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E&E Exam 4 > SA Endocrine Diseases > Flashcards

SA Endocrine Diseases Flashcards

1
Q

What is the most common endocrinopathy of cats?

A

Hyperthyroidism

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2
Q

What is the thyroid pathology of hyperthyroidism?

A

Adenomatous hyperplasia or adenoma resulting in autonomous production of thyroid hormones

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3
Q

T/F: Hyperthyroidism in cats most commonly involves both lobes but can be unilateral.

A

T

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4
Q

In a hyperthyroid cat, what do you expect to happen to the T4 and TSH levels?

A

Increased T4, decreased TSH

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5
Q

What are the most common signs associated with hyperthyroidism? (5 answers)

A

Weight loss with good appetite, PU/PD, vomiting, diarrhea, unkempt hair coat

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6
Q

In majority of cats with hyperthyroidism, you may hear a sinus tachycardia on auscultation. In some cases, you may hear a heart murmur or gallop rhythm. What does this suggest is occurring secondary to the hyperthyroidism?

A

HCM

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7
Q

Most hyperthyroid cats will have a __________ or __________ creatinine.

A

Normal or decreased

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8
Q

What is the most common cause of hypothyroidism in cats?

A

Iatrogenic after treatment of hyperthyroidism

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9
Q

Cats that develop worsening azotemia or new azotemia while on methimazole that have a low to low-normal T4 should have what other test performed?

A

cTSH

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10
Q

Why does a low T4 alone in a cat not confirm hypothyroidism?

A

Presence of nonthyroidal illnesses (CKD, neoplasia, diabetes, hepatic disease) can lower serum T4 in euthyroid cats

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11
Q

When should you evaluate a patient that had undergone radioiodine therapy for permanent iatrogenic hypothyroidism?

A

3 months after treatment or earlier if overt clinical signs of hypothyroidism develop or there is marked worsening of azotemia

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12
Q

What is the drug of choice for treating hypothyroidism in dogs and cats?

A

Levothyroxine

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13
Q

When should you administer levothyroxine in regards to feeding time?

A

Give without food 1 hour before a meal or 3 hours after a meal

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14
Q

Hypothyroidism can lead to a(n) increased/decreased GFR, which will improve/worsen kidney function and survival time.

A

Decreased, worsen

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15
Q

If cats being treated with methimazole have a low to low-normal T4 or develop a worsening azotemia, should you increase/decrease the dose of Methimazole and by what percentage?

A

Decrease dose by 25-50%

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16
Q

What is the treatment protocol for a cat that is still hypothyroid 6 months after treatment with radioiodine?

A

Treat regardless of presence of azotemia

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17
Q

What are the most common etiologies of canine hypothyroidism?

A

Lymphocytic thyroiditis and idiopathic thyroid atrophy

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18
Q

What is the most common signalment for canine hypothyroidism?

A

Young adult to middle aged medium to large-breed dogs

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19
Q

The general signs of canine hypothyroidism occur due to a(n) increased/decreased metabolic rate. (choose one)

A

Decreased

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20
Q

What are the general signs associated with canine hypothyroidism? 4 answers.

A

Lethargy, weakness, obesity, exercise intolerance

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21
Q

Describe the alopecia associated with canine hypothyroidism (location, bilateral/unilateral, pruritic or not, etc.)

A

Earliest loss occurs in areas of friction (neck and tail) and then becomes bilaterally symmetrical over trunk (spares head and distal extremities)

Non-pruritic unless secondary infection

Hyperpigmentation common

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22
Q

What is Myxedema?

A

Non-pitting edema that causes a puffy appearance of face (tragic facial expression); sometimes seen with canine hypothyroidism

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23
Q

What laboratory findings may you see on CBC/Chem associated with hypothyroidism in dogs?

A

Hypercholesterolemia and normocytic, normochromic, mild, non-regenerative anemia

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24
Q

How do you make a diagnosis of hypothyroidism in dogs?

A

History of clinical signs and low T4 with increased TSH

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25
Q

What is the most common test used to diagnose hypothyroidism?

A

T4

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26
Q

Why do nonthyroidal illnesses and lymphocytic thyroiditis pose a challenge when trying to diagnose hypothyroidism?

