EBCM Exam Two Flashcards
(205 cards)
1
Q
Asthmatic horses are typically young/middle/older (choose) aged horses.
A
(Middle and older)
2
Q
Pair the clinical signs with the progression of asthma in horses:
Moderate exercise intolerance
A - Severe disease
B - Early disease
C - Moderate disease
A
(B)
3
Q
Pair the clinical signs with the progression of asthma in horses:
Cough and mucoid nasal discharge
A - Severe disease
B - Early disease
C - Moderate disease
A
(C)
4
Q
Pair the clinical signs with the progression of asthma in horses:
Nostril flare and abdominal push
A - Severe disease
B - Early disease
C - Moderate disease
A
(A)
5
Q
Which form of equine asthma is associated with exposure to barn dust, hay dust or hay mold and is more commonly observed in winter?
A
(Typical equine asthma)
6
Q
Which form of equine asthma is associated with pasture, humidity, and hot temperatures and is observed in the south-eastern states such as Virginia?
A
(Summer Pasture Airway Obstructive Disease (SPAOD))
7
Q
What results from exposure to an inhaled irritant that causes bronchoconstriction and mucous hypersecretion?
A
(Airway neutrophilic inflammation)
8
Q
What in the history may distinguish between asthma and an infectious agent in horses?
A
(Exposure history (exposure to infectious agent → infectious; new environment/seasonal onset → asthma), clinical sign (fever → infectious; no fever → asthma), if other animals are affected or not, and onset (acute → infectious; gradual/chronic/recurring → asthma))
9
Q
What are the advantages of a transtracheal wash or brush?
A
(More representative and sterile)
10
Q
What is the advantage of a bronchiolar lavage?
A
(It is a more immediate assessment of inflammation in the lower airways)
11
Q
What type of drug are atropine, ipratropium bromide, and buscopan and which of them is the drug of choice for asthma and why?
A
(They are M3 receptor antagonists; ipratropium bromide is the drug of choice because it does not affect the GI tract like atropine and buscopan do (inhibits GI motility)) They are M3 receptor antagonists; ipratropium bromide is the drug of choice because it does not affect the GI tract like atropine and buscopan do (inhibits GI motility))
12
Q
How do alpha 2 agonists help with asthma?
A
(They block the release of AcH at the neuromuscular junction in the airway → reduces contraction; also increases mucous and water transport and generally promotes smooth muscle relaxation)
13
Q
How do beta 2 agonists help with asthma?
A
(When beta 2 receptors are activated they cause bronchodilation and increase mucous secretions and mucociliary clearance)
14
Q
What are the disadvantages to using systemic steroids for treatment of asthma?
A
(Systemic distribution affects overall immune response → more susceptible to infection, heavy parasite load, and skin disease; and increased risk for laminitis)
15
Q
If you perform a BAL because you want to see if you can stop administering corticosteroids to a horse with asthma, what would indicate that you cannot stop your treatments?
A
(Any presence of neutrophilic inflammation → clinical compromise will return once treatment is stopped)
16
Q
What are some ways to distinguish between inflammatory airway disease and asthma in horses?
A
(Age (IAD → young; asthma → middle to old age); history (IAD → no hx of recurring resp dz; asthma → recurring hx))
17
Q
What is the method of choice for identifying cytological changes that can indicate exercise induced pulmonary hemorrhage?
A
(BAL → you’ll be looking for hemosiderophages)
18
Q
What are the acute signs of equine respiratory viruses? 4 answers.
A
(High fever, general malaise, cough that often persists for several weeks, and clear to mucoid nasal discharge; some viruses can also acutely cause local lnn swelling/tenderness and limb/ventral edema)
19
Q
Pair the following time period in a viral infection with the suggestive clinical pathology that would be found during that time:
Acute
A - Mild to moderate neutrophilia
B - Leukopenia with mild to moderate lymphopenia
C - Monocytosis
A
A - Leukopenia with mild to moderate lymphopenia
20
Q
Pair the following time period in a viral infection with the suggestive clinical pathology that would be found during that time:
After several days
A - Mild to moderate neutrophilia
B - Leukopenia with mild to moderate lymphopenia
C - Monocytosis
A
A - Mild to moderate neutrophilia
21
Q
Pair the following time period in a viral infection with the suggestive clinical pathology that would be found during that time:
During early convalescence
A - Mild to moderate neutrophilia
B - Leukopenia with mild to moderate lymphopenia
C - Monocytosis
A
C - Monocytosis
22
Q
(T/F) Fibrinogen is always increased with viral respiratory infections in horses.
