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2. Adrenal Gland Flashcards

1
Q

Describe the location and structure of the adrenal glands

A

Adjacent to kidneys in retroperitoneum

Two functionally distinct zones;

i. Adrenal Cortex; glomerulosa, fasciculata, reticularis
ii. Adrenal Medulla

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2
Q

Describe the function of the adrenal zones

A

Adrenal Cortex: essential for life, produces 3 classes of steroid hormone;

i. glomerulosa: mineralocorticoids e.g. aldosterone
ii. fasciculata: glucocorticoids e.g. cortisol
iii. reticularis: androgens e.g. DHEAs, androstenedione

Adrenal Medulla: part of sympathetic NS, produces catecholamines, e.g. adrenaline/noradrenaline

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3
Q

What are the key hormones produced by the adrenal cortex?

A

Glucocorticoid: cortisol (from fasciculata)

Mineralocorticoid: aldosterone (from glomerulosa)

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4
Q

What are glucocorticoids and what is their function? Give an example of a glucocorticoid

A

Glucocorticoids = steroid hormones that bind glucocorticoid receptor (present on almost all vertebrate cells)

Functions:

  • immunological: part of feedback mechanism reducing some immune functions
  • e.g. inflammation: upreg anti/ downreg pro inflammatory proteins
  • role in development + homeostasis of T cells
  • metabolic: involved in glucose metabolism

E.g. cortisol

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5
Q

How is cortisol synthesised and regulated?

A

As part of the hypothalamic-pituitary-adrenocortical axis

Hypothalamus releases corticotrophin releasing hormone (CRH)

Pituitary is stimulated by CRH to produce adrenocorticotrophic hormone (ACTH)

Adrenal gland synthesises cortisol in response to ACTH stimulation

Cortisol exhibits negative feedback on ACTH release from pituitary + CRH from hypothalamus

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6
Q

Which hormone is an important precursor to ACTH and what adrenal disease symptom does it contribute to?

A

POMC (pro-opiomelanocortin) is a precursor to MSH (melanocyte stimulating hormone) + ACTH

Produced by anterior pituitary

Primary adrenal hypofunction (Addisons) = no cortisol synthesis from adrenal = increasing ACTH as no negative feedback;
- overproduction of POMC = MSH = hyperpigmentation in Addison’s disease

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7
Q

How can glucocorticoids (cortisol) be used therapeutically?

A

Adrenal insufficiency: low dose (physiologic replacement)

Immunosuppression: high doses;

  • allergic
  • inflammatory: asthma (inhaled 2nd line)/pain relief (except tendinopathies)
  • autoimmune disorders
  • post transplant: GvHD/rejection
  • heart failure
  • potential use in sepsis
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8
Q

What are the current findings on glucocorticoid therapy in CVD?

A

Link b/n heart disease + GC resistance;

  • polymorphism A3669G in exon 9 of GR gene associated with GC resistance
  • these pts have increased risk of coronary heart disease, enlarged hearts, systolic dysfunction, heart failure

Debate around use of GCs in;

  • decompensated heart failure to enhance response to diuretics (esp patients with refractory diuretic resistance with large doses loop diuretic)
  • treatment of patients with atrial fibrillation
  • can have beneficial cardiac effects e.g. improved contractility, inflammation reduction
  • strong risk factor for hypertension, atherosclerosis, diabetes mellitus, sodium and fluid retention
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9
Q

What is cortisol?

A
  • glucocorticoid
  • end product of HPA axis
  • medication = hydrocortisone
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10
Q

When is cortisol released?

A

In response to stress or low-blood glucose concentration

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11
Q

What are the functions of cortisol?

A

Range of physiogical functions

Metabolic; to regulate blood glucose

  • increased gluconeogenesis = raised blood sugar
  • increased hepatic glycogen storage
  • increased break down of plasma + muscle protein to amino acids (proteolysis)
  • increased release of glycerol + FFAs from adipose tissue (lipolysis) (some studies found suppression of lipolysis?)

Immunologic;

  • antiinflammatory effects
  • can weaken immune system
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12
Q

What is gluconeogenesis (GNG)?

A

Generation of glucose from non-carbohydrate carbon substrates

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13
Q

What is glycogenesis?

A

Formation of glycogen

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14
Q

How does cortisol increase GNG?

A

Enhances enzyme expression

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15
Q

How does cortisol increase glycogen storage?

A

Early fasting state: has indirect role in glycogenolysis: glycogen>glucose.

