Equine I Flashcards

1
Q

What is the function of platelets in hemostasis?

A

They form a platelet plug within about 5 minutes after vascular injury.

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2
Q

What are the three primary reactions of platelets after endothelial disruption?

A

Adhesion and shape change

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3
Q

What factor is necessary for platelet adhesion to the subendothelium?

A

Von Willebrand factor (vWF).

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4
Q

What is the final product of the coagulation cascade?

A

A cross-linked fibrin clot that stabilizes the platelet plug.

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5
Q

How does thrombin regulate clot formation?

A

Thrombin is absorbed into fibrin fibers and inactivated by anti-thrombin to prevent excessive clotting.

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6
Q

How does heparin work as an anticoagulant?

A

It binds to anti-thrombin and enhances its ability to prevent clot formation.

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7
Q

What are key clinical signs of platelet dysfunction?

A

Petechiae

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8
Q

What is the key test for primary hemostasis?

A

Platelet count and buccal mucosal bleeding time (BMBT).

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9
Q

At what platelet count do spontaneous bleeds typically occur?

A

Less than 30

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10
Q

What is the normal buccal mucosal bleeding time (BMBT)?

A

Less than 4 minutes.

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11
Q

What test is used to evaluate the intrinsic and common pathways?

A

Activated Clotting Time (ACT) and Activated Partial Thromboplastin Time (PTT).

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12
Q

What is the normal ACT range?

A

60-90 seconds.

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13
Q

Which clotting factors does ACT assess?

A

Prekallikrein

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14
Q

Which test is more sensitive for intrinsic pathway evaluation: ACT or PTT?

A

PTT is more sensitive than ACT.

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15
Q

What test is used to evaluate the extrinsic and common pathway?

A

Prothrombin Time (PT).

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16
Q

Which clotting factors does PT assess?

A

Factors X

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17
Q

What is the most common platelet disorder in Doberman Pinschers?

A

Von Willebrand’s Disease.

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18
Q

What is the inheritance pattern of Von Willebrand’s Disease in Dobermans?

A

Autosomal dominant with variable penetrance.

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19
Q

How is Von Willebrand’s Disease treated before surgery?

A

DDAVP (Desmopressin) 1μg/kg given 30 minutes before induction

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20
Q

What clotting factor is deficient in Hemophilia A?

A

Factor VIII.

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21
Q

What clotting factor is deficient in Hemophilia B?

A

Factor IX.

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22
Q

Which coagulation tests are elevated in Hemophilia A and B?

A

ACT and PTT.

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23
Q

What clotting disorder results from rodenticide toxicity?

A

Vitamin K deficiency.

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24
Q

Which clotting factors are affected by Vitamin K deficiency?

A

Factors II

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25
Q

Which coagulation tests are elevated in Vitamin K deficiency?

A

PT and PTT.

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26
Q

What is the half-life of Factor VII

A

making it an early indicator of Vitamin K deficiency?

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27
Q

How long does it take for clinical bleeding to develop in Vitamin K deficiency?

A

1-2 days.

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28
Q

What is the treatment for rodenticide toxicity?

A

Vitamin K1 for approximately 4 weeks.

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29
Q

Why should clotting times be rechecked after Vitamin K1 therapy?

A

To ensure the rodenticide has been completely eliminated.

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30
Q

What is the mnemonic for the common coagulation pathway?

A

2 x 5 x 1 = 10 (Factors II

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31
Q

What is the mnemonic for the intrinsic coagulation pathway?

A

I shop at Wal-Mart because everything is under $12. It is always $11.98 (Factors XII

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32
Q

What is the prognosis for hepatobiliary diseases in horses?

A

Variable; acute serum hepatitis has a guarded to poor prognosis

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33
Q

What is the most common cause of acute hepatitis and hepatic failure in horses?

A

Acute Serum Hepatitis (Theiler’s Disease).

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34
Q

What is Theiler’s Disease associated with?

A

Possible administration of tetanus antitoxin or other equine biologicals 4-10 weeks prior to onset.

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35
Q

What are the clinical signs of acute serum hepatitis?