A
(F, fibrinogen is usually normal if there is not secondary bacterial infection)
23
Q
(T/F) Modified live vaccines have a chance of stimulated cell mediated responses.
A
(T, killed vaccines have no chance of stimulated CMI)
24
Q
The equine respiratory panels that Davis, Cornell, and Idexx have available are which of the following tests:
A - ELISA
B - Virus neutralization
C - PCR
D - IHC
A
(C)
25
Are RNA or DNA viruses more fragile and less likely to survive in mucosal discharge?
(RNA (influenza and viral arteritis are RNA)
26
What are the common equine respiratory viruses? 4 answers.
(Equine influenza, equine herpesvirus 1, equine herpesvirus 4, and equine viral arteritis)
27
Antigenic drift/shift (choose) is the change of antigenicity within a viral subtype?
(Drift)
28
What is antigenic drift?
(The change of antigenicity within a viral subtype → mild change in surface antigens but they maintain the same category)
29
What is antigenic shift?
(Development of a new viral subtype → H3N8 versus H7N7)
30
Which type of equine influenza is associated with more severe disease?
(H3N8)
31
What is the incubation period for equine herpes virus?
(2-10 days)
32
(T/F) Most horses are infected with equine herpes virus by the age of 2 years old.
(T)
33
Which of the following transmission routes are viable options for herpes virus?
A - Fomites
B - Vertical
C - Direct contact
D - Recrudescence of infection
E - All of the above
F - None of the above
iykyk
(E)
34
Herpes virus can become latent in infected horses, where does it chillax waiting for a stressful period or corticosteroid usage to peek back out? 2 answers.
(Respiratory lympho-reticular system or the trigeminal ganglion)
35
There are multiple clinical syndromes that are associated with equine herpes virus, one of which is a typical upper respiratory tract infection, what are the other four clinical syndromes?
(Pulmonary vasculotropic infection (can be lethal, causes pulmonary edema), late-term abortion (primarily EHV-1), neonatal foal death (d/t interstitial pneumonia), and myeloencephalopathy)
36
Neurologic signs associated with herpes virus are due to mutation of which strain of herpes virus?
(EHV-1)
37
Abortions caused by equine herpes virus are early/mid/late (choose) term.
(Late term)
38
Broodmares should be vaccinated against herpes virus at what months of gestation to prevent abortion?
(5, 7, 9, 11)
39
If you are presented with an equine abortion case that occurred at 6 months of gestation, the mare currently has respiratory signs, and the fetus is autolyzed, what virus is your top differential?
(Equine viral arteritis → abortion occurs from 3-10 months of gestation, mare usually has resp signs at time of abortion and fetus is autolyzed, which herpes → always 5 months or greater into gestation, mares typically had resp signs a few weeks/months ago, and fetus will not be autolyzed)
40
Persistent infection of equine viral arteritis in stallions is dependent on the presence of which hormone?
(Testosterone)
41
Why might infection of the retropharyngeal lymph node with Strep equi equi not be associated with any swelling?
(Bc they can rupture into the medial floor of the guttural pouch and drain there)
42
What is the treatment for donkey lungworms (Dictyocaulus arnfieldi) that causes eosinophilia, which can be seen on a TTW?
(Ivermectin)
43
What are the three causes for pleural effusion in horses?
(Secondary to pulmonary lymphatic blockage by pneumonic exudate (i.e. secondary to pneumonia), secondary to thoracic neoplasia, and penetrating wound/trauma)
44
What type of history is often associated with infectious pleuritis?
(Stress, transport, recent viral infection, strenuous exercise, and general anesthesia)
45
Why may horses with pleuropneumonia be confused with horses with colic, laminitis, and/or myositis?
(Because they take up a base wide stance d/t pleurodynia)
46
What virus is equine multinodular pulmonary fibrosis associated with?
(EHV-5)
47
What is the most common neoplasia of the equine airway?
(Granular cell tumor)
48
(T/F) Inspiratory noise is always pathologic as it indicates narrowing of the upper airway lumen.
(T)
49
Stridor/stertor (choose) is associated with a low pitched sound.
(Stertor is associated with low pitched sounds, stridor is associated with high pitched sounds)
50
(T/F) Exercising expiratory sounds are normal at a trot, canter, and gallop.
(F, not at a trot, yes at a canter/gallop)
51
What is the primary diagnostic for upper airway cases?
