Quick Review Flashcards

Question

What is the cause of most fractures of the CT ? what happens to these fractures.

Answer 1

Most CT fractures occur in the absence of known trauma. these usually affect the maxillary CT and the most common pattern is a lateral slab fracture through the two lateral pulp cavities. the fracture space becomes filled with food, thus laterally displacing the smaller portion which may cause buccal lacerations. removal of the smaller loose fragments with forceps will usually resolve the problem in the short term but infection of the apex will later occur in a minority of CT.

Answer 2

Due to advanced infundibular caries. Deep seated infections of the alveolus and sinus frequently accompany these fractures in younger horses. complete extraction of the affected tooth and sinus lavage are required if sinusitis is present.

Answer 3

Non calcified epithelial tumours derived from the epithelium that forms enamel.

Answer 4

Haematogenous or lymphatic borne infections. (inflammation of pulp due to dental impaction may predispose). In upper CT - may be due to food accumulation and fermentation in cemental defects in the infundibulum (caries) leading to infection of the pulp or saggital fractures. Periapical abscessation of the lower CT commonly involves rostral ct in 1-2 years of eruption and may occur when there are eruption cysts in the early stages, infection usually remains confined to the apex, adjacent to the sinus tract and all the pulp cavities remain vital - antibiotics may suffice.

Answer 5

In young horses - cannot drain into oral cavity, but will affect supporting bones and drain from the apical aspect of the tooth. mandibular infections accompanied by unilateral mandibular swellings and external draining tracts. Infections of upper 6s and 7s will often develop focal swellings of the rostral maxilla. Infections of the caudal 4 maxillary CT generally results in a secondary sinusitis with the presence of a chronic malodorous unilateral nasal discharge. Apical infections that arise as an extension of deep periodontal disease from abnormal spaces surrounding the CT including supernumerary teeth, diastemata, developmental and acquired dental displacemets - will drai into the mouth.

Answer 6

Intra oral examination with mouth gag Radiographic evaluation of the dental apices (latero oblique projections) Scintigraphy or CT may provide conclusive evidence of apical infection If external sinus tract - obtain radiographs with a metallic probe in situ to define the infected area of the tooth. This procedure will also provide surgical landmarks, if the infected tooth is to be extracted by repulsion.

Answer 7

If a CT is infected. antibiotic therapy, maxillary sinus lavage - failure to respond to these - further clinical exam and definitive evidence of dental infection - then extraction.

Answer 8

Repulsion - high level of damage to alveolar and supporting bones. Lateral buccotomy technique - incision through skin and subcut tissues into alveolus under GA. Oral extraction Endodontics - treat CT infections by root canal therapy.

Answer 9

oral pain by quidding - dysmastication rather than inability to swallow. Fractures of mandible or premaxillary fractures. Disorders of the tongue due to paralysis of the 12th cranial nerve, or generalised neuro disorders such as botulism. Sharp wooden or metallic foreign bodies lodging in the tongue or oropharynx. Tumours of the oral cavity such as SCC.

Answer 10

``` Congenital neonatal neuromuscular pharyngeal dysfunction cleft palate guttoral pouch mycosis strangles infection botulism heavy metal poisoning nasopharyngeal foreign bodies nasopharyngeal tumours Guttoral pouch disease. ```

Answer 11

Masticated food flowing down both nasal cavities after eating and coughing due to aspiration of food material and saliva.

Answer 12

Aspergillus fumigatus. It can invade roof of the guttural pouch causing destructive changes and secondary bacterial infection.

Answer 13

``` depends on which erve affected; Cranial sympathetic - horners syndrome 7th - facial paralysis 9th -, 10th, 11th - pharyngeal paralysis 12th - toongue paralysis Internal carotid, internal maxillary artery, vein, external maxillary artery - Massive haemorrhage. (baloon or embolising coil needed). ```

Answer 14

Local anti mycotic treatment with Natamycin or enilconazole sprayed onto the roof of the pouch using self retaining or trans endoscopic catheters 2-3 times daily.

Answer 15

A sequel to strangles, with abscessation and drainage of the Retropharyngeal lymph nodes into the guttoral pouches, which have poor natural drainage. extensive swellings of the guttoral pouches can interfere with upper airway or swallowing, occasionally leading to stridor or dysphagia. chondroid formation occurs with more chronic cases. Chronic low grade purulent discharge - usually unilateral.

Answer 16

Endoscopically - collapse of the nasopharyngeal roof may be seen along with a purulent exudate draining from the affected pouches 7 pus, or chodroids. feed from the ground. lavage of pouches with dilute antiseptics. transendoscopic removal of chondroids or surgical drainage. using ventral approach.