Late fasting state: increases glycogenesis = liver takes up glucose not used by tissues for glycogen stores in case of starvation state.

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16
Q

How does cortisol have antiinflammatory effects?

A

Prevents release of pro-inflammatory substances

Increases release of anti-inflammatory substances

Believed to be protective to prevent overactivation of inflammatory response to infections (sepsis)

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17
Q

How does cortisol weaken the immune system?

A

Prevents T cell proliferation

Creates negative feedback loop on IL-1 - central roles in regulating immune responses

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18
Q

What is the steroid metabolism pathway for cortisol?

A

Cholesterol
v
Pregnenolone > 17a-hydroxypregnenolone
v v
Progesterone > 17a-hydroxyprogesterone
v
Cortisol

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19
Q

How is cortisol found in the body and why is it measured in the urine?

A

95% blood cortisol bound (mainly) to TRANSCORTIN (cortisol binding globulin)

Normal level free cortisol v. small (filtered at kidneys = excreted in urine)

Transcortin almost fully saturated at normal concentration: excess production = greatly increased excretion in urine
- 24H urine collection sensitive for increased cortisol secretion (BUT NOT DECREASED)

Both urine + serum cortisol measured by immunoassay

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20
Q

When should cortisol testing occur and why?

A

Cortisol levels fluctuate greatly but there is marked diurnal rhythm: morning=high/ night=low

Therefore blood draw 0800-0900h (peak levels)

Sometimes draw at 2300h (should be low) to detect loss of diurnal variation - early feature of Cushings

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21
Q

Are random cortisol levels of any use?

A

Random cortisol levels of little use but high levels exclude adrenal failure in sick pt

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22
Q

What factors may affect cortisol tests other than illness?

A

Stress during collection = increased levels

Use of synthetic glucocorticoids - interfere with some immunoassays

Time - marked diurnal variation

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23
Q

What type of assay is used to measure urine + serum cortisol?

A

Immunoassay

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24
Q

What is the basic principle of cortisol testing?

A

Hyperfunction tested by measuring cortisol during suppression

Hypofunction tested by measuring cortisol during stimulation

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25
Q

What is a mineralocorticoid? Give an example.

A

Steroid hormone - aldosterone (glomerulosa)

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26
Q

What is the main function of aldosterone?

A

Promote sodium reabsorption + potassium excretion in kidney

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27
Q

How are aldosterone levels controlled?

A

Primarily controlled through the renin-angiotensin system

But also;

  • ACTH can stimulate production to limited degree (minor role in normal secretion)
  • synthesis sensitive to changes in circulating potassium levels
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28
Q

Describe the renin-angiotensin-aldosterone system (RAAS)

A

Renin released from juxta glomerular cells (kidney) in response to various stimuli;

  • hypotension/decreased renal blood flow
  • hyperkalemia
  • hyponatremia

Renin catalyses conversion of angiotensinogen in plasma to angiotensin I

Angiotensin converting enzyme (ACE) converts angiotensin I to angiotensin II during passage through lungs

Angiotensin II stimulates aldosterone release from adrenal cortex

Aldosterone corrects hypotension/hyperkalemia/hyponatremia

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29
Q

How is aldosterone measured and what factors must be considered during test?

A

Plasma aldosterone varies with posture - measure after pt recumbent overnight + sometime after being upright

Plasma renin often measured with aldosterone (both measured by immunoassay)

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30
Q

What is Addison’s disease?

A

Primary adrenal insufficiency/hypocortisolism

Long term endocrine disorder - adrenal glands do not produce enough steroid hormone

Usually occurs slowly/can be acute (medical emergency)

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31
Q

What are the signs + symptoms of Addision’s disease?

A

Usually gradual development + non-specific

  • fatigue/weakness
  • anorexia/weight loss
  • dizziness/postural hypotension
  • hyperpigmentation (inc areas not exposed to sun)
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32
Q

What are the signs and symptoms of an acute adrenal crisis?

A

Severe hypovolaemia

Shock

Hypoglycaemia

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33
Q

What causes hyperpigmentation in primary adrenal sufficiency and why does it not occur in other forms?

A

Hyperpigmentation caused by melanocyte stimulating hormone (MSH)

POMC (pro-opiomelanocortin) is the precursor molecule for ACTH + MSH

POMC and therefore MSH are overproduced when there is no cortisol synthesis to provide negative feedback to reduce ACTH/CRH

In secondary and tertiary forms of adrenal hypofunction there is underproduction of POMC/ACTH/CRH

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34
Q

What are the causes of primary adrenal hypofunction (Addison’s)?

