Equine 3 Flashcards

1
Q

Equine herpesvirus myeloencephalopathy. Which statement is true?
 It is caused by EHV-2, on immuno-mediated basis, due to type 3 hypersensibilization
 It is caused by EHV-1, or sometimes by EHV-4, on an immune-mediated basis, due to type 3 hypersensibilization
 The symptoms can be seen in horses vaccinated against EHV because of immuno- complex based vasculitis
 In foals neurlogic signs are less frequent

A

B ?

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2
Q

Which disease most resembles rabies in horses?
 Tetanus
 Botulismus
 Equine Leukoencephalomalacia ELE
 Equine Meningoencephalitis THEME caused by Heamophilus somnus

A

c

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3
Q

Equine laryngeal hemiplegia/diagnosis?

 Grade 1: obvious asymmetry at test, no movements
 Grade 3: asynchronous movement, no complete opening
 Grade 1: asyncrhonicity, tremor, weak movements, complete open with
nasal occlusion
 Grade 3: synchronicity, complete closure and opening

A

B

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4
Q

COPD(RAO)
 Allergic disease
 Chronic fungal infection
 Chronic bacterial infection
 Chronic viral infection

A

A

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5
Q

Guttural pouch mycosis/signs?
 Unilateral nasal bleeding, fever, halitosis
 Bilateral nasal discharge, fever, cough
 Epistaxis, nasal discharge, dysphagia, laryngeal paralysis, Horner syndrome
 Swollen parotid region, loss of appetite, weightloss, cough

A

C

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6
Q

Resp rate of normal adult horse is:
 10-18 bpm
 20-28
 30-38
 40-48

A

A

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7
Q

Which method is suitable for tracheal fluid sampling?
 Aspiration via sterile catheter introduced through the endoscope
 Induced cough
 Aspiration through the accessory channel of the endoscope
 Collection of nasal discharge under sedation when the head is lowered

A

C

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8
Q

A tracheal wash sample is suitable:
 Culture
 Cytology
 Antibody sensitivity test
 All three

A

D

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9
Q

Thoracocentesis possible side effect:

A

Pneumothorax

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10
Q

Thoracocentesis location

A

 7-8th on left or 6-7th on right midway between shoulder and elbow.
 Cranial border of the rib to avoid blood vessels and nerves!

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11
Q

Nose bleed in racehorse
 Consequence of competition’s trauma
 Consequence of incidence of lung-bleeding
 Consequence of dope-using

A

B

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12
Q

Exercise induced pulmonary haemorrhage (EIPH

A

– Exhausting competitions
– Racehorses, three-day-eventers, show jumpers…

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13
Q

Nose bleed in racehorse reasons
 Trauma, haemorrhagic purpura, pharyngitis
 Nasal-tumor, dominant successions, coagulopathy
 Trauma, recessive thoroughbred-sick (EIPH), guttural pouch mycosis

A

C

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14
Q

Rhinitis in horse reasons
 Strangles, satratoxicosis, smoke-, dust inhalation
 Horse flu, fusariotoxicosis, gasterophilus larvae
 Strangles, fumonisin toxicosis, hypoderma larvas

A

A

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15
Q

Ethmoid haematoma
 Haematoma in region of nose or ethmoid, slow progression, nasal stridor, angiomatic tissue growth
 Haematoma in sphenoid bone, unilateral nasal discharge, nervous symtoms
 Haematoma in sphenoid bone, bilateral purulent nasal discharge, progressing in
weeks

A

A

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16
Q

Ethmoid hematome

A
  • Extensive angiomatous tissue overgrowth
  • Ethmoidal region, frontal and maxillar sinus
  • Cause: unknown, in older horses
  • Unilateral, bilateral
  • Signs: nasal discharge (changing quality, usually unilateral), halitosis, respiratory sounds,
    breathing abnormalities, periocular and/or facial swelling, headshaking, coughing
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17
Q

Maxillary sinusitis reasons in horse
 Rhinitis, trauma, sedentation of parasitic larvae
 Strangles, purulent periodontitis, rhinitis
 Infectious artheritis, gasterophilus, strangles

A

B

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18
Q

Maxillary sinusitis syptoms
 Nasal discharge on both sides which is haemorrhagic and purulent, facial deformation/pain, dyspnoe
 Haemorrhagic discharge with debris on both sides during lowering of head, maxillary pain, salivation
 Single side nasal discharge, region of maxillary pain, deformation

A

C

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19
Q

Guttural pouch tympany causes
 Congenital, a plica salingopharyngea hypertrophy, air-outflow blocked
 Hereditary, plica nsopharyngealis immaturity, intense air inflow into guttural
pouches
 Tumescence of plica nasopharyngealis, consequence of strangles, hypertrophy of
guttural pouches

A

A

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20
Q

Guttural pouch tympany symtoms
 Ballooning/pain of region of guttural pouches, dyspnea, regurgitation

 Ballooning, of region of guttural pouches, tympanic percussion sound, paroxysmal
cough

