Canine I Flashcards

1
Q

What is hypoadrenocorticism (Addisons Disease)?

A

A condition caused by inadequate production of glucocorticoids and mineralocorticoids by the adrenal glands.

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2
Q

What is the most common cause of Addisons Disease?

A

Idiopathic adrenocortical atrophy.

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3
Q

What electrolyte abnormalities are characteristic of Addisons Disease?

A

Hyponatremia

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4
Q

Why is Addisons Disease called ‘The Great Imitator’?

A

It can mimic many other diseases

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5
Q

What are the common acute clinical signs of Addisons Disease?

A

Hypovolemic shock

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6
Q

What are the common chronic clinical signs of Addisons Disease?

A

Waxing and waning illness

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7
Q

What cardiovascular abnormality is a key tip-off for Addisons?

A

Bradycardia despite cardiovascular collapse due to hyperkalemia.

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8
Q

What urine-specific gravity is typical in Addisonian dogs?

A

USG <1.030 due to lack of aldosterone.

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9
Q

What CBC finding is often absent in Addisons Disease?

A

Stress leukogram (which normally includes neutrophilia

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10
Q

What is the diagnostic test of choice for Addisons Disease?

A

ACTH stimulation test.

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11
Q

What result confirms Addisons Disease on an ACTH stimulation test?

A

Baseline and post-ACTH cortisol levels <2 ug/dL.

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12
Q

Which steroid does not interfere with ACTH testing?

A

Dexamethasone.

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13
Q

What ECG abnormalities are seen in Addisons Disease?

A

Tall tented T waves

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14
Q

What radiographic findings might suggest Addisons Disease?

A

Microcardia

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15
Q

What is the first step in treating an Addisonian crisis?

A

Rapid IV fluid therapy with 0.9% NaCl.

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16
Q

How does IV fluid therapy help in Addisons crisis?

A

Restores perfusion

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17
Q

What drug is used for cardioprotection in severe hyperkalemia?

A

Calcium gluconate.

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18
Q

Which drugs can shift potassium intracellularly in hyperkalemia?

A

Dextrose

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19
Q

What glucocorticoid is preferred in acute Addisons treatment?

A

Dexamethasone SP (does not interfere with ACTH testing).

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20
Q

What is the main glucocorticoid used for long-term Addisons management?

A

Prednisone or prednisolone.

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21
Q

What is the initial dose of prednisone in Addisons treatment?

A

0.5 mg/kg/day

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22
Q

What adjustment should be made to prednisone during times of stress?

A

Increase to 2-4 times the maintenance dose.

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23
Q

What are the two main mineralocorticoid replacement therapies?

A

Fludrocortisone (daily oral) and DOCP (injectable every 3-4 weeks).

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24
Q

What are the four major types of allergic skin diseases in dogs and cats?

A

Flea allergy dermatitis (FAD)

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25
Q

What is the predominant clinical sign of allergic skin disease?

A

Pruritus (itching).

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26
Q

How can you distinguish between food allergies and atopy based on clinical signs alone?

A

You cannot; their lesion distribution is identical.

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27
Q

Which type of allergy typically occurs in dogs under 1 year of age and in older dogs?

A

Food allergy.

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28
Q

At what age does atopic dermatitis typically present?

A

Between 1-3 years of age (full range: 6 months to 6 years).

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29
Q

Which allergic condition has no specific age predilection?

A

Contact allergy and flea allergy dermatitis (FAD).

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30
Q

Which allergies can be seasonal or non-seasonal depending on the allergen?

A

Atopy

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31
Q

Which type of allergy is exclusively non-seasonal?

A

Food allergy.

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32
Q

Which allergic condition typically has a rapid onset

A

often in warm weather?

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33
Q

Which allergic condition often has a gradual onset but may occasionally present suddenly?

A

Food allergy.

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34
Q

Which allergic condition typically affects the caudal half of the body

A

including the tail base

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35
Q

Which two allergic conditions have an identical lesion distribution (face

A

paws

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36
Q

Which allergic condition primarily affects hairless areas in contact with environmental allergens?

A

Contact allergy.

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37
Q

What type of primary lesion should be present in contact allergy?

A

Vesicles and erythematous papules.

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38
Q

What are the two primary reaction patterns of allergic skin disease in cats?

A

Miliary dermatitis and eosinophilic granuloma complex.

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39
Q

What are the three presentations of eosinophilic granuloma complex in cats?

A

Indolent ulcer (upper lip)

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40
Q

What are three possible distributions of flea allergy dermatitis in cats?

A

Caudal dorsal

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41
Q

How is flea allergy dermatitis (FAD) diagnosed?

