Equine Flashcards

1
Q
  • Is believed to play a role in the pathogenesis of equine sarcoidosis
A

Papillomavirus

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2
Q

What is the most common skin tumor of the horse

A

Sarcoids /fibrosarcomas - fibroblastic wart like skin lesions, often locally invasive and recurrent but not malignant

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3
Q

What are the recurrence rates of sarcoids that are surgically removed

A

50% - no single effective treatment, small lesions treated with benign neglect

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4
Q

What is colic and what are common signs

A

Abdominal pain - frequent pawing, kicking at abdomen with hindlegs, stretching out like to urinate, laying down, rolling, anorexia, muscle fascinations, flehman response

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5
Q

What is the flehman response

A

Upper lip curl - exposing smells to vomeronasal organs

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6
Q

Which horses are most affected by lipomas causing si disease and colic

A

Horses older than 20 years - lipoma on a stalk will twist causing strangulation

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7
Q

What is si volvulus

A

Twist in si causing strangulation at root of twist

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8
Q

Define intussuception

A

Invagination of one segment of intestine and its mesentery into the lumen of another piece of intestine

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9
Q

When is intussusception causing si disease and colic in horses likely to occur which part is most common

A

Common in younger horses, with diet changes, due to parasites like tapeworms - ileocecal most common

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10
Q

What is a mesenteric defect casing colic and si disease

A

Piece of si entrapped through aren’t in the mesentery causing strangulation

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11
Q

What is the epiploic foreman and what is the risk

A

A space between the greater and lesser omentums - risk of si entrapment

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12
Q

What are clinical signs of si disease in horses

A

Severe pain (analgesics don’t help), elevated heart rate, systemic shock, gastric reflux, rare palpable loops of si bowel

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13
Q

What will si intestinal disease look like on ultrasound

A

Dilated/nonmobile loops of si on trans abdominal ultrasound

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14
Q

What is a top differential for serosanguinous fluid with elevated proteins /WBC

A

Small intestinal disease

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15
Q

What are differentials for small intestinal disease in horses

A

Lipoma, volvulus , intussuption, herniation, mesenteric defect , anterior or proximal enteritis

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16
Q

What length of dead bowel leads you to a poor progress with si disease

A

Over 15 feet

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17
Q

What is Li volvulus / torsion

A

Severe form of colic, colon this then becomes ischemic then necrotic - can be fatal

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18
Q

What is the difference in treatment between small intestinal disease and large intestinal volulus treatment

A

Si - surgical resection and anastomosis
Li. - surgical correction rapidly (impossible almost to reset the LI)

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19
Q

What is the risk of surgically correcting Li volvulus

A

Risk of endotoxic shock when corrected

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20
Q

Which horses are more at risk of large intestinal volvulus

A

Older broodmares, just before partuition Or after, larger horses

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21
Q

What is the difference in clinical signs with si disease and Li volvulus

A

No gastric reflux in Li because Lester is too caudal and in Li you can actually palpate gas distension

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22
Q

What is colonic impaction , why does it occur and how is it often treated

A

Backup of fecal matter, often due to decreased water intake - medical management usually successful

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23
Q

What is worse - Li volvulus or colon impaction

A

Li volumes - colon impact mild colic signs and analgesia often helps

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24
Q

How do you treat colon impaction

A

Oral fluids and laxatives with either intermittent or indwelling nasogastric tube, using mineral oil , psyllium, Epsom salts

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25
Q

What commonly causes colic tympany or gas colic

A

Diet change or grain overload - but can happen anytime and spontaneously resolve

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26
Q

What are signs of colonic tympany and how do you treat

A

Mild to severe to spasmodic pain - treat with analgesics, sedation , iv and oral fluids

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27
Q

What is right dorsal colon displacement

A

Colon between cecum and right body wall

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28
Q

What is left dorsal colon displacement

A

Nephrosplenic entrapment - colon between left kidney and spleen the distends with gas

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29
Q

What is the treatment for nephrosplenic entrapment caused by colon displacement

A

Give phenylephrine IV - a sympathominetic that causes vasoconstriction to shrink the spleen and hopefully dislodge the colon

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30
Q

What does feeding alfalfa hay increase the risk of

A

Enteroliths (intestinal stones) due to mineral composition

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31
Q

What are enteroliths

A

Precipitation of struvite salts - magnesium ammonium phosphate, can block the small colon or transverse colon often

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32
Q

How does sand colic occur

A

Sand doesn’t pass well in manure so it settles in the ventral aspect of the colon

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33
Q

How can uw diagnose a sand colic

A

Might auscultate a fluid wave of sand in the ventral abdomen, mild intermittent pain

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34
Q

How do you diagnose sand colics/enteroliths

A

Positive fecal sand float , might see radiopaque sand or stores on abdominal rads

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35
Q

How do you treat sand colics

A

Frequent nasogastric ting with water, mineral oil, psyllium laxatives

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36
Q

How do you treat enteroliths

A

Enterotomy

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37
Q

Why do gastric ulcers occur in horses and where do they occur

A

Nonobstructive colic due to stress or prolonged time with an empty stomach - occur at the non glandular dorsal stomach (the squamous region of the stomach)

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38
Q

What are clinical signs of GI ulcers

A

Con continue eating and passing manure, intermittently colicky - cranky, no GI bleeding, often responds well to first dose of banamine/ analgesics but repeated use will worsen ulcers

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39
Q

How do you diagnose gastric ulcers and what is important to note

A

Fasted gastroscopy - reoccurrence common if lifestyle not addressed

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40
Q

How do you treat / prevent gastric ulcers

A

Oneprazole for several weeks to months, sucralfate - prevent by feeding alfalfa to reduce stomach acid and maximize roughage and turnout tire, reducing stress

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41
Q

What is the cause of both types of parasite associated colic and which horses are most affected

A

Improper or infrequent deworming - young horses most affected

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42
Q

Describe ascaria impaction casing parasite associated colic - what is the causative agent

A

Roundworms ( parascaris equorum)- occurs in young horses never previously dewormed then dewormed with a large dose of anthelmintics that caused a massive parasite die off then physical intestine blockage

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43
Q

Describe verminous arteritis or thromboembolic colic - what is the causative agent

A

Strongylus vulgaris parasite - migrates to cranial mesenteric artery, damage and immune system can form thrombus that cuts Off blood supply to the bowel causing infarction, cecum commonly

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44
Q

What are common causes of acute colitis

A

Infectious (salmonella, C perfringens or difficile, PHF, etc), non ininfectious (diet change or right dorsal colitis secondary to NSAID use), intestinal neoplasia

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45
Q

What is the causative agent of Potomac horse fever and what is often used to treat it

A

Neorickettsia risticii - tetracycline often used to treat

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46
Q

Which horses are most at risk for urolithiasis mimicking colic

A

Stallions and geldings - mares can form stones but are rarely obstructed

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47
Q

What stones usually cause urolitiasis in stallions and geldings

A

Calcium carbonate stones

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48
Q

Which horses are most at risk for uterine torsion that mimics colic

A

Mares late in gestation (7 months or so)

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49
Q

What helps diagnose uterine torsion in pregnant mares

A

Palpation of tight band of broad ligament over uterus palpable on rectal exam

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50
Q

What is the treatment for uterine torsion in pregnant mares

A

Anesthetize and roll over abdomen to stabilize fetus - surgery if unsuccessful

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51
Q

What would you expect to see in a horse that ingest sorghum? What is the treatment

A

Myelomalacia of the lower spinal cord causing pelvic limb incoordination and urine dribbling -no treatment rare to recover

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52
Q

Atrial sibrilkhor is most often associated with

A

Exercise intolerance in horses

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53
Q

What happens if a horse eats slafamine often found in moldy red clover

A

Causes hyper salivation

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54
Q

What is the most common ovarian tumor of horses

A

Granular theca cell tumor

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55
Q

Describe the causative agent of strangles in horse,

A

Strep equi equi - gram positive cocci bacteria with a large capsule

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56
Q

What would you expect to see if youvaspirated a lymph node in a horse with strangles

A

Purulent inflammation and gram positive cocci with large capsules

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57
Q

What is the causative agent of shaker foal syndrome

A

Closhidium botulinum

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58
Q

Describe shaker foal syndrome

A

Foul ingest spores of C. Botulinum that grow and make toxins in its intestines, leading to flaccid paresis or paralysis , decreased muscle tone, dyspnea, flaccid tongue

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59
Q

Which animals are most susceptible to tetanus

A

Horses and pigs

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60
Q

What is the causative agent of tetanus

A

Closhidium petani

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61
Q

Describe the pathogenesis of tetanus - does it work actively to invade wounds

A

Found widespread in soil and is introduced to patient through puncture wounds, castration sites, banding and dehorning - does not actively invade wounds, incubates for 10-21 dans tres produces a potent nervous system toxin

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62
Q

Tetanus is a - toxin

A

CNS

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63
Q

Once exposed to tetanus, will horse develop signs immediately

A

No - incubation period for 10- 21 days

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64
Q

What ave clinical signs of tetanus

A

Sawhorse stance, lock jaw causing inappetence, stiff tail, prolapsed third eyelid, flared nostrils, sensitivity to noise and movement

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65
Q

How do you diagnose tetanus

A

Based on clinical signs - no post mortem lesions

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66
Q

How do you treat tetanus ? How do you prevent it?

A

Antibiotics penicillin, tranquilization, tetanus antitoxin and supportive care - prevent with vaccination and do clean surgeries

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67
Q

Which botulism toxin are horses most susceptible to

A

Type B toxin

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68
Q

What is the caussitie agent of botulism and which toxins does it produce

A

Clostridium botulinum - produces toxins A, B or C

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69
Q

Describe the causative agent and patrogenesis of shaker foal syndrome

A

Clostridium botulinum - toxoinfectious form where toxins form in the git

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70
Q

What is the pathogenesis of botulism

A

Bacteria introduced through contaminated feed (dead cat or rabbit in feed or hay) where organism has produced high levels of toxins in feed - wound botulism is rare

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71
Q

What clinical signs can you expect with botulism

A

Muscle tremors, fascinations , ascending paralysis leading to respiratory paralysis and death, mydrinsis and ptosis, weak tongue

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72
Q

How do you diagnose botulism

A

Detect toxins in serum , intestines or feed -no postmortem signs

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73
Q

How do you treat botulism

A

No effective treatment - botulism antitoxin sometimes works in horses

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74
Q

How can you prevent botulism

A

Type B vaccine - 3 doses 4 weeks apart, booster mares before foaling

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75
Q

How long will clostridium protect foals from botulism

A

8-12 weeks

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76
Q

Define sheared heels

A

Asymmetry of heels due to imbalance of foot resulting in one heel hitting the ground before the other

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77
Q

What does monensin toxicity result in in horses

A

Cardiomyopathy and myocardial necrosis

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78
Q

What is normal fractional shortening in a horse (measure with an echo) and what value indicates a poor prognosis

A

30- 40% - less than 20% poor prognosis

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79
Q

What causes equine motor neuron disease, what signs do you see and how do you treat

A

Acquired neurodegenerative disease if horse is without pasture for 18 months - will see elevated muscle enzymes and low serum vitamin E, muscle wasting and fasiculations - supplement high lever of vitamin E

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80
Q

What are the 4 main equine nerve blocks used in lameness exams

A

Palmar digital , abaxial sesamoid block, low 4 point palmar block and high 4 point palmar block

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81
Q

Where is the proximal interphalangeal joint

A

Pastern joint - joint between p1 and p2

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82
Q

What is the distal interphalangeal joint

A

Coffin joint

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83
Q

What is the meta carpophalangeal joint

A

Fetlock joints

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84
Q

Where is metacarpal 2

A

Medial to the cannon bone (MC3)

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85
Q

Where is metacarpal 2

A

Medial to the cannon bone (MC3)

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86
Q

Where is metacarpal 4

A

Lateral to cannon bone ( MC3)

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87
Q

Where is metacarpal 1

A

Does not exist in horses (neither does metacarpal 5)

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88
Q

Describe the placement of the tendons / ligaments in the equine distal limb

A

Common digital extensor tendon is on the front of the limb, supensory ligament is directly on the bones, men deep next tendon, then superficial flexor tendon

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89
Q

Where is the palmar digital nerve block performed

A

Small amount of lidocaine placed between the medial and lateral palmar digital nerves , proximal to the cartilages of the hoof and on either side of P2

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90
Q

What do plantar and palmar mean

A

Plantar - rear facing hind limbs
Palmar - rear-facing forelimbs

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91
Q

How much desensitization does the palmar digital block

A

50 -70% of palmar/plantar part of the foot including the coffin joint (distal interphalamgeal joint)

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92
Q

If the palmar digital block and the abaxial sesamoid block both desensitize the medial and lateral palmar digital nerves, what is the difference

A

The palmar digital block is done on either side of P2, the abaxial sesamoid block is done around and above the proximal sesamoid bones

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93
Q

What is desensitized by the abaxial sesamoid block

A

Skin over the palmar pattern and distal dorsal pastern along foot, some partial desensitization of palmar fetlock - basically blocks everything below the fetlock

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94
Q

What nerves are blocked by the low 4 point palmar / plantar block

A

Medial/lateral palmar nerves, medial and lateral palmar metacarpal nerves

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95
Q

Where is the low 4 point palmar/planter block performed

A

Dorsolateral and dorsomedial to digital flexor tendan between the suspensory ligament and deep digital flexor tendon at level of the distal metacarpal bone, proximal to fetlock joint above the sesamoids, distal to the ends of the splint bones to reach the metacarpal nerves