A

Nonthyroidal illnesses can lower T4 in a euthyroid dog and lymphocytic thyroiditis creates T4 autoantibodies that can falsely elevate serum T4 in a true hypothyroid dog

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27
Q

What is the most accurate single test for diagnosis of hypothyroidism in dogs because it is less often affected by nonthyroidal illnesses but is used less frequently than T4 due to cost and availability?

A

Equilibrium dialysis assay (free T4)

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28
Q

What breeds tend to normally have lower T4 and fT4 levels than other breeds?

A

Sighthounds

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29
Q

Name 4 drugs/classes of drugs that can affect thyroid function tests (often lowers T4)

A

Corticosteroids, Sulfonamides, Phenobarbital, Clomipramine

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30
Q

If you suspect a dog has hypothyroidism but presents to you for being sick, when should you perform the thyroid function tests?

A

If you can, resolve illness before testing for hypothyroidism

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31
Q

T/F: Thyroiditis may or may not progress to hypothyroidism

A

T

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32
Q

What test is not affected by autoantibodies that can help you determine if a patient is truly hypothyroid or euthyroid?

A

fT4 by equilibrium dialysis

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33
Q

You have diagnosed a dog with hypothyroidism and have started him on Levothyroxine. When should you schedule a recheck? Be specific.

A

Recheck 6-8 weeks after starting treatment and measure serum levels 4-6 hours post-pill.

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34
Q

When can you tell owners they should start to see results once starting their dog on levothyroxine?

A

Increased activity, improved attitude, and weight loss in 1-2 weeks; dermatologic signs will require months to resolve

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35
Q

What should you do if a canine patient you are treating for hypothyroidism develops clinical signs of hyperthyroidism (PU/PD, panting, hyperactivity, polyphagia)?

A

Stop treatment for 2-3 days and then re-institute at 50-75% of original dose

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36
Q

A 6-year-old dog presents with central vestibular disease. A total T4 is below the reference range. What is your interpretation and recommendations?

A

Central vestibular signs can be seen with hypothyroid patients, but the low T4 may also be from nonthyroidal illness. Would recommend fT4 by ED +/- TSH

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37
Q

What are 2 signs that are specific to the hypercalcemia?

A

Generalized weakness and PU/PD

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38
Q

What are 5 general clinical signs that are non-specific to the hypercalcemia, but rather are related to the underlying disease?

A

Lethargy, anorexia, vomiting, diarrhea, and weight loss

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39
Q

With any elevation of hypercalcemia, what should be on your differential list?

A

Neoplasia

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40
Q

What is the most common cause of hypercalcemia in a dog/cat that feels well?

A

Spurious hypercalcemia

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41
Q

What are 4 causes for a spurious hypercalcemia?

A

Lipemic serum, hemolyzed serum, hemoconcentration (dehydration), or a young, growing animal

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42
Q

What can you do to distinguish hypercalcemia induced renal failure from renal failure induced hypercalcemia?

A

Measure ionized calcium

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43
Q

Explain how hypercalcemia can lead to azotemia (lack of perfusion to kidneys).

A

Excess calcium causes vasoconstriction to renal arteries -> azotemia

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44
Q

If azotemia is present and there is an increased ionized calcium, what is your interpretation?

A

Hypercalcemia induced renal failure

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45
Q

If azotemia is present and ionized calcium is normal, what is your interpretation?

A

Renal failure induced hypercalcemia

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46
Q

If the patient has repeatable hypercalcemia but not azotemia, do you still need to measure an ionized calcium?

A

No

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47
Q

What are 4 history/physical exam findings in addition to the hypercalcemia that would put neoplasia higher on your differential list?

A

Peripheral lymphadenopathy, palpable mass, long bone pain, and/or fever

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48
Q

What are 3 history/physical exam findings in addition to the hypercalcemia that would put granulomatous disease higher on your differential list?

A

Long bone pain, fever, and/or tachypnea/dyspnea/cough

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49
Q

What is the most common neoplasia in dogs and cats causing hypercalcemia?

A

Lymphoma

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50
Q

What are the 3 most common types of neoplasia causing hypercalcemia?

A

Lymphoma, apocrine gland adenocarcinoma of anal sac, and multiple myeloma

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51
Q

In a canine patient with hypercalcemia, what should always be included in your physical examination?

A

Rectal exam

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52
Q

What is the mechanism of hypercalcemia of malignancy?

A

Secretion of PTHrp, calcitriol, and/or cytokines by tumor cells

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53
Q

What is the typical calcium/phosphorus pattern and animal health (well vs. sick) associated with hypercalcemia of malignancy?