A

Acute depression

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36
Q

What are the microscopic findings in acute serum hepatitis?

A

Widespread hepatic necrosis

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37
Q

What is the treatment for acute serum hepatitis?

A

Supportive therapy: fluid therapy

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38
Q

What necropsy findings are observed in acute serum hepatitis?

A

Severe decrease in liver size

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39
Q

What is the prognosis for acute serum hepatitis?

A

Favorable if no severe hepatoencephalopathy; poor if there are signs of bleeding or hepatic encephalopathy.

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40
Q

What is chronic active hepatitis in horses?

A

Chronic inflammatory liver disease of unknown etiology.

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41
Q

What are potential causes of chronic active hepatitis?

A

Plant or chemical toxins

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42
Q

What are the clinical signs of chronic active hepatitis?

A

Progressive weight loss

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43
Q

What are the diagnostic findings in chronic active hepatitis?

A

Fibrosis in portal areas

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44
Q

How is chronic active hepatitis treated?

A

Corticosteroids

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45
Q

What is the prognosis for chronic active hepatitis?

A

Fair to good if mild fibrosis and response to steroids; poor if chronic hepatic changes or hepatic failure.

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46
Q

What causes pyrrolizidine alkaloid (PA) toxicity in horses?

A

Consumption of plants containing pyrrolizidine alkaloids (PA)

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47
Q

What are common plants that contain pyrrolizidine alkaloids?

A

Senecio spp.

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48
Q

What is the pathophysiology of PA toxicity?

A

Toxin is absorbed

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49
Q

What is the characteristic cellular change in PA toxicity?

A

Megalocytosis: hepatocytes enlarge as their cytoplasm expands without nuclear division.

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50
Q

What are the clinical signs of PA toxicity?

A

Weight loss

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51
Q

How is PA toxicity diagnosed?

A

History of consumption of PA-containing plants

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52
Q

What is the treatment for PA toxicity?

A

Remove PA-containing plants

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53
Q

What is the prognosis for PA toxicity?

A

Dependent on the degree of hepatic change.

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54
Q

What are common risk factors for laminitis?

A

Metabolic disease (Equine Cushing’s

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55
Q

What is the pathogenesis of laminitis?

A

Inflammation weakens the laminar projections

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56
Q

What are clinical signs of laminitis?

A

Rocked-back stance

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57
Q

What radiographic changes are seen in laminitis?

A

Coffin bone rotation

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58
Q

What is the initial treatment for laminitis?

A

Icing feet

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59
Q

What breeds are predisposed to navicular syndrome?

A

Quarter Horses

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60
Q

What are clinical signs of navicular syndrome?

A

Bilateral front limb lameness that switches between limbs after blocking

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61
Q

What radiographic findings are associated with navicular disease?

A

Increased nutrient foramina

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62
Q

What are treatment options for navicular syndrome?

A

Corrective shoeing (shortening toe

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63
Q

What tendons and ligaments are most commonly affected in equine lameness?

A

Suspensory ligament (especially proximally)

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64
Q

What is Degenerative Suspensory Ligament Desmitis (DSLD)?

A

A progressive failure of collagen repair in the suspensory ligament

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65
Q

How is tendonitis diagnosed?

A

Ultrasound showing focal anechoic lesions

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66
Q

What is the treatment for tendonitis?

A

Rest

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67
Q

What are common names for osteoarthritis based on location?

A

High ringbone (pastern joint OA)

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68
Q

What radiographic changes are seen in OA?

A

Osteophytes

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69
Q

What are treatment options for OA?

A

NSAIDs (phenylbutazone

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70
Q

What are risk factors for hoof abscesses?

A

Wet or muddy conditions

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71
Q

What are clinical signs of a hoof abscess?

A

Severe acute lameness (sometimes non-weight-bearing)

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72
Q

How is a hoof abscess treated?

A

Hoof soaking (Epsom salts

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73
Q

What are common clinical signs of a septic joint?

A

Severe lameness

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74
Q

How is a septic joint diagnosed?

A

Arthrocentesis with WBC >30

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75
Q

What is the treatment for septic arthritis?

