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Endocrine System > Adrenal Glands > Flashcards

Adrenal Glands Flashcards

1
Q

What hormones are produced by the adrenal gland?

A

Mineralocorticoids - aldosterone
Glucocorticoids - cortisol
Androgens

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2
Q

Which system controls the release of aldosterone from the adrenal gland?

A

Renin angiotensin system

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3
Q

Which system controls the release of cortisol and androgens from the adrenal gland?

A

The hypothalamic-pituitary-andrenocortico axis through the release of ACTH

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4
Q

What is adrenal insufficiency?

A

Inadequate adrenocortical function

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5
Q

What can cause primary adrenal insufficiency?

A

Addison’s disease
Adrenal tumours
Congenital adrenal hyperplasia

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6
Q

What can cause secondary adrenal insufficiency?

A

Lack of ACTH stimulation
Pituitary/hypothalamic disorders
iatrogenic

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7
Q

Congenital adrenal hyperplasia is an autosomal recessive condition where there is a lack of which enzyme?

A

21 hydroxyls

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8
Q

All steroid hormones are produced from which substance?

A

Cholesterol

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9
Q

How does a lack of 21-hydroxylase affect the synthesis of adrenal hormones?

A

Cannot synthesise aldosterone and cortisol so there is increased synthesis of androgens

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10
Q

What is the most common cause of primary adrenal insufficiency?

A

Addison’s disease

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11
Q

How much of the adrenal cortex needs to be destroyed in Addison’s disease in order for symptoms to develop?

A

90% of the cortex

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12
Q

What percentage of patient’s with Addison’s disease will have positive autoantibody tests?

A

70%

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13
Q

What other conditions are associated with Addison’s disease?

A

T1DM
Pernicious anaemia
Autoimmune thyroid disease

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14
Q

What are the symptoms of Addison’s disease?

A 
Anorexia
Weight loss
Fatigue / lethargy
Dizziness
Hypotension
Abdominal pain
Vomiting
Diarrhoea
Skin pigmentation
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15
Q

How are serum sodium and potassium concentrations affected by adrenal insufficiency and why is this the case?

A

Decreased aldosterone means less sodium reabsorption and less potassium excretion which can lead to hyponatraemia and hyperkalaemia

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16
Q

Why might a patient with adrenal insufficiency by hypoglycaemic?

A

Because decreased cortisol levels, decreases gluconeogenesis, decreases the effect of glucagon and increases the affect of insulin

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17
Q

Why is skin pigmentation seen in primary but not secondary adrenal insufficiency?

A

Because this is caused by increased ACTH levels which only occurs in primary insufficiency

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18
Q

Why are ACTH levels increased in primary adrenal insufficiency?

A

The lack of production of cortisol and androgens means that these hormones are not exhibiting a negative feedback effect on the hypothalamus and anterior pituitary and so these glands are releasing more CRH and thus more ACTH.

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19
Q

In an acute presentation of primary adrenal insufficiency treatment should not be delayed to confirm the diagnosis. T/F?

A

True

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20
Q

In the treatment of adrenal insufficiency, what drug is used to act as a cortisol replacement?

A

Hydrocortisone

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21
Q

In the treatment of primary insufficiency, what drug is used to act as a replacement for aldosterone?

A

Fludrocortisone

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22
Q

Why is fludrocortisone therapy not required in patients with secondary adrenal insufficiency?

A

Because this is an aldosterone replacement and since, in secondary insufficiency, only the production of cortisol and androgens are affected by the lack of ACTH, this is not needed.

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23
Q

How should treatment of a patient on long-term steroids be changed when they are ill?

A

Double the steroid dose

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24
Q

Steroid medication can be stopped suddenly. T/F?

A

False - this should never happen

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25
Q

Patients who take long-term steroid medication should carry an ID card. T/F?

A

True

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26
Q

What is the most common cause of secondary adrenal insufficiency?

A

Exogenous steroid use

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27
Q

How can exogenous steroid use lead to secondary adrenal insufficiency?

A

High doses of exogenous steroid act in a negative feedback loop to prevent the release of CRH and ACTH

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28
Q

How do the clinical features of secondary adrenal insufficiency differ from primary insufficiency?

