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 (169 cards)
1
Q
What is the most common abnormal cardiac rhythm noted in cats with hyperthyroidism?
A
(Sinus tachycardia)
2
Q
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?
A
(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)
3
Q
Why is it difficult to diagnose a hyperthyroid cat with kidney disease based on bloodwork?
A
(Bc hyperthyroidism will mask the typical presentation of kidney disease on blood work since it increases renal blood flow and GFR)
4
Q
What are the three possible reasons a cat may have a normal T4 or fT4?
A
(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)
5
Q
How does methimazole work to treat hyperthyroidism?
A
(It blocks thyroid peroxidase so there is no more thyroid hormone production)
6
Q
What are the two causes of primary hypothyroidism in dogs?
A
(Lymphocytic thyroiditis (autoimmune disease) or idiopathic atrophy of the thyroid gland)
7
Q
What laboratory finding being elevated in a dog with signs of hypothyroidism would indicate to you that you need to test them for hypothyroidism?
A
(Cholesterol, 75% of cases of hypothyroidism have concurrent hypercholesterolemia)
8
Q
Why is hypothyroidism often overdiagnosed?
A
(Bc nonthyroidal diseases lower T4, ppl see a low T4 and think hypothyroidism)
9
Q
What two possibilities are indicated if a dog has a serum T4 above the low normal range?
A
(The dog does not have hypothyroidism or there are T4 autoantibodies causing a false elevation)
10
Q
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?
A
(No, hypothyroid dogs can have a normal TSH so a normal TSH is not reliable in ruling out hypothyroidism)
11
Q
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?
A
(Breed, sighthound have lower T4 and fT4 than other breeds)
12
Q
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?
A
(The steroid use, drugs (corticosteroids, sulfonamides, phenobarbital, clomipramine) can decrease T4 and fT4)
13
Q
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?
A
(fT4 by equilibrium dialysis)
14
Q
What mechanism causes an animal to be PU/PD when they are hypercalcemic?
A
(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)
15
Q
What neuromuscular signs result from hypercalcemia altering the balance between negative and positive ions? Two answers.
A
(Generalized weakness and ileus)
16
Q
You are presented with an animal that has increased calcium, BUN, and creatinine on a routine chem. What additional test would you perform next?
A
(Ionized calcium)
17
Q
You are presented with an animal that has an increased calcium, BUN, creatinine, and ionized calcium, what does this indicate?
A
(That the animal has hypercalcemia due to a currently unknown underlying disease and also has subsequent renal failure)
18
Q
You are presented with an animal that has an increased calcium, BUN, and creatinine but a normal ionized calcium, what does this indicate?
A
(The animal is in renal failure and has subsequent hypercalcemia)
19
Q
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?
A
(Lymphoma, apical gland adenocarcinoma, and multiple myeloma)
20
Q
You suspect a cat has lymphoma, what do you expect to see in terms of their calcium and phosphorus?
A
(Hypercalcemia, cannot expect anything from phosphorus and cancer because cancers can cause hypophosphatemia hyperphosphatemia, or not affect phosphorus at all)
21
Q
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?
A
(Hypercalcemia and hyperphosphatemia)
22
Q
How does hypoadrenocorticism result in hypercalcemia?
A
(Dehydration → more albumin which binds calcium so there will be an innate increase in calcium)
23
Q
What does the hyperphosphatemia and hypovitaminosis D resultant of chronic renal failure result in that induces hypercalcemia?
A
(Hyperphosphatemia and hypovitaminosis D result in hypocalcemia which triggers excess PTH secretion which then induces hypercalcemia)
24
Q
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)?
A
(Vitamin D)
25
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)
26
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)
27
What do intravenous fluids, furosemide, and glucocorticoids do to treat hypercalcemia?
(All three promote calciuresis and glucocorticoids also inhibit bone calcium release)
28
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)
29
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)
30
You are presented with an azotemic dog with hypocalcemia, have you caught it early or late?
(Early)
31
How does pancreatitis induced hypocalcemia?