 Ballooning/palpation sensitivity of region of guttural pouches, incomplete dullness percussion sound, dysphagia

A

C
Nonpainful swelling, palpation, percussion (Viborg-triangle), uni/bilateral - Compression of the nasopharynx, labored breathing, dysphagia

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21
Q

Guttural pouch inflammation causes
 Infection through Wilson-duct, -with spread over, caused by anaerob bacteria
 Infection through Stenon-tunnel, consequence of strangles, caused by mycotic
disease
 Infection through Eustachion tube, or with spread over, caused by bacteria or mycotic disease

A

C

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22
Q

Guttural pouch inflammation symptoms
 During lowering of head purulent nasal discharge, ballooning of region of parotis, complications of nervous system
 Consistent, hemorrhagic, purulent nasal discharge, tumescence in the throat, extension of the head, head tilt, proprioceptional disorder
 Single side nasal discharge, sore tumescence in the sulcus jugularis, swallowing disorder

A

A

Purulent nasal discharge, painful, swollen region, labored breathing, dysphagia, extended neck - Chondroids

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23
Q

Dorsal displacement of the soft palate symptoms
 Exercise intolerance, sounds during expiration, diagnose in necrotized condition via endoscope
 Don’t cause exercise intolerance, sounds during expiration, diagnose in submaximal load via endoscope
 Cause exercise intolerance, sounds during expiration, diagnose in submaximal load via endoscope

A

C

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24
Q

Tracheal collapse
 Disease of ponies
 Congenital disease
 In big horses

A

A

Tracheal collapse
- Ponies, miniature horses
- Ligamentous part of trachea
- Negative pressure increases, other respiratory disoders in the background
- Circulus viciosus