A

Joint lavage

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76
Q

What is the prognosis for untreated septic arthritis?

A

Poor; secondary osteoarthritis leads to long-term lameness.

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77
Q

What are risk factors for OCD?

A

Rapid growth

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78
Q

What are common sites of OCD in horses?

A

Tarsus

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79
Q

How is OCD diagnosed?

A

Radiographs showing subchondral bone cysts

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80
Q

What is the treatment for OCD?

A

Conservative management in young horses

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81
Q

What are common sites of congenital flexural limb deformities?

A

Carpus and fetlock.

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82
Q

What are clinical signs of flexural deformities?

A

Contracted tendons preventing full extension

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83
Q

How are mild flexural deformities treated?

A

Splinting

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84
Q

What is the treatment for severe flexural deformities?

A

Desmotomy if unresponsive to conservative treatment.

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85
Q

What are risk factors for septic arthritis in foals?

A

Failure of passive transfer (IgG <800 mg/dL)

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86
Q

What are clinical signs of septic arthritis in foals?

A

Joint effusion

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87
Q

How is septic arthritis diagnosed?

A

Arthrocentesis with WBC >30

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88
Q

What is the treatment for septic arthritis in foals?

A

Systemic and intra-articular antibiotics (amikacin

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89
Q

What is a malunion?

A

A healed fracture in which anatomical bone alignment was not achieved or maintained during healing.

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90
Q

What is a common consequence of malunions in the appendicular skeleton?

A

Angular deformity.

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91
Q

What is the difference between minor and major angular deformities?

A

Minor: <10% in any plane or <10% loss of original length; Major: anything beyond this

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92
Q

What is a common site for malunions

A

and what problem can it cause?

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93
Q

What are common causes of malunions?

A

Improper treatment of original fracture

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94
Q

How is a malunion diagnosed?

A

Radiographs to determine extent of angular

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95
Q

What is a varus deformity?

A

Deviation of the segment axis towards the median sagittal plane.

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96
Q

What is a valgus deformity?

A

Deviation of the segment axis away from the median sagittal plane.

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97
Q

What is procurvatus?

A

Cranial bowing deformity in the sagittal plane.

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98
Q

What is recurvatus?

A

Caudal bowing deformity in the sagittal plane.

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99
Q

What is pronatus?

A

Internal rotation deformity in the axial plane.

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100
Q

What is supinatus?

A

External rotation deformity in the axial plane.

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101
Q

What is the treatment for malunions that cause functional problems?

A

Corrective osteotomy.

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102
Q

What is an important step before corrective osteotomy?

A

Preoperative planning.

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103
Q

What type of fixator can be used for bone lengthening and angular corrections?

A

Ring fixator.

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104
Q

What is an advantage of using a ring fixator in malunion correction?

A

Allows gradual stretching of muscles

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105
Q

What is Neonatal Isoerythrolysis (NI)?

A

A type II hypersensitivity reaction where maternal antibodies destroy a foal’s red blood cells (RBCs) after colostrum ingestion.

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106
Q

Which foals are most at risk for NI?

A

Foals born to multiparous mares.

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107
Q

At what age do foals typically present with NI?

A

Less than 7 days old

108
Q

What is a key clinical sign of NI?

A

Icteric mucous membranes and sclera.

109
Q

Which erythrocyte antigens are most commonly implicated in NI?

A

Aa and Qa factors.

110
Q

What type of hypersensitivity reaction is NI?

A

Type II hypersensitivity reaction.

111
Q

How do foals acquire maternal alloantibodies leading to NI?

A

By ingesting colostrum containing antibodies against their RBC antigens.

112
Q

What must be present for a foal to develop NI?

A

1) Neonatal RBC antigen inherited from the sire that the mare does not express

113
Q

How does a mare develop antibodies against RBC antigens?

A

Previous exposure through blood transfusion

114
Q

Why do mule foals have a higher incidence of NI?

A

Donkeys have a unique ‘donkey factor’ RBC antigen that horses do not express.

115
Q

What are the clinical signs of NI?