(Endoscopy)
52
Of the following diagnostic techniques, sort them into whether they would be more useful for sinus/nasal passage disease versus larynx/pharynx diseases:
Head radiographs
Dynamic/treadmill endoscopy
Watch during exercise
Head CT/MRI
Dental examination
Ultrasound
Head radiographs (Sinus/nasal passage)
Dynamic/treadmill endoscopy (Larynx/pharynx)
Watch during exercise (Larynx/pharynx)
Head CT/MRI (Sinus/nasal passage)
Dental examination (Sinus/nasal passage)
Ultrasound (Larynx/pharynx)
53
What procedure can be performed to provide an airway in a horse with a life-threatening URT obstruction?
(Tracheotomy)
54
Give causes for the following discharge presentations:
Serous discharge
Serous discharge (Viral respiratory infection, allergic rhinitis)
55
Give causes for the following discharge presentations:
Mucoid to purulent discharge
Mucoid to purulent discharge (Primary or secondary bacterial respiratory infection, sinusitis, tooth root abscess)
56
Give causes for the following discharge presentations:
Fresh hemorrhagic discharge
Fresh hemorrhagic discharge (Guttural pouch mycosis, trauma, lower airway causes such as exercise induced pulmonary hemorrhage)
57
Give causes for the following discharge presentations:
Old hemorrhagic discharge
Old hemorrhagic discharge (Ethmoid hematoma, lower airway causes such as necrotizing pneumonia)
58
Give causes for the following discharge presentations:
Discharge with feed
Discharge with feed (Choke, dysphagia d/t pharyngeal obstruction)
59
Give causes for the following discharge presentations:
Discharge with a fetid odor
Discharge with a fetid odor (Dental or chronic causes)
60
Is the sinus drainage angle rostral or caudal to the nasal septum termination?
(Rostral, so drainage from the sinus drainage angle will be unilateral)
61
Will discharge from the nostrils be unilateral or bilateral in guttural pouch disease with lots of discharge?
(Bilateral; I put the caveat of lots of discharge because it could be unilateral if there is minimal discharge that only drains down one side but something like GP mycosis induced hemorrhage will be bilateral bc the nasopharyngeal ostia are caudal to the termination of the nasal septum)
62
(T/F) Epidermal inclusion cysts, aka atheroma of false nostril, rarely obstruct the airway and are primarily a cosmetic problem.
(T)
63
Rare enlargement or failure of which muscle allows for alar fold collapse during exercise?
(Transversus nasi muscle)
64
Alar fold collapse is most common in which horse breeds?
(Standardbreds and saddlebreds)
65
Alar fold collapses are associated with noise during inspiration/expiration (choose).
(Both, inspiration mainly/- expiration)
66
(T/F) Alar fold collapses can cause reduced performance.
(T)
67
What is the purpose of performing a resting and/or dynamic endoscopy in cases of alar fold collapse?
(Rule out other causes of noise and exercise intolerance as alar fold collapses can occur in conjunction with other problems)
68
(T/F) There is evidence that nasal strips reduce peak inspiratory pressure and resistance when a horse is maximally exercising by pulling the dorsal conchal folds laterally and expanding the dorsal meatus.
(T)
69
Why is it optimal to close lacerations and wounds of the nares with a primary closure as opposed to second intention healing?
(Scarring can cause secondary stenosis, primary closures minimize scarring)
70
Paralysis of which cranial nerve leads to a lack of tone in the nostril(s) and may cause flutter or even collapse of the nostril?
(Facial nerve/CN VII)
71
(T/F) Nasal mucosal hemorrhage is rare and all other possible causes of epistaxis should be ruled out first.
(T)
72
When may the collection of blood vessels aka nasal varicosities that bleed in cases of nasal mucosal hemorrhage bleed?
(May bleed during turbulent airflow or randomly)
73
What radiographic projection should be taken in a case of wry nose to determine the degree of deviation?
(A dorsoventral radiograph of the nose)
74
What treatment is pursued in mild cases of wry nose?
(If no dyspnea or problems nursing in a foal, no treatment needed → reduce owner expectation for athleticism and will need to correct asymmetric growth of incisors as needed)
75
What treatment is pursued in severe cases of wry nose?
(Permanent or temporary trach and/or correction via premaxillary/maxillary osteotomy with internal or external fixation)
76
What results from a failure of bucconasal membrane rupture in early gestation?
(Choanal atresia, can be bilateral or unilateral, bilateral cases are fatal without trach)
77
How do the treatments for choanal atresia and choanal stenosis differ?
(Atresia → can relieved the atresia surgically with a laser or long instruments; stenosis → palliative care (can’t really widen the nasal passages))
78
What should you rule out prior to removing a nasal polyp via amputation with an OB wire?