(Bc calcium precipitates out of the blood into the inflammatory tissue around the inflamed pancreas)
32
What is the acute, emergent treatment for hypocalcemia?
(IV calcium gluconate)
33
What is the chronic treatment for hypocalcemia?
(PO calcium carbonate or calcitriol)
34
Is absolute hypoinsulinemia (a loss of beta cells), that occurs via immune-mediated destruction, type I or II diabetes mellitus?
(Type I diabetes mellitus)
35
Is relative hypoinsulinemia (an impairment of beta cells), with concurrent insulin resistance, type I or II diabetes mellitus?
(Type II diabetes mellitus)
36
Is type II diabetes insulin-dependent or non-insulin-dependent?
(Non-insulin-dependent)
37
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)
38
Through what three mechanisms does insulin deficiency promote hyperglycemia?
(Decreased tissue utilization of glucose, increased hepatic glycogenolysis, and increased hepatic gluconeogenesis)
39
What results from the exceedance of the renal tubular cell threshold to reabsorb filtered glucose?
(Glycosuria)
40
What results from the osmotic diuresis that is promoted by glycosuria?
(Polyuria)
41
What occurs compensatorily to the polyuria that follows glycosuria?
(Polydipsia)
42
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)
43
What occurs secondarily to the ‘starvation in the face of plenty’ that occurs in diabetic patients?
(Polyphagia)
44
What does the liver produce in the face of fatty acid mobilization that occurs secondarily to insulin deficiency?
(Ketone bodies)
45
(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)
46
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)
47
(T/F) In a diabetic animal, their ALP elevation should be greater than their ALT elevation.
(T)
48
Do you expect a diabetic animal to have a dilute or concentrated USG?
(Concentrated → glucose will artificially raise USG)
49
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)
50
What might you change based on the results of a glucose curve you perform on a diabetic patient?
(Dose and/or type of insulin)
51
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)
52
When would the ideal nadir occur in a diabetic patient’s glucose curve? Give a range.
(6-8 hours)
53
What is the ideal duration of insulin effect, which can be determined via a glucose curve in a diabetic patient?
(10-12 hours)
54
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)
55
What ocular clinical sign can result from diabetes mellitus in dogs?
(Bilateral cataracts)
56
What is the fiber and carbohydrate content of the diet that a diabetic dog should be on?
(High fiber, low carbohydrate)
57
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)
58
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))
59
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)
60
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)
61
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)
62
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)
63
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)
64
What are the three types of hyperadrenocorticism?
(Pituitary dependent, adrenal dependent, and iatrogenic)
65
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))
66
Do you expect a Cushingoid dog to have a dilute or concentrated (choose one) USG?
(Dilute, typically less than <1.020)
67
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))
68
If Cushing’s is high on your differential list (as in the dog has clinical signs that make you suspicious of HAC), which of the HAC screening tests would you reach for?
(Low dose dexamethasone suppression test/LDDST or the ACTH stimulation test)
69
How do you tell the difference between pituitary or adrenal-dependent HAC via ultrasound?
(With pituitary-dependent, adrenal glands will be symmetrical; with adrenal-dependent, one adrenal gland will have a mass and the other will be small)
70
What HAC screening test can be used to potentially differentiate between pituitary and adrenal-dependent HAC?
(LDDST, the presentation of the curve can possibly differentiate between PDH and ADH but not always)
71
What additional test can be used to differentiate between PDH and ADH, besides ultrasound and a LDDST?
(Endogenous ACTH/eACTH concentration → if within or above the reference range it indicates PDH, if it is lower than the reference range it indicates ADH)
72
What drug is used to treat both pituitary and adrenal-dependent HAC, when surgery is not an option?
(Trilostane → suppresses cortisol production in the adrenal gland)
73
What are the three types of hypoadrenocorticism?
(Typical, atypical, and iatrogenic)
74
Of the types of hypoadrenocorticism, which is the absence of both glucocorticoids and mineralocorticoids due to bilateral immune-mediated destruction of both the zona glomerulus and zona fasciculata?