A

Based on lesion distribution

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42
Q

Why is atopy diagnosed by exclusion?

A

Because intradermal and serum allergy testing cannot confirm a diagnosis; they are used for immunotherapy development.

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43
Q

What is the gold standard test for diagnosing food allergy?

A

An 8-12 week strict elimination diet trial using a hydrolyzed or novel protein diet.

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44
Q

Why are serum tests not recommended for diagnosing food allergies?

A

They are not accurate.

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45
Q

What test is used to diagnose contact allergy?

A

Patch testing.

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46
Q

What is the proper stepwise approach to diagnosing pruritus in dogs and cats?

A
  1. Rule out infectious causes (sarcoptes
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47
Q

What are the four main anti-pruritic drugs used in veterinary dermatology?

A

Apoquel (oclacitinib)

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48
Q

Why are anti-pruritic medications considered ‘Band-Aids’ in veterinary dermatology?

A

They provide relief from pruritus but do not cure the underlying cause.

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49
Q

What is the key cytokine responsible for pruritus in allergic dogs?

A

IL-31.

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50
Q

Which signaling pathway is activated by IL-31

A

leading to pruritus?

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51
Q

Which two anti-pruritic drugs act on the JAK/STAT pathway

A

but at different points?

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52
Q

How does Apoquel work?

A

Apoquel is a JAK inhibitor that preferentially targets JAK1

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53
Q

How does Cytopoint work?

A

Cytopoint is a monoclonal antibody that binds to IL-31

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54
Q

What is the mechanism of action of cyclosporin (Atopica)?

A

Cyclosporin is a calcineurin inhibitor that suppresses IL-2

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55
Q

How does prednisone reduce pruritus and inflammation?

A

Prednisone inhibits pro-inflammatory molecules and upregulates anti-inflammatory mediators like lipocortin-1.

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56
Q

How is Apoquel administered?

A

Orally

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57
Q

How is Cytopoint administered?

A

Subcutaneous injection given every 4-8 weeks.

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58
Q

How is cyclosporin administered?

A

Orally

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59
Q

How is prednisone administered?

A

Orally

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60
Q

Which three anti-pruritic drugs have a rapid onset of action (within 24 hours)?

A

Prednisone

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61
Q

Which anti-pruritic drug takes the longest to reduce pruritus?

A

Cyclosporin (4 weeks in dogs

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62
Q

Which anti-pruritic medication is the cheapest?

A

Prednisone.

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63
Q

Which two medications are moderately priced?

A

Apoquel and Cytopoint.

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64
Q

Which anti-pruritic drug is the most expensive

A

especially in large dogs?

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65
Q

What is a potential side effect of Apoquel related to immunosuppression?

A

Increased susceptibility to Demodex and other infections

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66
Q

Why should Apoquel not be given to dogs under one year of age?

A

Severe infections (e.g.

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67
Q

What are the common side effects of Cytopoint?

A

GI upset similar to the placebo group; appears to be well-tolerated with no observed hypersensitivity reactions.

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68
Q

What are some unique side effects of cyclosporin?

A

GI upset

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69
Q

How does cyclosporin affect diabetic patients?

A

It decreases pancreatic β-cell function

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70
Q

Why should cyclosporin not be used with ivermectin?

A

It inhibits P-glycoprotein

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71
Q

How can ketoconazole be used to reduce the cost of cyclosporin therapy?

A

Ketoconazole inhibits cytochrome P450

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72
Q

What are the most common side effects of prednisone?

A

PU/PD

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73
Q

Why should prednisone not be used with NSAIDs?

A

It increases the risk of GI ulceration and renal failure.

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74
Q

Is Apoquel recommended for use in cats?

A

No

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75
Q

Why should Cytopoint not be used in cats?

A

Cytopoint is a caninized monoclonal antibody

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76
Q

Which anti-pruritic drugs are commonly used in cats?

A

Cyclosporin and prednisolone (not prednisone

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77
Q

What is brachycephalic syndrome and what causes it?

A

A condition resulting from breeding short-faced (brachycephalic) dogs

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78
Q

Which three congenital abnormalities are characteristic of brachycephalic syndrome?

A

Elongated soft palate

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79
Q

Which two cat breeds are most commonly affected by brachycephalic syndrome?

A

Himalayans and Persians.

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80
Q

What is an elongated soft palate

A

and how does it contribute to airway obstruction?

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81
Q

What are stenotic nares

A

and how do they affect breathing?

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82
Q

What is a hypoplastic trachea

A

and which breed is most commonly affected?

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83
Q

What are some acquired components of brachycephalic syndrome due to increased airway resistance?

A

Everted laryngeal saccules

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84
Q

Which dog breeds are commonly affected by brachycephalic syndrome?