Answer 17

A neuromuscular defect or abnormal tissue fold at the nasopharyngeal ostium acts as a one way valve allowing air into but not out of guttoral pouches.

Answer 18

Radiography will show an enlarged air filled pouch and a ventral fluid line. A Foley catheter can be placed and distort the ostium into open position - or transendoscopic laser treatment. good prognosis.

Answer 19

Endoscopy will confirm the presence of pharyngeal dysphagia without any detectable underlying lesion. closer examination may also reveal weakness of the hindlimbs and a flaccid tail.

Answer 20

Distress, salivation, dysphagia, nasal discharge containing a food.

Answer 21

Sugar beet pulp or pelleted food. obstructs a variable distance of oesophageal lumen - large amounts of sugar bet pulp or dry unsoaked sugar beet pulp. Dehydratin, hypochloraemia will occur.

Answer 22

Unable to pass nasogastric tube, confirm endoscopically and by ultrasound and palpation.

Answer 23

Take off all bedding & starve. most cases will get better spontaneously or respond to treatment with spasmolytics and sedatives. conservative treatment is safe for up to 24 hours. if not cleared by then - iv corretion of hydration and gentle lavage f oesophagus by stomach tube in sedated horse with head lowered. Penicillin/metronidazole should be administered to help prevent aspiration pneumonia as som degree of aspiration is inevitable.

Answer 24

Congenital in foals up to 4 months or acquired secondary to gastroduodenal ulceration > fibrosis > stricture. contrast radiographs show delayed outflow. treatment - pyloromyotomy or bypass pylorus with gastrojejunostomy.