(Typical)
75
Is typical or atypical hypoadrenocorticism related to an ‘Addisonian crisis’?
(Typical)
76
Why is a patient who is presenting in an ‘Addisonian crisis’ typically bradycardic as opposed to tachycardic which is the typical response to hypovolemia?
(Bc animals with Addison's are hyperkalemic and potassium is a myocardial suppressant)
77
Why do Addisonian dogs typically have nonregenerative anemia on CBC?
(Cortisol is necessary for RBC maturation in the bone marrow and so if you don’t have any cortisol, as in an Addisonian dog, then the patient will not be making RBCs appropriately)
78
What chem abnormalities would you look for in an atypical Addisonian dog? Three answers.
(Hypoglycemia, hypoalbuminemia, and hypocholesterolemia)
79
In an atypical Addisonian dog, they may have hypoglycemia, hypoalbuminemia, and hypocholesterolemia.
What additional abnormalities would instead indicate a typical Addisonian dog? Three answers.
(Hyponatremia, hyperkalemia, and azotemia)
80
Do typical or atypical Addisonian dogs uncommonly present with megaesophagus?
(Can be both)
81
You want to test the baseline cortisol of a sick patient to rule out Addison’s, what value does their baseline cortisol need to be above to do that?
(A baseline cortisol of > 2 is not consistent with HOC)
82
What is the difference between starvation and anorexia due to illness in terms of the effects they have on the body?
(Starvation is associated with an attempt to preserve lean tissue by breaking down carbohydrates and fats prior to breaking down muscle; that does not occur with anorexia d/t illness and the animal will not be able to preserve their lean tissue)
83
An animal's BCS falling below what value indicates the need for nutritional support in a hyporexic or anorexic patient?
(< 4/9)
84
A recent unintended body weight loss of greater than what percentage indicates the need for nutritional support in a hyporexic or anorexic patient?
(> 10% BW)
85
What laboratory abnormalities in a hyporexic or anorexic patient indicates the need for nutritional support? Three answers.
(Hypoalbuminemia, anemia, and/or electrolyte abnormalities)
86
How much should you feed on day 1 of providing nutritional support to a hyporexic or anorexic patient?
(25-50% of current RER)
87
How long should your transition from feeding 25-50% RER to feeding 100% RER to a hyporexic or anorexic patient take?
(2-4 days if there are no complications such as vomiting or diarrhea)
88
What electrolyte abnormalities are associated with refeeding syndrome, that then need to be supplemented to combat the related negative effects?
(Hypophosphatemia and hypokalemia)
89
What is the transdermal serotonin antagonist appetite stimulant?
(Mirtazapine, there are other modes of administration but for the purpose of the question, I went with transdermal)
90
What is the ghrelin agonist appetite stimulant?
(Capromorelin; entyce for dogs and elura for cats)
91
Which method of enteral assisted feeding can you only feed liquids with and should be used for a week or less?
(Nasoesophageal or nasogastric tubes)
92
How long can esophagostomy tubes last?
(Months)
93
How long can gastrostomy tubes last?
(Life-long)
94
When should you start weaning/tapering tube feeding in a dog/cat hyporexic/anorexic patient?
(When the animal is consuming 75% of their RER)
95
When should you start weaning/tapering tube feeding in a horse hyporexic/anorexic patient?
(When the animal is consuming at least 1% their BW in dry matter)
96
When should you remove an enteral feeding tube in a dog/cat hyporexic/anorexic patient?
(When the animal is consuming 100% of their RER or BW gain/maintenance trend is established)
97
When should you remove an enteral feeding tube in a horse hyporexic/anorexic patient?
(When the animal is consuming 1.5% their BW in dry matter or BW gain/maintenance trend is established)
98
You are presented with a dog with an increased BUN and creatinine:
Their USG is 1.010, does this indicate pre-renal, renal, or post-renal azotemia?
(Renal)
99
You are presented with a dog with an increased BUN and creatinine:
Their USG is 1.035, does this indicate pre-renal, renal, or post-renal azotemia?
