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POD Exam II > Corticosteroids > Flashcards

Corticosteroids Flashcards

1
Q

Zona glomerulosa secretes:

A

Aldosterone.

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2
Q

Zona fasiculata secretes:

A

Cortisol (glucocorticoid).

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3
Q

Zona reticularis secretes:

A

DHEA and androstenedione.

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4
Q

Corticosteroid MOA:

A

Bind to cytoplasmic receptor, which is a ligand activated transcription factor.
- Takes time, not a rescue drug.

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5
Q

Glucocorticoid effects on metabolism:

A

Glucose regulation, induce hyperglycemia:
- Liver increases glucose synthesis and glycogen storage.
- Peripheral tissues: protein breakdown, decreased utilization of glucose, lipolysis, decreased uptake of glucose.
Fats, redistribution of body fats:
- Round face and back fat.
- Marked central obesity, reduced peripheral fats.

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6
Q

Glucocorticoid effects on calcium balance:

A

Induces a negative calcium balance, decreases calcium uptake in the gut, increase calcium secretion by the kidney.

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7
Q

Glucocorticoid effects on cardiovascular and blood:

A

Most glucocorticoids have some mineralocorticoid activity, sodium excretion can promote HTN.

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8
Q

Glucocorticoid effects on inflammation:

A

Reduces NF-kappa-B levels - inhibits:
- Proteolytic enzymes, vasoactive and chemoatractant factors.
- Pro-inflammatory enzymes such as COX-2 and NOS.
Stimulates the synthesis of lipocortin, inhibits phospholipase A2 activity, decreases arachidonic acid release and subsequent production of ecosanoids.
(Main non-endocrine use.)

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9
Q

Glucocorticoid effects on endocrine:

A
  • Inhibits TSH release, can lead to misinterpretation of TSH assays for hyperthyroidism.
  • Decrease serum levels of TBG.
  • Decreased T3 levels.
  • Inhibit growth via inhibition of IGF-1
  • Prolonged –> inhibits FSH and LH surges
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10
Q

Glucocorticoid effects on bone/connective tissue/skin:

A
  • Inhibits osteoblast function.
  • Decreases collagen and osteocalin synthesis.
  • Increased bone reabsorption (promotes osteoporosis).
  • Inhibits fibroblast function.
  • Decreased synthesis of collagen, fibronectin etc. (promotes stria and bruising).
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11
Q

Mineralocorticoid effects:

A

Water and ion balance:
- Increased Na/K ATpase expression on distal tubules and collecting duct to enhance Na+ and water reabsorption and K+ secretion.

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12
Q

Pseudo Cushing’s:

A

Physiological hypercortisolism associated with disorders other than Cushing’s syndrome:

  • Significant physical inflammatory stress.
  • Severe obesity.
  • Malnutrition, anorexia nervosa, intense chronic exercise.
  • Psychological stress, severe MDD
  • Chronic alcoholism.
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13
Q

Cushing syndrome - ACTH dependent:

A

Associated with excessive ACTH secretion leading to adrenocortical hyperplasia:

  • Cushing’s disease (pituitary hypersecretion of ACTH).
  • Ectopic secretion of ACTH by nonpituitary tumors.
  • Ectopic secretion of CRH by nonhypothalamic tumors.
  • Iatrogenic or factitious Cushing’s syndrome due to administration of exogenous ACTH.
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14
Q

Cushing syndrome - ACTH independent:

A

Iatrogenic or factitious Cushing’s syndrome.

  • Most commonly due to long term glucocorticoid use.
  • Adrenocortical adenomas and carcinomas.
  • Primary pigmented nodular adrenocortical disease (PPNAD).
  • Bilateral macronodular adrenal hyperplasia (BMAH).
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15
Q

Cushing’s syndrome - symptoms:

A
  • Central obesity, round “moon face”, “buffalo hump”.
  • Excessive sweating.
  • Muscle wastage.
  • Skin striae
  • Neurological complaints:
    • Euphoria.
    • Psychosis.
    • Depression.
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16
Q

Cushing’s syndrome - diagnosis:

A
  • Rule out exogenous glucocorticoids/pharmacological reasons.
  • 24 hour urine cortisol.
  • Late night salivary cortisol.
  • Dexamethasone test.
  • Metyrapone test.
17
Q

Dexamethasone test - low dose:

A

Differentiates if Cushing’s or not:

- If Cushing’s no suppression of cortisol.

