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07. Endocrine > 7.13 Diagnosis of Adrenal Gland Disorders > Flashcards

7.13 Diagnosis of Adrenal Gland Disorders Flashcards

1
Q

Describe the two major functional anatomy

A

They function as two independent systems

  • THE ADRENAL CORTEX: steroid hormone synthesis
  • THE ADRENAL MEDULLA: catecholamine synthesis
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2
Q

What are the major steroid hormones synthesised by the adrenal cortex?

A
  • Glucocorticoids (cortisol)
  • Mineralocorticoids (aldosterone)
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3
Q

What are the major catecholamines hormones synthesised by the adrenal medulla?

A

Adrenaline and noradrenaline

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4
Q

What are the disease states that involve the adrenal cortex?

A
  1. Cushing’s: overproduction of cortisol
  2. Addison’s: underprodution of cortisol
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5
Q

What is the major pathology involving the adrenal medulla?

A

Pheochromocytomas

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6
Q

Describe the histological features of the adrenal glands?

A

Medulla (the inside)

The Cortex: from outside to inside

  • Glomerulosa
  • Fasciculata
  • Reticularis
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7
Q

Where in the cortex do each of the major steroids get synthesised?

A

Glomerulosa - mineralocoricoids and aldosterone
Fasciculata - glucocorticoids (cortisol) + some androgens
Reticularis - sex steroids, androgens + some cortisol

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8
Q

What is the structure of the steroid hormones?

A

They are all steroids from cholesterol

  • Aldosterone & cortisol have the 4 ring structure common to all steroids
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9
Q

What is cortisol?

A

Cortisol = Also called Hydrocortisone

It is the endogenous hormone

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10
Q

What is cortisone?

A

Biological metabolite of cortisole/hydrocortisone, that is almost completely inactive

  • Very weak glucocorticoid
  • Metabolite of cortisol
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11
Q

What is aldosterone?

A

Another corticosteroid hormone which stimulates absorption of sodium by the kidneys and so regulates water and salt balance.

It is a Mineralocorticoid

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12
Q

What is the precursor molecule for the major corticosteroid hormones of the adrenal cortex: cortisol, aldosterone and sex hormones?

Describe the common pathway

A

Cholesterol

Cholesterol is converted to Pregnenolone

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13
Q

Three pathways from cholesterol, exist with each step tightly regulated such that the production of hormones is tightly controlled

Draw this pathway production of the corticosteroids

A
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14
Q

Will taking exogenous levels of the precursors in the synthesis pathway of corticosteroids increase the levels of the output hormones? Why or why not?

A

Because of the tight regulation, taking one of the precursers won’t necessarily increase the amount of the downstream hormones

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15
Q

What are the enzymes catalysing each step of the sythesis pathways for corticosteroids?

A
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16
Q

What are the four major actions of glucocorticoids?

A

It is especially important in times of acute stress - STRESS RESPONSE HORMONES to help maintain the body when homeostasis is challenged

  1. Stimulation of gluconeogenesis (liver)
  2. Mobilisation of amino acids (muscle)
  3. Stimulation of lipolysis (adipose tissues)
  4. Immunosuppression
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17
Q

What happens when there is an excess of cortisol in the body?

A
  • weight gain
  • wasting of muscle, skin and bone
  • hyperglycaemia (muscle amino acid → glucose)
  • hypertension (salt retention)
  • Inhibition of linear growth
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18
Q

What are the two major types of hypercoritsolism?

A
  • ACTH-dependent: when there is a problem with having too much stimulating hormone causing changes in cortisol production
  • ACTH-independent: when there are normal levels of the trophic hormone but the adrenal cortex is producing too much cortisol
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19
Q

What are the major types of ACTH-dependent hypercortisolism?

A
  • Pituitary adenoma (“Cushing’s disease”)
  • Ectopic ACTH syndrome
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20
Q

What are the major ACTH-independent?

A

“Cushing’s syndrome”

  • Adrenal adenoma or carcinoma
  • ACTH-independent nodular hyperplasia
  • Administration of glucocorticoids (common side effect of treatment)
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21
Q

Describe Cushing’s Disease

A

hyperadrenocortisolism (ACTH-dependent)

  • hypertension
  • apparent obesity
  • muscle wasting, thin skin, metabolic derangements (eg. diabetes)
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22
Q

What are the signs of Cushing’s Syndrome?

