Small Animal Medicine Exam V (42-49) Flashcards
What hormones are made by the hypothalamus?
What hormones are made by the anterior pituitary?
What hormones are made by the posterior pituitary?
What hormone is secreted in excess in a patient with acromegaly?
Draw out the normal hormone pathway for growth hormone.
What mediates the indirect anabolic effects of growth hormone? What are the effects?
What mediates the direct anabolic effects of growth hormone? What are the effects?
List the catabolic effects of growth hormone.
Describe the etiology of acromegaly in the feline.
Describe the etiology of acromegaly in the canine.
Describe the most common signalment for a cat with acromegaly.
What clinical signs do we see in feline acromegaly due to the anabolic effects of GH?
What clinical signs do we see in feline acromegaly due to the catabolic effects of GH?
What neurological signs secondary to acromegaly can we see in our feline patients?
What laboratory findings would you expect to see in a cat with acromegaly?
How do we diagnose feline acromegaly?
What should be some of our other differentials in a cat with suspect acromegaly?
What is the definitive treatment for feline acromegaly?
Describe the medical management of feline acromegaly.
What is the prognosis for feline acromegaly?
What is pituitary dwarfism? What is the etiology?
What are the clinical signs of pituitary dwarfism?
How do we diagnose pituitary dwarfism?
What are some endocrine and non-endocrine ddx for pituitary dwarfism?
What is the treatment for pituitary dwarfism?
What is the prognosis for pituitary dwarfism?
What is a normal amount of water intake and urine output for a dog/cat?
List the ddx for PU/PD.
Name some drugs that can cause PU/PD.
List the usual etiologies of PU/PD.
What is renal medullary solute washout?
What is central diabetes insipidus?
What is nephrogenic diabetes insipidus?
ADH (Vasopressin) is released when _____ or ____.
The main job of ADH is to reduce free water clearance, how does it do this?
List some causes of central diabetes insipidus.
List some causes of nephrogenic diabetes insipidus.
Describe the most common signalment for a patient with central diabetes insipidus.
Describe the most common signalment for a patient with nephrogenic diabetes insipidus.
What are some clinical signs and physical exam findings consistent with diabetes insipidus?
In general, how do we diagnose diabetes insipidus?
When and why should we perform specific diagnostic tests (beyond the minimum database) to confirm DI?
What specific diagnostic tests do we have to diagnose DI?
How can a patient’s response to desmopressin help us confirm DI?
Describe the first phase of the water deprivation test.
Describe the second phase of the water deprivation test.
How do we interpret the first phase of the water deprivation test?
How do we interpret the second phase of the water deprivation test?
How do we treat central DI?
How do we treat nephrogenic DI?
How do we treat psychogenic polydipsia?
What is the prognosis for idiopathic/congenital central DI?
What is the prognosis for traumatic central DI?
What is the prognosis for central DI secondary to tumors?
What is the prognosis for primary nephrogenic DI?
What is the prognosis for secondary nephrogenic DI?
What is the prognosis for psychogenic water consumption?
Draw out the HPA axis of cortisol secretion.
What is the role of the zona glomerulosa?
What is the role of the zona fasciculata?
What is the role of the zona reticularis?
List some factors that stimulate ACTH secretion and therefore cortisol secretion.
List some factors that inhibit ACTH secretion and therefore cortisol secretion.
List the general effects of cortisol/glucocorticoids.
What are the effects of cortisol on kidney and water balance?
What are the effects of cortisol on the cardiovascular system?
What are the effects of cortisol on the hemopoetic systems?
_____ is a disease syndrome resulting from abnormally elevated levels of circulating cortisol, either endogenous or exogenous in origin. It is classified as ____, ____, or ____.
Briefly describe pituitary dependent hyperadrenocortism.
Briefly describe tertiary hyperadrenocorticism.
Briefly describe primary adrenal hyperadrenocorticism.
Briefly describe iatrogenic hyperadrenocorticism.
Describe the most common signalment of a patient with Cushing’s.
What are the most common signs of Cushing’s disease?
What are the dermatological signs of Cushing’s disease?
Describe the clinical presentation of pituitary tumor syndrome causing secondary hyperadrenocorticism.
List some potential medical complications associated with hyperadrenocorticism.
