Small Animal Disease Flashcards
Covers: Small animal thyroid disease, Disorders of calcium and phosphorus regulation 1/2, Disorders of the endocrine pancreas 1/2, Obesity in small animals, Hyperadrenocorticism, Nutritional support for hyporexia/anorexia, Acute kidney disease, Chronic kidney disease, PU/PD, Hematuria/Pollakiuria/Stranguria 1/2/3, Urinary incontinence, Urolithiasis and Mucus plugs, and Urinary obstruction and Uroabdomen lectures
What is the most common abnormal cardiac rhythm noted in cats with hyperthyroidism?
(Sinus tachycardia)
You are reviewing the bloodwork on a cat you suspected to have hyperthyroidism (which is confirmed on the bloodwork) and notice the ALT is mildly elevated, what is your treatment protocol going to entail?
(Treat the hyperthyroidism and recheck blood work, if ALT is normal then you know it was elevated because of hyperthyroidism, if it is not normal you can then work up the cat for liver disease)
Why is it difficult to diagnose a hyperthyroid cat with kidney disease based on bloodwork?
(Bc hyperthyroidism will mask the typical presentation of kidney disease on blood work since it increases renal blood flow and GFR)
What are the three possible reasons a cat may have a normal T4 or fT4?
(Cat is not hyperthyroid, the cat has early or mild hyperthyroidism, or the cat has a concurrent nonthyroidal illness that is off-setting the increase in T4 into a normal range)
How does methimazole work to treat hyperthyroidism?
(It blocks thyroid peroxidase so there is no more thyroid hormone production)
What are the two causes of primary hypothyroidism in dogs?
(Lymphocytic thyroiditis (autoimmune disease) or idiopathic atrophy of the thyroid gland)
What laboratory finding being elevated in a dog with signs of hypothyroidism would indicate to you that you need to test them for hypothyroidism?
(Cholesterol, 75% of cases of hypothyroidism have concurrent hypercholesterolemia)
Why is hypothyroidism often overdiagnosed?
(Bc nonthyroidal diseases lower T4, ppl see a low T4 and think hypothyroidism)
What two possibilities are indicated if a dog has a serum T4 above the low normal range?
(The dog does not have hypothyroidism or there are T4 autoantibodies causing a false elevation)
You are going to be seeing a dog in the future and you have just received the history. The PE notes are handwritten so you know nothing of clinical signs but the blood work is printed. The dog has a low T4 and fT4 so you suspect hypothyroidism and luckily enough, they ran a TSH which was normal. Does that turn you away from a hypothyroidism diagnosis?
(No, hypothyroid dogs can have a normal TSH so a normal TSH is not reliable in ruling out hypothyroidism)
You are going to be seeing a dog in the future and you have just received the history. The PE notes are handwritten so you know nothing of clinical signs but the blood work is printed. The dog has a low T4 and fT4 so you suspect hypothyroidism and luckily enough, they ran a TSH which was normal.
It is a few days later and you are now seeing this dog, a 9-year-old MC greyhound, and his entire PE is WNL. What is the most obvious cause for the low T4 and fT4?
(Breed, sighthound have lower T4 and fT4 than other breeds)
You are going to be seeing a dog in the future and you have just received the history. The PE notes are handwritten so you know nothing of clinical signs but the blood work is printed. The dog has a low T4 and fT4 so you suspect hypothyroidism and luckily enough, they ran a TSH which was normal.
It is a few days later and you are now seeing this dog, an 11-year-old FS german shepherd. The only thing you note on PE is a healing hot spot and the owner tells you that it’s much better since she started the prednisone prescribed by the previous vet. What is the most obvious cause for the low T4 and fT4 now that you have seen the dog?
(The steroid use, drugs (corticosteroids, sulfonamides, phenobarbital, clomipramine) can decrease T4 and fT4)
What test is not affected by the presence of T4 autoantibodies, which is necessary to run in an animal with clinical signs but a normal T4?
(fT4 by equilibrium dialysis)
What mechanism causes an animal to be PU/PD when they are hypercalcemic?
(The excess calcium prevents the binding of ADH to its receptors in the kidney which results in polyuria and then the animal compensates with polydipsia)
What neuromuscular signs result from hypercalcemia altering the balance between negative and positive ions? Two answers.
(Generalized weakness and ileus)
You are presented with an animal that has increased calcium, BUN, and creatinine on a routine chem. What additional test would you perform next?
(Ionized calcium)
You are presented with an animal that has an increased calcium, BUN, creatinine, and ionized calcium, what does this indicate?
