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GINME > Week 8: Adrenal hypofunction > Flashcards

Week 8: Adrenal hypofunction Flashcards

1
Q

Adrenal problems for the clinician

7 listed

A
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2
Q

Clinical Case Vignette

A
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3
Q

Identify

A
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4
Q

Identify

A
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5
Q

Steroid hormone synthesis

A
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6
Q

Hydrocortisone AKA

A

Cortisol

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7
Q

How do steroid hormones work?

A
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8
Q

Describe the regulatory relationships of the HPA axis

A
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9
Q

Describe the circadian and ultradian variation in HPA activity

A
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10
Q

When should you measure cortisol for Cushing’s syndrome?

A

Midnight

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11
Q

When should you measure cortisol for adrenal insufficiency?

A

Morning so adrenals are usually high at this time

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12
Q

CRH is made in?

A

hypothalamus

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13
Q

How is CRH measured?

A

really diluted in systemic circulation so would have to get from the hypothalamus pituitary protal system

So instead we measure ACTH

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14
Q

Describe the free-hormone hypothesis

A

many steroids have a binding protein however the free portion of the steroid is the biologically active fraction

Usually, the protein-bound form can be high and total steroid count can seem high but it could be in the inactive protein-bound form

*Measure total not free*

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15
Q

one big issue with exoogenous corticosteroids

A

Negative feedback inhibition on ACTH of the Ant. Pit. causing adrenal insufficiency

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16
Q

Describe the regulation of aldosterone secretion

A

Angiotensin II is the main positive regulator for aldosterone secretion

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17
Q

Aldosterone secretion positive regulators

6 listed

A
  • Angiotensin II (main stimulatory regulator)
  • Hyperkalemia
  • Adrenocorticotropin
  • Hyponatremia
  • Angiotensin III
  • Aldosterone-stimulating factor
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18
Q

Negative regulators of Aldosterone secretion

2 listed

A
  • Atrial natriuretic factor
  • Dopamine
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19
Q

Things that promote renal secretion of renin

5 listed

A

↓ effective blood volume

↓ blood pressure

↓ [NaCl] and [K+] at the diistal tubule

↑ prostaglandins

β-adrenergic stimulation

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20
Q

Primary Adrenal insufficiency hormones deficient

A

No aldosterone and no cortisone

Combined cortisol and aldosterone deficiency

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21
Q

Secondary vs primary adrenal insufficiency

A

Primary

  • aldosterone and cortisol deficiency
  • High levels of ACTH (due to loss of cortisol feedback on the pituitary)

Secondary

  • Aldosterone is preserved
  • cortisol deficiency is deficient
  • low levels of ACTH
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22
Q

Adrenal medulla

A
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23
Q

SNS and the adrenal medulla

A
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24
Q

Describe the pathophysiology of adrenal disorders

A
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25
Q

Types of adrenal insufficiency

A
  • Primary means the target organ is deficient (Adrenals are non-functioning)
  • Secondary means other organ is failing to activate the target organ (pituitary not secreting ACTH to activate cortisol secretion by the adrenals)
  • Acute (ie adrenal hemorrhage or pituitary hemorrhage)
  • chronic
  • acute-on-chronic (has had adrenal insufficiency and some other problem occurs that causes an adrenal crisis) (hypotensions is the cardinal feature)
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26
Q

Primary AI epidemiolgy

A

Rare

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27
Q

Primary AI associations

A
  • Autoimmune
  • AIDS
  • Adrenoleukodystrophy (disorder of long-chain FAs that accumulate in the adrenals)
  • CAH (Congenital adrenal hyperplasia)
  • Fungal (histoplasmosis, Coxsie)
  • TB (probably most common cause worldwide)
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28
Q

Primary AI clinical presentation

A

GI symptoms prominent

  • Hyponatremia
  • Hyperkalemia
  • acidosis
  • eosinophilia
  • lymphocytosis
  • mild hypercalcemia
  • azotemia

Mineralocorticoid as well as glucocorticoid deficiency

  • hypotension
  • hyperpigmentation (almost pathognomonic)
  • weight loss
  • fatigue
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29
Q

Adrenoleukodystrophy description

A

(a disorder of long-chain FAs that accumulate in the adrenals)

30
Q

Adrenoleukodystrophy etiologies

A

X-linked syndrome

31
Q

CAH AKA

A

Congenital adrenal hyperplasia

32
Q

CAH etiologies

A

the common form is 21-hydroxylase deficiency so decreased ability to make cortisol

33
Q

Why hyperpigmentation for Primary AI

A

because the precursor of ACTH is proopiomelanocortin so high levels of ACTH cause hyperpigmentation of the skin

34
Q

Causes of Primary AI

7 listed

A
35
Q

Infectious causes of Primary AI

3 listed

A
  • TB
  • Coccidiomyocosis
  • histoplasmosis
36
Q

Autoimmune causes of Primary AI

A

Addison’s Disease

Polyglandular autoimmune disease

37
Q

CAH etiologies

A

Deficiencies of these enzymes

  • 17-hydroxylase
  • 11-hydroxylase
  • 21-hydroxylase
38
Q

Medications that can cause Primary AI

A
  • Abiraterone
  • Metyrapone
  • Ketoconazole
39
Q

Abiraterone MOA

A

used in prostate cancer because blocks first stemp is cortisol biosynthesis so it also blocks adrenal androgen production

40
Q

HPA axis and negative feedback mechanisms

A
41
Q

What is this?