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25
Laryngeal hemiplegia causes  Idiopathic, common in carthorse, frequent occurrence in paryngo-laryngitis  Hereditary, in rhinopneumonitis, idiopathic distal axonopathy,  Hereditary in Arabian horses, n. vagus nucleus trauma, idiopathic
B
26
Crycoarytenoideus dorsalis muscle innervatory problem (n. recurrens)
Generalized distal axonopathy - Causes: mechanical compression, inflammation, vitamin deficiency, paravenous injury, lead toxicity, organophosphate, toxicity, toxic plants, mycosis, neoplasia
27
Laryngeal hemiplegia symptoms  During inspiration beep sound-rattle, dyspnea, swallowing disorder  During expiration beep sound-rattle, expiration dyspnea, sore swelling of muscles of larynx  During inspiration stridor laryngis, fremitus laryngitis, barren larynx
C Signs: typical inspiratory stridor, poor performance, palpation ‘slap’ test, rest and exercise endoscopy
28
Laryngeal hemiplegia diagnosis  Endurance test, endoscope, “slap” test  Keeping horse stopped, US exam, endoscope  Endurance test, larynx x-ray, “slap” test
B
29
Laryngeal oedema causes  Allergy, pneumony, bee-sting  Laryngitis, hemorrhagic purpura, insect-sting  Hemorrhagic purpura, laryngeal paralysis, lead poisoning
B
30
Purpura hemorrhagica is a noncontagious, immune-mediated vasculitis of horses that is characterized by subcutaneous edema of the head, ventral abdomen, and limbs and by petechial hemorrhages of the mucous membranes
PURPURA HORSES HEMORRHAGES -Fill in the blank answers
31
Laryngeal oedema treatment  Prednisolone, laryngotomy, metronisazole  Laryngotomy, prednisolone, bromhexine inj  Prednisolone, tracheotomy, antihistamines
C
32
COPD diagnosis, complementary examination  TTL, atropine test, resp function exam, thorax x-ray  BAL-neutrophil %, atropine test, resp function exam, endoscopy  BAL and TTL-eosinophil %, thorax supersonic wave, lobelin test
B
33
COPD incidence  In older, stalled horses, giving mouldy hay  In free keeping horses, in hard working horses  In hereditary dispositional foals or horses
A
34
COPD etiology  Hereditary disposition, bacterial, viral bronchitis, race  Inspiration allergen (Micropolyspora faeni, Aspergillus spore), genetic predisposition  Allergic or bacterial resp disease hyperactivity
B
35
COPD pathogenesis Bronchitispneumoniaemphysema pulmonis Rhinitislaryngitisbronchitisallergen inspirationemphysema pulmonis  Hypersensitivity  neutrophils accumulating intraluminal  intraluminal fibrosis  emphysema
C
36
COPD 3rd grade CS  Frequent, light cough, dyspnea, border of lings shifting 1-2 ICS  Humid cough, broken-wind groove, border of lungs shifting 1⁄2 ICS  Paroxysmal cough, doubled expiration, border of lungs shifting 1 ICS
A
37
COPD 4th grade CS  Frequent paroxysmal cough, severe dyspnea, suffocating enlarged cardiac dullness  Frequent light cough, doubled expiration/broken-wing groove, border of lungs shifting back 2 ICS  Frequent aching cough, inspirational dyspnea
B
38
COPD tx with glucocorticoids  Inspiration glucocorticoids dispose to pododermatitis  The best is prednisolone PO  It is contraindicated to give them with bronchodilators
B
39
Bronchodilators in horse  Clenbuterol, salmeterol, albuterol  Albuterol, atropine, bromhexine  Clenbuterol, acetylcysteine, dembrexine
A
40
Mucolytics for horses  Atropine, terbutaline, dembrexine  Acetylcysteine, bromhexine, dembrexine  Terbutaline, celbuterol, dexamethasone
B
41
Acute alveolar pulmonary emphysema causes  Allergic rxn, heavy physical strain, glechoma hederacea (ground ivy) poisoning  Autoimmune rxn, pulmonary aspiration, threadworm larvae  Trichostrongylosis, allergy, aflatoxin poisoning
A CX:  Extreme work  Allergic reactions  toxicoses  Ground Ivy (Glechomahederacea) plant toxicosis
42
Acute alveolar pulmonary emphysema signs  Incr resp effort, caudal shift of lung border, dull-tympanic percussion sound  Serious dyspnea, 1-3 rib spaces shift of the lung border, cyanosis  Quick fatigue, epistaxis, tympanic percussion sound
B
43
Exercise induced pulmonary hemorrhage  Epistaxis in English thoroughbreds, frequently returns, causes anaemia  Pulmonary hemorrhage in racehorses, caseous necrosis of the lung’s lobe, exercise intolerance  Pulmonary hemorrhage after competition, recidivism, bleeding spontaneously stops
C
44
ronchitis-pneumonia origin of viral infection  EHV-1, equine influenza virus A, rhinovirus 2  Adenovirus A, equine reovirus A, equine arbovirus 1 and 2  Equine influenza virus 1 and 3, equine adenovirus, PI-B
A
45
Bacterial bronchitis pneumonia origin  Bordetella pneumoniae equi, Streptococcus pneumoniae equi, Chlamydia bronchiseptica  Streptococcus equi, Rhodococcus equi, Bordetella bronchiseptica  Mycoplasma hyopneumoniae equi, Chlamydophila equi, Corynebacterium pyogenes
B
46
Bacterial bronchitis pneumonia origin  Bordetella pneumoniae equi, Streptococcus pneumoniae equi, Chlamydia bronchiseptica  Streptococcus equi, Rhodococcus equi, Bordetella bronchiseptica  Mycoplasma hyopneumoniae equi, Chlamydophila equi, Corynebacterium pyogenes
