Cushing's Disease Flashcards
What is another name for Cushing’s Disease?
Hyperadrenocorticism
If the patient does not have ______ do not even investigate whether or not they have Cushing’s Disease.
PU/PD
What are the 2 broad categories of Cushing’s?
- Spontaneous
2. Iatrogenic
What are the 2 types of spontaneous Cushing’s Disease?
- Pituitary dependent (~85%)
2. Adrenal dependent (~15%)
What is the % chance that the reason an animal has Cushing’s is because of a tumor?
90%
What is the gold standard test for diagnosing Cushing’s Disease in dogs?
Low Dose Dex Suppression Test
With PDH (Pituitary Dependent) Cushing’s there is excessive stimulation of ______ and we subsequently get hyperplasia of the adrenal cortex.
ACTH
What are the 2 main layers that you get hyperplasia with, with PDH Cushing’s?
Zona Fasiculata and Zona Reticularis
The zona reticularis is responsible for production of what?
Sex steroids (androgens)
The zona fasiculata is responsible for production of what?
Glucocorticoids (cortisol)
What are the effects of glucocorticoids on the body?
Energy metabolism (generally catabolic, antagonistic to insulin: increase gluconeogenesis), water and electrolytes (alters Ca2+ metabolism, dec absorption and increase secretion in urine, causes PU/PD), cardiac and respiratory system (chronotropic and inotropic, increases beta adrenoreceptors, indirect cardiac effects through water/electrolyte metabolism), hematology (increased RBC lifespan, increased platelets, increased clotting/platelet function, “stress leukogram”), chemistry (ALP increases easily into the 1000’s, ALT, GGT, Cholesterol, Glucose MAY increase, normal or increased insulin with possibility for resistance, BUN, T3/T4 MAY decrease), nervous system (mental dependency, euphoria/depression, polyphagia, peripheral neuropathies), decrease fever (inhibition of PGE2 production in the thermoregulatory center, can mask a febrile response), skin (calcinosis cutis, thinning and weakening of skin, endocrine alopecia), musculoskeletal system (increase in osteoclast activity and decrease in osteoblast activity leads to osteoporosis and poor bone growth, depletion of cartilage matrix, inhibition of fibroblasts,) Reproductive system (fetal maturation, teratogenic can induce a cleft palate, induces abortions, or parturition, inhibit spermatogenesis, inhibit ovulation,) Gastrointestinal & Hepatic (GI ulcerations, fatty liver, pancreatitis.)
What are the clinical signs associated with Cushing’s Disease?
PU/PD, polyphagia, lethargy, excessive panting (can get mineralization of airways, and excessive fat will put pressure on the diaphragm), muscle weakness, obesity, bilateral truncal alopecia, hyperpigmented skin, pot belly, bacterial dermatitis, calcinosis cutis, development of thromboemboli due to increased synthesis of clotting factors, increased # of platelets, increased aggregation of platelets, excessive bruising, lack of estrus in intact females, soft testicles in males.
What does lab work usually show on Cushinoid patients?
Stress leukograms (neutrophilia, lymphopenia), Elevated ALP, increases in cholesterol, glucose, ALT, GGT, AST, bile acids, Decreased BUN & Creat., concentrated urine 1.022 or less down to Hyposthenuria (USG <1.010), UTIs, Glucosuria
On x-rays of a Cushanoid patient what might you expect to see but not necessarily find?
Increased amounts of fat in the abdominal cavity (throughout omentum), possibly mineralized adrenal glands, hepatomegaly, osteopenia, uroliths/nephroliths, full bladder.
How would you perform a LDDST?
Take a blood sample at time 0, then administer Dex-SP 0.015 mg/kg IV and dilute to 3 mL for small animals. After 4 hours collect another sample, and then after 8 hours collect another sample.
What is the LDDST measuring?
Cortisol concentration