A

hyperpigmentation from primary AI

42
Q

Evaluation of Primary AI

A
  • imaging of adrenals for hemorrhage or infiltrative disease, infections or malignant tumors
  • VLCFAs for adrenoleukodystrphy
  • Serological for autoimmune or congenital
43
Q

cortisol synthesis

A

Some babies from primary/secondary adrenal AI can have ambiguous genitalia from androgen dysfunction

look back at primary vs secondary to determine this because lecturer got a little lost

44
Q

Secondary adrenal insufficiency

A

ACTH deficiency

Insufficiency of ACTH or could be even higher up the axis tertiary etc.

45
Q

Chronic adrenotrophic hormone deficiency

A

leads to reversible atrophy of adrenal cortex

46
Q

Secondary/Tertiary AI epidemiology

A

Common & difficult to recognize clinically

47
Q

Secondary/Tertiary AI etiologies

A
  • hypopituitarism or isolated ACTH deficiency
  • exogenous corticosteroids
48
Q

Gold standard tests for Secondary/Tertiary AI

A
  • Insulin tolerance test
  • Metyrapone
49
Q

What to do from hypotension in the setting of Secondary/Tertiary AI

A

Empirical glucocorticoid replacement

50
Q

Describe the cortisol secretion rate as a function of ACTH concentration

A
51
Q

Chronic exogenous corticosteroids blunted cortisol response to ACTH

A

It is reversible and if needed, is managed with an intermediate-term ACTH replacement

52
Q

If there is long-term ACTH deficiency and a regular dose of ACTH is given why don’t you get a normal response

A

Because if there is long-term ACTH deficiency the response has been blunted and the adrenals don’t respond appropriately

53
Q

Scondary/Tertiary AI associations

A
  • Hypopituitarism (pituitary tumor removal, pituitary surgery, pituitary irradiation, pituitary apoplexy)
  • Cure after Cushing’s (pituitary tumor secreting ACTH if you cure the tumor th patient would immediately go into AI because of the long-term from endogenous cortisol negative feedback on ACTH) (will recover normal if wait long enough)
54
Q

Adrenal hormone synthesis pathways

A
55
Q

How does Secondary/Tertiary AI differ from Primary AI

A
  • No dehydration because mineralocorticoid activity remains intact (maintained by the renin-angiotensin axis in absence of ACTH)
  • No hyperpigmentation (because this is caused by ACTH overload)
  • Difficult to diagnose because (ACTH stimulation test is often positive but a significant % of false positives)
  • hypotension is less prominent
  • hyperkalemia not present (making aldosterone)
  • hyponatremia might be present
  • hypoglycemia is more common (glucocorticoids raise blood sugar)
56
Q

Treatment OF AI

6 listed

A

For #3 we don’t give aldosterone because hard to supplement so give Fludrocortisone in primary AI

give people Injectable dexamethasone for emergencies such as an adrenal crisis

57
Q

Clinical assessment of AI

A
  • Exogenous corticosteroids (Cushing’s-Like features)
  • Hyperpigmentation, hypotension, weight loss, orthostatic hypotension
  • Evidence of anterior pituitary deficiencies (especially secondary sexual characteristics)
  • Other clinical conditions that increase probability
  • Routine labs and imaging studies
58
Q

Diagnostics tests for AI

A
59
Q

How to monitor adrenocorticosteroid replacement therapy?

A

Just have to try your best because there’s no way to measure it reliably so try to mimic diurnal variations

60
Q

Adrenal Crisis AKA

A

Acute Adrenal Insufficiency

61
Q

Acute Adrenal Insufficiency AKA

A

Adrenal crisis

62
Q

Clinical features of adrenal crisis

A
63
Q

How to identify a patient with AI are critically ill

A
64
Q

CIRCI AKA

A

Critical Illness Related Corticosteroid Insufficiency

65
Q

Critical Illness Related Corticosteroid Insufficiency AKA

A

CIRCI

66
Q

Adrenal Crisis resistant to vasopressors

A

Adrenal insufficiency hypotension is resistant to vasopressors because glucocorticoids potentiate vasopressors so glucocorticoid deficiency can result in hypotensions that is resistant to vasopressor therapy

67
Q

Critical Illness Related Corticosteroid Insufficiency

A

HArd to interpret the cortisol because CBG levels frop so the % of free cortisol will have gone way up

Decreased cortisol clearance rates and increased cortisol production rates

68
Q

CIRCI & Septic shock

A
69
Q

CIRCI literature

A
70
Q

CIRCI Dx and Tx

A

GINME (63 decks)

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