CBLs 1 & 2 Flashcards
what is a stress (cortisol) leukogram in dogs
neutrophilia
lymphopenia
monocytosis
eosinopenia
Addison’s disease: Na and K levels
hyperkalemia
hyponatremia
Addison’s disease: glucose levels
hypoglycemia
Addison’s disease: cholesterol
hypocholesterolemia
Addison’s disease: CBC findings
NNN anemia
normal leukogram despite being sick (no stress leukogram bc no cortisol)
Addison’s disease: heart rate/rhythma
bradyarrhythmic
what tests are done to diagnose Addison’s disease
- ACTH stimulation test (good rule-out test)
- resting cortisol (good rule-in test)
what is the best liver function test
bile acids
Addison’s disease: cortisol concentration
low (<2)
Addison’s disease: aldosterone concentration
typical Addisons: low
atypical Addisons: normal
Addison’s disease: vasopressin concentration
high
(stimulated by dehydration)
Addison’s disease: insulin concentration
low
(hypoglycemic)
Addison’s disease: T4 concentration
low to normal
(possible euthyroid sick syndrome - mediated by more than just cortisol)
Addison’s disease: ACTH concentration
high
typical addisons
cortisol & aldosterone deficiency
- low aldosterone –> electrolyte imbalances (hyperkalemia, hyponatremia)
- low cortisol –> GI signs, leukogram changes, anemia, hypoglycemia, hypoalbuminemia, hypocholesterolemia
atypical addison’s
cortisol deficiency only
- normal aldosterone –> no electrolyte imbalances
- low cortisol (same signs as above)
how do you treat Addison’s disease
- fluids (bolus + CRI)
- 5% dextrose (bolus + CRI)
- exogenous cortisol
- percorten (exogenous aldosterone)
common causes of PU/PD
- diabetes mellitus
- hyperthyroidism
- renal disease
- hypercalcemia (hyperparathyroidism)
- Cushing’s
- diabetes insipidus (central)
- pyometra/pyelonephritis
- iatrogenic
- Addison’s
- hepatic insufficiency
- renal glucosuria
- hypokalemia
what are the mechanisms for the development of PU/PD (6 total)
- central DI
- primary nephrogenic DI
- secondary nephrogenic DI
- osmotic diuresis
- psychogenic
- multifactorial
how does central DI cause PU/PD
lack of ADH production in pituitary –> reduced water reabsorption in kidneys
how does primary nephrogenic DI cause PU/PD
congenital defect of ADH receptor –> reduced water reabsorption in kidneys
how does secondary nephrogenic DI cause PU/PD
- blocking of ADH release from pituitary
- blocking of ADH V2 receptors in collecting ducts
ex. Cushing’s, hypercalcemia, glucocorticoids, hypokalemia, bacterial endotoxins
how does osmotic diuresis cause PU/PD
something pulls water into the renal tubules
ex. diabetes mellitus, renal glucosuria, renal disease, post-obstructive diuresis, drugs
how does psychogenic mechanisms cause PU/PD
young, anxious dogs
how do multifactorial mechanisms cause PU/PD
ex. hyperthyroidism
- high RBF/GFR
- psychogenic
- downregulation of AQP
Hyperthyroidism: heart rate/murmurs
systolic murmur
tachycardia
often leads to HCM in cats
Hyperthyroidism: liver enzymes
reactive hepatopathy (elevated ALT)
what tests are used to diagnose hyperthyroidism
total T4
(free T4 and TSH less common)
other options: nuclear scintigraphy, cervical ultrasound, check PE for thyroid slip, fundic exam for hypertension signs
Hyperthyroidism: TSH levels
low (should be 0)
Hyperthyroidism: free T4 levels
high
Hyperthyroidism: total T4 levels
high
Hyperthyroidism: TGAA levels
normal (undetectable)
Hyperthyroidism: PTH levels
normal
(calcium levels should be normal)
T3 suppression test
administering exogenous T3 then measuring T3, total T4, and TSH
T3 suppression test in a euthyroid cat
expect DECREASE in total T4 and TSH
- exogenous T3 will suppress TSH and the production of T4
T3 suppression test in a hyperthyroid cat
expect NO CHANGE in total T4 and TSH
- loss of negative feedback on T4 due to primary hyperthyroid; administering T3 will not suppress T4 production
- TSH is already suppressed from excess T4, will still be low
reversible treatments for hyperthyroid
methimazole
limited iodine diet
irreversible treatments for hyperthyroid
radioactive iodine (gold standard)
thyroidectomy (less common in cats)
