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Endocrinology > Adrenal Gland Anatomy and Physiology > Flashcards

Adrenal Gland Anatomy and Physiology Flashcards

1
Q

What are cortioids derived from?

A

Steroids

Derived from enzymatic modification of cholesterol

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2
Q

Where are steroid enzymes location intracellularly?

A

Mitochondria and sER

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3
Q

Are steroids permeable or impermeable?

A

Freely-permeable to membranes

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4
Q

Can steroid enzymes be stored? Where

A

No. They are synthesised and immediately released

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5
Q

Are steroids water soluble?

A

No

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6
Q

What time of day is plasma concentration of steroid hormones highest?

A

Higher in the morning than at night (diurnal rhythm)

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7
Q

How is cortisol circulated?

A

95% is bound to proteins

- mainly cortisol-binding globulin

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8
Q

Where do the adrenal glands lie?

A

Between the superiomedial aspects of the kidneys and the diaphragmatic crura

Surrounded by connective tissue and perinephric fat

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9
Q

What are the adrenal glands?

A

Endocrine glands

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10
Q

What size and weight are the adrenal glands?

A

4-6cm

6-8geach

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11
Q

How many arteries supply the adrenal glands and where do they branch of?

A

3

  1. Superior suprarenal artery - from subphrenic artery
  2. Middle suprarenal artery - from abdominal aorta near the SMA
  3. Inferior suprarenal artery - from the renal artery
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12
Q

Describe adrenal venous drainage

A

Medullary vein emerges from the hilum of each gland forming the suprarenal vein which goings:
IVC on the R
RV on the L

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13
Q

Describe the nerve supply to the adrenal glands

A
  1. Colic plexus
  2. Thoracic splenchnic nerves

Act on the chromaffin cells in the adrenal medulla
- secrete (nor)adrenaline

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14
Q

Describe the histological layout of the adrenal glands

A

Fibrous capsule
______
Outer Cortex

  1. Zona glomerulosa
    - regulated by Ang II and K+
    - secretes mineralocorticoids (aldosterone) and glucocorticoids (cortisol)
    __
  2. Zona fasiculata
    - regulated by ACTH
    - secretes mineralocorticoids (aldosterone) and glucocorticoids (cortisol)
    __
  3. Zona reticularis
    - regulated by ACTH
    - secretes: androgens, DHEA, and DHEAs
\_\_\_\_\_
Inner medulla
- Chromaffin cells
- regulated by nerves: colic plexus and thoracic splanhnic nerves
- secretes: nor(adrenaline)
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15
Q

List the adrenal androgens and where are they secreted from?

A 
DHEA
Androstenedione
DHEA
DHEAs
Testosterone
  • zone reticularis
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16
Q

What areas secreted cortisol and aldosterone?

A

Zona glomerulosa and zona fasciculata

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17
Q

Sources of cholesterol?

A

Diet into circulation

De novo via acetyl CoA

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18
Q

What is the rate limiting step of cholesterol synthesis?

A

HMG-CoA Reductase enzyme

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19
Q

What is the first enzymatic step of steroid hormone synthesis?

A

Cholesterol –> pregnenolone

Via mitochondria P450 enzyme

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20
Q

What is the rate-limiting step of steroid hormone synthesis?

A

Transport of free cholesterol from cytoplasm to mitochondria by Steriodogenic Acute Regulatory Protein (StAR)

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21
Q

Where does steroid synthesis take place?

A

Mitochondria

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22
Q

What causes congenital adrenal hyperplasia?

A

21-hydroxylase deficiency
or
11-hydroxylase deficiency

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23
Q

Where are steroid receptors found?

A

Nucleus

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24
Q

How do steroid hormones act?

A

On nuclear receptors

Initiate transcription factors

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25
Q

What are the domains of the steroid receptors?

A

A/B - N-terminal: domain controls which gene is activated
C - DNA binding domain
D - hinge-region - controls movement of the receptor to the nucleus
E - ligand binding domain: binds steroid
F - C-terminal domain

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26
Q

Which domain on the steroid receptors do ligands bind?

A

E

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27
Q

Which domain on the steroid receptors control which gene is activated?