(Rule out an extension of a sinus cyst or involvement of the polyp with the dorsal or ventral nasal conchae → done via radiograph or endoscopy)
79
What is the treatment for fungal rhinitis in horses?
(Surgical debulking AND systemic antifungals (fluconazole or voriconazole)
80
What does the success of treatment of fungal rhinitis in horses depend on?
(Extent of the lesions, causative pathogen, and site of infection)
81
Infections with which fungal organism is common after sinus surgery in horses?
(Aspergillus)
82
(T/F) Nasal septal defects can be congenital or acquired.
(T, congenital makes sense, acquired can be from a conchal mass effect; surgery to resect nasal septum is difficult and associated with blood loss)
83
Which other sinus communicates with the ventral conchal sinus?
(Rostral maxillary sinus)
84
Which other sinuses communicate with the caudal maxillary sinus?
(Frontal and sphenopalatine)
85
What is the most common cause of secondary sinusitis?
(Dental-related sinusitis)
86
What is primary versus secondary sinusitis?
(Primary sinusitis is diagnosed when you cannot find any underlying cause of sinusitis, secondary sinusitis occurs secondarily to a primary disease process)
87
How do the treatments differ for acute versus chronic cases of primary sinusitis?
(Acute → broad spectrum antimicrobials for about a week; chronic (or acute cases that do not respond to broad spectrum abx) → sinus lavage, may need to repeat, and broad spectrum abx)
88
Which of the sinuses of the equine head can be accessed via a conchofrontal sinus trephination?
(Frontal, dorsal conchal, caudal maxillary, and sphenopalatine)
89
Which of the sinuses of the equine head can be accessed via a rostral maxillary sinus trephination?
(Rostral maxillary sinus and ventral conchal sinus)
90
Which of the sinus trephination sites can be utilized for through-through lavage?
(Caudal maxillary site)
91
Sinoscopy is performed via which sinus trephination site?
(Conchofrontal sinus)
92
What further tissue dissection must occur if you want to gain access to the rostral maxillary and ventral conchal sinuses with a frontonasal bone flap?
(You must fenestrate the maxillary septal bulla to gain access to those two sinuses via a frontonasal bone flap)
93
What radiographic view is best for finding the circular sinus cyst lesions?
(Oblique radiographs)
94
What occurs secondary to obstruction of sinus drainage which can occur if sinus cysts grow large enough?
(Sinusitis)
95
What might you see on radiographs of a horse with sinus neoplasia?
(Soft tissue or fluid opacity with loss of bone architecture)
96
What are the types of neoplasia that can affect horse sinuses?
(SCC, adenocarcinoma, fibroma, chondroma, hemangiosarcoma, and osteosarcoma)
97
What is the prognosis for sinus neoplasia with treatment?
(Poor → most are euthanized or have palliative care, tx is surgical resection and radiation typically)
98
Suture periostitis is more commonly a young/middle/old (choose) age horse problem.
(Young)
99
What radiographic view is best for observing suture periostitis and what would you look for?
(Oblique rads, will see a gap and periosteal proliferation at the facial sutures)
100
What is the purpose of administering antibiotics to an older horse with suture periostitis secondary to trauma?
(Prevention of secondary sinusitis)
101
Which imaging modality is particularly useful in cases of sinus fractures to look for the extent of damage?
(CT)
102
Is the intermittent epistaxis associated with progressive ethmoid hematomas more commonly unilateral or bilateral?
(Unilateral, bilateral possible if the animal is bilaterally affected but that is less common)
103
What diagnostic technique is best for progressive ethmoid hematomas and what will you expect to see?
(Endoscopy is diagnostic in most cases, will see a dark red to tan-brown encapsulated mass)
104
What is the purpose of performing radiographs in progressive ethmoid hematoma cases?
(To check for sinus involvement)
105
What is the most common first-line treatment for progressive ethmoid hematomas?
(Formalin injection, 25-50mls of 4-10% formalin adm via trans-endoscopic needle, repeated every 3-4 weeks for an average of 5 injections, continue until resolved)
106
Involvement of which sinus in cases of progressive ethmoid hematomas is the most common reason for recurrence?
(Sphenopalatine sinus)
107
Which vessel and cranial nerve are associated with the lateral compartment of the guttural pouch?
(CN7 and external carotid artery)
108
Which vessel and nervous structures are associated with the medial compartment of the guttural pouch?
(CN 9, 10, 11, and 12, sympathetic trunk, and the internal carotid artery)
109
What clinical signs may result from nerve dysfunction associated with the guttural pouches?
