Equine I Flashcards
(265 cards)
1
Q
What is the function of platelets in hemostasis?
A
They form a platelet plug within about 5 minutes after vascular injury.
2
Q
What are the three primary reactions of platelets after endothelial disruption?
A
Adhesion and shape change
3
Q
What factor is necessary for platelet adhesion to the subendothelium?
A
Von Willebrand factor (vWF).
4
Q
What is the final product of the coagulation cascade?
A
A cross-linked fibrin clot that stabilizes the platelet plug.
5
Q
How does thrombin regulate clot formation?
A
Thrombin is absorbed into fibrin fibers and inactivated by anti-thrombin to prevent excessive clotting.
6
Q
How does heparin work as an anticoagulant?
A
It binds to anti-thrombin and enhances its ability to prevent clot formation.
7
Q
What are key clinical signs of platelet dysfunction?
A
Petechiae
8
Q
What is the key test for primary hemostasis?
A
Platelet count and buccal mucosal bleeding time (BMBT).
9
Q
At what platelet count do spontaneous bleeds typically occur?
A
Less than 30
10
Q
What is the normal buccal mucosal bleeding time (BMBT)?
A
Less than 4 minutes.
11
Q
What test is used to evaluate the intrinsic and common pathways?
A
Activated Clotting Time (ACT) and Activated Partial Thromboplastin Time (PTT).
12
Q
What is the normal ACT range?
A
60-90 seconds.
13
Q
Which clotting factors does ACT assess?
A
Prekallikrein
14
Q
Which test is more sensitive for intrinsic pathway evaluation: ACT or PTT?
A
PTT is more sensitive than ACT.
15
Q
What test is used to evaluate the extrinsic and common pathway?
A
Prothrombin Time (PT).
16
Q
Which clotting factors does PT assess?
A
Factors X
17
Q
What is the most common platelet disorder in Doberman Pinschers?
A
Von Willebrand’s Disease.
18
Q
What is the inheritance pattern of Von Willebrand’s Disease in Dobermans?
A
Autosomal dominant with variable penetrance.
19
Q
How is Von Willebrand’s Disease treated before surgery?
A
DDAVP (Desmopressin) 1μg/kg given 30 minutes before induction
20
Q
What clotting factor is deficient in Hemophilia A?
A
Factor VIII.
21
Q
What clotting factor is deficient in Hemophilia B?
A
Factor IX.
22
Q
Which coagulation tests are elevated in Hemophilia A and B?
A
ACT and PTT.
23
Q
What clotting disorder results from rodenticide toxicity?
A
Vitamin K deficiency.
24
Q
Which clotting factors are affected by Vitamin K deficiency?
A
Factors II
25
Which coagulation tests are elevated in Vitamin K deficiency?
PT and PTT.
26
What is the half-life of Factor VII
making it an early indicator of Vitamin K deficiency?
27
How long does it take for clinical bleeding to develop in Vitamin K deficiency?
1-2 days.
28
What is the treatment for rodenticide toxicity?
Vitamin K1 for approximately 4 weeks.
29
Why should clotting times be rechecked after Vitamin K1 therapy?
To ensure the rodenticide has been completely eliminated.
30
What is the mnemonic for the common coagulation pathway?
2 x 5 x 1 = 10 (Factors II
31
What is the mnemonic for the intrinsic coagulation pathway?
I shop at Wal-Mart because everything is under $12. It is always $11.98 (Factors XII
32
What is the prognosis for hepatobiliary diseases in horses?
Variable; acute serum hepatitis has a guarded to poor prognosis
33
What is the most common cause of acute hepatitis and hepatic failure in horses?
Acute Serum Hepatitis (Theiler’s Disease).
34
What is Theiler’s Disease associated with?
Possible administration of tetanus antitoxin or other equine biologicals 4-10 weeks prior to onset.
35
What are the clinical signs of acute serum hepatitis?
Acute depression
36
What are the microscopic findings in acute serum hepatitis?
Widespread hepatic necrosis
37
What is the treatment for acute serum hepatitis?
Supportive therapy: fluid therapy
38
What necropsy findings are observed in acute serum hepatitis?
Severe decrease in liver size
39
What is the prognosis for acute serum hepatitis?
