The Adrenal Gland Flashcards

1
Q

What is the diagnostic test for determining priimary and secondary hyper-aldosteronism? Also, what values indicate a primary and secondary hyper-aldosteronism?

A

1) PRA (Plasma Renin Activity) & PAC (Plasma Aldosterone Concentration) Ratio 2) Primary Hyperaldosteronism (PAC/PRA of > 20:1) Secondary Hyperaldosteronism (PAC/PRA of ~ 10)

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2
Q

All congenital adrenal enzyme deficiences are characterized via what?

A

Adrenal Hyperplasia, due to positive feedback, increasing ATCH hormone levels

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3
Q

What are the expected lab values and presentation for a 17-a-hydroxylase enzyme deficiency?

A

Labs: Decreased Androstenedione & Cortisol Presentation: Males: Undescended testis Females: Lack of 2ndry sexual development

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4
Q

What are some lab findings and presentations for a 21-B-hydroxylase deficiency

A

Labs: Increased Renin Activity & Increased 17-hydroxy progesterone Presentation: Salt Wasting (in infancy) Precocoius puberty & Virilization

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5
Q

What are some lab values and presentation that would be found with a 11B-hydroxylase deficiency?

A

Labs: Increased DOC & BP (but decreased Aldosterone), Decreased Cortisol, and Increased Sex Hormones. Also seen would be decreased Renin activity (d/t increased DOC activity). Presentation: Virilization

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6
Q

What is the strongest form of exogenous cortisol?

A

Dexamethasone

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7
Q

What does a high mexthasone test differentiate between?

A

A pituitary tumor and a non pituitary tumor

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8
Q

What is Addison’s Disease?

A
  • Autoimmune disease of the Adrenal Gland (Decreased Cortisol and Aldosterone production)
  • Increased ACTH and CRH production
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9
Q

What is the mechanism behind hyperpigmentation in those with Addison’s Disease

A

1) Addison’s DIsease: Unable to produce Cortisol or Aldosterone; High ACTH levels
2) ACTH levels are then broken down, via post-translation modification of POMC –> a-MSH–> drives Melanin synthesis
3) Melanin accounts for the hyperpigmentation ]

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10
Q

What is Cosyntropin and what does it test for?

A

1) Cosyntropin (Synthetic ACTH)
2) Tests for Adrenal Insufficiency (1*, 2*, or 3*)

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11
Q

What are four possible causes of Primary Adrenal Insufficiency (Addison’s Disease)?

A

1) Autoimmune Disease
2) Adrenal Hemorrhage (d/t Anticoagulants or 2ndry to N. Meningitidis)
3) Infection: Tuberculosis & N. Meningitidis
4) Tumor Metastases to the Adrenal Gland

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12
Q

Which form of Adrenal Insufficiency, primary, secondary, or tertiary?

Also, what is the name of a hormone that can replace aldosterone production?

A

1) Primary (no produciton of Cortisol or Aldosterone)
2) Fludrocortisone

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13
Q

What is Conn’s Syndrome?

A

Adenoma of the Adrenal Cortex; releases excess Cortisol and Aldosterone

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14
Q

What is the rate limiting step in the synthesis of Catecholamines?

A

Tyrosine –> L-DOPA (via Tryosine Hydroxylase)

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15
Q

What is the purpose of circulating chromogranins?

A

They reduce the osmotic burden of storing Epi in chromaffin granules

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16
Q

In non neural tissues; most of the catecholamines will be degraded via what enzyme?

A

COMT

17
Q

In neural tissues the most prominent mechanism of catecholamine degradation occurs via what enzyme?

A

MOA (Monoamine Oxidase)

18
Q

What are the receptor affinities for the catecholamines in regards to B2, B1, and the rest of the receptors?

A

B2: High Affinity for Epi

B1: Equal Affinity

Rest: Higher affinity for NORI