18
Q

Dexamethasone test - high dose:

A

Differentiates type of Cushing’s:

  • ACTH undetectable but no suppression of cortisol: adrenal tumor.
  • ACTH elevated and no suppression of cortisol: ectopic ACTH syndrome.
  • ACTH normal to elevated and suppression of cortisol: Cushing’s disease.
19
Q

Cushing’s syndrome - pharmacological approach (2):

A
  1. Block and replace.
    - Patients with erratic cortisol secretion.
  2. Normalization.
    - Patients with invariant hypercortisolism.
20
Q

Ketoconazole:

A
  • Antifungal
  • At higher doses than antifungal therapy: inhibits CYP17.
    • Inhibits glucocorticoid and androgen synthesis.
  • Even higher doses: inhibits CYP11A1.
    • Inhibits corticotroph adenylate cyclase activation.
    • Reduces ACTH secretion at therapeutic doses.
  • Drug interactions: inhibits CYP1A2, CYP2C9, CYP3A4.
  • Co-administration with ergot derivatives, cisapride or triazolam is contraindicated –> fatal cardiac arrhythmias.
21
Q

Metyrapone:

A
  • MOA: selective inhibitor of CYP11B1 reducing the biosynthesis of cortisol.
  • Use: hypercorticism resulting from adrenal neoplasms or tumors producing ACTH; diagnostic test for Cushing’s syndrome.
  • Side effects: Hirsutism, nausea, headache, sedation and rash.
    • Hirsutism due to increased synthesis of adrenal androgens upstream from the enzymatic block.
22
Q

Mitotane:

A
  • Acts on CYP11B1 and CYLP11A1 enzymes.
  • Causes mitochondrial destruction and necrosis of adrenocortical cells.
  • Has long term effect.
  • Not used in pregnancy.
  • Need to supplement with exogenous glucocorticoids.
23
Q

Mifepristone (RU-486):

A
  • MOA: inhibits the release of the glucocorticoid receptor from the HSP chaperone proteins.
    • Reduces transcriptional effects of glucocorticoids.
    • Progesterone antagonist (abortion pill).
  • Use: controlling hypercortisolism in patients with Cushing’s syndrome caused by inoperable ACTH tumors, adrenal carcinomas unresponsive to other therapies.
  • Side effects: vaginal bleeding, headache, dizziness, abdominal pain, nausea, vomiting, diarrhea and abdominal cramps.
  • Drug interactions: increased metabolism of some drugs.
24
Q

Adrenal insufficiency - Primary:

A
  • Structural or functional deficiency of the adrenal cortex (Addison’s disease). High ACTH levels and low glucocorticoids and mineralocorticoids.
25
Q

Primary adrenal insufficiency treatment:

A

Combination of glucocorticoids and mineralocorticoids required.

  • Hydrocortisone or cortisone preferred.
  • Supplementation with fludrocortisone for mineralocorticoid effect.
26
Q

Cosyntropin test:

A

Used to determine between primary and secondary adrenal insufficiency.

  • Primary = ACTH levels high but low cortisol levels.
    • Symptoms: weakness, wt loss, anorexia, HTN, dark skin pigmentation, hyponatremia.
  • Secondary = baseline ACTH low and cortisol levels low
    • Symptoms: malaise, anorexia, no hyperpigmentation.
27
Q

Secondary adrenal insufficiency:

A

Pituitary or hypothalamic deficiency.

- Low ACTH and low-normal glucocorticoids/androgens, normal mineralocorticoids.

28
Q

Secondary adrenal insufficiency treatment:

A

Hydrocortisone, cortisone or prednisone.

- Mineralocorticoid not needed.

29
Q

Acute adrenal insufficiency:

A

Life threatening, should also consider isotonic NaCl and glucose therapy in conjunction with steroids.

30
Q

Congenital adrenal hyperplasia (CAH):

A
  • Deficiency in CYP21 most common.
  • Reduced levels of corticosteroids.
  • Increased 17-hydroxyprogesterone (clinical test), DHEA and androgens due to lack of feedback inhibition and excess ACTH.
  • Classic-severe deficit:
    • Females - pseudohermaphroditism.
    • Males - normal at birth, precocious puberty.
  • Non-classic: post puberty presentation.
  • Treat with corticosteroids, females with classic can be treated in utero.
31
Q

Aldosteronism:

A

Excessive production of aldosterone leading to HTN and hypokalemia.

  • Most common: aldosterone producing adenomas and bilateral idiopathic hyperaldosteronism.
  • Less common: Unilateral hyperplasia, adrenal hyperplasia, familial or pure aldosterone producing carcinomas and tumors.
  • Tx: Surgery, aldosterone antagonist.
32
Q

Spironolactone (aldactone) side effects:

A
  • Breast tenderness and menstrual irregularities in women.

- Impotence, decreased libido and gynecomastia in men.

33
Q

Most anti-inflammatory potent glucocorticoids (2):

A
  1. Betamethasone.

2. Dexamethasone.

34
Q

Glucocorticoid with the highest relative mineralocorticoid potency:

A

Fludrocortisone.

35
Q

Longest lasting (half-life) glucocorticoid:

A

Betamethasone.

Dexamethasone.

36
Q

Cortisol-cortisone shuttle:

A
  • HSD1 activates (cortisone –> cortisol).

- HSD2 deactivates (cortisol –> cortisone).

37
Q

Cushing’s syndrome common signs:

A
  • Cardio: HTN, edema, Na and water retention, hypokalemia.
  • CNS: euphoria, depression, psychosis, insomnia.
    Immune: increased susceptibility esp viral and fungal.
  • GI: peptic ulcer.
  • Metabolic: hyperglycemia, muscle catabolism, hyperlipidemia, altered fat deposition, striae.
  • Eye: cataracts, glaucoma.
  • Osteoporosis: negative Ca balance; inhibition of osteoblasts.

POD Exam II (20 decks)

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