(Prerenal or postrenal)
100
If you have determined your patient has prerenal azotemia, what should your next steps be?
(Rehydrate them and verify that the azotemia resolves)
101
If you have determined your patient has postrenal azotemia, what should your next steps be?
(Correct the obstruction/disruption, provide adequate fluid therapy, and verify the azotemia resolves)
102
Acute kidney injury/acute renal failure is associated with polyuria, oliguria, and/or anuria (choose correct answers).
(Oliguria and anuria)
103
What are the common causes of acute kidney injury in dogs and cats? Four answers.
(Ethylene glycol, NSAIDs, idiopathic, and leptospirosis (dog only))
104
What are the common in-hospital causes of acute kidney injury? Three answers.
(Anesthesia, medications, and sepsis)
105
Is AKI or CKD associated with hyperkalemia?
(AKI, CKD is associated with hypokalemia)
106
(T/F) Animals with AKI will typically present with a decreased body condition.
(F, good body condition, CKD patients present with a decreased body condition)
107
Over what time period should replacement fluids be administered to an AKI patient?
(Over 6 or less hours)
108
What is the treatment for leptospirosis, which should be given to dogs if there is any possibility of lepto?
(Injectable penicillin or ampicillin followed by oral doxycycline for 2 weeks)
109
What can be done to treat the hyperkalemia associated with AKI?
(Administer bicarbonate, this will correct the acidosis and the body will stop pulling potassium out of the cells (which is one of the causes of hyperkalemia in the first place))
110
What disease can result from decreased vitamin D production in a CKD patient?
(Renal secondary hyperparathyroidism, rarely causes clinical signs)
111
What results from the decreased erythropoietin production in CKD patients?
(Non-regenerative anemia)
112
(T/F) Renal therapeutic diets prolong survival of CKD patients.
(T)
113
What drug is used for controlling hypertension in cats with CKD?
(Amlodipine)
114
Give the difference in the history between polyuria and pollakiuria based on the questions below:
Volume of urine with each voiding?
(Pollakiuria - small amounts; polyuria - large amounts)
115
Give the difference in the history between polyuria and pollakiuria based on the questions below:
Frequency of needing to go out?
(Pollakiuria - more frequent; polyuria - less frequent)
116
Give the difference in the history between polyuria and pollakiuria based on the questions below:
Urination attempts when outside?
(Pollakiuria - multiple; polyuria - singular)
117
Give the difference in the history between polyuria and pollakiuria based on the questions below:
Other lower urinary tract signs?
(Pollakiuria - yes; polyuria - no)
118
Give the difference in the history between polyuria and pollakiuria based on the questions below:
Compensatory polydipsia?
(Pollakiuria - no; polyuria - yes)
119
If you are trying to determine if a patient is actually polyuric and you have the owner take multiple free catch specimens at home, what do you want all of their USGs to be to confirm polyuria?
(USG consistently < 1.020 = confirmative of polyuria)
120
You performed a CBC chem in a patient you have confirmed to have PU/PD, they have a neutrophilia, lymphocytosis, and a left shift, what disease process should be high on your differential list?
(This is a PU/PD patient with an inflammatory leukogram, indicates bacterial endotoxin/septicemia of some sort, pursue further diagnostics to figure out where the infection is located)
121
Do increased or decreased RBCs cause PU/PD?
(Increased → increased RBCs will impair ADH release from the pituitary gland)
122
You have a PU/PD patient with elevated liver values, primarily ALP, and a hypercholesterolemia with a normal glucose, what disease process is indicated?
(Hyperadrenocorticism, should pursue ACTH stim or LDDST)
123
An increased or decreased (choose one) potassium can cause PU/PD.
(Decreased → can indicate many diseases but include hyperaldosteronism, diabetic ketoacidosis, hepatic lipidosis, CKD, etc.)
124
An increased or decreased (choose one) calcium can cause PU/PD.
(Increased → can indicate primary hyperparathyroidism, granulomatous disease, hypoadrenocorticism, neoplasia, vitamin D toxicity, CKD, etc.)
