ED Flashcards

1
Q

Which hormone disorders can be a result of the gland itself?

A

→Graves disease

→Hashimoto

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2
Q

What disorders can be a result of adrenal hyperfunction?

A

→Excess cortisol (Cushing’s syndrome)

→Excess aldosterone (e.g. Conn’s syndrome)

→Adrenal insufficiency
Hypocortisolism
Lack of aldosterone and cortisol (Addison’s)

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3
Q

What is Conn’s syndrome?

A

→Aldosterone excess
primary hyperaldosteronism

→adrenal gland itself producing excess

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4
Q

What is Cushing’s syndrome?

A

→Cortisol excess

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5
Q

What is aldosterone secretion activated by?

A

→RAAS

→Increased plasma [K+]

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6
Q

What is RAAS activated by?

A

→Reduced renal perfusion

→Increased sympathetic activity

→Interpreted as fall in blood volume

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7
Q

What is useful in diagnosing primary hyperaldosteronism?

A

→plasma aldosterone/renin ratio

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8
Q

What are some roles of cortisol?

A

→Preserves plasma glucose

→promotes insulin resistance in muscles

→Promotes lipolysis, gluconeogenesis

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9
Q

What are some effects of excess cortisol?

A

→hyperglycemia,

→increased adiposity,
→hypertension,
→muscle wasting

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10
Q

What rises in absence of cortisol?

A

→ADH

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11
Q

What are the most common causes of Cushing’s syndrome?

A

→Exogenous glucocorticoids activate cortisol receptor

→Adrenal cortex atrophies with lack of ACTH stimulation

→Several days may be required for adrenal to become responsive to ACTH again

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12
Q

How is Cushing’s disease diagnosed?

A

→dexamethasone test

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13
Q

What is the dexamethasone test?

A

→After a dose of dexamethasone, cortisol levels often stay very high in people who have Cushing’s syndrome

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14
Q

In adrenal tumour what will the plasma ACTH be after dexamethasone test?

A

→low

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15
Q

In ectopic ACTH what would the level of ACTH be after dexamethsasone?

A

→very high

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16
Q

What is primary adrenal insufficiency?

A

→Addison’s disease- destruction of adrenal cortex

→Insufficient cortisol and aldosterone

17
Q

What is secondary adrenal insufficiency?

A

→Pituitary or hypothalamic disease

→Insufficient cortisol

18
Q

What is the primary stimulator for ADH?

A

→osmolarity

19
Q

What are the clinical features of Addison’s?

A
→Hypotension 
→Plasma [Na+]: normal to low
→Hyponatremia- increased ADH
→Plasma [K+]: normal to high
→High ACTH
→Elevated plasma renin
20
Q

Why is there hyperpigmentation in Addison’s?

A

→ACTH reacts with melanocytes receptors

21
Q

What are the hallmarks of Addison’s?

A

→high ACTH

→low cortisol

22
Q

What is used for ACTH testing?

A

→Synacthen

→Assess ability of adrenal to produce cortisol in response to ACTH

23
Q

What is involved in the short Synacthen test?

A

→Measure baseline cortisol (9am) and 30 min after 250 µg synacthen (synthetic ACTH) i.m.

→Adrenal insufficiency is excluded by an increase in cortisol of >200 nmol/L and/or a 30 min value >550

24
Q

What is involved in the Synacthen long test?

A

→Adrenal cortex ‘shuts down’ in absence of stimulation by ACTH – time needed to regain responsiveness

→3-day stimulation with synacthen

→In secondary (but not primary) adrenal insufficiency cortisol increases by >200 nmol/L over baseline

→Long test not often necessary since ACTH assay can distinguish