B
47
Mycotic bronchitis pneumonia origin  Pneumocystic carinii, Aspergillus species, Histoplasma equi  Coccidiodes equi, Pneumocystis carinii, Actinobaculum equi  Histoplasma capsulatum, Rhinosporidium seeberi, Coccidiodes immitis
C
48
Horses with compromised immune response – Parasites  Pneumocystis carinii  Parascaris equorum  Dyctiocaulus arnfieldi (donkeys, mules) – Fungi  Histoplasma capsulatum  Rhinosporidium seeberi  Coccidioides immitis  Aspergillus, Candida, Mucor, Rhizopus sp.  Cryptococcus neoformans
49
Horses with compromised immune response – Parasites  Pneumocystis carinii  Parascaris equorum  Dyctiocaulus arnfieldi (donkeys, mules) – Fungi  Histoplasma capsulatum  Rhinosporidium seeberi  Coccidioides immitis  Aspergillus, Candida, Mucor, Rhizopus sp.  Cryptococcus neoformans
50
Bronchopneumonia characteristics  Catarrhal style, bacterial origin, lobular extent  Catarrhal-purulent, bacterial origin, interstitial  Effusion, bacterial origin, interstitial
A
51
Viral pneumonia characteristics  Lobular interstitial, hepatic character, becoming chronic  Interstitial fibrosis and/or secondary bacterial infection hypoxia, acidosis
C
52
Croupous pneumonia stages  Yellow hepatisation  grey hepatisation  resolution  Fibrinous  haemorrhagic  hepatisation  crisis  Hyperaemia  hepatisation  resolution
C
53
Gangrenous pneumonia pathogenesis  Aspiration, putrid bronchitis  lung cavities  septicaemia  Pneumonia crouposa, exsudate  putrid bacteria  Metastasis or transmission; purulent localization in the lungs  infection with protease bacteria
A
54
Purulent pneumonia CS  Languor, serous-purulent nasal discharge, dullness with horizontal upper border by percussion, dyspnea  Weakness, purulent nasal discharge, dyspnea, whistling-wheezing resp sounds  Fever, bloody-frothy nasal discharge, dyspnea, dry cough, wide dullness
B
55
Croupous pneumonia CS  Peracute, racking cough, by mobbing stronger dyspnea, dullness with horizontal upper border, course within 1w  Course in 2-3w, freq becomes chronic, serous nasal discharge, dullness, catarrhal resp sounds  Acute course: 2w, high fever, serosanguinous nasal discharge, wide dullness, dyspnea/cyanosis
C High fever, nasal discharge: mucous, yellow or reddish, viscous – coughing: rare, painful, weak mixed, abnormal – auscultation: respiratory sounds, – percussion: atelectasis dullness
56
Gangrenous pneumonia CS  Within days fast general health decay  death, malodorous-putrid breath, smelly nasal discharge, dyspnea  Course in 1-2wfreq death, bloody-purulent nasal discharge, rapid, often cough, splashing sounds in the dullness area  Typically insp dyspnea, wide dullness, catarrhal resp sounds, long recovery
A
57
Aspiration pneumonia – localization of the dullness and resp sounds  Lower third of the chest, region of the cardiac basis  Caudal third of lungs, where the ventilation is bad  Craniodorsal part of the lungs
A
58
Pneumonia treatment – antibacterial agents  Ampicillin, lincomycin, ticarcillin, metronidazole  Amoxicillin, gentamycin, tilozin, cephalexin  Cephalexin, clindamycin, metronidazole, neomycin
B
59
Antibacterial drugs used in equine pneumonia  Amoxicillin - 30mg/kg/12h IV, IM  Ampicillin - 20mg/kg/8hIV, PO  Cefquinom - 1-2mg/kg/24h IV, IM  Gentamycin - 6.6mg/kg/24h IV  Kanamycin - 5-10mg/kg/24h IM, IV  Metronidazole - 25mg/kg/12h PO  Rifampin - 5-10mg/kg/12hPO  trimethoprim+sulfadiazine - 15-30mg/kg/12h IV,
60
Pleuropneumonia aerobic bacteria  Streptococcus pleuropneumoniae, Mycoplasma equi, Actinobacilus multiformis  Bacteroides fragilis, Klebsiella pneumonia, fusobacterium  Streptococcus equi, pasteurella, Actinobacillus equi
C
61
Pleuropneumonia anaerobic bacteria  Bacteroides fragilis, Clostridium sp., fusobacterium  Klebsiella equi, Fusobacterium virilise, Mycoplasma felis  Actinobacillus pneumonia, Clostridium multifactoralis, Bacteroides pleuropneumoniae
A
62
Pleuropneumonia CS  Whistling and wheezing resp sounds, cardiac dullness, discharge of transudate  Dullness with horizontal uppor border by percussion, no respiration, by puncture: exsudation  Discharge of inflammatory exsudate, loud catarrhal resp sounds, chest oedema
B
63
Pleuropneumonia treatment  Thoracocentesis, dexamethasone, sulfadimidine, aminophylline  Thoracocentesis, bromhexin, prednisolone, gentamicin  Antimicrobial therapy, flunixin-meglumide, lowering of the pleural exsudate
C
64
Equine pneumonia/treatment/antibacterial drugs  Ampicillin, lincomycin, metronidazole  Amoxicillin, gentamicin, metronidazole  Clindamycin, metronidazole, neomycin  Erythromycin, clarithromycin, amphotericin
B
65
COPD (RAO)/ Bronchoalveolar lavage sample  Neutrophils <2%, eosinophils >2%  Mast cells >20%  Eosinophils >2%, neutrophils >5%  Neutrophils >20%
D
66
Equine pneumonia/treatment/antibacterial drugs?  Ampicillin, lincomycin, metronidazole  Amoxicillin, gentamicin, metronidazole  Clindamycin, metronidazole, neomycin  Erythromycin, clarithromycin, amphotericin
B
67
