6 - ENDOCRINE DISORDERS: THE ADRENAL GLAND Flashcards

1
Q

CRH

A

Corticotropin Releasing Hormone

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2
Q

ACTH

A

AdrenoCortico Tropic Hormone

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3
Q

Adrenal cortex layers

A
  • zona glomerulosa
  • zona fasciculata
  • zona reticularis
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4
Q

zona glomerulosa

A

secreting aldosterone, control of renin from kidney.
Na rabsorption.
Production of mineralcorticoids

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5
Q

zona fasciculata

A

glucocorticoid secretion - cortisol

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6
Q

zona reticularis

A

secretion of sex hormones - androgen.
Precursor for testosterone and oestrogen.
Produces DHEA (precursor to androgens)

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7
Q

adrenal cortex

A

all hormones synthesised from cholesterol.

Has lots of LDL receptors to combine cholesterol and can act as store to synthesise hormones rapidly.

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8
Q

ALDOSTERONE

A
  • Regulates Na and K homeostasis
  • Secreted in response to low blood pressure/volume
  • Promotes Na reabsorption and K+ excretion in the kidney
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9
Q

Cortisol

A
  • Raises blood glucose
  • Increases lipid and protein breakdown
  • Resistance to stress
  • Immune response depression
  • Bound by cortisol binding protein in the blood
  • Highest levels 8am, lowest midnight.
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10
Q

DHEA

A

produced from zona reticularis

- precursor to androgens, tested for adrenal gland function

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11
Q

ANDROGENS

A

made from Dehydroepiandrosterone (DHEA)
Converted to testosterone in circulation, converted to oestrogen in ovaries if female
Secondary sexual characteristics
Prepubertal growth spurt

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12
Q

THE ADRENAL MEDULLA

A

• Produces adrenaline, noradrenaline (CATECHOLAMINES) from chromaffin cells in response to nervous stimulation.
• Fight/flight response
Not under control of ACTH from anterior pituitary.

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13
Q

Catecholamines (epinephrine and norepinephrine)

A

Line blood vessels, increase heart rate, force and pressure, increase glucose levels.

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14
Q

COMT (catechol-o-methyltransferase)

A

enzyme that breaks down catecholamines and Metabolises into metanephrine and normethanephrine.

  • broken down products seen in urine
  • assess quantity of adrenaline
  • cannot measure adrenaline as broken down too quick
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15
Q

Assess Adrenal function

A

Competitive ELISA - cortisol, aldosterone, DHEA, metanephrine
OR
2-site ELISA - plasma ACTH

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16
Q
Competitive ELISA
(cortisol, aldosterone, DHEA, metanephrine)
A
  • Antibody attached to well (specific for hormone X)
  • Patient’s serum added PLUS HRP labelled hormone X
  • TMB subsrate added
  • Yellow Colour development
  • This e.g. = low patient hormone X as few binding sites filled, high colour absorbance
17
Q

2-site ELISA

Measure plasma ACTH

A
  1. Antibody to ACTH in well.
  2. Serum added.
  3. C-terminal of ACTH binds to antibody in well.
  4. Antibody added to bind to N-terminal, linked to HRP enzyme.
  5. TMB substrate added, yellow colour change.
  6. High absorbance = more colour change. Directly proportional.
18
Q

Dexamethasone (glucocorticoid) suppression test

A

Looks like cortisol to body. Tests if cortisol production is regulated by negative feedback.
- dexamethasone inhibits ACTH release in healthy people, -ve feedback.
- If no decrease in cortisol, ACTH and CRH is still being released.
Pituitary tumour or ectopic ACTH source. Produced from tumour instead of anterior pituitary.

19
Q

Stress hormone pathway

A

Corticotropin-releasing hormone (hypothalamus),
Adrenocorticotropic hormone (ACTH) (anterior pituitary),
cortisol (adrenal gland).

20
Q

Synacthen test

A

Tests if adrenal gland responds to ACTH.

  • give patient IV synacthen, looks like ACTH
  • should stimulate cortisol production in adrenal gland.
  • measure cortisol, if no rise then suspect adrenal insufficiency.
21
Q

Adrenal cortical insufficiency

A

not producing enough hormones, aldosterone.

22
Q

Addison’s disease

A

destruction of both adrenal glands by autoimmune disease or infection.

23
Q

Adrenal cortical insufficiency symptoms

A

muscle weakness, tiredness, skin pigmentation, vomiting, sweating, hypotension, low blood Na.
High K causes cardia arythmias.
High ACTH to increase cortisol levels.
Precursor to ACTH causes pigmented skin.

24
Q

DIAGNOSTIC FINDINGS OF ADRENAL CORTICAL INSUFFICIENCY

A
Plasma ACTH higher than normal range
Plasma cortisol less than normal range
Synacthen test (ACTH analogue) – little, if any, increase in cortisol

If aldosterone production is decreased too:
Hyponatraemia (serum sodium low)
Hyperkalaemia (serum potassium high)
Uraemia – high levels of urea in blood (dehydrated)

25
Q

HYPERADRENALISM

A

excess cortical hormone secretione.g. Cushing’s syndrome

26
Q

Hyperadrenalism (Cushing’s syndrome) symptoms

A

muscle weakness, hypertension (cortisol stimulates mineralcorticoid leading to aldosterone effects), hirsutism (unwanted hair), central obesity, osteoporosis.

27
Q

Conn’s Syndrome (hyperaldosteronism)

A

Aldosterone in response to low blood pressure, cause water retention by reabsorption of Na.

symptoms:

  1. Hypertension
  2. Hypokalemia
  3. metabolic alkalosis
  4. decreased renin secretion
28
Q

SOME CAUSES OF HYPERADRENALISM

A
  • Adrenal cortical hyperplasia
  • Adrenal cortical adenoma
  • Adrenal cortical carcinoma
29
Q

Adrenal cortical hyperplasia

A

Increase in cell number
Increased ACTH stimulation, maybe tumour in pituitary gland.
Diagnosis = dexamethasone suppression test shows raised cortisol with no negative feedback

30
Q

Adrenal cortical adenoma

A
• May secrete excess cortisol (Cushing’s) or aldosterone (Conn’s)
• Yellow cut surface- stored cholesterol
• Diagnosis: ACTH not detectable
• If cortisol-secreting:
   - Cortisol increase
• If aldosterone-secreting
   - Plasma aldosterone high
   - Serum Na high
   - Serum K low
   - Urine K high
31
Q

Adrenal cortical carcinoma

A
• Yellow/white tumour
• Often secrete cortisol - Cushing’s 
• Often secrete androgens - hirsutism
• Diagnosis:
   - Cortisol increase 
   - DHEA increase
32
Q

PHEOCHROMOCYTOMA – ADRENAL MEDULLA TUMOUR

A

• Symptoms: sweating, headaches, palpitations, hypertension…
• Diagnosis:
- Increase in adrenaline/noradrenaline breakdown products (metanephrine and normetanephrine)