A

A/B

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28
Q

Describe steroid hormone MOA

A
  1. Steroid hormones diffuses through plasma membrane
  2. Binds to intracellular cytosolic receptor
  3. Receptor-hormone complex enters the nucleus and binds to a glucotocoid response element (DNA sequence) in the 5’ flanking region of the target gene
  4. Binding initiates gene transcription to produce mRNA
  5. mRNA is translocate to protein which mediates the effect-target cell response
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29
Q

What types of steroid receptors are there?

A 
Glucocorticoid receptors (GR)
Mineralocoritocoid receptors (MR)
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30
Q

Explains the distribution of steroid receptors

A
  1. Glucocorticoid receptors (GR)
    - widespread
  2. Mineralocoritocoid receptors (MR)
    - distal nephron
    - salivary glands
    - sweat glands
    - large intestine
    - brain
    - vascular tissue
    - heart
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31
Q

Cortisol can bind to MR
and cortisol concentration is higher than aldosterone

What mechanism if used to protect MR from illicit occupation by glucocortocoids?

A

Enzyme: 11beta-HSD II

  • Catalyses the conversion of cortisol (active) to cortisone (inactive)
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32
Q

What is the inactive form of cortisol?

A

Cortisone

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33
Q

How is cortisol converted to its inactive form?

A

Cortisone is its inactive form

Converted via 11b-HSDII

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34
Q

What common food can inhibit the enzyme that converts cortisol to its inactive form

A

Inactive form: cortisone
Converted by 11b-HSD II

Can be inhibited by liquorice

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35
Q

List effects of cortisol

A
  • stimulates gluconeogenesis in liver
  • permissive effect on glucagon
  • stimulates lipolysis in adipose tissue = FA is released
  • acts as insulin antagonist and suppresses the release of insulin
  • increases breakdown of skeletal muscle protein
  • immune suppression
  • changes mood
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36
Q

List actions of aldosterone

A
  • Na+ reabsorption + H2O

- K+ and H+ excretion

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37
Q

Where does aldosterone act?

A

MR in the principal cells of the DCT and CD in the kidney

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38
Q

What does aldosterone do in the kidney?

A
  • upregulates and activates basolateral Na/K-ATPases
  • upregulates ENaC - increasing apical membrane permeability to Na
  • stimulates K+ secretion into lumen
  • stimulate H+ secretion via H+-ATPase in the intercalated cells of the CD
39
Q

Describe aldosterone MOA in the kidney

A
  1. aldosterone bines to MR
  2. initiates cascade acting on the nucleus
  3. transcribes hormonal response elements
  4. mRNA transcription of ENaC, pumps etc…
  5. Na+ reabsorption + H2O
    + K+excretion
40
Q

How is adrenal steroid production regulated

A
  1. Cortisol and androgens - HPAA

2. Aldosterone - RAAS and [K+]plasma

41
Q

What is ACTH

A

Andogencoricotrophic hormone

42
Q

What kind or hormone is ACTH

A

39AA peptide

43
Q

What is ACTH formed from?

A

POMC

Pro-opiomelanocortin

44
Q

What hormones are secreted from POMC?

A

ACTH
gamma-MSH
Endorphins (lipotropins)

45
Q

What hormones trigger europhic effects and where are they released from?

A

B-endophin and met-enkephatin

POMC

46
Q

What’s the function of gamma-MSH?

A

Controls melanin pigmentation of the skin

47
Q

What activates RAAS?

A

Major regulator of aldosterone production

  • activated in response to decrease in BP and [Na+]plasma
48
Q

What is the direct effects of AngII

A

Vasoconstriction

49
Q

What is the indirect effects of AngII?

A

aldosterone + thirst

50
Q

What does RAAS do to BP

A

Increases BP

51
Q

What is the RAAS pathway?

A
  1. decrease in BP and [Na+] detected in JG-apparatus
  2. renin released from juxtaglomerular cells
  3. renin converts angiotensinogen to AngI
  4. ACE converts Ang I to Ang II
  5. Ang II acts on adrenal cortex to secrete aldosterone
  6. aldosterone acts on kidneys to retain sodium and water
52
Q

How does Ang II act on the adrenal medulla?

