Lab findings in Primary Adrenal Insufficiency 

elevated ACTH & renin

low levels of cortisol and aldosterone 

Lab findings in Secondary Adrenal Insufficiency 

Low ACTH and low cortisol

Aldosterone and renin are normal 

Primary Adrenal Insufficiency (Addison's disease)

destruction of the adrenal gland itself such as cortisol, aldosterone & adrenal androgens cannot be made 

Secondary Adrenal Insufficiency 

Adrenal glands are normal but ACTH production by the pituitary is impaired. 

*most common causes: exogenous glucocorticoid use, pituitary tumors, pituitary production, apoplexy (infarction), and infection 

Cortisol Low, 

ACTH High, 

Aldo Low

Primary Adrenal Insufficiency 

Cortisol Low, 

ACTH Low, 

Aldo NOrmal 

Secondary Adrenal Insufficiency 

Chronic or Acute:

wkness, fatigue, weight loss, anorexia, N/V, abdominal pain, orthostatic hypotension

Chronic 

*may progress to adrenal crisis 

Chronic or Acute

-muscle/joint/abdominal pain

postural hypotension, fever, hypotension, appearance of dehydration

Acute 

hyperpigmentation, salt craving, if autoimmune --> other autoimmune dzs (vitiligo & thyroid dz) 

Manifestations Specific to Primary AI

- Exogenous glucocorticoid use

- hx of pituitary disease 

-sx and symptoms of panhypopituitarism 

Clues suggestive of Secondary AI 

No aldosterone 

*like in 1st AI 

hyponatremia (lose Na+)

hyperkalemia (retain K+, H+)

ACTH stimulation test 

1) measure baseline cortisol level

2) give cortrosyn

3) measure serum cortisol 30-60 min after admid

4) normal response cortisol level>20 ug/dL 

ACTH stimulation test flow chart 

(talk it through) 

Cushing's Syndrome vs. Cushing's Disease 

Cushing's Syndrome: hypercortisolism

Cushing's Disease: hypercortisolism resulting from ACTH production by a pituitary source

Primary Hyperaldosteronism caused by: 

Conn's syndrome

Adrenal Hyperplasia 

Primary Hyperaldosterism

renin levels high or low 

Low 

Secondary Hyperaldosteronism 

High or Low Renin

Decreased RBF --> high Renin --> increased Aldosterone 

*causes: volume depletion, heart failure, cirrhosis, nephrotic syndrome 

-HTN (refractory to meds)

-hypokalemia

- metabolic alkalosis  (xss loss of H+)* I'm think this is the balance of trying to correct the hypoK+ by exchanging H for K out of cell

-muscle weakness

-polyuria, polydipsia 

Primary Hyperaldosteronism 

1) suspect dz

2) screen test (ARR)

3) Confirmatory Testing (aldosterone suppression test)

4) Localization 

Suppression Tests 

Saline supression test 

-Aldosterone <6: normal; Aldosterone > 10: hyperaldosteronism 

High Sodium Diet 

Aldosterone >14 abnl

Cushing Syndrome: Diagnostic Algorithm

Hyperaldosteronism Algorithm

unable to synthesize cortisol & aldosterone

progesterone & 17-OH progesterone

Salt wasting

Girls: ambiguous genitalia

Boys: precocious puberty & short stature

21 hydroxylase deficiency 

Cortisol cannot be synthesize

Androgens accumulate

11-deoxycorticosterone

Severe HTN 

11 Beta Hydroxylase deficiency 

Syndromes associated w/ Pheochromocytoma 

-NF type 1

-MEN 2a & 2b (mutations in RET protooncogenes)

-von Hipple Lindau dz 

Triad for pheochromocytoma 

HA, palpitations, diaphoresis 

biochemical dx for pheochromocytoma 

-plasma free metanephrines

-24 hr urine for catecholamines 

Algorithm for Adrenal Incidentaloma