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96
Q

What is desensitized by the low 4 point palmar/plantar block

A

Entire fetlock joint (metacarpophalangeal) and everything distal to it

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97
Q

What does the high 4 point or subcarpal block

A

Medial and lateral palmar nerves, medial and lateral palmar metacarpal nerves distal to carpus

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98
Q

Where do you do the high 4 point subcarpal block

A

Between the suspensory ligament and the deep digital flexor distal to carpus - also placed axial to the splint bones and abaxial to the suspensory ligament then towards the third metacarpal bone

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99
Q

What is desensitized by the high 4 point subcarpal block

A

Metacarpal region, entire fetlock (metacarpophalangeal ), and structures of digit

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100
Q

A horse with right front lameness that resolves 85% after performing a low 4 point block. Which area has the lameness

A

Metacarpophalangeal fetlock joint or below

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101
Q

A horse who’s lameness resolves after performing a palmar digital block most likely has a lameness where

A

Coffin joint or hoof

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102
Q

A horse with a lameness that resolves after performing an abaxial sesamoid block most likely has a lameness where

A

Fetlock or below

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103
Q

A horse with a lameness that resolves with a high four point subcarpal block most likely has a lameness where

A

Fetlock or digit or metacarpal bone

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104
Q

What is the only way to diagnose equine degenerative myeloencephalopathy

A

Histopath exam - lesions in caudal brainstem nuclei and spinal cord

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105
Q

What is the name for pinworms

A

Oxyuris equi

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106
Q

What lesions would you expect to see with pinworm infections (oxyuris equi)

A

Aloepecia around perineal region , tail rubbing

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107
Q

How do pinworms cause disease

A

Female pinworms crawl nt of anus and cement eggs around a perineal region

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108
Q

What is a common sequela to strangles caused by strep equi equi

A

Purpura hermorhagica - causing urticaria, edema, petechia, ecchymoses and vasculitis

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109
Q

Define urticaria

A

Skin condition causing raised welts

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110
Q

How do you treat sacroiliac luxations in horses

A

Untreatable -usually resolve over time with supportive care and NSAIDs but horse usually has limited movement after

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111
Q

What is the croup and what indicates good balance

A

Topline of horses hindquarters from hip to tail dock - must be same height as the withers for horse to balanced

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112
Q

What is the sacroiliac joint

A

Joint between the ilium of the pelvis and the sacrum of the spine

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113
Q

What is your top suspicion if you see a bump above the horses croup

A

Sacroiliac luxation

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114
Q

What is the causative agent of ringworm in equine

A

Trychophyton equinum

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115
Q

Describe lesions caused by dermatophilus congolensis and why they occur

A

Matted hair, supportive crusts, purulent exudate - bacteria enters under skin when it rains

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116
Q

What is another name for wobblers in horses

A

Cervical vertebral malformation

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117
Q

What is the causative agent of equine protozoal myeloencephalitis and when does it occur

A

Can occur at any age or breed - sarcocystis neurona

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118
Q

Who is the definitive host for sarcocystis neurona causing EPM in horses? What kind of host is the horse

A

Opossum definitive, horses are the aberrant hosts

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119
Q

How do horses become infected with EPM

A

Ingest sporocysts from opossums - only causes disease in some horses

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120
Q

What are clinical signs of EPM - equine protozoal myeloencephalitis

A

Ataxia, asymmetric atrophy, weakness, limb spasticity , maybe cranial nerve involvement

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121
Q

How do you diagnose EPM

A

Western blot, IFA, PCR

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122
Q

How do you treat EPM

A

Ponazuril or TMS with pyrethamine

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123
Q

What is the causative agent of equine herpes myeloencephalopathy and what type of disease does it cause

A

EHV I - respiratory 1 abortion and neuro disease associated with viral induced vasculitis in the CNS

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124
Q

What are clinical signs of equine herpes myeloencephalopathy

A

Hind limb ataxia or paresis, urinary incontinence, weak tail and anal tone , CN deficits, lethargy, recumbency, febrile episodes

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125
Q

How do you treat EHM - equine herpes myeloencephalopathy

A

Supportive care (padded stall to protect), evacuate bladder and rectum if needed, antiviral like acyclovir (efficacy variable)

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126
Q

When are you likely to see cases of cervical vertebral malformation /wobbler syndrome/ central stenotic instability

A

Young horses - 6 months to 3 years

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127
Q

What is your top differential in a yearling horse showing symmetrical ataxia

A

Cervical vertebral malformation

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128
Q

How can you differentiate cervical stenotic myelopathy from EPM based on clinical signs

A

Wobblers - symmetrical ataxia
EPM -asymmetric ataxia

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129
Q

What areas experience compression with wobblers syndrome

A

C3 - C4 or C4 - C5 (dynamic)
C5-C6 and C6-C7 (static)

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130
Q

What are clinical signs of wobblers syndrome in young horses

A

Hindlimb symmetric ataxia, proprioceptive deficits, weakness - young horses!

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131
Q

How do you diagnose wobblers

A

Saggital ratios - compare diameter of spinal cord with widest part of vertebral body, myelogram

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132
Q

How do you treat wobblers

A

Support, surgical correction but therapy is limited for sure

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133
Q

What is the causative agent of guttural pouch mylosis

A

Aspergillus

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134
Q

What causes equine degenerative myeloeneephalopathy

A

Occurs in yang horses due to lack of antioxidants like vitamin E and selenium in the diet

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135
Q

What causes equine degenerative myeloeneephalopathy

A

Occurs in yang horses due to lack of antioxidants like vitamin E and selenium in the diet

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136
Q

What does yellow star thistle ingestion lead to in horses and how do you treat

A

Dysphasia and other neuro signs - offer die due to dehydration or starvation, euthanasia often recommended

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137
Q

What is the causative agent of sweet itch? Where are lesions usually located

A

Cullcoides hypersensitivity ,occurs in warm months and lesions are usually due to self mutilation on the poll, mane, tail

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138
Q

Describe the muscles of the equine esophagus

A

Cranial 2/3 is striated muscle und caudal 1/3 is smooth mite

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139
Q

What is cushings disease in equine

A

Pituitary pars intermedia dysfunction

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140
Q

What is the most common cause of a pansystolic heart murmur with the point of maximum intensity on the right side

A

Ventricular septal defect

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141
Q

Why would terbutaline sulfate help diagnose anhidrosis

A

Beta 2 advenergic agonist that is supposed to stimulate sweat production - anhidrotic Norses will not over after intradermal injection of this

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142
Q

Describe parascaris equroum

A

Roundworm /ascarid affecting goals and yearlings - produce many eggs that are resistant and remain in the environment for years

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143
Q

What are clinical signs of equine cushings (ppid)

A

Lethargy, delayed shedding, abnormal sweating, laminitis

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144
Q

What is a common comorbidity of equine cushings that is associated with insulin dysregulation and can affect horses of any age

A

EMS - equine metabolic syndrome

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145
Q

What is a common comorbidity of equine cushings that is associated with insulin dysregulation and can affect horses of any age

A

EMS - equine metabolic syndrome

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146
Q

Why are horses with EMS at a greater risk for laminitis

A

Associated hyperglycemia (due to insulin disregulation)

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147
Q

Define poll evil - what is the causative agent

A

Brucella abortus - inflammation of the bursa adjacent to the nuchal ligament

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148
Q

Define fistulous withers - what is the causative agent

A

Brucella abortus - development of an open draining lesions over the supraspinous bursa

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149
Q

What does black walnut toxicity cause in horses

A

Laminitis

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150
Q

What is the causative agent of equine infectious anemia

A

Retrovirus

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151
Q

What is the causative agent of bacterial keratitis in horses

A

Pseudomonas

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152
Q

What happens with red maple leaf ingestion in horses

A

Hemolysis causing icteric mucus membranes , anorexia and mild intermittent colic

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153
Q

How does oak leaf ingestion affect horses

A

Causes diarrhea and abdominal pain

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154
Q

How is black walnut toxic to horses

A

Associated with laminitis

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155
Q

What heart arrhythmias are considered normal in horses

A

First and second degree AV block

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156
Q

What heart arrhythmias are considered normal in horses

A

First and second degree AV block

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157
Q

What is neonatal isoerythrolysis (Ni)

A

Destruction of a foals ABCs by all antibodies from the mare ingested through colostrum

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158
Q

What is neonatal isoerythrolysis (Ni)

A

Destruction of a foals ABCs by all antibodies from the mare ingested through colostrum

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159
Q

When are you most likely to see cases of neonatal isoerythrolysis

A

Foals less than 7 days old born to mares that have foaled once before

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160
Q

What type of immune reaction is Ni - neonatal isoerythrolysis

A

Type 2 hypersensitivity reaction between RBC antigens from foal and antigen specific antibodies from the mare ingested through colostrum

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161
Q

What antigens are most likely the cause of NI and where do they came from

A

Aa and Qa - foal antigens inherited from sire

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162
Q

How could a mare develop antibodies against RBC antigens

A

Must be exposed either through prior blood transfusions , exposure to fetal blood from placental abnormalities or exposure to fetal blood during partition

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163
Q

Which equid foal has a higher Chance of NI

A

Donkeys - unique donkey factor RBC antigen (mule foals)

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164
Q

What 3 things must happen for a foal to develop Ni (neonatal isoerythrolysis)

A
  1. Neonate RBC antigen not expressed by mare is inherited from the sire
  2. Mare has developed antibodies to specific manage RBC antigen
  3. Neonate ingests colostrum with antibodies
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165
Q

What are clinical signs of NI in foals

A

Indicate poor oxygen content in blood - icterus, hyperbilinbiremia, anemia, tachycardia, tachynpnea

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166
Q

What are clinical signs of NI in foals

A

Indicate poor oxygen content in blood - icterus, hyperbilinbiremia, anemia, tachycardia, tachynpnea

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167
Q

How do you diagnose Ni in foals

A

Clinical signs, cross match foal RBC with mare serum - jaundice foal agglutinates test between foal ABC, and mare colostrum

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168
Q

How do you treat NI in foals

A

Withhold colostrum, monitor PCV and perform blood transfuion if below 16%

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169
Q

What is the prognosis of foal Ni

A

Good if treated quick with blood transfusions - if anemic (PCV less than 10% ) more guarded

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170
Q

Define a malunion

A

Healed fracture where bone alignment was not achieved or maintained

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171
Q

What results if there is malunion of the appendicular skeleton after a fracture

A

Angular deformity

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172
Q

How can you differentiate between a minor and major angular deformity

A

Minor is a less than 10% difference in anyplane or 10% or less of the original length (everything else is major)

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173
Q

What is a common site for fracture malunion and what does it lead to

A

Pelvis - leads to barrowing of pelvic canal

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174
Q

Define physeal fractures

A

Growth plate fracture in long bones

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175
Q

Define Varus

A

Deviation of axis toward median plane

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176
Q

Define valgus

A

Deviation of axis away from median (latral)

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177
Q

Define procurvatus angular deformity

A

Cranial bowing

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178
Q

Define procurvatus angular deformity

A

Cranial bowing

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179
Q

Define recurvatus angular deformity

A

Caudal bowing

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180
Q

Define pronatus angular deformity

A

Internal rotation of axial plane

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181
Q

Define supinatus angular deformity

A

External rotation of axial plane

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182
Q

How do you fix a fracture malunion

A

Corrective osteotomy

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183
Q

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

A

Acute serum hepatitis / theilers disease

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184
Q

What causative agent is associated with theilers disease / acute serum hepatitis

A

Admin of the tetanus antitoxin possible - otherwise idiopathic (unidentified virus or plant toxin )

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185
Q

What causative agent is associated with theilers disease / acute serum hepatitis

A

Admin of the tetanus antitoxin possible - otherwise idiopathic (unidentified virus or plant toxin )

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186
Q

How do you definitively diagnose pyrrolizidine alkaloid toxicity

A

Based on observing fibrosis, megalocytosis and bile duct proliferation

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187
Q

What clinical signs would you expect with theilers disease

A

Acute depression , anorexia, severe icterus , photosensitization, hepatoencephalopathy, pica

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188
Q

How do you diagnose theilers disease/ acute serum hepatitis

A

Hepatic necrosis , informative cells with mononuclear cells and metrophil, in portal areas I proliferation of bile ducts

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189
Q

Define hepatoencephalopathy - if you see this with photosensitization Ina horse what is your top differential

A

Brain dysfunction due to liver dysfunction - theilers disease

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190
Q

What might you find on necropsy of a horse with theilers disease

A

Decrease in liver size, severe icterus

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191
Q

What clinical signs would you see with chronic active hepatitis

A

Progressive weight loss, intermittent fever , icterus, inappetence, photosensitization

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192
Q

How does hepatic disease cause photo sensitization

A

Hepatic disease allows pylloerythyn (produced in the stomach ) to re-enter circulation which causes a phototoxic reaction to occur under the skin

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193
Q

What are differentials for chronic active hepatitis

A

Plant or chemical toxins, environmental chemicals, ascending bacterial infections from billiary tract or immune mediated disease - basically anything causing a chronic inflammatory response

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194
Q

What would you see that could help diagnose chronic active hepatitis - what will the hepatocytes look like

A

Fibrosis in portal areas, cellular infiltrate and biliary hyperplasia - hepatocytes may be normal