125
You are presented with a PU/PD patient with hypoalbuminemia, hypocholesterolemia, low BUN, hypoglycemia, and mildly elevated liver values, what disease process is indicated?
(Hepatic insufficiency (lack of BUN can mess up the countercurrent multiplication in the kidney leading to PU/PD, with hepatic insufficiency cortisol can be elevated enough to cause PU/PD) → should pursue further diagnostics such as serum bile acids, AUS, and liver biopsy)
126
You are presented with a PU/PD patient with high normal kidney values, what disease process do you suspect and what test can you do to bring it higher or lower on your differential list?
(Early CKD, perform an SDMA (all the professors have been kinda eh about the SDMA but if you have a PU/PD patient with high normal kidney values, no other abnormalities and an increased SDMA, Dr. Bolton seems to like that for CKD))
127
You are presented with a PU/PD patient who is normoglycemic but glucosuric, does this rule out diabetes mellitus?
(Yes; it is instead primary renal glucosuria → something has damaged the proximal tubules and they are unable to absorb glucose appropriately so it shows up in the urine)
128
(T/F) You would ideally run a chem, UA, and T4 on all dogs and cats that present with PU/PD.
(F, in all cats yes but dogs you don’t need to run a T4 in because hypothyroidism does not cause PU/PD)
129
What five diseases are still viable diagnoses for a PU/PD patient with a completely normal minimum database?
(Early CKD, hyperadrenocorticism, hepatic insufficiency, psychogenic PD and diabetes insipidus)
130
Early CKD, hyperadrenocorticism, hepatic insufficiency, psychogenic PD and diabetes insipidus are still viable diagnoses for PU/PD in a patient with a normal minimum database.
What simple test that you should have already run to confirm the PU/PD is real can you go back and evaluate to bring some of the listed diseases higher or lower on your differential list?
(USG! If consistently isosthenuric (1.008-1.015) → CKD; if not consistently isosthenuric or hyposthenuria → hyperadrenocorticism, hepatic insufficiency, and psychogenic polydipsia; if consistently hyposthenuria → diabetes insipidus)
131
Give the differences in the values below between psychogenic PD and diabetes insipidus:
USG
(Psychogenic PD will have variable USGs (some hyposthenuria, some isosthenuric, some perfectly concentrated) while DI will have a consistently hyposthenuria USG)
132
Give the differences in the values below between psychogenic PD and diabetes insipidus:
Serum sodium
(Psychogenic PD will have low normal sodium while DI will have normal to higher sodium)
133
Give the differences in the values below between psychogenic PD and diabetes insipidus:
Water deprivation test response
(Psychogenic PD will have a concentrated urine after deprivation of water while DI will still have hyposthenuric urine until you administer ADH)
134
Why should you avoid immediately putting an intact male dog on antibiotics for a UTI without further diagnostics?
(Concurrent prostatitis can be the source of the UTI so you should look for this then treat appropriately)
135
Why should you avoid immediately putting a cat with a UTI on antibiotics without further diagnostics?
(Urinary tract infections are a common sequela of other diseases primarily CKD, you don’t want to treat and miss something else causing the UTI)
136
How quickly should clinical signs in a dog with a UTI improve after starting antibiotics +/- NSAIDs?
(48 hours)
137
(T/F) A lack of visible bacteriuria rules out a UTI.
(F, if there are other cells such as WBCs and clinical signs match, there likely is still a UTI, can try to perform a wright’s stain or a RapidBac Vet test prior to expensive culture to confirm)
138
(T/F) It is never normal for there to be bacteria present in a urine sample when obtained via a cystocentesis.
(F, can be bacteria present in the urinary tract that are not causing an infection/clinical signs; essentially, you do not need to treat animals with a bacteria on a UA if they do not have clinical signs)
139
Diagnostics for complicated UTIs or recurrent/persistent lower urinary tract signs in dogs and cats should include what two tests/techniques?