Equine laryngeal hemiplegia/ Diagnosis  Auscultation, "slap" test  Occlusion of the nostrils; US exam of the larynx; radiographic examination of the larynx  Endoscopy, palpation, "slap" test  Computed tomography, endoscopy
C
68
COPD(RAO)/Which statement is NOT true/horse?  Occasionally mild radiographic changes in the lungs: interstitial, bronchial, peribronchial pattern  Usually severe radiographic changes in the lungs: fibrosis, chronic oedema  Thoracic radiography mainly serves for differential diagnostic purposes  Bronchectasia and increased air content sometimes visible on chest x-ray
B
69
Tracheal collapse in horses/occurence  English thoroughbred horses  Large, jumping horses  Ponies, miniature horses  Large, draft horses
C
70
Aspiration pneumonia/localisation of dullness and abnormal respiratory sounds/horse?  Lower third of the thorax, over the heart base  The caudal third of the lungs, because of poor ventilation in this region  Craniodorsal part of the lungs  Caudodrosal lung quadrant
A
71
How can we treat pleuropneumonia in horses?  Thoracocentesis, dexamethasone, sulfadimidin, aminophylline  Thoracocentesis, bromhexin, prednisolone, gentamycin  Antimicrobial therapy, flunixin, meglumin, thoracic drainage  Thoracotomy, dexamethason, bromhexine
C
72
COPD (RAO)/Drugs/Horse  Clenbuterol, atropine, fluticazon  Albuterol, ipratropium, trilostane  Salmeterol, aminofillin, edrophonium  Antihistamines, aspirin
A
73
Caudal shift of the caudal lung border. It is characteristic for?  EGME  RAO  ELE(M)  FLUTTTD
B
74
Bronchitis-pneumonia/Etiology/Obligate pathogenic viruses/Horse  Equine herpesvirus-1 and 4, equine influenza virus-A, african horse sickness virus  Equine adenovirus, equine reovirus-1 and 3, african horse sickness virus  Equine herpesvirus-2, equine adenovirus, parainfluenza virus-3  Rhinovirus, herpesvirus, coronavirus
A
75
COPD (RAO) common occurrence:  In older horses kept in stables and getting mouldy hay  b) In horses kept on pasture and in horses performing hard exercise  c) In young foals after chronic respiratory infection  d) Most common in thoroughbreds, trotters and younger sport horses
A
76
Bronchodilators for horses  Ioperamid, albuterol, aminophylline (teophylline)  Albuterol, dimethyl-sulfoxide, bromhexin  Salbutanol, acetylcysteine, dembrexin  Clenbuterol, albuterol, aminophylline (theophylline)
D
77
Rhabdomyolytic myoglobinuria in horses  Disease with paralysis like locomotion disorder and myoglobinuria of untrained cold- blooded due to an extremely heavy work  Disease with paralysis like locomotion disorder and myoglobinuria of continuously working cold-blooded horse  Disease with paralysis like locomotion disorder and myoglobinuria of untrained racer due to an extremely heavy and uncommon exercise
B
78
myoglobinuria paralytica
myoglobinuria paralytica  In the past: Monday Morning Disease  Occurrence: in heavy-working draft horses, after 2-3 days rest, full feeding
79
Muscular degeneration myoglobin-micturition pathogenesis  2-3d rest in strong well-fed horses, then hard work within transition  1 week rest in well-fed horses, then hard work within transition  In undernourished, yoke horses, for the sake of grim-hard work
A
80
Muscular degeneration myoglobin-micturition pathogenesis  Muscular-glycogen incrlocal lactic acid incr + hypoxemiamuscular contraction incrzenker muscular paralysis + myoglobinuria  Hypoxia  muscular glycogen decoupling incr  local lactic acid incr  Zenker- muscular necrosisparalysis + myoglobinuria 81  Muscular glycogen synthesis incrlactic acid decroupling incr + hypoxemia muscular contraction decrmuscular bulgeZenker muscular paralysis + myoglobinuria
A
81
Muscular degeneration myoglobin-micturition symptoms  After the first interception within 2-3h: lameness, wobbly, drop down, rump muscular bulge, saw-horse position, brown-ruddy urine  After the first interception within 2-3h: serious lameness, wobbly, downfall, rump muscular bulge, pasty delicate muscular, brown ruddy urine  Normal walk, wobbly, downfall, rump muscular bulge, compact rubber delicate muscle, brown-ruddy urine
C
82
History, acute course, disorder of locomotion
Swollen, rigid, painful (gluteal) muscles) MYOGLOBINURIA(NEPHROSIs, renal failure)
83
Muscular degeneration myoglobin-micturition effects  Muscular atrophy, lameness, recumbencydeath ?  Claudication, debilitation, renal failure  Atrophic muscular slow degeneration, claudication, myocardosis
B
84
Muscular degeneration myoglobin-micturition prevention a) During rest days be aware of changing the feed, ensure the calm of the resting horse, gradual increase of the forage portion b) Half forage portion under rest days, ducting, after first interception humane loading? c) During rest days vitamin B supplement, be aware that the horses are under calm condition in their equerry, they have limitations under hard work in the first day
C Prevention: when resting – energy decrease, slight movement, gradual working after resting
85