(Facial nerve paralysis (eyelid, lip drooping, etc.), dysphagia d/t loss of soft palate function, laryngeal dysfunction, and horner’s syndrome)
110
Of the surgical correction options for guttural pouch tympany, which can be used for bilateral cases?
(Transendoscopic laser creation of a salpingopharyngeal fistula (drains air from both GPs); other surgical correction is a median septum fenestration but this is for unilateral cases (the abnormal air in the affect GP will drain out of the working ostia of the normal GP))
111
What age range is associated with guttural pouch tympany?
(Birth to one year old)
112
What causes guttural pouch tympany?
(The salpingopharyngeal ostium becomes a one-way valve so air can leak into the GP but cannot escape, what causes that to occur your guess is as good as mine)
113
What clinical signs can be seen in cases of GP empyema, which can occur as an extension of URT infections or when the retropharyngeal lnn bursts into the GP?
(Intermittent unilateral nasal discharge, lymph node enlargement, parotid swelling/pain, respiratory noise, and dysphagia)
114
What organism should be screened for in cases of GP empyema?
(Strep equi subsp. equi)
115
In a case of arterial hemorrhage secondary to guttural pouch mycosis, you should wait for what to occur prior to transporting the horse for treatment?
(Clotting and the bleeding to stop, don’t just throw them on a trailer while they’re still actively bleeding)
116
Why might you administer acepromazine to a horse with guttural pouch mycosis either before or after a bleeding event?
(Reduces blood pressure and will keep them calm)
117
What should you do prior to sedating a horse for endoscopy in cases of GP mycosis?
(Assess their systemic status, determine if systemically stable)
118
Explain the premise of placing surgical coils/plugs for treatment of GP mycosis.
(You’re stopping blood flow in the affected artery and starving the fungus)
119
Though the prognosis for GP mycosis is good when treated surgically, it is worse if what signs are present?
(Neurologic signs → head tilt, dysphagia, facial nerve paralysis)
120
What does medical treatment entail for temporohyoid osteoarthropathy and will medical tx improve neurological signs if they are present?
(Medical therapy entails antibiotics and anti-inflammatories for at least 3 weeks, no medical tx will not improve neurological signs)
121
What is the goal of surgical treatment of temporohyoid osteoarthropathy?
(Remove stresses on temporohyoid joint by removing part of the hyoid apparatus → ceratohyoidectomy to be specific)
122
Are the constrictor/elevator muscles or the dilator/tensor muscles of the soft palate important for inspiration?
(Dilator/tensor muscles, constrictor/elevator muscles important for swallowing)
123
Which of the cranial nerves innervate the muscles of the pharynx?
(CN 5, 9, and 10)
124
Lymphoid hyperplasia is more commonly a young/middle/old age horse problem.
(Young, 1-3 years of age, can occur in older horses secondary to inflammation)
125
What is the most common cause of upper airway obstruction in racehorses?
(Palatal dysfunction)
126
Dorsal displacement of the soft palate is associated with obstructing the airway during expiration or inspiration?
(Expiration, gurgling or flutter noise on expiration though can be silent)
127
What is caused by dorsal displacement of the soft palate that ultimately leads to reduced performance?
(Hypercarbia)
128
35% of horses have DDSP at rest which should correct itself if you make them swallow, if it does not correct itself, what should you evaluate the epiglottis for?
(Hypoplasia, epiglottic entrapment, and subepiglottic cysts)
129
Why does medical treatment for DDSP involve NSAIDs, corticosteroids, topical anti-inflammatory throat spray, and changing the environment to minimize dust/mold?
(One of the theories behind why horses get DDSP is inflammation causing neuromuscular dysfunction of the soft palate muscles and/or nerves so thought that if you reduce inflammation, it can treat the DDSP)
130
What are the goals of sternothyroideus tenotomy/tenectomy/myectomy and laryngeal tie-forward surgery, both of which are used for correction of DDSP?
(These surgical correction aim to move the position of the larynx forward so as to keep the soft palate below the epiglottis where is belongs)
131
What is the goal of a laser or thermal palatoplasty which is used for correction of DDSP?
(The resultant scarring is meant to stiffen the soft palate to prevent the dorsal billowing that leads to DDSP)
132
In cases of nasopharyngeal cicatrix there are often no clinical signs unless pharyngeal constriction occurs (variable URT noise and poor performance); those signs will be more severe if what laryngeal cartilage is involved?
(Arytenoid cartilages)
133
How do foals with nasopharyngeal dysfunction typically present and what should you do as soon as possible in those cases?