A

High tCa, high iCa, and normal or decreased PO4 (unless concurrent renal injury - then PO4 will be elevated);

Animal feels well; note that the calcium/phosphorus pattern can be anything with neoplasia!

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54
Q

What are the 2 most common causes of hypervitaminosis D?

A

Ingestion of cholecalciferol rodenticide or psoriasis cream (contains excessive vitamin D)

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55
Q

What is the calcium/phosphorus pattern associated with hypervitaminosis D? How does the animal feel overall?

A

High tCa, high iCa, and high PO4 (often have concurrent renal injury);

Animal feels sick

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56
Q

What are the 2 mechanisms of hypercalcemia due to typical hypoadrenocorticism in dogs?

A
  1. Hemoconcentration leads to hyperproteinemia (albumin) -> more calcium to measure
  2. Decreased GFR -> decreased renal clearance
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57
Q

What is the typical calcium/phosphorus pattern associated with typical hypoadrenocorticism in dogs and how do these patients feel?

A

High tCa, normal iCa, and high PO4 (due to concurrent prerenal azotemia);

Dog feels sick

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58
Q

What is the mechanism of renal failure induced hypercalcemia?

A

Secretion of excess PTH due to chronic renal secondary hyperparathyroidism (becomes autonomous)

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59
Q

Why does chronic kidney failure lead to hyperphosphatemia?

A

There is decreased renal clearance of phosphorus, so it gets reabsorbed in the blood -> hyperphosphatemia

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60
Q

Describe renal secondary hyperparathyroidism.

A

The last step in the synthesis of vitamin D occurs in the kidneys and requires PTH. Kidney failure -> less vitamin D produced -> less calcium absorption from the gut -> hypocalcemia -> stimulates PTH secretion from parathyroid glands -> restores normal calcium -> kidney failure still present, so parathyroid keeps secreting PTH (becomes autonomous) -> hypercalcemia

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61
Q

What is the typical calcium/phosphorus pattern associated with chronic kidney failure and how does the patient feel?

A

High tCa, normal iCa, and high PO4 (due to renal injury);

Patient can feel well or sick

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62
Q

What is the mechanism associated with granulomatous disease causing hypercalcemia?

A

Fungal organisms initiate a granulomatous (macrophage-based) inflammation around them, and those macrophages secrete calcitriol

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63
Q

What is the typical calcium/phosphorus pattern associated with granulomatous disease and how does the patient typically feel?

A

High tCa, high iCa, and normal or high PO4 (due to renal injury);

Patient feels sick usually

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64
Q

What is the mechanism of primary hyperparathyroidism in dogs?

A

Secretion of excess PTH by a parathyroid gland tumor (adenoma); kidneys are functioning as normal

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65
Q

What is the typical calcium/phosphorus pattern associated with primary hyperparathyroidism and how do those dogs typically feel?

A

High tCa, high iCa, and normal or low PO4 (almost never has renal injury);

Dogs will feel well

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66
Q

What is the second most common cause of hypercalcemia in cats and what is the typical pattern of calcium/phosphorus associated with it? How do the cats feel?

A

Idiopathic hypercalcemia;
High tCa, high iCa, and normal PO4;
Cats can feel well or sick

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67
Q

If your patient is hypercalcemic and primary hyperparathyroidism is at the top of your differential list, what would you do to diagnose it?

A

Measure iCa, PTH, and PTHrp

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68
Q

If your patient is hypercalcemic and the owner tells you there was an exposure to rat bait, what should you do to confirm this is hypervitaminosis D causing the hypercalcemia?

A

Measure serum 25-hydroxyvitamin D levels

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69
Q

What are 5 clinical signs related to hypocalcemia? (Do your best)

A

Muscle tremors/fasciculations, facial rubbing, stiff gait, behavior changes (restless, anxious, aggressive), and/or seizures

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70
Q

If you have a patient that is hypocalcemic, what should you rule out first?

A

Hypoalbuminemia

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71
Q

If your patient is hypocalcemic and has a history of recently whelping or is soon to whelp, what would be at the top of your differential list?

A

Eclampsia

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72
Q

If calcium is low and phosphorus is normal, what would be your top 3 differentials?

A

Acute pancreatitis, eclampsia, or malabsorptive GI disease

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73
Q

Are you more likely to see hyper- or hypocalcemia with chronic kidney failure?