A

Bulldogs

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85
Q

What are the common clinical signs of brachycephalic syndrome?

A

Exercise intolerance

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86
Q

How is brachycephalic syndrome diagnosed?

A

Physical exam

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87
Q

What imaging modality can be used to evaluate a hypoplastic trachea?

A

Thoracic radiographs.

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88
Q

Why should an oral exam be performed under anesthesia when diagnosing brachycephalic syndrome?

A

To properly assess elongated soft palate

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89
Q

What is the surgical treatment for an elongated soft palate?

A

Resection to normal size

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90
Q

What is the treatment for stenotic nares?

A

Wedge resection of the nasal fold.

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91
Q

What is the treatment for hypoplastic trachea?

A

There is no effective treatment; management focuses on treating other abnormalities to improve breathing.

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92
Q

Why is accurate diagnosis essential before treating laryngeal collapse?

A

It should be distinguished from laryngeal paralysis

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93
Q

What is the best treatment option for advanced laryngeal collapse?

A

Permanent tracheostomy.

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94
Q

How are everted laryngeal saccules treated?

A

Removal using traction with hemostats or Allis tissue forceps.

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95
Q

What is a major post-operative risk following surgery for elongated soft palate?

A

Life-threatening airway obstruction due to excessive swelling.

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96
Q

What is dilated cardiomyopathy (DCM)?

A

A primary myocardial disease characterized by cardiac enlargement and impaired systolic function.

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97
Q

Which breeds are predisposed to DCM?

A

Doberman

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98
Q

What are the early clinical signs of DCM?

A

Fainting

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99
Q

Why can DCM be difficult to diagnose early?

A

Many dogs are asymptomatic until they suddenly develop symptoms of heart failure.

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100
Q

What are the signs of left-sided congestive heart failure (CHF) in DCM?

A

Respiratory distress.

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101
Q

What is collapsing trachea?

A

A condition where the tracheal rings weaken

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102
Q

Can collapsing trachea be a primary condition or secondary to another disease?

A

It can be primary or secondary to cardiopulmonary disorders such as heart failure or chronic bronchitis.

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103
Q

What are the two types of collapsing trachea?

A

Fixed or dynamic.

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104
Q

Which dog breeds are most commonly affected by collapsing trachea?

A

Small breeds

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105
Q

At what age do clinical signs of collapsing trachea typically appear?

A

Around 7 years of age.

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106
Q

What are the early clinical signs of collapsing trachea?

A

Mild productive cough and exercise intolerance.

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107
Q

What are the advanced clinical signs of collapsing trachea?

A

Honking cough

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108
Q

What triggers dyspnea in dogs with collapsing trachea?

A

Excitement or anxiety.

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109
Q

What common physical characteristic is seen in many dogs with collapsing trachea?

A

Obesity.

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110
Q

What structural abnormalities contribute to collapsing trachea?

A

Weak or redundant dorsal tracheal membrane and hypoplastic or fibrodystrophic cartilaginous rings.

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111
Q

When does extrathoracic (cervical) tracheal collapse occur?

A

On inspiration.

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112
Q

When does intrathoracic tracheal collapse occur?

A

On expiration.

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113
Q

What clinical test can be performed during a physical exam to suggest collapsing trachea?

A

Tracheal palpation

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114
Q

What radiographic finding is associated with collapsing trachea?

A

Flattened trachea.

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115
Q

What is the most useful diagnostic test for evaluating collapsing trachea in an awake patient?

A

Fluoroscopy in lateral recumbency.

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116
Q

What advanced diagnostic test allows visualization of collapsing bronchi?

A

Endoscopy.

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117
Q

Why is it important to first identify and treat primary upper respiratory conditions before addressing collapsing trachea?

A

Treating conditions such as stenotic nares

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118
Q

What concurrent disease should be ruled out before treating collapsing trachea?

A

Cardiac disease.

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119
Q

Why is surgery less successful if bronchial collapse is present?

A

Surgical treatment is less effective in these cases

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120
Q

What are three main components of medical management for collapsing trachea?

A

Weight loss

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121
Q

What is dorsal tracheal membrane plication

A

and when is it used?

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122
Q

Why is dorsal tracheal membrane plication not commonly performed?

A

Most mild cases are managed medically.

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123
Q

What are the potential complications of intratracheal stenting for collapsing trachea?

A

Stent fracture

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124
Q

What is the success rate of intratracheal stenting when performed correctly?

A

Up to 80%.

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125
Q

What materials have been attempted for external tracheal support?

A

Plastic rings

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126
Q

Why is external tracheal support not commonly used?

A

Results have been inconsistent.