Favorable if no severe hepatoencephalopathy; poor if there are signs of bleeding or hepatic encephalopathy.
40
What is chronic active hepatitis in horses?
Chronic inflammatory liver disease of unknown etiology.
41
What are potential causes of chronic active hepatitis?
Plant or chemical toxins
42
What are the clinical signs of chronic active hepatitis?
Progressive weight loss
43
What are the diagnostic findings in chronic active hepatitis?
Fibrosis in portal areas
44
How is chronic active hepatitis treated?
Corticosteroids
45
What is the prognosis for chronic active hepatitis?
Fair to good if mild fibrosis and response to steroids; poor if chronic hepatic changes or hepatic failure.
46
What causes pyrrolizidine alkaloid (PA) toxicity in horses?
Consumption of plants containing pyrrolizidine alkaloids (PA)
47
What are common plants that contain pyrrolizidine alkaloids?
Senecio spp.
48
What is the pathophysiology of PA toxicity?
Toxin is absorbed
49
What is the characteristic cellular change in PA toxicity?
Megalocytosis: hepatocytes enlarge as their cytoplasm expands without nuclear division.
50
What are the clinical signs of PA toxicity?
Weight loss
51
How is PA toxicity diagnosed?
History of consumption of PA-containing plants
52
What is the treatment for PA toxicity?
Remove PA-containing plants
53
What is the prognosis for PA toxicity?
Dependent on the degree of hepatic change.
54
What are common risk factors for laminitis?
Metabolic disease (Equine Cushing's
55
What is the pathogenesis of laminitis?
Inflammation weakens the laminar projections
56
What are clinical signs of laminitis?
Rocked-back stance
57
What radiographic changes are seen in laminitis?
Coffin bone rotation
58
What is the initial treatment for laminitis?
Icing feet
59
What breeds are predisposed to navicular syndrome?
Quarter Horses
60
What are clinical signs of navicular syndrome?
Bilateral front limb lameness that switches between limbs after blocking
61
What radiographic findings are associated with navicular disease?
Increased nutrient foramina
62
What are treatment options for navicular syndrome?
Corrective shoeing (shortening toe
63
What tendons and ligaments are most commonly affected in equine lameness?
Suspensory ligament (especially proximally)
64
What is Degenerative Suspensory Ligament Desmitis (DSLD)?
A progressive failure of collagen repair in the suspensory ligament
65
How is tendonitis diagnosed?
Ultrasound showing focal anechoic lesions
66
What is the treatment for tendonitis?
Rest
67
What are common names for osteoarthritis based on location?
High ringbone (pastern joint OA)
68
What radiographic changes are seen in OA?
Osteophytes
69
What are treatment options for OA?
NSAIDs (phenylbutazone
70
What are risk factors for hoof abscesses?
Wet or muddy conditions
71
What are clinical signs of a hoof abscess?
Severe acute lameness (sometimes non-weight-bearing)
72
How is a hoof abscess treated?
Hoof soaking (Epsom salts
73
What are common clinical signs of a septic joint?
Severe lameness
74
How is a septic joint diagnosed?
Arthrocentesis with WBC >30
75
What is the treatment for septic arthritis?
Joint lavage
76
What is the prognosis for untreated septic arthritis?
Poor; secondary osteoarthritis leads to long-term lameness.
77
What are risk factors for OCD?
Rapid growth
78
What are common sites of OCD in horses?
Tarsus
79
How is OCD diagnosed?
Radiographs showing subchondral bone cysts
80
What is the treatment for OCD?
Conservative management in young horses
81
What are common sites of congenital flexural limb deformities?
Carpus and fetlock.
82
What are clinical signs of flexural deformities?
Contracted tendons preventing full extension
83
How are mild flexural deformities treated?
Splinting
84
What is the treatment for severe flexural deformities?
Desmotomy if unresponsive to conservative treatment.
85
What are risk factors for septic arthritis in foals?
Failure of passive transfer (IgG <800 mg/dL)
86
What are clinical signs of septic arthritis in foals?
Joint effusion
87
How is septic arthritis diagnosed?
Arthrocentesis with WBC >30
88
What is the treatment for septic arthritis in foals?
Systemic and intra-articular antibiotics (amikacin
89
What is a malunion?