Answer 25

``` stomach - no uodenum - attached to right body wall - no Jejunum - long mesojeunum - YES Ileum - no Ileocaecal junction - no ```

Answer 26

Certain diets eg Bermuda grass hay or with severe ascarid infestation in young horses possibly related to tapeworm. treatment is decompression. good prognosis.

Answer 27

Lymphosarcoma. Thickening of intestinal wall > complete/partial obstruction. weight loss. Resect affected portion. Often multifocal. poor prognosis.

Answer 28

Most common cause. mature/obese animals. lipoma often suspended n a single fibrous band attached to the mesentery > encircles a bowel segment > strangulates intestinal vasculature.

Answer 29

Rotation of all/some of the jejunum about its attachment in the doorsal abdomen at the cranial mesenteric arterial root. often severe pain and poor prognosis due to amount of gut affected. may be secondary to other lesions causing distension.

Answer 30

Invagination of proximal intussusceptum into distal intussucipiens > simple obstruction initially then strangulating as more gut entrapped and arterial supply is drawn in. May involve any segment of bowel but jejuno-jejunal intussusceptions more common in foals. Ileo caecal associated with tapeworm infestation.

Answer 31

Mesenteric vascular thrombi - result of the migration of strongylus vulgaris larvae > vascular infarction of a segment of SI which can be extensive. these lesions - formerly the most common cause of SI colics have become rarer since the widespread use of avermectins.

Answer 32

Epiploic foramen - caudal vena cava, caudate liver lobe, pancreas, hepatic portal vein. Gut entrapped cranial to liver > may be no abnormal rectal findings. Inguinal /scrotal - swollen inguinal region. Palpate per rectum. Herniation through a mesenteric rent - broodmare after parturition. Gastrosplenic ligament - rare Umbilical hernia Diaphragmatic hernia - congenital or major trauma

Answer 33

only apex and part of body exteriorisable at laparotomy.

Answer 34

primary impaction or secondary to motility disorer, common in hospitalised patients .g after GA or repeated sedation. Surgery needed if no response to medical treatment because caecum is prone to spontaneously rupture. Surgery - evacuation & caecal bypass because condition often recurs.

Answer 35

Caecum > RVC> LVC > LDC > RDC > Transverse colon > small colon. Left colons - highly mobile, displacements and torsions occur commonly

Answer 36

colon becomes entrapped between dorsal aspect of spleen and nephro splenic ligament adjacent to the left kidney. total or partial obstruction and variable pain. surgery to reduce displacement - prognosis generally good.

Answer 37

The left colons migrate around the body of the caecum (clockwise or anticlockwise). if no volvulus - good (70-80%).

Answer 38

Often around caeco colic junction > whole colon involved. can be 180 degrees to 360 degrees (strnagulating). Rapid deterioration due to massive endotoxaemia. - surgical correction and colonic resection needed. guarded prognosis.

Answer 39

Mineralised enteroliths tend to obstruct narrow transverse colon. Treatment - surgical removal of the enteroliths via an enterotomy carries a good prognosis.

Answer 40

graded 1-4. grades 3&4 - guarded prognosis because the mesorectum tears. If mild - clean and resect affected mucosa & replace, provided the seromuscular layer is intact. Prolapse >25-30cm - probable mesocolon rupture > more aggressive surgery needed - refer.

Answer 41

Usually occur during rectal palpation. graded 1 - depending on depth. grade one - mucosa only, grade 2- muscularis only, grade 3- mucosa and muscularis and grade 4- all layers. grade 4 results in abdominal contamination with faeces.

Answer 42

Sedate, give epidural or larve volume of local anaesthetic per rectum,c areful evacuation and packing of the rectum to prevent further contamination, broad spectrum antibiotics non steroidal anti inflammatories then referral/surgery in the cases of severe lesions. grade 3 &4 carry guarded prognosis.

Answer 43

Repeat episodes of colic - especially in first year post surgery. Continuing endotoxaemia/dehydration. Ileus - (20% prevalence) may result from inflammation (peritonitis, handling at sugery, systemic effects of endotoxaemia), distension, or denervation (grass sickness). Ileus causes further distension and pain & dehydration if SI or impaction if LI affected. diagnosis - rectal or abdominal ultrasound > distended SI loops with little movement, nasogastric intubation > reflux. Incisional drainage/infections/hernations.(10-40% prevalence). Prediposes horses to incisional herniation at a later date. Adhesions - usually weeks after surgery - fibrinous then fibrous adhesions may cause intestinal obstruction, strangulation etc and recurrence of colic. prevention is by careful tissue handling, use of anti adhesion therapy eg heparin, peritoneal lavage, carboxymethylcellulose.

Answer 44

Careful examinatio for scrotal herniatioon. if present - closed castration must be performed. Horses sometimes castrated standing using IV sedation and analgesia along with local anaesthesia of the scrotum and cord. sometimes lcal anaesthetic is also injected directly into the testes. The anaesthetised scrotal area is thoroughly prepared using a disinfectant solution an a long deep midline cranio caudal incision is made over each anaesthetised testis through ventral skin, subcutaneous scrotal tissues and then through the external tunic, thus allowing extrusion of the testes directly to the outside. sectioning the avascular caudal ligament will help exteriorise the testes. The spermatic cord is simultaneously transected and crushed using an emasculator which should be kept in place for 2-4 minutes. absorbable ligatures can be placed on the spermatic cord but the surgical site is not sterile.

Answer 45

Increase risk of haemorrhage, eventration and infection are present.

Answer 46

Incision only through skin and subcutaneous tissue but not through external vaginal tunic must be performed if inguinal herniation is suspected. closed technique prevents post operative gut prolapse /herniiation. Transfixing ligatures very effective at achieving haemostasis and thus the other major post operative complication (haermorrage) rarely occurs with closed. Older animals have larger testicular vasculature so should be castrated using ligatures under GA. More thorough preparation of the surgical site is possible and post operative infections are also less common. Can be performed through a single or two separate scrotal incisors. having incised the skin and dartos care is taken not to incise the shiny white external tunic, which is dissected from the surrounding fascia along the spermatic cord. Transfixing ligatures are inserted into the cord which is then emasculated a further 2cm distal to the ligature.

