Adrenal Flashcards

1
Q

Cortisol Effects

A

Gluconeogenesis
Proteolysis
Lipolysis –> up FFAs
90% is protein bound

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2
Q

HPA axis

A

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

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3
Q

Glucocorticoid Effects on Protein, Fibroblasts, Bone, Adipose, RBC

A

Proteolysis = proximal muscle weakness
Fibroblasts decreased = Thin skin, easy bruising
Osteoporosis (opposes Vit D & Ca absorb)
Centripetal fat, moon facies, buffalo hump
Polycythemia

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4
Q

Glucocorticoid Effect on HR, EF, other hormones, inflammation, immunity, menses, hair

A

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

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5
Q

Mineralcorticoid

A

Aldosterone
absorb Na, secrete K+ and H+
Metab in liver
Renin secreted in JGA to low Na/volume –> AT to AT I -> ATII -> aldosterone

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6
Q

Sex Steroids

A

DHEA(S)
Stimulated by ACTH
Adrenal primary for females, but less potent for males

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7
Q

Steps of Catecholamines

A

Splanchnic nerve release ACh -> binds nicotinic (gated-fast) & muscarinic (Gq-slower) -> Epi -> binds alpha (1Gq, 2Gi) & beta (Gs) receptors

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8
Q

Aldosterone formation

A

Pregnalone (from cholesterol via 20,22 desmolase) -> aldosterone (requires 21- hydroxylase

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9
Q

Cortisol formation

A

17-prenenolonecortisol (requires 21- hydroxylase

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10
Q

Primary Adrenal Insufficiency

Sx

A

autoimmune (70-80% i.e. Addison’s),
infectious (TB, 10-20%)
Vitiligo, pigmentation
Fatigue, weakness, myalgias, anorexia, salt craving

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11
Q

Primary AI stages

A
  1. Increased Renin, normal aldo
     2. Decreased cortisol response to ACTH
     3. Stage 2 plus high plasma ACTH
     4. Clinically overt AI
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12
Q

Primary AI Lab findings

A

HyperK, Hyponatremia, hypoglycemia, hypercalcemia
 Eosinophilia
Cortisol 100 pg/ml

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13
Q

Secondary AI

A

Defect in CRH release from hypothalamus OR ACTH release from pituitary.
Fatigue, weakness, myalgias, anorexia, salt craving, dizziness, abd pain,

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14
Q

Secondary AI Lab Findings

A

Hyponatremia
Hypoglycemia, hypercalcemia  Eosinophilia
Cortisol

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15
Q

Primary Aldosteronism

A

High aldosterone  HTN, hypokalemia and metabolic alkalosis
Most from Adenoma & Idiopathic hyperaldosteronism
Check if hypokalemia, severe HTN, or young

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16
Q

Primary Aldo Labs

A

High PA
Oral Salt Loading/High Na diet high aldo in urine
IV Saline Infusion high PA

17
Q

Primary Aldo Tx

A

Surgery for Adenomas

Aldo Antagonists plus HTN Meds

18
Q

Pheochromocytoma

A

Tumor causing hypercatecholamine secretion
Can be MEN 2A/B, VHL, NF
HA +Sweating + Palpitations

19
Q

Pheochromocytoma Lab

A

Urine metanephrines, catecholamines, normetanephrine
Plasma metanephrines,
Easy to find on MRI, CT, etc

20
Q

Pheochromocytoma Tx

A

Preop: Alpha blockers, then beta-blockers OR Ca blockers alone
Adrenalectomy