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Management of GI and Endocrine Conditions > Lecture 24 - Adrenal Glands > Flashcards

Lecture 24 - Adrenal Glands Flashcards

1
Q

Where do the adrenal glands sit?

A

on top of the kidneys

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2
Q

What do the adrenal glands consist of?

A

an outer layer called the cortex and an inner layer called the medulla

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3
Q

What is each adrenal gland essentially?

A

two glands in one because the cortex and the medulla and functionally and structurally different

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4
Q

What are the 3 layers of the adrenal gland?

A

outer = zona glomerulosa

middle = zona fasciculata

inner = zona reticularis

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5
Q

What do the cells in the 3 layers contain?

A

different compliments of enzymes involved in the synthesis of adrenal hormones

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6
Q

What are adrenocorticoids?

A

refers to their site of origin (adrenal cortex) and steroid nature

mineralocorticoids and glucocorticoids

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7
Q

Mineralocorticoids?

A

primarily aldosterone

secreted by cells in the zona glomerulosa

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8
Q

What do mineralocorticoids do?

A

promote Na+ resorption and K+ excretion in kidneys

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9
Q

Glucocorticoids?

A

primarily cortisol

secreted by cells in the zona fasciculata

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10
Q

What do glucocorticoids do?

A

regulate the body’s response to stress

regulate glucose levels and have anti inflammatory effects as well

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11
Q

What do mineralocorticoids affect?

A

water and electrolyte balance

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12
Q

When is there overlap of activity of hormones?

A

when their structures are similar

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13
Q

Why are synthetic steroids constructed?

A

to enhance the mineralocorticoid and glucocorticoid activity of the drug

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14
Q

Sex hormones?

A

primarily androgens

zona reticularis and fasciculata

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15
Q

What do sex hormones regulate?

A

reproductive function

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16
Q

What do adrenal androgens stimulate in females?

A

the sex drive

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17
Q

Where else are sex hormones produced?

A

gonads

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18
Q

What does the adrenal medulla contain?

A

chromaffin cells which secrete catecholamines

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19
Q

Adrenal medulla hormones?

A

80% adrenaline

20% noradrenaline

> 1% dopamine

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20
Q

What is the primary stimulus for adrenal medulla hormones?

A

neural stimulus

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21
Q

What is cortisone?

A

a metabolite or synthetic form of cortisol

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22
Q

What is cortisol secretion controlled by?

A

the hypothalamic-pituitary-adrenal axis

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23
Q

What does the hypothalamus secrete?

A

Corticotrophin releasing hormone (CRH)

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24
Q

What does CRH do?

A

Acts on the anterior pituitary

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25
Q

What does the anterior pituitary secrete?

A

adrenocorticotrophic hormone (ACTH)

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26
Q

What does ACTH do?

A

acts on the adrenal cortex to stimulate secretion of cortisol

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27
Q

When can the amount of cortisol secreted be increased?

A

under situations of increased stress such as trauma, surgery, sleep deprivation

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28
Q

What do elevations in cortisol levels do?

A

have a negative feedback effect on the hypothalamus and the anterior pituitary

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29
Q

As the blood level of cortisol increases it…?

A

inhibits the secretion of CRH and ACTH

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30
Q

What do cortisol levels show?

A

diurnal variation

daily cycle

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31
Q

When do cortisol levels peak?

A

in the morning when we wake up

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32
Q

When are cortisol levels at their lowest?

A

at night (midnight)

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33
Q

What is urinary free cortisol?

A

the blood free cortisol that is circulated and subsequently filtered through the glomerulus into urine during a 24 hour period

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34
Q

What must be done to get an accurate representation of cortisol levels?

A

urine must be collected over a 24 hour period

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35
Q

How is homeostasis maintained?

A

by the negative feedback mechanism

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36
Q

What are stressors most effective in stimulating cortisol secretion?

A

noxious stimuli such as surgery, trauma, infection, shock, pain, extreme temps, anxiety

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37
Q

Why is cortisol sometimes called the stress hormone?

A

it regulates the changes in the body that occur in response to stress

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38
Q

What is cortisol?

A

the main glucocorticoid in humans

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39
Q

Where are the receptors for cortisol?

A

found in many tissues

they are steroid hormones and can cross the cell membranes

intracellular receptors

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40
Q

What do most of the effects of cortisol involve?

A

interactions with intracellular receptors, the complex then enters the nucleus and acts as a transcription factor

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41
Q

What are the effects of cortisol?

A

increase circulating glucose levels

maintain normal responsiveness of blood vessels to vasoconstrictive stimuli

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42
Q

What other areas does cortisol have effects on?