(That the animal has hypercalcemia due to a currently unknown underlying disease and also has subsequent renal failure)
You are presented with an animal that has an increased calcium, BUN, and creatinine but a normal ionized calcium, what does this indicate?
(The animal is in renal failure and has subsequent hypercalcemia)
Hypercalcemia of malignancy is one of the more common causes of hypercalcemia in both dogs and cats. What are the three types of cancer that are more commonly found in cases of hypercalcemia?
(Lymphoma, apical gland adenocarcinoma, and multiple myeloma)
You suspect a cat has lymphoma, what do you expect to see in terms of their calcium and phosphorus?
(Hypercalcemia, cannot expect anything from phosphorus and cancer because cancers can cause hypophosphatemia hyperphosphatemia, or not affect phosphorus at all)
An owner brought their dog to your emergency clinic because they ingested dCon (which you google and find it is a cholecalciferol rodenticide) and you run blood work. What changes do you expect to see in calcium and phosphorus?
(Hypercalcemia and hyperphosphatemia)
How does hypoadrenocorticism result in hypercalcemia?
(Dehydration → more albumin which binds calcium so there will be an innate increase in calcium)
What does the hyperphosphatemia and hypovitaminosis D resultant of chronic renal failure result in that induces hypercalcemia?
(Hyperphosphatemia and hypovitaminosis D result in hypocalcemia which triggers excess PTH secretion which then induces hypercalcemia)
What do macrophages secrete that can induce hypercalcemia when an animal has granulomatous disease (which is a general category of diseases that induce a macrophage response such as fungal or specific parasitic infections)?
(Vitamin D)
You are presented with a hypercalcemic dog that has hypophosphatemia, normal kidney values, and a PE WNL; first, what do you think that information indicates and second, what additional test would you perform?
(Primary hyperparathyroidism is indicated so you can measure PTH levels, they should be high)
What are the indications for treatment of hypercalcemia? Three answers.
(Hypercalcemia induced renal failure is present, high risk of tissue mineralization, and/or if there are clinical signs of hypercalcemia present)
What do intravenous fluids, furosemide, and glucocorticoids do to treat hypercalcemia?
(All three promote calciuresis and glucocorticoids also inhibit bone calcium release)
Are the neuromuscular clinical signs related to hypocalcemia (muscle tremors and/or fasciculations, facial rubbing, stiff gait, behavior changes, and/or seizures) typically episodic or continuous?
(Continuous)
In an animal with a protein-losing enteropathy, is it expected that they will have hypocalcemia?
(Yes, a significant portion of total calcium is bound to albumin so if the animal is hypoproteinemic as they would be with protein-losing enteropathy, then you can expect them to also be hypocalcemic)
You are presented with an azotemic dog with hypocalcemia, have you caught it early or late?
(Early)
How does pancreatitis induced hypocalcemia?
(Bc calcium precipitates out of the blood into the inflammatory tissue around the inflamed pancreas)
What is the acute, emergent treatment for hypocalcemia?
(IV calcium gluconate)
What is the chronic treatment for hypocalcemia?
(PO calcium carbonate or calcitriol)
Is absolute hypoinsulinemia (a loss of beta cells), that occurs via immune-mediated destruction, type I or II diabetes mellitus?
(Type I diabetes mellitus)
Is relative hypoinsulinemia (an impairment of beta cells), with concurrent insulin resistance, type I or II diabetes mellitus?
(Type II diabetes mellitus)
Is type II diabetes insulin-dependent or non-insulin-dependent?
(Non-insulin-dependent)
Beta cells will secrete insulin in the face of glucotoxicity induced by an insulin-resistant disease/drug/factor, this leads to deposition of what substance in the islets?
(Amyloid → leads to amyloidosis)
Through what three mechanisms does insulin deficiency promote hyperglycemia?
(Decreased tissue utilization of glucose, increased hepatic glycogenolysis, and increased hepatic gluconeogenesis)
What results from the exceedance of the renal tubular cell threshold to reabsorb filtered glucose?
(Glycosuria)
What results from the osmotic diuresis that is promoted by glycosuria?
(Polyuria)
What occurs compensatorily to the polyuria that follows glycosuria?
(Polydipsia)
Why does a diabetic animal lose weight?
(Lack of an ability to utilize glucose for cellular energy and storage → starvation in the face of plenty)
What occurs secondarily to the ‘starvation in the face of plenty’ that occurs in diabetic patients?
(Polyphagia)
What does the liver produce in the face of fatty acid mobilization that occurs secondarily to insulin deficiency?
(Ketone bodies)
(T/F) Cells cannot use ketone bodies and that is why you get the severe clinical illness of diabetic ketoacidosis.