A 
Autoimmune destruction of adrenal gland
Tuberculosis
Tumour metastasis in adrenal
Adrenal hemorrhage
Amyloidosis
Hemochromatosis
Removal of adrenals
Meningicoccal septicaemia
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35
Q

What are the most common causes of primary adrenal hypofunction (Addison’s)?

A

Autoimmune destruction of adrenal gland

  • 90%
  • most common cause in developed world

Other causes total 10%

Tuberculosis is most common in developing world

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36
Q

What causes autoimmune destruction of the adrenal gland in primary adrenal hypofunction?

A

Immune reaction against enzyme 21-hydroxylase (cytochrome p450) involved in biosynthesis of steroids aldosterone + cortisol

37
Q

What are the causes of secondary adrenal hypofunction?

A

Sudden withdrawal of GC drugs/failure to increase GC during stress (e.g. illness/surgery)

Hypopituitarism = decreased ACTH stimulation

38
Q

Why does suddenly withdrawing from GC drugs or failure to increase them during times of stress result in secondary adrenal hypofunction?

A

Treatment suppresses normal function of H-P-A axis

It takes a long time to become self-sufficient in GC production again

Will not produce enough excess for stress

39
Q

What are the clinical differences between primary and secondary adrenal hypofunction?

A 
No hyperpigmentation (ACTH low)
No renal Na wasting (only cortisol deficient not aldosterone)
40
Q

How is Addison’s disease treated?

A

Maintenance;

  • replace missing cortisol = hydrocortisone/prednisone tablets/prednisolone
  • replace missing aldosterone = fludrocortisone
  • i.e. lifelong GC/MC replacement therapy mimicking physiologic concentrations

Carry med-alert bracelet etc in case of emergency

Carry injectable cortisol kit for emergencies

Increase medicine in times of illness/surgery/dental

Acute crisis;

  • IV GCs, large volumes saline solution with dextrose (glucose)
  • usually rapid improvement, wean to maintenance dose
41
Q

What are the biochemical features of adrenal hypofunction and what causes them?

A

Hyponatremia/hyperkalemia: related to aldosterone deficiency

Hyperuremia (urine excretion products in blood): loss of sodium at kidneys = ECF volume depletion/dehydration = no urine output

Hypoglycaemia: related to cortisol deficiency

42
Q

How is adrenal hypofunction diagnosed?

A

9am plasma cortisol;

  • <50nmol/L virtually diagnostic of adrenal failure
  • > 450nmol/L excludes adrenal failure

SynACTHen = synthetic ACTH analogue;
- used to test capacity of adrenal cortex response to ACTH (stimulation test)

Further testing to establish primary or secondary;

  • long/depot synACTHen test = cortisol increased in secondary not primary
  • measurement of ACTH levels = increased in primary/ decreased in secondary
43
Q

Describe the process in a synACTHen stimulation test for hypofunction diagnosis

A
  • measure basal cortisol level
  • administer synACTHen
  • cortisol measured 30 mins later
  • cortisol should rise >450nmol/L
44
Q

What is adrenocortical hyperfunction and what two syndromes result?

A

Adrenocortical hyperfunction is the overexpression of the products of the adrenal cortex

Causing;

  • overproduction of GCs (cortisol) = Cushing’s syndrome
  • overproduction of MCs (aldosterone) = Conn’s syndrome
45
Q

What is Cushing’s syndrome?

A

A collection of signs + symptoms due to prolonged exposure to cortisol/other GCs

Primarily excess cortisol

46
Q

What are the clinical features of Cushing’s?

A

Depend on aetiology but primarily excess cortisol

Cortisol + precursors have some MC activity;

  • excess MC = hypertension (hypernatremia), hypokalemic acidosis (hypokalemia)
  • synthetic GCs have no MC activity = these features not present in iatrogenic Cushing’s

Excess androgen symptoms e.g. hirsuitism in females

Generally;

  • baldness/facial hair in females
  • acne
  • moonface/plethoric cheeks
  • buffalo hump
  • hypertension
  • osteoporosis
  • skin thinning
  • easy bruising
  • poor wound healing
  • increased abdominal fat
  • abdominal striae
  • avascular necrosis of femoral head
  • muscle weakness
47
Q

List the causes of Cushing’s syndrome

A

Pituitary adenoma: ACTH secreting tumour (60-70%)

Ectopic ACTH secretion by various tumours e.g. bronchial carcinoma + carcinoid tumours

Adrenal adenoma/carcinoma: excess GC

Iatrogenic Cushing’s: exogenous GC therapy

48
Q

What are the difficulties with Cushing’s diagnosis?

