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Adrenal disorders Flashcards

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1
Q

the medulla of the adrenal gland is

A

primitive nerve tissue

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2
Q

the cortex of the adrenal gland is

A

endocrine tissue (deep you o the sweeter its gets

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3
Q

Zona glomerulosa

A

Salt and water- mineralocorticoids

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4
Q

Zona fasciculata

A

Sugar -glucocorticoids

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5
Q

Zona reticularis

A

Sex- androgen

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6
Q

Disorders of the adrenal cortex

A

Adrenal insufficiency’s

Cushing’s

Hyperaldosteronism

Congenital adrenal hyperplasia (CAH)

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7
Q

Disorders of the adrenal medulla

A

Pheochromocytoma (dusty coloured cell of a tumour)

Paraganglioma (pheochromocytoma outside the adrenal gland)

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8
Q

Presentation of adrenal medulla disease (noradrenaline/ adrenaline)

A
  • Excessive catecholamine secretion
  • Acute episodes
  • Sweating
  • Palpitations
  • High or low BP
  • Collapse
  • SUDDEN DEATH
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9
Q

Biochemical assessment of adrenal medulla

A
  • 24h urine catecholamines
    • Adrenaline
    • NA
    • Dopamine
    • 3-methoxy-tyramine
  • Usually measure breakdown products of catecholamines- Metanephrines24 h urine metanephrines
    • Metadrenaline
    • Normetadrenaline
  • Plasma metanephrines (more sensitive than 24h urine)
    • Avoid certain foods: coffee, coke, bananas, chocolate, vanilla
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10
Q

Clinical presentation of adrenal cortex disease: Cortisol (lack of glucocorticoid) deficiency

A

weakness, tiredness, weight loss, hypoglycaemia

*Cortisol does the opposite to insulin*

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11
Q

Clinical presentation of adrenal cortex disease: Mineralocorticoid (aldosterone) deficiency

A

– dizziness, hypotension, low Na, high K

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12
Q

Clinical presentation of adrenal cortex disease: Androgen deficiency– e.g. Addisons

A
  • In women- low libido and loss of body hair in women
    • Testosterone only produced in adrenal gland in women
  • In men- no symptoms because produced in testosterone
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13
Q

Clinical presentation of adrenal cortex disease: Cortisol excess

A
  • Weight gain and cushingoid features (cushing’s syndrome)
  • Diabetes
  • Bone weakness
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14
Q

Clinical presentation of adrenal cortex disease: Mineralocorticoid excess (aldosterone)-

A

high BP and low K

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15
Q

Clinical presentation of adrenal cortex disease: androgen excess

A

increased male characteristics in women

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16
Q

ACTH excess from pituitary

A
  • Skin pigmentation due to melanocyte stimulation
  • Pigmentation seen in Addisons and ACTH- driven cushings
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17
Q

Biochemical assessment of adrenal cortex: Suspected adrenal hormone deficiency

A
  • Electrolytes- low Na, high K in aldosterone deficiency
  • 0900 basal cortisol- low when it should be high
  • Stimulation test- inject synthetic ACTH (synacthen)
  • ACTH stimulates cortisol
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18
Q

Biochemical assessment of adrenal cortex :Suspected adrenal hormones excess

A
  • Electrolyte- high BP, low K
  • Midnight cortisol- high, should be low
  • 24h urine cortisol- high
  • Suppression test- failure to suppress
  • Androgens and derivatives – high
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19
Q

Radiological assessment of adrenal disease

CT scan

A
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20
Q

Radiological assessment of adrenal disease

MRI scan

A
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21
Q

Radiological assessment of adrenal disease

functional imaging - MIBG scan

A
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22
Q

Radiological assessment of adrenal disease

functioning imaging - PET scan

A
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23
Q

adrenal cortex disorders are related to which hormones

A

aldosterone, cortisol and androgens

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24
Q

Hperaldosteronisms

A

A condition in which there is excessive production of aldosterone.