A healed fracture in which anatomical bone alignment was not achieved or maintained during healing.
90
What is a common consequence of malunions in the appendicular skeleton?
Angular deformity.
91
What is the difference between minor and major angular deformities?
Minor: <10% in any plane or <10% loss of original length; Major: anything beyond this
92
What is a common site for malunions
and what problem can it cause?
93
What are common causes of malunions?
Improper treatment of original fracture
94
How is a malunion diagnosed?
Radiographs to determine extent of angular
95
What is a varus deformity?
Deviation of the segment axis towards the median sagittal plane.
96
What is a valgus deformity?
Deviation of the segment axis away from the median sagittal plane.
97
What is procurvatus?
Cranial bowing deformity in the sagittal plane.
98
What is recurvatus?
Caudal bowing deformity in the sagittal plane.
99
What is pronatus?
Internal rotation deformity in the axial plane.
100
What is supinatus?
External rotation deformity in the axial plane.
101
What is the treatment for malunions that cause functional problems?
Corrective osteotomy.
102
What is an important step before corrective osteotomy?
Preoperative planning.
103
What type of fixator can be used for bone lengthening and angular corrections?
Ring fixator.
104
What is an advantage of using a ring fixator in malunion correction?
Allows gradual stretching of muscles
105
What is Neonatal Isoerythrolysis (NI)?
A type II hypersensitivity reaction where maternal antibodies destroy a foal’s red blood cells (RBCs) after colostrum ingestion.
106
Which foals are most at risk for NI?
Foals born to multiparous mares.
107
At what age do foals typically present with NI?
Less than 7 days old
108
What is a key clinical sign of NI?
Icteric mucous membranes and sclera.
109
Which erythrocyte antigens are most commonly implicated in NI?
Aa and Qa factors.
110
What type of hypersensitivity reaction is NI?
Type II hypersensitivity reaction.
111
How do foals acquire maternal alloantibodies leading to NI?
By ingesting colostrum containing antibodies against their RBC antigens.
112
What must be present for a foal to develop NI?
1) Neonatal RBC antigen inherited from the sire that the mare does not express
113
How does a mare develop antibodies against RBC antigens?
Previous exposure through blood transfusion
114
Why do mule foals have a higher incidence of NI?
Donkeys have a unique 'donkey factor' RBC antigen that horses do not express.
115
What are the clinical signs of NI?
Tachycardia
116
What determines the severity of NI in foals?
The amount of maternal antibodies absorbed via colostrum.
117
What are key diagnostic findings in NI?
Hyperbilirubinemia and anemia.
118
How is NI confirmed?
Cross-matching the foal’s RBCs with the mare’s serum (Jaundice Foal Agglutination Test).
119
What is the treatment for NI if recognized in the first 24 hours?
Withhold dam’s colostrum
120
What is the treatment for NI after 24 hours of age?
Monitor PCV; if PCV < 12%
121
What supportive care should be provided to foals with NI?
Minimize stress and exercise
122
What is the prognosis for foals with NI?
Good with proper treatment
123
Why is client education important in NI cases?
To prevent recurrence in future pregnancies.
124
What risk does severe anemia (<10% PCV) pose in NI?
Limited time to acquire blood for transfusion
125
What is the purpose of diagnostic nerve blocks in equine lameness exams?
To localize the source of lameness by desensitizing specific regions of the limb.
126
Where is the palmar digital nerve block administered?
Around the medial and lateral palmar digital nerves between the proximal sesamoid bones and just proximal to the cartilages of the foot.
127
What areas are desensitized by the palmar digital nerve block?
50-70% of the palmar/plantar aspect of the foot
128
Where is the abaxial sesamoid block administered?
Around the medial and lateral palmar digital nerves over the abaxial surface of the proximal sesamoid bones.
129
What areas are desensitized by the abaxial sesamoid block?
Skin over the palmar pastern
130
Which nerves are blocked in the low four-point block?
Medial and lateral palmar nerves and medial and lateral palmar metacarpal nerves.
131
Where is the low four-point block administered?
Palmar nerves: between the suspensory ligament and deep digital flexor tendon; Palmar metacarpal nerves: just distal to the end of the splint bones.
132
What areas are desensitized by the low four-point block?