A
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23
Q

What is the pathophysiology of the straie in Cushing’s syndrome?

A

Stretch marks as the growth of the the abdomen by stretching causes thinning of the skin above (as well as proteolysis by the cortisol of CT on the skin) and blood vessels under show

24
Q

What is a chronic sign of Cushing’s Syndrome?

A

Fat deposition in the face and abdomen and muscle wasting in the arms and legs causing a characteristic “lemon on toothpicks” appearance

25
Q

In endocrinology, is radiology or biochemical testing examined first?

A

Always look at biochemical tests first because they give a better indication of the activity of a gland. An enlarged or atrophic gland doesn’t always mean pathology

Eg. 5% of the population have small pituitary glands, doens’t necessarily cause pathology

26
Q

What are the 3 main steps of testing in endocrinology?

A
  1. Biochemical Testing first then radiology
  2. Repeat the test
  3. Do not measure random hormones (need to know what you are measuring)
27
Q

Why is it important to conduct repeat tests?

A

Normal hormone levels are in constant flux (Assays are not perfect)

28
Q

What kind of Hormone tests can be performed? [5]

A
  • hormone and trophic hormone
  • stimulation if underactive
  • suppresion if overactive
  • regulated reagent and hormone (ca/PTH), glc/insulin
  • 24hr urine assay
29
Q

There are 2 main examples of assaying the hormone and its regulated metabolite, what are they?

A
  • Ca & PTH
  • Glucose & insulin
30
Q

What is a more accurate way of testing hormone levels?

Give 4 major examples

A

Assaying the hormone and the trophic factor

  • T4 and TSH
  • Cortisol and ACTH
  • Oestrogen and FSH/LH
  • Testosterone and LH
31
Q

What is involved in Investigation of suspected Cushing’s?

A
  • 24h urine free cortisol
  • Check diurnal variation: serum cortisol & plasma ACTH at 0800 and midnight
  • Check that negative feedback loop is working: dexamethasone supp’n test
  • cranial MRI/ adrenal CT as indicated
32
Q

Describe the rationale behind the dexamethasone suppression test

A

Dexamethasone is a cortisol analogue that aims to suppress the pituitary gland by acting to increase the negative feedback.

If the secretion of ACTH from the pituitary gland is suppressed then pituitary function is normal. If it doesn’t then there is abherrant production of ACTH.

33
Q

What happens when there is not enough cortisol in the body? (Hypocortisolism) [6]

A
  • GI symptoms (anorexia, nausea, vomiting, diarrhea, weight loss)
  • low blood pressure (salt wasting)
  • darkening of the skin (if ACTH secretion is stimulated)
  • muscle weakness (both skeletal and cardiac muscle)
  • increased susceptibility to infection
  • death
34
Q

Can a person live without cortisol?

A

The person is still in the ‘viable’’ mode but adding stress causes everything to fall apart.

35
Q

Explain the GIT symptoms (anorexia, nausea, vomiting, diarrhea, weight loss) of hypocortisolism

A

Shift of salt and water across the bowel

36
Q

Why is there darkening of the skin in hypocortisolism?

A

High ACTH levels due to lack of negative feedback causing other proteins and peptides related to ACTH to increase

Increased secretion causes stimulation of melanocytes in the skin (leading to pigmentation)

37
Q

What are some causes of adrenal insufficiency (the adrenal cortex doesn’t produce enough cortisol)

A
  • Genetic: Enzyme defect in cortisol biosynthesis
  • Genetic: metabolic defect: adrenoleukodystrophy
  • Autoimmune adrenal destruction
  • Infectious disease: adrenal destruction by tuberculosis (other countries)
38
Q

What is Addison’s Disease?

A

Adrenal insufficiency due to destruction of adrenals, usually by tuberculosis (autoimmune in Australia).

The salt-wasting state results in low serum sodium and high serum potassium

39
Q

What is vitiligo?

A

A chronic skin condition characterized by portions of the skin losing their pigment. It occurs when skin pigment cells die or are unable to function.

40
Q

What kind of diagnostic signs can be seen on examination of a person for Addison’t Disease?

