Exam 4- Hypoadrenocorticism in Dogs

what is the casual name for hypoadrenocorticism

addisons disease

give a VERY brief overview of hypoadrenocorticism

• due to cortisol and aldosterone deficiency

• clinical signs are often GI related, but may include hypovolemic shock

• diagnose based on electrolyte abnormalities and ACTH stimulation test

what is produced in the different parts of the adrenal cortex

• glomerulosa = mineralcorticoids

• Fasciciulata= glucocorticoids, sex hormones

• reticularis= glucocorticoids, sex hormone

• GFR= salt, sugar, sex

what are the peripheral effects of cortisol

• gluconeogenesis/glycogenolysis

• maintenance of vascular tone

• stimulation of erythropoiesis

• anti-inflammatory

• adaption to stress

generally describe aldosterone

• regulated by RAAS

• released in response to hypovolemia, hyperkalemia

• increases NA and Cl reabsorption to increase BP

• increases K and H+ ecretion

what are the types of hypoadrenocorticism

• primary = adrenal gland lesion (most common)

• secondary= pituitary gland lesion (rare, low ACTH)

• tertiary? low CRH

• iatrogenic (chronic steroids, mitotane/trilostane)

what is the general hormonal failure seen with primary hypo-AC

• both mineralocorticoid and glucocorticoid deficiency

what is atypical Addisons

• eunatremic, eukalemic hypoadrenocorticism

• electrolytes within normal limits

what is the etiology of primary hypo-AC

• immune mediated most common

• iatrogenis via mitotane, trilostane

• neoplasia

• granulomatous disease

what is the electrolyte imbalance seen with typical hypi-AC

increased K

decreased NA

what are causes of iatrogenic hypo-ac

• treatment of cushings with mitotane and trilostane

• chronic steroid use causing adrenal atrophy, hypoadrenocortical crisis

what are causes of atypical addisons

• adrenal cortical destruction sparing the glomerulosa (thus allowing aldosterone)

• early typical

• aldosterone deficient but compensating

• secondary, ACTH deficiency

what signalment is associated with hypo-ac

• young to middle aged

• females

  • poodles, great danes, west highland whites, saint bernards, Nova Scotia Duck Tolling Retrievers (Catch)

what is the history and clinical signs with hypo-Ac

• non-specific

• ADR

• acute or chronic

• waxing/waning that is worse with stress, responds to fluids and or steroids

• decreased appetite, weight loss, V/D, lethargy and weakness, PU/PD, collapse, rarely seizures, megaesophagus

what diagnostics are used for hypo-ac

• physical

• CBC

• chemistry with electrolytes

• UA

• rads

• ECG

• ACTH stimulation test

what may be seen on a PE for hypo-AC

• nonspecific

• depression/weakness

• diarrhea/melena

• dehydration

• ± hypovolemic shock

• bradycardia in the face of hypovolemia aka relative brady

what are common lab findings for hypo-ac

• hyperkalemia

• hyponatremia

• increased BUN and creatinine

• urine SG <1.030

• hypocholesterolemia

what are less common lab findings for hypo-ac

• hypercalcemia

• hypoalbumemia

• hypoglycemia

• anemia

• eosinophlia/lymphocytsos

• lack of stress leukogram

what are your differentials for increased K and decreased Na

• AKI/urinary obstruction

• whipworm infestation

• thoracic effusion/ascites

• ACE-inhibitors

what are your differentials for only increased K

• acidosis

• iatrogenic

• artifact
  -separate serum ASAP
  -hemolysis
  -thrombocytosis
  -leukocytosis

• DKA

describe the effect of different increases in serum potassium

• normal <5.5

• mild 5.5-7.0

• moderate 7-9 = weakness, cardiac issues

• severe >9 ofte fatal

what are the ECG abnormalities with hypekalemia in order of severity

• spiked T wave

• decreased P, R wave amplitudes

• increased P, P-R, QRS duration

• loss of P wave

• marked bradycardia with heart block, severe arrhythmias and cardiac arrest

what are the clinical signs more unique to cortisol deficit

• V/D

• hypoglycemia

what are the clinical signs more unique to aldosterone deficit

• PU/PD

• hyperkalemia, hyponatremia

what other diagnostic abnormalities may be present with hypo-ac

• rads may show microcardia, megaesophagus

• US adrenal size

• ECG= bradycardia, increased T wave amplitude, widened QRS complex, flattened P wave

what is the only way to definitively diagnose hypo-ac

• ACTH stimulation test

  • goal is maximal stimulation of the adrenal to detect ANY function

what is the proceduce for ACTH stimulation test

• take serum pre-sample

• give cosyntropin IV (1ug/kg, 250 max dose)

• take serum post-sample 1 hr later

what are the potential downsides to ACTH testing

• interactions with prednisone and other steroids (assay interference)

• any glucocorticoid causes axis suppresion

• expensive

how do you interpret the post sample from ACTH stimulation testing

• post <2.0 is diagnostic if no exposure to glucocorticoids

• >2 is NOT addisons

• 2-5 may be due to steroid use

how is baseline cortisol used for hypo-ac diagnosis

can only be used to rule out if baseline is above 2-3ug/dL

what is the clinical use of baseline cortisol

• cannot diagnose, can only rule out

• less expensive

• time, can only be used on non-critical pt

how is atypical addison’s diagnosed

• clinical signs similar
  -shck is rare, GI signs may be mos specific, isolated hypoglycemic seizures, megaecopahgus

• will see same bloodwork issues EXCEPT normal K and Na

• definitive requires ACTH stimulation test