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Medicine I > Hypoadrenocorticism > Flashcards

Hypoadrenocorticism Flashcards

1
Q

OBJ: Understand adrenal gland functional anatomy and regulation

A
  • see picture
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2
Q

OBJ: Understand the pathological bases for Hypoadrenocorticism

A
  • Destruction of adrenal cortex
    • immune-mediate adrenalitis/adrenal atrophy (most common)
      • lowers GC and MC production
    • Infiltrative diseases (granuloma, amyloidosis
      • same size /bigger gland but decreased functional ability
  • Adrenal suppression by exogenous GC’s
    • Iatrogenic
    • adrenal gland can shrink due to disuse
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3
Q

OBJ: Know the clinical signs and laboratory findings of Hypoadrenocorticism

A
  • Waxing and waning illness
  • Loss of appetite - weight loss
  • lethargy/depression
  • Vomiting/diarrhea
  • PU
  • weakness
  • Regurgitation/abdominal pain
  • Mild anemia
  • lack of stress leukogram
  • Azotemia
  • Electrolyte abnormalities
    • usually hyponatremia and hyperkalemia
      • Na+/K+ ratio <27:1
  • dilute USG
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4
Q

OBJ: Understand the diagnostic approach to Hypoadrenocorticism

A
  • ACTH stimulation test
    • synthetic ACTH used
    • Dogs with Addisons show no increase in cortisol after admin
      • their adrenal gland does not work so there is no response to the extra ACTH
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5
Q

OBJ: Know and understand the treatment of a patient with Hypoadrenocorticism

A
  • Fix crisis
    • glucocorticoid, mineralocorticoid both injectable
  • Maintain healthy
    • can move to long lasting oral glucocorticoid and mineralocorticoid
  • Monitor for life:
    • electrolyte balance
    • clinical signs
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6
Q

Which hormones are released from the adrenal gland? give specific areas and examples

A
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7
Q

How is cortisol secretion regulated?

A
  • ACTH secretion is pulsatile
  • ACTH secretion influenced by:
    • feeding
    • Physiologic / environmental stress
      • pain, trauma, hypoxia, pyrogens, cold exposure, surgery
  • HYPERadrenocorticism - excess cortisol
  • HYPOadrenocorticism - cortisol and aldosterone deficiency
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8
Q

What are the two types of hypoadrenocorticism? how are they different?

A
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9
Q

What are causes of adrenal cortex destructuion?

A
  • Immune-mediated adrenalitis / adrenal atrophy
    • most common - possibly genetic?
  • Infiltrative diseases (ex granuloma, amyloidosis)
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10
Q

What are the results of adrenal suppression by exogenous Glucocorticoids?

A

Usually GC deficiency, sometimes aldosterone deficiency

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11
Q

What are the consequences of Adrenal Failure?

A
  • See signs at 85% loss
  • Cortisol deficiency - multisystemic
    • inappetence, weight loss, lethargy, GI signs, hypoglycemia, hypercalcemia
  • Aldosterone deficiency - salt and water
    • Electrolyte disturbances
      • hypoNa, HypoCl, HyperK
    • Decreased plasma volume
    • Polyuria and inc water loss
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12
Q

What affects does a cortisol deficiency have on the body?

A
  • Multisystemic
    • Inappetence
    • Weight loss
    • Lethargy
    • GI signs
    • hypoglycemia
    • Hypercalcemia
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13
Q

What affects does aldosterone deficiency have on the body?

A
  • Salt and water affects:
    • Electrolyte disturbances
      • Hyponatremia, hypocloremia, hyperkalemia
    • Decreased plasma volume
    • Polyuria and increased water loss
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14
Q

What are the patient factors that can play a role in hypoadrenocorticism?

A
  • “young dog” disease
    • mean age 4.5yo @ diagnosis
  • Genetic influences based on:
    • breed susceptibility, pedigree analysis, genomic studies
  • In early stages - basal hormone secretion is sufficient unless stressed
    • may be “ill” with non-specific signs
    • “waxing and waning”
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15
Q

What are the most common signs of hypoadrenocorticism?

A
  • Loss of appetite
  • Lethargy/depression
  • vomiting / diarrhea
  • Polyuria
  • Weakness
  • Weight loss
  • Regurgitation / abdominal pain
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16
Q

What is an “Addisonian crisis”

A
  • Severe hypoadrenocorticism
  • Progression of disease
  • Severe signs caused be electrolyte distrubances and volume depletion
    • Bradycardia
    • Weak pulses
    • Poor perfusion
    • Hypothermia
    • Shock
    • Melena
    • Collapse
    • Seizure
17
Q

What changes are seen on a CBC of a patient with hypoadrenocorticism?

A
  • Mild anemia
  • Lack of a ‘stress leukogram’
    • important observation in a ‘critical’ patient
18
Q

What changes are seen on serum chemistry of a patient with hypoadrenocorticism

A
  • Azotemia - elevated BUN and creatinine
  • Electrolyte abnormalities
    • Hyponatremia and hypochloremia - aldosterone deficiency
    • Hyperkalemia - aldosterone deficiency and acidosis
    • Addison’s usually causes both!
  • Na+/k+ ration (normal > 27:1)
    • < 27:1 is suspicious; < 20:1 strongly suspicious
  • Other: hypoglycemia, hypercalcemia, hypoalbuminemia, acidosis
19
Q

What changes on a urinalysis are seen in a patient with hypoadrenocorticism? Why?

A
  • USG often dilute (<1.030) despite dehydration
    • Aldosterone deficiency - Sodium and Chloride losses cannot take place without concurrent loss of water
20
Q

What is hypoadrenocorticism commonly misdiagnosed as? why?

A
  • Renal failure
    • Azotemia + dehydration + dilute urine
21
Q

How can a diagnosis of hypoadrenocorticism be confirmed?

