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OU Module Endo Fall 2018 > Disorders and Treatment of the Adrenal Gland Exam 1 > Flashcards

Disorders and Treatment of the Adrenal Gland Exam 1 Flashcards

1
Q

What are the layers of the adrenal gland?

A
  • capsule
  • cortex
  • medulla
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2
Q

What are the zones of the cortex and what do they secrete?

A
  • Zona glomerulosa -> mineralocorticoid secretion
  • Zona fasciculate ->cortisol secretion
  • Zona reticularis -> androgen secretion
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3
Q

What is the adrenal medulla responsible for secreting?

A

catecholamines

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4
Q

Explain the HPA axis

A
  • CRH released from hypothalamus
  • stimulates release of ACTH (aka corticotropin) from anterior pituitary
  • stimulates adrenal cortex to release adrenal hormones
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5
Q

Cortisol

A
  • Release is primarily controlled by HPA axis.
  • main glucocorticoid in humans (AKA: hydrocortisone)
  • Regulates physiologic stress response
  • Increases when needed (e.g., illness)
  • Secreted in diurnal circadian rhythm (Peaks in early morning, Nadir around mid-night)
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6
Q

Aldosterone

A
  • Release is primarily controlled by renin-angiotensin-aldosterone system, not the HPA axis.
  • Angiotensin II Receptors, Type 1 are present in adrenal gland.
  • Regulates blood pressure control, electrolyte homeostasis
  • Aldosterone promotes water retention, salt retention, and potassium excretion
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7
Q

Androgens

A

Androgen precursors are released and converted in target organs (e.g., gonads) to active sex steroids (progesterone, testosterone).

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8
Q

Clinical presentation of Cushing’s

A
  • Central obesity
  • Facial rounding (moon face)
  • Abdominal striae (often red/purple colored)
  • Thin skin
  • Dorsocervical fat accumulation (“buffalo hump”)
  • Supraclavicular fat pad
  • Glucose intolerance/hyperglycemia
  • Hypertension in 75-85%
  • Gonadal dysfunction/amenorrhea
  • Osteoporosis
  • Myopathy/myalgia
  • Hirsutism (in females)
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9
Q

Pathophysiology of Cushing’s

A

Excessive levels of glucocorticoids from: Endogenous overproduction by the adrenal glands OR Exogenous glucocorticoid administration

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10
Q

Endogenous Causes of Cushing’s

A
  • ACTH-dependent

- ACTH-independent

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11
Q

Endogenous Causes of Cushing’s: ACTH-dependent

A
  • Excess glucocorticoids are produced due to overproduction of ACTH
  • Pituitary Adenoma: chronic ACTH stimulates adrenal glands -> bilateral adrenal hyperplasia (BAH)
  • Ectopic (non-pituitary) ACTH-Secreting tumors: tumors that secrete CRH; often an endocrine tumor
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12
Q

Endogenous Causes of Cushing’s: ACTH-independent

A
  • o overproduction of ACTH.

- Caused by direct adrenal stimulation (as with Adrenal Adenoma, Adrenal Carcinoma)

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13
Q

What are the different treatment options for Cushing’s?

A
  • Surgery: Tumor resection, Adrenalectomy

- Pharmacologic therapy

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14
Q

Adrenalectomy

A
  • Must replace glucocorticoids for 6-12 months post-op (if unilateral adrenalectomy) or lifelong if bilateral
  • Hydrocortisone ± fludrocortisone
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15
Q

When can pharmacologic therapy be used in adjunct?

A
  • Peri-operatively while preparing for surgery & waiting for clinical response to surgery.
  • Incomplete surgery/incomplete resection
  • Rarely used without surgery, but can be for those who aren’t surgical candidates.
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16
Q

Exogenous Causes of Cushing’s

A
  • Induced by MEDS: glucocorticoids (oral, intravenous, topical, intranasal, etc…), progestins
  • The most common type of Cushing’s Syndrome (med-induced).
  • Treatment – wean off or dose reduce glucocorticoids if possible.
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17
Q

What are the classes of drugs that can be used to treat Cushing’s?

A
  • Steroidogenesis inhibitors
  • Adrenolytic agents
  • Neuromodulators of ACTH release
  • Glucocorticoid receptor blocking agents
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18
Q

Treatment for Cushing’s: Steroidogenesis inhibitors

A
  • Metyrapone

- Ketoconazole

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19
Q

Treatment for Cushing’s: Adrenolytic agents

A

Mitotane

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20
Q

Treatment for Cushing’s: Neuromodulators of ACTH release

A

Cyproheptadine

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21
Q

Treatment for Cushing’s: Glucocorticoid receptor blocking agents

A

Mifepristone (RU-486)

22
Q

Metyrapone

A
  • Inhibits 11 β-hydroxylase (this is the enzyme that converts 11-deoxycortisol to cortisol)
  • ADR: androgen side effects (hirsutism, acne), BP / electrolyte abnormalitites
23
Q

Mitotane

A
  • Inhibits 11-hydroxylation of 11-desoxycortisol and 11-desoxycorticosterone in the adrenal cortex, thereby inhibiting cortisol and corticosterone synthesis
  • ADR: lethargy, somnolence, nausea, diarrhea,
    hypercholesterolemia, prolonged bleeding time
24
Q

Cyproheptadine

A
  • Decreases ACTH secretion

- ADR: dizziness, blurred vision, anticholinergic ADR’s (sedation, weight gain)

25
Q

Mifepristone (RU-486)

A
  • Inhibits dexamethasone suppression; increases endogenous cortisol & ACTH
  • ADR: hypokalemia, peripheral edema, headache, arthralgia, nausea, fatigue
  • Contraindication: pregnancy (can abort baby)
26
Q

What are the types of hyperaldosteronism?