A

Tachycardia

116
Q

What determines the severity of NI in foals?

A

The amount of maternal antibodies absorbed via colostrum.

117
Q

What are key diagnostic findings in NI?

A

Hyperbilirubinemia and anemia.

118
Q

How is NI confirmed?

A

Cross-matching the foal’s RBCs with the mare’s serum (Jaundice Foal Agglutination Test).

119
Q

What is the treatment for NI if recognized in the first 24 hours?

A

Withhold dam’s colostrum

120
Q

What is the treatment for NI after 24 hours of age?

A

Monitor PCV; if PCV < 12%

121
Q

What supportive care should be provided to foals with NI?

A

Minimize stress and exercise

122
Q

What is the prognosis for foals with NI?

A

Good with proper treatment

123
Q

Why is client education important in NI cases?

A

To prevent recurrence in future pregnancies.

124
Q

What risk does severe anemia (<10% PCV) pose in NI?

A

Limited time to acquire blood for transfusion

125
Q

What is the purpose of diagnostic nerve blocks in equine lameness exams?

A

To localize the source of lameness by desensitizing specific regions of the limb.

126
Q

Where is the palmar digital nerve block administered?

A

Around the medial and lateral palmar digital nerves between the proximal sesamoid bones and just proximal to the cartilages of the foot.

127
Q

What areas are desensitized by the palmar digital nerve block?

A

50-70% of the palmar/plantar aspect of the foot

128
Q

Where is the abaxial sesamoid block administered?

A

Around the medial and lateral palmar digital nerves over the abaxial surface of the proximal sesamoid bones.

129
Q

What areas are desensitized by the abaxial sesamoid block?

A

Skin over the palmar pastern

130
Q

Which nerves are blocked in the low four-point block?

A

Medial and lateral palmar nerves and medial and lateral palmar metacarpal nerves.

131
Q

Where is the low four-point block administered?

A

Palmar nerves: between the suspensory ligament and deep digital flexor tendon; Palmar metacarpal nerves: just distal to the end of the splint bones.

132
Q

What areas are desensitized by the low four-point block?

A

Entire metacarpophalangeal (fetlock) joint and all structures distal to this joint.

133
Q

Which nerves are blocked in the high four-point (subcarpal) block?

A

Medial and lateral palmar nerves and medial and lateral palmar metacarpal nerves just distal to the carpus.

134
Q

Where is the high four-point block administered?

A

Palmar nerves: between the suspensory ligament and deep digital flexor distal to the carpus; Palmar metacarpal nerves: axial to the splint bones and abaxial to the suspensory ligament.

135
Q

What areas are desensitized by the high four-point block?

A

Metacarpal region

136
Q

If a horse’s lameness resolves by 85% after a low four-point block

A

what is the most likely location of the problem?

137
Q

Why is a general understanding of equine nerve blocks important for the NAVLE?

A

To correctly answer questions about which block anesthetizes which area

138
Q

What are common clinical signs of pneumonia in horses?

139
Q

What history factors predispose horses to pneumonia?

A

Extended transport

140
Q

What is pleuropneumonia?

A

Pneumonia with significant accumulation of fluid and fibrin in the pleural cavity.

141
Q

What is aspiration pneumonia

A

and what causes it?

142
Q

What are common bacterial causes of pneumonia?

A

Streptococcus zooepidemicus (Gram+)

143
Q

What viruses predispose horses to bacterial pneumonia?

A

Equine Herpes Virus

144
Q

What fungal pathogens may cause pneumonia?

A

Coccidiodes

145
Q

What are common clinicopathologic abnormalities in equine pneumonia?

A

Leukopenia (acute) to leukocytosis (chronic)

146
Q

What diagnostic tests are used for pneumonia?

A

Thoracic radiography

147
Q

What radiographic findings are common in pneumonia?

A

Radiopacity of cranial-ventral or caudal-ventral thorax

148
Q

What ultrasonographic findings are common in pleuropneumonia?

A

Free pleural fluid

149
Q

What are key components of pneumonia treatment?

A

Antimicrobials

150
Q

What antibiotics are commonly used for bacterial pneumonia?