A

In secondary insufficiency there is no skin pigmentation and aldosterone production is intake so there is no hyponatraemia or hyperkalaemia

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29
Q

What is the name of the clinical syndrome where there is an excess of cortisol?

A

Cushing’s syndrome

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30
Q

What is the annual incidence of Cushing’s syndrome?

A

2 in a million

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31
Q

Women are more likely to get Cushing’s disease than men. T/F?

A

True

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32
Q

What are the clinical features of Cushing’s syndrome?

A

Abdominal striae, central fat deposition, bruising, thinning of the limbs, buffalo hump, moon face, poor wound healing, red face, euphoria, tendency to avascular necrosis

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33
Q

What are the possible causes of ACTH dependent Cushing’s syndrome?

A

Pituitary adenomas
Ectopic ACTH
Ectopic CRH

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34
Q

Ectopic ACTH secretion (from somewhere other than the pituitary) is most commonly caused by a tumour in which tissue?

A

The lung

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35
Q

What are the possible causes of ACTH dependent Cushing’s syndrome?

A

Adrenal adenomas
Adrenal carcinomas
Nodular hyperplasia

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36
Q

What tests can be used to establish cortisol excess in patient’s with suspected Cushing’s syndrome?

A

Dexamethasone supression testing
measure 24 hr urinary free cortisol
measuring late night salivary cortisol

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37
Q

In the investigation of Cushing’s syndrome, once cortisol excess has been established, the cause of the excess must be determined. This is done by measuring ACTH levels. If ACTH levels are undetectable then what further investigations are required?

A

Adrenal CT to look for an adrenal tumour

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38
Q

In the investigation of Cushing’s syndrome, once cortisol excess has been established, the cause of the excess must be determined. This is done by measuring ACTH levels. If ACTH levels are normal or high then what further investigations are required?

A

Pituitary MRI to look for pituitary ACTH-secreting tumour

If this is negative then a chest/abdominal/pelvic CT can be done to look for an ectopic ACTH secreting tumour

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39
Q

What surgical procedures may be used in the management of Cushing’s syndrome?

A

Transphenoidal pituitary surgery

laparoscopic adrenalectomy

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40
Q

Cushing’s syndrome can be managed medically in the short term. What drugs are used for this purpose?

A

Metrypaone

Ketoconazole

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41
Q

Iatrogenic steroid use is the most common cause of Cushing’s syndrome. T/F?

A

True

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42
Q

Prolonged high dose steroid therapy causes chronic suppression of pituitary ACTH which causes adrenal atrophy. T/F?

A

True

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43
Q

What percentage of cases of hypertension are secondary to another condition?

A

10%

44
Q

What is the most common cause of secondary hypertension?

A

Primary aldosteronism

45
Q

What can cause primary aldosteronism?

A

Single adrenal adenoma

Bilateral adrenal nodules

46
Q

What are the clinical features of primary aldosteronism?

A

Significant hypertension
Hypokalaemia
Alkalosis

47
Q

In primary aldosteronism, how are renin levels affected?

A

Renin is supressed

48
Q

Renin suppression is characteristic of primary aldosteronism. How can this be tested for?

A

By giving an IV saline load

49
Q

If a patient has a single adrenal adenoma causing primary aldosteronism, how can this be managed?

A

By unilateral laparoscopic adrenalectomy

50
Q

In cases of bilateral adrenal hyperplasia causing primary aldosteronism, surgery cannot be used. How is this managed instead?

A

Mineralocorticoid receptor blocks such as spironolactone or eplerenone
Blockers of sodium reabsorption in the kidney such as amiloride

51
Q

What condition of the adrenal medulla can cause secondary hypertension?

A

Phaeochtomocytomas

52
Q

What is a phaeochromocytoma?

A

A catecholamine secreting tumour of the adrenal medulla

53
Q

What symptoms can result from a phaeochromocytoma?

A 
Hypertension (may be intermittent)
Episodes of headache
Palpitations
Pallor
Sweating
54
Q

How is a phaeochromotcytoma diagnosed?

