Week 9 Lecture 5 Evaluating Adrenal Function PDF

Identifying adrenal function - Normal hypothalamic -- pituitary -- adrenal gland regulation of cortisol release - In the hypothalamus the hormone CRH is released stimulates pituitary gland to release ACTH goes to adrenal glands to stimulate production of cortisol when c...

Identifying adrenal function - Normal hypothalamic -- pituitary -- adrenal gland regulation of cortisol release - In the hypothalamus the hormone CRH is released stimulates pituitary gland to release ACTH goes to adrenal glands to stimulate production of cortisol when cortisol is produced, there is neg feedback to tell the hypothalamus to stop producing CRH and tell the pituitary gland to stop releasing ACTH - Diagnosis of hyperadrenocorticism - Identify a case with clinical signs with consistent blood and UA results - Screening test to confirm P has hyperadrenocorticism - If we can, use a localizing test to determine the cause - If it is pituitary dependent or adrenal or iatrogenic - Pituitary dependent hyperadrenocorticism - There is a mass in the pituitary gland (it is autonomous) which secretes lots of ACTH despite neg feedback hyperplastic adrenal glands and produce lots of cortisol cortisol will try to do the neg feedback to the pituitary gland to stop producing ACTH but since this mass is autonomous, it does whatever it wants and keeps producing ACTH - High cortisol, high ACTH - Adrenal dependent hyperadrenocorticism - There is a mass in the adrenal glands produces a lot of cortisol the normal adrenal gland (one without a mass) will not produce any cortisol and the normal adrenal gland will become atrophied ACTH is decreased because the neg feedback is telling the pituitary gland to stop producing ACTH due to excess cortisol because ACTH secretion will promote even more cortisol release - High cortisol, low ACTH - Iatrogenic hyperadrenocorticism - P gets corticosteroid therapy chronically add into the pituitary gland as neg feedback reduction of ACTh production reduction of cortisol production adrenal glands become atrophic due to not producing cortisol - Also has effect on hypothalamus - Variable cortisol, low ACTH - Hyperadrenocorticism in dogs - See PU/PD - Polyphagia - Abdominal enlargement - Thin skin, alopecia - Hyperpigmentation, comedones, calcinoses cutis with time - Muscle wastage - Panting - High BP - Insulin resistance with diabetes mellitus - CNS signs with macroadenoma - Hyperadrenocorticism in cats - Rare - PU/PD - Diabetes mellitus secondary to insulin resistance - Polyphagia - Thin skin -- so fragile it can tear - Alopecia - Potbellies - Muscle atrophy - Hyperadrenocorticism in horses - Most cases are pituitary pars intermedia dysfunction - Neurodegenerative condition - Hirsutism -- get hairy - PU/PD - Muscle wastage - Hyperhidrosis (sweaty) - Recurrent laminitis -- overlaps with metabolic syndrome too - Potbellies - Infertility - Normal horses show seasonal variation in cortisol and ACTH levels - Hematology findings with Hyperadrenocorticism - Stress leukogram - Mainly about lymphopenia - Mature neutrophilia because the cells get older in circulation - Mild monocytosis in dogs - Eosinopenia - Mild thrombocytosis - Lipemic blood sample - Lymphopenia - High cortisol levels can cause sequestration in lymph nodes, spleen and bone marrow - High cortisol levels also cause lysis of lymphocytes - Mature neutrophilia - High cortisol levels can cause increased marrow release coming from the storage pool which is why you will see mature neutrophils (segmented) and not immature (band) - Decreased emigration into tissues - Shift from marginating to circulating pool so the neutrophils are attached to the vessels go into circulating pool - Monocytosis in dogs - Shift from marginating to circulating pool - Eosinopenia - Margination or sequestration in tissues - Can have inhibition of marrow release and IL-5 - Biochemistry findings with hyperadrenocorticism - Elevated ALP - Due to induction of corticosteroid isoform in dogs - Steroid hepatopathy may cause compression of bile canaliculi between hepatocytes bile struggles to get out decreased efflux of bile elevated ALP with corticoid isoform in dogs - Elevated ALT - Steroid hepatopathy with secondary glycogen accumulation in hepatocytes and membrane becomes more permeable / stretched allows escape of ALT - Elevated GGT - Steroid hepatopathy - Induction of this enzyme - Hypercholesterolemia and hypertriglyceridemia - Stimulation of VLDL synthesis in the liver - Stimulation of hormone sensitive lipase - Inhibition of lipoprotein lipase through insulin antagonism decrease of metabolism of lipids - Hyperglycemia - Due to insulin antagonism - Decreased GLUT-4 transporters which are the glucose receptors in different tissues - Stimulation of gluconeogenesis - Stimulation of glucagon release - Low total T4 -- euthyroid sick syndrome - Mild uremia (prerenal azotemia) - Routine UA findings with hyperadrenocorticism - Poorly concentrated urine - Inhibition of ADH action and release - Mild proteinuria - Glomerular hypertension caused by aldosterone - UTI - Suppression of immune response -- prone to infections - Poorly concentrated urine - Testing options for hyperadrenocorticism in dogs and cats - Screening tests to confirm diagnosis - Urinary cortisol-creatinine ratio - Highly sensitive test -- detects more than 75% of cases - Poor specificity as it can be elevated with stress or illness - To improve specificity, test 2 free catch morning samples collected at home (to minimize stress) - Normal in dogs UCCR \