A

Penicillin or cephalosporin + aminoglycoside; metronidazole for anaerobes.

151
Q

What anti-inflammatory drug is commonly used for pneumonia?

A

Flunixin meglumine (Banamine) for fever

152
Q

Why should laminitis prevention be considered in pneumonia cases?

A

Endotoxemia from bacterial infection can trigger laminitis.

153
Q

When is thoracocentesis or an indwelling chest tube indicated?

A

When large amounts of pleural fluid accumulate in pleuropneumonia.

154
Q

What is the prognosis for pneumonia in horses?

A

Fair to good with aggressive treatment; worse for anaerobic infections and complicated cases.

155
Q

What factors worsen prognosis in pleuropneumonia?

A

Development of laminitis

156
Q

What is another name for Recurrent Airway Obstruction (RAO) in horses?

157
Q

What age group of horses is typically affected by RAO?

A

Middle-aged to older horses (>7-8 years old).

158
Q

What are the primary clinical signs of RAO?

A

Increased respiratory effort (especially expiratory)

159
Q

What environmental factors contribute to RAO?

A

Exposure to molds

160
Q

What is the primary pathological change in RAO?

A

Bronchoconstriction and accumulation of mucus and neutrophils in the airways

161
Q

How is RAO typically diagnosed?

A

Based on signalment

162
Q

What bronchoalveolar lavage (BAL) fluid findings support a diagnosis of RAO?

A

Increased neutrophils; normally

163
Q

What are Curshmann’s spirals

A

and what do they indicate?

164
Q

Are thoracic radiographs useful in diagnosing RAO?

165
Q

What is a key finding on arterial blood gas analysis in RAO?

A

Significant hypoxemia.

166
Q

What is the primary treatment approach for RAO?

A

Environmental control and medications to manage inflammation and bronchoconstriction.

167
Q

What environmental changes help manage RAO?

A

Avoid stabling

168
Q

Which corticosteroids are used for RAO treatment?

A

Dexamethasone and prednisolone to reduce airway inflammation.

169
Q

Which bronchodilators are used for RAO treatment?

A

Clenbuterol and albuterol to relieve bronchoconstriction.

170
Q

How can RAO medications be administered?

171
Q

What is the long-term prognosis for RAO?

A

Good with proper management

172
Q

What is the causative agent of Strangles?

A

Streptococcus equi ssp. equi.

173
Q

How is Strangles transmitted?

A

Inhalation or ingestion of respiratory secretions from infected horses.

174
Q

What are key clinical signs of Strangles?

175
Q

What severe complication can occur with repeated exposure to Strangles?

A

Purpura hemorrhagica (immune-mediated vasculitis).

176
Q

What is the best diagnostic test for acute Strangles?

A

PCR or bacterial culture from nasal swab

177
Q

What is the primary treatment for uncomplicated Strangles?

A

Supportive care; antibiotics (penicillin

178
Q

How does Equine Herpesvirus (EHV) persist in horses?

A

Latent infection reactivates during stress

179
Q

What are key clinical signs of EHV?

180
Q

How is EHV diagnosed?

A

PCR from nasal swab.

181
Q

How is EHV prevented?

A

Vaccination every 6 months in high-risk horses; pregnant mares vaccinated at 5

182
Q

What is the primary mode of transmission for Equine Influenza A?

A

Inhalation of aerosolized virus from respiratory secretions.

183
Q

What are clinical signs of Equine Influenza?

184
Q

How is Equine Influenza diagnosed?

A

PCR from a nasal swab.

185
Q

What is the primary treatment for Equine Influenza?

A

Supportive care

186
Q

How can Equine Influenza be prevented?

A

Vaccination every 6 months for high-risk horses.

187
Q

What is the suspected pathophysiology of EIPH?

A

High capillary pressure from high cardiac output causes capillary wall failure and bleeding into airways.

188
Q

What is the most common clinical sign of EIPH?

A

Epistaxis during or after intense exercise.

189
Q

How is EIPH diagnosed?

A

Endoscopy within 2 hours of exercise or bronchoalveolar lavage showing hemosiderophages.