A

Hypercalcemia

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74
Q

Are you more likely to see hyper- or hypocalcemia with acute kidney injury and urinary tract obstruction?

A

Hypocalcemia

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75
Q

What is the mechanism of hypocalcemia caused by acute pancreatitis?

A

Calcium precipitation with saponified peripancreatic fat

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76
Q

What is the mechanism of hypocalcemia caused by eclampsia?

A

Mobilization of calcium into milk production and/or fetal skeletal development

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77
Q

What is the mechanism of hypocalcemia caused by malabsorptive GI disease in dogs?

A

Poor intestinal calcitriol absorption and/or calcitriol loss bound to albumin

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78
Q

What is the mechanism of hypocalcemia caused by owners using a phosphate containing enema (aka fleet enema)?

A

Phosphorus is absorbed by colonic wall -> body responds with mass law effect -> rapidly dropping calcium levels

79
Q

What is the mechanism of hypocalcemia caused by acute kidney injury or urinary tract obstruction?

A

Acute drop in GFR -> hyperphosphatemia -> mass law driven hypocalcemia

80
Q

What is the mechanism of hypocalcemia caused by primary hypoparathyroidism in dogs?

A

Secretion of no PTH by immune-mediated destruction of the parathyroid gland

81
Q

What is the typical calcium/phosphorus pattern associated with primary hypoparathyroidism in dogs?

A

Low tCa, low iCa, and high PO4

82
Q

If you are concerned for hypoparathyroidism, what should you do to confirm it?

A

Measure iCa, PTH, and PTHrp

83
Q

If you are concerned for acute pancreatitis, what should you do to diagnose it?

A

Perform abdominal ultrasound and/or PLI

84
Q

With hypocalcemia and hypercalcemia, what should your goals of treatment be?

A

Treat the underlying disease

84
Q

With hypocalcemia and hypercalcemia, what should your goals of treatment be?

A

Treat the underlying disease

85
Q

When is acute, emergent (and non-specific) therapy indicated for treatment of hypocalcemia?

A

When clinical signs of hypocalcemia are present

86
Q

What is used for acute, emergent treatment of hypocalcemia?

A

Calcium gluconate IV (slow and “to effect”)

87
Q

What treatment is used for chronic hypocalcemia or life-long therapy?

A

Calcium carbonate (TUMs) PO and/or calcitriol PO

88
Q

What is the treatment protocol for acute and emergent cases of hypercalcemia? (3 answers)

A

IV fluids (0.9% NaCl), furosemide (once euhydrated), and glucocorticoids;

All promote calciuresis and steroids will also inhibit bone Ca2 release

89
Q

Why might we see an unconcentrated urine (USG <1.035) in a cat with hyperthyroidism?

A

Thyroid hormone increases renal blood flow and GFR and make the animals PU/PD

90
Q

Is an unconcentrated urine in a suspected hyperthyroid cat definitive for thyroid disease or kidney disease?

A

No, can be <1.035 for either one (can’t differentiate)

91
Q

Why might creatinine be low in a hyperthyroid patient?

A

Muscle wasting

92
Q

What is your interpretation of a cat that has clinical signs associated with hyperthyroid disease, but the patient’s TT4 is mid to high normal and high fT4?

A

Could be early/mild hyperthyroid or concurrent nonthyroidal illness

93
Q

How do you get a definitive diagnosis of hyperthyroidism in cats?

A

By documenting persistently elevated thyroid hormones in a cat with at least one or more clinical signs of hyperthyroidism

94
Q

What is your interpretation of a cat with clinical signs associated with hyperthyroidism but the TT4 is low to low-normal and the fT4 is high?

A

Likely euthyroid with nonthyroidal illness

95
Q

In order to know the kidney function in a hyperthyroid cat, we must remove the effects of thyroid disease. How do we do this?

A

Treat with Methimazole and assess kidney function 4 weeks after the cat becomes euthyroid

96
Q

What are 4 treatment options for hyperthyroid cats?

A

Methimazole, Surgical thyroidectomy, radioiodine therapy, or iodine-restricted diet

97
Q

What is the mechanism of methimazole?

A

Blocks thyroid peroxidase -> no more thyroid hormone production

98
Q

How long does Methimazole take to become effective?

A

2-4 weeks (still already made thyroid hormones in the body)

99
Q

If within the first 3 months of hyperthyroid treatment the cat develops GI signs with oral methimazole, what can you do to still manage the thyroid disease?