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195
Q

How do you treat chronic active hepatitis and why

A

Corticosteroids because it is a chronic information response in the liver - treat the inflammation - but if it is due to bacterial cholongiohepatitis you would use antibiotics

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196
Q

What is the cause of pyrrolizidine alkaloid toxicity in horses

A

Chronic progressive intoxication from consuming plants with PAs - senecio crotalaria and heliotropium

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197
Q

Describe Tre pathophys of PA toxicity - pyrrolizidine alkaloid toxicity

A

Toxin absorbed by git then liver where it is metabolized to pyrroles which have an antibiotic effect (hepatocytes can’t divide) I leading to megalocyte formation - these cells will tra die and be replaced by connective and fibrous tissue - makes live unusable pretty much

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198
Q

What clinical signs would you see with PA toxicity - pyrrolizidine alkaloid

A

Weight loss, icterus, photosensitization

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199
Q

If u are presented with a horse with icteric muss membranes and sclera , a history of weight loss, And photosensitization - what are your top 3 differentials

A

Theilers disease (acute serum hepatitis), chronic active hepatitis, pyrrolizidine alkaloid toxicity

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200
Q

What family does west nile virus belong to

A

Flavovirus

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201
Q

What family of viruses does eee, wee and vee belong to

A

Alphavirus genus , togavirus family

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202
Q

Since its out break in 1999,- has been a leading cause of human and viral encephalitis

A

West Nile virus

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203
Q

How is West Nile virus transmitted

A

WNV infected mosquito bites a horse - mosquitos became infected by birds and vice versa

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204
Q

What results from a horse infected with WNV? What clinical signs might you see

A

Low grade viremia (short duration) - depressed mentation, fever, ataxia, weakness, made fascinations, recumbency

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205
Q

Will all horses infected with WNV develop clinical signs

A

No - not all will develop clinical signs , if horse is vaccinated signs are vocally Vera mild

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206
Q

What will CSF look like in a horse infected with WNV

A

High protein concentration and mononuclear pleocytosis

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207
Q

How can you confirm a diagnosis of WNV

A

Igm antigen capture ELISA / virus isolation and plaque reduction neutralization

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208
Q

What is the prognosis of WNV

A

Mortality of 33% - many recover

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209
Q

Who are vectors for togavirus encephalitis (EEE, WEE, VEE)

A

Mosquitos - bite Asymptomatic birds, small mammals then bite horses

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210
Q

What are clinical signs of the togavirus encephalitis

A

Fever, depression, sleeping sickness, anorexia, proprioceptive deficits, hyperesthesia, cerebral/CN deficits, propulsive walking, head tilt

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211
Q

How do you diagnose EEE, VEE, WEE

A

Abnormal CSF (high protein, pleocytosis), serology

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212
Q

Describe the prognosis for togavirus encephalitis

A

EEE has high mortality (75%), WEE and VEE are lower(20-80%)- horse may have residual neuro deficits

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213
Q

Describe the prognosis for togavirus encephalitis

A

EEE has high mortality (75%), WEE and VEE are lower(20-80%)- horse may have residual neuro deficits

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214
Q

How is strangles (strep equi equi ) spread - bacterial!

A

Respiratory secretions that are then inhaled or ingested

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215
Q

What clinical signs do you expect with strangles in horses

A

Fever, mucopurelent nasal discharge, enlarged lymph nodes (particularly submandibular), pupura hemorrhagica (severe edema, petechiae, septicemia), chondroids

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216
Q

What is guttural pouch empyema

A

Usually secondary to strangles - bacterial infection causes the thin lining of the guttural pouch to be inflammed and the pouch to then fill with thick pus

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217
Q

What is bastard strangles

A

Strangles infection that spreads to internal organs causing abscesses

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218
Q

What is pupura hemorrhagica

A

Hemorrhage or edema due to an allergic reaction - causes aseptic vasculitis and swelling of blood vessels leading to petechia, septicemia, etc

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219
Q

why would a horse with strangles develop a secondary pupura hemorrhagica

A

Either repeated exposures to natural infections or vaccination

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220
Q

What are chondroids and why do they offer occur

A

Can be caused by a strangles infection - solidified caseous material /stones in guttural pouches that persist for years if not removed and can cause bacterial shedding

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221
Q

How can you diagnose strangles

A

PCR from nasal swab , guttural pouch lavage - if acute
Serology for liters - if chronic

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222
Q

What do high antibody titers for strangles on serology indicate

A

Chronic infection - either pupura hemorrhagic or bastard strangles

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223
Q

What is contraindicated when treating strangles and why

A

Antibiotics like penicillin or ceftiofur - they allow bacteria to hide which prolong, clearance and recovery, onlynuse in severe cases

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224
Q

How should you treat Strangles

A

Most infections clear on their own - savage guttural pouches, instill penicillin, antiinflammatories, and supportive care

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225
Q

How can horses become carriers for strangles infection and how can they her it

A

Can be persistent carriers if abscesses or chondroids remain, can also shed without showing any signs - should have 3 negative nasal PCRs before cleared

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226
Q

How can you prevent spread of strangles

A

Isolate + biosecurity measures - vaccine with mlv intranasal or killed IM

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227
Q

There is an outbreak of strangles on a farm - do you recommend vaccinating the healthy horses

A

No- vaccines + natural exposure increases the risk for pupura hemorrhagica which can be fatal

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228
Q

There is an outbreak of strangles on a farm - do you recommend vaccinating the healthy horses

A

No- vaccines + natural exposure increases the risk for pupura hemorrhagica which can be fatal

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229
Q

What can occur if EHV 1 mutates

A

It can mutate to the wild type /neurogenic type causing neurologic disease (equine herpes myeloencephalopathy)

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230
Q

What can occur if EHV 1 mutates

A

It can mutate to the wild type /neurogenic type causing neurologic disease (equine herpes myeloencephalopathy)

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231
Q

What are clinical signs of EHV 1 and 4

A

Fever, cough, mucopurelent nasal discharge , abortions in pregnant mares, secondary pneumonia

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232
Q

What can be a source of subclinical spread for EHV

A

Vaccinated horses with a more mild infection

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233
Q

How do you diagnose EHV

A

PCR of nasal discharge

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234
Q

How should you vaccinate horses for ehv

A

MLV intranasal or IM killed - give biannual vaccines to mares during pregnancy to prevent abortions

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235
Q

What is another name for equine rhinopneumonitis

A

EHV I or 4

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236
Q

What is the causative agent of equine herpes myeloencephalopathy

A

EHV 1 or 4

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237
Q

What viral infection looks just like EHV except it does not cause abortions in pregnant mares usually ( spread through respiratory secretions, same vaccine protocol, same treatment, nasal swab pcr to diagnose)

A

Require influenza A

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238
Q

What is thought to be the cause of EIPH and what predisposes horses

A

Likely in high speed event horses with lung damage or chronic infections - high pressure and high cardiac output cause capillary wall collapse and hemorrhage

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239
Q

How can you treat EIPH

A

Give furosemide a few hours before an event to decrease interstate pressure and hemorrhage

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240
Q

What risk factors predispose to recurrent airway obstruction / heaves

A

Warm dry environment, barn with pour ventilation, little turnout

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241
Q

How does RAO / heaves cause disease

A

Causes inflammation of lower airways leading to bronchospasm, excess mucus production and airway remodeling that on lead to obstructin

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242
Q

What are clinical signs of heaves / RAO

A

Tachypnea or dyspnea, respiratory noise, flared nostrils , cough, wheeling noise on end exhalation, have line on abdomen - otherwise fne asymptomatic between flare ups usually

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243
Q

How can you diagnose rao / heaves

A

BAL cytology (increased neutrophils), clinical signs

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244
Q

How can you diagnose rao / heaves

A

BAL cytology (increased neutrophils), clinical signs

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245
Q

How do you treat rao/heaves

A

Environmental modification mostly 1 corticosteroids to decrease inflammation, bronchodilators

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246
Q

What is almost always the cause of sinusitis

A

Usually secondary to a dental problem

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247
Q

Which teeth are usually involved in sinusitis? which sinus

A

08-11 but 09 is most common - sinus affected depends on tooth affected

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248
Q

What are clinical signs of sinusitis

A

Chronic unilateral mucopurelent nasal discharge that is foul smelling that goes away with antibiotics but then came back when you stop

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249
Q

How do you diagnose sinusitis

A

Rule out other causes with nasal PCR and nasal endoscopy - then head and dental rads and CT

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250
Q

Which nerve is affected during laryngeal paralysis and why

A

Left recurrent laryngeal nerve because it is the longest equine nerve

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251
Q

What is the pathophysiology of laryngeal hemiparesis /recurrent laryngeal nerve paralysis/ roarer

A

Idiopathic neuropathy of left recurrent laryngeal nerve causing the left arytenoid cartilage to fail to abduct during inspiration leading to partial or full obstruction

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252
Q

What are clinical signs of laryngeal hemiparesis

A

Upper respiratory noise on inspiration during exercise, exercise intolerance, poor performance

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253
Q

How do you diagnose laryngeal hemi paresis

A

Upper endoscocopy while horse is exercising and in sedated

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254
Q

When are you likely to see R. Equi infections

A

Foals 1-3 months old - gradual unset but often have significant disease before clinical signs develop

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255
Q

How easy is R. Equi to get rid of

A

Not easy -lives in soil and can be endemic for years on farms

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256
Q

What are clinical signs seen with R. Equi infections in foals

A

Pyogranulomatous bronchopneumonia, fever , lethargy, anorexia, poor weight gain -if disseminated it can cause septic arthritis / uveitis, etc

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257
Q

How can you diagnose R. Equi infection in foals

A

Transtacheal wash and cytology - will see intracellular rods , abscesses on thoracic rads

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258
Q

How do you treat R. Equi infection

A

Rifampin and azithromycin for 4-10 weeks

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259
Q

How can farms help prevent R. Equi infections

A

Endemic farms can treat foals with R. Equi hyper immune plasma at birth then again 1 month of age

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260
Q

What are predisposing factors for pleuropneumonia / shipping fever in horses

A

Thing a horses head up during transport which decreases ability to clear airways, extended duration of transport - maybe infectious respiratory disease

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261
Q

What are predisposing factors for pleuropneumonia / shipping fever in horses

A

Thing a horses head up during transport which decreases ability to clear airways, extended duration of transport - maybe infectious respiratory disease

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262
Q

What are clinical signs of pleuropneumonia /shipping fever in horses

A

Severe fever, dyspnea, decreased lung sounds ventrally, nasal discharge, reluctance to move due to pleural pain from fluid accumulation

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263
Q

How can you diagnose pleuropneumonia

A

Thoracic rads to check for pleural effusion / clinical signs

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264
Q

How can choke ( gastro esophageal obstruction) present as a respiratory disease

A

May begin as bilateral green nasal discharge or coughing, gagging,

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265
Q

What happens if choke is not treated within 6 - 12 hours

A

Aspiration pneumonia risk a lot higher

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266
Q

How can youdiagnose choke

A

Inability to pas a nasogastric tube and clinical signs

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267
Q

How can youdiagnose choke

A

Inability to pas a nasogastric tube and clinical signs

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268
Q

How do you treat choke

A

Sedation to lower head and decrease risk of aspiration pneumonica ,gentle lavage via a nasogastric tube

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269
Q

How do you treat choke

A

Sedation to lower head and decrease risk of aspiration pneumonica ,gentle lavage via a nasogastric tube

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270
Q

What is founder? Describe its pathophysiology

A

Laminitis - inflammation causing laminar projections /lamellae in the hoof capsule to be inflamed and weak - when laminate are weak, the deep digital flexor tendon will pull the coffin bore to rotate toward the palmar aspect (tippy toe) - coffin bone en sink lower in the hoof

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271
Q

What often predisposes to laminitis /founder

A

Metabolic disease, obesity, equine cushings disease, excess grain intake, endotoxemic diseases ( colitis, grain overload, inorganic steroid induced)

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272
Q

Which limbs are usually affected by laminitis

A

Front limbs

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273
Q

What clinical signs would you see with founder/ laminitis

A

Increased digital pulses, rocked back stance, walking on eggshells, positive to pressure at the toe, difficulty picking up hoof due to pain

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274
Q

What might you see on radiographs of a laminitis case

A

Coffin bore rotated at a palmar angle, decreased sole depth at point of the coffin bone , osteophyte ski tip at point of coffin bone

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275
Q

What might you see on radiographs of a laminitis case

A

Coffin bore rotated at a palmar angle, decreased sole depth at point of the coffin bone , osteophyte ski tip at point of coffin bone

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276
Q

What diagnostic tool is contraindicated in cases of laminitis

A

Nerve blocks -lead to increased temporary weight bearing which can make it worse

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277
Q

What diagnostic tool is contraindicated in cases of laminitis

A

Nerve blocks -lead to increased temporary weight bearing which can make it worse

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278
Q

How do you treat laminitis / founder

A

Ice/cool the feet , antiinflammatories, fashioned boots and a deeply bedded stall, trimming to derogate the toe and decrease heel angle. - tenotomy for chronic cases , weight loss plan to keep low sugar, low starch hay and grain

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279
Q

Which breeds are over represented for navicular syndrome and why

A

Paints, quarter horses - small feet

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280
Q

What is navicular syndrome

A

Any source of pain from the navicular bone or attached ligaments - osteophytes on the mericular bore will care pain on the deep digital flexor tendon where it attaches to bottom of coffin bone

