Adrenal Disorders Pharamcology Flashcards

1
Q

Anatomic parts of adrenal gland with hormones it produces

A

Outer cortex

  • cortisol
  • vasopressin
  • aldosterone
  • DHEA

Inner medulla
- catecholamines (NE and epinephrine)

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2
Q

Cortisol and aldosterone effects

A

Cortisol

  • Raises plasma glucose levels and stimulates gluconeogenesis
  • inhibits glucose uptake except in the brain
  • Promotes protein catabolism
  • Promotes lipolysis and fat redistribution in the body
  • enhances catecholamine effects on blood vessels (HTN)
  • decreases osteogenesis and promotes osteoporosis
  • immunosupression and anti-inflammation

Aldosterone

  • alters sodium and water in the renal collecting duct
  • synthesis and secretion regulated by angiotensin 2 at AT1 receptors on zona glomerulosa cells
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3
Q

Cushing syndrome

A

Excess glucocorticoids
(especially cortisol)

Symptoms:

  • obesity
  • hyperglycemia and HTN
  • osteoporosis
  • muscle weakness
  • hirsutism
  • buffalo hump and strain on abdomen
  • poor wound healing
  • moon-like facies

Treatment:

  • surgical adrenal tumor with HRT therapy (hydrocortisone and cortisone)
  • can also use: metyrapoine, aminoglutethimide, ketoconazole
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4
Q

3 drugs used to treat Cushing syndrome

A

On top of hydrocortisone or cortisone treatment

1) metyrapone:
- 11-B hydroxylase enzyme inhibitor

2) aminoglutethimide
- inhibits conversion of cholesterol -> pregneolone (chemical adrenalectomy)

3) ketoconazole
- inhibits synthesis of all hormones in testes and adrenal cortex

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5
Q

Primary hyperaldosteronism

A

Excess aldosterone secretion caused by adrenal tumors

Symptoms:

  • edema
  • fluid/electrolyte disturbances
  • HTN

Treatment:

  • surgical adrenal resection with fludrocortisone HRT
  • Also can use spironolactone (antagonizes aldosterone)
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6
Q

Addison’s disease

Adrenal hormone deficiency

A

Caused by multiple causes but all result in insufficiency of cortisol and aldosterone levels

Symptoms:

  • weakness
  • emanciation
  • hypoglycemia
  • hyperpigmentation of skin
  • hyperkalemia
  • hyponatremia
  • hypotension

Treatment: HRT with hydrocortisone/cortisone and fludrocortisone

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7
Q

What is the diurnal rhythm of cortisol release

A

Highest levels are in the morning/waking up

Lowest levels found at night

very closely related to sleep-wake cycle

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8
Q

How does stress regulate cortisol release

A

The Stress descending central pathways increases CRH release from the hypothalamus.

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9
Q

How does angiotensin 2 affect aldosterone secretion

A

Angiotensin 2 binds to AT1 receptors on zona glomerulosa cells

1) Regulates conversion of cholesterol -> pregneolone Via desmolase enzyme activity
2) Regulates conversion of corticosterone -> aldosterone via aldosterone synthase

Aldosterone effects are increase sodium reabsorption and potassium excretion via Na/K exchanger

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10
Q

DHEA

A

Produced by the zona reticularis in the adrenal cortex

In males = produces testosterone and is primary androgen throughout life

In females = induces puberty effects but under normal conditions is clinically insignificant after puberty

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11
Q

Glucocorticoid receptors (GRs)

A

Nuclear receptor family of transcription factors
- reside in the cytoplasm in an inactive form until steroid binding occurs (then it translocates to the nucleus to up-regulate transcriptions of glucocorticoid responsive elements (GREs). This upregulates glucocorticoid production while also inhibiting cycloxygenase 2, nitric oxide and inflammatory cytokine production

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12
Q

Mineralcorticoid receptors (MRs)

A

Ligand-activated transcription factors and bind to very similar hormone responsive elements
- are expressed in epithelial tissues involved in electrolyte transport (kidney,colon, salivary glands, etc) and in the heart, vasculature and adipose tissue

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13
Q

What is the purpose of the dexamethasone test

A

Diagnosing Cushing syndrome

Inject a patient with dexamethasone (contains potent glucocorticoid action but little Mineralcorticoid action)
- administer in the evening before bed and then measure in the morning

Normal functional HPA axis = ACTH release and cortisol levels are suppressed

Cushing syndrome = ACTRH levels are suppressed but cortisol levels will remain elevated

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14
Q

Corticosteroid toxicity

A

Occurs with cessation of chronic steroid use of acute high dose use

If abruptly stopped, results in acute Addison’s disease
- because of this tapered dose is required instead of going cold turkey (requires several weeks to months to taper off and minor ACTH and cortisol levels)

Withdrawal syndrome symptoms:

  • fever
  • myalgia
  • arthralgia
  • malaise
  • *Continued use of high dose corticosteroids in high doses
  • fluid electrolytes
  • HTN
  • hyperglycemia
  • increased susceptibility to infections
  • peptic ulcers, osteoporosis
  • myopathy
  • cataracts and growth arrest
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15
Q

What are the three most common characteristics of physical signs associated with excess glucocorticoid use

A

Fat redistribution (buffalo hump)

Striae (collagen rearrangement)

Ecchymoses (poor wound healing)

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