Describe the prevalence of hyperadrenocorticism in the cat.
What are some PE findings we may see in a cat with hyperadrenocorticism?
What clinical pathology findings can we find in our canine patients with Cushing’s disease?
What clinical pathology findings can we find in our feline patients with Cushing’s disease?
What may you find on radiographs of a patient with Cushing’s disease?
What may you find on abdominal ultrasound of a patient with Cushing’s disease?
What is the role of MRI and CT in a patient with Cushing’s disease?
What are the different diagnostic and differentiation tests we have to help us diagnose hyperadrenocorticism?
Differentiate between sensitivity and specificity when it comes to diagnostic testing.
Describe the Urine-Cortisol-Creatinine Ratio (UCC) as a diagnostic test for hyperadrenocorticism.
Describe the LDDS test as a diagnostic test for hyperadrenocorticism.
Describe the ACTH stimulation test as a diagnostic test for hyperadrenocorticism.
____ is the screening test of choice for hyperadrenocorticism according to the 2012 ACVIM Consensus Statement.
Describe the abdominal ultrasound as a differentiation test for hyperadrenocorticism.
Describe the HDDS test as a differentiation test for hyperadrenocorticism.
Describe the endogenous ACTH level as a differentiation test for hyperadrenocorticism.
A majority of dogs with classic Cushing’s disease screened with ____ or ____ will have at least one positive test.
What is atypical Cushing’s disease?
What questions should we ask and answer prior to deciding to treat a patient with Cushing’s disease?
Describe trilostane (Vetoryl) as a treatment from hyperadrenocorticism.
You started a Cushing’s patient on trilostane, how do we monitor the patient’s response and disease progression?
What adverse reactions are associated with Trilostane?
Describe mitotane/lysodren as a treatment for Cushing’s disease.
You started a Cushing’s patient on mitotane/lysodren, how do we monitor the patient’s response and disease progression?
Describe an adrenalectomy as a treatment for Cushing’s disease.
Describe radiation as a treatment for Cushing’s disease.
What are some key client education points we should rely when we diagnose Cushing’s disease?
Describe infections as a secondary complication to Cushing’s disease.
Describe muscle weakness as a secondary complication to Cushing’s disease.
Describe neuropathies as a secondary complication to Cushing’s disease.
Describe systemic hypertension as a secondary complication to Cushing’s disease.
Describe proteinuria as a secondary complication to Cushing’s disease.
Describe bladder calculi as a secondary complication to Cushing’s disease.
Describe dystrophic calcification as a secondary complication to Cushing’s disease.
Describe diabetes mellitus as a secondary complication to Cushing’s disease.
Describe pancreatitis as a secondary complication to Cushing’s disease.
Describe biliary mucoceles as a secondary complication to Cushing’s disease.
Describe thromboembolisms as a secondary complication to Cushing’s disease.
What CNS signs can we see in our Cushing’s patients?
What nutroceuticals can we use to support our patients with Cushing’s disease?
How should we monitor disease progression in our patients with Cushing’s disease?
The parasympathic system has ____ receptors while the sympathic nervous system has ____ receptors.
List the different circumstances which require regulation by adrenal medullary secretions.
What are the effects of the release of epinephrine by the adrenal gland medulla?
What is a pheochromocytoma?
What are the most common clinical signs associated with a pheochromocytoma?
How do we diagnose pheochromocytomas?
How do we treat pheochromocytomas?
What is the prognosis for a patient with a pheochromocytoma?
Describe the pathway that triggers the release of angiotensin I which eventually initiates the release of aldosterone.
T/F: The role of ACTH in aldosterone secretion is significant.
What is the role of extracellular fluid volume in regulation aldosterone secretion?
What is the role of K+ concentration in regulating the secretion of aldosterone?
Describe the pathogenesis of primary/idiopathic hypoadrenocorticism.
Describe the pathogenesis of secondary hypoadrenocorticism.
Describe the most common signalment for a canine/feline with Addison’s disease.
Describe the most common history and clinical signs that you make see in a patient with Addison’s disease.
What physical exam findings will you often find in a patient with Addison’s disease?
What CBC findings will you often see in a patient with Addison’s disease?
What biochemistry findings will you often see in a patient with Addison’s disease?