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127
Q

Why is medical management preferred over surgical intervention for collapsing trachea?

A

Surgical interventions have a high risk of complications

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128
Q

What are the signs of right-sided CHF in DCM?

A

Abdominal distension due to ascites.

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129
Q

What is the gold standard diagnostic test for DCM?

A

Echocardiography.

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130
Q

What echocardiographic findings are characteristic of DCM?

A

Systolic dysfunction (poor contractility and shortening fraction).

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131
Q

What is a controversial treatment recommendation for subclinical DCM?

A

Some cardiologists recommend ACE inhibitors and/or pimobendan for early-stage cardiac dilation.

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132
Q

What are the treatment options for ventricular tachycardia in dogs with DCM?

A

Sotalol

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133
Q

What is another name for familial arrhythmogenic cardiomyopathy (ARVC)?

A

Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC).

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134
Q

Which breed is primarily affected by ARVC?

A

Boxers.

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135
Q

What is the primary clinical sign of ARVC?

A

Syncope.

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136
Q

What causes sudden death in dogs with severe ARVC?

A

Ventricular premature complexes (VPCs) leading to fatal arrhythmias.

137
Q

How is ARVC diagnosed?

A

24-hour Holter monitor to assess the frequency of VPCs.

138
Q

Why is a 24-hour Holter monitor recommended over a brief ECG in diagnosing ARVC?

A

A brief ECG may overestimate or underestimate the frequency of VPCs due to their intermittent nature.

139
Q

What are the three levels of severity in ARVC?

A

1) Asymptomatic dogs with VPCs

140
Q

How many VPCs in 24 hours warrant treatment for ARVC?

A

More than 1000 VPCs per 24 hours

141
Q

What are the two main treatment options for symptomatic ARVC (syncope)?

A

Sotalol or a combination of mexiletine and atenolol.

142
Q

How should ARVC dogs with systolic dysfunction and heart failure be treated?

A

As dogs with DCM.

143
Q

What nutritional supplement is sometimes recommended for ARVC?

A

L-carnitine.

144
Q

What is the function of the cranial cruciate ligament (CCL)?

A

Prevents cranial drawer

145
Q

Where does the cranial cruciate ligament originate?

A

Medial surface of the lateral femoral condyle.

146
Q

Where does the cranial cruciate ligament insert?

A

Craniomedial surface of the tibial plateau beneath the intermeniscal ligament.

147
Q

Which dog breeds are predisposed to cranial cruciate ligament disease?

148
Q

What are the typical clinical signs of CCL rupture?

A

Acute or chronic lameness that does not improve with rest and may improve mildly with NSAIDs.

149
Q

What is the ‘positive sit test’ for CCL rupture?

A

The dog sits with the knee rotated outward.

150
Q

What are the two primary orthopedic tests for diagnosing CCL rupture?

A

Cranial drawer test and tibial thrust test (tibial compression test).

151
Q

What is a medial buttress

A

and why is it significant in CCL rupture?

152
Q

What radiographic findings support a diagnosis of CCL rupture?

A

Joint effusion

153
Q

What is the lateral suture (extracapsular) repair technique for CCL rupture?

A

A heavy suture is placed around the fabella and through the tibia to mimic the CCL.

154
Q

What is a limitation of extracapsular repair for CCL rupture?

A

The suture may stretch

155
Q

What is the tibial plateau leveling osteotomy (TPLO) procedure?

A

An osteotomy is performed at the proximal tibia

156
Q

Why does TPLO not restore the cranial cruciate ligament?

A

It biomechanically stabilizes the leg without directly repairing the ligament.

157
Q

What is the tibial tuberosity advancement (TTA) procedure?

A

A cut is made along the cranial tibia

158
Q

Which surgical procedure is considered the ‘gold standard’ for CCL repair?

159
Q

Does any CCL repair completely prevent osteoarthritis?

160
Q

Can strict cage rest be used instead of surgery for CCL rupture?

161
Q

What is a major disadvantage of conservative management (cage rest) for CCL rupture?

A

Progression of arthritis is likely greater compared to surgical repair.

162
Q

What is hyperadrenocorticism (Cushing’s Disease)?

A

A condition caused by excessive cortisol production due to pituitary or adrenal tumors.

163
Q

What are the two most common causes of Cushing’s Disease?

A

Pituitary-dependent hyperadrenocorticism (PDH) and adrenal tumors (AT).

164
Q

What is the most common form of Cushing’s Disease?

A

Pituitary-dependent hyperadrenocorticism (PDH)

165
Q

What is iatrogenic Cushing’s Disease?

A

Hyperadrenocorticism caused by prolonged steroid administration.

166
Q

What are the key clinical signs of Cushing’s Disease in dogs?