A
  • ACTH stimulation test
    • Dogs with Addison’s show NO increase in cortisol after administration of exogenous ACTH
    • Affected dogs usually have a “flat stim” test
      • low baseline cortisol and low cortisol after ACTH
22
Q

are aldosterone levels assessed in Addison’s patients?

A
  • NO
    • deficiency is inferred by electrolyte abnormalities
23
Q

What are some infrequently used tests for Hypoadrenocorticism?

A
  • Endogenous ACTH
    • elevated in primary hypoadrenocorticism but not used for diagnosis
  • Basal (resting) cortisol level
    • used to screen suspicious cases for hypocortisolemia
    • low result is consistent with hypoadrenocorticism but NOT DIAGNOSTIC
  • Aldosterone concentration
    • Not routinely measured; can confirm mineralocorticoid deficiency
    • Aldosterone overlaps between normal dogs and dogs with hypoadrenocorticism
    • Basal and ACTH-stimulated samples measured
    • Occasionally used in elevation of atypical disease
24
Q

What is the treatment for Hypoadrenocorticism?

A
  • Initial hormone replacement
    • patient is dehydrated, inappetence and in crisis
    • Glucocorticoid - usually injectables
    • Mineralocorticoid
      • Na containing crystalloid - replaces volume
      • Improves BP
  • Maintenance hormone replacement
    • Patient is stable, hydrated, eating
    • Glucocorticoid - oral
    • Mineralocorticoid supplement
      • injectable long-acting product
      • Oral Product
  • Glucocorticoid replacement:
    • Acute therapy - use injectable glucocorticoid
      • Dexamethasone 0.05 - 0.1 mg/kg IV
      • Prednisolone sodium succinate (alternative)
    • Chronic therapy - daily therapy with oral glucocorticoid
      • Prednisone - Physiologic dose is 0.2 - 0.4 mg/kg/day
      • Increase dose if anticipate stressful event
      • Can safely double dose for several days
      • Only treatment needed for atypical Addison’s Disease
  • Mineralocorticoid Replacement
    • Administer immediately after diagnosis
    • Maintenance therapy for life
    • DOCP - Deoxycorticosterone pivalate
      • 2.2 mg/kg IM or SC every 21-30 days
      • Max dose 50mg/dog/dose
      • Slow release of mineralocorticoid
      • No GC activity
      • Single dose is not harmful if dog does not have Addison’s
    • Fludrocortisone (Florinel®)
      • Has minor GC activity
      • Dose 0.015 - 0.02 mg/kg/day
      • Poor absorption
      • ~50% of dogs treated with fludrocortisone will not require additional GC
25
Q

What long term monitoring has to be done for patients with hypoadrenocorticism?

A
  • Serial evaluation of electrolytes
    • First month after diagnosis; weekly beginning 2-weeks after first DOCP dose
    • As needed until the patient’s effective dose and interval is determined
    • Every 3 - 4 months thereafter
    • Adjust mineralocorticoid dose and dosing interval based on electrolyte results
  • Serial evaluation of clinical signs
    • Owners’ observation helpful
    • Deficiencies result in subtle manifestations
    • If not “ doing quite right” adjust daily GC dose
    • MC adjustment if GC adjustment doesn’t correct
  • No Role for serial ACTH stim tests
26
Q

How can we reduce the cost of treating hypoadrenocorticism patients for owners?

A
  • Get good control
    • Reduce hospital costs
    • Healthy patient
  • Work to find minimal effective dose
  • Shop around for best price
    • on-line vet pharmacies
  • Owner administers DOCP at home
    • must be part of long-term monitoring program with veterinarian
27
Q

What is the treatment for an Addisonian Crisis?

A
  • Volume replacement
    • death due to vascular collapse and shock
    • Restore volume using 0.9% NaCl
    • Avoid rapid replacement if Na is <125 mEq/L
  • Hormone replacement after initial fluid bolus
    • Glucocorticoid replacement - complete ACTH stim test before GC are given
    • Mineralocorticoid replacement
  • Treat hyperkalemia if needed
    • administer calcium gluconate
  • Treat acidosis if needed
    • administration of bicarbonate
    • rarely needed
28
Q

How is hyperkalemia treated during an Addisonian crisis?

A
  • Specific therapy usually not needed
    • often corrects with volume replacement and increased urine production
  • Severe or life-threatening hyperkalemia requires immediate treatment
    • Signs include bradycardia and arrhythmia
    • Options:
      • 10% Calcium gluconate
        • 0.5 - 1.0 mg/kg IV SLOW over 10 - 20 minutes with continuous ECG monitoring
        • 15 - 30 minutes for onset of action
        • Cardioprotective effect - protects against K+ but doesn’t directly reduce serum K+
      • Dextrose + Humulin-R (regular insulin)
        • 1 - 2 mls/kg of 50% dextrose IV and 0.125 - 0.5 units regular insulin/kg IV
        • follow with glucose CRI
29
Q

What is the prognosis of canine Hypoadrenocorticism?

A
  • Excellent
    • if owners are educated
    • compliance is excellent
    • close follow-up is maintained
30
Q

What is the Etiology of feline Hypoadrenocorticism?

A
  • Primary - rare
    • suspected to be immune-mediated
  • Secondary
    • iatrogenic causes
      • adrenal suppresion due to megestrol acetate or glucocorticoids
31
Q

How if Feline Hypoadrenocorticism diagnosed?

A
  • ACTH stimulation test
    • 0.125mg/cat
    • blood samples taken before, 30 and 60 minutes post injection
32
Q

How are canine and feline Hypoadrenocorticism similar?

A
  • similar clinical signs
  • similar laboratory abnormalities
  • similar treatments

Medicine I (43 decks)

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