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SA Medicine Endocrine > Hypoadrenocorticism > Flashcards

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
Q

Pathophysiology of non-regenerative anemia in Addison’s

A
  • Steroids play a role in erythropoiesis, so chronically can have an anemia
26
Q

Common Urinalysis in Addison’s

A
  • Isosthenuria even with dehydration (60%)
27
Q

Pathophysiology of isosthenuria in Addison’s

A
  • Medullary washout due to low sodium
28
Q

Common chemistry panel findings in Addison’s

A
  • Hyponatremia
  • Hyperkalemia
  • Azotemia
  • Hyperphosphatemia
29
Q

Less common chemistry panel findings in Addison’s

A
  • Hypercalcemia (unknown mechanism)
  • Hypoalbuminemia (GI loss, possible hepatopathy)
  • Hypoglycemia (lack of glucocorticoids)
  • Hypocholesterolemia (melena, GI signs can lead to hypocholesterolemia)
  • Elevated liver enzymes
30
Q

Clinical signs of Addison’s associated with Cortisol deficit

A
  • Vomiting Diarrhea
  • Hypoglycemia
  • Maintenance of vascular tone
31
Q

Clinical signs of Addison’s associated with Aldosterone deficit

A
  • Polyuria/polydipsia (possible some contribution from glucocorticoids)
  • Hyperkalemia
  • Hyponatremia
32
Q

General signs of Addison’s that are a combination of the Aldosterone and Cortisol signs

A
  • Lethargy/Weakness
  • Collapse
  • Hypovolemic shock
33
Q

Na:K ratio with Addison’s

A
  • 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
Q

Baseline cortisol <2 µg/dL Meaning

A
  • 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
Q

Baseline cortisol >2 µg/dL Meaning

A
  • NOT Addison’s
36
Q

ACTH stim overview for Addison’s

A
  • Gold standard
37
Q

ACTH Stim Test Protocol

A
  • Give cosyntropin IV and measure cortisol 1 hr post administration
38
Q

ACTH Stimulation tests consistent with Addison’s

A
  • 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
Q

Treatment for Acute Addisonian crisis

A
  • 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
Q

Rationale for fluids in Addison’s

A
  • 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
Q

How long will treatment for Addison’s last?

A
  • LIFELONG TREATMENT NEEDED
42
Q

What are the mainstays of treatment for chronic Addison’s?

A
  • Glucocorticoids (prednisone): oral
  • Mineralocorticoid (DOCP or Percortin): IM injection
  • Glucocorticoid and Mineralocorticoid (Florinef): oral
43
Q

Prednisone treatment for Addison’s

A
  • Daily administration
  • Give at physiologic doses (~0.1-0.25 mg/kg/day)
  • Increase dose during stressful or exciting events
44
Q

DOCP treatment frequency

A
  • Given every 25-30 days
45
Q

Price of DOCP

A
  • $$$$$
46
Q

Florinef frequency

A
  • Daily
47
Q

Florinef overview

A
  • Fludricortisone acetate
  • Glucocorticoid and mineralocorticoid
  • Difficult to manipulate tablet size
48
Q

Florinef challenges

A
  • Can be difficult to accurately dose for glucocorticoid amount
  • May be too much for some
  • Others may need additional prednisone
49
Q

Florinef cost

A
  • Often less expensive than DOCP
50
Q

Monitoring for DOCP

A
  • 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
Q

Glucocorticoid monitoring

A
  • 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
Q

Prognosis of Addison’s

A
  • 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

SA Medicine Endocrine (8 decks)

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