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HPA Axis disorders Flashcards

1
Q

What hormones are released by the anterior pituitary gland?

A

TSH
ACTH
FSH and LH
GH
Prolcatin

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2
Q

What hormones are released by the posterior pituitary gland?

A

Oxytocin
ADH

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3
Q

What is the main blood supply to the adrenal gland?

A

Superior adrenal artery - from the inferior phrenic artery
Middle adrenal artery - abdominal aorta
Inferior adrenal artery - from renal arteries

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4
Q

What is the main venous drainage of the adrenal gland?

A

Right adrenal vein into the IVC
Left adrenal vein into the left renal vein

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5
Q

What are the different layers of the adrenal gland?

A

Capsule
Cortex =
Zone glomerulosa
Zona fasciculata
Zona reticularis
Medulla

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6
Q

What does each section of the adrenal cortex secrete?
What is the basic function of this?

A

Zona glomerulosa - mineralcorticoids - salt - inc blood pressure
Zona fasiculata - corticosteroids (some androgens) - sugar - stress and inc bg
Zona reticularis - androgens (some corticosteroids) - sex - sexual development

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7
Q

What does the medulla of the adrenal gland do?

A

has chromaffin cells which secrete catecholamines - flight or fight response
Also secrete enkephalins - pain control

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8
Q

What is the adrenal axis? (HPA)

A

Hypothalamus releases CRH
Stimulates anterior pituitary to release ACTH
Stimulates adrenal glands to release cortisol
Cortisol has negative feedback effect to suppress CRH + ACTH

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9
Q

What is cortisol?
Where is it produced?
Trends in levels?

A

A steroid hormones - glucocorticoid - released from zona fasiculata of adrenal gland in response to stress and hypoglycemia.
Diurnal variation - peaks in mornings, lowest in evenings

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10
Q

What are the different actions of cortisol within the body?

A

Increase alterness
Inhibits bone formation
Raises blood glucose
Inhibits immune system
Increases metabolism
Anti-inflammatory effects

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11
Q

Give an overview of the Renin-Angiotensin-Aldosterone system

A

JG cells - in afferent arterioles in the kidney release enzyme renin in response to low BP
Converts angiotensinogen (liver) to angiotensin 1.
ACe (lungs) converts to angiotensin 2
Angiotensin 2 = vasoconstriction = inc BP
Angiotensin 2 = stimulates the release of aldosterone from adrenal glands

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12
Q

What are the effects of aldosterone in the nephron?

A

Increase Na+ reabsorption from the distal tubule
Increase K+ secretion from distal tubule
Increase H+ secretion from the collecting duct
Water follow sodium by osmosis - leading to increased intravascular volume and inc BP

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13
Q

What electrolyte abnormality is seen in aldosterone receptor antagonists?

A

Hyperkalemia

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14
Q

What are the two types of corticosteroids?

A

Glucorticoids e.g cortisol
Mineralcorticoids e.g aldosterone

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15
Q

What is the function of glucorticoids?

A

Increase alertness
Anti-inflammatory
Inhibits immune system
Inhibits bone formation
Raises blood glucose
Increases metabolism

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16
Q

What are the effects of mineral corticoids?

A

Increase intravascular volume to increase blood pressure
Causes sodium to be adsorbed and potassium to be excreted.

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17
Q

Give some examples of synthetic corticosteroids and where they sit on the glucorticoids/mineralcorticoid spectrum

A

Mainly gluc some mineral - prednisolone
50/50 = hydrocortisone
Fully gluc -dexamethosome, beclometasone
Fully mineral with some gluc - fludrocortisone

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18
Q

How can we reduce the adverse effect of chronic use of systemic steroids?

A

Avoid oral preparation whre possible
Use lowest effective dose for the shortest amount of time
Optimise and pre-existing co-morbidities
Monitor patients for adverse effects
Add a PPI for patients also receiving NSAIDs/Anti-coagulants
Doses should always be tapered down rather than stopped abruptly

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19
Q

At what stage of use do steroid become dangerous?