Answer 47

Usual to have blood dripping from the scrotal wound foor up to 30 mi but should be in countable drops rather than a steady drip stream or spurt - the latter may indicate testicular artery has not been properly crushed or ligated. Pack with sterile gauze and observe if this reduces haemorrhage. if it does - this may just indicate that connective tissue seepage or subcut vasculature bleeding was the cause of the haemorrhage. If not - this indicates continuing haemorrhage from the testicular artery. Crush artery with forceps, if still not stopped bleeding - must give GA and explore. MUST BE GIVEN TETANUS ANTIITOXIN IF NOT VACCINATED. Some degree of post operative woound infection is common. If severe, affected horses will be febrile, have a swollen scrotum and prepuce and be stiff in their hindquarters. scrotal woounds should be large enough to allw clots to drain out. Low grade strep zooepidemicus infections will drain and normally resolve within a week. Prophylatic antibiotics are given by some. less common infection that may occur is about a week later with strep zoooepidemicus - development of infected granulation tissue protruding from the wound. - Needs digitally or gentle curettage by irrigation and penicillin administered. infection of the spermatic cord is funiculitis and grossly infected cord may need to be resected. A more long term spermatic cord infection is termed scirrhous cord which can rarely occcur often due to a staphylococcus infection. this will present may months later as a very firm scrotal swelling with purulent draining tracts, sometimes temporarily appearing and disappearig, especially following antibiotic treatment. Horses will invariably develop post operational oedema of the scrotum, prepuce. Hand walking or slow riding exercise, two or three times a day will help reduce such swellings and stiffness. Especially in stalions and older hoses post operative NSAIDS are indicated. Evisceration is poossible after an open castration. Most frequently just the omentum. If evisceration occurs after you have left te premises the owners hsould e tolt to protect and elevate the gut in a clean sheet - one should then replace the prolapsed guts into scrotum and suture the scrotum. the horse should then immediately be referred to an appropriate referral centre.

Answer 48

Ultrasnography of the inguinal anal can determine if a retained testis is in the canal or abdmen. surgery on a cryptorchid must be performed under GA r by standing lapaorscopy. If horses over 3yo a resting plasma oestrone sulphate assay may be performed, if younger horse <3yo two blood samples are required one prior to and one after HCJ injection. a significant rise in testosterone indicates the presence of a functional testes in the animal.

Answer 49

Injection of tincture of iodine into or cautery of the lumen of the urachus with silver nitrate can be used to treat cases that persist beyond a week. Ligation may lead to abscessation and should be aovoided. A persistent patent urachus may lead to omphalophlebitis, purulent umbilical discharge, Abscessation of the urachus and cystitis and should be investigated by ultrasound and treated surgically.

Answer 50

Calcium carbonate calculi - have a sharp spiculated surface. Can become very large >1kg and mechanically irritate the bladder.

Answer 51

Frequent urination, haematuria, tail swishing, colic and straining. Occasionally smaller calculi will exit the bladder and can fully obstruct the urethra. Rectal exam will confirm. Passage of endoscope or urinary catheter. Palpation of peis and ultrasound. Remove via midline laparotomy. Urethral calculi - administration of spasmolytics/analgesics.

Answer 52

An epidermoid cyst can develop in the false nostril lining, resulting in facial swelling int he area of the naso maxillary notch. These do not cause nasal airflow obstruction. Treatment is cosmetic.

Answer 53

Flesh alar fold attached between the ventral concha and false nostril and occasionally can collapse during fast work and cause airflow obstruction and noise. diagnosis can be confirmed by suturing the alar folds too the nostrils bilaterally and assess if this stops noise.

Answer 54

Exercise induced pulmonary haemorrhage. | May also be due to haemorrhage from trauma, guttoral pouch mycosis or ethmoid haematoma.

Answer 55

Intubation or endoscope - passed into middle meatus - turbinates or ethmoturbinates traumatised. Or from ventral meatus if a wide tube is used or inadequate lubriaction. May occur due to a tear of rectus capitis muscles. (trauma to the head region after a heavy fall)

Answer 56

adencarcniomas, osteogenic sarcomas. usually very malignant, older animals. Local inflammation and secondary infection occur. Chronic unilateral purulent nasal discharge, malodorous breath, secondary sinus empyema, unilateral submandibular lymph node enlargement, nasal airflow obstuction, facial swelling, halitosis.

Answer 57

Aspergillus fumigatus or pseudallescheria boydii.

Answer 58

Unilateral malodorous mucopurulent nasal discharge and unilateral lymphadenitis, occasionally epitaxis. Mouldy cheese like white yellow or black coloured plaques on the turbinates or ethmoturbinates on endoscopy.

Answer 59

remove any large fungal plaques prior to topical therapy with natamycin or enilconazole solutions. treatment is usually successful. Confirmation can be made ia nasal swabs with isolation of a heavy pure growth of potentially pathogenic fungus.

Answer 60

Infection of the first 2-3 maxillary cheek teeth usually results in a swelling with a discharging sinus tract n the affected side of the face, rostro dorsal to the facial crest. A small percentage will hwoever, discharge medially into the nasal caviyt, leading t a unilateral purulent malodorous nasal discharge. endoscopy may reveal a purulent granuloma or pus in the rostro lateral aspect of the middle meatus.

Answer 61

An ethmoid haematoma is a haemorrhagic polyp with the histological appearance of a haematoma. these lesions which usually occur in adult horses generally protrude rostrally into the nasal cavity frm the ethmoturbinates, less commonly they grow laterally or dorsally into the sinuses. they bleed in small amounts over very long periods. mucopurulent as well as hemorrhagic nasal discharge may occur. most common cause of chronic unilateral epistaxis in the horse.

Answer 62

Repeated transendoscopic intra lesional formalin injections - surgical excision is traumatic with a less favourable long term prognosis.

Answer 63

