortisol
    *these 2 are the main ones
  • RAAs, AVP, GH (when stressed, thyroid hormones decreased)
40
Q

how does the SNS and adrenaline react to stress

A
  • increase cardiac output and ventilation
  • divert blood flow to muscles and heart
  • mobilisation of glycogen and fat stores
  • fight or flight
    *need cortisol for this to happen (permissive action of cortisol)
41
Q

how does cortisol react to stress

A
  • breaks down proteins and fats
  • shift from protein and fat stores in favour of expanded glycogen stores (in case stress situation is prolonged) and plasma glucose availability
  • amino acids available for tissue repair if physical damage
  • in stress-activated immune responses (acute infection) cortisol protects body against damage from potential over-activation of immune defence mechanisms (anti-inflammatory/immunosuppressive effect)
  • cortisol is a good hormone normally as it’s for everyday functioning
42
Q

what does prolonged elevated cortisol levels lead to (chronic)

A
  • muscle wasting (catabolic effect on muscle)
  • hyperglycaemia
  • GI ulcers (decreased prostaglandins so decreased mucus and increased acid production)
  • impaired immune response (due to anti-inflam and immunosuppressive effects of high cortisol)
43
Q

what syndrome can excess glucocorticoid cause

A

Cushing’s syndrome

44
Q

what disease can adrenal insufficiency cause

A

Addison’s disease

45
Q

what is the main cause of Cushing’s syndrome

A
  • exogenous glucocorticoid: high-dose, long-term use of glucocorticoids
  • most common cause = excessive steroid medication use
46
Q

primary defect causing Cushing’s syndrome (endocrine cause)

A
  • adrenal tumour: autonomous secretion of cortisol
  • ACTH and CRH levels are low due to -ve feedback from high cortisol levels
47
Q

what is the most common cause of Cushing’s syndrome - secondary (endocrine cause)

A
  • Cushing’s disease: ACTH-secreting pituitary tumour in anterior pituitary
  • excessive ACTH production
  • ACTH levels remain high as the tumour cells have impaired responsiveness to negative feedback from high cortisol levels

*syndrome = excess but can be from anywhere

48
Q

what is another secondary defect causing Cushing’s syndrome (endocrine cause)

A
  • ectopic ACTH-producing tumour (small cell lung/pancreatic/ovarian tumour etc)
  • ectopic tumour cells lack feedback control
  • we see a decrease in CRH and ACTH when lots of cortisol activates -ve feedback
49
Q

what signs and symptoms of Cushing’s syndrome does altered fat deposition cause

A
  • truncal obesity
  • ‘moon’ face
  • dorsal fat pad ‘buffalo hump’
50
Q

what signs and symptoms of Cushing’s syndrome does breakdown of protein, muscle wasting, loss of collagen cause

A
  • thin skin which is easily bruised
  • muscle weakness (hypokalaemia also)
  • poor wound healing
  • skinny arms and legs
  • purple striae (stretch marks with truncal obesity)
51
Q

what signs and symptoms of Cushing’s syndrome does immunosuppression cause

A
  • skin infections
52
Q

what signs and symptoms of Cushing’s syndrome does mental changes cause

A
  • sleep disturbances
  • depression
53
Q

what signs and symptoms of Cushing’s syndrome does altered bone metabolism cause

A
  • hypertension due to excess mineralocorticoid activity and sodium and water retention
  • diabetes due to hyperglycaemia and insulin resistance
  • osteoporosis
54
Q

treatment of Cushing’s syndrome

A
  1. localisation of tumours (anterior pituitary - MRI, adrenal - abdominal CT/MRI scan, bronchial tumour - chest x-ray, ACTH-secreting tumours - octrescan)
  2. surgery or radiotherapy
  3. drugs to inhibit steroidogenesis eg: metyrapone, trilostane

Pre-operative (preparation for surgery) OR palliative (if can’t remove tumour, improve QoL)
(rarely used for long-term therapy)

55
Q

what causes primary adrenal insufficiency in Addison’s disease

A
  • rare, chronic condition due to failure of adrenal glands (adrenal cortex)
  • gradual destruction of adrenal tissue (often autoimmune or by HIV or TB)

*main cause is autoimmune

56
Q

what are the levels of the 3 adrenal hormones in Addison’s disease

A
  • low aldosterone
  • low cortisol
  • low androgens
  • elevated ACTH as -ve feedback not activated (CRH levels also high)
57
Q

symptoms of Addison’s disease

A
  • postural hypotension
  • muscle weakness
  • fatigue
  • lethargy
  • hyponatraemia
  • hyperkalaemia
  • increased pigmentation
  • loss of appetite/unintentional weight loss
  • nausea, vomiting

*due to loss of glucocorticoid/mineralocorticoid activity

58
Q

what causes increased pigmentation in Addison’s disease

A
  • increased melanin content in skin
  • increased ACTH release results in increased melanocyte-stimulating hormone levels
  • hyperpigmentation seen in skin creases (knuckles and knees), old scars, gums and inside of the cheek
59
Q

what can you test for adrenal failure

A
  • decreased cortisol and increased ACTH levels
  • synacthen test (stimulation test): give ACTH, cortisol should go up
  • adrenal auto-antibodies (if suspect auto-immune disease)
60
Q

treatment for adrenal failure

A
  • life-long hormone replacement
  • glucocorticoid: hydrocortisone (20mg AM, 10mg PM to mimic diurnal variation) and
    mineralocorticoid: fludrocortisone (daily)

*higher doses of glucocorticoids are given during times of illness or major stress (e.g. surgery)

61
Q

what causes secondary adrenal insufficiency in Addison’s disease

A
  • lack of ACTH production (tumour, damage to pituitary)
  • low cortisol, with normal aldosterone levels (RAAs intact)
  • or due to excessive exogenous glucocorticoid use (secondary adrenal suppression) as activates -ve feedback loop and we get a decrease in ACTH
  • often in patients with long-term, high-dose glucocorticoid use
  • suppression of ACTH levels leading to suppression &
    atrophy of adrenal cortex (so low endogenous cortisol)
62
Q

what can excess exogenous glucocorticoids lead to

A
  • cushingoid appearance: truncal obesity, dorsocervical fat pads, striae and secondary adrenal suppression
63
Q

what happens when there is a sudden withdrawal of exogenous steroid

A
  • symptoms of acute adrenal insufficiency: fatigue, nausea, vomiting, anorexia, weight loss, hypotension, myalgia
  • due to lack of endogenous cortisol activity
  • looks like Addison’s disease
64
Q

what is classified as an adrenal crisis

A
  • acute adrenal insufficiency & expressed when patient is under stress (e.g. infection) as not making enough cortisol
  • leads to hypotension, circulatory failure, potentially death
  • medical emergency
  • urgent treatment: i.v. fluids, hydrocortisone to replace cortisol (i.v, then oral)

ENDOCRINE (17 decks)

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