Muscular degeneration myoglobin-micturition what to do  Try to rig up the recumbent horse to put up to walk, give it vitamin B, blood-letting  Transfer the recumbent horse to its equerry and place it to a hammock, abet the healing with blood-letting and vit B inj  Immediately terminate the work, grooming, give it NaHCO3, flunixin-meglumide, if a horse cannot stand up, it has a big change to die
C
86
Muscular degeneration (myalgia) incidence in horse tying up  Racehorse under hard/drastic load, stress, individual sensibility  Racehorses with hard loading without training, after transport, inherited individual sensibility  Syndrome under horse transportation or racing, it’s familiar in studs, the individual sensibility has a big lead in it
A
87
Muscular degeneration (myalgia) symptoms in horse  Claudication, drop with comedown, hobbyhorse attitude  Racehorses with hard loading without training, after transport, inherited individual sensibility  Breast-, loins-, thigh muscular to be swollen and to be stiff, serious and irreversible lameness, renal failure
C
88
Pathophysiology of post-exercise myopathy (myoglobinuria paralytica)/Horse?  Muscular-glycogen ↑ -> local lactic acid ↑ -> vasoconstriction due to hypoxaemia -> Zenker type myopathy -> muscular-paralysis + myoglobinuria  Hypoxia -> anaerobe glycolysis ↑-> local lactic acid ↑ -> myonecrosis -> + myoglobinuria + tubulonephrosis  Hypoxia -> anaerobe glycolysis ↑ -> local lactic acid ↑ -> Zenker type myopathy -> + myoglobinuria + immune-mediated glomerulonephritis
A
89
hypoxia in the muscles  muscle spasm  ischemia  local lactic acid cc. ↑
90
myopathy  myoglobinaemia  myoglobinuria cardiac muscle myopathy, tubulonephrosis
91
Physical properties of horse urine  Mucous containing mucin, muddy, rich in Ca-carbonate  Streams easily, contains mucin, translucid, contains Mg-P  Streams with difficulty, contains protein, translucid, contains Ca-Oxalate
B
92
Cause of renal infarction  Large necrosis, hemophilic area in cortex of kidney, embolia renalis, migration of Strongylus vulgaris 0 thrombosis – embolia  Circumscribed infarct with hemorrhagic area in kidney, embola in arteria renalis, migration of Strongylus vulgaris – thrombosis – embolia
B Wandering strongylus vulgaris larvae ! kidney ! endarteritis –Z thrmbosus for example embolus ! (occlusion) of renal arteries ! renal infarct Other embolus from endocarditis: embolic nephritis
93
Renal infarct CS  Deterioration of hematuria, colic, renal failure  Serious hematuria – shock – bleeding out  Sudden occurrence of large amount of urine, enlarged kidneys
C Clinical signs - acute haematuria - dullness - anaemia (fatal bleeding rare) - rectal findings: enlarged kidney, fremitus renal artery
94
Causes of nephrotoxicosis from drugs or chemicals  Gentamicin, hemoglobin/myoglobin, heavy metals  Aminoglycosides, glucocorticoids, Pb, Hg, Se  Cephalosporins, NSAID’s, aflatoxin
A
95
Causes of nephrotoxicois  myoglobinemia (myoglobinuria), hemoglobinemia  nonsteroid/steroid antinflammatorics (flunixin, phenylbutazone)  antibiotics (e.g. neomycin, gentamicin) + water deprivation!  endotoxemia  Hg-, As-, Se-, Cd- compounds → necrosis  Vitamin K3, D2 and D3 toxicity
96
Causes of vitamin nephropathy  Calciferol, riboflavine, menadion, nikotinacid  Menadion-natrium, ergocalciferol, cholecalciferol  Tocoferol, menadion-natrium, calciferol
B
97
Plants and drugs causing nephrosis acuta  Aflatoxin, ochratoxin, tetracyclines, gentamicin, levamisole  Fumonisin, aflatoxin, plants rich in oxalate, aminoglycosides, cephalosporins  Mycotoxins, plants rich in oxalate aminoglycosides, monensin
C
98
Severe acute nephrosis/combined aetiology/horse?  Endotoxaemia + repeated flunixin meglumine + dehydration  Endotoxinaemia + repeated flunixin meglumine + overdosed HAES-infusion  Repeated flunixin meglumine + NSAID + cephalosporins  Clostridium botulinum toxin + repeated furosemide infections
A
99
Skin: Which statement describes sycosis horses?  Folliculitis on the back due to the untended saddle  Folliculitis long hair follicles on the hock, dorsal margin of the neck, root of the tail  Painful pustulous skin disease appearing on the skin of neck, back due to poor handling
B
100
Characteristics of urticaria in horses?  Can be caused by inhaled allergens (fungi), rounded wheals on the skin within minutes or hours. Usually fast healing, but it might reoccur  Can be caused by inhaled allergens (dust), rounded wheals on the skin within days. Always fast healing  Can be caused by fodder (e.g. oat), rounded wheals on the skin always together with small bleedings of mucosa membranes (nose, mouth)  Caused by nettle plant, allergic reaction with pruritus and alopecia, rapid regeneration
A
101
Etiology of secondary photodermatitis in horses?  Uptake of photosensibilizing plants  Accumulation of phylloerythrin (from chlorophyll) caused by hepatic insufficiency  Retention of photosensibilizing substances because of renal failure  Contact dermatitis caused by pasture plants phylloerythrin
B
102
Horse with photosensitivity on the pigmentless/white skin areas is usually related to a liver problem in the  background – check for liver disease (blood sampling)  Liver can’t eliminate phyerythrin?? (found in plants)