A

> 5mg pred for 4w+ - risk of HPA axis suppression and adrenal crisis if physiologically stressed
Short erm use increase 30 day risk of sepsis, VTE and fractures

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20
Q

How do exogenous steroids affect the HPA axis?

A

Mimic endogenous cortisol - act as negative feedback signal to reduce ACTH secretion
Less stimulation of adrenal gland so less endogenous cortisol
Persistent suppression leads to adrenal gland atrophy -> unable to produce adequate cortisol even after exogenous source has been removed = adrenal insufficiency

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21
Q

What are the sick day rules for steroids?

A

During acute physiological stress (infection or surgery)
Long term steroid dose should be increases
To meet increased requirements of body - adrenal gland suppressed so not able to produce

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22
Q

What are the side effects of long term corticosteroid use?

A

Cataracts
Ulcers
Skin thinning/brusing, straie
HTN
Infection - oral thursh
Necrosis of the femoral head
Glucose elevation
Osteoporosis/obesity
Immunosuppression and impaired wound healing
Depression/mood changes

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23
Q

Define adrenal insufficiency

A

When the adrenal glands do not produce enough steroid hormones - cortisol and aldosterone

may also affect androgens and catecholamines

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24
Q

What are the risk factors for adrenal insufficiency?

A

Female
Autoimmune disease
Hyper-coagulable states
Adrenal haemorrhage (warfarin and DOACs)

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25
Q

What is the common presentation of adrenal insufficiency?

A

Fatigue
Muscle Weakness
Dizziness and Fainting
Muscle cramps
Thirst and craving salts
Weight loss
Abdominal pain
Depression
Reduced libido
Loss of pubic hair
Hypotension
Hypoglycemia
Hyponatremia, hyperkalemia

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26
Q

What are some signs that can occur in adrenal insufficiency?

A

Postural hypos
Bronze hyperpigmentation of the skin (skin creases and the oral mucosa) - ACTH stimulates melanocytes

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27
Q

What are the key clinical features of addisons disease?

A

Bronze pigmentation of the skin
Changes in distribution of body hair
GI disturbances
Weakness
Weight loss
Postural Hypos
Hypoglycemia

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28
Q

What are the signs of an adrenal crisis?

A

Profound fatigue
Dehydration
Vascular collapse decreases BP
Renal shutdown - decreased serum Na and inc Serum K

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29
Q

What are the primary causes of adrenal insufficiency?

A

Damaged adrenal glands - cortisol and aldosterone mostly affected
Autoimmune (70%) - addisons disease
Infections
Medications
Metastatic
Adrenal Haemorrhage
Familial
Infiltrative diseases

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30
Q

What is meant by central adrenal insufficiency?

A

Secondary and tertiary causes (aka not the adrenal gland)

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31
Q

What are the secondary causes of adrenal insufficiency?

A

Tumours - pituitary adenoma
Surgery to pituiary
radiotherapy
Sheehans syndrome
Trauma

Mechanism:
Damage to the pituitary gland
Inadequate ACTH secretion
Less stimulation of adrenals
Less cortisol produced

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32
Q

What are the causes of tertiary adrenal insufficiency?

A

Usually long term corticosteroid causes suppression of the hypothalamus
Abrupt stop of exogenous steroids - hypothalamus remains suppressed

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33
Q

What is a key difference between peripheral and central adrenal insufficient?

A

Peripheral - low cortisol and aldosterone
Central - low cortisol only, aldosterone remains normal as the RAAS system is not affected by the Hypothalamus or pituitary gland

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34
Q

How can blood tests be used to differentiate between primary, secondary and tertiary adrenal insufficiency?

A

Primary - low cortisol, high ACTH, renin high, aldosterone low
Secondary - low cortisol, low ACTH, high CRH, renin normal, aldosterone normal
Tertiary - low cortisol, low ACTH, low CRH

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35
Q

What bedside investigations should be done for suspected adrenal insufficiency?

A

Lying standing BP
Capillary blood glucose

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36
Q

How bloods should be done for suspected adrenal insufficiency?