167
Q

What is the hallmark clinical sign of equine Cushing’s Disease?

A

Hirsutism (abnormally long

168
Q

Why does Cushing’s cause a pendulous abdomen?

A

Due to muscle wasting and hepatomegaly.

169
Q

What bloodwork abnormalities are commonly seen with Cushing’s Disease?

A

Stress leukogram (neutrophilia

170
Q

What is the most commonly used diagnostic test for Cushing’s Disease?

A

Low-dose dexamethasone suppression test (LDDST).

171
Q

How does the LDDST diagnose Cushing’s Disease?

A

Plasma cortisol is measured before and at 4 and 8 hours after IV dexamethasone; most dogs with Cushing’s have 8-hour cortisol levels >1.4 µg/dL.

172
Q

How can the LDDST differentiate between PDH and AT?

A

Dogs with PDH often show some suppression at 4 hours (<50% of baseline)

173
Q

What is the ACTH stimulation test used for?

A

Diagnosing Cushing’s and monitoring therapy effectiveness.

174
Q

What is the expected result of an ACTH stimulation test in a Cushing’s dog?

A

Exaggerated cortisol response after ACTH administration.

175
Q

Why is abdominal ultrasound useful for diagnosing Cushing’s Disease?

A

It helps differentiate PDH (bilaterally enlarged adrenal glands) from AT (unilateral adrenal mass).

176
Q

What is the Urine Cortisol:Creatinine Ratio used for?

A

It has high sensitivity but low specificity; a negative result rules out Cushing’s.

177
Q

What is the role of endogenous ACTH testing?

A

Differentiating PDH (high plasma ACTH) from AT (low ACTH).

178
Q

What is the high-dose dexamethasone suppression test used for?

A

To differentiate PDH from AT in additional cases not diagnosed by LDDST.

179
Q

What is atypical Cushing’s Disease?

A

A form where dogs have normal LDDST results but abnormal 17-hydroxyprogesterone levels.

180
Q

What is the treatment of choice for PDH?

A

Medical management with Mitotane (o

181
Q

How does Mitotane treat Cushing’s?

A

It causes adrenocorticolysis (partial chemical adrenalectomy).

182
Q

What monitoring is required with Mitotane treatment?

A

ACTH stimulation tests to avoid hypoadrenocorticism.

183
Q

How does Trilostane work?

A

It is an oral steroid analogue that inhibits cortisol and aldosterone synthesis.

184
Q

What are alternative treatments for Cushing’s Disease?

A

Selegiline (not recommended) and Ketoconazole (associated with side effects).

185
Q

What surgical options exist for Cushing’s?

A

Adrenalectomy for adrenal tumors and hypophysectomy for pituitary tumors (rarely performed in North America).

186
Q

What is the treatment of choice for equine Cushing’s Disease?

A

Pergolide mesylate

187
Q

What is diabetes mellitus?

A

An endocrine disorder caused by inadequate insulin production or peripheral insulin resistance.

188
Q

What are the two primary presentations of diabetes mellitus?

A

Healthy diabetic and severe diabetic ketoacidosis (DKA).

189
Q

What are the key clinical signs of diabetes mellitus?

190
Q

What are less common clinical signs that may suggest diabetes?

A

Plantigrade stance in cats (diabetic neuropathy) and cataracts in dogs.

191
Q

What are the clinical signs of severe DKA?

192
Q

How is diabetes mellitus diagnosed?

A

Based on clinical signs

193
Q

Why is stress hyperglycemia a concern when diagnosing diabetes in cats?

A

Stress can cause transient hyperglycemia and sometimes glucosuria

194
Q

What additional bloodwork abnormalities are common in diabetic patients?

A

Metabolic acidosis

195
Q

What are the ancillary tests used to evaluate long-term glycemic control?

A

Fructosamine and glycosylated hemoglobin.

196
Q

What is the primary treatment for healthy diabetic animals?

A

Insulin injections

197
Q

Which species require insulin therapy for diabetes?

A

All dogs and 90% of cats.

198
Q

What are examples of intermediate and long-acting insulins used for diabetes management?

199
Q

Why are blood glucose curves important in insulin therapy?

A

To ensure proper insulin potency and duration while avoiding the Somogyi effect.

200
Q

What oral hypoglycemic drug is most commonly used in veterinary medicine?

A

Glipizide (Glucotrol).

201
Q

Why is the efficacy of oral hypoglycemics in veterinary patients controversial?

A

They may reduce insulin requirements but are not consistently effective.

202
Q

What type of diet is recommended for diabetic dogs?

A

High-fiber

203
Q

What type of diet is recommended for diabetic cats?