103
Photosensitisation/which statement is not true?  Hypericum perforation (st. johns wort) causes primary photosensitization  Fagopyrum esculentum & lupinus albus cause secondary photosensitisation  Hepatogenous photosensitisation is characterised by phylloerythrin accumulation  The colchicine does not cause photosensitization
B
104
Secretolytics for horses?  Atropine, terbutaline, dembrexine  Acetylcysteine, bromhexine, dembrexine  Terbutaline, clenbuterol, dexamethasone  Clenbuterol, albuterol, dembrexine
B
105
Atrial fibrillation in horses treatment:  Quinidine sulphate  Procainamide  Lidocaine
A
106
Atropine toxicosis/horse/treatment?  Pilocarpine  Physostigmine  Metoclopramide  Lidocaine
B
107
Intestinal motilisers for horses (prokinetics)  Flunixin meglumine, metoclopromaide  Neostigmine, lidocaine  Xylazine, neostigmine  Morphine, neostigmine, lidocaine
B
108
IV lidocaine is used in the treatment of postoperative ileus in people and has been shown to be useful in treating ileus and proximal duodenitis-jejunitis in horses
109
EIPH/ horse/ therapy  Furosemide  Antibiotics  Non-steroid anti-inflammatory drugs  Glucocorticoids  Vitamin C
A
110
COPD (RAO)/Drugs/Horse?  Clenbuterol, atropine, fluticazon  Albuterol, ipratropium, trilostane  Salmeterol, aminofillin, edrophonium  Antihistamines, aspirin
A
111
Secretolytics for horses?  Atropine, terbutaline, dembrexine  Terbutaline, imodium  Terbutaline, clenbuterol  Acetylcysteine, bromhexine
D
112
Glucocorticoids for horses (in RAO/COPD)?  Beclometazon, triameinolone, fluticazon  Bromhexine, dembrexine, dobutrex  Albuterol, clenbuterol, salmeterol  Atropine, ipratropium bromide, scopolamine bromide
A
113
Neonatal pharyngeal weakness/foal?  Clinical signs: milky nasal discharge, bruxism, fever  Physiologic up to 2-4 weeks of age  Treatment with calcium  Treatment with antibiotics and NSAIDs
B
114
EGUS/clinical signs/foals/NOT true?  Diarrhoea  Salivation  Colic  Fever
D
115
General therapy in equine hepatitis diseases?  Diet low in carbohydrates, vitamin B, folic acid, lactulose  Diet restricted in protein, glucose iv., insulin, B-vitamins, antioxidants  Diet low in lipids, insulin, heparin  Diet high in lipids, vitamin E
B
116
Causes and features of Tyzzer-disease in horses?  Listeria monocytogenes-caused meningoenphalitis  Actinobacillus equulis infection, septicaemia in foals  Clostridium piliforme acute hepatitis in foals  Clostridium botulinum, hepatocencephalopathy in foals
C
117
General therapy in equine hepatic diseases?  Diet low in carbohydrates, vitamin B6, folic acid, lactulose  Diet restricted in protein, glucose iv, insulin, B-vitamins, antioxidants  Diet low in lipids, insulin, heparin  Diet high in lipids, vitamin E
B
118
Additional diagnostic methods in Equine hepatic diseases:  Ultrasound examination, Ultrasound guided biopsy  Ultrasound examination, ultrasound guided liver biopsy  Doppler ultrasound, radiography, diagnostic laparotomy  Creatinine clearance test, Bromsulphthalein, clearance test
B
119
Large Strongyles may cause?  Thromboembolism  Chronic diarrhoea  Intussusceptions  Gastric ulceration
A
120
Chorioptes mange affects horses'?  Head  Limbs  Mane  Ventral abdomen
B
121
Blood-sucking lice in horses:  Haematopinus asini can cause anaemia in foals  Linognathus vituli causing anaemia and weakness  Hippobosca equienea; can cause anaemia in adult horses
A
122
Blister beetle causes?  Intussusception, anaemia, hypokalaemia  Diarrhoea, haematuria, hypomagnesemia, hypocalcaemia  Diarrhoea, myocardial necrosis, hypochloraemia, hypermagnesemia  Gastric ulceration, oliguria, invagination
B
123
Ethmoid hematoma/cause?  Traumatic injury of the ethmoid region (e.g. nasogastric tubing)  Secondary to hemostatic problems  Angiomatous tissue overgrowth  Neoplastic origin
124
Curative treatment of hypovolaemic shock in horses  Perfusion, isotonic infusion 10-20 ml/ttkg/24h, dextran  40-50ml hypertonic infusion/24h, perfusion  40-60 ml/ttkg Ringer-liquor; fast infusion, dextran-liquor, plasma inf.
C
125
Haemolytic anaemia causes in horses  Infectious anaemia, babesiosis, leptospirosis, immune-/autoimmune processes  Infectious anaemia, leptospirosis, listeriosis, immune-/autoimmune processes  Infectious anaemia, horse plague, strangles, immune processes
A
126
Haemolytic syndrome of foals ?  Destruction of the equine foetus, in 1-w posprandially weakness, haemolyticus icterus  death  Immunogenetic origin, after colostral uptake, 1/2-3d postprandially, haemolysis, icterus  Blood type incompatibilitydestruction of the fetus in the uterus, icterus at birth, haemoglobinuria, unviability
B
127
Congenital coagulopathies in horses  Haemophilia-A and –B, in stallions; von Willebrand disease: recessive inheritance, in mares  Haemophilia B: Belgian horses and ponies; von Willebrand disease: symptoms in elderly horses  Haemophilia-A: recessively inherited in stallions; von Willebrand-disease: recessively inherited, independent from sex
C
128