A

immune system, nervous system and kidneys

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43
Q

What are the pharmacological actions of cortisol?

A

anti-inflammatory and immunosuppressant

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44
Q

When are glucocorticoids best known for pharmacological effects?

A

when administered as doses that exceed the normal physiological levels, at these dosages they have more potent effects

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45
Q

What are the primary actions of cortisol?

A

to maintain normal concentrations of the enzymes necessary for the breakdown of proteins, fats and glycogen and the conversion of amino acids to glucose in the liver

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46
Q

What is cortisol necessary for survival during?

A

prolonged fasting periods

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47
Q

In the absence of cortisol what happens?

A

the resulting decrease in gluconeogenesis can lead to death by hypoglycaemia once glycogen stores have been depleted

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48
Q

Tissue effects of cortisol?

A

decrease glucose uptake and amino acid uptake

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49
Q

Adipose tissues effects of cortisol?

A

increase lipolysis

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50
Q

Muscle and other tissue effects of cortisol?

A

increase protein breakdown and decrease protein synthesis

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51
Q

Liver effects of cortisol?

A

increased gluconeogenesis

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52
Q

What is the presence of glucocorticoids essential to?

A

the body’s ability to mobilise fuels in response to signals from other hormones e.g. glucagon and insulin

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53
Q

Generally cortisol causes?

A

increase plasma levels of glucose, fatty acids and amino acids

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54
Q

What is transactivation?

A

the glucocorticoid receptor forms a homodimer and it binds to specific DNA responsive elements on the gene, activating gene transcription

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55
Q

What is transrepression?

A

glucocorticoid receptor complexes with the other transcription factors and prevent them from binding to target genes and expressing genes they would normally up regulate

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56
Q

What is cortisol an agonist for?

A

the glucocorticoid receptor

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57
Q

When is the glucocorticoid receptor in its active form?

A

when it forms a complex with heat shock proteins

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58
Q

What happens to the glucocorticoid receptor once it has had its effect?

A

it is exported back into the cytoplasm of the cell and forms a complex with the heat shock proteins again and waits to be reactivated

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59
Q

What is Addison’s disease?

A

adrenocortical insufficiency

60
Q

What is Addison’s disease due to?

A

destruction or dysfunction of the entire adrenal cortex

61
Q

What does Addison’s disease affect?

A

glucocorticoid and mineralocorticoid function

62
Q

When does the onset of Addison’s disease occur?

A

when 90% or more of both adrenal cortices are destroyed

63
Q

Prevalence of Addison’s disease?

A

40-60 cases per 1 million

64
Q

Who is Addison’s disease most common in?

A

adults aged 30-50

65
Q

Symptoms of Addison’s disease?

A

darkening areas of the skin (hyperpigmentation)

extreme fatigue

unintentional weight loss and decreased appetite

low blood pressure (light headedness and fainting)

GI disturbance

salt craving

low blood glucose

66
Q

Why does Addison’s disease cause hyperpigmentation?

A

due to increased level of adrenal corticotrophic hormone acting on melanocytes increasing production of melanin

67
Q

What does the salt craving in addison’s disease relate to?

A

mineralocorticoid deficiency

68
Q

What do patients with Addison’s disease usually present with?

A

glucocorticoid or mineralocorticoid deficiency

69
Q

What is Addison’s disease classed as?

A

primary adrenal insufficiency

70
Q

What causes Addison’s disease?

A

autoimmune destruction of the gland (85% of cases)

adrenal glands are damaged and can no longer produce sufficient cortisol, aldosterone secretion is often insufficient as well

71
Q

What else can cause Addison’s disease?

A

infections (tuberculosis, HIV, syphilis, cryptococci)

invasion (neoplastic, fibrosis, sarcoidosis, amyloidosis)

haemorrhage (waterhouse-friderichsen syndrome)

72
Q

What is adrenal gland failure in haemorrhage caused by?

A

bleeding in the gland itself

commonly associated with severe bacterial infection of the adrenal gland

73
Q

What are the levels of hormones like in addison’s disease?

A

decreased secretion of cortisol causes a lack of negative feedback

this means there is increased secretion of corticotrophin releasing hormone and adrenocorticotrophic hormone

74
Q

Why is there decreased cortisol secretion in Addison’s disease?

A

the adrenal cortex has been completely destroyed

75
Q

Treatment of Addison’s disease?

A

hydrocortisone (sometimes longer acting prednisolone or dexamethasone)

fludrocortisone (mineralocorticoid)

76
Q

What is needed in treatment of Addison’s disease?

A

glucocorticoid and mineralocorticoid replacement

77
Q

Dose of fludrocortisone?