(Diagnostic imaging of some sort and a urine C/S)
140
How is the treatment for a complicated UTI different if the source is prostatitis in an intact male dog? Three answers.
(The drugs will be different (you need a lipid soluble abx), the timeline will be different (treat for 2-3 weeks instead of just 7-14 days), and you need to reduce their testosterone)
141
What IV antimicrobial combination is often used prior to receiving results of your CS in a patient with pyelonephritis?
(Ampicillin and enrofloxacin)
142
Prostatic neoplasia more commonly affects castrated or intact (choose one) male dogs.
(Castrated)
143
Prostatitis more commonly affects castrated or intact (choose one) male dogs.
(Intact)
144
(T/F) If you can palpate the prostate in a castrated dog, it almost certainly has prostate cancer.
(T)
145
What is the primary treatment for benign prostatic hyperplasia/trophy?
(Neuter)
146
(T/F) The detrusor muscle and the internal urinary sphincter are smooth muscle while the external urinary sphincter is skeletal muscle.
(T)
147
Larger or smaller (choose one) dogs tend to get IVDD of their lower spine which can lead to urinary incontinence (and a plethora of other lower motor neuron lesions).
(Larger; smaller dogs tend to get cervical IVDD)
148
(T/F) Incontinence in a neurologically normal adult female spayed dog with concentrated non-inflammatory urine is almost always urethral sphincter mechanism incompetence.
(T)
149
What nerve sends signals to the brain to let it know that the bladder is stretching due to filling and also is the nerve that is used to trigger the detrusor muscle to contract?
(Pelvic nerve)
150
What nerve does the brain use to tell the internal sphincter to contract and the detrusor muscle to relax?
(Hypogastric nerve)
151
What nerve does the brain use to tell the external sphincter to contract?
(Pudendal nerve)
152
When you want to urinate, what nerves are inhibited to allow urination to occur?
(The hypogastric and pudendal nerves need to be inhibited so that everything can relax appropriately)
153
What is the typical presentation of struvite stones on radiography?
(Large, rounded, smooth, and radiopaque)
154
What type of stone is more common in female dogs?
(Struvite stones)
155
(T/F) Struvite uroliths are induced by UTIs in dogs and cats.
(F, not in cats (it is thought to be diet caused in cats))
156
Why should antibiotics be started prior to surgery to remove stones? Two answers.
(Prevent infection of the abdominal cavity and non-infected tissue heal better than infected tissue)
157
What should always be performed after removing/dissolving uroliths surgically/medically?
(Perform diagnostic imaging)
158
What are the characteristics of the diets that are used for dissolution and prevention of struvite stones? Three answers.
(Low protein, acidifying, and high sodium)
159
What sex is typically impacted with feline mucus plugs?
(Males)
160
Of struvite and calcium oxalate crystals, which are acidic to neutral?
(Calcium oxalate)
161
What drug can be administered to animals with recurrent calcium oxalate crystals that binds calcium to try and prevent their formation?
(Hydrochlorothiazide)
162
What is the mainstay for prevention of calcium oxalate stones?
(Increase water intake)
163
What diagnostic imaging can be used to visualize ammonium urate/biurate uroliths? Two answers.
(Ultrasound and/or contrast radiography)
164
What diet and medication is used for dissolution and prevention of urate stones in non-shunt patients?
(Hill’s u/d diet and allopurinol)
165
Nephroliths and ureteroliths are associated with what age of animals?
(Geriatric)
166
What stone type is most commonly indicated in nephroliths or ureteroliths?
(Calcium oxalate)
167
(T/F) Most urinary obstructions are of the lower urinary tract and if they are complete blockages, will cause uremia in 24-48 hours.
(T)
168
What are the most common causes of urinary obstruction in small animals? Four answers.
(Feline idiopathic cystitis, uroliths, mucus plugs, and tumors)
169
What drugs can be administered to a patient with potassium greater than 7.5 meq/L or a symptomatic hyperkalemic patient?
(Insulin/glucose, albuterol, calcium gluconate, and bicarbonate)