A

Switch to transdermal methimazole

100
Q

What is a common side effect that tells us the cat is becoming intolerant to methimazole?

A

Facial pruritis

101
Q

What is the follow up protocol for starting cats on Methimazole?

A

Recheck patient in 4 weeks (CBC, Chem, UA, T4);
Recheck again in 2 months if T4 normal and no side effects;
Then periodically if stable

102
Q

What are the risks associated with surgical thyroidectomy? (2 answers)

A

Hypothyroidism and hypoparathyroidism (hypocalcemia -> life threatening)

103
Q

T/F: Radioiodine emits beta particles that destroys abnormal thyroid tissue but spares normal tissue.

A

T

104
Q

What monitoring is involved when radioiodine is used as treatment for hyperthyroidism?

A

Chemistry, UA, T4/TSH 1- month post-treatment, and again at 3 months and 6 months.

105
Q

If clients opt to use an iodine-restricted diet, how long after starting the diet should they see clinical signs improve?

A

Appx. 4 weeks

106
Q

Can cats that are not hyperthyroid eat iodine-restricted diets?

A

Yes, but the food is expensive

107
Q

What cells of the endocrine pancreas are responsible for making insulin?

A

Beta cells

108
Q

Which type of diabetes is more common in the dog? What about in the cat?

A

Dog = Type I diabetes mellitus
Cat = Type II diabetes mellitus

109
Q

Which type of diabetes is considered insulin-dependent?

A

Type I diabetes mellitus

110
Q

With type I diabetes mellitus there is a loss of beta cells, resulting in a(n) relative/absolute hypoinsulinemia. (Choose one)

A

Absolute

111
Q

With type II diabetes mellitus, there is impairment of the beta cells, resulting in a(n) relative/absolute hypoinsulinemia. (Choose one)

A

Relative

112
Q

What causes type I diabetes mellitus in dogs?

A

Immune-mediated destruction (“insulitis”)

113
Q

What causes type II diabetes mellitus in cats?

A

Often concurrent disease causing insulin resistance

114
Q

What are 5 potential causes of insulin resistance that could contribute to type II diabetes mellitus?

A

Genetic factors, obesity, insulin-antagonistic drugs (i.e. progesterone or glucocorticoids), endocrinopathies (insulin-antagonistic disease), and diseases secreting inflammatory cytokines (IL-1, IL-6, TNF alpha; pancreatitis, aspiration pneumonia, bacterial gallbladder infection, etc.)

115
Q

Diabetes mellitus occurs due to an insulin deficiency, which promotes hyperglycemia. Why does hyperglycemia occur? (3 answers)

A

Decreased tissue utilization of glucose, increased hepatic glycogenolysis, and increased hepatic gluconeogenesis

116
Q

Why does glucosuria occur in a diabetic dog/cat?

A

Amount of glucose exceeds the renal threshold of proximal tubule to reabsorb the filtered glucose, so it spills out into the urine

117
Q

What are the 4 clinical signs associated with diabetes mellitus in dogs and cats?

A

PU/PD, weight loss, and polyphagia

118
Q

Why are diabetic patients PU/PD?

A

Glucose is an osmotically active substance, and water follows anything that is osmotically active. Glucose spills into the urine, so water follows -> polyuria. There is a compensatory polydipsia to maintain hydration

119
Q

Why do diabetic animals lose weight?

A

Lack of an ability of cells to utilize glucose for energy and storage -> weight loss

120
Q

What is normal blood glucose in the dog and cat?

A

Dog = 80-120 mg/dL
Cat = 80-140 mg/dL

121
Q

When the body cannot utilize glucose for energy, what will it use as an alternative source of energy to provide to the cells?

A

Fat to form ketones in the liver

122
Q

What is a complication of diabetes mellitus that occurs as a result of some other insulin-resistant disease in the body?

A

Diabetic ketoacidosis

123
Q

How will a DKA patient present to you?

A

Vomiting, diarrhea, not eating, lethargic, etc.

124
Q

Like glucose, what is another osmotically active substance that can lead to acidosis when produced in large quantities?

A

Ketone bodies

125
Q

Diabetic patients can have increased liver enzymes on blood chemistry. Will ALT or ALP be more elevated?

