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Endocrinology > Adrenal > Flashcards

Adrenal Flashcards

1
Q

What are the layers of the adrenal gland?

A 
(superficial) 
capsule
cortex
medulla
(deep)
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2
Q

What are the three zones of the cortex? What do they secrete?

A

Zona glomerulosa-mineralocorticoids
Zona fasciculata- glucocorticoids
Zona reticularis- adrenal androgens

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3
Q

What is contained in the adrenal medulla? What is secreted?

A

chromaffin cells secrete catecholamines, medullary veins, splanchnic (sympthetic) nerves

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4
Q

What are the corticosteroids made from in the adrenal cortex?

A

cholesterol

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5
Q

Whatis the end corticosteroid from

a) z. glomerulosa
b) z fasciculata
c) z. reticularis

A

a) aldosterone
b) cortisol
c) DHEA and androstendione

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6
Q 
How is the production of
a) aldosterone
b) cortisol
c) androgen
regulated?
A

a) RAAS and plasma K+
b) hypothalamus and ant. pit.
c) hypothalamus and ant. pit

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7
Q

What is the cortisol/androgen axis?

A

Hyp: CRH+
Pit: ACTH+
Adrenal cortex:Cortisol

NB, negative feedback

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8
Q

How does the RAAS system work?

A 
Fall in BP
Renin released from kidneys
Turns angiotensinogen to angiotensin 1
ACE turn it to angiotensin 2
(vasoconstriction=direct)
Angiotensin 2 causes aldosterone to be released from adrenal
Aldosterone increases salt retention (indirect)
BP rises
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9
Q

What is the mechinism of action in corticosteroids?

A

Steroid hormones binds to intracellular receptor

DNA is bound to affect transcription

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10
Q

What are the metabolic affect of cortisol?

A

increase blood sugar
increased lipolysis (central distribution)
increased proteolysis

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11
Q

What are the CVS effects of cortisol?

A

Increased CO
Increased BP
increased renal blood flow and GFR

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12
Q

What are the MSK effects of cortisol?

A

accelerates osteoporosis
reduced serum Ca2+
reduced collagen
reduced wound healing

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13
Q

What are the immunological effects of cortisol?

A

reduced capillary permeabilty
reduced leukocytes
reduced macrophages
reduced cytokines

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14
Q

What are the main uses of corticosteroids?

A

suppress inflammation
suppress immune system
replacement treatment

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15
Q

Where are Mineralocorticoid receptors found?

A

kidneys
salivary glands
gut
sweat glands

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16
Q

What are the effects of aldosterone?

A

K+/H+ excretion
increased Na+ reabsorption
BP regulation
Regulates ECF volume

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17
Q

What can cause adrenal insuffieciency?

A

Inadequate adrenal function
Primary insufficiency
Secondary insufficiency

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18
Q

What are causes of primary adrenal insufficiency?

A

Addison’s
Congenital adrenal hyperplasia
Adrenal TB
Malignancy

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19
Q

What can cause secondary adrenal insufficiency?

A

lack of ACTH stimmulation
iatrogenic steroids
Pituitary/Hypothalamic disorders

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20
Q

What is the commonest cause of primary adrenal insufficiency?

A

Addison’s

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21
Q

What is the aetiology of addison’s?

A

Autoimmune destruction of adrenal cortex
Autoantibodies in 70%
Low cortisol levels

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22
Q

How much of the adrenal will be destroyed before symptoms of addison’s appear?

A

90%

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23
Q

With what other conditions is addison’s associated?

A

T1DM
Pernicious anaemia
Autoimmune thyroid

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24
Q

What are the symptoms of addison’s?

A 
Anorexia
Weight loss
Fatigue
Dizziness
Low BP
Abdo pain
Vomiting
Diarrhoea
Skin pigmentation (ACTH)
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25
Q

What are the diagnositic features of addison’s?

A 
low Na+
high K+
Anbormal synacthen
Hypoglycaemia
Increased ACTH
increased renin/reduced alsdosterone
Adrenal sutoantibodies
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26
Q

What dynamic test would be used to test for addison’s? How does it work?

A

Short SynATCHen test

  • measure before and 30 mins after iv ACTH injection
  • before >250nmol, after>480 is normal
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27
Q

What is the management for addison’s?

A

Hydrocortisone to replace cortisol( IV if unwell, 15-30mg daily, mimic diuinal rhythm)
Fludrocortisone to replace aldosterone (monitor BP and K)

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28
Q

What education do patients treated for adrenal insufficiency need?

A

sick day rules
do not stop suddenly
wear identification

29
Q

How is secondary adrenal insufficiency characterised?

A

lack of CRH or ACTH

30
Q

What is the most common cause of secondary adrenal insufficiency?

A

exogenous steroids

mimcs negative feedback

31
Q

How is secondary adrenal insufficiency different to addison’s?

A 
Pale skin (no inc ACTH)
Aldosterone intact (no RAAS involvement)
32
Q

How is secondary adrenal insufficiency treated?

A 
Hyrdocortisone only 
(no need for fludrocortisone)
33
Q

How is cushing’s syndrome defined?