A

High-protein

204
Q

What is the primary treatment for severe DKA?

A

Aggressive IV fluid therapy and insulin administration.

205
Q

Which type of insulin is used for treating severe DKA?

A

Regular insulin (fast-acting)

206
Q

Why is frequent blood glucose monitoring necessary in DKA treatment?

A

To achieve gradual reduction in blood glucose and prevent complications.

207
Q

When is bicarbonate therapy indicated in DKA patients?

A

If metabolic acidosis is severe and not improving with IV fluids.

208
Q

Why is it important to identify and treat concurrent infections in diabetic patients?

A

Infections can worsen insulin resistance and lead to diabetic ketoacidosis.

209
Q

What is elbow dysplasia?

A

An umbrella term for multiple congenital abnormalities affecting the elbow.

210
Q

What are the four conditions included in elbow dysplasia?

A

Ununited anconeal process (UAP)

211
Q

Which dog breeds are commonly affected by elbow dysplasia?

A

German Shepherds

212
Q

What are the key clinical signs of elbow dysplasia?

A

Forelimb lameness

213
Q

What radiographic sign suggests fragmentation of the medial coronoid process (FCP)?

A

Sclerosis of the ulna and degenerative changes above the anconeal process.

214
Q

What is the typical age of onset for ununited anconeal process (UAP)?

A

4-12 months of age.

215
Q

What is the best radiographic view to diagnose UAP?

A

Flexed lateral projection of the elbow.

216
Q

What is the primary surgical treatment for UAP?

A

Excision of the anconeal process.

217
Q

What causes osteochondrosis dissecans (OCD) of the humeral condyle?

A

Abnormal endochondral ossification leading to thickened cartilage and flap formation.

218
Q

What is the most common radiographic finding in OCD of the elbow?

A

Lesion on the medial aspect of the humeral trochlea with visible flattening and subchondral bone defect.

219
Q

What is the preferred treatment for OCD of the humeral condyle?

A

Arthroscopic surgical removal of the flap and debridement of subchondral bone.

220
Q

What is the most common breed affected by fragmented medial coronoid process (FCP)?

A

Labrador Retrievers.

221
Q

Why is FCP difficult to diagnose radiographically?

A

The fragment is often not visible

222
Q

What imaging modality is preferred for diagnosing FCP?

A

CT or arthroscopy.

223
Q

What is the treatment of choice for FCP?

A

Arthroscopic removal of the fragment.

224
Q

What is elbow incongruity?

A

A mismatch in joint surface alignment

225
Q

Why is elbow incongruity difficult to diagnose on radiographs?

A

It is highly dependent on positioning and can be subjective.

226
Q

What imaging modality is more accurate for diagnosing elbow incongruity?

227
Q

What surgical procedure may be attempted to correct elbow incongruity?

A

Ulnar osteotomy

228
Q

How many cranial nerves are there?

229
Q

What is the function of CN I (Olfactory Nerve)?

A

Mediates the sense of smell.

230
Q

How is CN I tested?

A

By observing the patient sniff around.

231
Q

What is the function of CN II (Optic Nerve)?

A

Carries visual signals from the retina to the occipital lobe of the brain.

232
Q

How is CN II tested?

A

Menace response

233
Q

What is the function of CN III (Oculomotor Nerve)?

A

Motor to extraocular muscles (dorsal

234
Q

How is CN III tested?

A

Observing for physiologic nystagmus when turning head and pupillary light reflex (PLR).

235
Q

What is the function of CN IV (Trochlear Nerve)?

A

Motor to dorsal oblique extraocular muscle

236
Q

How is CN IV tested?

A

Observing for dorsolateral rotation of the pupil.

237
Q

What is the function of CN V (Trigeminal Nerve)?

A

Motor to mastication muscles; sensory to eyelids

238
Q

How is CN V tested?

A

Palpating masticatory muscles

239
Q

What is the function of CN VI (Abducens Nerve)?

A

Motor to lateral rectus and retractor bulbi muscles.

240
Q

How is CN VI tested?

A

Corneal retraction

241
Q

What is the function of CN VII (Facial Nerve)?

A

Motor to facial expression muscles

242
Q

How is CN VII tested?

A

Menace response

243
Q

What is the function of CN VIII (Vestibulocochlear Nerve)?

A

Sensory for hearing and head position.

244
Q

How is CN VIII tested?

A

Hearing assessment

245
Q

What is the function of CN IX (Glossopharyngeal Nerve)?

A

Motor and sensory to the pharynx for swallowing

246
Q

How is CN IX tested?

A

Gag reflex and observing for dysphagia.

247
Q

What is the function of CN X (Vagus Nerve)?

A

Innervates larynx

248
Q

How is CN X tested?

