Hypoadrenocorticism Flashcards

1
Q

Hormone

A
  • chemical messenger
  • Secreted from a ductless gland
  • Emptied directly into the circulation
  • Transported by blood to alter the function of a target organ
  • Usually has multiple actions
  • Present in small concentrations
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2
Q

Relative proportions of each zone of the adrenal gland

A
  • Zona glomerulosa (15%)
  • Zona fasciculata (75%)
  • Zona reticularis (10%)
  • Medulla
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3
Q

Hormone secreted by zona glomerulosa

A

Aldosterone

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4
Q

Hormone secreted by zona fasciculata

A

Cortisol

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5
Q

Hormone secreted by zona reticularis

A

Sex hormones

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6
Q

Hormone(s) secreted by adrenal medulla

A

Epinephrine and Norepinephrine

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7
Q

Peripheral effects of cortisol

A
  • Vascular tone
  • Gluconeogenesis/Glycogenolysis
  • Stimulation of erythropoiesis
  • Anti-inflammatory
  • Adaptation to stress
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8
Q

What system regulates Aldosterone?

A
  • RAAS
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9
Q

What is aldosterone released in response to?

A
  • Hypovolemia, hyponatremia, hyperkalemia

- Via Angiotensin II

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10
Q

Primary functions of Aldosterone (electrolytes)

A
  • Increased sodium and chloride reabsorption (SAVE SODIUM)

- Increased potassium and hydrogen secretion (PEE POTASSIUM)

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11
Q

Primary (adrenal gland lesion) cause of hypoadrenocorticism (#1 cause)

A
  • Immune mediated destruction of adrenal cortex
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12
Q

How much of the adrenal cortex must be destroyed for clinical signs (usually)?

A
  • > 85-90% of adrenal cortical destruction

- Most cases are 95%

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13
Q

Other primary (adrenal gland lesion) causes of hypoadrenocorticism

A
  • Iatrogenic destruction
  • Drugs (mitotane, trilostane)
  • Suppression by exogenous steroids
  • Neoplasia
  • Granulomatous disease
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14
Q

Secondary causes of hypoadrenocorticism (Pituitary gland lesion)

A
  • RARE

- Decreased ACTH

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15
Q

Typical Addisonian

A
  • Destruction of zona glomerulosa and fasciculata

- Deficiency of cortisol (glucocorticoid) and aldosterone (mineralocorticoid)

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16
Q

Atypical Addisonian

A
  • Destruction of zona fasciculata only (?)
  • Signs of cortisol deficiency only
  • No electrolyte changes
  • This is why you can’t rule out Addison’s even if you don’t see changes in electrolytes
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17
Q

Does atypical really exist?

A
  • May be another mechanism allowing for maintenance of electrolytes even without aldosterone present
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18
Q

Typical age of Addisonian patients

A

Young to middle aged

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19
Q

Typical sex of Addisonian patients

A

Females may be more predisposed

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20
Q

Typical breeds of Addisonian patients

A
  • Standard poodles***
  • Portuguese water dog
  • Nova Scotia Duck Tolling Retriever
  • Bearded Collie
  • Others: Great Danes, Westie, Saint Bernard, etc.
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21
Q

Acute signs of Addisonian crisis

A
  • May present recumbent, shocky

- Threatening crisis

22
Q

Chronic signs of Addison’s

A
  • “waxing and waning”
  • History of GI signs, etc., that resolve on their own with supportive care (especially fluids)
  • PU/PD, weakness/lethargy, weight loss
23
Q

Physical exam findings of Addison’s

A
  • Non-specific findings
  • Changes may be vague or absent
  • Weakness, dehydration, pale mucous membranes, decreased pulse strength, bradycardia, hypothermia
24
Q