What radiographic findings will you often see in a patient with Addison’s disease?
What EKG findings will you often see in a patient with Addison’s disease?
How do we use baseline cortisol levels and ACTH stimulation tests to confirm Addison’s disease?
Describe the treatment for an Addisonian patient in an acute crisis.
Describe DOCP as a maintenance treatment for Addison’s disease.
Describe fludrocortisone acetate as a maintenance treatment for Addison’s disease.
Describe glucocorticoids as a maintenance treatment for Addison’s disease.
____ is the reference drug when we use to compare all glucocorticoids to.
What is the prognosis for a patient with Addison’s disease?
What is primary hyperaldosteronism?
What is secondary hyperaldosteronism?
Describe hypokalemia as a clinical signs of hyperaldosteronism.
Describe hypernatremia as a clinical signs of hyperaldosteronism.
How do we diagnose hyperaldosteronism?
How do we treat hyperaldosteronism?
What is the prognosis for a patient with hyperaldosteronism?
What is feline hyperthyroidism?
____ is one of the most common endocrine disorders in cats.
Feline hyperthyroidism
What are the different etiologies of feline hyperthyroidism?
What are the risk factors associated with feline hyperthyroidism?
Describe the most common signalment of a patient with feline hyperthyroidism.
What clinical signs, relative to appearance and behavior, will you see in a cat with hyperthyroidism?
What may you find on a thyroid exam of a cat with feline hyperthyroidism?
What clinical signs, relative to the GIT, will you see in a cat with hyperthyroidism?
What clinical signs, relative to the renal system, will you see in a cat with hyperthyroidism?
What clinical signs, relative to the cardiovascular system, will you see in a cat with hyperthyroidism?
Describe the apathetic (atypical) form of feline hyperthyroidism.
You have an older cat with a history of losing weight, increased appetite , and PU/PD. What are your ddx?
What clinical pathology changes would you expect to find in a cat with feline hyperthyroidism?
What would you expected the T4 and T3 levels to be in a cat with feline hyperthyroidism?
What would you expected the free T4 levels to be in a cat with feline hyperthyroidism?
Describe the role of radionuclide thyroid scanning to diagnose feline hyperthyroidism.
What are the 3 treatment options for a cat with hyperthyroidism?
According to the AAFP, what should be our treatment goal when we treat for feline hyperthyroidism?
How do we treat the cardiovascular effects of feline hyperthyroidism?
How do we treat the renal effects of feline hyperthyroidism?
How does diet play a role in our treatment for feline hyperthyroidism?
List the different anti thyroid medications that we use to treat feline hyperthyroidism.
What is the MOA of methimazole (thiamazole) in our treatment of feline hyperthyroidism?
What are the different available formulations of methimzole (thiamazole)?
Describe the clinical use and timeframe of improvement when we use methimazole (thiamazole) to treat our hyperthyroid feline patients.
What adverse effects are associated with methimazole?
Describe the MOA of radioactive iodine in treating our hyperthyroid feline patients.
What are some of the different outcomes of radioactive iodine when treating hyperthyroid cats?
What are some of the disadvantages of radioactive iodine when treating hyperthyroid cats?
Describe surgery as a treatment option for cats with hyperthyroidism. What is the most serious complication?
What is the prognosis for a cat with hyperthyroidism?
Describe the etiology of canine hyperthyroidism. What are the clinical signs?
How do we diagnose and treat canine hyperthyroidism? What is the prognosis?
How do we diagnose and treat canine hyperthyroidism? What is the prognosis?
What is hypothyroidism?
Describe the regular pathophysiology of thyroid hormones in the body.
What is primary hypothyroidism? Name the different etiologies.
What is secondary hypothyroidism?
What is tertiary hypothyroidism?
What are some of the causes of congenital hypothyroidism?
List some of the normal physiologic effects of thyroid hormones.
Describe the most common signalment for a patient with hypothyroidism.
What are some of the metabolic clinical signs of hypothyroidism?
What are some of the dermatological clinical signs of hypothyroidism?
What are some of the reproductive clinical signs of hypothyroidism?
What are some of the neuromuscular clinical signs of hypothyroidism?
What are some of the cardiovascular clinical signs of hypothyroidism?