A

ALP > ALT (vacuolar hepatopathy due to excess fat mobilized in body)

126
Q

What changes do you expect to see on a blood chemistry in patients suspected to have diabetes mellitus? 4 answers.

A

Hyperglycemia, increased liver enzymes, hypercholesterolemia, and hypertriglyceridemia

127
Q

If a patient is PU/PD, what would you expect their USG to be? Does this rule apply to diabetics? Why or why not?

A

Would expect it to be dilute (hyposthenuric); glucose artificially elevates USG, so we will see a concentrated urine in diabetic patients (>1.020) or isosthenuric because water follows glucose and can dilute the urine

128
Q

What criteria does a patient need to make a diagnosis of diabetes mellitus?

A

Appropriate clinical signs, persistent fasting hyperglycemia, and persistent fasting glucosuria

129
Q

In uncomplicated cases of diabetes mellitus, what is the first choice of insulin for cats?

A

Glargine (aka Lantus, Sanofi)

130
Q

In uncomplicated cases of diabetes mellitus, what is the first choice of insulin for dogs? 2 answers.

A

NPH (Novolin N, Humulin N) OR Lente (Vetsulin)

131
Q

If we are using insulin to treat DKA, do we want short-acting or long-acting insulin?

A

Short-acting

132
Q

For all long-acting insulin types, how do we typically dose it? (Don’t be specific with number)

A

Dosed twice daily after a meal

133
Q

If a glucose curve shows uncontrolled numbers, but the owner describes an animal that is doing well at home and not showing clinical signs, should you change the insulin dose?

A

No

134
Q

When should you perform a glucose curve in a diabetic patient?

A

During initial 1-2 months following diagnosis (to get animal regulated) and/or anytime a diabetic animal becomes poorly regulated

135
Q

What is a blood glucose curve used to determine?

A

If/what adjustments to the insulin TYPE or DOSE are needed

136
Q

Following an insulin type change or dose adjustment, when should a recheck blood glucose curve be performed?

A

7-10 days following change

137
Q

What test can be performed to differentiate between stress hyperglycemia and true diabetes mellitus?

A

Measure fructosamine

138
Q

What is a somogyi response?

A

Insulin “overdosing” that occurs when the insulin dose increases based on spot BG -> results in either rapid decrease in BG or absolute hypoglycemia -> body responds by secreting insulin-antagonizing hormones -> very profound rebound hyperglycemia

139
Q

What are 3 additional clinical signs specific to dogs with diabetes mellitus?

A

Bilateral cataracts, poor haircoat, and abdominal distension (lipid accumulation in liver -> hepatomegaly -> abdominal distension)

140
Q

What are the goals for treating diabetes mellitus in dogs and cats? 3 answers

A

Eliminate owner-observed clinical signs, prevent hypoglycemia, and minimize cataract formation

141
Q

What type of diet is recommended for diabetic dogs?

A

High fiber, low simple carbohydrate diet

142
Q

What are 2 additional clinical signs of diabetes mellitus that are specific to cats?

A

Plantigrade stance and poor haircoat

143
Q

Your feline patient you suspect has diabetes mellitus has a mild to moderate increase in BG (<270 mg/dL), no concurrent glucosuria, and the fructosamine was normal. What is your interpretation?

A

Stress hyperglycemia

144
Q

What diet is recommended for a diabetic cat?

A

High protein, low simple carbohydrate diet and restrict calories if planned weight loss secondary to obesity is needed

145
Q

What is the ability to induce diabetic remission based on? 2 answers.

A

Insulin resistance is rapidly treated or removed (if present) and/or reversal of glucotoxicity via early initiation of insulin therapy

146
Q

When does diabetic remission usually occur in the cat?

A

During the first 3-4 months of therapy

147
Q

Can dogs go into diabetic remission?

A

No - will require insulin injections for the rest of their life

148
Q

What is the name for the endocrine disease in dogs in which the adrenal gland is making excess cortisol?

A

Hyperadrenocorticism aka Cushing’s

149
Q

Which type of hyperadrenocorticism is more common: Pituitary dependent or adrenal dependent?

A

Pituitary dependent

150
Q

Describe pituitary dependent hyperadrenocorticism

A

Benign (adenoma) tumor or hyperplasia of pituitary secretes excess ACTH -> stimulates adrenal gland to make excess cortisol -> results in endogenous cortisol secretion

151
Q

Describe adrenal dependent hyperadrenocorticism

A

Benign (adenoma) or malignant (carcinoma) tumor of adrenal gland that makes excess cortisol -> excess endogenous cortisol secretion

152
Q

How do dogs get iatrogenic hyperadrenocorticism?