A

Na+ = low
K+ = high
Urea and creatinine = raised

Morning cortisol - falsely normal
ACTH, Renin, cortisol, aldosterone

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37
Q

What auto-antibodies are present in Addison’s disease?

A

Adrenal cortex Ab
21-hydroxylase Ab

38
Q

What imaging may be done in suspected adrenal insufficiency?

A

CT/MRI of the adrenal glands
MRI - pituitary - not routine

39
Q

What special test should be done in suspected adrenal insufficiency?

A

Short synACTHen test

40
Q

What happens in the short synACTHen test?

A
  1. Baseline serum cortisol
  2. give synthetic ACTH (synacthen)
  3. Repeat cortisol 30 mins

If cortisol >420nmol/L indicates adequate adrenal gland response
If less - primary adrenal insufficiency.

41
Q

What is a common source of ectopic ACTH secretion?

A

small cell lung cancer - neuroendocrine cells - paraneoplastic syndrome

42
Q

What is the management of adrenal insufficiency?

A

Replacement steroids:
Hydrocortisone - replace cortisol
Fludrocortisone - replace aldosterone

Steroid ID card, ID tag, emergency letter to alert emergency services
Sick day rules education
Emergency IM hydrocortisone supply with patient education

43
Q

What is an adrenal (addisonian) crisis)?
How does it present?

A

Life-threatening - severe adrenal insufficiency
May be first presentation or triggered by infection/trauma
Present - reduced consciousness, severe hypotension, hypoglycemia, hyponatremia, hyperkalemia

44
Q

How do you manage adrenal (addisonian) crisis?

A

ABCDE - treat as appropriate
IM/IV hydrocortisone 100mg stat followed by infusion or 6hrly doses
IV fluid resus
Correct hypoglycemia
Monitor electrolytes and fluid balance

45
Q

What is the relevant epidemiology of Addisons disease?

A

peak 30 to 40yrs
Twice as common in females

46
Q

What acid-base abnormality commonly occurs in Addisons disease?

A

Metabolic acidosis

47
Q

What are the major aetiologies of addisons disease + primary adrenal insufficiency?

A

Autoimmune adrenalitis - destruction of the adrenal cortex, isolated or part of a syndrome
Infection - TB, fungal, HIV and cytomegalovirus
Genetic disorders - CYP21A2 - congenital adrenal hyperplasia, AIRE.
Metastatis infiltartions - lungs, breast or melanoma mets
Adrenal haemorrhage
Medication - prolonged glucocorticoids (suppress HPa axis)

48
Q

What are some important differential diagnosis for Addisons disease?

A
  1. insufficiency secondary to pituitary disease - hyperpigmentation does not occur, and aldosterone levels tend to be preserved.
  2. Adrenal TB -also have fever and night sweats, adrenal calcification
  3. Sepsis - acute adrenal dysfunction, hypotensive
49
Q

What are some common complications of Addisons disease?

A

Adrenal crisis = severe hypotension, hypoglycemia, altered mental status
Chronic - fatigue, weight loss, electrolyte imbalances
Osteoporosis - from long term glucorticoids
Infections - increased susceptibility due to impaired immune function, prompt recognition and treatment is required

50
Q

What is the most common cause of secondary HTN?

A

Hyperaldosteronism
Presents in up to 10% of patients

51
Q

When should hyperaldosteronism by tested for as a cause of HTN?

A

Younger (under 40yrs)
Fail to respond to treatment
Low potassium (may still be normal)

52
Q

How does hyperaldosteronism present?

A

Headache
Muscle weakness
Fatigue
Resistant hypertension
Signs of hypokalemia = cardiac arrhythmias (and muscle weakness)
Metabolic alkalosis = vomiting, nausea, light-headed or confused.
Polyuria and polydipsia.

53
Q

What are the different causes of primary hyperaldosteronism?
What is it?

A

Adrenal glands too much aldosterone, inc BP, decrease renin

Bilateral adrenal hyperplasia (most common)
Adrenal adenoma secreting aldosterone (Conn’s syndrome)
Familial hyperaldosteronism (rare)

54
Q

What is secondary hyperaldosteronism?
what are the common causes?