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281
Q

What is navicular syndrome

A

Any source of pain from the navicular bone or attached ligaments - osteophytes on the mericular bore will care pain on the deep digital flexor tendon where it attaches to bottom of coffin bone

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282
Q

Which feet are usually affected by navicular syndrome

A

Front feet bikteally usually - but one foot will be worse ( and lameness will be worse when initial is blocked)

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283
Q

You perform a palmar digital nerve block on a horse with a lower limb lameness that then shifts to the other limb. what is your top differential

A

Navicular syndrome

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284
Q

What diagnostics indicate navicular syndrome

A

Positive pressure at heels, palmar digital nerve block causing shifting leg lameness

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285
Q

What will navicular syndrome look like on radiographs

A

Normally looks like a Reverse Oreo (central medulla is darker and less dense) - with navicular disease, the navicular bone will be enlarged and have increased nutrient dense former, medulla has increased density - in severe cases the medulla and cortex are indistinguishable - will tho see osteophytes

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286
Q

What is breakover in horses

A

The point where the horse pivots from when pushing heels

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287
Q

How can you treat navicular syndrome and what is the goal

A

Trim to improve breakover, increase heel angle to take pressure off tendons, wedge or heel pad/ biphosphonate injection to decrease osteoclast action labor for osteoblast action)

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288
Q

What tendons are most likely affected by tendinitis or desmitis

A

Suspensory ligament, deep digital flexor tendon and superficial digital flexor tendon

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289
Q

Define desmitis

A

Inflammation of a ligament

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290
Q

Define desmitis

A

Inflammation of a ligament

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291
Q

Describe DSLD - degenerative suspensory ligament desmitis/ disease pathophysiology

A

Progressive failure of collagen fiber repair in the suspensory ligament apparatus, causing a gradual enlargement but weakening of the suspensory ligament, leading to a fetlock drop (bilaterally)

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292
Q

What clinical signs might you see with desmitis or tendonitis

A

Swollen tendon or tendon sheath , painful on palpation, lameness at a trot but almost always weight bearing

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293
Q

How do you diagnose tendonitis or desmitis and what will you see

A

Ultrasound - focal anechoic lesions or abnormal fiber pattern if chronic

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294
Q

How do you treat tendonitis or desmitis

A

Neurectomy, PRP, shockwave therapy

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295
Q

How do you treat tendonitis or desmitis

A

Neurectomy, PRP, shockwave therapy

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296
Q

What does a positive to flexion test mean

A

Obvious lameness for 3-5 strides while horse trots a straight line after flexing the limb

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297
Q

What is the pathogenesis of osteoarthritis

A

Degeneration of articular cartilage due to trauma/synovitis - joint fluid loses viscosity which increases shock leading to remodeling and osteophyte formation - can fracture and form fragments leading to joint stress

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298
Q

What is high ringbone

A

Pastern joint OA

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299
Q

What is low ringbone

A

Coffin joint OA

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300
Q

Differentiate between bone spavin and bog spavin

A

Bone spavin - hock joint OA (intertarsal)
Bog spavin - tibiotarsal joint effusion

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301
Q

What predisposes a horse to subsolar / hoof abscesses

A

Week hoof, moist environment , poor hoof hygiene - all allow bacteria to travel intofoot and proliferate deep in hoof

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302
Q

What predisposes a horse to subsolar / hoof abscesses

A

Week hoof, moist environment , poor hoof hygiene - all allow bacteria to travel intofoot and proliferate deep in hoof

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303
Q

What clinical signs would you expect to see with a subsolar abscess

A

Almost non weight bearing lameness, positive to hoof testers , heat in hoof, gray purulent drainage

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304
Q

What will a sub solar abscess look like on rads

A

Big gas pocket on rads

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305
Q

What is contraindicted for treating subsolar abscesses and why

A

Systemic antibiotics not used because limited blood supply to superficial hoof means poor antimicrobial penetration

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306
Q

How does a laceration leading to a septic joint or tendon cause lameness

A

Initially due to pain of the joint capsule - then continues due to distention and pressure on the joint capsule as WBC and inflammatory markers increase effusion

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307
Q

How does a laceration leading to a septic joint or tendon cause lameness

A

Initially due to pain of the joint capsule - then continues due to distention and pressure on the joint capsule as WBC and inflammatory markers increase effusion

308
Q

What does joint fluid look like

A

Straw colored, stringy between fingers

309
Q

What will a septic joint look like when analyzing the joint fluid

A

Increased protein and cellularity - WBC over 30,000 with 80% neutrophils and total protein over 4

310
Q

When are you likely to see cases of OCD (osteochondritis dissecans)

A

1-2 year old horses , large or fast growing breeds, or horses on an improperly balanced diet (poor ca to p ratio)

311
Q

What is OCD - osteochordritis dissecans

A

Failure of normal endochondral ossification - cartilage at articular surface fails to ossify

312
Q

What is OCD - osteochordritis dissecans

A

Failure of normal endochondral ossification - cartilage at articular surface fails to ossify

313
Q

What joints are commonly affected by OCD lesions

A

Tarsus, stifle, fetlock

314
Q

What clinical signs might you see with OCD

A

Joint effusion, lameness at the trot

315
Q

What is likely the cause of congenital flexural limb deformities and which areas are most commonly affected

A

Intrauterine mal positioning, dysmaturity - carpus and fetlock take most common

316
Q

What are common clinical signs of congenital flexural limb deformity

A

Inability to extend limb, knuckling over, walking on heels with toe in air, fetlock extension

317
Q

Head, neck and muzzle fesiculations in the horse are highly suggestive of

A

WNV - but most infections are undetected or asymptomatic

318
Q

Head, neck and muzzle fesiculations in the horse are highly suggestive of

A

WNV - but most infections are undetected or asymptomatic

319
Q

When are you likely to see cases of WNV and why

A

Late summer or fall in warm climates - mosquitos are vectors for this disease

320
Q

When are you likely to see cases of WNV and why

A

Late summer or fall in warm climates - mosquitos are vectors for this disease

321
Q

List the neurolgic ataxia grading scale (0-5)

A

0 - normal
I- normal at rest deficits seen with manipulative tests
2- mild deficit at normal gait, more pronounced with manipulative tests
3. Obvious at all gaits
4 - obvious at all gain, falls easily
5- recumbent

322
Q

Out of the causes of equine encephalitis (EEE, WEE, VEE) which are core vaccines

A

EEE and wee are core vaccines

323
Q

Which cause of equine encephalitis can be zoonotic

A

VEE

324
Q

What is your top differential for a horse experiencing sleeping sickness - head pressing, circling, etc

A

Equine encephalitis - eee, VEE, WEE

325
Q

What are common signs of sleeping sickness in horses

A

Head pressing, blindness, circling, ataxia, recumbency, coma, seizures

326
Q

What occurs when EHV I mutates to the wild type and what predisposes the horse

A

Equine herpes myeloencephalitis -frequent travelling or exposure to other hoses

327
Q

What occurs when EHV I mutates to the wild type and what predisposes the horse

A

Equine herpes myeloencephalitis -frequent travelling or exposure to other hoses

328
Q

EHM causes - and is readily -

A

Vhswlihs in CNS - readily contagious

329
Q

What are clinical signs of EHM

A

Ataxia, paresis of hind end , urinary incontinence loss of tail tore

330
Q

What are clinical signs of EHM

A

Ataxia, paresis of hind end , urinary incontinence loss of tail tore

331
Q

How do you diagnose EHM

A

Nasal swab PCR

332
Q

You suspect a horse was EHM - should nw vaccinate for EHV (since the causative agent is EHV1)

A

No- not effect because it is a mutation of EHV1

333
Q

EHVI normally causes -

A

Respiratory disease

334
Q

What is the definitive host for equine protozoal myeloencephalitis (EPM) and how is it transmitted

A

Opossums - pass sporoust in feces which are ingested by the horse , access the CNS, and cause multifocal damage

335
Q

What is the causative agent of equine protozoal myeloencephalitis

A

Sarcocystis neurona - lately also neospora Hughesi

336
Q

What are clinical signs of EPM

A

Chronic vague signs - unilateral hind end atrophy, shifting leg lameness , animals often BAR

337
Q

What are clinical signs of EPM

A

Chronic vague signs - unilateral hind end atrophy, shifting leg lameness , animals often BAR

338
Q

Exposure to - is common, disease is rare

A

EPM / sarcocystis neurona

339
Q

How can you diagnose EPM

A

CSF titers more accurate than serology titers

340
Q

How can you treat EPM? what is important to remember about treatment

A

Ponazuril for about 6 months - treatment usually improves clinical signs but relapse is common

341
Q

Describe tetanus pathophysiology in the horse - what is the incubation period

A

C. Petani enters through a wound (anaerobic) - proliferates to release a neurotoxin that travels to the CNS I incubation about 1-3 weeks

342
Q

What ate clinical signs of tetanus in horses (horses particularly sensitive)

A

Stiff spastic gait, raised head and tail, extreme noise and light hyperesthesia, third eyelid prolapse/ recumbeas I lockjaw

343
Q

How do you treat tetanus in the horse

A

Penicillin and tetanus antitoxin

344
Q

What are the 3 forms of rabies

A

Furious (cerebral), dumb (brain stem), paralytic (spinal cord )

345
Q

Describe the furious form of rabies

A

Aggressive behavior, self mutilation, vocalization

346
Q

Describe the furious form of rabies

A

Aggressive behavior, self mutilation, vocalization

347
Q

Describe the dumb form of rabies

A

Somnolence, dementia, dysphagia ,ataxia

348
Q

Describe the paralytic form of rabies

A

Progressive ascending paralysis

349
Q

How do horses usually become infected with C. Botulinum

A

Ingestion through silage, round hay bales, poorly stored forage

350
Q

How does C botulinum cause disease

A

Toxin blocks ACH release at neuromuscular junction preventing electrical signals

351
Q

What are clinical signs of botulism

A

Symmetrical flaccid paralysis, gradually progressive weakness, respiratory paralysis, ileus, colic , dysphagia, poor tongue tone

352
Q

What is cauda equina and what is the pathogenesis

A

Polyneuritis equi - granulomatous perineuritis of CN and peripheral nerves triggered by an immune mediated event Dre to bacterial or viral infection

353
Q

What is cauda equina and what is the pathogenesis

A

Polyneuritis equi - granulomatous perineuritis of CN and peripheral nerves triggered by an immune mediated event Dre to bacterial or viral infection

354
Q

What clinical signs do you expect to see with cauda equina / polyneuritis equi

A

Hind end issues - urinary incontinence, flaccid tail
Cranial nerve deficits - depressed PLR, maseter atrophy, tongue weakness, head tilt , difficulty swallowing

355
Q

What is the prognosis of caudal equine/ polyneuritis equi

A

Poor long term - usually diagnose with a necropsy

356
Q

What causes equine degenerative myeloencephalopathy (edm)

A

Vitamin E deficiency and a genetic component

357
Q

What causes equine degenerative myeloencephalopathy (edm)

A

Vitamin E deficiency and a genetic component

358
Q

When are you likely to see cases of EDM and what clinical signs would you expect

A

Young horses - dull, quiet, symmetrical ataxia in all legs

359
Q

What occurs during EDM (equine degenerative myeloencephalopathy) and what is the prognosis

A

Neuroaxonal dystrophy - rarely successful to supplement with vitamin E

360
Q

What disease occurs due to chronic vitamin E deficiency in adult horses and what occurs

A

Equine motor neuron disease - peripheral motor neuron cell death

361
Q

What disease occurs due to chronic vitamin E deficiency in adult horses and what occurs

A

Equine motor neuron disease - peripheral motor neuron cell death

362
Q

What are 2 biggest differences between equine degenerative myeloencephalopathy and equine motor neuron disease

A

Both are due to vitamin E deficiency but EDM occurs in young horses and causes ataxia in all limbs and EMND is chronic in adult horses and does not cause ataxia

363
Q

What are clinical signs of equine motor neuron disease

A

Weakness , low head carriage, high tail carriage, muscle atrophy, good appetite with weight and muscle loss

364
Q

What is another name for wobblers

A

Cervical vertebral malformation or cervical stenotic myelopathy

365
Q

What is another name for wobblers

A

Cervical vertebral malformation or cervical stenotic myelopathy

366
Q

What is wobblers / cervical stenotic myelopathy and who does it mostly affect

A

Compressive lesion in the vertebral column - affects large fast growing breed, like warmbloods and thoroughbreds

367
Q

Differentiate between type 1 and type 2 cervical stenotic myelopathy

A

Type 1 - congenital malformation in young hoses
Type 2 - osteoarthritis in older horses

368
Q

Differentiate between type 1 and type 2 cervical stenotic myelopathy

A

Type 1 - congenital malformation in young hoses
Type 2 - osteoarthritis in older horses

369
Q

Which part of the vertebral column is usually affected by wobblers / cervical stenotic myelopathy

A

C3 - C7

370
Q

Why is ataxia usually worse in hindlimbs with wobblers

A

Hindlimb innovation is superficial on the spinal Cord (compressed more)

371
Q

Describe clinical signs of wobblers / cervical stenotic myelopathy

A

Ataxia (worse in hindlimbs), pour performance - gradual onset

372
Q

What are possible causes for pseudo narcolepsy in horses

A

Behavioral /anxiety or pain causing a reluctance to lay down

373
Q

What clinical signs might you see to make you suspect pseudonarcolepsy

A

Knuckling on front fetlocks, rocking back with head in a low position, chronic abrasions on dorsal fetlocks

