Hypoadrenocorticism Flashcards
describe the broad hypoadrenocorticism
- umbrella term for naturally-occurring, spontaneous, or iatrogenic reduced function of the adrenal cortex
- results in glucocorticoid deficiency, mineralocorticoids deficiency, or both
describe primary hypoadrenocorticism
- loss of at least 90% of adrenocortical function
- naturally-occurring or spontaneous
-often immune-mediated
-less commonly due to: neoplasia, infarction, infection, hemorrhage, or necrosis - iatrogenic:
-surgery, bilateral adrenalectomy
-drugs: trilostane, mitotane
describe atypical addison’s
- cortisol deficiency
- normal electrolytes with normal or decreased aldosterone
-at least 10% will develop aldosterone deficiency
describe secondary hypoadrenocorticism
- glucocorticoid deficiency due to a lack of eACTH
-NO electrolyte abnormalities - naturally occurring/spontaneous:
-post-adrenalectomy of functional/cortisol-producing tumor
-hypophysectomy - iatrogenic: abrupt withdrawal of
-chronic/high dose glucocorticoids
-progestins
describe aldosterone
secretion stimulated by:
- hypovolemia, hypotension: via RAAS
- kyperkalemia: direct
actions:
1. principal cells: sodium and water absorption, potassium excretion
2. intercalated cells: hydrogen excretion
describe signalment of Addison’s
- most common breeds:
-standard poodles!!!
-portuguese water dog
-nova scotia duck tolling retriever
-bearded collie - other breeds:
-basset hound, airedale terrier, great dane, rottweiler, soft-coated wheaten terrier, springer spanial, st. bernard, westies
-also mfin goldendoodle (muppet ass) - median age: 4 years
- potential predisposition for females
describe clinical signs of addison’s
due to low cortisol:
1. decreased stress response: lethargy, hypoglycemia
2. GI health: vomiting, diarrhea
3. decreased vascular tone: hypotension, weakness
due to low aldosterone:
1. decreased sodium and water absorption: polyuria, hypovolemia
2. decreased K and H secretion: hyperkalemia, bradycardia, and acidosis
signs are intermittent (the great pretender!!)
1. episodic GI signs: anorexia, V/D, regurg if megaesophagus, melena, hematochezia, esp if after stress
2. PU/PD
3. lethargy, weakness, trembling
Acute Addisonian/Adrenal crisis:
1. collapse, hypovolemic shock
2. acute onset GI signs
3. hypoglycemic seizures
4. esp after stress
describe physical exam for addison’s
- nothing pathognomonic or specific
- chronic: poor BCS
- acute:
-near death
-hypothermia
-bradycardia
-dehydrated or hypovolemic
describe CBC of addison’s
- LACK OF A STRESS LEUKOGRAM
-no neutrophilia, or disproportionately low neutrophilia for severe disease
-lymphocytosis
-eosinophilia
- non-regenerative anemia
-sometimes masked by hemoconcentration!!
describe the chemistry of addison’s
- hyperkalemia
- hyponatremia
-Na:K <24-27 - azotemia
- liver enzyme decrease
- metabolic acidosis
- decreased GFR
+/- hyperphosphatemia - decreased calciuresis
+/- hypercalcemia - decreased gluconeogenesis
+/- hypoglycemia - chronic enteropathy/decreased hepatic production
+/- hypoalbunimeia
+/- hypocholesteremia
what are differentials for hyperkalemia and hyponatremia that must be ruled out when suspect addison’s?
diseases:
1. acute renal failure
2. urinary tract obstruction
3. uroabdomen
4. whipworms, trichuriasis
5. severe GI disease
6. peritoneal effusion
7. chylothorax
8. diabetic ketoacidosis
9. CHF
10. hepatic failure/cirrhosis
11. primary polydipsia
drugs:
1. furosemide
2. spironolactone
3. ACE-inhibitors (enalapril)
4. angiotensin R blockers, telmisartan
describe urinalysis of addison’s
USG <1.030
-disproportionately dilute for presentation
dehydrated but diluted!!
why is addison’s called the great pretender?
