What is the diagnostic test for determining priimary and secondary hyper-aldosteronism? Also, what values indicate a primary and secondary hyper-aldosteronism?
1) PRA (Plasma Renin Activity) & PAC (Plasma Aldosterone Concentration) Ratio 2) Primary Hyperaldosteronism (PAC/PRA of > 20:1) Secondary Hyperaldosteronism (PAC/PRA of ~ 10)
All congenital adrenal enzyme deficiences are characterized via what?
Adrenal Hyperplasia, due to positive feedback, increasing ATCH hormone levels
What are the expected lab values and presentation for a 17-a-hydroxylase enzyme deficiency?
Labs: Decreased Androstenedione & Cortisol Presentation: Males: Undescended testis Females: Lack of 2ndry sexual development
What are some lab findings and presentations for a 21-B-hydroxylase deficiency
Labs: Increased Renin Activity & Increased 17-hydroxy progesterone Presentation: Salt Wasting (in infancy) Precocoius puberty & Virilization
What are some lab values and presentation that would be found with a 11B-hydroxylase deficiency?
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
What is the strongest form of exogenous cortisol?
What does a high mexthasone test differentiate between?
A pituitary tumor and a non pituitary tumor
What is Addison’s Disease?
- Autoimmune disease of the Adrenal Gland (Decreased Cortisol and Aldosterone production)
- Increased ACTH and CRH production
What is the mechanism behind hyperpigmentation in those with Addison’s Disease
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 ]
What is Cosyntropin and what does it test for?
1) Cosyntropin (Synthetic ACTH)
2) Tests for Adrenal Insufficiency (1*, 2*, or 3*)
What are four possible causes of Primary Adrenal Insufficiency (Addison’s Disease)?
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
Which form of Adrenal Insufficiency, primary, secondary, or tertiary?
Also, what is the name of a hormone that can replace aldosterone production?
1) Primary (no produciton of Cortisol or Aldosterone)
What is Conn’s Syndrome?
Adenoma of the Adrenal Cortex; releases excess Cortisol and Aldosterone
What is the rate limiting step in the synthesis of Catecholamines?
Tyrosine –> L-DOPA (via Tryosine Hydroxylase)
What is the purpose of circulating chromogranins?
They reduce the osmotic burden of storing Epi in chromaffin granules
In non neural tissues; most of the catecholamines will be degraded via what enzyme?
In neural tissues the most prominent mechanism of catecholamine degradation occurs via what enzyme?
MOA (Monoamine Oxidase)
What are the receptor affinities for the catecholamines in regards to B2, B1, and the rest of the receptors?
B2: High Affinity for Epi
B1: Equal Affinity
Rest: Higher affinity for NORI