A

Gag reflex

249
Q

What is the function of CN XI (Spinal Accessory Nerve)?

A

Innervates cranial cervical muscles.

250
Q

How is CN XI tested?

A

Rarely assessed and rarely a clinical problem.

251
Q

What is the function of CN XII (Hypoglossal Nerve)?

A

Motor to the tongue.

252
Q

How is CN XII tested?

A

Observing tongue movement

253
Q

What are two common disorders affecting cranial nerves?

A

Idiopathic trigeminal neuritis and idiopathic facial nerve paralysis.

254
Q

What are key signs of idiopathic trigeminal neuritis?

A

Peracute onset of dropped jaw

255
Q

How is idiopathic trigeminal neuritis treated?

A

Supportive care

256
Q

What are key signs of idiopathic facial nerve paralysis?

A

Acute onset of inability to blink

257
Q

What are differentials for idiopathic facial nerve paralysis?

A

Otitis media

258
Q

What is the treatment for idiopathic facial nerve paralysis?

A

Tear supplementation

259
Q

What is the prognosis for idiopathic facial nerve paralysis?

A

Fair; complete recovery is rare

260
Q

What are some mnemonic aids for remembering cranial nerves?

A

See Wikipedia for a list of over 20 mnemonics for cranial nerves.

261
Q

What other disorders can affect cranial nerves?

A

Focal or multifocal central nervous system lesions of any etiology.

262
Q

What are the primary systemic fungal diseases in veterinary medicine?

A

Histoplasmosis

263
Q

What organism causes histoplasmosis?

A

Histoplasma capsulatum.

264
Q

Which regions are endemic for histoplasmosis?

A

Ohio River Valley and East of Mississippi River.

265
Q

How is histoplasmosis transmitted?

A

Inhalation of fungal spores from decaying vegetation

266
Q

What are the common clinical signs of histoplasmosis?

267
Q

What is the preferred diagnostic method for histoplasmosis?

A

Urinary antigen test or cytology of cutaneous lesions.

268
Q

What is the primary treatment for histoplasmosis?

A

Itraconazole for 2-3 months (continued 1-2 months post clinical signs).

269
Q

What organism causes blastomycosis?

A

Blastomyces dermatitidis.

270
Q

Which species is more susceptible to blastomycosis?

271
Q

What is the primary mode of blastomycosis transmission?

A

Inhalation of spores from pigeon feces and soil in the Pacific Northwest.

272
Q

What are the clinical signs of blastomycosis?

273
Q

What is a characteristic nasal presentation in cats with blastomycosis?

A

Roman nose appearance (nasal bridge swelling).

274
Q

What is the best diagnostic method for blastomycosis?

A

Cytology: Round

275
Q

What is the primary treatment for blastomycosis?

A

Amphotericin B +/- fluconazole for 3-5 months to a year.

276
Q

What organisms cause cryptococcosis?

A

Cryptococcus neoformans and Cryptococcus gattii.

277
Q

Which regions are endemic for cryptococcosis?

A

Southwestern U.S. after heavy rainfall

278
Q

What are the common clinical signs of cryptococcosis?

279
Q

What is the preferred diagnostic method for cryptococcosis?

A

Cytology: Spherules with double walls and endospores.

280
Q

What are the treatment options for cryptococcosis?

A

Ketoconazole or Itraconazole for at least 3 months; Amphotericin B for refractory cases.

281
Q

What organism causes Valley Fever?

A

Coccidioides immitis.

282
Q

What region is endemic for Valley Fever?

A

Southwestern U.S. (Arizona

283
Q

How is Valley Fever transmitted?

A

Inhalation of fungal spores from soil

284
Q

What are the clinical signs of Valley Fever?

A

Respiratory distress

285
Q

What is the best diagnostic method for Valley Fever?

A

Serology and cytology of draining tracts.

286
Q

What is the primary treatment for Valley Fever?

A

Fluconazole or Itraconazole for 6-12 months.

287
Q

What organism causes heartworm disease?

A

Dirofilaria immitis.

288
Q

How is heartworm transmitted?

A

By mosquito bites

289
Q

Where do adult heartworms reside in the host?

A

Pulmonary artery and right ventricle.

290
Q

How long can adult heartworms live?

A

Several years.

291
Q

What bacterial symbiont has been identified in heartworms?

A

Wolbachia.

292
Q

What are the primary clinical signs of heartworm disease in dogs?

A

Exercise intolerance

293
Q

What are the acute clinical signs of heartworm disease in cats?

A

Salivation

294
Q

What is HARD in feline heartworm disease?

A

Heartworm Associated Respiratory Disease

295
Q

What are chronic clinical signs of heartworm in cats?