``` 1 - primary infective sinusitis 2 - dental apical infection or oro fistula 3 maxillary sinus cyts 4 - sinus neoplasia 5 - mycotic sinusitis 6 - sinus trauma 7 - intra sinus PEH lesions ```

Answer 64

Unilateral purulent nasal discharge, unilateral submandibular lymph node enlargement, possibly unilateral facial swelling, nasal airflow obstruction or epiphora, endoscopy will show discharge emanating from the naso maxillary aperture. direct endoscopy of the paranasal sinuses is possible through a small external sinus opening made under Local anaesthesia usually into the frontal sinus.

Answer 65

The sinuses have poor natural drainage - mucosal inflammation with URT infections and simultaneous increased mucus production and decililation of the sinus epithelial cells results in less effective drainage. if secondary bacteiral infection occurs > sinus empyema. This can occur transiently with URT infections or due to inspissation of pus it may become chronic.

Answer 66

antibiotics sinus lavage via frontal sinus trephine Indwelling tubing with lukewarm dilute iodine or saline for 5-6 days. Transendoscopic or surgical removal under standing sedation.

Answer 67

Caused by infection of the apices of the upper 8s and 11s that lie within the maxillary sinuses. A copious and malodorous nasal discharge is often present and halitosis if infection involves the crown. Lateroblique radiographs of most value. CT optimal diagnostic. Extraction indicated.

Answer 68

these mucoid filled cysts develop int he maxillary and occasionally i the frontal sinuses. they can occur in all age groups including foals, very marked facial swelling and epiphora is a feature. cofirm by radiography. homogenous rounded radiodense cysts sometimes visible. surgically remove.

Answer 69

Multiple large lymphoid follicles in the naspharynx. very common in young horse. regresses with maturity. normal adult horses have small follicles. not a cause of poor performance. Enlarge with respiratory infection.

Answer 70

The free margin of the soft palate should normally be positioned tightly underneath the base of the eipglottis. if the soft palate displaces dorsally to the epiglottis, this will cause airflow obstruction with the production of loud abnormal gurgling expiratory and inspiratory noises & PP.

Answer 71

Dynamic overground or high speed treadmill endoscopy. Displacing palate transiently during resting endoscopy is not a good indicator that DDSP occurs at exercise. some DDSP affected horses show ulceration of caudal border of soft palate.

Answer 72

Primary dysfunction of intrinsic palate muscles - thermal cautery of palatal tissue. Dysfunction of thyro hyoid muscle - tie forward surgery Excessive caudal retraction of the larynx - Myectomy of strap muscles, sternothyroid tenectomy at insertion in thyroid cartilage. Associated with damage to pharyngeal branch of vagus nerve - rest, treat concurrent inflammation Non specific sign of hypoxaemia or exhaustion towards the end of strenuous work - rest, improve fitness.

Answer 73

very rare compared to intermittent. often secondary to other diseases e.g epiglottic entrapment or sub epiglottic cysts. Others are due to congenital or acquired neuromuscular dysfunction of the soft palate or epiglottic muscles. Affected horses make loud and continuous gurgling noises at rest or at low level of exercise and may be mildly dysphagic.

Answer 74

the rostral free aspect of the epiglottis becomes trapped in a pouch of mucosa that develops from the mobile sub epiglottic mucosa. Entrapment may be permanent/intermittent/exercise induced. if permanent, entrapping membrane and possibly the epiglottic cartilage may be swollen and ulcerated. Permanent or intermittent SP often occurs secondary to epiglottic entrapment.

Answer 75

Abnormal expiratory oiises occur as air fills the pouch during expiration. on endoscopy an entrapped epiglottis loses normal flat, serrated appearance and becomes rounded, thickened, reddened or ulcerated. The normally prominent blood vessels on the dorsal aspect are now not visible. Treat by sectioning the entrapping membrane per nasum or per os using a hooked bistoury, or transendoscopic laser.

Answer 76

Rare congenital structures mainly seen in standardbreds. they can deviate epiglottis dorsally causing airflow obstruction and possibly dysphagia, depending on the degree of epiglottic distortion.

Answer 77

Occasionally an abnormally dorsally angled epiglottis may be observed in resting horses without the presence of a sub epiglottic cyst. rarely seen as a dynamic disorder during high speed treadmill endoscopy where epiglottis sucked back towards laryngeal lumen.

Answer 78

The mobile folds between the arytenoids and epiglottis will sometimes become displaced medially into the airway during fast work and cause turbulence and noise.

Answer 79

Unilateral idiopathic degenerative neuropathy of the left recurrent laryngeal nerve which innervates the intrinsic laryngeal muscles. Loss of abductor dysfunction occurs first but causes no clinical signs, but adductor muscle dysfunction - cricoarytenoideus dorsalis causes an inability to fully open the larynx during exercise. Occasionally unilateral laryngeal paralysis is caused by guttoral pouch mycosis or damage to the recurent laryngeal nerves in the cervical area.