374
Q

What clinical signs might you see to make you suspect pseudonarcolepsy

A

Knuckling on front fetlocks, rocking back with head in a low position, chronic abrasions on dorsal fetlocks

375
Q

What are the names for heaves

A

Recurrent airway obstruction, chronic obstructive pulmonary disease (copd), broken wind, hay sickness

376
Q

What clinical signs might you see with recurrent airway obstruction

A

Increased respiratory rate, increased expiratory effort, cough, exercise intolerance, weight loss, heave line

377
Q

What occurs in recurrent airway obstruction to cause disease

A

Bronchoconstriction and accumulation of mucus and neutrophils within the airway

378
Q

What occurs in recurrent airway obstruction to cause disease

A

Bronchoconstriction and accumulation of mucus and neutrophils within the airway

379
Q

When are you likely to see cases of rao / copd and why

A

Older horses, stalled in a born in the winter being fed hay probably due to dust, mold or fungi in the environment

380
Q

Hypertrophy of which muscle leads to a leaves line

A

External abdominal oblique muscle

381
Q

Hypertrophy of which muscle leads to a leaves line

A

External abdominal oblique muscle

382
Q

What could you hear on physical exam in a horse with RAO/Hay sickness

A

Wheezes and crackles

383
Q

What should bal fluid of a healthy horse look like

A

Mostly macrophages

384
Q

What will bal fluid look like in a case of heaves

A

Increased number of neutrophils

385
Q

What will bal fluid look like in a case of heaves

A

Increased number of neutrophils

386
Q

What are curshmanns spirals and what disease would it indicate

A

Inspirated mucus plugs on cytology - suggestive of RAO

387
Q

What are curshmanns spirals and what disease would it indicate

A

Inspirated mucus plugs on cytology - suggestive of RAO

388
Q

What can you treat RAO/COPD with medically

A

Corticosteroids (Dexamethasone and prednisolone) to decrease inflammation and bronchodilators like albuterol

389
Q

Where do sarcocysts of sarcocystis, neurona develop in the intermediate host

A

Skeletal muscle

390
Q

The horse is a - host that ingests sporocysts of sarcocystis neurona

A

Dead end / aberrant host

391
Q

Is sarcocystis neurona rare in horses

A

Exposure is common but only a minor population develops neurologic signs if the parasite reaches the CNS

392
Q

A defining clinical sign of equine protozoal myeloencephalitis that differentiates it from cervical vertebral malformation is

A

Asymmetric ataxia

393
Q

What are 2 possible diagnostic tests to identify EPM

A

Positive western blot analysis of CSF or IFA testing

394
Q

What are 3 primary treatments for EPM

A

TMS, ponazuril, nitrazoxinade

395
Q

What are 3 primary treatments for EPM

A

TMS, ponazuril, nitrazoxinade

396
Q

What amount of maternal antibodies is enough to prevent sepsis

A

IGG antibodies over 800 mg/dl

397
Q

What amount of maternal antibodies is enough to prevent sepsis

A

IGG antibodies over 800 mg/dl

398
Q

What is sirs and what are clinical signs

A

Systemic inflammatory response - sepsis - clinical signs include tachycardia , tachypnea, leukopenia, over 10%band neutrophils

399
Q

What confirms a sirs infection (systemic inflammatory response )

A

2 or more clinical Signs - tachycardia, tachypnea, leukopenia, over 10% of band neutrophils

400
Q

What is the most common isolate cultured from foals with neonatal sepsis

A

E. Coli

401
Q

How are SARS and sepsis related

A

If SARS is caused by an infection it becomes sepsis

402
Q

How can you diagnose sepsis in neonatal foals

A

Positive bacterial cultures / blood cultures - check for aerobic growth and anaerobic growth , can collect 2-3 times

403
Q

What are some common clinical signs of sepsis in regnatal foals

A

Jaundice, swollen joints, hypovolemia, hypoglycemia, acidemia, high serum lactate

404
Q

What sort of things are included in a sepsis score for foals

A

Hypoglycemia, fpt, prematurity, CBC results, toxic neutrophils

405
Q

What are common secondary complications to neonatal sepsis

A

Septic arthritis, thrombophlebitis, septic physitis, omphalophlebitis, diarrhea

406
Q

What type of bacteria is strep equi and is it normal flora of the respiratory tract

A

Gram positive Beth hemolytic strep - is not a normal inhabitant of the respiratory that

407
Q

What is the drug of choice to treat strangles

A

Penicillin

408
Q

What is the drug of choice to treat strangles

A

Penicillin

409
Q

Strep equi is highly - and frequently causes _

A

Contagious - herd outbreaks

410
Q

Describe the pathogenesis of strangles

A

Bacteria adheres to epithelial cells of mucosa and replicates in lymph nodes where it establishes in the pharyngeal region 1 casing lymph node absessation and drainage

411
Q

Which lymph nodes are affected with strangles? Bastard strangles?

A

Intermandiular and retro pharyngeal - if bastard strangles the internal lymph nodes will be affected

412
Q

What are clinical signs of strangles

A

Serous to mucopurlent nasal discharge, fever, inappetence, firm lymphadenopathy, trouble breathing due to airway compression

413
Q

What club path abnormalities could you see with strangles

A

Hyperfibrinogeremia, neutrophilic leutocytosis

414
Q

Describe rhodococcus equi as a bacteria - is it normal fora

A

Gram positive facultative intracellular coccobacillus - is not normal flora but is gammon environmental pathogen that can cause widespread disease (readily aerosolized in dry dusty peroids)

415
Q

What is the treatment for r. Equi infections in foals 1-6 months old

A

Rifampin mixed with a macrolide (erithyromycin or azithromycin)

416
Q

Why does R. Equip often cause severe pneumonia before owners notice signs

A

Foals inhale bacteria early in life but onset is slow and insidious

417
Q

Describe the pathogenesis of R. Equi infections in foals

A

Bacteria is inhaled from dusty environments then invades alveolar macrophages where my replicate and cause progranulomatous pneumonia and pulmonary abscessation

418
Q

Describe the pathogenesis of R. Equi infections in foals

A

Bacteria is inhaled from dusty environments then invades alveolar macrophages where my replicate and cause progranulomatous pneumonia and pulmonary abscessation

419
Q

Why would a foal infected with R. Equi have diarrhea or signs of colic

A

Can develop ulcerative colitis or mesenteric lymphadenitis

420
Q

What clinical signs can you see with R. Equi infection

A

Intermittent fever, weight loss, inappetence, wheezes and crackles on thoracic auscultation, cough, increased respiratory effort

421
Q

What would be abnormal on Clin path of a foal infected with R. Equi

A

Hyperfibrogenemia, neutrophilic leukocytosis

422
Q

What are possible secondary complications of R. Era infection in foals

A

Osteomyelitis, septic arthritis, joint effusion , internal abscessation

423
Q

What are some ways to detect R. Equip infection earlier

A

Monitor elevations in temp, routine CBC screening to check for leukocytosis

424
Q

What clinical signs indicate lower respiratory tract involvement

A

Cough, nasal discharge, increased respiratory rate (effort, exercise intolezie

425
Q

What can predispose horses to developing pneumonia

A

Extended transport, exposure to a lot of horses, stressful events like anesthesia

426
Q

What is the relationship between pneumonia and pleuropneumonia

A

Pleuropneumonia occurs in conjunction with pneumonia - causes significant accumulation of fluid and fibrin in the thoracic cavity

427
Q

What is the relationship between pneumonia and pleuropneumonia

A

Pleuropneumonia occurs in conjunction with pneumonia - causes significant accumulation of fluid and fibrin in the thoracic cavity

428
Q

Clinical signs like cough, fever and increased respiratory rate effort lead you to suspect

A

Pneumonia

429
Q

What clin path abnormalities might you see with pneumonia

A

Hyperfibrinogenemia, hyperglobulinenia, anemia, leukopenia or leukocytosis it chronic

430
Q

What would thoracic rads look like for a horse with pneumonia or pleuropneumonia

A

Cranial ventral or caudal ventral radio opacity

431
Q

Consider treating with - in a horse with pneumonia caused by anaerobes

A

Metronidazole

432
Q

What is habronemiasis and what does it cause

A

Parasitic disease causing aberrant cutaneous migration of nematode larvae

433
Q

What is habronemiasis and what does it cause

A

Parasitic disease causing aberrant cutaneous migration of nematode larvae

434
Q

What is the most common cause of cutaneous ulcerative granulomas in the horse

A

Habronemiasis

435
Q

Which 3 nematodes cause habronemiasis / summer sores

A

Habronema muscae, habronema majus, draschia megastoma

436
Q

Who are the intermediate hosts of habroremiasis (explain)

A

Flies - stable fly and house fly - fly maggots ingest larvae found in feces (where the nematode develops into L3 (the infective stage), area flies go to moist areas on the horse to deposit larvae (wounds or mucous membranes)

437
Q

Where do adult nematodes causing habronemiasis or summer sores reside and how are eggs passed

A

Inhabit the stomach then eggs are passed in the feces

438
Q

Where are lesions commonly seen in horses infected with habronemiasis /summer sore

A

Medial canthus, nostrils, vulva, teats, commissures of lips and wounds

439
Q

When will you see cases of hebronemiasis

A

Summer - summer sores

440
Q

What clinical signs might you see with habronemiasis /summer sores

A

Ulcerative granulomas on skin and moist areas, intense pruritis due to a hypersensitivity reaction to the nematodes

441
Q

What other differentials must be ruled out when diagnosing habronemiasis / summer sores

A

Other causes of nodules and masses - neoplasia, eosinophilic granulomas

442
Q

What other differentials must be ruled out when diagnosing habronemiasis / summer sores

A

Other causes of nodules and masses - neoplasia, eosinophilic granulomas

443
Q

How can you prevent habronemiasis

A

Ivermectin or moxidectin - eliminates nematodes in stomach

444
Q

How do you diagnose habronemiasis

A

Deep skin scoping, smear, biopsy

445
Q

If the gutteral pouches in horses don’t have a known function, why do we care so much about the disease they cause

A

The GP contains vital structures like cranial nerves, internal and external Carotid , maxillary arteries

446
Q

If the gutteral pouches in horses don’t have a known function, why do we care so much about the disease they cause

A

The GP contains vital structures like cranial nerves, internal and external Carotid , maxillary arteries

447
Q
  • Is congenital and causes non painful air filled swelling in the throat latch region in young foals
A

Guttural pouch tympany

448
Q

What is guttural pouch empyema and what is it usually caused by

A

Accumulation of purulent exudate secondary to respiratory infections - usually strangles

449
Q

The GP communicates with the -

A

Pharynx

450
Q

The GP communicates with the -

A

Pharynx

451
Q

What separates the medial and lateral guttural pouches

A

Stylohyoid bone

452
Q

What separates the medial and lateral guttural pouches

A

Stylohyoid bone

453
Q

What structures are associated with the guttural pouches

A

Cranial nerves 7, 9, 10, 11, 12 , sympathetic trunk, internal and external carotid, maxillary arteries

454
Q

What is thought to cause gutteral pouch tympany in foals

A

An extra mucosal flap at the pharynx opening acting as n one way value allowing air to get trapped

455
Q

What is thought to cause gutteral pouch tympany in foals

A

An extra mucosal flap at the pharynx opening acting as n one way value allowing air to get trapped

456
Q

What clinical signs might you see with gp tympany

A

Soft non painful swelling on the throat, respiratory sterter or dysphagia, aspiration premonia

457
Q

What clinical signs might you see with gp tympany

A

Soft non painful swelling on the throat, respiratory sterter or dysphagia, aspiration premonia

458
Q

How can you treat GP tympany

A

If unilateral, fenestrate the septum between the medial and lateral gp - if bilateral, surgical correction of the pharynx

459
Q

What clinical signs might you see with GP empyema

A

Nasal discharge, regional lymph node enlargement, dysphagia, film masses palpable (if chronic - chondroids!)

