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GERR > Lecture 21 + 22: Adrenal Glands > Flashcards

Lecture 21 + 22: Adrenal Glands Flashcards

1
Q

what tissues make up the adrenal gland

A 
adrenal cortex (outer) 
adrenal medulla (inner)
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2
Q

what category of hormones does each tissue of the adrenal gland produce

A

cortex - corticosteroids

medulla - catecholamines

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3
Q

name the three Zona that make up the cortex and the type of hormones they secrete

A
  • glomerulosa (outer) = mineralocorticoids
  • fasciculata (middle) = glucocorticoids
  • reticularis (inner) = adrenal androgens
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4
Q

why do the three Zona of the adrenal cortex secrete different types of hormones

A

each zone possesses different enzymes involved in the manufacture of these hormones

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5
Q

what are all corticosteroids formed from

A

cholesterol

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6
Q

what hormone stimulates the conversion of cholesterol to pregnenolone

A

ACTH (adrenocorticotrophic hormone)

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7
Q

what is the rate limiting step in synthesis of steroid hormones

A

conversion of cholesterol to pregnenolone

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8
Q

what peptide hormone is necessary for synthesis of aldosterone

A

Angiotensin 2 - activates aldosterone synthase enzyme

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9
Q

where are most steroid hormone receptors found

A

inside cell within cytoplasm and within nucleus

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10
Q

what type of effects do steroid hormones have when binding to receptors inside cell

A

genomic effects - either activate or inhibit transcriptase in DNA

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11
Q

what makes the adrenal medulla different from the normal sympathetic nervous pathway

A
  • normal SNS –> preganglionic neuron extending from spinal cord and terminating on postganglionic neuron which then goes on to innervate organs and tissues
  • adrenal medulla –> no axon accompanying postganglionic cell body so ganglionic cell bodies within adrenal medulla release chemical transmitter directly into circulation upon appropriate stimulation
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12
Q

what is the principal output of the adrenal medulla

A

adrenaline/epinephrine

also secretes some noradrenaline/norepinephrine

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13
Q

where are most receptors for catecholamines found and why

A

on cell surface membrane because catecholamines are hydrophilic

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14
Q

what effect do catecholamines have on the cell they bind to

A

non-genomic effect –> cause alterations in proteins; enzymes or ion channels –> leads to target cell response

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15
Q

what is the principal stimulus for cortisol secretion

A

stress e.g. physical, emotional, chemical

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16
Q

outline the process by which cortisol is released

A
  • stress acts on hypothalamus
  • CRH (corticotropin releasing hormone) released
  • stimulates corticotrophins in ant. pit. to secrete ACTH
  • ACTH stimulates zona fasciculata to secrete cortisol
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17
Q

what is the second stimulus for cortisol secretion

A

diurnal rhythm for cortisol secretion

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18
Q

when are ACTH levels at their lowest

A

at night when sleeping appx 1-3am

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19
Q

when are peak ACTH levels

A

in the morning when you wake up appx 7-9am

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20
Q

what time would you measure Cortisol levels if suspecting excess cortisol

A

at night between 12-3am –> if levels are high (when should be low) the excess is likely

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21
Q

when is the pulsatile secretion of cortisol also inversed

A

in patients who might work night shifts –> awake sleep cycle is inversed

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22
Q

name a binding protein for cortisol in the blood

A

transcortin

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23
Q

describe the binding of cortisol and transcortin in the blood in normal cortisol levels

A
  • most cortisol in blood (85%) bound to transcortin
  • transcortin almost fully saturated
  • free cortisol levels are low
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24
Q

describe the binding of cortisol and transcortin in the blood in high cortisol levels

