PRIMARY AND SECONDARY ADDISON'S DISEASE PATHOPHYSIOLOGY GROUP I-1

SECONDARY
-Removal of a nonendocrine
corticotropin-secreting tumor
Legend:
-Autoimmune disease
-Long-term corticosteroid therapy
-Pituitary tumors or infection
Symptoms -Bleeding in the pituitary
Pathophysiology /Manifestations -Genetic diseases that affect the way the
pituitary gland develops or functions.
-Surgical removal of the pituitary to treat other
conditions
PRIMARY
-Traumatic brain injury link -Idiopathic
Causes/Risk -Tuberculosis
Diagnosis -Removal of both adrenal glands
factors
-Hemorrhage into the adrenal gland
-Neoplasm
-Infections (HIV, histoplasmosis, meningococcal
Decreased/suppressed pneumonia, cytomegalovirus)
Pituitary
Note production of CRH by the Decrease in
infiltration/destruction
hypothalamus digestive enzymes Abdominal
due to low cortisol pain, N/V,
Anorexia

Impaired or Significant
suppressed function of the bilateral damage to the
pituitary gland adrenal glands Decreased Malaise, muscle
serum dehydroepia Decreased weakness (can't lift legs
ndrosterone sulfate axillary and against resistance)
(DHEAS), testosterone, Decreased
pubic hair
androste libido
decreased Atrophy of Secondary adrenal Adrenal
production of ACTH by the nedione Decreased
adrenal gland insufficiency develops cortex function is
pituitary gland impaired cortisol mediated Hypoglycemia
gluconeogenesis and (60)
Decreased androgen glycogenolysis
Decrease androgen levels in women (adrenal
production from the zona glands are their primary Low
Low ACTH reticularis source) Increased urine
cortisol-releasing Increased Kidneys reabsorb
serum levels Addison's water, increasing output (15
hormone (CRH) from ADH release to 20 ml/hr, dark
Disease/Adrenal hypothalamus total body water
Insufficiency Decrease cortisol yellow)
production from the zona
fasciculata Lack of cortisol-driven Diminished
Increased
vasoconstriction of blood peripheral pulses,
Adrenal Crisis vasodilation
vessels pale & cool skin
References Decreased serum levels
of adrenal steroid hormones Decrease Low
Sgaggi, S. (2015, May 25). Central adrenal insufficiency: Pathogenesis and clinical findings | calgary guide. The Calgary Guide to exert positive feedback effect serum cortisol BP (80/48), Compensatory
Understanding Disease. Retrieved March 31, 2022, from on pituitary gland postural mechanism to
https://calgaryguide.ucalgary.ca/Central-Adrenal-Insufficiency---Pathogenesis-and-Clinical-Findings/ Signs of increase BP
dehydration, High dizziness
Patients could present
with many severe symptoms of BUN Hyponatremia
Sgaggi, S. (2021, October 2). Primary adrenal insufficiency: Clinical findings | calgary guide. The Calgary Guide to Understanding Increased production
Disease. Retrieved March 31, 2022, from https://calgaryguide.ucalgary.ca/primary-adrenal-insufficiency-clinical-findings/ Increased adrenal insufficiency, e.g low blood levels (123)
serum levels of adrenocorticotropic pressure refractory to fluid Tachycardia
Water follows sodium -->
of ACTH hormone (ACTH) by resuscitation (126 bpm)
Nicolaides, N. C. et. al. (2017). Adrenal Insufficiency. Endotext. https://www.ncbi.nlm.nih.gov/books/NBK279083/ the pituitary gland Increase excretion of water
Hypochloremia
Decrease aldosterone production (88)
Platnich, J. (2013). Central Adrenal Insufficiency: Pathogenesis and Clinical Findings.
from the zona glomerulosa
http://calgaryguide.ucalgary.ca/wp-content/uploads/2015/05/Central-Adrenal-Insufficiency-Pathogenesis-and-Clinical-Findings.jpg Decrease sodium resorbed from
Coincidental increase Decrease sodium channel Increase
kidney tubules ---> Increase sodium
in melanocyte-stimulating and NA/K ATpase expression on salt craving
hormone (MSH) by the excretion
Wilkins, W. L. (2018). Pathophysiology made incredibly easy (incredibly easy series) (6th ed.). LWW. principle cells of kidney
pituitary due to
Decrease serum Hyperkalemia
decrease in cortisol Decrease potassium pumped
aldosterone (6.6)
into kidney tubules --> Increase potassium
retained in serum
NOTE: Aldosterone is not affected in Tall T-waves
MSH triggers the increased
production of melanin by the secondary Addison's disease as it is
melanocytes of the skin predominantly controlled by the RAAS Metabolic
Decrease excretion of hydrogen
and not ACTH. Potassium may be normal Acidosis
ions from kidneys
or low due to vomiting.

Hyperpig
mentation
of skin and mucosal
membranes (inner arms &
genitalia, bluish-black
spot on lips)