A

Excessive renin stimulates the release of axcessive aldosterone -> caused by disproportionately low BP in the kidneys

Renal artery stenosis (atherosclerosis)
Heart Failure
Liver cirrhosis and ascities

55
Q

What bedside investigations should be done for hyperaldosteronism?

A

Blood pressure
ECG

56
Q

What bloods should be done for hyperaldosteronism?

A

K+ = low
Na+ = raised/normal
Blood gas - metabolic alkalosis (raised bicarb)
Serum aldosterone
Aldosterone to renin ratio = primary high aldo and low renin, secondary high aldosterone and high renin

57
Q

What imaging should be done for hyperaldosteronism?

A

CT/MRI of the adrenal gland - hyperplasia or tumour
Renal artery imaging (Doppler, CT angiogram, MR-angiograpghy) for renal artery stenosis

58
Q

What special tests may be done in hyperaldosteronism?

A

Adrenal vein sampling
Taking blood for both adrenal veins to locate which side is producing more aldosterone.

59
Q

What is the treatment for hyperaldosteronism?

A

Eplerenone and spironolactone - aldosterone antagonists
Treatment of the underlying causes:
- surgical removal of adrenal adenoma
- percutaneous renal artery angioplasty via the femoral artery to treat renal artery stenosis.

60
Q

What is the relevant epidemiology of primary hyperaldosteronism?

A

Peak incidence of 40-50yrs
Equal between men and women

61
Q

What is the relevant pathophysiology of hyperaldosteronism?

A

Excessive secretion of aldosterone from the adrenal cortex - independently of the RAAS system
Acts on mineralcorticoid receptors in distal tubles and CD of kidney - inc Na+ reabsorption and potassium secretion
Net effect is water retention leading to increased blood volume (HTN and fluid retention) and hypertension - hypokalemia.
Activates PANS due to hypertension - bradycardia and low CO - however insufficient to compensate for high BP.
Renin suppressed

62
Q

What is the first line investigation for primary hyperaldosteronism?

A

Aldosterone/renin ratio

63
Q

What are some important differentials for primary hyperaldosteronism?

A

Secondary - normal renin
Cushing - central obesity, moon facies, purple striae and hirsutism
Pheochromocytoma - episodic headaches, diaphoresis, palpitations.

64
Q

Define cushing syndrome /cushing disease

A

Prolonged high levels of glucorticoid (cortisol) in the body

65
Q

What is the difference between Cushing syndrome and crushing disease?

A

Cushing syndrome = clinical manifestation of pathological hypercortisolism
Cushing disease = pituitary adenoma, secreting excessive ACTH, thus stimulating excess cortisol release from adrenal glands/

66
Q

What are the two forms of Cushings?

A

Exogenous or iatrogenic = medication or substance containing cortisol
Endogenous = body produced too much cortisol

67
Q

What are the three forms of endogenous cushing?

A

Cushing disease - pituitary tumour (adenoma most common) secrete ACTH
Ectopic - paraneoplastic syndrome - ACTH released from small cell lung cancer or pancreatic cancer
Adrenal gland - tumour/hyperplasia

68
Q

What is the relevant epidemiology of Cushing disease?

A

Rare
Affect 10-15 people per million every year
More common in women
People aged 20-50yrs.

69
Q

What is a key sign of ACTH elevation?

A

Hyperpigmentation
Stimulates melanocytes to produce melanin

70
Q

What are some physiological causes of hypercortisolism?

A

Physical stress
Malnutrition
Alcoholism
Depression
Pregnancy
Metabolic syndrome

71
Q

What are the different metabolic effects of Cushing syndrome?

A

Hypertension
Cardiac hypertrophy
Type 2 Diabetes
Dyslipidaemia
Osteoporosis

72
Q

What is the general presentation of Cushing syndrome?

A

Enlarged fat pad ‘buffalo hump)
Insomina
Anxiety and depression
Limb wasting
Easy bruising
Abdominal striae
Central obesity
Hirsutism
Round ‘moon’ face

73
Q

What bedside investigation should be done for Cushing syndrome?