A

Cushingoid features common in general public (hypertension, obesity)

Cushing’s relatively rare (<5million/year)

Pseudo-cushing’s can occur in alcoholism + severe depression
- pt appears cushingoid but also exhibits similar biochem abn

Exclude iatrogenic cause - need thorough drug history

49
Q

What are the 2 steps of a Cushing’s diagnosis?

A
  1. Initial screening tests to identify hypercortisolism

2. Tests to find cause of high cortisol

50
Q

Name the tests used to screen for hypercortisolism

A

3 main tests;

  1. 24H urinary free cortisol (UFC)
    - normal <210nmol/24H
    - usually used by GPs in NI
  2. Overnight dexamethasone suppression test
  3. 48H low dose dexamethasone suppression test
    - both normal = plasma cortisol <50nmol/L @0900h
51
Q

What other useful screening tests can be used for hypercortisolism? Describe them.

A

Insulin hypoglycaemia test;

  • cortisol should rise >500nmol/L in response to hypoglycaemia
  • rise not seen even in mild cushings
  • pseudocushings do respond
  • hypoglycaemia-associated risks = contraindicated in various pts

Loss of cortisol secretion diurnal pattern;

  • 11pm cortisol <100nmol/L excludes cushings
  • 11pm test must be done as inpt + stress avoided to prevent false positives (not practical for screen test)
  • pulsatile secretion in both normal + abn states = false positives + negatives common
52
Q

Describe the UFC screening test for hypercortisolism

A

Increased UFC (>210nmol/24H) seen in cushings but also pseudocushings + extreme obesity

Care needed as incomplete collection = falsely low levels

Measurement of cortisol:creatinine ratio may help avoid problems with inaccurate urine collections

53
Q

Describe the dexamethasone suppression tests used to screen for hypercortisolism

A

Dexamethasone: synthetic GC

  • binds cortisol receptors in pituitary = suppression of ACTH release
  • in normal pt suppression of ACTH release = suppression of cortisol by adrenals

Overnight dexa supp test;

  • 1mg dexa tablet @ 11pm
  • 9am cortisol measured: <50nmol/L normal
  • failure to suppress = cushings/false positive (pseudo-cushings/stress)

48H low dose dexa supp test;

  • 0.5mg dexa every 6hrs for 2 days
  • cortisol measured morning after last dose
  • levels normally suppress <50nmol/L
  • fewer false positives with this method
54
Q

What 3 main tests are used to find the cause of hypercortisolism/cushings?

A
  1. High dose dexamethasone suppression test
  2. Plasma ACTH measurement
  3. Cortico-trophin releasing hormone (CRH) test
55
Q

Describe the high dose dexamethasone test used to find the cause of cushings

A

Patient given 2mg dexa every 6hrs for 48hrs

Plasma cortisol measured;

  • day 1: 0900h before 1st dose (basal level)
  • day 2: 0900h
  • day 3: 0900h 6hr after last dose

Cushing’s disease (pit tumour) = cortisol usually suppresses to <50% of pretreatment value

Failure to suppress = adrenal tumour/ectopic ACTH source

56
Q

Describe the plasma ACTH measurement used to find the cause of cushings

A

Ectopic ACTH source = very high ACTH

Cushings disease (pit tumour) = moderately elevated

Adrenal tumour = low

57
Q

Describe the CRH test used to find the cause of cushings

A

Used to distinguish b/n cushings disease (pit tumour) + ectopic ACTH secretion

Pt given dose of IV CRH then ACTH + cortisol measured at intervals; -15, 0, 15, 30, 45, 60, 90, 120 mins

Interpretation;

  • pituitary source: cortisol rise from basal to peak >20%
  • pituitary source: ACTH rise from basal to peak >50%
  • ectopic ACTH secretion (+adrenal tumours): usually no response

Problems;

  • 10% pts with cushings disease do not respond to CRH but usually show suppression to HDDST
  • 10% of ectopic ACTH syndrome may respond to CRH but fail to suppress with dexa
58
Q

What other useful tests help determine cause of hypercorticolism?