296
Q

What is the preferred diagnostic test for heartworm disease in dogs?

A

Heartworm antigen test detecting adult female worms.

297
Q

What test can detect microfilaria but is less sensitive than the antigen test?

A

Modified Knott’s test.

298
Q

What are common thoracic radiographic findings in canine heartworm disease?

A

Right-sided cardiac enlargement (‘reverse D’ shape) and enlarged pulmonary arteries.

299
Q

What additional lab findings are seen in canine heartworm disease?

A

Proteinuria and eosinophilia.

300
Q

Why can feline heartworm antigen tests yield false negatives?

A

Low worm burden or all-male infections.

301
Q

What test indicates exposure but not necessarily infection in cats?

A

Heartworm antibody test.

302
Q

What imaging modality can confirm heartworms in cats?

A

Thoracic radiographs and echocardiography.

303
Q

What is the echocardiographic appearance of heartworms?

A

Double-lined echodensity in the heart.

304
Q

What is the treatment of choice for heartworm disease in dogs?

A

Melarsomine.

305
Q

What is the current recommended melarsomine treatment protocol?

A

A single injection followed by two injections 24 hours apart after 1 month.

306
Q

Why is strict confinement important during heartworm treatment?

A

To reduce the risk of thromboembolic disease.

307
Q

What antibiotic is used to target Wolbachia bacteria in heartworms?

A

Doxycycline (or azithromycin

308
Q

Why is the ‘slow-kill’ method using monthly preventatives not recommended?

A

It allows adult worms to persist

309
Q

Why is melarsomine not used to treat heartworm in cats?

A

Cats do not tolerate melarsomine well.

310
Q

What is the primary treatment approach for feline heartworm disease?

A

Symptomatic management with corticosteroids

311
Q

What are the available oral heartworm preventatives?

A

Ivermectin (Heartgard) and Milbemycin (Sentinel).

312
Q

What are the available topical heartworm preventatives?

A

Selamectin (Revolution) and Moxidectin/Imidacloprid (Advantage Multi).

313
Q

What is the general recommendation for heartworm prevention?

A

Monthly administration of preventatives year-round.

314
Q

What is heat stroke?

A

A life-threatening emergency caused by excessive heat load overwhelming the body’s ability to dissipate heat.

315
Q

Which dog breeds are predisposed to heat stroke?

A

Obese and brachycephalic breeds.

316
Q

What is the primary method of heat dissipation in dogs?

317
Q

How can heat stroke be differentiated from a true fever?

A

True fever is caused by pyrogens

318
Q

What are the key clinical signs of heat stroke?

319
Q

What organ systems can be affected by heat stroke?

A

Cardiovascular

320
Q

What is the critical temperature threshold for heat stroke complications?

A

Approximately 106°F.

321
Q

What environmental conditions increase the risk of heat stroke?

A

High temperatures

322
Q

What is the primary goal of emergency heat stroke treatment?

A

Normalizing body temperature while addressing cardiovascular compromise

323
Q

What are the recommended cooling methods for heat stroke?

A

Soaking fur with tepid water

324
Q

Why should cooling efforts be stopped at 103°F?

A

To avoid peripheral vasoconstriction and rebound hypothermia.

325
Q

Which controversial cooling methods should be used cautiously?

A

Ice packs to the groin/axilla

326
Q

What are the ABCs of emergency treatment for heat stroke?

327
Q

What is the importance of securing an airway in heat stroke cases?

A

Ensures adequate breathing and heat dissipation via panting.

328
Q

Why is oxygen supplementation beneficial in heat stroke treatment?

A

It reduces the work of breathing but should not interfere with panting.

329
Q

What cardiovascular interventions are used in heat stroke patients?

A

Rapid IV crystalloid or colloid administration

330
Q

How should neurologic complications from heat stroke be managed?

A

Monitor for hypoglycemia

331
Q

What coagulation abnormalities should be monitored in heat stroke cases?

332
Q

What renal parameters should be monitored in heat stroke patients?

A

Electrolytes

333
Q

How can acute renal failure be treated in heat stroke patients?

334
Q

Why is urine alkalinization recommended in some heat stroke cases?

A

To prevent myoglobin precipitation in the kidneys in cases of rhabdomyolysis.

335
Q

What gastrointestinal complications are common with heat stroke?

336
Q

How should GI complications be managed in heat stroke patients?

A

IV fluid replacement

337
Q

What is the prognosis for heat stroke?

A

Guarded; 25-50% of patients may not survive due to complications such as DIC

338
Q

What is the key factor for survival in heat stroke cases?

A

Aggressive treatment within the first 24 hours significantly improves prognosis.