(Respiratory distress and dysphagic, need to perform a tracheotomy asap, also check for FPT)
134
Why is the prognosis poor to grave for cleft palates in horses?
(Repair has a high chance of dehiscence due to tension, grave prognosis if hard palate involved)
135
Laryngeal hemiplegia is associated with an expiratory or inspiratory obstruction?
(Inspiratory)
136
What does your choice of treatment for laryngeal hemiplegia depend on?
(The job of the horse, conservative appropriate for non-athletic horses, surgical for athletic horses)
137
Of the surgical options for laryngeal hemiplegia (prosthetic laryngoplasty and ventriculocordectomy), which primarily prevents noise?
(Ventriculocordectomy, prosthetic laryngoplasty improves exercise intolerance by tying back the arytenoid cartilage)
138
(T/F) Once the cricoarytenoid dorsalis muscle has lost its function, it cannot be regained.
(F, can be re-innervated overtime, usually 12 months)
139
What is the difference between laryngeal hemiplegia and arytenoid chondropathy?
(Laryngeal hemiplegia is loss of innervation to the CAD causing the inability to abduct the arytenoid cartilage, arytenoid chondropathy is deformation of the arytenoid cartilage due to infection)
140
What imaging modality is useful in determining if a horse has laryngeal hemiplegia versus arytenoid chondropathy?
(Ultrasound, will see an abnormally shaped/enlarged arytenoid with arytenoid chondropathy or an atrophied cricoarytenoid lateralis muscle with laryngeal hemiplegia)
141
What structures cover the epiglottis in cases of an entrapped epiglottis?
(Aryepiglottic folds and subepiglottic mucosa)
142
What is the treatment for an epiglottic entrapment?
(Axial midline division of the subepiglottic mucosa that is covering the epiglottis, make sure to not cut the epiglottis)
143
What electrolyte channels open during phase 0 of a cardiac action potential?
(Sodium voltage gated channels)
144
What electrolyte channels opened and closed during phase 1 of a cardiac action potential?
(Sodium close, potassium open)
145
Calcium channels are open/closed (choose) and potassium channels are open/closed (choose) during phase 3 of a cardiac action potential?
(Calcium channels are closed, and potassium channels are open)
146
Where does electrical activity in the heart start?
(Sinoatrial node)
147
Depolarization of which part of the heart is represented by the P wave in an ECG wave?
(Atrial depolarization)
148
Depolarization of the ventricles is indicated by what portion of an ECG wave?
(QRS complex)
149
Repolarization of the ventricles is indicated by what portion of an ECG wave?
(T wave)
150
Describe the placements of the ECG leads in a lead I base-apex ECG, be specific.
(White (negative) is placed at the point of the shoulder on the right side of the animal, black (positive) is placed in the axilla on the left side of the animal (at the apex of the heart), and red (ground) can be placed anywhere on the left side of the animal)
151
What should you evaluate when looking at an ECG of an animal?
(Heart rate, RR interval, P and QRS relationship (P before every QRS? Normal PR interval?), and complex morphology)
152
(T/F) It is normal for the P wave to be biphasic in a horse as long as it shows consistency.
(T, bc the atrium is large and it can take awhile for the entire atrium to depolarize)
153
A horse is considered to be in sinus tachycardia when their heart rate is above what value?
(50 bpm)
154
How can you determine if a bradyarrhythmia is caused by high parasympathetic tone associated with a resting horse or a pathology?
(Exercise the horse to increase sympathetic tone, if its gone then it was physiologic, if it is still present it is pathologic)
155
Describe a sinus arrhythmia.
(Variable RR interval, each QRS is normal and preceded by a P wave, and the pauses are less than or equal to two normal P-P intervals)
156
What is the most common non-pathologic cardiac arrhythmia in horses?
(2nd degree AV block)
157
What is the difference between a 2nd degree AV block and an advanced 2nd degree AV block?
(2nd degree AV block is an occasional P wave not followed by a QRS wave, advanced 2nd degree AV block is two or more P waves not followed by a QRS complex; important to note that ALL QRS complexes are preceded by a P wave in these abnormal ECGs)
158
Describe a 3rd degree AV block.
(P waves present but have no association with QRS complexes, QRS complexes are wider with an irregular R-R interval)
159
What is the difference between 2nd degree AV blocks and premature atrial complexes?
1) the heart rate, will be slow with 2nd degree AV blocks and fast with premature atrial complexes
2) the pathology, 2nd degree AV blocks are normal SA node depolarizations that just don’t trigger the AV node and ventricles whereas premature atrial complexes are when sites of the atrium besides the SA node depolarize spontaneously, which can then trigger or not trigger the ventricles as well)
160
What is the most common pathologic arrhythmia in horses?