A
  • transcortin quickly saturated
  • greatly increased free cortisol
  • urinary free cortisol (UFC) high
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25
Q

what could high UFC indicate

A

adrenal disorder

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26
Q

outline the actions of glucocorticoids

A
  • mainly catabolic reactions

muscle

  • -> breakdown prot. to a.a. (a.a. then converted to gluc. in liver)
  • -> i.e. net loss of a.a. so favours -ve nitrogen balance

liver

  • -> gluconeogenesis of a.a.
  • -> glycogenesis (when gluc. levels high) ANABOLIC

fat cells
–> lipolysis

immune system and inflammation

  • -> suppresses - decreases no. of WBC and their motility/action
  • -> reduction in inflammatory mediators
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27
Q

what is the only anabolic action of cortisol

A

glycogenesis in liver when glucose levels are high

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28
Q

describe cortisol’s role in adaptation to stress

A
  • directly promotes rapid supply of glucose to tissues

- permissive hormone

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29
Q

describe how cortisol is a permissive hormone

A
  • needs to be present for other hormones to work optimally
  • affects other counter regulatory hormones
  • required for expression of adrenergic and angiotensin 2 receptors in CVS
  • –> cortisol needed to maintain normal BP
  • –> cortisol important in body’s response to hypertension + hypovolaemia
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30
Q

what is a counter regulatory hormone

A

hormone whose actions oppose the action of insulin

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31
Q

what is Cushing’s syndrome

A

glucocorticoid excess / hypercorticolism

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32
Q

name some causes of Cushing’s syndrome

A
  • hypothalamic tumour
  • ant. pit. tumour
  • adrenal tumour
  • ectopic tumour
  • iatrogenic Cushing’s syndrome –> exogenous glucocorticoids
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33
Q

what cause of Cushing’s syndrome is most likely

A

ant. pit. tumour 60-70% of cases –> known as Cushing’s disease (secondary level disorder)

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34
Q

Where is the most likely place to find an ectopic ACTh tumour in the body

A

in the lung

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35
Q

describe hormone levels in 2nd hypersecretion due to hypothalamic problem

A
  • high CRH
  • high ACTH
  • high cortisol
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36
Q

describe hormone levels in 2nd hypersecretion due to ant. pit. problem

A
  • low CRH
  • high ACTH
  • high cortisol
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37
Q

describe hormone levels in 1st hypersecretion due to problem in adrenal cortex

A
  • low CRH
  • low ACTH
  • high cortisol
38
Q

describe some of the features of Cushing’s syndrome

A
  • deposition of fat in face and abdomen
  • thin limbs
  • abdominal striae
  • bruising of skin
  • thinning of skin and BV
  • pink in face
  • moon face
  • dorsal cervical fat pad
39
Q

outline the effects of Cushing’s syndrome on carbohydrate metabolism

A
  • hyperglycaemia –> adrenal diabetes

- ^ in BP due to cortisol binding to mineralocorticoid receptors

40
Q

outline the effects of Cushing’s syndrome on protein metabolism

A
  • protein shortage –> muscle weakness
  • striae / stretch lines
  • easy bruising and thinning skin
41
Q

outline side effects for patients who take exogenous glucocorticoids

A
  • osteoporosis incl. pathological fractures
  • immune suppression
  • delayed healing of fracture and soft tissue injuries
42
Q

how does cortisol impact calcium metabolism

A
  • reduces uptake of calcium from GIT

- increases reabsorption of calcium from bone and excretion

43
Q

outline signs and symptoms of Cushing’s syndrome using mnemonic CUSHING

A

C - central obesity, collagen fibre weakness, comedones

U - UFC + glucose ^

S - striae, suppressed immunity

H - hypercorticolism, hypertension, hyperglycaemia, hypercholestorolaemia

I - iatrogenic

N - noniatrogenic (neoplasms)

G - gluc. intolerance, growth retardation

44
Q

to which cause of Cushing’s syndrome does ‘Cushing’s disease’ specifically refer to

