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STEP 8: EndoRepro PATHOMA FA > Pilch_AdrenalDrugs > Flashcards

Pilch_AdrenalDrugs Flashcards

1
Q

What is the administration method of GC and MC?

A

ALL ORALLY BIOAVAILABLE

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2
Q

Is there a natural form of GC? MC?

A

YES GC: Natural form of GC = Cortisol [hydrocortisone]

NO MC: Synthetic form of MC = FLUDROCORTISONE

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3
Q

What are the “CUSHINGOID EFFECTS” of GC?

A
  1. Glc metabolism - Hyperglycemia
  2. Fat metabolism - Central obesity (Moon facies, back hump, truncal obesity)
  3. Protein and bone metabolism - Catabolic (muscle wasting) + osteoporosis
  4. Immunosuppression - Opportunistic infection + Poor wound healing
  5. HTN
  6. Androgenic effects - Hirsutism + excessive sweating + acne
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4
Q

When does GC toxicity manifest itself as Cushingoid effects?

A

> 2 wks of therapy

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5
Q

What is the #1 most common opportunistic infection that pts taking GC therapy are most susceptible to? #2?

A 
#1 = Candida albicans fungal infection 
#2 = Aspergillus fungal infection
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6
Q

Which prototypical GC has a short half-life, intermediate half-life, and long half-life?

A

SHORT: HYDROCORTISONE
INTERMEDIATE: PREDNISONE
LONG: DEXAMETHASONE

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7
Q

What is the classic replacement therapy of CHRONIC primary adrenocortical insufficiency?

A

GC (Hydrocortisone) + MC (Fludrocortisone)

*GC by itself is not enough to maintain BP

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8
Q

What are the 3 immediate steps of therapy for ACUTE primary adrenocortical insufficiency?

A
  1. LARGE PARENTERAL (IV) doses of HYDROCORTISONE - Oral dose won’t act quick enough since acute causes are life-threatening
  2. Fluid electrolyte abnormality correction
  3. Treat the underlying precipitating cause (e.g. infection, traum, hemorrahge)
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9
Q

When an ACUTE ADRENAL INSUFFICIENCY pt stabilizes, what is the regimen of treatment? What is the basis for this?

A

Ween the pt off of the HYDROCORTISONE because there could be SERIOUS WITHDRAWAL if hydrocortisone is cold-turkey stopped

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10
Q

What are 3 ways to assess the adequacy of corticosteroid replacement therapy?

A

2 Sx and 1 Hormone:

  1. HYPERPIGMENTATION resolution
  2. ELECTROLYTE resolution
  3. Plasma ACTH - Should NOT be suppressed, but should also be moderate levels
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11
Q

What is the main reason for testing AM ACTH levels in pts with corticosteroid therapy?

A

Mainly to prevent possible overtreatment

Overtreatment can cause SUPPRESSED ACTH

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12
Q

What is the most common mutated enzyme for CONGENITAL ADRENAL HYPERPLASIA? What is there a buildup of as a result?

A

21B-HYDROXYLASE (90% of pts) - Buildup of precursors that get shunted toward the ANDROGEN PATHWAY

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13
Q

What is the classic CP of CONGENITAL ADRENAL HYPERPLASIA in FEMALES, if not treated in utero with GC?

A

VIRILIZED EXTERNAL GENITALIA

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14
Q

What is the classic CP of CONGENITAL ADRENAL HYPERPLASIA in MALES, if not treated in utero with GC?

A

At birth: NORMAL

Later: Develop PRECOCIOUS PUBERTY

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15
Q

In pregnancies at high CAH risk, how can fetuses be protected from genital abnormalities?

A

ORAL ADMINISTRATION of DEXAMETHASONE to the mother -> Negative feedback to ACTH -> Reduces shunting + Massive surge of ACTH-mediated adrenal hyperplasia

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16
Q

What is the LONG-TERM REPLACEMENT therapy of pts with classical CAH? What is the basis for each?

A

GC (PREDNISONE) + MC (FLUDROCORTISONE)

  1. PREDNISONE = INTERMEDIATE ACTING GC (use this for alternate-day therapy to get GREATER ACTH suppression WITHOUT increasing growth inhibition) - Not too short (inadequate ACTH suppression), not too long (too much ACTH suppression)
  2. FLUDROCORTISONE - Also given because GC (cortisol) is insufficient by itself in maintaining BP
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17
Q

What is the GC potency and MC potency of DEXAMETHASONE? What is its half-life? What type of therapy is DEX mostly used for?

A

HIGH GC potency, barely any (0) MC potency
LONG half-life
Mostly used as treatments of pregnancies with HIGH RISK of CAH by oral administration to the mother

18
Q

Why does GC dosage have to be carefully monitored for classical CAH?

A

Dosage needs to be adjusted to maintain normal growth and bone maturation
**Excess cortisol can reduce linear growth in children and cause osteoporosis

19
Q

What is the most common cause of CUSHING SYNDROME?

A

EXOGENOUS CORTICOSTEROIDS

20
Q

What is the most common cause of ENDOGENOUS Cushing syndrome?

A

CUSHING DISEASE - ACTH-secreting pituitary adenoma causing bilateral adrenal hyperplasia (BAH)

21
Q

What is the treatment regimen of CUSHING SYNDROME due to exogenous corticosteroids?

