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Endocrinolgy > Adrenal > Flashcards

Adrenal Flashcards

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1
Q

What is the average size and weight of an adrenal gland?

A

average size: 2-3cm wide, 4-6cm long and 1cm thick
mean weight: 4g irrespective of age, sex or weight
- At autopsy the adrenal gland may weigh up to 22g

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2
Q

What hormones are made in the adrenal gland in each region?

A

medulla: adrenaline and noradrenaline
cortex - steroid hormones:
● Zona glomerulosa - mineralocorticoid - aldosterone
● Zona fasciculata - glucocorticoid cortisol cortisol
● Zona reticularis - adrenal androgens - androstenedione dehydroepiandrosterone acetate (DHEA), (testosterone?)

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3
Q

What happens to the adrenal androgens?

A

Converted in to sex hormones in the periphery

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4
Q

How is cortisol synthesis regulated?

A
  • hypothalamus: CORTICOTROPIN RELEASING HORMONE (CRH) (41aa’s). CRH stimulates corticotrophs in anterior pituitary to produce to produce ADRENOCORTICOTROPIC HORMONE (ACTH) (39 amino acids).
  • ACTH stimulates the adrenal cortex to synthesize and release cortisol.
  • Cortisol feeds back on the corticotrophs of the anterior pituitary to decrease ACTH release and on the hypothalamus to inhibit release of CRH.
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5
Q

How are steroid hormones synthesised?

A

All steroid hormones - derived from cholesterol.
ACTH - G-protein coupled receptor - activates adenyl cyclase - - - increase in cAMP levels.
- activates protein kinase A
- activates cholesteryl ester hydrolase (CEH) which liberates cholesterol from lipid droplets.
- also stimulation of cholesterol 20,22-hydroxylase (desmolase) which is the first enzyme in the pathway and is the rate limiting step. This leads to increased synthesis of cortisol

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6
Q

Why can’t the zona glomerulosa synthesise cortisol?

A

Zona glomerulosa - lacks - 17-alpha-hydroxylase enzyme - Needed to make cortisol

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7
Q

Is the mitochondria involved in the synthesis of cortisol?

A

Yes

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8
Q

What percentages of cortisol in plasma are free, CBG bound, Albumin bound?

A

10%
75%
15%

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9
Q

What percentages of aldosterone in plasma are free, CBG bound, Albumin bound?

A

30-50%
5-10%
25 – 50%

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10
Q

What the mechanism of steroid receptor activation

A
  • Steroid hormones interact with nuclear receptors.
  • Steroid hormone enters cells by diffusion
    binds to cytoplasmic receptor.
  • This leads to dissociation of Heat Shock Protein (hsp90) from the receptor.
  • The hormone-receptor complex dimerises and is translocated to nucleus.
  • The complex binds to hormone responsive element (HRE) on DNA
  • increase in mRNA production and subsequently to increased protein synthesis.
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11
Q

What are the metabolic effects of glucocorticoids

A
  • decrease glucose uptake
  • decrease glucose use
  • increase gluconeogenesis
  • hyperglycaemia
  • decrease protein synthesis
  • increase protein breakdown - muscle wasting
  • decrease Ca2+ absorption in gut
  • increase Ca2+ excretion in kidney
  • decrease activity of osteoblasts
  • increase activity of osteoclasts - osteoporosis
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12
Q

What a the anti inflammatory effects of glucocorticoids?

A 
early phase: vs. redness, heat, pain, swelling late phase: vs. wound healing, repair, proliferation
- decreases:
expression of COX2 (cyclo-oxygenase 2)
cytokine production 
complement in plasma 
nitric oxide (NO) production 
histamine release 
IgG production 
increases: 
annexin-1 (lipocortin-1) which inhibits phospholipase A2 (PLA2)
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13
Q

How is the prevention of cortisol activation of mineralocorticoid receptors achieved?

A

cortisol and aldosterone have same affinity for mineralocorticoid receptor
11betaHSD converts cortisol to cortisone (inactive)
11betaHSD - 11-beta-hydroxysteroid dehydrogenase
11betaHSD2 isoform expressed in aldosterone sensitive tissues

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14
Q

What are the adverse affects of glucocorticoids?

A 
suppression of response to infection
suppression of endogenous glucocorticoid production
metabolic effects
osteoporosis
iatrogenic Cushing's syndrome
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15
Q

What Is the difference between Cushing’s disease and Cushing’s syndrome?