What are some of the gastrointestinal clinical signs of hypothyroidism?
What are some of the ocular clinical signs of hypothyroidism?
What clinical signs will you see in puppies with hypothyroidism?
What clinical pathology changes would you expect to find in a patient with hypothyroidism?
How do we use thyroid hormone level testing to confirm hypothyroidism?
Many factors can decrease baseline thyroid hormone measurements. What are the most common factors?
What are the effects of glucocorticoids on tT4, fT4, and cTSH?
What are the effects of sulfonamides on tT4, fT4, and cTSH?
What are the effects of phenobarbital on tT4, fT4, and cTSH?
What are the effects of carprofen on tT4, fT4, and cTSH?
What are the effects of clomipramine on tT4, fT4, and cTSH?
What is non-thyroidal illness (NTI)?
What is tT4? What are the advantages and disadvantages to using it as diagnostic tool?
What is baseline fT4? Describe its role as a diagnostic tool.
Describe baseline cTSH tests as a diagnostic tool.
Describe TSH and TRH tests as a diagnostic tool.
How does lymphocytic thyroiditis affect thyroid testing?
What is the preferred initial diagnostic plan for a patient you suspect may have thyroid pathology?
What are the different screening tests we perform on breeding dogs with and without thyroid pathology clinical signs?
What is the treatment for a patient with hypothyroidism?
How do we monitor our patient’s response to hypothyroid treatment?
What should we do if our patients fail to respond to hypothyroid treatment?
When should we consider decreasing our hypothyroid patient’s levothyroxine medication?
What are the different calcium concentrations/fractions found in the body?
What is the role of PTH in calcium metabolism?
“GOSHDARNIT my patient is hypercalcemic” is a common pneumonic used to help us list the differentials for hypercalcemia. What does it mean?
List some of the different granulomatous causes of hypercalcemia.
List some of the different osteolytic causes of hypercalcemia.
List some of the different spurious causes of hypercalcemia.
Briefly describe how hyperparathyroidism leads to hypercalcemia.
Briefly describe how hypervitaminosis leads to hypercalcemia.
Briefly describe how Addison’s disease leads to hypercalcemia.
Briefly describe how renal secondary hyperparathyroidism leads to hypercalcemia.
Briefly describe how neoplasia leads to hypercalcemia.
Briefly describe idiopathic hypercalcemia.
Temperature induced _____ can lead to hypercalcemia.
Identify the anatomy.
Fill in the blanks.
Differentiate between primary and secondary hyperparathyroidism.
Describe the most common signalment for a dog with primary hyperparathyroidism.
Describe the most common signalment for a cat with primary hyperparathyroidism.
What are the clinical signs of primary hyperparathyroidism in the dog?
What are the clinical signs of primary hyperparathyroidism in the cat?
What physical exam findings may you find in a patient with hyperparathyroidism?
What general tests do we have to help us diagnose hyperparathyroidism?
What specific tests do we have to help us diagnose hyperparathyroidism?
What are your primary DDx for hypercalcemia in cats and dogs?
What is the treatment for primary hyperparathyroidism?
Describe the pathogenesis of renal secondary hyperparathyroidism.
Why is high PTH bad?
Why is high cellular calcium bad?
What is the treatment for renal secondary hyperparathyroidism?
What are the effects of calcitriol on PTH?
Calcitriol has two main types of actions, what are they?
What are the functions of calcitriol?
Describe the general guidelines to calcitriol dosing.
What are the traditional thoughts on when to stop calcitriol treatment?
Describe the prevalence of renal secondary hyperparathyroidism in the cat.
Describe the prevalence of renal secondary hyperparathyroidism in the dog.
What is the relation between renal secondary hyperparathyroidism and appetite?
What are the causes of nutritional secondary hyperparathyroidism?
What are the effects of nutritional secondary hyperparathyroidism?
Briefly describe adrenal secondary hyperparathyroidism.
What is hypoparathyroidism? What are the consequences and treatment?
Briefly describe the causes and consequences of transient hypoparathyroidism.
Describe the most common signalment for a dog with primary hypoparathyroidism.
Describe the most common signalment for a cat with primary hypoparathyroidism.
What are the clinical signs of primary hypoparathyroidism ?