A

50mcg - 300mcg

78
Q

Dose of hydrocortisone?

A

15-30mg given as a divided dose e.g. 10mg on waking, 5mg at noon, 5mg in early evening

79
Q

Why is hydrocortisone given in divided doses?

A

so the glucocorticoid replacement resembles the natural cycle release

80
Q

What does the dose depend on?

A

the body weight, absorption and metabolism

81
Q

What might require an increased glucocorticoid dose?

A

intercurrent illness (infections)

dose should be doubles

if vomiting/diarrhoea, parenteral administration should be given

82
Q

How long is the treatment of Addison’s disease?

A

life long

83
Q

Secondary adrenal insufficiency?

A

lack of ACTH secretion from pituitary

84
Q

Tertiary adrenal insufficiency?

A

lack of corticotrophin releasing hormone secretion from hypothalamus

85
Q

Adrenal gland function in secondary and tertiary?

A

adrenal gland is functioning properly, there is just a lack of stimulation

86
Q

What do patients with secondary and tertiary not show?

A

hyperpigmentation or cravings for salt

87
Q

What can secondary or tertiary adrenal insufficiency also be due to?

A

glucocorticoid drug therapy or if glucocorticoid medication is stopped too abruptly

suppression of the hypothalamus-pituitary-adrenal axis by long term corticosteroid use in patients

88
Q

Na+ and K+ levels in secondary and teriary?

A

normal

89
Q

Treatment for secondary and tertiary adrenal insufficiency?

A

glucocorticoid (hydrocortisone) but mineralocorticoid is unnecessary

90
Q

Why is treatment with mineralocorticoid unnecessary in S & T?

A

the adrenal gland itself is working fine

91
Q

Why can the adrenal gland shrink?

A

if ACTH is reduced, the production of cortisol will be reduced, eventually resulting in shrinking of adrenal glands

92
Q

Therapeutic use of glucocorticoids?

A

replacement therapy in corticosteroid insufficiency

93
Q

Use of glucocorticoids in acute inflammatory disease?

A

bronchial asthma

anaphylaxis and angioedema

acute fibrosing alveolitis

94
Q

Use of glucocorticoids in chronic inflammatory disease?

A

connective tissue disease (systemic lupus)

renal disorders (glomerulonephritis)

hepatic disorders (chronic active hepatitis)

GI disorders (IBD)

95
Q

use of glucocorticoids in neoplastic disease?

A

myeloma

lymphomas

lymphocytic leukaemias

96
Q

Use of glucocorticoids in miscellaneous disorders?

A

bells palsy

sarcoidosis

organ transplantation (as an immunosuppressant)

97
Q

What do glucocorticoid drugs do?

A

they suppress the hypothalamus and anterior pituitary

98
Q

What does suppression of the hypothalamus and anterior pituitary do?

A

reduces CRH and ACTH levels

99
Q

How long can it take the hypothalamic-pituitary-adrenal axis to return to normal?

A

a year

100
Q

Examples of glucocorticoid drugs?

A

prednisolone

dexamethasone

hydrocortisone

beclomethasone

101
Q

What is a glucocorticoid withdrawal regime?

A

no single withdrawal regime

102
Q

What does a withdrawal regime depend on?

A

patients response to withdrawal, disease being treated and the intended duration of treatment

103
Q

What courses of oral corticosteroids can be stopped abruptly?

A

short courses (<3 weeks)

104
Q

What should gradual withdrawal be considered for?

A

those who have received >3 weeks treatment

received repeated courses of treatment

received >40mg of prednisolone daily >1 week

105
Q

What happens if withdrawal symptoms are reported?

A

a higher dose is resumed and the withdrawal is continued at a slower rate

106
Q

What are patients whose medication is stopped abruptly or not increase during illness at risk of?

A

adrenal crisis

107
Q

What is adrenal crisis?

A

sudden severe worsening symptoms of adrenal insufficiency symptoms

108
Q

Symptoms of adrenal crisis?

A

sudden, severe pain in the lower back, abdomen or legs

severe vomiting and diarrhoea

dehydration

low blood pressure

loss of consciousness

109
Q

Why is it important a patient with adrenal crisis gets treated immediately?

A

it can result in death

110
Q

What should a patient with adrenal insufficiency wear?

A

a medical alert bracelet

111
Q

What is Cushing’s syndrome?

A

hypersecretion of cortisol (hypercortisolism)

patients have too much cortisol in the body

112
Q

What can long term elevations of cortisol do?

A

have harmful effects on many organ systems throughout the body

113
Q

What is Cushing’s syndrome a result of?

A

prolonged exposure to elevated levels of cortisol in the body

114
Q

What can Cushing’s syndrome cause?