A

Measuring urinary catecholamines

CT scan of the adrenal glands

55
Q

How is a phaeochromotcytoma managed?

A

Adrenalectomy with preoperative treatment with alpha one and beta one antagonists

56
Q

Why are steroid hormones not stored but immediately released?

A

Because they are lipid soluble and freely permeable to the cell membrane

57
Q

Since steroid hormones are not water soluble they are carried by proteins in the blood. What protein carried cortisol?

A

Corticosteroid binding globulin

58
Q

Where is the cell are steroid hormones produced?

A

Mitochondria and smooth ER

59
Q

Why are the adrenal glands yellow in colour?

A

They have a high cholesterol content

60
Q

What is the term for the arrangement of the vessels in the adrenal gland whereby the blood reaches the outer surface of the gland before entering and supplying each layer?

A

Centripetal blood flow

61
Q

The right suprarenal vein drains to…?

A

The IVC

62
Q

The left suprarenal vein drains to…?

A

The left renal vein

63
Q

What type of cells exist in the adrenal medulla?

A

Chromaffin cells

64
Q

What nerves supply the adrenal cortex?

A

Nerves from the coeliac plexus and greater splanchnic nerves

65
Q

What is the arrangement of cells in the zona glomerulosa of the adrenal cortex?

A

Small clusters of cells

66
Q

Which layer of the adrenal cortex produces the mineralocorticoids (aldosterone)?

A

Zona glomerulosa

67
Q

How are the cells arranged in the zona fasciculata of the adrenal cortex?

A

Large cells arranged in cords

68
Q

What hormones are produced by the zona reticularis of the adrenal cortex?

A

DHEA
Androstenedione
Small amounts of cortisol

69
Q

What enzyme controls the rate limiting step in the process of de novo synthesis of cholesterol for acetyl coA?

A

HMG-CoA reductase

70
Q

In the pathway of steroid hormone production, what is cholesterol first converted to?

A

Pregnenolone

71
Q

What is required as a cofactor in the conversion of cholesterol to pregnenolone?

A

Cytochrome P450

72
Q

Where is the cell does conversion from cholesterol to pregnenolone take place?

A

Mitochondria

73
Q

What protein carries out the transport of free cholesterol from the cytoplasm into the mitochondria?

A

Steroidogenic acute regulatory protein (StAR)

74
Q

In the pathway of steroid hormone synthesis from cholesterol, which conversion steps take place in the mitochondria?

A

Cholesterol to pregnenolone

11-deoxycorticosterone to corticosterone to 18-OH- corticosterone to aldosterone

11- Deoxycotisol to cortisol

75
Q

Which enzyme is responsible for the conversion of cholesterol to pregnenolone?

A

Side chain cleavage enzyme desmolase

76
Q

Which enzymes is responsible for the conversion of pregnenolone to progesterone?

A

3beta HSD

77
Q

Which enzyme is responsible for the conversion of progesterone to 11-deoxycorticosterone and also for the conversion of 17-OH progesterone to 11-deoxycortisol?

A

21-hydroxylase

78
Q

What conversion steps is the enzyme 17 alpha hydroxylase responsible in the steroid hormone synthesis pathway?

A

pregnenolone to 17-OH- pregnenolone to DHEA

Progesterone to 17-OH-progesterone to andostenedione

79
Q

What conversion steps is the enzyme 11 beta hydroxylase responsible in the steroid hormone synthesis pathway?

A

Conversion of 11-deoxycorticosterone to corticosterone

Conversion of 11-deoxycortisol to cortisol

80
Q

What conversion steps is the enzyme aldosterone synthase responsible in the steroid hormone synthesis pathway?

A

Corticosterone to 18-OH-corticosterone to aldosterone

81
Q

What is the function of the A/B domain of the steroid nucleus receptor superfamily?

A

Controls which domain is activated

82
Q

D is the hinge region of the steroid nuclear receptor superfamily. What does this do?

A

Controls movement of the receptor to the nucleus

83
Q

To which domain of the steroid nuclear receptor superfamily does the ligand bind to?

A

E

84
Q

Describe the binding of a steroid hormone to its receptor and how this causes an effect?