190
Q

What is the primary treatment for EIPH?

A

Furosemide (Lasix) administered before events to reduce pulmonary capillary pressure.

191
Q

What is the pathogenesis of RAO?

A

Inflammation and bronchoconstriction caused by dust

192
Q

What are the classic clinical signs of RAO?

A

Chronic cough

193
Q

How is RAO definitively diagnosed?

A

Bronchoalveolar lavage cytology showing increased neutrophils.

194
Q

What is the most important aspect of RAO management?

A

Environmental modification to reduce dust exposure.

195
Q

What is the most common cause of primary sinusitis in horses?

A

Dental disease (infection of cheek teeth).

196
Q

What are the key clinical signs of sinusitis?

A

Unilateral mucopurulent nasal discharge

197
Q

How is sinusitis diagnosed?

A

Radiographs

198
Q

What is the treatment for sinusitis?

A

Tooth extraction and sinus lavage.

199
Q

What is the cause of laryngeal hemiparesis?

A

Idiopathic neuropathy of the left recurrent laryngeal nerve.

200
Q

What are clinical signs of laryngeal hemiparesis?

A

Inspiratory noise (roaring) during exercise

201
Q

How is laryngeal hemiparesis diagnosed?

A

Endoscopy of the upper airway.

202
Q

What is the treatment for severe cases of laryngeal hemiparesis?

A

Laryngoplasty (‘tie-back’ surgery).

203
Q

What age group is most affected by Rhodococcus equi?

A

Foals 1-3 months old.

204
Q

What are clinical signs of Rhodococcus equi pneumonia?

205
Q

How is Rhodococcus equi diagnosed?

A

Transtracheal wash cytology and culture

206
Q

What is the treatment for Rhodococcus equi?

A

Rifampin and a macrolide (azithromycin

207
Q

What is a major risk factor for pleuropneumonia?

A

Extended transportation with poor ventilation and tied heads.

208
Q

What are clinical signs of pleuropneumonia?

209
Q

How is pleuropneumonia diagnosed?

A

Thoracic ultrasound showing pleural effusion

210
Q

What is the treatment for pleuropneumonia?

A

IV antibiotics

211
Q

What condition can mimic a respiratory disease but is actually gastrointestinal?

A

Esophageal obstruction (choke).

212
Q

What are clinical signs of choke?

A

Bilateral nasal discharge with feed material

213
Q

How is choke diagnosed?

A

Failure to pass a nasogastric tube into the stomach.

214
Q

What is the treatment for choke?

215
Q

What is the primary age range for foals affected by Rhodococcus equi?

A

Foals between 1-6 months of age.

216
Q

How is Rhodococcus equi typically acquired?

A

Inhalation of the organism from a dusty environment.

217
Q

What is the primary pathogen causing Rhodococcus equi infection?

A

Rhodococcus equi

218
Q

Where does Rhodococcus equi replicate in infected foals?

A

Inside alveolar macrophages

219
Q

What are the main clinical signs of Rhodococcus equi infection?

A

Intermittent fever

220
Q

What are the common clinicopathologic abnormalities associated with Rhodococcus equi?

A

Neutrophilic leukocytosis and hyperfibrinogenemia.

221
Q

What imaging findings are characteristic of Rhodococcus equi pneumonia?

A

Ultrasonographic evidence of pulmonary abscesses or characteristic radiographic pulmonary abscesses.

222
Q

What is the gold standard for confirming Rhodococcus equi pneumonia?

A

Transtracheal wash with bacterial culture of Rhodococcus equi.

223
Q

What is the treatment of choice for Rhodococcus equi pneumonia?

A

A macrolide (erythromycin

224
Q

What supportive care measures are important in treating Rhodococcus equi?

A

NSAIDs for inflammation

225
Q

What are some complications of Rhodococcus equi infection?

A

Abdominal abscessation

226
Q

What neurologic complication can Rhodococcus equi cause?

A

Intervertebral abscess resulting in neurologic deficits such as weakness and ataxia.

227
Q

What is the prognosis for foals diagnosed and treated early for Rhodococcus equi pneumonia?