A

metabolic complications - type 2 diabetes (insulin resistance)

excessive bone resorption (osteoporosis)

hypertension

115
Q

Symptoms of Cushing’s syndrome?

A

moon face

bruisability

red striation

pendulous abdomen

poor wound healing

red cheeks

fat pads

thin skin

higher blood pressure

thin arms and legs

116
Q

Most specific symptoms of Cushing’s syndrome?

A

bruising easily, muscle weakness and ruddy complexion

117
Q

What causes 65-70% of Cushing’s syndrome cases?

A

pituitary tumour leading to increased secretion of adrencorticotrophic hormone (CUSHINGS DISEASE)

118
Q

What causes 15-20% of Cushing’s syndrome cases?

A

adrenocortical tumours (benign or malignant) or bilateral adrenal hyperplasia or dysplasia

(tumour within the adrenal gland itself)

119
Q

What causes 10-15% of Cushing’s syndrome cases?

A

tumours external to the hypothalamic-pituitary-adrenal axis (ectopic adrenocorticotrophic hormone secretion)

120
Q

Adrenocorticotrophic (ACTH) dependent Cushing’s syndrome?

A

body is making too much ACTH

due to pituitary tumour or ectopic tumour producing ACTH (tumour in another part of the body)

121
Q

Adrenocorticotrophic independent Cushing’s syndrome?

A

ACTH level is low due to negative feedback

adrenal glands are making too much cortisol by itself

due to adrenal tumour or adrenal hyperplasia

122
Q

What type of cushing’s syndrome is typically seen in pratice?

A

Iatrogenic (drug related or exogenous)

123
Q

What other treatment can cause Cushing’s syndrome?

A

glucocorticoid treatment

prednisolone
hydrocortisone
dexamethasone

124
Q

Route of administration causing cushing’s syndrome?

A

occurs irrespective of route

route does not matter

125
Q

What type of treatment can cause Cushing’s syndrome?

A

prolonged and use of potent drugs

126
Q

What are glucocorticoids metabolised by?

A

CYP450 enzymes

127
Q

What is CYP3A4 important for?

A

metabolism or cortisol and glucocorticoids

128
Q

What can drugs that inhibit CYP450 enzymes do?

A

prolong the action of glucocorticoids (itraconazole, ritonavir, antidepressants)

these may decrease metabolism of cortisol and cause Cushing’s syndrome

129
Q

What are cortisol and other glucocorticoids?

A

CYP3A4 inducers, which means they could increase the metabolism of other drugs being taken concurrently

130
Q

Surgery to treat Cushing’s syndrome?

A

removal of pituitary gland (or ectopic source of ACTH)

removal of adrenal glands

131
Q

When might surgery be an option?

A

in cases of bilateral adrenal hyperplasia - bilateral adrenalectomy might be used

132
Q

What can surgery result in?

A

adrenal insufficiency and require lifelong hormone replacement therapy

133
Q

What is an effective treatment of Cushing’s disease?

A

reducing the size of the pituitary gland

134
Q

Treatment for drug induced Cushing’s disease?

A

gradual withdrawal for the causative drug

aim to discontinue the use of the causative drug if possible

135
Q

When surgery cannot be done or is unsuccessful what should be used as treatment?

A

medication

this often occurs with ectopic adrenocortiotrophic hormone or metastatic adrenal carcinoma

136
Q

What is mifepristone (RU486)?

A

a high affinity non selective glucocorticoid receptor antagonist

137
Q

What can mifepristone do?

A

restore glucose tolerance (60%) and lower blood pressure (43%)

DOESNT REDUCE CORTISOL LEVELS

138
Q

What are the goals of treating Cushing’s syndrome?

A

reversal of clinical features, normalisation of the cortisol levels and long term control without recurrence

139
Q

What is metyrapone?

A

a drug that inhibits 11-beta-hydroxylase enzyme

140
Q

What does 11beta-hydroxylase do?

A

converts 11-deoxycortisol to cortisol

141
Q

What does inhibiting 11beta-hydroxylase do?

A

reduced body’s ability to produce cortisol

142
Q

What is metyrapone effective for?

A

short and long term treatment of Cushing’s syndrome

143
Q

What does metyrapone require?

A

dose titration and careful clinical and biochemical monitoring

disturbances of K+ levels were reported

144
Q

What are the side effects of metyrapone?

A

primarily GI but long term use has been associated with hirsutism and hypertension

145
Q

What is another 11 beta hydroxylase inhibitor currently undergoing clinical trial?

A

LCI1699

Management of GI and Endocrine Conditions (24 decks)

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