Adrenal Flashcards
Cortisol Effects
Gluconeogenesis
Proteolysis
Lipolysis –> up FFAs
90% is protein bound
HPA axis
CRH (hypothalamus) -> ACTH (pituitary) -> cortisol (adrenals)
CRH binds Gs -> up cAMP -> ACTH -> binds Gs in zona fasciculata -> up cAMP -> up cortisol & pregneolone & LDL uptake -> cortisol inhibts CRH & ACTH
Glucocorticoid Effects on Protein, Fibroblasts, Bone, Adipose, RBC
Proteolysis = proximal muscle weakness
Fibroblasts decreased = Thin skin, easy bruising
Osteoporosis (opposes Vit D & Ca absorb)
Centripetal fat, moon facies, buffalo hump
Polycythemia
Glucocorticoid Effect on HR, EF, other hormones, inflammation, immunity, menses, hair
Up HR & EF
Potentiates other hormones (more NE & Epi)
Inhibits phospholipase A2 = can’t make LT or PG
Decreases T cell fxn & proliferation
Amenorrhea
Hirsuitism
Mineralcorticoid
Aldosterone
absorb Na, secrete K+ and H+
Metab in liver
Renin secreted in JGA to low Na/volume –> AT to AT I -> ATII -> aldosterone
Sex Steroids
DHEA(S)
Stimulated by ACTH
Adrenal primary for females, but less potent for males
Steps of Catecholamines
Splanchnic nerve release ACh -> binds nicotinic (gated-fast) & muscarinic (Gq-slower) -> Epi -> binds alpha (1Gq, 2Gi) & beta (Gs) receptors
Aldosterone formation
Pregnalone (from cholesterol via 20,22 desmolase) -> aldosterone (requires 21- hydroxylase
Cortisol formation
17-prenenolonecortisol (requires 21- hydroxylase
Primary Adrenal Insufficiency
Sx
autoimmune (70-80% i.e. Addison’s),
infectious (TB, 10-20%)
Vitiligo, pigmentation
Fatigue, weakness, myalgias, anorexia, salt craving
Primary AI stages
- Increased Renin, normal aldo
2. Decreased cortisol response to ACTH
3. Stage 2 plus high plasma ACTH
4. Clinically overt AI
Primary AI Lab findings
HyperK, Hyponatremia, hypoglycemia, hypercalcemia
Eosinophilia
Cortisol 100 pg/ml
Secondary AI
Defect in CRH release from hypothalamus OR ACTH release from pituitary.
Fatigue, weakness, myalgias, anorexia, salt craving, dizziness, abd pain,
Secondary AI Lab Findings
Hyponatremia
Hypoglycemia, hypercalcemia Eosinophilia
Cortisol
Primary Aldosteronism
High aldosterone HTN, hypokalemia and metabolic alkalosis
Most from Adenoma & Idiopathic hyperaldosteronism
Check if hypokalemia, severe HTN, or young