(F, cells can use ketone bodies it’s just that there is such an overproduction of them that they accumulate outside of cells and then can cause severe clinical illness)
Besides hyperglycemia, what other chem values would you not be surprised to see elevated on a diabetic animal’s chem?
(Hypercholesterolemia, hypertriglyceridemia, and increased liver enzymes)
(T/F) In a diabetic animal, their ALP elevation should be greater than their ALT elevation.
(T)
Do you expect a diabetic animal to have a dilute or concentrated USG?
(Concentrated → glucose will artificially raise USG)
You are rechecking a diabetic dog that you are treating. You are looking at their urine on the microscope and notice occasional WBCs, RBCs, and bacteria on the slide. The dog had no clinical signs of a UTI. Should you prescribe this dog antibiotics to prevent a kidney infection?
(No, there is no reason to prescribe abx as this subclinical bacteria has not been shown to infect the kidneys)
What might you change based on the results of a glucose curve you perform on a diabetic patient?
(Dose and/or type of insulin)
When is a fructosamine test indicated?
(When you are trying to determine if an animal has stress hyperglycemia versus true diabetes mellitus → it will be elevated only in cases of true diabetes mellitus)
When would the ideal nadir occur in a diabetic patient’s glucose curve? Give a range.
(6-8 hours)
What is the ideal duration of insulin effect, which can be determined via a glucose curve in a diabetic patient?
(10-12 hours)
What results from insulin ‘overdosing’, which usually results from inaccurate blood glucose curves or spot checks?
(Somogyi response → a rapid decrease in blood glucose or a slow decrease that peaks in the hypoglycemia range)
What ocular clinical sign can result from diabetes mellitus in dogs?
(Bilateral cataracts)
What is the fiber and carbohydrate content of the diet that a diabetic dog should be on?
(High fiber, low carbohydrate)
What three things must occur for a cat to be considered to be in diabetic remission?
(Clinical signs are resolved, blood glucose is normalized, and the insulin administration has been discontinued)
What two instances does the ability to induce diabetic remission depend on?
(Insulin resistance is rapidly treated/removed and/or the glucotoxicity is reversed (via early initiation of insulin therapy))
You assessed Turtle the cat to be a 7/9 BCS and 8 kgs and you inform the owner their cat should ideally be a 5/9:
Calculate the target weight in pounds for this cat.
(~14lbs → 7-5 = 2; 17.6lbs x .10 = 1.76; 1.76 x 2 = 3.5; 17.6 - 3.5 = ~14lbs)
You assessed Turtle the cat to be a 7/9 BCS and 8 kgs and you inform the owner their cat should ideally be a 5/9:
Using the accurate equation for RER, what is Turtle’s RER?
(333 kcal → 8kgs^0.75 = 4.75; 4.75 * 70 = ~333 kcal)
You assessed Turtle the cat to be a 7/9 BCS and 8 kgs and you inform the owner their cat should ideally be a 5/9:
Using the rapid estimate for RER, what is Turtle’s RER?
(310 kcals → 8kgs x 30 = 240; 240 + 70 = 310 kcal)
You assessed Turtle the cat to be a 7/9 BCS and 8 kgs and you inform the owner their cat should ideally be a 5/9:
If her favorite Temptation treats are 2kcal per treat, what is the maximum number of treats she can receive in a day (based on the accurate RER of 333 kcal)?
(~16 treats → 333 kcal * .10 = 33 kcal; 33/2 = ~16 treats)
You assessed Turtle the cat to be a 7/9 BCS and 8 kgs and you inform the owner their cat should ideally be a 5/9:
How long will it take Turtle to reach her ideal BCS if she needs to lose 3.5 lbs to get there?
(10-20 weeks or 2.5-5 months → for the low end: 17.6lbs x 0.02 = 0.352; 3.5lbs/0.352 = ~10 weeks; for high end: 17.6lbs x 0.01 = 0.176; 3.5lbs/0.176 = ~20 weeks)
What are the three types of hyperadrenocorticism?
(Pituitary dependent, adrenal dependent, and iatrogenic)
What changes in the liver values do you expect to see on a chem of a dog with suspected Cushing’s disease?
(ALT can be normal to increased; ALP must be increased (since it has a cortisol isoenzyme, if ALP is not increased that will push Cushing’s lower on your differential list))
Do you expect a Cushingoid dog to have a dilute or concentrated (choose one) USG?
(Dilute, typically less than <1.020)
What is the purpose of the urine cortisol:creatinine ratio test?
(To rule out HAC → this test can tell you ‘this dog does not have HAC’ but it cannot tell you ‘this dog has HAC’ (so it is highly sensitive but unspecific))