Entire metacarpophalangeal (fetlock) joint and all structures distal to this joint.
133
Which nerves are blocked in the high four-point (subcarpal) block?
Medial and lateral palmar nerves and medial and lateral palmar metacarpal nerves just distal to the carpus.
134
Where is the high four-point block administered?
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
What areas are desensitized by the high four-point block?
Metacarpal region
136
If a horse's lameness resolves by 85% after a low four-point block
what is the most likely location of the problem?
137
Why is a general understanding of equine nerve blocks important for the NAVLE?
To correctly answer questions about which block anesthetizes which area
138
What are common clinical signs of pneumonia in horses?
Cough
139
What history factors predispose horses to pneumonia?
Extended transport
140
What is pleuropneumonia?
Pneumonia with significant accumulation of fluid and fibrin in the pleural cavity.
141
What is aspiration pneumonia
and what causes it?
142
What are common bacterial causes of pneumonia?
Streptococcus zooepidemicus (Gram+)
143
What viruses predispose horses to bacterial pneumonia?
Equine Herpes Virus
144
What fungal pathogens may cause pneumonia?
Coccidiodes
145
What are common clinicopathologic abnormalities in equine pneumonia?
Leukopenia (acute) to leukocytosis (chronic)
146
What diagnostic tests are used for pneumonia?
Thoracic radiography
147
What radiographic findings are common in pneumonia?
Radiopacity of cranial-ventral or caudal-ventral thorax
148
What ultrasonographic findings are common in pleuropneumonia?
Free pleural fluid
149
What are key components of pneumonia treatment?
Antimicrobials
150
What antibiotics are commonly used for bacterial pneumonia?
Penicillin or cephalosporin + aminoglycoside; metronidazole for anaerobes.
151
What anti-inflammatory drug is commonly used for pneumonia?
Flunixin meglumine (Banamine) for fever
152
Why should laminitis prevention be considered in pneumonia cases?
Endotoxemia from bacterial infection can trigger laminitis.
153
When is thoracocentesis or an indwelling chest tube indicated?
When large amounts of pleural fluid accumulate in pleuropneumonia.
154
What is the prognosis for pneumonia in horses?
Fair to good with aggressive treatment; worse for anaerobic infections and complicated cases.
155
What factors worsen prognosis in pleuropneumonia?
Development of laminitis
156
What is another name for Recurrent Airway Obstruction (RAO) in horses?
Heaves
157
What age group of horses is typically affected by RAO?
Middle-aged to older horses (>7-8 years old).
158
What are the primary clinical signs of RAO?
Increased respiratory effort (especially expiratory)
159
What environmental factors contribute to RAO?
Exposure to molds
160
What is the primary pathological change in RAO?
Bronchoconstriction and accumulation of mucus and neutrophils in the airways
161
How is RAO typically diagnosed?
Based on signalment
162
What bronchoalveolar lavage (BAL) fluid findings support a diagnosis of RAO?
Increased neutrophils; normally
163
What are Curshmann’s spirals
and what do they indicate?
164
Are thoracic radiographs useful in diagnosing RAO?
No
165
What is a key finding on arterial blood gas analysis in RAO?
Significant hypoxemia.
166
What is the primary treatment approach for RAO?
Environmental control and medications to manage inflammation and bronchoconstriction.
167
What environmental changes help manage RAO?
Avoid stabling
168
Which corticosteroids are used for RAO treatment?
Dexamethasone and prednisolone to reduce airway inflammation.
169
Which bronchodilators are used for RAO treatment?
Clenbuterol and albuterol to relieve bronchoconstriction.
170
How can RAO medications be administered?
Orally
171
What is the long-term prognosis for RAO?
Good with proper management
172
What is the causative agent of Strangles?
Streptococcus equi ssp. equi.
173
How is Strangles transmitted?
Inhalation or ingestion of respiratory secretions from infected horses.
174
What are key clinical signs of Strangles?
Fever
175
What severe complication can occur with repeated exposure to Strangles?
Purpura hemorrhagica (immune-mediated vasculitis).
176
What is the best diagnostic test for acute Strangles?
PCR or bacterial culture from nasal swab
177
What is the primary treatment for uncomplicated Strangles?