A

pituitary adenoma

45
Q

in adult patient w/ diagnosed Cushing’s disease, which treatment is preferred…

  1. bilateral adrenalectomy
  2. unilateral adrenalectomy
  3. resection of pituitary tumour
A
  1. pituitary tumour resection
46
Q

give two important roles of RAAS

A
  • critical regulator of blood volume and systemic vascular resistance
  • important in long term regulation of BP
47
Q

name two main stimuli for ^ aldosterone production

A
  • ^ K+ conc in ECF –> directly stims adrenal cortex to produce aldosterone
  • Angiotensin 2 –> directly stimulates adrenal cortex to produce aldosterone
48
Q

what zone of adrenal cortex produces aldosterone

A
  • zona glomerulosa
49
Q

when is angio 2 increased

A
  • Na+ deficiency
  • dehydration
  • haemorrhage (drop in blood volume –> decrease in BP –> decreases renal blood flow); juxtaglomerular cells produce renin
50
Q

outline actions of aldosterone (mineralocorticoid effect)

A
  • ^ Na+ and H2O reabsorption
  • ^ K+ and H+ exertion in urine
  • ^ blood volume
  • BP returns to normal
51
Q

describe the effects of aldosterone deficiency

A
  • ^ loss of Na+ and H2O in urine
  • -> dehydration
  • -> plasma depletion
  • -> hypotension
  • renal retention of K+ and hyperkalaemia
  • -> ^ cardiac excitability
  • -> ventricular fibrillation
  • renal retention of H+
  • -> metabolic acidosis
52
Q

describe the difference between primary and secondary hypoaldosteronism

A

primary = problem in adrenal gland

secondary = problem in kidney –> reduced renin production

53
Q

what is Conn’s syndrome

A

primary hyperaldosteronism - over production of aldosterone due to problem in adrenal glands

54
Q

what is the most common cause of Conn’s syndrome

A

adrenal adenoma (75% cases)

55
Q

outline effects of Conn’s syndrome

A
  • hypertension
  • hypokalaemia (due to ^ Na+ retention)
  • hypervolaemia
  • metabolic alkalosis (^ H+ loss)
56
Q

what is secondary hyperaldosteronism

A

overactivity of RAAS

57
Q

main difference between primary and secondary hyperaldosteronism

A 
primary = low renin levels 
secondary = high renin levels
58
Q

what is Addison’s disease

A

primary adrenocortical insufficiency

–> destruction of both adrenal cortices

59
Q

why does Addison’s disease have to be the destruction of both adrenal cortices

A

if only one adrenal cortex is destroyed the other will hypertrophy and hyperplasia can take over

60
Q

what usually causes Addison’s disease

A

autoimmune destruction of adrenal cortices

–> autoantibodies attack adrenal cortex tissue

61
Q

what are some rarer causes of Addison’s disease

A
  • haemorrhage
  • TB
  • malignancy
62
Q

what is adrenal/addisonians crisis

A

acute drop in hormone secretion from adrenal cortex

63
Q

outline effects of a lack of glucocorticoids

A
  • hypoglycaemia
  • reduced fat and protein metabolism
  • weight loss
  • poor exercise tolerance
  • poor stress tolerance –> death
64
Q

outline effects of a lack of mineralocorticoids

A
  • reduced Na+, ^ K+ and H+
  • hypovolaemia
  • reduced CO –> circulatory collapse –> shock –> death
65
Q

outline effect of lack of adrenal androgens

A
  • no effect in males –> testosterone produced in testes

- in women can cause mood changes

66
Q

what is secondary adrenocortical insufficiency

A
  • pituitary/hypothalamic abnormality rustling in insufficient ACTH
  • can have sudden withdrawal of glucocorticoid drugs
  • failure to ^ glucocorticoids during stress
67
Q

give some signs and symptoms of Addison’s disease

A
  • bronze pigmentation of skin (hyperpigmentation)
  • hypoglycaemia
  • changes in body hair distribution
  • GI disturbances
  • weight loss
  • weekness
  • postural hypotension
68
Q

give some signs/symptoms of adrenal crisis

A
  • profound fatigue
  • dehydration
  • vascular collapse –> low BP
  • renal shut down
  • low serum Na+
  • ^ serum K+
69
Q

which combination of biochemical disturbances is the classical finding in a patient with untreated Addison’s disease