Answer 80

history - the type of noise and its onset in relation to fast work. RLN may be progressive in some. affected horses make an abnormal INSPIRATORY noise at exercise plus possibly poor performance. Palpate the dorsal laryngeal area for evidence of laryngeal muscle atrophy. Endoscopy at rest including during nasal occlusion and after swallowing.e valuate for asymmetry and asynchrony. laryngeal function graded from 1 normal to 4 total hemiparesis. do not evaluate in a sedated horse. Listen to respiratory sounds during fast exercse. treadmill or overground endoscopy do not correlate. Ultrasonography of the ipsilateral cricoarytenoideus muscle can show characteristic changes.

Answer 81

Mild cases - perform a vocalcordectomy or ventriculectomy or ventriculocordectomy to prevent vocal fold obstruction at work surgically or using a transendoscopic laser. Severe cases need a tieback - a prosthesis mimics action of CAD muscle to permanently abduct the left arytenoid. complications include loss of surgical abduction, coughing due to aspiration tracheitis due to lack of aduction during swallowing, post operative wound ifectios.

Answer 82

Hepatic encephalopathy, organophosphate or lead poisoning, GA.

Answer 83

Rare congenital abnormality with variable abnormal missing cricopharyngeal, thyroid and cricoid cartilage unilaterally or bilterally.

Answer 84

Occurs in small pony breeds and donkeys. Caused by a cartilage deformity or degeneration of the dorsal trachealis ligament that may cause separation of the tracheal mucosa from dorsal ligament. affected ponies show stridor, dyspnoea, exercise intolerance or may be undiagnosed due to low workload. If the problem is cervical trachea this causes an inspiratory noise whilst intra thoracic obstructions cause expiratory obstruction.

Answer 85

Usually performed on the standing horse under local. the upper third of cervical trachea where most superficial. skin prep. Local anaesthetic infiltrated. elevate head. 15cm midline skin ad Subcut incision. Incise muscle. Separation of the muscle over 7-8cm length the reveals the trachea. Lower horses head to normal position. A transverse stab incision is made int the annular ligament and this will induce a loud inspiratory noise as air rushes into trachea. extend incision on both sides to create a large opening. insert tracheostomy tube.

Answer 86

the most common neoplasm affecting the horse. they are benign but can be locally aggressive. they are fibroma type structures. the aetiology is unknown but BPV or similar viral cause suspected. some evidence that they can be spread by flies.

Answer 87

head groin prepuce axillae and neck. >80% of horses with sarcoids have more than 1 lesion.

Answer 88

Occult - area of slightly thickened skin with a roughened surface, often hairless and very slow growing. Verrucous warty sarcoid - dry horny and cauliflower like, hairless and can have either a broad base or a stalk. Fibroblastic sarcoid - resembles proud flesh, can be firm and nodular in its surface and may be ulcerated. Mixed - mix between any types. Nodular - entirely under the skin, easily shelled out. Malevolant sarcoids - Rare, most aggressive type - tumours spread extensively through the skin with cords of tumour tissue interspersed with nodules and ulcerating fibroblastic lesions.

Answer 89

Many treatments available.not one is very effective. 1. do nothing - if not causing interference, or ulcerated. 2. surgery - up to 40% recurrence. better results (80%) if wide margins taken or used to debulk large lesions. Laser surgery also good as seals blood vessels and lymphatics as it cuts. ligation or elastration of stalks of pedunculated sarcoids sometimes effective. 3. Cryosurgery - effective for lesions with limited size and deth, may cause extensive damage to surrounding structures and scarring. 4. BCG injection - very succesfull for perocular sarcoids, poor rate elsewhere, 2-3 injections several weeks apart, unknown mechanism of action. 5. Radiation - best results but very expensive and restricted, difficult around eyes or joints. 6. topical cytotoxic therapy - AW-4LUDES = secret formula applied topically on several occasions. obtained on case by case basis fom leahurst. Causes skin necrosis and scarring. 7. Intralesional chemotherapy 0 cisplatin or 5 flouracil 8 combination therapy best results.

Answer 90

( may change from benign > malignant). Leave alone- unless causing a problem Excision - wide and check margins. may be curative for discrete dermal lesions or helpful for debulking large lesions. Cryotherapy - may need to repeat, combine with debulking Cimetidine - systemic oral treatment. TID for 3 months. Chemotherapy - intralesional cisplatin on at least 2 occasions.

Answer 91

Uv radiation, chronic irritation, previous wound, smegma, penile SCC. usually around the head / eye r external genitalia (vulva , penis) particularly non pigmented sk. Lesions are productive (papillary appearance) or erosive (nodular plaques and ulceration. locally invasive, slow to metastasise. may travel to local lymph nodes then the lung.