A

Not much diagnostically relevant information from looking at the patient, mostly thin and sometimes pigmented

Pigmentation of the gums: a pathopneumonic sign (if you have it, you have Addison’s)

41
Q

What happens when there is an adrenal gland excess? [8]

A
  • premature pubic hair
  • hirsutism (excessive hair), acne
  • enlargement of penis or clitoris (child)
  • behavioural changes
  • linear growth spurt
  • rapid epiphyseal fusion (child) - thus stunted adult
  • muscular habitus
  • deepening of voice.
42
Q

Describe the impact of adrenal cortex testosterone production in females vs. males

A

The adrenal cortex makes a small amount of testosterone:

  • in males this amount has no effect (the amount from the testes is much more significant)
  • in females, changes could have significant effects
43
Q

What is Congenital adrenal hyperplasia?

A

A autosomal recessive defect that occurs due to 21-hydroxylase deficiency in 90% of cases.

This enzyme is cruicial to the synthetic pathway to cortisol, a lack of enzyme the adrenal won’t make enough cortisol causing increase in ACTH driving the rest of the pathway to the other pathways (androgens)

44
Q

What are major consequences of having a 21-hydroxylase deficiency?

A
  • variable impairment of cortisol and aldosterone biosynthesis
  • prenatal ACTH stimulation → adrenal hyperplasia
  • ↑androgen → virilisation
45
Q

What are the three different presentations that congenital adrenal hyperplasia in females?

A
  • Infant with ambiguous genitalia OR
  • premature pubic hair & enlarged clitoris OR
  • adolescent hirsutism and acne
46
Q

Describe the 2 presentations of congenital adrenal hypertrophy in males

A
  • Adrenal crisis in a baby aged 2-3 weeks OR
  • Premature sexual development at age 2-3 years
47
Q

What are the main two steps that are catalysed by 21-hydroxylase?

A
  • Conversion of 11 deoxycorticosterone to corticosterone (which is then converted to aldosterone)
  • Conversion of 17 OH Progesterone to 11 deoxycortisol (which is converted to cortisol)
48
Q

What is the rational for having the sexual changes appearing in congenital adrenal hyperplasia?

A

The lack of the hormone causes there to be a back up of the major precursors of the pathway. This paired with a lack of negative feeback (increasing amounts of ACTH) drives the pathway down the third 21-hydroxylase independent pathway: production of testosterone

49
Q

Why is there enlargement of the adrenal glands in congenital adrenal hyperplasia?

A

Lack of production of cortisol and aldosterone removes negative inhibition leading to increased production of ACTH causing trophic (growth and hyperplasia) of the glands

50
Q

Cortisol is a glucocorticosteroid. Describe some clinical uses of it

A
  • Replacement therapy for inadequate production diseases: pituitary disease, Addison’s disease
  • Glucocorticoids have potent anti- inflammatory and immunosuppressive properties. Used as drugs to treat inflammatory conditions eg. arthritis, dermatitis, asthma, autoimmune diseases
51
Q

What are the two stimulators (triggers) for aldosterone release?

A
  • Increase [K+] in extracellular fluid
  • Angiotensin II (RAAS)

produced by the adrenal cortex and regualtes salt, water and potassium balance

52
Q

What are the main actions of aldosterone?

A

Aldosterone regulates [Na+], [K+] in extracellular fluids

  • increased resorption of Na+
  • increased resorption of water
  • increased excretion of K+ from the kidney distal tubule
53
Q

What happens when there is excess aldosterone?

A
  • hypertension (salt retention)
  • weakness (hypokalaemia)
54
Q

What happens if there is aldosterone deficiency?

A
  • dehydration, salt depletion & postural
  • hypotension: cardiac arrhythmias (hyperkalaemia)
55
Q

We can survive without cortisol for a while, but can’t survive without mineralocorticoids, why is this?

A

Removal of the adrenal glands leads to death within just a few days, due principally to a loss of mineralocorticoid activity.

Because of the important role of electrolyte balance

56
Q

What is Conn’s Syndrome?

A

Mineralocorticoid excess

  • Main cause: Adrenocortical tumour secreting aldosterone
  • Presents with hypertension or with weakness due to low potassium
  • high sodium, low potassium, low renin
  • cured by surgery
57
Q

What is Pheochromocytoma?

A

A tumour of adrenal medulla causing excess of the catecholamines

Episodes of severe hypertension and cardiac disorders due to the episodic release of the hormones. Diagnosis: measuring adr and nor adre (or metabolites) in the urine over 24hrs

07. Endocrine (10 decks)

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