A

Cushing’s disease - ectopic tumour - ACTH, cortisol

Cushing’s syndrome - more common - drug induced

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16
Q

What are the clinical manifestations of Cushing’s syndrome?

A 
easy bruising 
poor wound healing 
muscle wasting 
thinning of skin 
increased abdominal fat
buffalo hump 
moon face 
osteoporosis 
obesity 
increased appetite 
increased susceptibility to infection 
cataracts
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17
Q 
What are the percentage frequencies of the following clinical features of Cushing's disease or syndrome? Obesity
Hypertension
Hirsutism
Striae
Acne
Bruising
Neuropsychiatric effects
Menstrual disorders
Impotence
Glucose intolerance
Diabetes
A 
Obesity 90 
Hypertension 85 
Hirsutism 75 
Striae 50 
Acne 35 
Bruising 35 
Neuropsychiatric effects 85 
Menstrual disorders 70 
Impotence 85 
Glucose intolerance 75 
Diabetes 20
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18
Q

What are the treatments for Cushing’s syndrome?

A
  • Metryrapone 11-beta-hydroxylase
  • Ketoclonazone inhibits steroid biosynthesis
  • Pasireotide (somatostatin analogue) SSTR5 agonist (Receptors highly expressed in tumours - shut down ACTH production) - Mifeprestone - glucocorticoid receptor antagonist
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19
Q

What are the clinical manifestations of Addison’s disease?

A 
muscular weakness 
low blood pressure 
depression
anorexia
loss of weight
Fatigue
Gastrointestinal disturbances
hypoglycaemia
Hyper pigmentation 
Salt cravings
Postural symptoms
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20
Q

What are the percentage frequencies of these clinical manifestations of Addison’s disease?
Weakness, fatigue, anorexia, weight loss
Hyper-pigmentation
Hypotension
Gastrointestinal disturbances
Salt craving
Postural symptoms

A 
Weakness, fatigue, anorexia, weight loss 100
Hyperpigmentation 92
Hypotension 88
Gastrointestinal disturbances 56
Salt craving 19
Postural symptoms 12
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21
Q

In pre-menopausal women what percentage of androstenedione is derived from the adrenal and is converted in peripheral tissue to oestrogen and testosterone?
What effect can excess androgen secretion have in women?

A

In the pre-menopausal woman 50% of androstenedione is derived from the adrenal and is converted in peripheral tissue to oestrogen and testosterone. Excess secretion of these androgens in women can lead to hirsutism and virilisation.

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22
Q

What ‘advantage can obesity have in post-menopausal women?

A

In the post-menopausal woman, with the regression of the ovary, the main oestrogen in oestrone, peripheral conversion of androgen to oestrogen takes place in adipose tissue

  • the production of oestrone is higher in the obese postmenopausal woman than in the thin woman.
  • obese women suffer less from high testosterone in Cushing’s
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23
Q

What are the effects of aldosterone and what is spironolactone?

A

Effects in kidney
Increased number of sodium channels in apical membrane
Increase in Na +/K +ATPase in basolateral membrane
Spironolactone: Aldosterone antagonist , Used as K+ sparing diuretic

