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Medicine Year 2 > Endocrine Topic 5 - Adrenal Glands > Flashcards

Endocrine Topic 5 - Adrenal Glands Flashcards

1
Q

Which diseases are often associated with Addison’s disease?

A

Other autimmune diseases e.g. T1DM, thyroid, pernicious anaemia

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2
Q

Describe the mechanism of action of ACTH

A
  • Binds to 7TMD G protein coupled receptor
  • Conformational change - adenyl cyclase, increases cAMP, PKA activation, Ca2+ influx
  • Rapid and long-term actions
    • Rapid - stimulation of cholesterol delivery to mitochondria
    • Long-term - transcription of genes coding for steroidogenic enzymes
  • Increases cortisol/androgen production
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3
Q

Describe the formation of ACTH

A
  • Peptide hormone formed from cleavage of pro-opiomelanocortin (POMC) in corticotropes in anterior pituitary
  • Lipotropin (beta endorphin precursor), beta endorphin and metencephalin (opiod peptides - reduce pain, euphoria) and melanocyte stimulating hormone also released
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4
Q

How can primary and secondary adrenal insufficiency be distinguished?

A
  • Short synacthen test
    • Primary = low cortisol after ACTH
    • Secondary = high cortisol after ACTH
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5
Q

Describe the structure of the zona fasciculata

A
  • Large cells arranged in cords - spongiocytes (appear empty)
  • Parallel organisation - fenestrated capillaries run alongside
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6
Q

Describe the hypothalamic-pituitary-adrenal axis

A
  • Time of day (circadian), stress or illness stimulate release of corticotrophin releasing hormone (CRH) from the hypothalamus
  • CRH stimulates adrenocorticotrophic (ACTH) hormone from the anterior pituitary
  • ACTH stimulates cortisol/androgen release from the adrenal cortex
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7
Q

Describe the mechanism of action of steroid hormones

A
  • Diffuse through plasma membrane
  • Bind to intracellular cytosolic receptor - steroid receptor
  • Receptor-hormone complex moves into nucleus, binds to glucocorticoid response element (DNA sequence) in 51 flanking region of target genes
  • Binding causes gene transcription of mRNA sequences, translation produces proteins which modulate the response
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8
Q

What activates the renin-angiotensin system?

A

Activated in response to low BP and/or high plasma potassium

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9
Q

Describe the affinity of steroid hormone receptors for steroid hormones

A
  • Mineralocorticoid receptor = aldosterone > deoxycorticosterone > corticosterone > cortisol > dexamethasone
  • Glucocorticoid receptor = dexamethasone > corticosterone > cortisol = aldosterone
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10
Q

What are the actions of the renin-angiotensin system?

A

Renin leads to production of angiotensin II - direct (vasoconstriction) and indirect (thirst/aldosterone) methods of increasing blood pressure

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11
Q

Describe the structure of the adrenal medulla

A
  • Chromaffin cells, medullary veins, splanchnic nerves
  • Rounded cords with large secretory cells
  • Blood from capillaries/sinusoids of cortex and arterioles from capsule
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12
Q

Describe the embryological origin of the adrenal glands

A
  • Cortex - genital ridge (mesoderm)
  • Medulla - neural crest (sympathetic nerve system) - ectoderm
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13
Q

List the types of steroid receptor

A
  • Glucocorticoid receptor - widespread
  • Minerlocorticoid receptor - distal nephron, salivary glanfs, sweat glands, large intestine
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14
Q

Describe the venous drainage of adrenal glands

A
  • Left adrenal vein, drains to left renal vein
  • Right adrenal vein, drains to inferior vena cava
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15
Q

Define Addison’s disease

A
  • Primary adrenal insufficiency
  • Autoimmune destruction of adrenal cortex - 90% destroyed before symptomatic, autoantibodies in 70%
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16
Q

How are steroid hormones formed?

A
  • All synthesised from cholesterol - taken up from circulation (as LDL through LDL receptors then esterified to free cholesterol) or synthesised de novo from acetyl coA (rate limiting enzyme is HMG coA reductase)
  • Rate limiting step - cholesterol transported from cytoplasm into mitochondria by steroidogenic acute regulatory protein (StAR)
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17
Q

Which hormones are produced by each part of the adrenal glands?

A
  • Cortex
    • Zona glomerulosa - mineralocorticoids e.g. aldosterone
    • Zona fasiculata - glucocorticoids e.g. cortisol
    • Zona reticularis - adrenal androgens e.g. DHEA, DHEAS
  • Medulla
    • Catecholamines - adrenaline, noradrenaline
18
Q

How is adrenal insufficiency managed?

A
  • Hydrocortisone as cortisol replacement
    • If unwell IV
    • Then 15-30mg daily - split dose (oral tablets)
    • Mimic diurnal rhythm
  • Fludrocortisone as aldosterone replacement
    • Monitor BP and plasma K+
  • Education - increase dose when unwell
    • Cannot stop suddenly
    • Need identification to show long-term steroid treatment
19
Q

How does the action of angiotensin II lead to aldosterone release?