Answer 92

Infection - bacteria prolong inflammatory phase of wound healing, may produce collagenases which decrease wound strength. Excess movement - particularly over high motion joints in the limbs. Large skin defects - may just require more time if epithelisatio is occuring. Presence of foreign body/necrotic tissue - inadequately debrided wounds, bone fragment remaining or bony Sequestrum post injury. Excessive granulation tissue - proud flesh. limbs > trunk wounds. horses > pnies. V difficult for epithelium to grow over it once protruding higher than wound edge. Systemic disease of the patient - cachexia, cushings.

Answer 93

Remove necrotic tissue, foreign bodies, give topical ad systemic antibiotics. Immobilise to stop excess movements in a robert jones bandage or bandage and cast. Skin graft possible if large skin defect. Bandage with moderate pressure for excessive granulation tissue - excision of excess tissue, cut back to just below the surrounding skin surface - note granulation tissue can bleed a lot. Topical steroids - CARE ON AN INFECTED WOUD. reduces granulation tissue but also slows epithelisation too so don't use for too long. biological dressings e.g amnion, skin grafts can reduce granulation tissue production. Cauterising compounds - copper sulphate, silver nitrate salicylic acid DO NOT USE.

Answer 94

need a fresh or granulating wound If granulating - debride granulation tissue which reduces bacterial contamination. do not consider graft if infection present. consider topical treatment of recipient site after initial debridement. streps and pseudomonas often a problem so consider silver sulfadiazine.

Answer 95

1. History - concurrent disease, what is the horse used for, vaccination, insurance, previous lameness, duration and severity of lameness, any trauma, when was horse last shod. 2. Observe at rest- assess weight bearing, look for swellings, foot 3. Observe while moving - at walk, at trot, on lunge on soft and hard ground, use hoof testers once lameness is confirmed, flexion tests 4. Palpate and maipulate- 5. Diagnostic nerve/joint blocks - anaesthesia of sensory nerves to localise region of pain. 6. Diagnostic imaging - radiographs, ultrasound, nuclear scintigraphy, MRI, CT - after a region of interest has been identified.

Answer 96

It will trot with its head nodding DOWN when the SOUND limb lands, as it tries to shift the weight off the painful limb.

Answer 97

A horse with a unilateral hindlimb lameness wil show an increased excursion of the gluteal region on the lame side at the trot. IF severe a hindlimb lameness will result in a head nod mimicking lameness of the ipsilateral forelimb.

Answer 98

Most f the sole. usually do not lose dorsal coronary bad sensation. If performed distally unlikely to alleviate pain from the proximal interphalageal joint but will do so if needle is inserted mid pastern.

Answer 99

All of the hoof capsule, proximal interphalangeal joint, palmar pastern region including sesamoidean ligaments, DDFT, SDFT, distal part of tendon sheath.

Answer 100

Hereditary Diet - methioine, biotin etc increase hoof growth Environment - wet horn weak, ammonia rots horn, formalin damages hoof wall horn Farriery - lack of farriery may cause imbalance. nail placement affects function. imbalance predisposes to cracks.

Answer 101

Toe angle equals pastern angle, toe angel equals heel agle, heels the same length and height. equal distribution of weight.

Answer 102

The nail has penetrated the sensitive tissues of the foot at the time of shoeing.

Answer 103

they protect the hoof wall against wear & tear and improve performance, and give additional support on slippery surfaces, but they add weight, they restrict expansion of foot during loading an cause problems if done incorrectly.

Answer 104

A clinical manifestation of different pathological processes in the navicular bone, flexor surface of NB, DIP joint, DDFT, navicular suspensory ligaments, impar ligament. Due to increased pressure between the DDFT and NB in a flat foot with along toe/low heel - leading to remodelling of the NB - sclerosis,thickening sc bone and inflamation of the NB. analogous to degenerative joint disease.

Answer 105

Insidious onset, frequent stumbles, reluctant to work on circle, may point one foot, shortened stride at the trot, often bilateral lameness which is accentuated on the hard circle, diagnostic analgesia: will improve to PDNB, DIP and NB block. Take Upright navicular (dorsoproximal palmarodistal) and skyline navicular views (palmaroproximal palmarodistal oblique).

Answer 106

Foot care - support the heel, relax the DDFt. NSAIDS vasodilators Intra articular or intra bursal corticosteroids - contra indicated if DDFT lesion present. Tiludronate - reduces osteoclast activity. Surgery - desmotomy of suspensory lig, decompression of navicular medullary cavity, neurectomy - 74% sound at 1year.

Answer 107

most common cause of lameess, typically acute lameness, typically increase of digital pulse, any insult to the sole ca create a ideal medium for bacterial growth. Chronic cases may preset with cellulitis and systemic infection. Increase of digital pulse, use hoof testers and warm poultice, radiographs - may see gas shadow, antibiotics and anti inflammatories can be contraindicated.