(Afib)
161
(T/F) All of the appropriate waves (P, QRS, and T) will be present on an ECG of a horse with atrial fibrillation, the P waves will just be at a much higher rate and will not be associated with QRS complexes.
(F, there will be a lack of P waves, this is the hallmark of Afib)
162
What structural heart disease is thought to be associated with atrial fibrillation in horses?
(Progressive atrial enlargement → as the larger the atria become, the less organize the electrical activity is thought to be; only issue is some horses without structural heart dz have afib so true etiology is unknown atm)
163
What electrolyte deficiency is thought to be associated with atrial fibrillation in horses?
(Hypokalemia)
164
What endocrine disorder is thought to be associated with atrial fibrillation in horses?
(Hyperthyroidism)
165
What things will affect the prognosis of conversion to NSR and maintenance of NSR in horses with afib?
(The duration of which they have had afib and heart size)
166
Why do horses with afib have suboptimal cardiac output?
(They lack atrial contribution to ventricular filling, leads to the development of exercise intolerance and increased heart rate (>220 bpm) to compensate for decreased cardiac output)
167
What other arrhythmia can result from the decreased cardiac output and decreased cardiac muscle oxygenation associated with afib in racehorses?
(Premature ventricular complexes)
168
What medical therapy can be used to convert horses in afib to NSR?
(Quinidine sulfate → sodium channel blocker that also affects potassium channels, prolongs the refractory period and slows action potential conduction)
169
The progressively increased shocks applied for transvenous electrocardioversion must be delivered precisely on which wave of the ECG complex?
(The R wave)
170
What are premature ventricular complexes and are they associated with (aka what causes them but they don’t want to say cause because they haven’t proven it)?
(VPCs are premature, abnormal QRS complexes that are not preceded by a P wave, they are associated with colic, electrolyte abnormalities, myocarditis, and exercise)
171
Ventricular tachycardia is considered how many or more PVCs in a row?
(3 or more PVCs in a row)
172
Is uniform or multiform ventricular ectopy worse?
(Multiform; uniform is when all QRS complexes look the same (still abnormal but they are all at least similarly abnormal, this means they are sourced from the same location), multiform is when there are different types of QRS complexes, this means there are multiple portions of the ventricles sending out electrical impulses and if two were to go at the same time, bye bye life)
173
Pair the following class of antiarrhythmic drug to 1) the type of blocker it is and 2) the phase it works on:
Class I
Potassium channel blockers
Beta blockers
Calcium channel blockers
Sodium channel blockers
Phase 0
Phase 1/3
Phase 2
Phase 4
(Phase 0, sodium channel blockers → lidocaine, quinidine)
174
Pair the following class of antiarrhythmic drug to 1) the type of blocker it is and 2) the phase it works on:
Class II
Potassium channel blockers
Beta blockers
Calcium channel blockers
Sodium channel blockers
Phase 0
Phase 1/3
Phase 2
Phase 4
(Phase 4, beta blockers → sotalol)
175
Pair the following class of antiarrhythmic drug to 1) the type of blocker it is and 2) the phase it works on:
Class III
Potassium channel blockers
Beta blockers
Calcium channel blockers
Sodium channel blockers
Phase 0
Phase 1/3
Phase 2
Phase 4
(Phase 1/3, potassium channel blockers → sotalol)
176
Pair the following class of antiarrhythmic drug to 1) the type of blocker it is and 2) the phase it works on:
Class IV
Potassium channel blockers
Beta blockers
Calcium channel blockers
Sodium channel blockers
Phase 0
Phase 1/3
Phase 2
Phase 4
(Phase 2, calcium channel blockers → magnesium sulphate is a physiologic calcium channel blocker)
177
What is the treatment of choice for torsades de pointes and digitalis toxicity?
(Magnesium sulphate)
178
What is the difference between innocent, functional, and pathologic murmurs?
(Innocent and functional occur in the absence of structural cardiac disease, pathologic is associated with structural cardiac dz; innocent associated with an unknown origin, functional occurs with dehydration, colic, fever → resolves when you resolve the inciting cause)
179
Decrescendo murmurs are classic for which heart pathology?
(Aortic regurgitation)
180
You hear a murmur between S1 and S2 on the left side of a horse, what is most likely to be the problem?
(Mitral valve regurgitation → most common left sided systolic murmur in horses)
181
You hear a murmur between S1 and S2 on the right side of a horse, what is most likely to be the problem?