What physical exam findings would you expect to find in a patient with primary hypoparathyroidism?
How do we diagnose primary hypoparathyroidism?
What are your differentials for hypocalcemia in the dog/cat?
Describe the treatment for primary hypoparathyroidism.
What is the prognosis for a patient with primary hypoparathyroidism?
List some of the different causes of PTH independent hypercalcemia.
What would you expect the total calcium, ionized calcium, intact PTH, vit D, phosphorus, and PTHrP levels to be in a patient with primary hyperthyroidism?
What would you expect the total calcium, ionized calcium, intact PTH, vit D, phosphorus, and PTHrP levels to be in a patient with malignant hypercalcemia?
What would you expect the total calcium, ionized calcium, intact PTH, vit D, phosphorus, and PTHrP levels to be in a patient with primary hypoadrenocorticism?
What would you expect the total calcium, ionized calcium, intact PTH, vit D, phosphorus, and PTHrP levels to be in a patient with CKD?
What would you expect the total calcium, ionized calcium, intact PTH, vit D, phosphorus, and PTHrP levels to be in a patient with primary hypervitaminosis D (calcitriol or calcitriol analogue)?
What would you expect the total calcium, ionized calcium, intact PTH, vit D, phosphorus, and PTHrP levels to be in a patient with hypervitaminosis D (D2 or D3 toxicity)?
What would you expect the total calcium, ionized calcium, intact PTH, vit D, phosphorus, and PTHrP levels to be in a patient with granulomatous disease?
What would you expect the total calcium, ionized calcium, intact PTH, vit D, phosphorus, and PTHrP levels to be in a cat with idiopathic hypercalcemia?
Differentiate between type I and type II DM.
Differentiate between insulin dependent and non-insulin dependent diabetes mellitus.
Essentially all dogs have ____ diabetes mellitus at the time of presentations; ____ diabetes mellitus is uncommon.
What are the causes of diabetes mellitus in dogs?
Describe the pathogenesis of diabetes mellitus in the dog.
Describe the prevalence of diabetes mellitus in the cat. What are the different types and some predisposing factors?
Provide a brief overview of feline type II diabetes.
Describe amylin as a risk factor for DM.
Describe obesity as a risk factor for DM.
Describe physical inactivity as a risk factor for DM.
Describe gender as a risk factor for DM.
Describe age as a risk factor for DM.
Describe genetic predisposition as a risk factor for DM.
Describe medication/diet as a risk factor for DM.
What are they metabolic hallmarks and consequences of type II DM?
_____ requirements fluctuate in approximately 20% of cats with DM.
Describe the common signalment for a dog with diabetes mellitus.
Describe the common signalment for a cat with diabetes mellitus.
Describe the most common clinical presentation for a patient with diabetes mellitus.
What is a diabetic neuropathy? What are the causes and treatment?
How do we make our presumptive diagnostics of DM?
What would you expect to see on the CBC of a patient with diabetes mellitus?
What would you expect to see on the biochemistry of a patient with diabetes mellitus?
What would you expect to see on the urinalysis of a patient with diabetes mellitus?
Describe the role of fructosamine in diagnosing diabetes mellitus.
Describe the role of glycolated hemoglobin in diagnosing diabetes mellitus.
What are some reasons to utilize fructosamine and glycosylated hemoglobin assays in diabetic patients?
What are the primary goals of treatment for patients with diabetic mellitus?
Describe the role of nutrition in managing patients with diabetes mellitus.
What are the differences in feline nutrition that help us manage diabetic patients?
What is the carnivore connection theory?
Cats may not be metabolically adapted to ingest _____.
What dietary recommendations should we make for diabetic cats?
Describe the role of exercise as a multimodal treatment option for patients with diabetes mellitus.
_____ do NOT substitute the use of insulin, cannot reverse beta cell glucose toxicity and are backed by limited veterinary data.
What are the 4 classes of oral hypoglycemic agents?
Describe the use of acarbose (precose) as a treatment option for a patient with diabetes mellitus.
Describe the use of troglitazone (rezulin) as a treatment option for a patient with diabetes mellitus.
Describe the use of vanadium as a treatment option for a patient with diabetes mellitus.
Describe the use of chromium picolinate as a treatment option for a patient with diabetes mellitus.
