Please enable JavaScript.
Coggle requires JavaScript to display documents.
Canine Cushing's syndrome (Signalment (History/clinical signs…
Canine Cushing's syndrome
Chronic exposure of cortisol
catabolic effect on fat, carbohydrates
insulin resistence
gluconeogenic
anti-inflammatory effect
blood pressure regulation
causes
80-85% due to microadenoma at pituitary (pituitary dependent)
15-20% due to microadenoma at adrenal gland (adrenal-dependent)
Normally: corticotrophs stimulated by CRH from hypothalamus will produce and secrete ATCH that circulates to adrenal glands and binds to zona fasiculata of adrenal cortex, stimulating these cells to secrete cortisol.
Negative feedback of cortisol will decrease CRH/ATCH secretion at Hypothalamus/anterior pituitary
Pituitary dependent has a failure of negative feedback control so an increase of cortisol and ATCH. The adrenal glands work even harder, resulting in hypertrophy and hyperplastic bilateral adrenal glands
Adrenal dependent cases are due to excessive secretion of cortisol independent of pituitary signal, which results in inhibition of ATCH secretion. Atrophy of contralateral adrenal gland that does not have tumor as it lacks stimulation.
Remove that tumor and the atrophied adrenal glands might not be able to keep up with needs.
Signalment
Middle age/old dogs 6-16 yrs
more likely in females
more likely to see PDC in small breeds (less so in AD)
History/clinical signs
PU/PD/PP (stressed= need more)
Urinate (due to ADH inhibition of anterior pituitary by excess cortisol, less water can be taken back into the body by aquaporin channels) more meaning the dog needs to drink more to stay hydrated
Central and/or nephrogenic diabetes insipidus
Water consumption of normal dog is 40-60ml/kg/day, with cushings 2-10 times normal levels as a compensatory mechanism to combat plasma osmolarity increase from water loss stimulation of osoreceptors of hypothalamus
Normally: Anterior hypothalamus osmol receptors respond to decrease in osmolarity by increasing thirst (and secreting ADH to insert water channels and increased reuptake of water).
Increase glomerular filtration rate due to cortisol vasodilation of afferent arterioles to increase renal blood flow and GFR
Tumor compression of posterior hypothalamus
Polyphagia is a direct effect of the glucocorticoids in the brain (unique to dogs)
Panting, lameness and exercise intolerance
Fat redistribution: accumulation of liver and mediastinum decrease lung volume and puts pressure on the diaphragm
Hepatomegaly: due to fat accumulate vacuolization, increase glycogen accumulation and hepatic vacuolization
Mineralization of interstitial lung tissue affects oxygen profusion, causing hypoxia
Intercostal muscles undergo catabolic effect of their protein that decreases ability to take in more air
Lameness/exercise intolerance results from wasting of other muscles as protein is catabolized (cruciate rupture is common)
Muscle atrophy, pendulous abdomen,
Hair loss of neck, trunk, tail and caudal aspect of legs (spontaneous hair loss due to glucocorticoids inhibition of anagen (resting phase of hair, lack of adherence to wall) and thin skin due to catabolic effect of GC on protein/fat (leading to predisposition to infection), and calcinosis cutis as increase of protein catabolism leafs to the formation of the organic matrix that attacts and binds calcium and phsophorus
Complications
Glucocorticoids: increase sectrion of cortisol with a weak mineralocorticoid effect of sodium retention, increase vascular sensitivity to pressures, reduction of vasodilators such as prostaglandins, increases levels of endothelin-1
Diabetes mellitus: GC are gluconeogenic, decrease insulin response of peripheral tissues (only 5-10% of dogs/70-80% cats develop this, it is more common to have hyperglycemia)
Asymptomatic UTI due to dilute urine, inhibition of neutrophil and macrophage to bladder mucosa, lower UTI leads to pyelonephritis (antibiotic resistance concerns will dictate that we don't treat asymptomatic patients)