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1. Internal Medicine I > 14. Glucocorticoid deficiency and overproduction, Addison's and Chusing's > Flashcards

14. Glucocorticoid deficiency and overproduction, Addison's and Chusing's Flashcards

1
Q

What are the physiological causes of glucocorticoid excess?

A
  • Stress,
  • pregnancy,
  • prolonged and intensive physical activity
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2
Q

What are some pathological causes of glucocorticoid excess?

A
  • Iatrogenic Cushing’s syndrome,
  • Cushing’s syndrome
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3
Q

What are some complications of Cushing’s syndrome?

A
  • Cardiovascular (MI, HT, hypokalemia),
  • Neuropsychiatric (depression, anxiety),
  • Metabolic (diabetes, hepatic steatosis, obesity),
  • Reproductive (infertility)
  • Skin (skin thinning, poor wound healing)
  • Thromboembolic
  • Muskuloskeletal (osteoporosis, myopathy)
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4
Q

What is the prevalence of Cushing’s disease? At what age does it usually occur? M/F ratio?

A

The prevalence is 39/million. It can occur at any age, but it is most frequent between 25-45 years. The female/male ratio is 3-4/1.

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5
Q

What is the prevalence of ACTH-dependent forms of endogenous Cushing’s syndrome in adulthood?

A

70%

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6
Q

What is the most common form of ACTH dependant Cushing syndrome?

A

Pituitary adenoma (aka Cushing’s disease)

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7
Q

What is the prevalence of adrenal tumours in endogenous Cushing’s syndrome?

A

23%

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8
Q

What are the most common concomitant disorders in patients with Cushing’s?

A
  • High blood pressure
  • Hyperglycemia
  • Osteoporosis
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9
Q

What are the main signs to differenciate between Cushing’s syndrome and simple obesity?

A
  • Skin thinning, easy bruising
  • Myopathy
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10
Q

What are the laboratory tests used for the diagnosis of cortisol excess in Cushing’s syndrome?

A
  • Urinary free cortisol,
  • midnight serum cortisol,
  • midnight salivary cortisol,
  • low dose dexamethasone suppression test.
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11
Q

What is the interpretation in the short (overnight) dexamethasone test?

A

Normal if < 1,8 microg/dl (<50 nmol/l).

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12
Q

What are the different forms of dexamethasone suppression test?

A
  • Once (midnight, short, overnight)
  • Repeated (two days, standard, long test / liddle test)
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13
Q

What are the different doses of dexamethasone used in the short dexamethasone suppression test?

A

Low-dose: 1 mg,
High-dose: 8 mg,

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14
Q

What are the laboratory tests used for the differential diagnosis of ACTH-dependent hypercortisolism?

A
  • Basal ACTH,
  • high-dose dexamethasone suppression test,
  • CRH test.
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15
Q

What does a high dose decamethasone suppression test tell us?

A

It tells us wether the problem is from the pituitary (Cushing’s disease) or a different site in the body (ectopic)

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16
Q

What is the difference in the progression of Cushing’s disease and ectopic ACTH syndrome?

A
  • Cushing’s disease has a slow progression
  • Ectopic ACTH syndrome has a rapid progression, with myopathy and hyperpigmentation
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17
Q

How is the serum ACTH in Cushing’s disease and in ectopic ACTH syndrome?

A
  • Cushing’s : normal / elevated
  • Ectopic : high / very high
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18
Q

Which of the 2 types of Cushing’s syndrome can be suppressed in dexmethasone testing?

A

Cushing’s disease can be suppressed (aka invisible) in high dose testing

19
Q

What is inferior petrosal sinus sampling?

A

Sampling the ACTH levels directly from veins that drain the pituitary to then compare with peripheral blood levels

20
Q

What is the treatment for ACTH-producing pituitary adenoma in Cushing’s syndrome?

A
  • Surgical intervention with transsphenoidal adenomectomy
  • Drugs : inhibition of ACTH secretion or steroid biosynthesis inhibitors
  • Pituitary radiation
  • Bilateral adrenalectomia
21
Q

What is the medical treatment for inhibiting ACTH secretion?

A
  • Carbergoline : D2 agonist
  • Pasireotide : somatostatin analog
22
Q

What are some steroid synthesis inhibitors used in the treatment of ACTH producing pituitary adenomas?