A
  1. GPCR
  2. Cascade: PLC-PIP2-IP3-DAG
  3. Increased IC Ca2+
  4. Transcription of StAR (Steriodogenic Acute Regulatory Protein)
  5. Cholesterol uptake into mitochondria
  6. Biosynthesis
53
Q

What blood biochemical change apart from sodium decrease can trigger aldosterone?

A

increase [K+]ec

54
Q

What is primary aldosteronism?

A

Increase levels of aldosterone

55
Q

What does primary aldosteronism lead to (biochemically)?

A
  • increase Na reabsorption = hypernaturaemia
  • volume expansion
  • hypokalaemia
  • alkalosis
  • low plasma renin activity
  • hypertension
56
Q

What can cause primary aldosteronism?

A
  • aldosterone-producing adenoma (unilateral)

- bilateral adrenal hyperplasia

57
Q

What syndrome results from increased levels of cortisol?

A

Cushing’s Syndrome

58
Q

What are the typical features seen in Cushing’s syndrome

A
  • weight gain
  • moon face
  • increased BP
  • red raddy face
  • buffalos hump
  • stomach strech striae
59
Q

What are the cause of Cushing’s syndrome?

A

ACTH-producing pituitary adenoma

60
Q

What, apart from pituitary adenoma, can cause hypersecretion of cortisol?

A

Cortisol-producing adrenal adenoma

or
Iatrogenic

61
Q

What is Addison’s disease?

A

Primary adrenal insufficiency or hypoadrenalism
Autoimmune
Inability of adrenal gland to make cortisol and aldosterone

62
Q

What are the common clinical characteristics of Addison’s?

A 
Fatigue
Cachexia
Low mood
Loss of appetite 
Weight loss
Increased thirst
Pigmentation
63
Q

Give a few examples of what can cause primary adrenal insufficiency

A

Autoimmune (Addison’s)
TB
Viral
Malignancy

64
Q

What is primary adrenal insufficiency

A

Inadequate adrenocortical function

Inability to increase steroid hormone production

65
Q

What are the characteristics of congenital adrenal hyperplasia

A
  • ambiguous genitalia
  • precocious puberty
  • hirsutism
  • amenorrhea
  • mentrural irregularities
66
Q

What kind of disease is congenital adrenal hyperplasia?

A

Autosomal recessive
lack of 21-hydroxylase activity
deficiency of cortisol and aldosterone
increased adrenal androgens

67
Q

What biochemical feature would you expect in congenital

adrenal hyperplasia

A

Increase ACTH - in an attempt to compensate but this drives cholesterol biosynthesis down 17-hydroxylase pathways generating increased androgens

Decreased cortisol and aldosterone

68
Q

How is secondary adrenal insufficiency caused?

A
  • lack of ACTH stimulation
  • iatrogenic (excess exogenous steroid)
  • pituitary/hypothalamic disorders
69
Q

What is Addison’s disease?

A

Commonest cause of primary adrenal insufficiency

- autoimmune destruction of adrenal cortex

70
Q

How much of the adrenal cortex would be destroyed in Addison’s before patient is symptomatic?

A

> 90%

71
Q

What are the common clinical features of Addisons

A 
Anorexia
Weight loss
Fatigue/lethargy
Dizziness
Decreased BP
Abdominal pain
Vomiting
Diarrhorea
Skin pigmentation
72
Q

Why do you get an increased ACTH in Addison’s?

A

Amplified negative feedback of cortisol due to lack of cortisol production

73
Q

Dx Addison’s

A
  • Suspicious biochemistry: decreased Na+, increased K+, hypoglycaemia, acidosis
  • Impair cortisol response to synthetic ACTH (syn-ACTH-en)
  • Elevated ACTH causes skin hyperpigmentation (POMC)
  • Adrenal autoantibodies
  • Increased renin
  • Decreased Aldosterone
74
Q

What is the biochemistry of addisons

A
  • Suspicious biochemistry: decreased Na+, increased K+, hypoglycaemia, acidosis
75
Q

Describe the synthetic ACTH test

A

Impaired cortisol response test

synACTHen
- measure plasma cortisol before and 30minutes after IV injection

Normal (cortisol levels):

  • baseline: >250nmol/L
  • post-ACTH >480nmol/L
76
Q

Why is there hypotension and electrolyte imbalance in Addisons

A

Mineralocorticoid deficiency

  • Decrease aldosterone = Decreased Na+ and increase K+
  • Decreased water reabsorption = hypovolaemia = hypotension

*dehydration is the most common cause of orthostatic hypotension

77
Q

What causes hyperpigmentation in Addisons?

