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Endocrinology > Lec 9 The HPA axis - Clinical aspects > Flashcards

Lec 9 The HPA axis - Clinical aspects Flashcards

1
Q

What type of cells release peptidergic hormones transported by the the pituitary portal system?

A

Neurosecretory cells

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2
Q

Give examples of neurosecretory cells which release peptidergic hormones transported by the pituitary system to the pituitary gland.

A

Median eminence

Hypothalamus

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3
Q

What is the enzyme which converts cortisone into cortisol?

A

11 beta hydroxysteroid dehydrogenase

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4
Q

List the effects of glucocorticoids

A 
Maintenance of homeostasis during stress
Regulation of blood pressure 
Formation of bone and cartilage 
Energy balance and metabolism
Anti-inflammatory 
Cognitive function, memory and conditioning
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5
Q

What is one of the effects of an individual not producing enough cortisol?

A

They will have an altered circadian rhythm

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6
Q

What is the name of the enzyme that converts testosterone to oestrogen?

A

Aromatase

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7
Q

In vitro, because cortisol and aldosterone both have the same affinity for the mineralocorticoid receptor (MR), how if specify conferred?

A

Through a “pre-receptor” mechanism

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8
Q

Which enzyme inactivates cortisol?

A

11-beta-hydroxysteroid dehydrogenase

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9
Q

Where is 11 beta hydroxysteroid dehydrogenase (11B-HSD2) found?

A

In the kidneys

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10
Q

Why is cortisol inactivated to cortisone in the some tissues?

A

So that you can prevent cortisol from having an effect in some tissues and allow aldosterone to have an effect

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11
Q

What is the function of 11 Beta HSD enzymes?

A

They allow for tissue specificity by “gating” the GC access to nuclear receptors

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12
Q

What do 11beta HSD enzymes allow to happen?

A

Amplification of GC signals to target tissues and blocking of the signal to non target tissues

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13
Q

What is Cushing’s syndrome?

A

Excessive production or presence of excess cortisol

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14
Q

What other factors are associated with Cushing’s Disease?

A 
Weight gain
Hypertension
Insulin resistance 
Neuropsychiatric problems 
Osteoporosis
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15
Q

What is the pathogenesis of Cushing’s Syndrome?

A 
Excess cortisol due to:
Pituitary adenoma: ACTH secreting cells 
Adrenal tumour: adenoma/ carcinoma
Ectopic source of ACTH: carcinoid, paraneoplastic e.g. small lung cancer
Iatrogenic: steroid treatment
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16
Q

What are the clinical features of Cushing’s syndrome?

A 
Central obesity with thin arms and legs 
Fat deposition over upper back (buffalo hump)
Rounded 'moon' face 
Thin skin - easy bruising 
Hirsutism 
Hypertension
Diabetes 
Psychiatric manifestations 
Osteoporosis
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17
Q

What is Addison’s disease

A

An endocrine disorder caused by too little cortisol

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18
Q

What happens to the patient in Addison’s disease?

A

Gradually falls off in general health
Becomes languid and weak
Indisposed to physical or mental exertion
The body wastes
Slight pain referred to the stomach
Occasional actual vomiting
Discoloration of the skin - Ibiza tan - really dark tan due to ACTH influencing melanin production

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19
Q

What is the pathogenesis in Addison’s disease?

A

Primary adrenal insufficiency
Usually autoimmune in the UK
Rare causes may be metastases or TB
Decreased production of all adrenocortical hormones

20
Q

What may be other causes of hypoadrenalism?

A

Secondary to pituitary disease (rare)
Iatrogenic - steroid hormone given for long time, high dose and then suddenly stopped at a time of stress - the adrenal glands would not be able to keep up

21
Q

What are the clinical features of Addison’s disease?

A

Malaise, weakness, anorexia, weight loss
Increased skin pigmentation
Hypotension, postural hypotension
Hypoglycaemia
Not enough cortisol to mobilise glucose and keep blood sugar levels up

22
Q

What are the two type of Autoimmune Polyendocrine Syndromes?