A
  • Etomidate
  • Metyrapone
  • Osilodrostat
23
Q

What is the potential complication of pituitary irradiation?

A

Panhypopituitarism.

24
Q

What are some of the known ectopic tumors that can produce ACTH?

A
  • Bronchial tumors,
  • Pheochromocytoma,
  • Gastrinoma,
  • Other neuroendocrine tumours
25
Q

Which imaging techniques can be used for differentiating ACTH-producing tumors?

A
  • MRI
  • CT
  • PET-CT
  • Somatostatin receptor scintigraphy

(all this is less good than inferior petrosal sinus sampling)

26
Q

What are the treatment options for ectopic Cushing’s syndrome?

A
  • Surgical removal,
  • steroid-biosynthesis inhibitors,
  • chemotherapy,
  • inhibition of ACTH secretion (somatostatin-analog),
  • isotope therapy
27
Q

What are the clinical manifestations of cortisol-producing adrenal tumors?

A
  • Cushing’s syndrome,
  • abdominal pain,
  • mineralocorticoid excess (DOC): hypertension, hypokalaemia, alkalosis,
  • androgen excess: severe hirsutism, virilism,
  • estrogens : gynecomastia, uterine bleeding
28
Q

What are the treatment options for cortisol-producing adrenal tumors?

A
  • Surgical removal,
  • laparoscopic adrenalectomy
29
Q

What is the peri-and postoperative management for patients undergoing surgical removal of cortisol-producing adrenal tumors?

A

Patients are at risk of adrenal insufficiency and should receive iv. hydrocortisone continued by per os replacement.

30
Q

What is the drug treatment for adrenocortical cancer?

A

o’p’DDT : a steroid-biosynthesis inhibitor that has a cytolytic effect on adrenocortical cells. It is usually administered lifelong in combination with hydrocortisone and other drugs (EDP-M).

31
Q

What is the glucocorticoid receptor antagonist used in the drug treatment of cortisol excess?

A

Mifepristone

32
Q

What is glucocorticoid insufficiency?

A

A state of inadequate cortisol production, either due to
1. Primary failure of the adrenal cortex
2. Lack of stimulation of adrenal cortex by ACTH

33
Q

What is primary adrenal insufficiency?

A

The lack of gluco-and mineralocorticoids due to adrenal destruction.

34
Q

What is the etiology of primary adrenal insufficiency?

A
  • autoimmune (70%),
  • tuberculosis (20%),
  • other (10%) - mycotic infections, amyloidosis, lymphoma, adrenal hemorrhage, ACTH-resistance.
35
Q

What are the most common signs and symptoms of chronic adrenal insufficiency?

A
  • Fatigue,
  • anorexia,
  • gastrointestinal symptoms
  • salt craving,
  • orthostatic hypotension,
  • musculoskeletal pain.
36
Q

What are the most common laboratory features of chronic adrenal insufficiency?

A
  • electrolytes : Hyponatremia, hyperkalemia, alkalosis,
  • hormones : low serum cortisol (unresponsive to iv. ACTH), elevated ACTH, low serum aldosterone, and increased plasma renin activity.
37
Q

What is the laboratory diagnosis for adrenal insufficiency?

A

Basal serum cortisol levels below 5 microg/dl (140 nmol/l) confirm the diagnosis, while levels above 20 microg/dl (550 nmol/l) exclude it.

38
Q

What is the recommended glucocorticoid replacement therapy for chronic adrenal insufficiency?

A
  • Glucorticoid replacement
  • Mineralocorticoid replacement
39
Q

What is the recommended daily dose of hydrocortisone for glucocorticoid replacement therapy?

A

15-30 mg/day, in 2-3 doses.

40
Q

What is the recommended daily dose of fludrocortisone for mineralocorticoid replacement therapy?

A

50-150 ug/day, in 1-2 doses.

41
Q

What is the recommended treatment for Addisonian crisis?

A

100 mg hydrocortisone bolus, followed by slow infusion of hydrocortisone at 100-200 mg/day for the first day, along with physiological saline infusion

42
Q

What is autoimmune polyendocrine syndrome?

A

rare, inherited disease in which the immune system attacks its own tissues (glands)

43
Q

Hormonal features of cortisol-producing adrenal tumors

A

Suppressed ACTH, non-suppressible serum cortisol.

1. Internal Medicine I (20 decks)

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