A

Imaging;

  • adrenal/abdominal CT
  • pituitary MRI scan
  • chest x-ray for tumours

Selective venous sampling for ACTH to reveal source of secretion (1977 paper);

  • selective catheterisation + venous sampling
  • localises ACTH secretion
  • samples pit venous drainage using Seldinger technique from a femoral approach
  • ACTH determined in L + R inferior petrosal sinuses + compared to peripheral venous samples drawn at same time
  • increased conc. ACTH in neck vs peripheral suggests pit source
59
Q

How is Cushings treated?

A

Depends on cause.

Adrenal adenoma/carcinoma = surgically removed/resected

Cushing’s disease (pit adenoma);

  • transphenoidal hypophysectomy
  • or if adrenals semi-autonomous: bilateral adrenalectomy + pituitary irradiation
  • appropriate steroid/replacement therapy needed after both

Presurgery/if not amenable to surgery = drugs to block cortisol synthesis, e.g. metyrapone

Ectopic ACTH = treat cause, e.g. tumour removal

Iatrogenic cushing’s = review/adjust treatment

60
Q

What is Conn’s syndrome?

A

Primary hyperaldosteronism

Rare condition (1 million/year)

61
Q

What are the clinical features of Conn’s?

A

Hypertension (accounts for up to 10% of hypertension)
- due to sodium retention at kidneys

Muscle weakness
Tetany (spasms)
Paraethesiae (pins + needles)
Polydipsia + polyuria
 - all due to hypokalemia as a result of increased renal potassium excretion

Many pts asymptomatic: identified by hypokalemia during hypertension investigation

62
Q

What are the causes of primary aldosteronism (Conn’s)?

A

Adrenal adenoma (majority ~75%)
Bilateral hyperplasia of zona glomerula (~2/3 pts in some studies)
Adrenal carcinoma (rare)
GC-suppressible hyperaldosteronism;
- rare autosomal dominant inherited condition
- aldosterone secretion under control of ACTH
Other causes;
- mimicked by excess liquorice/carbenoxone ingestion

63
Q

Why does excess liquorice ingestion cause Conn’s?

A

Liquorice = carbenoxone

Inhibits 11B-hydroxysteroid dehydrogenase that converts cortisol to inactive cortisone

Excess cortisol exerts MC effects

64
Q

What causes secondary hyperaldosteronism?

A

More common than primary aldosteronism

Overactivity of renin-angiotensin-aldosterone system (RAAS)

Common causes;

  • heart failure
  • liver cirrhosis
  • nephrotic syndrome

Less common;

  • renal artery stenosis
  • Na wasting nephritis
  • Barrter’s syndrome
  • Renin-secreting tumour
65
Q

What other names are primary and secondary hyperaldosteronism known by?

A

Primary = hyporeninemic hyperaldosteronism (release of aldosterone from adrenal despite no renin stimulation)

Secondary = hyperreninemic hyperaldosteronism (overactive RAAS system)

66
Q

What are the typical lab findings in Conn’s?

A

Hypokalemia (excreted in urine)
- urine K+ inappropriately high (>30mmol/24H) for low serum K+ in pt not on diuretics

Plasma sodium usually high-normal/slightly above ref range (usually lower in secondary)

67
Q

How is Conn’s diagnosed?

A

Recumbent + ambulatory plasma aldosterone + renin;

  • basal measurement taken after 8h recumbency on waking in morning
  • Conn’s = high plasma aldosterone/low plasma renin activity

Measurement after ambulatory for 4 hrs useful in distinguishing cause

Imaging techniques;
- CT scan of adrenals

Selective blood sampling

68
Q

What is the treatment for Conn’s?

A

Dependent on cause

Adrenal adenoma/carcinoma;

  • surgically removed/resected
  • pts awaiting sirgery given spironolactone

Bilateral adrenal hyperplasia;
- treated w/ spironolactone (diuretic that antagonises action of aldosterone)

GC-suppressible hyperaldosteronism;
- treated with dexamethasone

69
Q

What is CAH?

A

Congenital adrenal hyperplasia (CAH) = a group of metabolic disorders of adrenal steroid hormone synthesis

70
Q

What causes CAH?

A

Mutation of enzymes mediating biochem synthesis of steroids

71
Q

What are the features of CAH?

A

Depends on enzyme deficiency

72
Q

What is the most common cause of CAH?