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24
Q

See table on synthetic steroid in adrenal - basic notes

A

-

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25
4 classifications of adrenal disorders
– Hypofunction – Hyperfunction – Cancer – Genetic conditions
26
3 Types of hypofunction adrenal disease
– Hypothalamo-pituitary disease – Primary adrenal failure (Addison's disease - destruction of cortex) – Congenital adrenal hyperplasia
27
How does an adrenal gland appear on a CT scan?
Thin structure with lateral and medial limbs
28
From where do the cells of the adrenal medulla originate?
Migratory neural crest cells
29
Aetiology of Adrenal Failure/ Primary adrenal insufficiency? | 9 causes
* Autoimmune (polyglandular failure) * Granulomatous infiltration (TB, sarcoid etc) * Haemorrhage * Fungal infection Fungal * AIDS * Congenital adrenal hyperplasia * Metastatic disease * Adrenalectomy * Toxic drugs
30
Causes of secondary adrenal insufficiency?
* Cessation of exogenous steroids | * Hypothalamo-pituitary hypofunction - Surgery - Radiotherapy - Tumours - Genetics
31
What are the common features of Addison's disease?
``` Weakness - 100% Weight loss - 100% Pigmentation - 95% Postural hypotension - 25% Anorexia - 95% Nausea - 95% Abdominal pain - 30% ```
32
What are the uncommon features of Addison's disease?
Vitiligo - 20% Salt craving - 15% Hypoglycaemia - (in adults) - less than 1% Aches and pain - 10%
33
Treatment of adrenal failure?
• Emergency, life-threatening adrenal crisis: – ICU care – Fluids, sodium IV hydrocortisone @ high dose – IV hydrocortisone @ high dose • Maintenance treatment – Glucocorticoid (hydrocortisone, prednisolone) – Mineralcorticoid (fludrocortisone) – ?DHEA
34
What is Congenital adrenal hyperplasia CAH and what are its consequences?
• Recessive defect in cortisol biosynthesis leading to: - elevated ACTH - adrenomegaly - excess androgens Commonest defect = 21 OH enzyme – Commonest defect Features: – Salt-wasting crises – Precocious puberty in boys – Masculinisation of females leading to ambiguous genitalia at birth
35
List the clinical manifestations of congenital adrenal hyperplasia CAH
``` Classic CAH - presents in neonate Non-classic CAH - presents in adolescence or adulthood Urogenital sinus Labial fusion Scotilization of labia majora Clitoromegaly Penile enlargement Precocious adrenarche Bone age advancement Rapid growth Acne Hirsutism Menstrual abnormalities Infertility - this is the spectrum ```
36
How is CAH treated?
* In utero ideally * Use glucocorticoids to suppress ACTH * Antiandrogens * Mineralocorticoid * Genitoplasty – Controversial wrt age, degree of operation – Gender assignment
37
What are the clinical manifestations of Addison's disease (glucocorticoid deficiency)?
``` Muscle fatique and chronic weakness Depression psychosis Nausea anorexia Hypoglycemia ```
38
What are the clinical manifestations of Cushing's disease (glucocorticoid excess)?
``` Hyperglycemia Elevated blood pressure Obesity (thin limbs, fat trunk) Wasting of skeletal muscle Poor wound healing Mood swings (depression/euphoria) hallucinations ```
39
What is the aetiology of Cushing's disease/syndrome?
ACTH - dependent 80%: – Pituitary adenoma (Cushing's disease) – Ectopic (neuroendocrine tumour) ACTH - independent 20%: – Adrenal adenoma – Adrenal carcinoma – Carney' syndrome (PPNAD)
40
Diagnosis of adrenal Cushing's syndrome?
``` • Circadian serum cortisol (nmol/l) – 0900 604 – 1800 626 – 2400 677 • Plasma ACTH levels (ng/l) – 0900 s so ACTH stays high ```
41
What is the treatment of Cushing's?
Treatment • Laparoscopic adrenalectomy • Replacement GC – Hydrocortisone – Periodic withdrawal • Many of the features improve – BP, diabetes, psychological disturbance may continue
42
What effect does noradrenaline have on force of myocardial contraction,Systolic blood pressure and Diastolic pressure?
Increases them all
43
What effect does adrenaline have on force of myocardial contraction,Systolic blood pressure and Diastolic pressure?
Increases the first 2 | Usually little effect on latter
44
What affect do adrenaline and noradrenaline have on heart rate?
Adrenaline: increases Noradrenaline: decreases because of reflexes
45
What is the effect of adrenaline on the blood flow to skin, mucous membranes, gut, brain, skeletal muscle?
``` skin - decreases mucous membranes - decreases gut - decreases brain - increases skeletal muscle - increases ```
46
What is the effect of noradrenaline on the blood flow to skin, mucous membranes, gut, brain, skeletal muscle?