A

Reduce dosage of GC GRADUALLY to prevent acute withdrawal Sx

22
Q

How long does it take for the normal baseline function of the hypothalamic-pituitary adrenal axis to restore?

A

2-12mo for HPA axis to restore

Another 6-9mo for cortisol levels to normalize

23
Q

What is the first-line treatment of CUSHING SYNDROME?

A

SURGICAL RESECTION OF TUMOR producing ACTH or cortisol

24
Q

What are the Tx options if the tumor responsible for Cushing Syndrome is inoperable?

A

Radiotherapy
Bilateral adrenalectomy
Pharmacotherapy

25
Q

What are the two types of drugs that can be used in the management of CUSHING SYNDROME/DISEASE to normalize CORTISOL production?

A
  1. ADRENAL BLOCKERS

2. ACTH ANTAGONISTS

26
Q

What are the 2 specific types of ADRENAL BLOCKERS used for the Tx of CUSHING SYNDROME/DISEASE?

A
  1. BLOCK SYNTHESIS of adrenal steroids = KETOCONAZOLE

2. BLOCK GC RECEPTOR = MIFEPRISTONE (GC-R antagonist)

27
Q

What are the 2 specific types of ACTH antagonists used for the Tx of CUSHING SYNDROME/DISEASE?

A
  1. DA-R AGONIST = CABERGOLINE

2. SOMASTOSTATIN (SST) AGONIST = PASIREOTIDE

28
Q

At what level (hypothalamus, AP, or adrenal) do CABERGOLINE and PASIREOTIDE act at?

A

Level of the HYPOTHALAMUS (agonize DA and SST) that send inhibitory signals to PRL/TSH and GH/TSH, respectively

29
Q

Which syndromes are these SOMATOTROPIN-R AGONISTS used for: OCTEOTRIDE, LANREOTIDE, and PASIREOTIDE?

A

OCTEOTRIDE and LANREOTIDE: GH-secreting ADENOMAS (e.g. GIGANTISM before epiphyses close in prepuberty children, ACROMEGALY after epiphyses close)

PASIREOTIDE: CUSHING SYNDROME/DISEASE

30
Q

What is the most common cause of PRIMARY ALDOSTERONISM?

A

CONN SYNDROME =

ADRENAL ADENOMA hyper-secreting aldosterone

31
Q

What are the pharmacotherapy Tx options of PRIMARY ALDOSTERONISM?

A

MINERALOCORTICOID RECEPTOR ANTAGONISTS = SPIRONOLACTONE + EPLERENONE

32
Q

Can a pt with PRIMARY ALDOSTERONISM discontinue his/her SPIRONOLACTONE or EPLERENONE medication?

A

NO, NOT unless the adrenal adenoma tumor is resected bec HTN and HYPOKALEMIC states will return

33
Q

Pt was initially on SPIRONOLACTONE, but switched to EPLERENONE bec he/she did not like the side effects associated with spironolactone. Describe the physiology of this occurrence.

A

SPIRONOLACTONE is great at inhibiting aldosterone, but has OFF-target side effects due to cross-reactivity with ANDROGEN/PROGESTERONE receptors -

EPLERENONE is MC-R specific and thus free of sex hormone side effects

34
Q

What are some of the possible side effects of SPIRONOLACTONE?

A

Cross-reactivity with androgen and progesterone receptors -> GYNECOMASTIA, DECREASED LIBIDO, IMPOTENCE, IRREGULAR MENSES

35
Q

What kind of tumor is a PHEOCHROMOCYTOMA? What does it secrete?

A

Neuroendocrine tumor of the ADRENAL MEDULLA derived from CHROMAFFIN cells

Secretes LOTS of NE/E

36
Q

What are the clinical findings of PHEOCHROMOCYTOMA

A

HTN + Elevated HR + Palpitations

37
Q

What is the standard protocol for treating a PHEOCHROMOCYTOMA? What does one need to be careful about particular with this Tx plan?

A

SURGICAL RESECTION of tumor BUT super important to stabilize BP and Pulse with medication prior to resection

Bec tumor is sensitive to touch -> Massive SURGE of NE/E -> Life-threatening

38
Q

What is the main goal of pharmacotherapy associated with a PHEOCHROMOCYTOMA?

A

Keeping the BP and HR under control while the surgical resection is being conducted

39
Q

What is the primary class of drug used prior to a PHEOCHROMOCYTOMA resection? What are the two other classes that may be used in the management?

A
  1. ALPHA-BLOCKERS**
  2. BETA-BLOCKERS (only after alpha-blockers) - pre-operative management
  3. CATECHOLAMINE BIOSYNTHESIS (Tyr Hydroxylase) INHIBITOR - management for pheo-associated HTN
40
Q

Name the ALPHA BLOCKERS used for PHEOCHROMOCYTOMA pre-operative management.

A

-ZOSINS

PHENOXYBENZAMINE, DIBENZYLINE, PRAZOSIN, TERAZOSIN, DOXAZOSIN

41
Q

Name the BETA BLOCKERS used for PHEOCHROMOCYTOMA pre-operative management.

A

ATENOLOL
METOPROLOL
PROPANOLOL

42
Q

Name the catecholamine biosynthesis inhibitor used for management of PHEO-associated HTN

A

METYROSINE

STEP 8: EndoRepro PATHOMA FA (7 decks)

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