A

24hr urinary free cortisol
Capillary blood glucose

74
Q

What bloods should be done for Cushing syndrome investigations?

A

FBC - raised WCC
U&Es - low K+ if adrenal adenoma also secreting aldosterone
ACTH serum level
Morning cortisol

75
Q

What imaging should be done for Cushing syndrome investigation?

A

MRI for brain pituitary adenoma
CT chest for small cell lung cancer
CT abdomen for adrenal tumours

76
Q

What special tests should be done for suspected Cushing syndrome?

A

Dexamethasone suppression test
Diagnose endogenous cushing syndrome
Normal - dex suppress cortisol due to negative feedback on the HPA axis
Lack of cortisol suppresion = Cushing syndrome

77
Q

What are the different types of dexamethosone suppresion test?
How does this help diagnose the type of Cushings?

A

All detect endogenous cushings
1. Low dose overnight - lack of suppresion = cushing
2. Low does 48hr test - lack of suppresion = cushing
3. High dose 48hr test - higher dose can suppress Cushing disease (Pituitary adenoma) but not adrenal adenoma or ectopic ACTH.

78
Q

What are the common complications of Cushing Syndrome?

A

Hypertension
Osteoporosis
Fractures
Stroke
Diabetes Mellitus
Frequent infections
Heart attack
Thromboembolism

79
Q

What is the typical surgical treatment for Cushing syndrome?

A

Trans-sphenoidal resection of pitutary tumour
Surgical removal of adrenal tumour
Surgical removal or paraneoplastic tumour e.g SCLC
Bilateral adrenalectomy - followed by lifelong steroid replacement therapy

80
Q

What medication may be given to help treat Cushing syndrome?

A

Metyrapone - reduce production of cortisol in the adrenals
Ketoconazole - steroidogenic inhibitor - endogenous disease.

LOW CONCERN

81
Q

What is Nelsons syndrome?

A

Development of an ACTH producing pituitary tumour following bilateral adrenalectomy
Due to lack of cortisol negative feedback

Causes:
Skin pigmentation
Bitemporal hemianopia
Lack of other pituitary hormones

82
Q

What is the most common cause of Cushing syndrome?

A

Exogenous - long term corticosteroid therapy

83
Q

What are the first line investigations for Cushing syndrome?

A

Low dose dexamethsone suppresion test
24hr urinary free cortisol
late night salivary cortisol

84
Q

Define acromegaly

A

Clinical manifestation of excessive growth hormone secretion after the fusion of the epiphysis
Leading to large extremities and characteristic faces

85
Q

Define gigantism

A

The clinical manifestation of excessive growth hormone secretion before the fusion of the long bone epiphysisis
Characterised by tall stature
Paediatric condition

86
Q

What are the most common causes of acromegaly?

A

Pituitary adenoma - most common
Ectopic GHRH or GH from a tumour

87
Q

How does acromegaly present?

A

Excessive soft tissue growth - frontal bossing, large ears, large nose, large protruding jaw (prognathism), large tongue
If pituitary adenoma cause - bitemporal hemianopia

88
Q

What investigations should be done for acromegaly?

A

Growth hormone should NOT be done - unreliable fluctuates throughout the day
IGF-1 -serum, indicates GH levels
GH suppresion test = glucose drink should suppress GH
MRI pituitary - pituitary adenoma (note may be too small to see)

89
Q

What are some common complications of acromegaly?

A

Cardiomyopathy
Hypertension
Type 2 diabetes
Carpal tunnel syndrome
Arthiritis
Colonic polyps

89
Q

What is the management for acromegaly?

A

Trans-sphenoid resection of pituitary tumour
Radiotherapy may be offered

Surgical removal or paraneoplastic tumour (lung or pancreas)

90
Q

What medication may be given to treat acromegaly?

A

Pegvisomant - GH receptor antagonist
Somatostatin analogues - octreotide - block GH release
Dopamine agonist - bromocriptine - block GH release

Med 2 (4 decks)

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