A

Excess exogenous cortisol administration from prescribing steroids

153
Q

What are the common clinical signs associated with hyperadrenocorticism? (Do your best)

A

PU/PD, truncal alopecia (non-pruritic), polyphagia, abdominal distension, panting, muscle wasting/weakness

154
Q

Why are Cushingoid patients PU/PD? (2 answers)

A

Excessive cortisol inhibits ADH binding to its receptor in the kidney -> water is not retained -> PU/PD;
Also inhibition of ADH release from posterior pituitary

155
Q

Why do Cushingoid patients have abdominal distension?

A

Hepatomegaly (“steroid hepatopathy”) that occurs due to glycogen accumulation in liver

156
Q

What can you expect so see on a CBC/Chem of a patient with hyperadrenocorticism?

A

CBC - stress leukogram, thrombocytosis

Chem -normal to mild hyperglycemia, increased ALP > ALT, hypercholesterolemia, hypertriglyceridemia

157
Q

What would you expect the USG to be in a patient with hyperadrenocorticism? Is there protein present, too?

A

USG <1.020; proteinuria; potentially UTI because they are more prone like diabetic patients

158
Q

What are the 3 screening tests for hyperadrenocorticism?

A
  1. Urine Cortisol:Creatinine Ratio (UC:CR)
  2. Low dose dex suppression test (LDDST)
  3. ACTH stim test
159
Q

When would you want to perform a urine cortisol:creatinine ratio in a dog?

A

If you want to rule out Cushing’s (aka when you don’t think the animal has HAC)

160
Q

You perform a urine cortisol:creatinine ratio on a dog and the test came back negative (below reference range). What is your interpretation? What if the test came back positive (above reference range)?

A

Negative - This animal does not have Cushing’s

Positive - may have Cushing’s, need to run another test

161
Q

If you perform a low dose dex suppression test in a normal animal, what would you expect their cortisol level to be?

A

Should be less than the reference interval (complete suppression)

162
Q

You perform a low dose dex suppression test in a dog you suspect has hyperadrenocorticism. The results show a 4 and 8-hour cortisol that is above the reference interval, and both numbers are increased >50% of 0-hour cortisol. What is your interpretation?

A

This animal likely has HAC; don’t know if it is pituitary dependent or a functional adrenal tumor

163
Q

What drug is administered to a patient for an ACTH stimulation test?

A

Cosyntropin

164
Q

You perform an ACTH stimulation test in an animal you suspect has Cushing’s. The 1-hour cortisol is above the reference interval. What is your interpretation?

A

This is consistent with HAC

165
Q

Are you more likely to have false positives for HAC with the LDDST or the ACTH stim test?

A

LDDST has more false positives than ACTH stim test

166
Q

If you have an animal that is very stressed in hospital but you want to run a test to confirm if he/she has Cushing’s, what test would you run to get the most accurate results? (i.e., one that is not affected by stress)?

A

ACTH stim test best;

LDDST could give you a false positive if patient is stressed in hospo

167
Q

What diagnostic can you perform to differentiate between pituitary dependent and adrenal dependent HAC?

A

Abdominal ultrasound

168
Q

What do you look for on abdominal ultrasound to differentiate pituitary dependent vs. adrenal dependent HAC?

A

Adrenal dependent -> look for adrenal tumor; other adrenal gland will be atrophied

Pituitary dependent -> both adrenals will be enlarged (no tumor on adrenal glands)

169
Q

You perform a LDDST on a dog you suspect has Cushing’s. Both the 4 and 8-hour post Dex samples are above the reference range but one or both is/are less than 50% of the 0-hour cortisol. What is your interpretation?

A

This patient likely has pituitary dependent HAC because there is some suppression of cortisol.

170
Q

What is the drug of choice for treating Cushing’s disease in dogs? What is its mechanism of action?

A

Trilostane (Vetoryl) -> suppresses cortisol production in the adrenal gland

171
Q

What is the ideal method of treatment for pituitary dependent vs. adrenal dependent HAC?

A

Pituitary dependent -> treat with Trilostane for rest of life;

Adrenal dependent -> ideally, surgery to remove tumor. But, can still use trilostane

172
Q

What is the ideal method of treatment for pituitary dependent vs. adrenal dependent HAC?

