Exam 8: L.2 Adrenal/Addison's Flashcards
Anterior pituitary (Adenohypophysis)
1) Vascular!
2) Releases:
- ACTH (to adrenal gland), MSH, TSH, FSH, LH, GH, prolactin
Posterior pituitary (neurohypophysis)
1) neural!
2) Releases:
- oxytocin, ADH (vasopressin)
Adrenal gland anatomy
1) adrenal cortex
- zona glomerulosa (G) SALT - aldosterone
- zona fasciculata (F) SUGAR - cortisol
- zona reticularis (R) SEX - androgens
2) adrenal medulla
- releases epinephrine and norepinephrine
Aldosterone
1) deficiency: hypoadrenocortiscism (Addison’s disease)
Note: usually have decreased cortisol with decreased aldosterone
Cortisone
1) deficiency: hypoadrenocortiscism (Addison’s disease)
excess: hyperadrenocortiscism (Cushing’s syndrome)
Note: usually have decreased cortisol with decreased aldosterone
Aldosterone
1) secreted in response to:
A) hyponatremia*, hypotension, hypovolemia
-mediated by angiotensin II
-potent vasoconstrictor
B) hyperkalemia
Biologic half-life = roughly 20 minutes
Renin-Angiotensin-Aldosterone pathway
Dehydration/Na+ deficiency/hemorrhage = => decrease in blood volume = = >decrease in blood pressure = = > JG cells in kidneys release renin = = >renin converts angiotensinogen from liver into angiotensin I ==> ACE in the lungs converts this to angiotensin II = = > vasoconstriction of arterioles/aldosterone release = = >sodium and water retention = => increased blood volume = = >blood pressure increases to normal
Aldosterone effects on sodium and potassium
1) aldosterone release stimulated by a drop in ECF/Na+/BP
- result= sodium and water resorption = increase ECF volume
2) aldosterone release stimulated by increase in potassium
- renal potassium excretion = blood potassium levels decrease
Remember
Cortisol is secreted from zona fasciculata in response to ACTH
Role of physiologic glucocorticoids
1) metabolism
- increase gluconeogenesis/glycogenolysis
- increased fatty acid mobilization
- decrease protein synthesis
- opposite actions of insulin!
2) CNS: stimulates appetite, sensory acuity
3) vasculature: maintains normal blood pressure and volume/role in vascular constriction
4) G.I. tract: maintains normal perfusion/motility
5) immune system
- inflammatory/numerous
- stress response/stress leukogram
Glucocorticoids
Excess: Cushing’s
deficiency: Addison’s
Addison’s vs. Cushing’s
1) vascular volume, blood pressure
-Addison’s: hypotension*
-Cushing’s: hypertension
2) G.I. tract
-Addison’s: ileus
3) complete blood count
-Addison’s: lack stress leukogram
-Cushing’s: stress leukogram
4) serum glucose levels
-Addison’s: hypoglycemic
Cushing’s: hyperglycemic
Hypoadrenocortiscism
1) primary (adrenal gland based)
- most common etiology (usually due to immune mediated disease or idiopathic atrophy and fibrosis)
- loss of functional adrenocortical tissue
* *85-90% loss before clinical signs noted!
Hypoadrenocortiscism: typical signalment
1) females >males (70: 30)
2) medium to large breed dogs
3) younger age at diagnosis (2-7 years)
4) standard poodle genetics may predispose
Hypoadrenocortiscism: presenting complaints
1) no pathognomonic signs-“great imitator”
2) may have waxing and waning course
3) vague complaints (poor appetite, depressed, weight loss, vomiting, diarrhea)
Hypoadrenocortiscism: physical exam findings
1) dehydration-may be severe!
2) bradycardia (hyperkalemia)
3) melena/hematochezia
4) hypothermia
Stress Leukogram
Neutrophilia, lymphopenia, eosinopenia
Hypoadrenocortiscism: minimum database
(May be normal)
1) lack of stress leukogram (92%)
2) hypoglycemia, hypercalcemia, hyponatremia hypercalcemia (cortisol is important for calcium excretion), azotemia
Hypoadrenocortiscism: classic finding
Low Na:K ratio
1) hyponatremia: hypercalcemia
- result of ALDOSTERONE deficiency
- Na:K ratio <24-27:1
Hyperkalemia
Hyperkalemia: May cause a tented T wave, QRS widening, loss of P waves, SLOW heart rate
In severe cases it may cause a widened QRS, loss of P wave, asystole, ventricular fibrillation
Confirming Dx: ACTH stimulation test
gold standard diagnostic test
1) collect baseline/resting cortisol level
2) inject ACTH
3) collect one hour cortisol level
- typical result is flatline (normal animal would be an increase)
- basal cortisol >2.0 ug/dl helps rule out hypoadrenocortiscism
ACTH stimulation test: interference
1) exogenously administered steroids = problems
- suppression of normal adrenal glands
- certain steroids will be measured as cortisol (prednisone)
If you must administer corticosteroids prior to performing ACTH stimulation test, DEXAMETHASONE should be used
Hypoadrenocortiscism: therapy-hormone replacement
1) glucocorticoids (prednisone)
- physiologic dose: ~0.1-0.22 mg/kg/day PO
2) Mineralocorticoids
- oral Florinef (fludrocortisone acetate)
Hypoadrenocortiscism: monitoring and long-term maintenance
Recheck the physical exam, renal panel, and electrolytes every 2 weeks for the 1st month
-find the lowest dose that keeps electrolytes normal