460
Q

What would you see on rads of GP empyema

A

Fluid line in the guttural pouches

461
Q

What is guttural pouch mycosis

A

Fungal plaques that develop in the GP resulting in clinical signs due to involvement of valor and neural structures

462
Q

What is guttural pouch mycosis

A

Fungal plaques that develop in the GP resulting in clinical signs due to involvement of valor and neural structures

463
Q

Why does gp mycosis occur

A

Unknown - aspergillosis plays a role, often causes erosion of the wall of the arteries leading to epistaxis of Nero signs if the cranial nerves are affected

464
Q

What clinical signs might you see with GP mycosis

A

Hemorrhage / epistasis , dysphasia, horners syndrome or facial nerve paralysis - depends on what structures, are affected

465
Q

What clinical signs might you see with wobblers / cervical vertebral malformation

A

Symmetric ataxia, paresis, spasticity, worse in hindlimbs - wide base stance/ proprioceptive deficits/ toe dragging , stumbling, circumduction of hindlimbs

466
Q

What is the sagittar radio on clerical radiographs

A

Measuring the smallest sagital diameter of the vertebral canal of each cervical vertebra then dividing by the width of the hernial aspect of vertebral body at in widest point

467
Q

What is the sagittar radio on clerical radiographs

A

Measuring the smallest sagital diameter of the vertebral canal of each cervical vertebra then dividing by the width of the hernial aspect of vertebral body at in widest point

468
Q

What should the sagittal ratio be for a healthy horse

A

Over 52% from C4-C6 or over 56% for C7

469
Q

What commonly causes EIPH and which horses are most often affected

A

Horses performing strenuous exercise, intense bouts of exercise - thoroughbreds, quarter horses Or standardbred horses

470
Q

What commonly causes EIPH and which horses are most often affected

A

Horses performing strenuous exercise, intense bouts of exercise - thoroughbreds, quarter horses Or standardbred horses

471
Q

What is the most obvious clinical sign of exercise induced pulmonary hemorrhage

A

Epistaxis

472
Q

What are possible pathophysiology of EIPH

A

Stress failure of pulmonary capillaries during intense exercise or rupture of pulmonary capillaries

473
Q

Is eiph related to duration or intensity of exercise

A

Intensity (duration is not found to matter)

474
Q

What is often used as a treatment for eiph

A

Giving lasix prior to intense exercise

475
Q

Which lung fields are most affected by EIPH

A

Caudadorsal lung fields

476
Q

Will you see epistaxis in all horses with EIPH? What other clinical signs could you see

A

Not all - decreased performance, labored breathing , coughing, loss of speed

477
Q

How can you diagnose eiph

A

Endoscopy or cytologic exam of bal fluid (will see hemosideraphages or erythrocytes)

478
Q

Is furosemide to treat EIPH permitted by race officials

A

Yes as long as it is given 4 hours prior to the race

479
Q

What commonly occurs secondary to placentitis

A

Abortion in the later stages of pregnancy

480
Q

What commonly occurs secondary to placentitis

A

Abortion in the later stages of pregnancy

481
Q

What is the most common viral cause of abortion in nurses

A

Equine herpes virus 1

482
Q

What is the most common viral cause of abortion in nurses

A

Equine herpes virus 1

483
Q

When does EHVI typically cause abortion,

A

Late gestation

484
Q

What is the best way to prevent abortions caused by equine herpes virus

A

Vaccinate pregnant mares at months 5,7 and 9

485
Q

What is the most common cause of non infectious abortion in horses

A

Twin fetuses - typically absorbed during gestation

486
Q

What is the most common route for bacteria causing placentitis

A

Ascending infection allowing bacteria to be introduced into the uteroplacental unit

487
Q

How does placentitis cause abortion in the mare

A

Ascending infection leads to inflammation and placental detachment at cervical region - placental thickening and separation from endometrium

488
Q

What are typically the causative agents of placentitis in the pregnant mare

A

Strep zoo epidemicus, E. Coli, pseudomonas, aeruginosa, klebsiella (ifbacterial), aspergillosis if fungal

489
Q

What ave some options with treating placntiti, in the pregnant mare

A

Antimicrobial, flunixin meglumine (NSAID), progesterone to promote uterine dormancy, clenbuterol to suppress uterine motility

490
Q

What are some viral causes of abortions in pregnant mares

A

Equine viral arteritis, EHV 1 or EHV4

491
Q

Other man abortions what can EHVI result in

A

Subclinical to clinical abortions

492
Q

How does EHVI cause abortions

A

Fetus infected during a viremic episode which cases rapid placental detachment

493
Q

How is the fetus infected with EHVI

A

Either through chorionic vasculature or inhalation of infected amniotic fluid

494
Q

How is the fetus infected with EHVI

A

Either through chorionic vasculature or inhalation of infected amniotic fluid

495
Q

What will an aborted fetus due to EHVI look like

A

Small necrotic foci on the liver, necrotizing bronchiolitis or intranuclear inclusion bodies on histology

496
Q

What will an aborted fetus due to EHVI look like

A

Small necrotic foci on the liver, necrotizing bronchiolitis or intranuclear inclusion bodies on histology

497
Q

What will a foal born infected with EHV 1 look like / show signs of

A

Don’t survive more than a few hours / days, signs of respiratory distress, icterus, fever, lethargy

498
Q

How can you confirm an EHVI infection

A

Indirect immunoflouresence, per, virus isolation

499
Q

Why do twin fetuses in the mare almost always cause abortion

A

Diffuse microcotyledonary placentation of the mare, limited endometrial surface available for the allantochorion to attach, both fetuses compete for adequate nutrition and placentation

500
Q

What is umbilical torsion in the mare and what happens as a result

A

Fetus rotates in the amniotic sac which twists the umbilical cord causing constriction of normal flow, edema, hemorrhage, thrombosis

501
Q

Your clinician tries to give your horse clindamycin - what do you do

A

Scream - clindamycin on kill a horse with diarrhea

502
Q

What is a common non pathologic heart arhymmia in healthy horses that requires no treatment

A

Second degree AV block

503
Q

Describe what you’ll see with 2nd degree AV block in a horse

A

Slow to normal heart rate (25-40), normal QRS, p waves not followed by a QRS complex every time

504
Q

How can yo confirm your suspicion of 2nd degree AV block in a horse

A

Jog them - if it goes away when the heart rate is increased it is a non pathological second degree AV block

505
Q

How can yo confirm your suspicion of 2nd degree AV block in a horse

A

Jog them - if it goes away when the heart rate is increased it is a non pathological second degree AV block

506
Q

What is the most common pathologic arrhythmia in horses

A

Atrial fibrillation

507
Q

What is the most common pathologic arrhythmia in horses

A

Atrial fibrillation

508
Q

Describe atrial fibrillation

A

Normal to elevated heart rate, normal QRS, r-r interval irregular, no p waves (instead see fibrillation waves)

509
Q

Define r-r interval

A

Space between the rs in two successive QRS complexes - measures ventricular rate

510
Q

What are gbrilkation waves caused by

A

Upper atrial chambers of the heart beating chaotically and irregularly

511
Q

What clinical signs can you see with atrial fibrillation in horses

A

Exercise intolerance, poor performance - may see none at all or horse man have an underlying heart condition

512
Q

What can be used to treat atrial fibrillation in horses? What are the disadvantages

A

Quinidine sulfate - lot of side effects like diarrhea , colic, laminitis, arrhythmogenic,

513
Q

What can be used to treat atrial fibrillation in horses? What are the disadvantages

A

Quinidine sulfate - lot of side effects like diarrhea , colic, laminitis, arrhythmogenic,

514
Q

Do you have to treat cases of atrial fibrillation

A

No- sometimes an incidental finding you can just monitor horse, especially if just a pasture horse

515
Q

What is another name for equine cushings disease

A

Pituitary pars intermedia dysfunction

516
Q

When are you likely to see cases of pituitary pars intermedia dysfunction/ equine cushings and what clinical signs might you see

A

Older horses (15-20 years) - see hirsutism (excessive hair), pu/pd, hyperglycemia, chronic laminitis, muscle washing

517
Q

What is your top differential for a horse with an increased haircoat that is older (15 years or so)

A

Pituitary pars intermedia dysfunction - PPID equine cushings

518
Q

How can you diagnose PPID in horses

A

Dexamethasone suppression test - dex is supposed to suppress cortisol I or ACTH levels

519
Q

How do you treat PPID in horses

A

Pergolide (a dopamine agonist), supportive care

520
Q

How can you evaluate if a foal has absorbed enough colostrum from mare

A

Check igg antibodies in blood or serum

521
Q

What values can you use to determine failure of passive transfer in a foal? How do youtest

A

Test with ELISA snap test for a quick answer
Over 800 igg levels - adequate
400 - 800 - partial failure
Les man 400 - complete failure

522
Q

Define foal septicemia

A

Bacteremia (bacteria in the blood) along with sirs (systemic informatory response syndrome)

523
Q

Define foal septicemia

A

Bacteremia (bacteria in the blood) along with sirs (systemic informatory response syndrome)

524
Q

What are clinical signs of sirs in foals

A

Tachycardia, tachypnea, hypo or hyperthermia, leukocytosis or leukopenia, presence of band neutrophils

525
Q

What predisposes to septicemia in foals

A

FPT mostly , salmonella infections, overcrowding

526
Q

Give examples of gram positive organisms that can cause foal septicemia

A

Strep, enterococcus, acinetobacter

527
Q

What are examples of gram negatives that can cause foal septicemia

A

Klebsiella, salmonella , pseudomonas

528
Q

Which bacteria is most often isolated in foal septicemia

A

E. coli (gram negative)

529
Q

Which bacteria is most often isolated in foal septicemia

A

E. coli (gram negative)

530
Q

What clinical signs can you see with foal septicemia

A

Weakness, hypovolemia, tachycardia, tachypnea, hypo or hyper thermia, diarrhea

531
Q

Which antimicrobials are often used to treat foal septicemia

A

Beta lactams and aminoglycosides (amikacin)

532
Q

What are the Shock organs in the horse - what does this mean

A

Lungs and colon - if horse experiences something like graphylachi shock the signs you might see will be respirator and GI (dyspnea, severe respiratory distress, diarrhea)

533
Q

What are the Shock organs in the horse - what does this mean

A

Lungs and colon - if horse experiences something like graphylachi shock the signs you might see will be respirator and GI (dyspnea, severe respiratory distress, diarrhea)

534
Q

Would you give ketamine to a horse who you want to relax their muscles more

A

No - ketamine can cause hypertonic (try guanifesin)

535
Q

Would you give ketamine to a horse who you want to relax their muscles more

A

No - ketamine can cause hypertonic (try guanifesin)

536
Q

What are risks of guanifesin toxicity

A

Increased muscle rigidity, severe cardiac and respiratory distress

537
Q

What are risks of guanifesin toxicity

A

Increased muscle rigidity, severe cardiac and respiratory distress

538
Q

What are the key components of TPN (total parental nutrition)

A

Carbohudster (like dextrose), proteins (amino acids) , lipids

539
Q

What are the key components of TPN (total parental nutrition)

A

Carbohudster (like dextrose), proteins (amino acids) , lipids

540
Q

What is another name for greasey heel /scratches - describe it

A

Chronic seborrheic dermatitis of palmar/plantar aspect of the pastern

541
Q

What is another name for greasey heel /scratches - describe it

A

Chronic seborrheic dermatitis of palmar/plantar aspect of the pastern

542
Q

What can cause summer sores in horses

A

Habronema or draschia - stomach worms in the horse

543
Q

What can cause summer sores in horses

A

Habronema or draschia - stomach worms in the horse

544
Q

Describe sweet itch

A

Caused by culcoides and a type I hypersensitivity reaction causing intense pruritis and self trauma lesions

545
Q

What is Sweeney in horses

A

Shoulder atrophy due to damage to he suprascapular nerve innovating the spinus muscles (Supra and infra)

546
Q

What does lethal white syndrome in foals born to paint horses lead to

A

Agangliosis of intestines leading to hypo motility, megacolon, constitution, colic and death

547
Q

Describe clinical signs of equine influenza

A

Affects a large group, rapid onset of fever, lethargy, weakness, and cough

548
Q

Describe clinical signs of equine influenza

A

Affects a large group, rapid onset of fever, lethargy, weakness, and cough

549
Q

What is diagnostic for a foal with uroperitoneum

A

Abdominal creatinine is twice as high as seam creatinine

550
Q

Intermittent lameness and bulging at the metacarpal region is specific for

A

Tendinitis or a bowed tendon

551
Q

Describe classical signs of equine metabolic syndrome

A

Severe obesity and clinical or subclinical laminitis

552
Q

What does it mean when a horse has require metabolic syndrome

A

They have a higher than normal insulin level in blood

553
Q

What does it mean when a horse has require metabolic syndrome

A

They have a higher than normal insulin level in blood

554
Q

What are common clinical signs of a horse presenting with colic

A

Flank watching, pawing, inappetence, rolling, stretching out, tucked abdomen

555
Q

What are non git causes for signs that present similar to colic

A

Liver disease or torsion, pancreatitis, ovarian pain, peritonitis, uterine pain

556
Q

What are non abdominal cavity reasons for a horse to present with signs similar to colic

A

Pleuropneumonia, neuro disease like equine motor neuron disease or tying up/ rhabdomyalosis

557
Q

What are non abdominal cavity reasons for a horse to present with signs similar to colic

A

Pleuropneumonia, neuro disease like equine motor neuron disease or tying up/ rhabdomyalosis

558
Q

What clinical signs would you expect to see in a foal presenting with colic

A

Disinterest in nursing, teeth grinding , tail flagging, straining to defecate, lying on side with front legs folded

559
Q

What clinical signs would you expect to see in a foal presenting with colic

A

Disinterest in nursing, teeth grinding , tail flagging, straining to defecate, lying on side with front legs folded

560
Q

What are differentials for a less severe colic (mild presentation/signs)

A

Gas colic, gastric ulcers, large colon impaction

561
Q

What clinical signs of colic indicate a less severe case of colic due to something like gas colic

A

Inappetence, flank watching, decreased manure production, lifting upper lip, lying down more than usual, pawing

562
Q

What clinical signs of colic indicate a less severe case of colic due to something like gas colic

A

Inappetence, flank watching, decreased manure production, lifting upper lip, lying down more than usual, pawing

563
Q

What are differentials for a more severe presenting colic

A

Small intestine strangulating lesion, large colon displacement or volvulus - need surgery!