Most common CBC changes with Addison’s

A
  • No stress leukogram (92%)
  • Eosinophilia (20%)
  • Lymphocytosis (10%)
  • Non-regenerative anemia (27%) - may be masked by dehydration
25
Pathophysiology of non-regenerative anemia in Addison's
- Steroids play a role in erythropoiesis, so chronically can have an anemia
26
Common Urinalysis in Addison's
- Isosthenuria even with dehydration (60%)
27
Pathophysiology of isosthenuria in Addison's
- Medullary washout due to low sodium
28
Common chemistry panel findings in Addison's
- Hyponatremia - Hyperkalemia - Azotemia - Hyperphosphatemia
29
Less common chemistry panel findings in Addison's
- Hypercalcemia (unknown mechanism) - Hypoalbuminemia (GI loss, possible hepatopathy) - Hypoglycemia (lack of glucocorticoids) - Hypocholesterolemia (melena, GI signs can lead to hypocholesterolemia) - Elevated liver enzymes
30
Clinical signs of Addison's associated with Cortisol deficit
- Vomiting Diarrhea - Hypoglycemia - Maintenance of vascular tone
31
Clinical signs of Addison's associated with Aldosterone deficit
- Polyuria/polydipsia (possible some contribution from glucocorticoids) - Hyperkalemia - Hyponatremia
32
General signs of Addison's that are a combination of the Aldosterone and Cortisol signs
- Lethargy/Weakness - Collapse - Hypovolemic shock
33
Na:K ratio with Addison's
- K is high and Na low with "Typical Addison's" (Na:K ratio <27) - Electrolytes normal with "Atypical Addison's (can still progress to clinical form) - There are other things that can cause a ratio <27 (NOT PATHOGNOMONIC)
34
Baseline cortisol <2 µg/dL Meaning
- If cortisol <2 µg/dL = NOT DIAGNOSTIC - need ACTH stimulation to confirm - YOU WOULD HAVE TO COMMIT TO STIM-ING THE ANIMAL! - Very suspicious but NOT diagnostic
35
Baseline cortisol >2 µg/dL Meaning
- NOT Addison's
36
ACTH stim overview for Addison's
- Gold standard
37
ACTH Stim Test Protocol
- Give cosyntropin IV and measure cortisol 1 hr post administration
38
ACTH Stimulation tests consistent with Addison's
- Most Addisonian patients have pre and post cortisol values <1 µg/dL - Value <2 µg/dL = Addison's - Value >2 µg/dL = Not Addison's
39
Treatment for Acute Addisonian crisis
- IV fluids, supportive, and symptomatic care - Get all blood work and perform an ACTH stim test - If you are suspicious of Addison's and patient is unstable, then start glucocorticoids - Ideally perform stim first, but if you can't then use dexamethasone (NOT PRED)
40
Rationale for fluids in Addison's
- Volume replacement - Fluids will likely also help correct electrolyte imbalances - Be cautious about correcting sodium too rapidly - Wait until sodium levels are safe to administer a mineralocorticoid (otherwise you can correct sodium too quickly, which is also dangerous)
41
How long will treatment for Addison's last?
- LIFELONG TREATMENT NEEDED
42
What are the mainstays of treatment for chronic Addison's?
- Glucocorticoids (prednisone): oral - Mineralocorticoid (DOCP or Percortin): IM injection - Glucocorticoid and Mineralocorticoid (Florinef): oral
43
Prednisone treatment for Addison's
- Daily administration - Give at physiologic doses (~0.1-0.25 mg/kg/day) - Increase dose during stressful or exciting events
44
DOCP treatment frequency
- Given every 25-30 days
45
Price of DOCP
- $$$$$
46
Florinef frequency
- Daily
47
Florinef overview
- Fludricortisone acetate - Glucocorticoid and mineralocorticoid - Difficult to manipulate tablet size
48
Florinef challenges
- Can be difficult to accurately dose for glucocorticoid amount - May be too much for some - Others may need additional prednisone
49
Florinef cost
- Often less expensive than DOCP
50
Monitoring for DOCP
- Check electrolytes 14 days after starting - Then check every 25-30 days to determine maximal duration possible between injections - Once controlled - check electrolytes every 6 months
51
Glucocorticoid monitoring
- Based on clinical signs - If pred side effects seen (PU/PD, polyphagia), may need to decrease dose - If GI signs then may be too low
52
Prognosis of Addison's
- Good - Quality of life can be excellent with vigilance and proper care - Medications need to be given correctly and on schedule to prevent crisis and possible death - Can be cost prohibitive as medications are expensive