Supportive care; antibiotics (penicillin
178
How does Equine Herpesvirus (EHV) persist in horses?
Latent infection reactivates during stress
179
What are key clinical signs of EHV?
Fever
180
How is EHV diagnosed?
PCR from nasal swab.
181
How is EHV prevented?
Vaccination every 6 months in high-risk horses; pregnant mares vaccinated at 5
182
What is the primary mode of transmission for Equine Influenza A?
Inhalation of aerosolized virus from respiratory secretions.
183
What are clinical signs of Equine Influenza?
Fever
184
How is Equine Influenza diagnosed?
PCR from a nasal swab.
185
What is the primary treatment for Equine Influenza?
Supportive care
186
How can Equine Influenza be prevented?
Vaccination every 6 months for high-risk horses.
187
What is the suspected pathophysiology of EIPH?
High capillary pressure from high cardiac output causes capillary wall failure and bleeding into airways.
188
What is the most common clinical sign of EIPH?
Epistaxis during or after intense exercise.
189
How is EIPH diagnosed?
Endoscopy within 2 hours of exercise or bronchoalveolar lavage showing hemosiderophages.
190
What is the primary treatment for EIPH?
Furosemide (Lasix) administered before events to reduce pulmonary capillary pressure.
191
What is the pathogenesis of RAO?
Inflammation and bronchoconstriction caused by dust
192
What are the classic clinical signs of RAO?
Chronic cough
193
How is RAO definitively diagnosed?
Bronchoalveolar lavage cytology showing increased neutrophils.
194
What is the most important aspect of RAO management?
Environmental modification to reduce dust exposure.
195
What is the most common cause of primary sinusitis in horses?
Dental disease (infection of cheek teeth).
196
What are the key clinical signs of sinusitis?
Unilateral mucopurulent nasal discharge
197
How is sinusitis diagnosed?
Radiographs
198
What is the treatment for sinusitis?
Tooth extraction and sinus lavage.
199
What is the cause of laryngeal hemiparesis?
Idiopathic neuropathy of the left recurrent laryngeal nerve.
200
What are clinical signs of laryngeal hemiparesis?
Inspiratory noise (roaring) during exercise
201
How is laryngeal hemiparesis diagnosed?
Endoscopy of the upper airway.
202
What is the treatment for severe cases of laryngeal hemiparesis?
Laryngoplasty ('tie-back' surgery).
203
What age group is most affected by Rhodococcus equi?
Foals 1-3 months old.
204
What are clinical signs of Rhodococcus equi pneumonia?
Fever
205
How is Rhodococcus equi diagnosed?
Transtracheal wash cytology and culture
206
What is the treatment for Rhodococcus equi?
Rifampin and a macrolide (azithromycin
207
What is a major risk factor for pleuropneumonia?
Extended transportation with poor ventilation and tied heads.
208
What are clinical signs of pleuropneumonia?
Fever
209
How is pleuropneumonia diagnosed?
Thoracic ultrasound showing pleural effusion
210
What is the treatment for pleuropneumonia?
IV antibiotics
211
What condition can mimic a respiratory disease but is actually gastrointestinal?
Esophageal obstruction (choke).
212
What are clinical signs of choke?
Bilateral nasal discharge with feed material
213
How is choke diagnosed?
Failure to pass a nasogastric tube into the stomach.
214
What is the treatment for choke?
Sedation
215
What is the primary age range for foals affected by Rhodococcus equi?
Foals between 1-6 months of age.
216
How is Rhodococcus equi typically acquired?
Inhalation of the organism from a dusty environment.
217
What is the primary pathogen causing Rhodococcus equi infection?
Rhodococcus equi
218
Where does Rhodococcus equi replicate in infected foals?
Inside alveolar macrophages
219
What are the main clinical signs of Rhodococcus equi infection?
Intermittent fever
220
What are the common clinicopathologic abnormalities associated with Rhodococcus equi?
Neutrophilic leukocytosis and hyperfibrinogenemia.
221
What imaging findings are characteristic of Rhodococcus equi pneumonia?
Ultrasonographic evidence of pulmonary abscesses or characteristic radiographic pulmonary abscesses.
222
What is the gold standard for confirming Rhodococcus equi pneumonia?