564
Q

What clinical signs indicate a more severe case of colic

A

Kicking at abdomen, sweating, stretching, rolling or trying to roll, lying in lateral with legs tucked) throwing themselves down on the ground

565
Q

What clinical signs indicate a more severe case of colic

A

Kicking at abdomen, sweating, stretching, rolling or trying to roll, lying in lateral with legs tucked) throwing themselves down on the ground

566
Q

What risk factors predispose a horse to colic

A

More time in a stall, sudden alterations in diet or management, high levels ofconcentrated feed with low levels of forage 1 previous colic history or recent deworming

567
Q

What risk factors predispose a horse to colic

A

More time in a stall, sudden alterations in diet or management, high levels ofconcentrated feed with low levels of forage 1 previous colic history or recent deworming

568
Q

What is the epiploic foramen and what can predispose a horse to colic due to entrapment in this former

A

Hole between the liver and the pancreas - horses who wind suck or crib bite are predisposed to this

569
Q

What is the epiploic foramen and what can predispose a horse to colic due to entrapment in this former

A

Hole between the liver and the pancreas - horses who wind suck or crib bite are predisposed to this

570
Q

A more who recently foaled presents with colic signs - what is your top differential

A

Large colon Volvulus

571
Q

A more who recently foaled presents with colic signs - what is your top differential

A

Large colon Volvulus

572
Q

What are 4 types of colic

A

Strangulating, nonstrangulating, incomplete obstruction or complete obstruction

573
Q

Describe strangulating colic and what occurs

A

Either an external compression stops blood flow or there is a 360 torsion of blood vessels that causes revitalization of the gut, acute and extreme pain, systemic compromise and usually a complete obstruction

574
Q

Describe a nonstangulating colic

A

Intelluminal obstruction, inflammation, ulceration or displacement causing varying degrees of pain

575
Q

Describe a nonstangulating colic

A

Intelluminal obstruction, inflammation, ulceration or displacement causing varying degrees of pain

576
Q

Describe an incomplete obstruction causing colic

A

Ingesta, gas and intestinal secretions ion still pass through git but at a reduced rate, will see more mild intermittent colic signs, can progress to complete obstructin

577
Q

Describe a complete obstruction causing colic

A

Ingesta, gas, etc pool in front of the obstruction casing viscous distention and pain, then severe abdominal distraction causing respiratory distress and reduced cardiac return

578
Q

What are differentials for non strangulating colics

A

Gastric impaction or ulceration, equine gastric ulcer syndrome, ileal impaction, ascarid impaction, intossucception , right or left dorsal displacement , large colon impaction, enteroliths, gas colic, colitis

579
Q

What are differentials for non strangulating colics

A

Gastric impaction or ulceration, equine gastric ulcer syndrome, ileal impaction, ascarid impaction, intossucception , right or left dorsal displacement , large colon impaction, enteroliths, gas colic, colitis

580
Q

What are differentials for strangulating colics

A

Large colon volvulus, si lipoma, epiplpic foramen entrapment, diaphragmatic hernia

581
Q

What are the 4 main parts of a colic work up

A

Distance exam, physical exam , pass nasogastric tube , abdominal palpation per rectum - after this interpret bloodwork, ultrasounds, abdominocentesis

582
Q

What is colic face I what does it look like

A

Lesions above the TMJ or above the eyes, swollen eyelids - may see concurrent lesions on limbs and pelvis too

583
Q

What is colic face I what does it look like

A

Lesions above the TMJ or above the eyes, swollen eyelids - may see concurrent lesions on limbs and pelvis too

584
Q

What does colic face indicate if yo see it in a horse

A

Severe GI compromise /rupture

585
Q

Should you sedate a horse showing signs of severe colic and shock before fluid resuscitation

A

No- if in shock the sedation can cause the horse to decompensate - fluid therapy to stabilize first

586
Q

What sedation is mostly used for sedating colic patients and why

A

Xylazine - lasts 20 mins

587
Q

What sedation is mostly used for sedating colic patients and why

A

Xylazine - lasts 20 mins

588
Q

What can you give if xylzine is not enough to sedate your colicky horse and that does this mean

A

Demotomidire with or without butorphanol - means the pain/colic is severe enough to warrent surgery

589
Q

Describe how to pass a nasogastric tube

A

Measure from nare to eye, lube the tube then pass through the ventral meatus until half of what you measured, have handle bend head down as far as it will go to pass time to the esophageal sphincter where the nurse should swallow, then keep passing tube into stomach

590
Q

What are a few ways you can check to make sure you passed the nasogastric tube correctly

A

You can palpate the tube in the esophagus above the left jugular vein, aspiration on the tube I (is not a stand alone check) or shake the ventral neck of the horse and should hear tube rattle in the trachea

591
Q

What are a few ways you can check to make sure you passed the nasogastric tube correctly

A

You can palpate the tube in the esophagus above the left jugular vein, aspiration on the tube I (is not a stand alone check) or shake the ventral neck of the horse and should hear tube rattle in the trachea

592
Q

After passing a nasogastric tube - how do you get reflux out of it

A

Use a funnel and gravity flpw with 4-5 pumps of plain warm water to start a siphon - the funnel is to help prevent over filling of the stomach

593
Q

How is net reflux calculated - what volume is significant

A

Over 4 L is significant - total amount of water we put in deducted from total reflux that came out is the net reflex

594
Q

How is net reflux calculated - what volume is significant

A

Over 4 L is significant - total amount of water we put in deducted from total reflux that came out is the net reflex

595
Q

What can indicate post op ileus in a horse

A

A net reflex over 4L or over 2L per hour

596
Q

What can indicate post op ileus in a horse

A

A net reflex over 4L or over 2L per hour

597
Q

What can you do if a colicky horse is difficult to rectally palpate

A

Give lidocaine to reduce staining and provide analgesia or bucospam (antispasmolytic )

598
Q

What can you do if a colicky horse is difficult to rectally palpate

A

Give lidocaine to reduce staining and provide analgesia or bucospam (antispasmolytic )

599
Q

What can you palpate on rectal exam in a horse

A

Reprovtact, pelvic brim, caudal aorta, left kidney , nephrosplenic space, spleen, pelvic flexure , cecal base

600
Q

What point of care tests can help you determine dehydration and/or severity of colic

A

PCV and TS - PCV over 65% poor prognosis, low TP indicates protein loss due to git compromise

601
Q

What is a normal blood lactate? What value could support a diagnosis of severe colic

A

Lactate normally is less than 2 I might be 5-7 if severe colic with a poor prognosis

602
Q

What does endotoxemia mean in a horse

A

Endotoxins in the blood - with severe inflammation or infection high numbers of bacteria release a significant number of endotoxins into the bloodstream which then cause damage to surrounding tissue organs

603
Q

What blood count can indicate endotoxemia due to colic or rupture and why

A

Less than 3000 cells with or without a left shift - sudden infection en drop the body’s WBC count before body has line to increase WBC in response

604
Q

What acid base change would you expect with colic and why

A

Acidosis due to increased lactate

605
Q

What acid base change would you expect with colic and why

A

Acidosis due to increased lactate

606
Q

Describe how to perform an abdominocentesis in horses

A

Perform to the right of midline on the ventral abdomen, inject 2% lidocaine into abdominal wall , make a stab incision all the way through the external rectus sheath / insert cannula through gauze then the stab incision until a the drops flow out - collect clean sample!

607
Q

Describe the appearance of normal abdominal fluid

A

Straw colored, translucent red newspaper through it

608
Q

Describe the meaning of cloudy abdominal fluid

A

Suggests increase proteins or cells

609
Q

What does serosanguinous abdominal fluid suggest and what does it look like

A

Suggests devitalized small intestine or intestinal damage from strangulation - looks red but lighter than blood

610
Q

What does serosanguinous abdominal fluid suggest and what does it look like

A

Suggests devitalized small intestine or intestinal damage from strangulation - looks red but lighter than blood

611
Q

What does turbid abdominal fluid suggest

A

High WBC or peritonitis

612
Q

What does turbid abdominal fluid suggest

A

High WBC or peritonitis

613
Q

If abdominal fluif has feed material inside it or a fetid odor - what does that indicate

A

GI Rupture

614
Q

How long does it take bank mire to take effect

A

45 minutes

615
Q

How long does it take bank mire to take effect

A

45 minutes

616
Q

What is important to note about giving bucospan in horses

A

Antispasmodic that makes rectal exams much easier but will increase heart rate by 30 %

617
Q

What is important to note about giving bucospan in horses

A

Antispasmodic that makes rectal exams much easier but will increase heart rate by 30 %

618
Q

What should be your feeding plan when initially treating a colic

A

Remove hay for 6-12 hours, Refeed slowly (25 - 50-75- 100) then restart for 2 days

619
Q

What should be your feeding plan when initially treating a colic

A

Remove hay for 6-12 hours, Refeed slowly (25 - 50-75- 100) then restart for 2 days

620
Q

Define exostosis

A

Bone spur

621
Q

What are wind puffs

A

Digital flexor tendon sheath effusion

622
Q

What conditions ave exacerbated when circling with the injured limb on the inside of the circle

A

Navicular syndrome, osteoarthritis, subsolar bruises

623
Q

Which conditions are exacerbated when circling with the injured limb on the outside

A

Proximal suspensory ligament desmitis, suspensory branch desmitis , collateral ligament desmitis

624
Q

Which conditions are exacerbated when circling with the injured limb on the outside

A

Proximal suspensory ligament desmitis, suspensory branch desmitis , collateral ligament desmitis

625
Q

What signifies a successful perineural nerve block

A

Over 80% reduction in lameness in 5 minutes (max 10)

626
Q

What condition in horses is similar to ruminants

A

Hyperlipemia / hyperlipidemia in ponies and mini horses

627
Q

Describe hyperlipidemia in ponies/ mini horses

A

Primary disease leading to anorexia, then fat accumulation in plasma and liver

628
Q

What is the biggest difference between ketosis in ruminants and hyperlipemia in mini horses

A

Equids do not form ketones like ruminants so they accumulate triglycerides

629
Q

What is the biggest difference between ketosis in ruminants and hyperlipemia in mini horses

A

Equids do not form ketones like ruminants so they accumulate triglycerides

630
Q

What is the most common case of maxillary sinusitis in horses

A

Tooth root abscess - often first molars involved

631
Q

What is the most common case of maxillary sinusitis in horses

A

Tooth root abscess - often first molars involved

632
Q

What are top differentials for a foal with a dull mentation , decreased suckling and weakness /ataxia

A

Neonatal maladjustment syndrome (dummy foals), sepsis, hypoglycemia

633
Q

What are top differentials for a foal with a dull mentation , decreased suckling and weakness /ataxia

A

Neonatal maladjustment syndrome (dummy foals), sepsis, hypoglycemia

634
Q

How can you treat dummy foals

A

Supportive care, they will usually recur on their own in 3-5 days

635
Q

Premolar 1 is also called the

A

Wolf tooth

636
Q

Premolar 1 is also called the

A

Wolf tooth

637
Q

How is African horse sickness primarily transmitted

A

Culcoides flies mostly, could also be from mosquitos

638
Q

How is African horse sickness primarily transmitted

A

Culcoides flies mostly, could also be from mosquitos

639
Q

What clinical signs can you see with African horse sickness

A

Pulmonary form - acute respiratory distress, coughing, sweating, foaming at the nostrils
Cardiac form - edema of head and face ( particularly the supraorbital fossa), abdominal pain, depression

640
Q

Which form of African horse sickness is usually fatal

A

Pulmonary form

641
Q

Which form of African horse sickness is usually fatal

A

Pulmonary form

642
Q

How is strongyloides westi transmitted - how can you prevent it

A

Through moms milk to foal - treat post partum mares with ivermectin

643
Q

Where are strongyloide westi worms found and what do they cause

A

Found in small intestine, cause diarrhea in foals

644
Q

Where are strongyloide westi worms found and what do they cause

A

Found in small intestine, cause diarrhea in foals

645
Q

What is Sweeney

A

Suprascapular nerve paralysis - causing muscle atrophy of Supra and infraspinatous muscles caring shoulder lateral luxation

646
Q

What would you expect to see in a cow with pyelonephritis

A

Arched back, tail swishing, large and painful kidneys on rectal exam, cloudy and bloody urine

647
Q

What organisms can cause septicemia in foals

A

E. Coli , pasteurella, actinobacillus

648
Q

What organisms can cause septicemia in foals

A

E. Coli , pasteurella, actinobacillus

649
Q

Where does the low 4 point block provide analgesia too

A

Methcarpophalongeal(fetlock joint and lower

650
Q

Where does the low 4 point block provide analgesia too

A

Methcarpophalongeal(fetlock joint and lower

651
Q

What is me causal agent of summer sores and how does it cause disease

A

Habronema - stomach worm larvae deposited in feces where maggot flies eat them then deposit at susceptible areas on skin (moist areas, mucus membranes , damaged skin) causing eosinophilic granulomas

652
Q

What is me causal agent of summer sores and how does it cause disease

A

Habronema - stomach worm larvae deposited in feces where maggot flies eat them then deposit at susceptible areas on skin (moist areas, mucus membranes , damaged skin) causing eosinophilic granulomas

653
Q

Acute death with thrombosis of the cranial mesenteric artery leads you to suspect

A

Strongylus vulgaris

654
Q

Acute death with thrombosis of the cranial mesenteric artery leads you to suspect