A

Type I

Type II

23
Q

Describe Type 1 autoimmune polyendocrine syndromes

A

Rare
Onset in infancy
AIRE gene
Common phenotype = Addison’s disease
Hypoparathyroidism
Candidiasis

24
Q

Describe Type 2 APES

A

More common but still rare
Onset infancy to adulthood
Polygenic
Common phenotype:
Addison’s
Type 1 diabetes
Autoimmune thyroid disease

25
Q

Name some autoimmune diseases that may occur together

A 
Type 1 diabetes 
Autoimmune thyroid disease 
Coeliac disease 
Addison's disease 
Pernicious anaemia 
Alopecia
Vitiligo
Hepatitis
Premature ovarian failure 
Myasthenia gravis
Gestational/ post partum thyroiditis
26
Q

What should you have a high index of suspicion with?

A

Additional autoimmune endocrine disorders
e.g. T1DM with malaise, fatigue and weight loss ? Addison’s
or T1DM with non specific GI symptoms or diarrhoea ?coeliac

27
Q

When could you consider screening?

A

In patients with T1DM and or Addison’s disease

28
Q

What screens would you consider?

A

Coeliac screen

Thyroid function tests

29
Q

How would you assess the HPA axis

A

Basal tests
Blood Cortisol/ACTH
Urine cortisol
Saliva cortisol

30
Q

What dynamic tests could you do?

A

Stimulated or suppressed

31
Q

What is an example of a suppressed test?

A

Dexamethasone - a synthetic glucocorticoid

32
Q

How does a dexamethasone suppression test work?

A

Dexamethasone is a potent steroid
So there should be very low levels of cortisol - suppression of cortisol production
But in pts with Cushing’s they don’t have the suppression because the causes of Cushing’s don’t behave physiologically therefore they continue to pump out ACTH and cortisol

33
Q

What tests could you do to check for Cushing’s?

A

24 hour urinary free cortisol - “area under the curve”
Midnight cortisol saliva measurement
9am ACTH paired with cortisol measurement

34
Q

What tests could you do to check for Addison’s?

A

9am cortisol
SynACTHen test - adrenal response to ACTH - trophic effect of ACTH on adrenals
Insulin intolerance test
U&E - decreased sodium increased potassium in Addison’s
Glucose concentration - decreased

35
Q

What are the two golden rules with endocrine conditions?

A
  1. Never start investigating a patient for an endocrine condition unless their symptoms and signs suggest they may have it - due to risk of false positives
  2. Do not image an endocrine glands unless there is a diagnosis established biochemically
36
Q

Once you have estabished pt has Cushing’s biochemically, what imaging would you do?

A

CXR
MRI pituitary
CT adrenals

37
Q

What imaging would you do on an Addison’s pt?

A

Nothing - don’t need imaging unless you are concerned they have TB or metastatic cancer

38
Q

What is the management for Cushing’s Syndrome?

A

Surgerical: Transphenoidal adenectomy or Adrenalectomy

Pituitary radiotherapy

39
Q

What is the management for Addison’s

A

Glucocorticoid replacement therapy - usually hydrocortisone or prednisolone

Mineralocorticoid replacement therapy - fludrocortisone

40
Q

What do patients with secondary adrenal insufficiency have for management?

A

GC replacement therapy only - no need for fludrocortisone

41
Q

What needs to be considered in dosing of GCs?

A

Dose needs to be increases to cover “stresses” e.g. illness such as flu
Operations/ post op period
Pts may need IV or IM steroid if nil by mouth and vomiting - unable to take orally

42
Q

Patients might be on long term high dose steroids for a number of reasons/conditions, name some

A

Severe asthma,
COPD
Temporal arteritis
Polymyalgia rheumatic

43
Q

Why would pts be on these high dose long term steroids?

A

For their anti-inflammatory, immunosuppressive effects

44
Q

What can happen to the endogenous adrenal functions of patients on long term high dose steroid therapy?

A

Their endogenous adrenal function may be suppressed

45
Q

Why is it significant that they may have suppression of their endogenous adrenal function?

A

They wouldn’t be able to mount an adequate stress response
They should ensure that the steroids are not stopped suddenly
If the pt needs an operation, they need increased steroid cover
They should be given a Steroid Treatment Card to remind them and their doctors that they’re on steroids

Endocrinology (11 decks)

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