Haemorrhagic purpura causes  Immune complex production in chronic purulent processesimmune-originated vasculitisplasma and blood outflow  Immune disease in horses after viral infections immune complex forming immune-originated vasculitisplasma and blood outflow  Autoimmune disease, immune complex formation  vasculitis of autoimmune originplasma and blood outflow
A
129
Aetiology and pathogenesis:  Long lasting purulent inflammation (e.g. strangles)  Immune complex (IgA + antigen) deposition on vessel walls ! vascular lesion,  extravasation of blood and plasma into tissues  Leukocytoclastic vasculitis (hypersensitivity vasculitis)
130
Haemorrhagic purpura symptoms  Haemorrhages, haematomas, “elephant leg”, “hippo head”, hypovolaemia  Haemorrhages in the mucous membranes, skin oedema, oedema of the head, leg, ventral abdominal hypoproteinemia  Urticaria, haemorrhages, exsudation under the skin and in coelomae, hypovolaemic shock
B
131
First symptoms of haemorrhagic purpura, localisation  Glottis, conjunctiva  Internal nasal wings, lips  Mucosa of the praeputium, outer genital organs
B
132
Haemorrhagic purpura treatment  NSAID treatment, transfusion, isotonic infusion, ABs  Glucocorticoid treatment, transfusion, infusion of glucose, heparin  Treatment of purulent process (abscess), dexamethasone, blood plasma IV, ABs to treat the original matter
C
133
Thrombophlebitis therapy in horse  Locally: ice packing, parenteral: prednisolone, ABs, operation: phlebotomy  Locally: iodine paste, parenteral: NSAID-drugs, ABs, operation, phlebotomy  Locally: prednisolone-paste, parenteral: heparin, ABs, operation: phlebotomy, transplantation from v. femoralis
C
134
Thrombophlebitis prevention in horse  In case of several IV injections rotating, using correct IV catheter, heparin flush through the catheter  Compliance with the regulation of IV application, catheter sterilization/heparin, we do not ive tissue-irritant materials IV  Keep the asepsis, applicating tissue irritant material to the vein is allowed only when also use heparin, use vein needle as thin as possible
C
135
Hyperlipaemia of mares occurrence  Lipemic blood plasma is a symptom characteristic of a metabolic disease of Arabian mares, which occurs often after exercise  In this serious metabolic disease, that occurs mainly in mares before parturition, hyperlipaemia is the main symptom, blood triglyceride >5-6mmol/L  The around parturition often occurring lipidaemia is a symptom suggesting hepatopathy
B
136
Hyperlipaemia of mares pathogenesis  In draft mares, pregnancy, physical overload, malnutrition  Idiopathic disposition, low energy nutrition, in the last trimester of pregnancy, wasting disease  Breed disposition, pregnancy, obesity, stress, anorexia
C
137
Hyperlipaemia of mares symptoms?  Colic  weakness, hepatocerebral syndrome, lipermic plasma  Colic, fever, icterus, weakness, disturbed plasma  Lack of appetite, diarrhea, icterus, nervous signs, bloody-disturbed plasma Depression, anorexia, colic, lethargy, abnormal gait, hepatoencephalopathy (coma), recumbency, death
A
138
Hyperlipaemia of mares treatment  Antispasmodic/sedatives, in case of colic: walking, high energy nutrition, infusion several times  Stall rest, 4h long drip infusion/Ringer solution + glucose, artificial nutrition, liver protective therapy  Gentle treatment, regular walking, glucose infusion several times, insulin, heparin
B
139
Hyperlipaemia of mares prevention and prognosis  Suitable management and nutrition, avoid exercise during pregnancy. Reacts good to therapy.  Good nutrition during pregnancy, vitamin supplementation. It is mostly favourable without treatment.  Avoid fattening during pregnancy, avoid stress and predisposing diseases. Therapy is often ineffective, high death risk.
C
140
Yellow fat disease and steatosis horse  Fat tissue discoloration, degeneration, and steatitis mainly in pony foals  Yellow discoloration of SC fat tissue in overfed horses. Icterus, swelling in the fat tissue.  In lg breed, fat horses. Yellow swellings in the skin, formation of increments, icterus
A
141
Yellow fat disease and steatosis pathogenesis  Fat degeneration and steatitis because of Fe- and E-vitamin deficiency, Fe- and/or Se- deficient nutrition, formation of glutathione-peroxidase decr  Lesions of adipocytes because of fatty acid peroxidases at the embryonic stage, Se or E-vitamin deficiency, food rich in peroxidases  In areas lacking Se, without Fe-replacement in case of dominance of oxiperoxidases: adipocytes degeneration and necrosis
B
142
Yellow fat disease and steatosis symptoms  Muscle weakness, gradually slowing movement, SC oedema, painful movement of neck.  Skin discoloured into yellow; yellow, palpable, sensitive swellings on the head + neck  Muscle weakness, foal paralysis, painful movement of the head and neck, painful swellings on the neck
A
143
Yellow fat disease and steatosis treatment and prevention  High energy/carbohydrate food, Se and E-vitamin replacement, analgesics  Liver protective therapy, glucose infusions, analgesics  Food rich in fibre, analgesics, spasmolytics, physiotherapy
A