A
  • Binds to 7TMD G-coupled receptor
  • Activates phospholipase C
  • Hydrolyses PIP2 to IP3 and DAG
  • IP3 causes stored calcium to be released
  • Increased calcium activates Ca2+ calmodulin dependent protein kinases (CaMKs), causes StAR transcription, increased cholesterol movement into the mitochondria
  • Increased aldosterone production
20
Q

Describe the innervation of the adrenal glands

A

Coeliac plexus and thoracic splanchnic nerves (innervate chromaffin cells)

21
Q

Describe the structure of the zona glomerulosa

A

Clusters of small cells, dark granules, close association with blood vessels

22
Q

Describe the gross structure of the adrenal glands

A
  • Endocrine glands (4-6cm, 6-8g) - rich blood supply
  • Pyramidal
  • Yellow due to high cholesterol
  • Outer cortex and inner medulla
    • Outer cortex - zones, secrete different hormones
    • Inner medulla - embryologically/histologically distinct
23
Q

Define Cushing’s syndrome

A
  • Excess cortisol production
  • High mortality, rare
  • More common in women - 20-40 years old
24
Q

How is Addison’s disease diagnosed?

A
  • Biochemistry - low Na+, high K+, hypoglycaemia
  • Short synacthen test
    • Measure plasma cortisol before and 30 minutes after ACTH injection
    • Normal - baseline >250nmol/L, post-ACTH >480nmol/L
  • ACTH level - high
  • Renin high, aldosterone lw
  • Adrenal autoantibodies
25
Q

Why does skin pigmentation occur in Addison’s disease

A

High levels of ACTH (no negative feedback) - bind to melanocortin 1 receptors on the surface of dermal melanocytes

26
Q

List the effects of cortisol

A
  • Increased gluconeogenesis
  • Permissive effect on glucagon
  • Increased lipolysis in adipose tissue to produce free fatty acids (used for energy or in gluconeogenesis)
  • Insulin antagonist
  • Increased skeletal muscle protein breakdown
  • Memory, learning, mood
  • Immune suppression
27
Q

Describe the arterial supply of the adrenal glands

A
  • Superior adrenal artery - inferior phrenic artery
  • Middle adrenal artery - abdominal aorta
  • Inferior adrenal artery - renal arteries
28
Q

Describe the histological layers of the adrenal glands

A
  • Mature adipose tissue surrounds for protection
  • Fibrous capsule
  • Zona glomerulosa
  • Zona fasciculata
  • Zona reticularis
  • Medulla
29
Q

Describe the structure of the zona reticularis

A
  • Smaller cells, haphazard arrangement
  • Stain darker, less lipids
30
Q

List the effects of aldosterone

A
  • Bind to mineralocorticoid receptors on principle cells of DCT and collecting ducts
  • Upregulates Na+/K+ ATPase, ENaC, H+/ATPase (intercalated cells), K+ secretion into lumen, SGK-1 (increased Na+/K+ ATPase)
  • Causes
    • Increased Na+ reabsorption by the kidneys, therefore increased water reabsorption and an increase in BP
    • Increased K+ excretion by the kidneys
    • Increased H+ excretion by the kidneys
31
Q

How is hormone production in the adrenal gland regulated?

A
  • Androgens regulated by ACTH
  • Glucocorticoids regulated by ACTH
  • Mineralocorticoids regulated RAS
32
Q

Describe the causes of Cushing’s syndrome

A
  • ACTH dependent
    • Pituitary adenoma (68%)
    • Ectopic ACTH - carcinoid/oma
    • Ectopic CRH
  • ACTH independent
    • Adrenal adenoma
    • Adrenal carcinoma
    • Nodular hyperplasia
33
Q

What is the cause of iatrogenic Cushing’s syndrome?

A
  • Prolonged high dose steroid therapy, usually oral (can be inhaled/injected)
    • In asthma, rheumatoid arthritis, inflammatory bowel disease, transplants etc.
  • Chronic suppression of ACTH production and adrenal atrophy
  • Unable to respond to stress/illness - need extra doses when ill
  • Cannot stop steroid therapy suddenly - gradual withdrawal of steroid therapy if 4-6+ weeks
34
Q

Describe the clinical features of Cushing’s syndrome

A
  • Euphoria (or depression/psychosis)
  • Hypertension
  • Buffalo hump
  • Thinning of skin
  • Wasting of arm + leg muscles
  • Easy bruising
  • Avascular necrosis of femoral head
  • Increased abdominal fat
  • Moon face and red cheeks
  • Cataracts
  • Striae
35
Q

How is Cushing’s syndrome managed?

A
  • Surgical - removal of ACTH source
    • Transphenoidal pituitary surgery
    • Laproscopic adrenalectomy
  • Medical - metyrapone/ketaconazole - inhibit cortisol production, short-term
36
Q

List the clinical features of Addison’s disease

A
  • Anorexia
  • Weight loss
  • Pre-syncope
  • Low BP (postural hypotension)
  • Abdominal pain
  • Vomiting
  • Diarrhoea
  • Skin pigmentation
37
Q

Where are the adrenal glands located?

A

In abdomen, superior to kidneys

Retroperitoneal

38
Q

How is Cushing’s syndrome diagnosed?

A
  • Establish cortisol excess
    • Dexamethasone suppression testing
    • 24 hr urinary free cortisol
    • Late night salivary cortisol
  • Establish course of cortisol excess
    • Measure ATCH
      • Undetectable - adrenal scan
      • Normal/high - CRH stimulation test
        • No change - CT chest/abdomen/pelvis - ectopic
        • Exaggerated rise in ACTH - pituitary MRI
39
Q

What causes secondary adrenal insufficiency?

A
  • Pituitary/hypothalamus tumour/exogenous steroid use (predisolone, dexatriethasone, inhaled corticosteroid)
  • No skin darkening, no need for fludrocortisone
40
Q

Compare cortisol and aldosterone concentration

A
  • High concentration of cortisol compared with aldosterone
  • Cortisol converted to cortisone (inactive), catalysed by 11 beta-hydroxysteroid dehydrogenase in selected tissues e.g. kidneys to allow aldosterone to function

Medicine Year 2 (41 decks)

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