Exam 8: L.2 Adrenal/Addison's

Question 1

Anterior pituitary (Adenohypophysis)

Answer 1

1) Vascular!
2) Releases:
- ACTH (to adrenal gland), MSH, TSH, FSH, LH, GH, prolactin

Question 2

Posterior pituitary (neurohypophysis)

Answer 2

1) neural!
2) Releases:
- oxytocin, ADH (vasopressin)

Question 3

Adrenal gland anatomy

Answer 3

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

Question 4

Aldosterone

Answer 4

1) deficiency: hypoadrenocortiscism (Addison’s disease)

Note: usually have decreased cortisol with decreased aldosterone

Question 5

Cortisone

Answer 5

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

Note: usually have decreased cortisol with decreased aldosterone

Question 6

Aldosterone

Answer 6

1) secreted in response to:
  A) hyponatremia*, hypotension, hypovolemia
    -mediated by angiotensin II
    -potent vasoconstrictor
  B) hyperkalemia

Biologic half-life = roughly 20 minutes

Question 7

Renin-Angiotensin-Aldosterone pathway

Answer 7

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

Question 8

Aldosterone effects on sodium and potassium

Answer 8

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

Question 9

Remember

Answer 9

Cortisol is secreted from zona fasciculata in response to ACTH

Question 10

Role of physiologic glucocorticoids

Answer 10

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

Question 11

Glucocorticoids

Answer 11

Excess: Cushing’s
deficiency: Addison’s

Question 12

Addison’s vs. Cushing’s

Answer 12

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

Question 13

Hypoadrenocortiscism

Answer 13

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!

Question 14

Hypoadrenocortiscism: typical signalment

Answer 14

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

Question 15

Hypoadrenocortiscism: presenting complaints

Answer 15

1) no pathognomonic signs-“great imitator”
2) may have waxing and waning course
3) vague complaints (poor appetite, depressed, weight loss, vomiting, diarrhea)

Question 16

Hypoadrenocortiscism: physical exam findings

Answer 16

1) dehydration-may be severe!
2) bradycardia (hyperkalemia)
3) melena/hematochezia
4) hypothermia

Question 17

Stress Leukogram

Answer 17

Neutrophilia, lymphopenia, eosinopenia

Question 18

Hypoadrenocortiscism: minimum database

Answer 18

(May be normal)

1) lack of stress leukogram (92%)
2) hypoglycemia, hypercalcemia, hyponatremia hypercalcemia (cortisol is important for calcium excretion), azotemia

Question 19

Hypoadrenocortiscism: classic finding

Answer 19

Low Na:K ratio

1) hyponatremia: hypercalcemia
- result of ALDOSTERONE deficiency
- Na:K ratio <24-27:1

Question 20

Hyperkalemia

Answer 20

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

Question 21

Confirming Dx: ACTH stimulation test

gold standard diagnostic test

Answer 21

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

Question 22

ACTH stimulation test: interference

Answer 22

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

Question 23

Hypoadrenocortiscism: therapy-hormone replacement

Answer 23

1) glucocorticoids (prednisone)
- physiologic dose: ~0.1-0.22 mg/kg/day PO
2) Mineralocorticoids
- oral Florinef (fludrocortisone acetate)

Question 24

Hypoadrenocortiscism: monitoring and long-term maintenance

Answer 24

Recheck the physical exam, renal panel, and electrolytes every 2 weeks for the 1st month
-find the lowest dose that keeps electrolytes normal

Question 25

Addisonian Crisis

Answer 25

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**!

Question 26

Addisonian crisis: therapy

Answer 26

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)

Question 27

Dexamethasone dose

Answer 27

Prednisone dose divided by 7!

Question 28

Atypical Addisonian

Answer 28

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

Question 29

Atypical Addisonian: therapy

Answer 29

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

Question 30

Feline hypoadrenocortiscism (Addison’s Disease)

Answer 30

Much more rare than canine disease!