A

95% due to 21-hydroxylase deficiency (1 in 15000 live births in UK)

73
Q

Describe 21-hydroxylase deficiency

A

21-hydroxylase converts progesterone into aldosterone precursor + 17a-hydroxyprogesterone into cortisol precursor
- deficiency = no/little cortisol + aldosterone

21-hydroxylase deficiency may be partial/complete;
- complete presents shortly after birth = severe salt losing state due to deficient cortisol/aldosterone

Lack of cortisol = lack of negative feedback to pit = increased ACTH = drives androgen synthesis

74
Q

What causes 21-hydroxylase deficiency?

A

Autosomal recessive disease (male=female frequency)

75
Q

How can 21-hydroxylase deficiency be diagnosed in the lab?

A

High levels of 17a-hydroxyprogesterone secreted

76
Q

Describe the signs and symptoms of classical CAH (21-hydroxylase deficiency)

A

Lacks cortisol + aldosterone
- predisposes 3/4 severely affected to adrenal crisis with dehydration/shock/death if not properly diagnosed + treated

Excess adrenal androgen production begins in early fetal life;

  • may lead to virulisation/ambiguous genitalia in baby girls
  • continued androgen excess = precocious puberty in boys
77
Q

Describe the signs and symptoms of non-classical CAH (21-hydroxylase defiency)

A

Partial enzyme deficiency;

  • some cortisol production
  • normal aldosterone
  • lower levels adrenal androgens

Milder, non-life threatening form of CAH

Manifests later in childhood/young adult life;

  • no ambiguous genitalia in girls
  • premature development of pubic hair
  • menstrual irregularities
  • hirsuitism
  • severe acne
  • ~10% fertility problems

Ashkenazi jews = highest prevalence

78
Q

What other rarer forms of CAH exist and how rare are they?

A

Other forms account for <5% CAH cases

11B-hydroxylase deficiency (5%)

  • increased MC + androgen
  • hypertension due to accumulation of 11-deoxycorticosterone + excessive androgen production

17-hydroxylase (v rare)
- increased MC, decreased androgen

18-hydroxylase (v rare)
- decreased MC + androgen

3B-hydroxyhydrogenase ( v rare)

Delta5 isomerase (v rare)

79
Q

How is CAH diagnosed?

A

Hormone measurement

Clinical evaluation: history + PE

Newborn screening (USA): high false +ve rate

80
Q

How is CAH treated?

A

Generally steroid replacement therapy;

  • GC - oral hydrocortisone/prednisolone/dexamethasone
  • MC - fludrocortisone (classical CAH)
  • restores inhibition = decreased androgens

Additional treatments to optimise growth by delaying puberty/bone maturation

81
Q

What conditions can affect the adrenal medulla?

A

Pheochromocytoma

82
Q

What is a pheochromocytoma?

A

A tumour of the adrenal medulla (usually) secreting catecholamines

  • usually noradrenaline (some = large amounts adrenaline)
  • rare but treatable cause of hypertension (0.5%)
83
Q

Where are pheochromocytomas found?

A

Usually in the adrenal medulla (90%)

Extra adrenal: 10%

84
Q

Are pheochromocytomas malignant?

A

10% are malignant

85
Q

What are the signs + symptoms of a pheo?

A
  • Hypertension associated with vasomotor symptoms (anxiety/sweating/palpitations)
  • Headache
  • Pallor
  • Tremor
  • Abdominal pain
86
Q

What are the major clinical effects of a pheo?

A

If increased noradrenaline;

  • v high BP
  • slow heart rate
  • increased sweating
  • increased blood glucose

If increased adrenaline;

  • slightly increased/decreased BP
  • rapid heart rate
  • increased sweating
  • apprehension
  • increased blood glucose
87
Q

How is a pheo diagnosed?

A

Measurement of urinary metanephrines (BHSCT);

  • 1x 24H urinary metanephrine collection
  • used to require 2x 24H for urinary catecholamines
  • if +ve but potentially interfering drugs: repeat after drug washout
  • if still abn then measure plasma metanephrines + confirm with clonadine

Clonadine suppression test;

  • 97% sensitivity
  • pt must be relaxed
  • insert IV cannulae
  • after 30 minutes baseline sample collected for plasma catecholamines
  • administer 0.3mg clonadine orally
  • collect blood for catecholamines after 3 hours
  • requires decrease of >50% in plasma adrenaline + noradrenaline
88
Q

What is clonadine + what does it do?

A

Clonadine;

  • drug that stimulates alpha 2 receptors in brain stem
  • binding has sympathetic effect
  • suppresses release of noradrenaline
89
Q

What is the treatment for a pheochromocytoma?

A

Surgical removal of tumour

ug biochemistry (14 decks)

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