Exam 8: L.2 Adrenal/Addison's Flashcards Preview

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Flashcards in Exam 8: L.2 Adrenal/Addison's Deck (30):

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



1) deficiency: hypoadrenocortiscism (Addison's disease)

Note: usually have decreased cortisol with decreased aldosterone



1) deficiency: hypoadrenocortiscism (Addison's disease)
excess: hyperadrenocortiscism (Cushing's syndrome)

Note: usually have decreased cortisol with decreased 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



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
-stress response/stress leukogram



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



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: 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


Addisonian Crisis

1)*recognition and early intervention is critical*
2) result of:
-hypoglycemia (deficiency of cortisol)
-hyperkalemia and hyponatremia (deficiency of aldosterone)
-profound dehydration and hypotension (deficiency of cortisol and aldosterone)
3) most life-threatening component!
-Vascular collapse in shock ==> most important component of therapy is IV fluid replacement**!


Addisonian crisis: therapy

1) 0.9% NaCl -shock rate if necessary
2) monitor blood pressure, urine output, sensible and insensible fluid losses
3) IV dextrose if hypoglycemic
4) ECG monitoring (hyperkalemia)
5) glucocorticoid and mineralocorticoid supplementation (be aware how glucocorticoid choice may influence ACTH stim test)


Dexamethasone dose

Prednisone dose divided by 7!


Atypical Addisonian

1) typical Addisonian
-glucocorticoid and mineralocorticoid deficient
2) atypical Addisonian
-*glucocorticoid deficient only
-mineralocorticoid levels and functions are maintained!
-Electrolytes are normal!!** (Tricky to diagnose)
3) atypical Addisonian
-signs due to glucocorticoid deficiency
-neuropathy, myopathy, gastrointestinal, decreased appetite


Atypical Addisonian: therapy

1.) Glucocorticoid replacement
2) NO need to supplement mineralocorticoids
- Monitor electrolytes: it may/may not progress to typical form of disease


Feline hypoadrenocortiscism (Addison's Disease)

Much more rare than canine disease!