can resemble a lot of diseases with its:
-vague, intermittent, or chronic GI signs
-PU/PD
-lymphocytosis or eosinophilia
-renal azotemia
-increased liver enzymes
-hypoglycemia in isolation
diagnosis may require you to pick up on subtle clues to save a life!
describe differences in bloodwork/labs of atypical addison’s
- no hyperkalemia or hyponatremia
- less likely to present with hypovolemia shock
-fewer are azotemic or azotemia is less severe - less hemoconcentrated:
-anemia is more common
-lower serum albumin concentrations - cholesterol concentrations are lower:
-reflect more chronic disease since harder to diagnose potentially
describe imaging for addison’s
- abdominal imaging for GI signs:
-radiographs: hypovolemia and microhepatica
-ultrasound: smaller adrenal glands - thoracic radiographs:
-microcardia
-reduced caudal vena cava
+/- megaesophagus
describe diagnostic tests for addison’s
- screening tests with 100% Sn
-basal cortisol concentration: >2mg/dL excludes cortisol deficiency! <2mg/dl = MUST perform SCTHST to confirm - definitive diagnostic test:
-ACTH stim test
-pre and post often <1.0mcg/dL
others:
1. aldosterone concentration:
-performed on pre/0hr and post/1hr cortisol samples
-electrolytes are a poor indicator of aldosterone concentrations!
- basal cortisol to eCTH ratio (CAR)
-alternate way to help confirm diagnosis
-need a more user friendly eACTH assay though - eACTH for primary versus secondary disease
-primary/common: high
-secondary/rare: low
describe emergency treatment for addison’s hypovolemia
hypovolemia: fluid resuscitation is THE most important therapy!
IV fluid therapy: 10-15ml.kg bolus over 15-30min, reassess, and readmin PRN
fluid type:
1. saline or 0.9% NaCl previously favored BUT
-high Na concentration may increase Na too fast
-goal is <0.5mEq/kg/hr or 12mEq/day
-osmotic demyelination syndrome
-acidifying
- LRS or normosol-R:
-contains buffer
-Na concentration lower than 0.9% NaCl
-trivial K and Ca concentrations
describe emergency treatment for addison’s hypotension and hypoglycemia
- IV dexamethasone with NO mineralocorticoid content
-10x more potent that prednisone! - give IV fluids BEFORE perform ACTH stimulation
- can also give single dexamethasone injection beforehand
-avoid correct diagnosis on a dead patient, treat the patient first, then try to diagnose - for hypoglycemia:
-bolus then add to fluids - for severe anemia (like with a GI bleed):
-give blood products (packed RBCs)
describe signs of hyperkalemia on an ECG
progressive:
1. increased T wave amplitude
- shortened Q-T interval
- decreased P wave amplitude
- prolonged P-R interval
- absent P wave (sinoatrial standstill)
- severe bradycardia
- asystoly
describe treatment of hyperkalemia if fluid therapy is insufficient
- severe hyperKa : >9.0 mEq/L causes life-threatening arrhythmias
- calcium gluconate is cardioprotective but does NOT decrease K
- regular insulin and dextrose: drives K into cells
- DOCP: once re-perfused
-desoxycorticosterone pivalate
describe maintenance glucocorticoid replacement for an addison’s patient
- prednisone:
-0.2-0.4 mg/kg/day PO initially, then wean to lowest effective dose over weeks-months
-most end up needing <0.1mg/kg/day
-increase to 0.5mg/kg before and after stressful events
lifelong therapy!! canNOT combine with NSAIDs
describe DOCP as mineralocorticoid replacement
monitoring:
1. recheck electrolytes after 10-14d
-dose typically adequate
- recheck again at 25d
-to determine if dosing interval acceptable
lifelong therapy and EXPENSIVE
-monitory electrolytes to see if can extend dosing interval
-but REMEMBER for atypical addison’s continue to monitor electrolytes every 3-4 moonths for progression to typical disease!
describe fludrocortisone
- 0.02mg/g PO daily
- monitoring:
-titrate weekly dose based on: electrolytes and clinical signs, many patients required higher doses over time
-contains small amts of glucocorticoids so beware or cushingoid