``` skin - decreases mucous membranes - decreases gut - decreases brain - may increase slightly skeletal muscle - little or no effect ```
47
Does adrenaline affect anxiety?
Yes - increases the sensation of anxiety
48
Does noradrenaline affect anxiety?
No
49
What affect does adrenaline have on the blood levels of glucose, lactic acid, fatty acids?
- Glucose: Raised - Lactic acid: Markedly increased - Fatty acids: Somewhat increased
50
What affect does noradrenaline have on the blood levels of glucose, lactic acid, fatty acids?
- Glucose: Little effect - Lactic acid: Slightly increased - Fatty acids: Increased
51
STIMULI WHICH CAUSE EPI/NORAdrenaline RELEASE?
* Stressful situations * Hypoglycemia (dietary or disease induced) * Postural hypotension * Exercise
52
What is Phaeochromoctoma and what is its aetiology?
``` • Tumour of the adrenal medulla(typically benign, typically cystic?) – Secreting NA or A – 10 % bilateral - 10 % malignant – 10 % part of a genetic condition: • MEN 2 • Von Hippel Lindau • NF- 1 SDH ```
53
How does Phaeochromoctoma present?
* Headaches * Palpitations * Sense of Doom * Chest pain * Sweating * Weight loss
54
How can you diagnose Phaechomoctoma?
• Plasma or urine assessment of levels of A, NA or their products – VMA / HMMA – Metanephrins - almost exclusively used – Imaging • Nuclear medicine – MIBG • Radiology – CT/ MRI
55
Treatment of Phaechomoctoma?
* Surgical removal after – Pretreatment with alpha and B blockade • Phenoxybenzamine * Doxazosin first then propranolol
56
PHYSIOLOGICAL EFFECTS OF ALDOSTERONE?
``` Regulation of water and electrolyte balance - Decreases cellular K+ - increases cellular Na+ in kidney: - Increases Na+ reabsorption - Decreases K+ reabsorption - Increases H+ secretion ```
57
Volume-feedback loop between angiotensin 2 and aldosterone?
``` • Action of angiotensin II on aldosterone results in negative feedback • 2 critical systems are regulated: – 1) sodium homeostasis ) – 2) regulation of arterial pressure: • Vasular smooth muscle • NA release • ADH • Volume expansion ```
58
What is the action of aldosterone?
• Aldosterone binds to the type 1 mineralocorticoid receptor – Increasing the number of “open” sodium channels channels - Increased sodium resorption • Negative gradient in the lumen – Consequent secretion of K and H
59
What are the clinical features of Conn's syndrome (primary hyperaldosteronism)?
– Hypertension, often difficult, younger people – Spontaneous or diuretic associated hypokalaemia – Oedema = rare • Hypernatraemia, hypomagnesaemia, alkalosis, DI, neuromuscular symptoms
60
What are the features of aldosteronism?
* Often non-specific, hypertension * Hypokalaemia related to renal potassium wasting * Classical: hypertension, hypokalaemia & alkalosis
61
What causes secondary aldosteronism?
–Renovasular | –Gitelmans, Barrters pseudo, nephrotic, cirrhotic, CCF
62
What are the usual clinical manifestations do primary hyperaldosteronism?
* Hypertension * Hypokalemia * Hypervolemia (without peripheral edema) * Metabolic alkalosis
63
What are the 'other' clinical manifestations/effects do primary hyperaldosteronism?
-Due to hypertension: •Headaches •Retinopathy (rare) -Due to hypokalemia: •Neuromuscular symptoms (cramps, paresthesias, weakness) •Nephrogenic diabetes insipidus •Cardiac arrhythmia •Glucose intolerance / impaired insulin secretion -Due to direct actions of aldosterone on the cardiovascular system: •Cardiac Hypertrophy/Fibrosis •Vascular smooth muscle hypertrophy •Due to a reset osmostat •Mild hypernatremia
64
What are the subtypes of Primary hyperaldosteronism?
* Aldosterone producing adenoma (60%) * Bilateral adrenal hyperplasia (30-40%) * Glucocorticoid-remediable aldosteronism (1-3%) * Unilateral adrenal hyperplasia * Adrenal carcinoma
65
What do you know about Aldosterone producing adenoma?
* Small – 0.-2 cm * Women > men * Histology- difficult= benign cortical adenoma * CT appearance- low HU
66
Diagnosis of primary aldosteronism?
• Biochemical screening – PRA, aldosterone= PA/ PRA
67
Confirmation of primary hyperaldosteronism?
* Measurement of PRA (suppressed) and aldosterone (high) in salt-replete individuals * Salt loading * Suppression with fludorocortisone * Catheter studies for selective venous sampling
68
Treatment of Conn's syndrome?
``` • Remove the adenoma – Open or laparoscopic • Drug treatment: – Spironolactone – Eplerenone – Amiloride + others ```

Endocrinolgy (8 decks)

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