A

The steroid hormone diffuses through the pm and binds to its intracellular cytosolic receptor and the receptor-hormone complex then enters the nucleus and binds to the glucocorticoid response element which initiates gene transcription to produce mRNA which is translated to proteins which mediate the effects on the target cell

85
Q

Glucocorticoid receptors are widespread throughout the body. T/F?

A

True

86
Q

Where in the body are mineralocorticoid receptors found?

A 
Distal nephron
Salivary glands
Sweat glands
Large intestine
Brain vascular tissue
Heart
87
Q

To which substance is the affinity of glucocorticoid receptors highest?

A

Dexamethasone

88
Q

To which substance is the affinity of mineralocorticoid receptors highest?

A

Aldosterone

89
Q

There is a much higher level of circulating cortisol than aldosterone so cortisol will bind to mineralocorticoid receptors (MR). How is illicit occupation by glucocorticoids of the MRs in the kidney stopped?

A

By the enzyme 11 beta HSD 2 which catalyses the conversion of cortisol to the inactive cortisone

90
Q

What are the effects of cortisol on the body?

A

Increases gluconeogenesis in the liver
Permissive effect on glucagon
Acts as an insulin antagonist
Increases breakdown of skeletal muscle protein
Has a role in memory, learning, mood and immune suppression

91
Q

What are the effects of aldosterone on the body?

A

Increases sodium and water reabsorption with concomitant potassium and hydrogen excretion in the distal tubule and collecting ducts of the kidney
stimulates sodium and water reabsorption form the gut, salivary glands and sweat glands in exchange for potassium

92
Q

Describe how aldosterone is able to exert its action?

A

It binds to its receptor and is translocated into the nucleus where it binds to HREs to act as a transcription factor which creates mRNA transcripts of SGK-1, ENaC and Na/K-ATPase to promote sodium reabsorption and potasisum secretion

93
Q

Cortisol release follows a circadian rhythm. Thus, when are cortisol levels highest?

A

In the morning

94
Q

What type of hormone is ACTH?

A

Peptide hormone

95
Q

ACTH is formed by the cleavage of…?

A

POMC

96
Q

What other molecules are formed as by-products in the synthesis of ACTH?

A

Lipotropin
Beta endorphin
Met-enkephalin
Melanoycte stimulating hormone

97
Q

How does ACTH act on the adrenal gland to increase the synthesis of cortisol and androgens?

A

Binds to a GPCR which stimulates adenylyl cyclase ceasing an increase in cAMP, activation of PKA and a calcium influx.
This stimulates cholesterol delivery to the mitochondria and increases transcription go genes coding for steroidogenic enzymes

98
Q

How does angiotensin II act on the adrenal gland to increase the synthesis of aldosterone?

A

It binds to a GPCR to activate phospholipase C which hydrolyses PIP2 to form IP3 and DAG
IP3 causes the release of stored calcium to activate calcium calmodulin dependent protein kinases with stimulate the transcription of StAR and cholesterol uptake into the mitochondria to increase aldosterone production

99
Q

How will an increase in serum potassium concentration affect aldosterone secretion?

A

It will increase aldosterone secretion

100
Q

Where does the superior suprarenal artery come from?

A

Inferior phrenic artery

101
Q

Where does the middle suprarenal artery come form?

A

Direct branch of the abdominal aorta

102
Q

Where does the inferior suprarenal artery come from?

A

The renal artery

103
Q

Which plasma protein is cortisol bound to?

A

Corticosteroid binding globulin - transcortin

104
Q

Which plasma protein is aldosterone and dehydroepiandrosterone?

A

Bound to albumin

105
Q

Cortisol plays a key role is adaptation to stress. How is cortisol secretion affected by stress?

A

Increased

106
Q

How does cortisol exert anti-inflammatory and immunosuppressive effects?

A

Blocks production of inflammatory chemokine (prostaglandins and leukotrienes)
suppresses the migration of neutrophils to the injured site
Inhibits proliferation of fibroblasts
Interfere with antibody production in lymphocytes

107
Q

The use of corticosteroid replacement therapy aims to mimic endogenous hormonal secretion. T/F?

A

True

Endocrine System (12 decks)

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