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25
Primary hyperaldosteronism:
excess aldosterone production due to a defect in the adrenal cortex. Commonoest form of endocrine hypertension. 1. Bilateral idiopathic adrenal hyperplasia 2. Or Aldosterone-secreting adenoma (Conns syndrome)
26
diagnosis of primary hyperaldosteornism
* Hypertension and hyperkalaemia * Elevated aldosterone independent of RAAS (suppressed renin) * Scan- shows adrenal adenoma or bilateral hyperplasia
27
Secondary hyperaldosteronism:
* excess aldosterone production due to o**veractivity of the RAAS** * Renin- producing tumour or renal artery stenosis
28
signs and symptoms of hyperaldosteronism
* High blood pressure * Left ventricular hypertrophy * Stroke * Hypernatremia * Hypokalaemia
29
treatment of hyperalsteronism
* Dependent on cause * **Surgical treatmen**t for aldosterone-secreting adenomas or * **Spironolactone** (a mineralocorticoid receptor agonists) can be used for other causes
30
what is a disorder cause dby excessive exposure to cortisol
cushing's syndrome
31
causes of cushing's syndrome can be
exogenous or endogenous
32
exogenous causes of cushing's syndrome
main cause is being prescribed glucocorticoids
33
endogenous causes of main cause cushing's syndrome
* **Cushing’s disease:** benign pituitary adenoma that secretes ACTH * **Adrenal cushing’s:** Adrenal tumour secreting glucocorticoids * **Non- pituitary-adrenal tumours producing ACTH and/ or CRH** (e.g. small cell lung cancer- very rare)
34
Signs and symptoms of Cushing’s syndrome
* Moon shaped face * Buffalo hump * Abdominal obesity * Striae * Acute weight gain * Hyperglycaemia – increased gluconeogenesis * Hypertension- mineralocorticoid effects of excess cortisol
35
Non- pituitary-adrenal tumours producing ACTH and/ or CRH
e.g. small cell lung cancer- very rare
36
sterid drugs have the same effects as
higher levels of cortisol \***steroid dosage should always be decreased gradually and never stopped suddenly\***
37
adrenal cushins syndrome
ACTH is suppressed- ACTH independent * Unlike pituitary and ectopic ACTH
38
symptoms of ## Footnote Adrenal Cushing’s syndrome
* Androgenic symptoms may be present * Hirsutism * Acne * Greasy skin * Virilising features in large tumours * Androgenic alopecia * Deep voice * Clitoromegaly (abnormal enlargement of the clitoris)
39
treatment of adrenal cushing syndrome
* Adrenalectomy- laparoscopic * Large tumours need open surgery
40
Androgens are partially regulated by
ACTH and CRH.
41
androgens promote
Promote axillary and pubic hair growth in both males and females
42
43
androgens and males
* In prepubescent males dehydroepiandrosterone (DHEA) released from the adrenal glands is converted to testosterone in the testes. * After puberty this production is insignificant as the testes themselves release testosterone
44
androgens and females
* Adrenal androgens promote libido and are converted to oestrogen in tissues * After menopause this is the only source of oestrogen in the body (not in ovaries)
45
Genital ambiguity in female infants caused by which genetic defect
deficiency of the 21-hydroxylase enzyme
46
deficiency of the 21-hydroxylase enzyme results in and can cause what
decreased glucocorticoid and mineralocorticoid production * Precursor of these hormones- **17a-hydroxypregnenolone** is therefore diverted to **more androgen synthesis** (e.g. testosterone) * Can also cause **salt wasting crises-** high rate of sodium lost
47
ACTH and steroid suppression: ACTH deficiency
* Occurs in any case of hypopituitarism * Similar symptoms to primary adrenal failure * No pigmentation as ACTH not raised * No hyperkalaemia as no mineralocorticoid deficiency * Hyponatraemia due to effect of cortisol on free water excretion
48
ACTH and steroid suppression: Steroid induced hypoadrenalism
* ACTH suppressed with long-term steroids * Abrupt withdrawal can cause hypo-adrenal crisis * Important to consider if an unwell patient is on steroids
49
which adrenal disorder is reffered to as *Primary adrenal insufficiency*
**Addisons disease**
50
Addisons disease
hypocortisolism
51
causes of Addisons disease
* Destructive atrophy of the adrenal glands by autoimmune response * Fungal infections * Adrenal cancer * Adrenal haemorrhage * TB (in old times- good time lol)
52
Addisons disease signs and symptoms
* Postural hypotension * Lethargy * Weight loss * Anorexia * Increased skin pigmentation hypoglycaemia
53
addisons disease and hyperpigmentation
* Decrease in cortisol * Reduced negative feedback on the anterior pituitary * More POMC produced to synthesis ACTH * POMC also produces alpha-MSH * Increase in MSH= increase in melanin synthesis- hyperpigmentation * ACTH can also activate melanocortin receptors on melanocytes- hyperpigmentation
