Cushings/Addisons Flashcards
Know the different divisions of the adrenal cortex and what is produced there.
Zona Glomerulosa - aldosterone.
Zona Fasciculata - cortisol
Zona Reticularis - 17-ketosteroids and cortisol.
Breed and age incidence of cushing’s
Toy and mini breeds, poodle and dachshunds have increased incidence.
Age 3-13 years (8y avg).
What is exogenous/iatrogenic cushing’s?
Caused by giving large doses of glucocorticoids. Tx is slowly weaning off of the meds and giving the adrenals time to start producing again.
Physical features of cushing’s
Pot bellied
Thin skin, esp on abdomen
Truncal, bilateral, symmetrical alopecia.
Occ, calcinosis cutis.
Cushing’s functional adrenal tumor incidence and pathophys-
15-20% of cases.
Tumor causes excessive amounts of cortisol to be produced/released. This DOES feed back to the pituitary and cause a decrease in ACTH.
Pituitary-dependent cushing’s incidence and pathophysiology
80-85% of cases.
Feedback loop is damaged by tumor and ACTH continues to be released despite high cortisol levels.
Clinical signs of cushing’s disease
PU/PD, polyphagia, weight gain, weakness/lethargy, hyperpigmentation of skin and hair, testicular atrophy, and hepatomegaly. Physical appearance changes.
Cushinoid dogs are ____coagulable.
Hypercoagulable.
Lab findings for cushing’s
Stress leukogram (lymphopenia, eosinopenia, neutrophilia and monocytosis).
^Chol, ALP, ALT.
Proteinuria, +/- UTI.
Endocrine dx of cushing’s
ACTH stim test LDDT HDDT Plasma ACTH Urine cortisol/Cr ratio
ACTH stimulation test evaluation
Elevated - cushing’s
Depressed - addison’s
Abdominal U/S could then be done to see if adrenal tumor present for cushinoid animals.
OPDDD (AKA - lysogren, mitotane)
Used in dogs only. Cat rapidly metabolize so ineffective. Phenobarb makes ineffective as well b/c of P450.
- Cytotoxic to all layers of adrenal cortex.
- If ACTH >10 reload dose.
- drug tox - depression, weakness, v/d, anorexia. Stop med until signs abate then restart on lower dose.
Trilostane
Used in dogs and cats. Most popular drug used for PDH.
1-2 mg/kg BID, titrate to effect (as high as 3mg/kg BID)
Cushinoid cat
Etiology similar to dogs. Many diabetic, testing is the same but interpretation difficult.
LDDST interpretation
- Failure of suppression by atleast 50% base cortisol level by 4-8hrs is diagnostic for cushing’s disease — either PDH or ADH.
- 30% of PDH patients will have suppression of cortisol by 4 hrs and increase by 8 hrs.
HDDST interpretation
Used to differientiate PDH from ADH.
*PDH - cortisol level <50% baseline at 4-8hrs post-dex..
ACTH stimulation test interpretation
Measures response to synthetic ACTH.
- If pre and post <2 ug/dl - hypoadrenocorticism.
- If post is >18 patient is cushinoid but a HDDST or abdominal ultrasound needs to be done to deterine if PDH or ADH.
Incidence of addison’s
Not common, but frequently undiagnosed.
No known sex predilection.
Most common in young dogs <5yr.
Causes of adrenal insuffiency
Iatrogenic Infiltrative - dz, cancer, mycosis. Infartion Pituitary insufficiency OPDDD induced Idiopathic Autoimmune destruction
Electrolyte abnormalities associated with hypoaldosteronism
Decreased Na and Cl
Increased K
S/S of acute addisonian crisis
Hx of wt loss, lethargy, anorexia, +/- GI signs.
Dog presents weak or lateral recumbent.
Mentally dull.
Bradycardia, weak femoral pulses.
Lab findings with acute addison’s crisis
► ± ↓ Neuts ► ± ↑ Eos ► ± ↑ Lymphs ^^^Insensitive ► ↑ K+ ► ↓ Na ► ↑ BUN ► ↓ Glu (rare) ► ↓ HCO3
Other causes of decreased Na and increased K - pseudoaddison’s
renal disease
GI disease
DKA, HNKD,
Chylothorax
Dx of addisons
Gold standard is ACTH stim test.
Na/K <20
Plasma aldosterone
Low in most addisonian dogs.
Low blood levels are independent of serum Na and K levels…. sometimes Na and K can be normal despite low aldosterone due to independent compensatory mechanisms.
A patient presents in what you believe is an addisonian crisis. How do you treat and Dx at the same time?
Begin IV NaCl. Collect resting serum cortisol blood.
Give Cortrosyn IV.
Give dexamethasone IV.
Collect 2nd serum cortisol at 1 hr.
Goals of treating addisonian crisis
Restore volume.
Provided glucocorticoid.
Pred Na succinate or dexamethasone.
Provide mineralcorticoid.
Florinef or DOCP
Reverse marked hyperkalemia.Maintenance tx for addison’s
Florinef or DOCP
+/- Prednisone
Periodic Na/K eval.
What is DOCP?
Percorten-C. Tx for addison’s.
Contains only mineralocorticoid. Need to give pred with.
*OD = hypokalemic myopathy. Tx w/ KCl in fluids.
What is Florinef?
Treatment for addison’s. Has both glucocorticoid and mineralcorticoid activity. Occ need to supplement with pred.
Atypical addision’s
Chronic lethargy, weakness, poor appetite, wt loss.
Normal Na/K despite low aldosterone. Absent to minimal ACTH-induced cortisol response.
Tx of atypical addison’s
If lytes normal: Pred
If lytes ABnormal: Pred w/ florinef (DOCP) OR percorten-V.
What is important to remember when managing an addisonian patient?
Any medical or surgical stress will warrent the use of significant supplemental doses of glucocorticoids.
Comparison between typically and atypical addison’s
Typical |Atypical Na+ ↓ N or ↓ K+ ↑ N or ↑ Cl- ↓ N or ↓ BUN ↑ N Cortisol ↓ ↓ Glucose N, ↓ ↑ N or ↓