A

Pituitary dependent -> treat with Trilostane for rest of life;

Adrenal dependent -> ideally, surgery to remove tumor. But can still use trilostane

173
Q

What disease in dogs occurs as a result of a deficiency of cortisol only or of cortisol and aldosterone?

A

Hypoadrenocorticism (aka Addison’s Disease)

174
Q

Describe typical hypoadrenocorticism

A

Absence of glucocorticoids and mineralocorticoids; more common than atypical

175
Q

Describe atypical hypoadrenocorticism

A

Absence of glucocorticoids ONLY; bilateral immune mediated zona glomerulosa destruction ONLY

176
Q

Describe iatrogenic hypoadrenocorticism

A

Due to abrupt discontinuation of exogenous glucocorticoids or side effect of a drug used to treat hyperadrenocorticism (mitotane, trilostane)

177
Q

What are the common signs of typical hypoadrenocorticism?

A

PU/PD, hypovolemic shock (PU without the PD) +/- bradycardia; can also have signs of atypical hypoadrenocorticism but these predominate

178
Q

What are the common signs of atypical hypoadrenocorticism? (There’s many, do your best)

A

Vomiting, diarrhea, weight loss, hemorrhage, poor appetite, lethargy, weakness, seizures

179
Q

Why might an Addisonian be PU/PD?

A

PU/PD occurs due to osmotic diuresis secondary to chronic Na+ loss through the kidneys (lack of aldosterone)

180
Q

Why would an Addisonian patient have bradycardia?

A

Due to hyperkalemic induced effects on cardiac myocyte depolarization and repolarization

181
Q

Addisonian crisis occurs due to a lack of _____________, which leads to a loss of sodium and water, causing the patient to become hypovolemic and present with signs of shock.

A

Aldosterone

182
Q

Patients with typical Addison’s disease have a deficiency of both cortisol and aldosterone. What do you expect the sodium and potassium concentrations in the blood?

A

Hyponatremia and hyperkalemia

183
Q

What would you expect to see on a CBC in a patient with hypoadrenocorticism?

A

CBC - mild to moderate nonregenerative, normochromic and normocytic anemia, lack of stress leukogram, and normal platelets

184
Q

What changes on serum chemistry from an Addisonian patient would you expect to see that mimics renal failure? 5 answers.

A

Prerenal azotemia, hypercalcemia, hyponatremia, hyperkalemia, and mild metabolic acidosis

185
Q

What changes on serum chemistry from an Addisonian patient could you see that mimics hepatic insufficiency or protein losing enteropathy? (5 answers)

A

Hypoglycemia, hypoalbuminemia, increased liver enzymes, hypocholesterolemia, and normal sodium and potassium (could be increased if typical Addison’s due to aldosterone deficiency too)

186
Q

What would you expect the USG of a patient with hypoadrenocorticism to be?

A

Dilute urine (USG 1.008-1.020)

187
Q

A dog comes in for regurgitation and you diagnose him/her with megaesophagus. What endocrine disorder must you rule out?

A

Addison’s Disease

188
Q

You perform bloodwork on a patient and need to rule out renal failure vs. hypoadrenocorticism. You perform a baseline cortisol, and it is less than 2. What is your interpretation?

A

This likely isn’t renal failure, but it still could be HOC.

189
Q

You suspect a dog may have hypoadrenocorticism and decide to run an ACTH stim test. The results from the 1-hour cortisol is <2ug/dL. What is your interpretation?

A

This result is consistent with HOC

190
Q

A patient presents to you and you aren’t entirely sure if the patient has hypoadrenocorticism or something else. What test should you run?

A

Baseline cortisol

191
Q

A patient presents to you and HOC is your top differential based on exam findings and clinical signs. What test should you do to confirm?

A

ACTH stimulation test

192
Q

What are the treatment recommendations for patients experiencing an Addisonian crisis?

A

IV fluid therapy & electrolyte correction (if life threatening), ACTH stim test, corticosteroid replacement (often Dexamethosone), mineralocorticoid replacement (DOCP aka Percorten)

193
Q

What are the treatment recommendations for patients with stable HOC?

A

Resting cortisol -> ACTH stim test, corticosteroid replacement (Prednisone), mineralocorticoid replacement (DOCP aka Percorten injection given every 25-28 days)

E&E Exam 4 (5 decks)

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