A
  • hyponatraemia
  • hypoglycaemia
  • hyperkalaemia
70
Q

in Addison’s disease where would you normally see hyperpigmentation

A
  • areas where skin is thinner
  • palmar creases
  • gums
  • buccal mucosa
  • ridges of nails
  • lips
  • areola of nipples
  • old scars turn darker
71
Q

why do you get hyperpigmentation with Addison’s disease

A
  • adrenal failure
  • reduced adrenal hormones
  • ^ ACTH
  • ^ alpha MSH
  • ^ melanocyte stimulation
  • hyperpigmentation
72
Q

what is the adrenal medulla composed of

A

modified post ganglionic sympathetic neurons

73
Q

what is the neurotransmitter located at the preganglionic neuron for both sympathetic and parasympathetic nerves

A

acetylcholine

74
Q

when acetylcholine from preganglionic nerves bind to nicotinic receptors on post ganglionic nerves, what is released from the post gang. (answer for both PNS and SNS)

A

PNS = ACh

SNS = noradrenaline

75
Q

list some effects of SNS stimulation

A
  • pupil dilation
  • lower volume of thicker saliva
  • activates heart ^ contractility and HR
  • relaxes bronchi
  • inhibits digestive activity
  • stim gluc release by liver
  • adrenaline and noradrenaline secretion from kidney
  • relaxes bladder
  • contracts rectum
76
Q

compare and contrast effects of catecholamines and SNS activity

A

Adrenal Stim:

  • generalised effects as hormones travel through blood
  • exerts effects in all cells
  • delay in beginning
  • prolonged effects

SNS Activation:

  • more localised effects due to direct innervation
  • some organs/tissues have no innervation
  • immediate effects
  • rapid decay when activation ceases
77
Q

what cells secrete catecholamines

A

chromaffin cells of adrenal medulla

78
Q

what are catecholamines derived from

A

amino acid tyrosine

79
Q

give examples of catecholamines

A
  • dopamine
  • noradrenaline
  • adrenaline
80
Q

what is the majority hormone produced in adrenal medulla

A

adrenaline

81
Q

describe how SNS stimulation causes release of adrenaline/noradrenaline from adrenal medulla

A
  • postganglionic nerve releases ACh
  • binds to nicotinic receptors on surface of chromaffin cells
  • depolarisation of chromaffin cell
  • granules in cell containing adrenaline/noradrenaline fuse with plasma membrane
  • exocytosis into blood
82
Q

what is the trigger for release of adrenaline and noradrenaline

A

stress

83
Q

describe metabolism of catecholamines

A

rapidly inactivated by:

  • reuptake by extraneuronal sites
  • metabolised by monoamine oxidase (MAO) or catechol-O-methyltransferase (COMT)
  • conjugation with glucuronide in liver (excreted in urine and bile)
  • direct filtration into urine
84
Q

describe the MoA of catecholamines

A
  • receptor (G-prot linked adrenergic) mediated

- peripheral effects depend upon type and ratio of receptors in target tissues

85
Q

what type of adrenergic receptor does noradrenaline have more affinity for

A

alpha

86
Q

what type of adrenergic receptor does adrenaline have more affinity for

A

beta

87
Q

describe the location of the different types of adrenergic receptors

A
  • A1 = vascular
  • A2 = presynaptic
  • B1 = heart
  • B2 = smooth muscle
  • B3 = fat
88
Q

which adrenergic receptor only binds to adrenaline

A

B2

89
Q

give the effect of the different adrenergic receptors on cAMP production

A

A2 - decreases
B1 - ^
B2 - ^

90
Q

name the disorder assc w/ adrenomedullary dysfunction

A

pheochromocytoma (catecholamine secreting tumour)

91
Q

give some signs and symptoms of pheochromocytoma

A
  • hypertension
  • headache
  • sweating
  • palpitations
  • chest pain
  • anxiety
  • gluc. intolerance
  • ^ metabolic rate
92
Q

in which cell type do pheochromocytomas originate

A

chromaffin

GERR (46 decks)

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