A

Fair to good

228
Q

How can Rhodococcus equi infection be prevented in breeding farms?

A

Administer hyperimmunized plasma early in life

229
Q

Why is prophylactic macrolide use no longer recommended for Rhodococcus equi prevention?

A

Due to potential antibiotic resistance and questionable efficacy.

230
Q

What routine monitoring can aid in early detection of Rhodococcus equi pneumonia?

A

Regular measurement of body temperature and respiratory rate

231
Q

What is neonatal sepsis in foals?

A

A systemic disease caused by circulating microorganisms and their products.

232
Q

At what age does neonatal sepsis typically occur in foals?

A

During the neonatal period

233
Q

What are the primary routes of bacterial introduction in neonatal foals?

A

Inhalation

234
Q

What is the most important factor in preventing neonatal sepsis?

A

Adequate passive transfer of maternal antibodies (IgG >800 mg/dL).

235
Q

What is the most common bacterial isolate in neonatal foal sepsis?

236
Q

What are other common bacterial causes of neonatal sepsis?

A

Streptococcus

237
Q

What are the primary clinical signs of neonatal sepsis?

238
Q

What are key clinicopathologic abnormalities in neonatal sepsis?

A

Leukopenia

239
Q

What diagnostic test definitively confirms neonatal sepsis?

A

Positive blood culture with bacterial identification and antimicrobial susceptibility testing.

240
Q

What is a sepsis score in neonatal foals?

A

A point-based system that assigns values to abnormalities such as hypoglycemia

241
Q

What are the main components of neonatal sepsis treatment?

A

Fluid therapy

242
Q

What is a key complication of neonatal sepsis?

A

Septic arthritis

243
Q

What is the prognosis for neonatal sepsis?

A

Guarded to good with early aggressive treatment; complications may worsen prognosis.

244
Q

What is a major concern regarding neonatal sepsis treatment?

A

The cost of intensive care can be substantial for the client.

245
Q

What is the causative agent of Strangles in horses?

A

Streptococcus equi.

246
Q

What type of bacteria is Streptococcus equi?

A

Gram-positive

247
Q

What age group is most commonly affected by Strangles?

A

Young horses (<2-5 years old).

248
Q

How is Strangles transmitted?

A

Direct contact with purulent discharge from infected horses or contaminated equipment.

249
Q

Where does Streptococcus equi establish infection in horses?

A

Pharyngeal mucosa and local lymph nodes (intermandibular and retropharyngeal).

250
Q

Why is Strangles named as such?

A

Severe lymphadenopathy may occlude the airway

251
Q

What is the incubation period for Strangles?

252
Q

What are the hallmark clinical signs of Strangles?

253
Q

Which lymph nodes are most commonly affected in Strangles?

A

Intermandibular

254
Q

What clinicopathologic abnormalities are associated with Strangles?

A

Neutrophilic leukocytosis and hyperfibrinogenemia.

255
Q

How is Strangles diagnosed?

256
Q

When is penicillin recommended in Strangles treatment?

A

If the horse is febrile without lymph node abscessation or has been recently exposed.

257
Q

Why should penicillin be avoided once lymph node abscessation has occurred?

A

It may slow abscess maturation; treatment should focus on abscess drainage.

258
Q

How should mature abscesses be managed?

A

Hot packing to promote maturation

259
Q

What additional management strategies are needed for a Strangles outbreak?

260
Q

What is Bastard Strangles?

A

A form of internal abscessation affecting mesenteric or other lymph nodes.

261
Q

What are the clinical signs of Bastard Strangles?

A

Chronic intermittent colic

262
Q

What is Purpura Hemorrhagica?

A

Immune-mediated vasculitis resulting in limb and head edema

263
Q

What complication occurs when purulent material collects in the guttural pouch?

A

Guttural Pouch Empyema

264
Q

What are the consequences of septicemia in Strangles?

A

Occasional CNS involvement leading to encephalopathy and poor prognosis.

265
Q

What is the prognosis for Strangles?

A

Good; most horses recover uneventfully and develop strong immunity