Describe the use of metformin (glucophage) as a treatment option for a patient with diabetes mellitus.
Describe the use of glipizide (glucotrol) as a treatment option for a patient with diabetes mellitus.
Describe the use of glimepiride (amaryl) as a treatment option for a patient with diabetes mellitus.
Describe the use of glucagon-like peptide 1 analogue as a treatment option for a patient with diabetes mellitus.
Describe the use of bexacat (bexagliflozin tablets) as a treatment option for a patient with diabetes mellitus.
Describe the use of senvelgo as a treatment option for a patient with diabetes mellitus.
How do we categorize the different types of insulin?
Describe e the onset, peak, and duration of regular (crystalline) insulin.
Describe the onset, peak, and duration of NPH insulin.
Describe e the onset, peak, and duration of PZI insulin.
What are the different insulin preferences for dogs/cats?
What is the most common type of insulin we use in veterinary medicine (origin)?
What should be your initial insulin therapy for dogs with diabetes mellitus?
What should be your initial insulin therapy for cats with diabetes mellitus?
Describe the use of PZI insulin in cats.
Describe the use of glargine insulin.
Diabetic cats treated with twice daily _____ have better glycemic control and a higher probability of remission than cats treated with twice daily ____ or ____.
Describe the use of detemir insulin.
Describe the use of insulin pumps to help treat diabetes mellitus.
What are the general guidelines to initiation insulin therapy in our patients with diabetes mellitus?
Glycemic control (in our diabetic patients) is defined as _____.
Describe the home management for an owner whose dog/cat has diabetes mellitus.
Describe how to perform a blood glucose curve at home.
What are the advantages of glucose monitors?
What are some factors that affect the accuracy of glucose monitors?
Draw out the ideal blood glucose curve.
Draw out the blood glucose curve consistent with an insufficient insulin dose.
Draw out the blood glucose curve consistent with an inappropriate duration of insulin action.
Draw out the blood glucose curve consistent with a somogyi effect.
Describe the pathogenesis of the somogyi effect on the BG curve.
Draw out the blood glucose curve consistent with insulin resistance.
List some of the potential causes of insulin resistance.
Assess this BG curve.
What are the general guidelines to monitoring a blood glucose curve?
What are some owner management errors that can lead to an unregulated diabetic patient?
What are the different initial, intermediate, and long term regulation parameters/tests we have to assess our diabetic patients?
What should be included in the routine management of a patient with diabetes mellitus?
Describe hypoglycemia as a potential complication when treating patients with diabetes mellitus.
____ is the most common clinical sign when treating a patient with diabetes mellitus.
Describe insulin overdose as a potential complication when treating patients with diabetes mellitus.
Describe a shorten duration of insulin as a potential complication when treating patients with diabetes mellitus.
Describe inadequate insulin absorption as a potential complication when treating patients with diabetes mellitus.
Describe insulin antibodies as a potential complication when treating patients with diabetes mellitus.
How can concurrent disease affect insulin treatment in a diabetic patient?
What are the risk factors associated with an insulin overdose?
What are the clinical signs associated with an insulin overdose?
What is the treatment and prognosis associated with an insulin overdose?
When evaluating the BG curve, if the NADIR is too high you should ____.
When evaluating the BG curve, if the insulin is too short acting you should _____.
When evaluating the BG curve, if notice a Somogyi effect, you should ______.
Describe the use and importance of urine glucose monitoring to monitor a diabetic patient.
List the indications for a glycosylated blood proteins in your diabetic patients.
Analyze the blood glucose and serum fructosamine.
Analyze the blood glucose and serum fructosamine.
Analyze the blood glucose and serum fructosamine.
Analyze the blood glucose and serum fructosamine.
Analyze the blood glucose and serum fructosamine.
For a cat with diabetes mellitus, the primary goal of therapy is _____.
List the positive predictors for remission in cats with diabetes mellitus.
List the factors that have not been shown to affect remission in a diabetic cat.
Briefly describe how we manage diabetic remission in the cat.
What is considered “tight regulation” of the diabetic cat?
List some keys factors that affect the prognosis for a cat with diabetes mellitus. What is the median survival time?
List some negative prognostic factors for a cat with diabetes mellitus.