A
  • Primary

- Secondary

27
Q

What are the causes of hyperaldosteronism: primary?

A

Caused by bilateral adrenal hyperplasia or aldosterone-producing adenoma

28
Q

What are the causes of hyperaldosteronism: seondary?

A
  • ona Glomerulosa is stimulated by a non-adrenal factor.
  • Most common – Renin-Angiotensin-Aldosterone System stimulation:
    + Heart failure, cirrhosis, 3rd trimester of pregnancy, menses, renal artery stenosis.
29
Q

Clinical presentation of hyperaldosteronism

A
  • Hypertension (more difficult to treat or resistant)
  • Weakness, fatigue, paresthesias, headache
  • Polydipsia / polyuria
  • Hypokalemia
  • Hypomagnesemia
  • Hypernatremia
30
Q

What are the treatment options for hyperaldosteronism

A
  • Surgery

- Pharmacotherapy

31
Q

Surgery option

for hyperaldosteronism

A

removal of aldosterone producing adenoma

32
Q

Pharmacotherapy for hyperaldosteronism

A
  • Eplerenone (Inspra®)

- Spironolactone (Aldactone®)

33
Q

Eplerenone brand name and dose

A
  • Inspra
  • Starting dose: 25-50 mg QD
  • Typical dose: 50mg BID
34
Q

Eplerenone contraindications

A
  • Renal insufficiency (SCr > 2.0 mg/dL in men

- > 1.8 mg/dL in women) Hyperkalemia

35
Q

Eplerenone ADR’s

A
  • Hyperkalemia

- Renal dysfunction

36
Q

Eplerenone drug interactions

A
  • CYP 3A4 substrate

- Caution with strong inhibitors/inducers

37
Q

Spironolactone brand name and dose

A
  • Aldactone
  • Starting dose: 25 mg QD
  • Typical dose: 50-400 mg QD
38
Q

Spironolactone contraindications

A
  • Renal insufficiency (SCr > 2.5 mg/dL)

- Hyperkalemia

39
Q

Spironolactone ADR’s

A
  • Hyperkalemia
  • Renal dysfunction
  • Gynecomastia
40
Q

Clinical presentation of adrenal insufficiency

A
  • Hyponatremia, hyperkalemia, elevated BUN
  • Hyperpigmentation of areas where friction is more likely (Palms of hands, dorsal foot; More common in primary; secondary insufficiency will have pale pigment.)
  • Weight loss/anorexia
  • Depression
  • Dehydration
  • Salt craving
  • Hypotension
  • Nausea / vomiting
41
Q

What are the two types of adrenal insufficiency?

A
  • Primary

- Secondary

42
Q

adrenal insufficiency: primary

A
  • aka Addison’s disease
  • destruction of all 3 zones of the adrenal cortex
  • can be autoimmune
  • Ketoconazole inhibit cortisol synthesis
  • meds can accelerate cortisol metabolism
43
Q

What are medications that can accelerate cortisol metabolism?

A
  • Phenytoin
  • rifampin
  • phenobarbital
44
Q

adrenal insufficiency: secondary

A
  • Loss of glucocorticoid secretion
  • Most common cause is extended or chronic exogenous steroid administration, which causes suppression of the HPA axis
  • manifests when glucocorticoids are stopped / decreased or during times of increased physiologic stress
  • HPA suppression occurs after approximately 2 weeks of supra-physiologic doses of corticosteroids
45
Q

What are the different treatment options for adrenal insufficiency?

A
  • replacement of cortisol

- replacement of mineralocorticoids

46
Q

treatment of adrenal insufficiency: replacement of cortisol

A
  • hydrocortisone, prednisone, cortisone
  • needed in both primary and secondary
  • corticosteroids given twice daily; goal: use lowest effective dose to mimic diurnal adrenal rhythm
  • hydrocortisone: 15-25 mg orally; 67% in the AM, 33% 6-8 hours later
47
Q

treatment of adrenal insufficiency: replacement of mineralocorticoids

A
  • for primary only
  • Fludrocortisone (Florinef) replacing aldosterone
  • used in combination with cortisol replacement
  • potent salt-retaining activity
  • if hypertension develops, reduce to 0.05 mg daily
48
Q

Fludrocortisone ADRs

A
  • hypertension
  • hypokalemia
  • hyperglycemia
  • edema
49
Q

Acute Adrenal Insufficiency other names

A
  • aka Adrenal Crisis, Addisonian Crisis

-

50
Q

Acute Adrenal Insufficiency clinical presentation

A
  • Nausea, vomiting
  • Dehydration: Hyponatremia
  • More severe – can lead to significant neurologic sequelae (seizures)
  • Hypotension
  • Hyperkalemia: Increased risk of ventricular arrhythmias
  • Reduced cardiac function
51
Q

What are the different treatment options for acute adrenal insufficiency?

A
  • IV hydrocortisone
  • 100 mg IV bolus, followed by 50-100 mg Q 8 hours
  • Reduce to 25-50 mg Q6-8 hours until patient is stabilized
  • treat same as chronic adrenal insufficiency once patient is stabilized

OU Module Endo Fall 2018 (27 decks)

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