Transtracheal wash with bacterial culture of Rhodococcus equi.
223
What is the treatment of choice for Rhodococcus equi pneumonia?
A macrolide (erythromycin
224
What supportive care measures are important in treating Rhodococcus equi?
NSAIDs for inflammation
225
What are some complications of Rhodococcus equi infection?
Abdominal abscessation
226
What neurologic complication can Rhodococcus equi cause?
Intervertebral abscess resulting in neurologic deficits such as weakness and ataxia.
227
What is the prognosis for foals diagnosed and treated early for Rhodococcus equi pneumonia?
Fair to good
228
How can Rhodococcus equi infection be prevented in breeding farms?
Administer hyperimmunized plasma early in life
229
Why is prophylactic macrolide use no longer recommended for Rhodococcus equi prevention?
Due to potential antibiotic resistance and questionable efficacy.
230
What routine monitoring can aid in early detection of Rhodococcus equi pneumonia?
Regular measurement of body temperature and respiratory rate
231
What is neonatal sepsis in foals?
A systemic disease caused by circulating microorganisms and their products.
232
At what age does neonatal sepsis typically occur in foals?
During the neonatal period
233
What are the primary routes of bacterial introduction in neonatal foals?
Inhalation
234
What is the most important factor in preventing neonatal sepsis?
Adequate passive transfer of maternal antibodies (IgG >800 mg/dL).
235
What is the most common bacterial isolate in neonatal foal sepsis?
E. coli.
236
What are other common bacterial causes of neonatal sepsis?
Streptococcus
237
What are the primary clinical signs of neonatal sepsis?
Weakness
238
What are key clinicopathologic abnormalities in neonatal sepsis?
Leukopenia
239
What diagnostic test definitively confirms neonatal sepsis?
Positive blood culture with bacterial identification and antimicrobial susceptibility testing.
240
What is a sepsis score in neonatal foals?
A point-based system that assigns values to abnormalities such as hypoglycemia
241
What are the main components of neonatal sepsis treatment?
Fluid therapy
242
What is a key complication of neonatal sepsis?
Septic arthritis
243
What is the prognosis for neonatal sepsis?
Guarded to good with early aggressive treatment; complications may worsen prognosis.
244
What is a major concern regarding neonatal sepsis treatment?
The cost of intensive care can be substantial for the client.
245
What is the causative agent of Strangles in horses?
Streptococcus equi.
246
What type of bacteria is Streptococcus equi?
Gram-positive
247
What age group is most commonly affected by Strangles?
Young horses (<2-5 years old).
248
How is Strangles transmitted?
Direct contact with purulent discharge from infected horses or contaminated equipment.
249
Where does Streptococcus equi establish infection in horses?
Pharyngeal mucosa and local lymph nodes (intermandibular and retropharyngeal).
250
Why is Strangles named as such?
Severe lymphadenopathy may occlude the airway
251
What is the incubation period for Strangles?
2-7 days.
252
What are the hallmark clinical signs of Strangles?
Fever
253
Which lymph nodes are most commonly affected in Strangles?
Intermandibular
254
What clinicopathologic abnormalities are associated with Strangles?
Neutrophilic leukocytosis and hyperfibrinogenemia.
255
How is Strangles diagnosed?
History
256
When is penicillin recommended in Strangles treatment?
If the horse is febrile without lymph node abscessation or has been recently exposed.
257
Why should penicillin be avoided once lymph node abscessation has occurred?
It may slow abscess maturation; treatment should focus on abscess drainage.
258
How should mature abscesses be managed?
Hot packing to promote maturation
259
What additional management strategies are needed for a Strangles outbreak?
Isolation
260
What is Bastard Strangles?
A form of internal abscessation affecting mesenteric or other lymph nodes.
261
What are the clinical signs of Bastard Strangles?
Chronic intermittent colic
262
What is Purpura Hemorrhagica?
Immune-mediated vasculitis resulting in limb and head edema
263
What complication occurs when purulent material collects in the guttural pouch?
Guttural Pouch Empyema
264
What are the consequences of septicemia in Strangles?
Occasional CNS involvement leading to encephalopathy and poor prognosis.
265
What is the prognosis for Strangles?
Good; most horses recover uneventfully and develop strong immunity