A

excess cortisol secretion

34
Q

what is the etiology of cushing’s?

A

women

20-40years

35
Q

What are the symptoms of cushing’s?

A

easy bruising
striae
facial plethora
proximal muscle weakness

36
Q

What are the adrenal causes of cushing’s?

A

adrenal adenoma/carcinoma

37
Q

What is the most common cause of Cushing’s?

A

iatrogenic high dose steroids=chronic suppression of ATCH and adrenal atrophy

38
Q

What is primary aldosteronism?

A

Autonomus production of aldosterone independent of regulators(angiotensin 2/K)

39
Q

What are the CVS actions of aldosterone?

A 
increased cardiac collagen
increased sympathetics
Na+ retention
Cytokine synthesis
Altered endothelial function
40
Q

What are the CVS responses to aldosterone?

A

inc BP

  • LVH
  • Atheroma
41
Q

What are the clinical features of primary aldosteronism?

A

Significant hypertension
Hypokalaemia
Alkalosis

42
Q

What are the causes of primary aldosteronism?

A 
adrenal adenoma (Conn's syndrome)
Bilateral hyperplasia (commonest)
Genetic mutation (KCNJ5 channel)
Unilateral hyperplasia(rare)
43
Q

How is primary aldosteronism diagnosed?

A

1) -measure ARR (aldosterone renin ratio)
- >750 then saline suppression test
- failure to suppress saline by 50%=PA

2) confirm subtype
- Adrenal CT
- adrenal vein sample to confirm adenoma s true source

44
Q

How is primary aldosteronism managed?

A

Surgical laproscopic adrenalectomy if adenoma.

Spironolactone if bilateral hyperplasia (MR antagonist)

45
Q

What is congenital adrenal hyperplasia?

A

defect with enzymes in steroid pathway

46
Q

What is the most common enzyme deficiency in CAH?

A

21a hydroxylase

47
Q

How is CAH diagnosed?

A

Basal/stimulated 17-OH progesterone levels

48
Q

How do males with CAH classically present?

A

Adrenal insufficiency (2-3 weeks)
poor weight gain
Addison’s biochemical pattern

49
Q

How do females with CAH classically present?

A

genital ambiguity

50
Q

What is the non-classical presentation of CAH?

A 
Hirsuites
Acne
Oligomaenhorroea
Precocious puberty
Infertility/subfertility
51
Q

What is the principles of treatment of CAH in children?

A

Timely recognition
Gluco/mineralocorticoid replacement
surgical correction
Acheive maximum growth potential

52
Q

What are the principles of treatment in CAH adults?

A

Control androgen excess
Restore fertility
Avoid steroid overreplacement

53
Q

What is the weight of an adrenal gland in healthy adults?

A

4g

54
Q

What is phaeochromocytoma?

A

rare tumour of adrenal medulla
Increased catecholamines
10% tumour

55
Q

Why do adrenals look brown in phaeochromocytoma?

A

chromaffin cells reduce chrome salts to metal chromium

56
Q

Why is it important to diagnose phaeochromocytoma?

A

Curable hypertension
surgical risks
pregnancy risks
potentially fatal

57
Q

What are the symptoms of phaeochromocytoma?

A 
Triad: hypertension (50%paroxysmal), headache, sweating
palpitations
breathless
constipation
anxiety
weight loss
58
Q

What are the signs of phaeochromocytoma?

A 
hypertension
postrual hypotension (50%)
pallor
arrythmia
pyrexia
59
Q

What are the biochemical abnormalities in phaeochromocytoma?

A 
hyperglycaemia
low K
raised Hb
mild hypercalcaemia
lactic acidosis
60
Q

Who should be investigated for phaeochromocytoma?

A

family memebers with syndromes
resistant hypertension
<50 yrs patient with HT
HT and Hyperglycaemia

61
Q

How can phaeochromocytoma be confirmed?

A

confirm catecholamine excess

Urine catecholamine samples 2x24hr

62
Q

How can you identify the source of catecholamine excess in phaeochromocytoma?

A

MRI
PET
MIBG scans

63
Q

How is phaeochromocytoma treated?

A

alpha and beta blockade
fluid+/- blood replacement
total excision where possible
chemotherapy if malignant

64
Q

What conditions are associated with phaeochromocytoma?

A

Multiple endocrine neoplasia 2
Succinate dehydrogenase mutations
Neurofibromatosis
Tuberose sclerosis

65
Q

What is MEN2?

A

Autosomal dominant
mutation of tyrosine kinase receptor

associated:MTC, parathyroid hyperplasia, bilateral phaeochromocytoma

66
Q

What is Von Hippel Lindau syndrome?

A

Mutation HIF1-a
Autosomal dominant
Vascular tumour
SDH genes stabilise HIF1-a

67
Q

What are the signs of neurofibromatosis?

A

Axillary freckling
Cafe au lait patches
Neurofibromas

68
Q

What is the apperance of phaeochromocytoma?

A

Zellballen (cells form nests)

69
Q

Where do phaeochromocytomas metastasise to?

A

bones
regional lymph nodes
liver
lung

Endocrinology (17 decks)

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