A

Strongylus vulgaris

655
Q

What is the causative agent of Potomac horse fever

A

Neoricketssia risticii

656
Q

What is the causative agent of Potomac horse fever

A

Neoricketssia risticii

657
Q

What is the causative agent of rain scald

A

Dermatophilus Congolesis - bacterial

658
Q

What is the causative agent of rain scald

A

Dermatophilus Congolesis - bacterial

659
Q

Where will you see chorioptes equi lesions in horses what does it look like

A

Mites often in feathered hair around the fetlock - causes a pruritic dermatitis leading to formation of papules, crusts thickened skin and alopecia

660
Q

How do you treat chorioptes equi

A

Ivermectin (like with other mites)

661
Q

How do you treat chorioptes equi

A

Ivermectin (like with other mites)

662
Q

What structures cross the guttural pouches

A

Internal carotid, sympathetic trunk and cranial nerves 7,9,10, 11 and 12

663
Q

When and with what breeds are you likely to see cerebellar abiotrophy

A

Arabians 1-6 months old

664
Q

What is your top differential in a colicky horse that produces a large volume of net reflux and looks to be recovered after gastric decompression

A

Proximal enteritis or duodenitis/ proximal jejunitis

665
Q

What is your top differential in a colicky horse that produces a large volume of net reflux and looks to be recovered after gastric decompression

A

Proximal enteritis or duodenitis/ proximal jejunitis

666
Q

What are normal synovial fluid values

A

Total protein - less than 2.5
TNCC - less than 500
Over 90% monocular cells on cytology

667
Q

What are normal synovial fluid values

A

Total protein - less than 2.5
TNCC - less than 500
Over 90% monocular cells on cytology

668
Q

What clinical sign of Cushings can you see in horses that you wouldn’t see in dogs

A

Hirsutism - an abnormally long wavy hair coat

669
Q

Describe cushings in horses

A

Pituitary pars intermedia dysfunction - distinction of pituitary leads to excess ACTH, then excess cortisol production

670
Q

Describe cushings in horses

A

Pituitary pars intermedia dysfunction - distinction of pituitary leads to excess ACTH, then excess cortisol production

671
Q

What is the causative agent of contagious equine metritis - what do you do if you suspect it

A

Taylorella equigenitalis - I’m because it is supposed to be indicated in the US

672
Q

What is the causative agent of contagious equine metritis - what do you do if you suspect it

A

Taylorella equigenitalis - I’m because it is supposed to be indicated in the US

673
Q

Red maple leaf toxicity causes - in mares

A

Heinz body anemia

674
Q

What is thorough pin

A

Effusion of the tarsal sheath - sheath of deep digital flexor tendon

675
Q

Describe a parascavis equorum egg

A

Spherical, dark brown, single zygote in the middle

676
Q

Describe a parascavis equorum egg

A

Spherical, dark brown, single zygote in the middle

677
Q

What is swelling of the tibiotarsal joint called

A

Bog spavin

678
Q

What is swelling of the tibiotarsal joint called

A

Bog spavin

679
Q

How do you treat bog spavin

A

You don’t if it isn’t causing any clinical abnormality - swelling will usually reoccur anyways if you drain it

680
Q

How do you treat bog spavin

A

You don’t if it isn’t causing any clinical abnormality - swelling will usually reoccur anyways if you drain it

681
Q

What is the most common cause of genital infections in horses

A

Pneumovagina - causing vaginitis and endometritis

682
Q

What is the most common cause of genital infections in horses

A

Pneumovagina - causing vaginitis and endometritis

683
Q

What is the Achilles tendon in the horse

A

Common calcaneon tendon with the gastrocnemius tendon, biceps femoris tendon, and semi tendininosus muscle

684
Q

What is the Achilles tendon in the horse

A

Common calcaneon tendon with the gastrocnemius tendon, biceps femoris tendon, and semi tendininosus muscle

685
Q

What is pathopneumonic for myotonia in the horse

A

Dive bomber sounds on ECG - repitini firing after contraction of muscles

686
Q

In what breeds do you see HYPP

A

Quarter horses, paints and Appaloosas

687
Q

In what breeds do you see HYPP

A

Quarter horses, paints and Appaloosas

688
Q

A stallion presents with a unilaterally enlarged testicle that palpates firm - what is your top differential

A

Seminoma

689
Q

A stallion presents with a unilaterally enlarged testicle that palpates firm - what is your top differential

A

Seminoma

690
Q

Describe the life cycle of gastrrophilus in horses (the horse bot fly)

A

Eggs deposited early summer on body (cannon bone, abdomen. , shoulders), horse licks and ingests them somehow and larvae have hooks where they attach in the git, ten are passed in feces a months later and burner in the soil

691
Q

Describe the life cycle of gastrrophilus in horses (the horse bot fly)

A

Eggs deposited early summer on body (cannon bone, abdomen. , shoulders), horse licks and ingests them somehow and larvae have hooks where they attach in the git, ten are passed in feces a months later and burner in the soil

692
Q

Do you treat the horse bot fly - if so what do you se

A

You don’t have to because they may not cause clinical disease - but they can cause stomatitis, colic, stress so should anywhere with Ivermectin

693
Q

Do you treat the horse bot fly - if so what do you se

A

You don’t have to because they may not cause clinical disease - but they can cause stomatitis, colic, stress so should anywhere with Ivermectin

694
Q

What is imidocarb used for in horses

A

Treating babesiosis

695
Q

What is imidocarb used for in horses

A

Treating babesiosis

696
Q

What is combined immunodeficiency and who is usually affected

A

Arabian foals mostly - heritable immunodeficiency of b and T lymphocytes

697
Q

How do Arabian foals with combined immunodeficiency often present

A

A foal whose maternal antibodies are starting to wane presents a repeated infections or bouts of pneumonia that are responsive to antibiotics but reoccur when stopped

698
Q

Lymphosarcomas commonly occur where in the horse

A

Intestines

699
Q

Lymphosarcomas commonly occur where in the horse

A

Intestines

700
Q

The most common neoplasia of the equine stomach is

A

SCC

701
Q

The most common neoplasia of the equine stomach is

A

SCC

702
Q

What clinical condition occurs with scratches

A

Chronic seborrhic dermatitis on the palmar or plantar aspect of the pastern

703
Q

What clinical condition occurs with scratches

A

Chronic seborrhic dermatitis on the palmar or plantar aspect of the pastern

704
Q

What is the risk of giving tetanus antitoxin if not needed

A

Theilers disease

705
Q

What is the risk of giving tetanus antitoxin if not needed

A

Theilers disease

706
Q

What is the causative agent of tyzzers disease

A

Closhidium piliforme

707
Q

Describe the pathogenesis of tyzzers disease

A

Neonatal foals ingests mares manure leading to intestinal overgrowth of clostridium piliforne, casing acts hepatic necrosis with septicemia resulting in acute coma and death, nearly 100% fatal

708
Q

How do you diagnose tyzzers disease in neonate foals

A

Fecal PCR

709
Q

Define physitis

A

Swelling around growth plates in long bones

710
Q

Pergolide is a- used to -

A

Dopamine agonist used to suppress pituitary hormone secretion (ppid in horses)

711
Q

What are the 3 A’s of EPM

A

Asymmetry, ataxia, atrophy

712
Q

What clinical signs are you likely to see with rescue toxicity in pregnant mares

A

Increased thickness of placenta keeping foals from breaking out on their own, stillbirths, agalactia

713
Q

What clinical signs are you likely to see with rescue toxicity in pregnant mares

A

Increased thickness of placenta keeping foals from breaking out on their own, stillbirths, agalactia

714
Q

Why do you more commonly see ulceration on the squamous cell region of the equine stomach compared to the glandular region

A

Glandular region secretes mucus to protect itself

715
Q

Why do you more commonly see ulceration on the squamous cell region of the equine stomach compared to the glandular region

A

Glandular region secretes mucus to protect itself

716
Q

What is a good way to tell the difference between listeriosis infection and polioencephalomalacia

A

Polio does not cause cranial nerve deficits - listeriosis does due to microabscesses on cranial nerve roots

717
Q

What is a good way to tell the difference between listeriosis infection and polioencephalomalacia

A

Polio does not cause cranial nerve deficits - listeriosis does due to microabscesses on cranial nerve roots

718
Q

Surcocustis neurons is a causative agent of

A

EPM

719
Q

Surcocustis neurons is a causative agent of

A

EPM

720
Q

When are horses resistant to infection with Rhodococcus unless immunocompromised

A

By 6 months - maternal antibodies are protective until 2 months so unlikely to see it then

721
Q

When are horses resistant to infection with Rhodococcus unless immunocompromised

A

By 6 months - maternal antibodies are protective until 2 months so unlikely to see it then

722
Q

A leaning forward stance is indicative of what in horses

A

Navicular disease

723
Q

What is a common sequela to anterior enteritis

A

Laminitis

724
Q

What is a common sequela to anterior enteritis

A

Laminitis

725
Q

What is a common sequela to anterior enteritis

A

Laminitis

726
Q

Pupusa hemorrhagica is a _ resulting from -

A

Vasculitis resulting from type 3 immune hypersensitivity after a strep equi infection

727
Q

Pupusa hemorrhagica is a _ resulting from -

A

Vasculitis resulting from type 3 immune hypersensitivity after a strep equi infection

728
Q

How do you diagnose EDM

A

Only confirm on necropsy by seeing diffuse degeneration of white matter - low serum vitamin E levels with clinical signs are suggestive

729
Q

How do you diagnose EDM

A

Only confirm on necropsy by seeing diffuse degeneration of white matter - low serum vitamin E levels with clinical signs are suggestive

730
Q

What is immunodiffusion

A

Coggins test

731
Q

What is immunodiffusion

A

Coggins test

732
Q

How is equine infectious anemia spread

A

Blood sucking flies

733
Q

How is equine infectious anemia spread

A

Blood sucking flies

734
Q

What is the causative agent of sweet itch

A

Type I hypersensitivity to culicoides

735
Q

What is the causative agent of sweet itch

A

Type I hypersensitivity to culicoides

736
Q

What is Sweeney

A

Shoulder atrophy due to suprascapular nerve injury

737
Q

What are clinical signs of gutteral pouch mycosis

A

Unilateral or bilateral mucous nasal discharge, intermittent epistaxis, facial paralysis, horners syndrome

738
Q

Describe clinical signs of hebroneimiasis in horses and why they occur

A

Larvae of habronemia stomach worms cause a hypersensitivity reaction leading to non healing reddish brown lesions on legs, velum, prepuce or face

739
Q

How do you treat habronemiasis lesions

A

Ivermectin, corticosteroids, wound cleaning and fly management

740
Q

What is the causative agent of Potomac horse fever

A

Neorickettsial risticci

741
Q

What is the causative agent of Potomac horse fever

A

Neorickettsial risticci

742
Q

What type of parasite is anoplocephala perfoliata

A

Require tapeworm associated with colic

743
Q

What type of parasite is anoplocephala perfoliata

A

Require tapeworm associated with colic

744
Q

What clinical affect does anoplocephala perfioliata have in horses

A

High numbers can lead to mechanical obstruction , mucosal damage, necrotic ulcers leading to intestinal hyper peristalsis and illoceal interceptions

745
Q

What is a common sequela of strep equip infection or vaccination

A

Pupura hemorrhagica

746
Q

What is a common sequela of strep equip infection or vaccination

A

Pupura hemorrhagica

747
Q

Pupura hemorrhagica results from

A

Type 3 hypersensitivity

748
Q

What is a keratoma

A

Mass on the inside hoof wall

749
Q

What is a keratoma

A

Mass on the inside hoof wall

750
Q

What does club foot look like

A

Contracture of distal interphalageal joint leading to a shortened toe and steep hoof wall

751
Q

What does club foot look like

A

Contracture of distal interphalageal joint leading to a shortened toe and steep hoof wall

752
Q

Phenoxybenzamine is a - that can be used to treat- , why

A

Alpha adrenergic antagonist - promotes vasodilation and blood flow to digits to treat laminitis

753
Q

How do you treat bone spavin (OA of distal intertarsal joint)

A

Joint arthrodesis - Bally progresses and will do this naturally if you don’t do it

754
Q

What is ringbone

A

Osteoarthritis of phalanges

755
Q

Melting ulcers in horses indicate - and are usually caused by

A

Infection in the stroma, usually caused by pseudomonas

756
Q

Melting ulcers in horses indicate - and are usually caused by

A

Infection in the stroma, usually caused by pseudomonas

757
Q

A horse with muscle fascinations that is ataxic makes you think of

A

West Nile virus

758
Q

A horse with muscle fascinations that is ataxic makes you think of

A

West Nile virus

759
Q

How do you diagnose WNV

A

Serum igm elisa-can tell active infection even if the horse has been vaccinated

760
Q

Estrus in a mare lasts

A

2-10 days, average of 6

761
Q

How do you treat pupura hemorrhagic

A

High dose of dexmetmasone with penicillin to kill off remaining strep equi

762
Q

You see a mini horse colicking - what is your top differential

A

Small colon impaction

763
Q

The cranial 2/3 of horse esophagus is - muscle , with the last third being - muscle

A

Cranial - striated muscle
Caudal - smooth muscle

764
Q

How does clostridium piliforme affect nursing foals

A

Tyzzers disease - cross the permeable immature gut causing acute hepatic necrosis and septicemia

765
Q

Colic signs with parascaris equorum eggs indicate what

A

Intestinal impaction

766
Q

Pruritic dermatitis lesions around the fetlock and foot, particularly in draft horses, lead you to suspect -

A

Choriopties equi (equine mange)