A

Increased ACTH
Increased POMC
POMC = pro-opiomelanocortin

78
Q

What causes hypoglycaemia in Addisons

A

Decreased cortisol

79
Q

What natural conditions could give rise to cortisol?

A

Pregnancy and contraceptive pill

80
Q

Tx Addisons

A
  • Hydrocortisone (cortisol replacement)

- Fludrocortisone (aldosterone replacement)

81
Q

What clinical feature distinguishes between primary and secondary adrenal insufficiency?

A

In secondary there is no increase in ACTH (there’s a lack of ACTH) so there is no hyperpigmentation (POMC)

And during an aldosterone production test, aldosterone is working as its regulated by RAAS

82
Q

What are the causes of Cushing’s syndrome?

A

MAIN: oral steroids

Endogenous causes are rare
- 80% are due to increase ACTH - pituitary adenoma (Cushing’s disease)

  • ACTH-dependent
    1. pituitary adenoma
    2. ectopic ACTH - carcinoid/carcinoma
    3. Extopic CRH
  • ACTH-independent: decreased ACTH due to negative feedback
    1. adrenal adenoma
    2. adrenal carcinoma
    3. nodular hyperplasia
83
Q

Why is random plasma cortisol not an effective way to Dx Cushing’s?

A

May be misleading as illness, time of day, and stress (e.g. venepuncture) influence cortisol levels

84
Q

How would you Dx Cushing’s?

A

Step 1: establish cortisol excess

  1. Overnight dexamethasone suppression test
    - 1mg oral steroid
    - if normal: should decrease ACTH and cortisol due to negative feedback
    - in Cushing’s: No cortisol is suppressed
  2. 24-hour urinary free cortisol (alternative)
    - excess cortisol will exceed availability plasma capacity of plasma binding globulin (cortisol binding globulin)
    - unbound cortisol is filtered freely into urine
    - either 24hr assessment or cortisol:Cr ratio
  3. Midnight salivary test of cortisol
    - 11pm-midnight
    - in normal people cortisol level is very low at this time
    - in cushings it is very high due to loss of circadian rhythm

Step 2: Establish the source of cortisol excess

  1. undetectable ACTH
    - adrenal CT = positive adrenal adenoma/carcinoma
  2. normal/high ACTH
    - do CRH stimulation test
    a) no change in ACTH = CT chest/abdominoplevic region = actopic ACTH
    b) exaggerated rise in ACTH = pituitary MRI = adenoma
85
Q

Tx Cushing’s Syndrome?

A
  1. medical
    - inhibit cortisol production (Metyrapone)
  2. Surgical
    - Trans-sphenoidal pituitary surgery
    - laproscopic adrenalectomy
    - excise ATCH source
86
Q

What is the 2nd commonest cause of hypertention?

A

Primary aldosteronism

87
Q

What causes primary aldosteronism?

A

Single or bilateral adrenal adenoma

88
Q

Dx primary aldosteronism

A
  1. biochemistry:
    - increase aldosterone
    - decrease renin
    - decreased K+
    - increased Na+
  2. suppression test
    - IV saline
    - attempt to suppress aldosterone
  3. Adrenal CT
89
Q

Management primary aldosteronism

A
  1. Surgical
    - adrenal adenoma: unilateral laparoscopic adrenalectomy
    - cures hypokalaemia
    - cures hypertension (30-70% cases)
  2. Medical
    - in bilateral adrenal hyperplasia
    - MR antagonist - spironolactone
    - amiloride (inhibit ENaC)
90
Q

What is phechromocytoma?

A

Catecholamine-secreting tumours of the adrenal medulla

91
Q

What is the clinical consequence of phechromocytoma?

A 
Hypertension
Headaches
Palpitations
Pallor
Sweating
92
Q

Dx phechromocytoma

A
  • Measure urinary catecholamines and metabolites

- CT adrenals

93
Q

Tx phechromocytoma

A

alpha1 +/- beta1 antagonists

Endocrinology (11 decks)

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