54
maintenance treatment of Addisons disease
* **Lifelong replacement** * Glucocorticoid: hydrocortisone, prednisolone * Mineralocorticoid: fludrocortisone * **Education** * Double dose of glucocorticoid at time of illness * Emergency HC injection if vomiting * Steroid card and bracelet
55
Addisonian crisis
Life threatening emergency due to adrenal insufficiency
56
causes of addisonian crisis
* Abrupt steroid drug withdrawal * Severe stress * Salt depravation * Infection * Trauma * Cold exposure * Over exertion
57
addisonian crisis signs and symptoms
Collapse Nausea Vomiting Pyrexia Hypotension Vascular collapse
58
addisonian crisis treatment
fluid replacement and cortisol
59
Diagnosis of suspected adrenocortical disease
* Measurement of cortisol and ACTH * Measurement of 24hr urinary excretion of cortisol and its breakdown products * Dynamic function tests
60
dynamic functions test for adrenocortical disease
Dexamethasone suppression test and ACTH stimulation test
61
Dexamethasone suppression test
Suppression of plasma cortisol by \>50% is characteristic of Cushing’s disease, but suppression doesn’t normally occur in adrenal tumour or ectopic ACTH production
62
ACTH stimulation test
Admission of Synacthen would normally increase plasma cortisol, and a normal response to this usually excludes Addison’s disease
63
Congenital adrenal hyperplasia (CAH)
is a group of rare inherited autosomal recessive disorders characterized by a deficiency of one of the enzymes needed to make specific hormones.
64
CAH effects which organs
adrenal glands located at the top of each kidney
65
Normally, the adrenal glands are responsible for producing three different hormones:
1. corticosteroids, which gauge the body's response to illness or injury; 2. mineralocorticoids, which regulate salt and water levels; and 3. androgens, which are male sex hormones.
66
In CAH an enzyme deficiency will make the body unable to produce one or more of these hormones, which in turn will result in
the overproduction of another type of hormone precursor in order to compensate for the loss.
67
The most common cause of CAH is
the absence of the enzyme 21-hydroxylase.
68
Congenital adrenal hyperplasia (CAH) can cause
adrenal crisis and ambiguous genitalia * Block in adrenal cortex pathway * Presentation depends on enzyme defect * Lack of enzyme leads to: * Low cortisol and aldosterone * High male hormones (androgens)
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signs of Congenital adrenal hyperplasia (CAH)
* Hypotension * Hyponatraemia * Hyperkalaemia * Hypoglycaemia * Virilisation – development of male body parts
71
treatment of CAH
* Treat adrenal crisis * Determine sex of baby * Longer term GC and MC * Corrective surgery
72
Disorders of adrenal medulla
- Phaeochromocytoma and paraganglioma
73
- Phaeochromocytoma and paraganglioma is
Genetic disorder * Familial causes * Multiple endocrine neoplasia type 2- MEN\_2 * Von Hippel- Lindau- VHL * Neurofibromatosis type 1- NF1 * Associated disease * MEN-2= medullary thyroid cancer and hyperparathyroidism * VHL= renal cancer, angiomas
74
symptoms of ## Footnote Phaeochromocytoma and paraganglioma (think high A/NA)
* Acute episodes * Sweating * Panic attacks * Palpitations * High or low BP * Collapse
75
Phaeochromocytoma
Tumour of adrenal medulla
76
Paraganglioma
Extra-adrenal tumour- chromaffin tissue origin
77
Phaeochromocytoma and paraganglioma : acute crisis
Hypertensive crisis Encephalopathy Hyperglycaemia Cardiac arrhythmias Sudden death
78
Phaeochromocytoma and paraganglioma : investigatiosn
* 24h urine metanephrines * 2-3 x collections needed * Plasma metanephrine * Neuro-endocrine marker: Chromogranin A
79
radiological investigations of Phaeochromocytoma and paraganglioma
80
Management of Phaeochromocytoma and paraganglioma
* **α-blockade** phenoxybenzamine * **β-blockade** bisoprolol * **surgical excision**
81
alpha blockade- phenoxybenzamine
always do an alpha-block before b-block
82
why always do an always do an alpha-block before b-block
Unopposed alpha stimulation can cause hypertensive crisis
83
surgical excision of phaeochromocytoma and paraganglioma
* Perioperative management * Specialist anaesthetic team * Risk of crisis during operation * Maximal vasodilaton and filling with IV fluids
84
Pheochromocytoma secretes
catelcholamine s(mainly NA) stains dark with chromium salts
85
Signs and symptoms of Pheochromocytoma
* Severe hypertension * Headaches * Palpitation * Diaphoresis * Anxiety * Weight loss * Elevated blood glucose
86
Paraganglioma
Extra-adrenal tumour (chromaffin tissue origin)
87
spiralactone
diuretic to reduce bp e.g. heart failure

Endocrinology (12 decks)

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