(Tricuspid valve regurgitation → most common right sided systolic murmur in horses)
182
You hear a murmur between S2 and S1 on the left side of a horse, what is most likely to be the problem?
(Aortic valve regurgitation → most common left sided diastolic murmur in horses)
183
What are the causes of mitral regurgitation?
(Valvular dysplasia, degenerative thickening of the leaves, ruptured chordae tendineae, and endocarditis)
184
Regurgitation at which valve is the most common cause of congestive heart failure in horses?
(Mitral, but mild MR is associated with a normal athletic performance and life expectancy so monitoring is extremely important bc it can progress to CHF, cardiac u/s annually)
185
What are the causes of aortic regurgitation in horses?
(Age related valvular degeneration or valvular prolapse)
186
Why is tricuspid regurgitation a common finding in equine athletes?
(Bc as they exercise regularly, the right side of the heart becomes more robust and muscular which can cause tricuspid regurg)
187
What are the goals for treatment of valvular regurg?
(Decrease cardiac work by decreasing afterload (by decreasing systemic vascular resistance), slow progression of cardiac chamber enlargement (kinda goes hand in hand with decreasing cardiac work), and improve cardiac contractility)
188
What type of drug is benazepril and what does it do for the heart?
(ACE inhibitor, decreased afterload, improves systolic function and cardiac output, and slows cardiac remodeling via an unknown mechanism)
189
What type of drug is digoxin and what does it do for the heart?
(Cardiac glycoside, increases parasympathetic tone therefore reducing vasoconstriction and slowing the heart rate which helps to improve stroke volume (lower heart rate allows for greater diastolic filling which increase end-diastolic volume which increase stroke volume (stroke volume = end-diastolic volume minus end-systolic volume))
190
What is the most common congenital cardiac anomaly in horses?
(Ventricular septal defects)
191
What is the normal flow of blood through a PDA, what can cause it to reverse, and what results from the reversal?
(Normal flow → aorta to pulmonary artery; causes of reversal → if defect is large and/or chronic and if pulmonary hypertension is present; results of reversal → cyanosis +/- syncope)
192
What are the characteristics of a restrictive ventricular septal defect that is associated with a good prognosis for athleticism?
(Size of less than 2.8 cm and a shunt speed of faster than 4 m/s (indicates normal pressure differential b/w right and left heart))
193
How do horses with infective endocarditis commonly present?
(Fever, weight loss, inflammatory leukogram with hyperfibrinogenemia and hyperglobulinemia, and may have concurrent arrhythmias)
194
What are the three types of pericarditis?
(Effusive, fibrinous, and constrictive)
195
What clinical signs result from cardiac tamponade, which can occur in horses with constrictive pericarditis?
(Increased heart and resp rate, increased jugular pulses, weak arterial pulses, and ventral edema)
196
What would you look for on a CBC in a horse with pericarditis to indicate infection versus idiopathic/neoplastic?
(Leukocytosis and increased acute phase proteins (SAA, fibrinogen) would indicate infection)
197
What diagnostic imaging modality is best for cases of pericarditis?
(Ultrasound → look for fluid/fibrin in the pericardial space)
198
What is the purpose of submitting blood for a cardiac troponin test?
(cTNI is a marker for myocardial damage, will help to guide therapy depending on severity of damage to the heart)
199
What are the normal values for protein and TNCC for pericardial fluid?
(Protein < 2.5 g/dL, TNCC < 1500 x 106/L)
200
Describe the difference between the pericardial fluid in an idiopathic versus bacterial pericarditis case.
(Idiopathic → increased protein and non-degenerate neutrophils; bacterial → degenerate neutrophils, may see bacteria)
201
What are the most common toxic causes of myocarditis in horses?
(Cardiac glycoside plants specifically oleander, cantharidin formed by blister beetles, and ionophores such as monensin or lasalocid)
202
What deficiency is associated with nutritional myodegeneration?
(Vitamin E and/or selenium deficiency, both help to protect cells against free radicals, chronic deficiencies lead to fibrosis of muscles that are constantly in work i.e. heart, prognosis is guarded but some can improve with tx)
203
Why is an ECG and echocardiogram indicated in myocarditis cases?
(ECG to identify cardiac arrhythmias, echo to image the myocardium and calculate fractional shortening to get information about cardiac output)
204
Fractional shortening that persists over a few weeks at what percent or lower in cases of myocarditis indicate a poorer prognosis?
(20%, normal is 30-45%)
205
What are the clinical signs associated with aortic rupture?
(Besides per acute death? Colic, tachycardia, sweating, and a continuous murmur, all shortly followed by death)