Answer 108

release infection & allow adequate drainage, deridement of necrotic tissue, poultice until the infection is controlled, warm bath with povidone and magnesium salt. Tetanus prophylaxis. Antibiotics and anti inflammatories can be contraindicated.

Answer 109

Bruise of sole at specific location: medial angle much more common than latera. usually due to pressure from heel of shoe either shod too short, shoe left on too long, dorsopalmar foot imbalance. Excessive heel loading leads to bruises/subsolar abscess. Bandage or poultice/corrective trim - re shoe.

Answer 110

Common emergncy. rule out sepsis of synovial structures. commonly result in Subsolar abscesses. use radiographs, synovoocentesis, navicular bursa contrast study, MRI. Subsolar abscess is localised usng hoof testers - pare tract to release pus.

Answer 111

White line is a weak region due to the soft horn. a combination f bacteria and fungi produce separation of the white line. this occasionally produces lameness. typically an incidental finding. white line becomes filled with poor quality infected tissue. often secondary to laminitis. advanced cases cause instability of pedal bone or infection of laminae.

Answer 112

A benign, hyperplastic keratin mass which arises from the epidermal keratin producing cells and originates at any point in the hoof wall and sole. it is a space occupying tumour, often causes recurrent hoof abscesses. Causes a disruption in the hoof architecture and allows bacterial infection and recurrent abscess. May cause pressure necrosis and resorbtion of pedal bone margin leading to characteristic radiographic lucency.

Answer 113

an infection of the frog caused by wet environment, by fusibacterium necrophorum. black sticky discharge & terrible smell present. can result in under run sole and limb oedema. contracted heels may predispose to the condition. Trim affected parts of the frog ad move to a dry environment. Give antiseptic foot baths (povidone iodine)

Answer 114

Due too a penetrating injury to the sole involving P3 a chronic subsolar abscess, blunt trauma.

Answer 115

Surgical debridement standing or under GA. Curettage of infected pedal bone. packing the area with antibiotic impregnated swab. regional perfusion with antibiotics. systemic antibiotics and anti inflammatory.

Answer 116

chronic pododermatitis of the germinal layers. gram negative bacterial infection of the stratum germinatum of the frogs epidermis. causes hypertrophic dermatitis of the frog and the bulbs of the heels.

Answer 117

collateral cartilage infection - as a result of a hoof wall crack puncture wound, chronic abscess, or heel laceratio. causes a severe degree of lameness until adequate drainage is established. Causes chronic sepsis with intermittent purulent discharge above the coronary band.

Answer 118

Important to rule out sepsis of the synovial structures - Assess DDFT, collateral cartilages, navicular bursa, impar ligamnet, DFTS.

Answer 119

Ungular cartilages | DIPJ/NB/DFTS

Answer 120

Check depth and direction of penetration BEFOORe removing object provided there is no risk of object penetrating further - do dorsopalmar and lateromedial radiographs. Mark entry wound on sole. Possible structures involved include NB, DIPJ, DFTS, DDFT, P3, digital cushion. - Can do synoviocentesis, contrast arthrography, MRI.

Answer 121

With sterile saline (0.9%) - optimal lavage. OR 1tbsp table salt + 600ml water, or 0.05% chlorhexidine or povidone iodine. always lavage with saline after using these. avoid scrub solutions. use pressure 10-15PSI - 30ml syringe with a 19g needle.

Answer 122

perform promptly, minimise contamination, use tension relieving suture patterns/techniques, not if infected, drains if dead space. always try too perform primary closure of the eyelid/distal limb wounds.

Answer 123

Aim to minimise oedema with firm even pressure, absorb exudate, maintain temperature and moisture, allow gaseous exchange, immobilise the woound, protect from further contamination and trauma. 1 - primary dressing - chooose non adherent dressings. Meloln for on exudative. Allevyn for exudative. calcium alginates for healing by 2nd intention. collagen dressings foor healing by 2nd intention. hydrgels for contaminated wounds, hydrocolloids, manuka honey, amnion. 2.- secondary layer - use cotton wool or gamgee, absorbs exuate, secures primary layer, supports and protects. 3- Tertiary layer - vetrap, secures provides support and pressure.

Answer 124

Accessory carpal, medial malleolus, flexor tendons, gastrocneumius tendon.

Answer 125

If the horse sustains an injury or manifests an illness or disease that is so severe as to warrant immediate destruction to relieve incurable and excessive pain and that n other options of treatment are available to the horse at that time. hopeless prognosis incldes; complete fractures of the radius or humerus if horse >300kg, long bone fractures with severe soft tissue damage, complete femoral or tibial fractures in adult, severely contaminated fractures.

Answer 126

``` Haemorrhage/anaemia Trauma malnurition NSAIDS Corticosteroids (slow) Cocurrent disease Cachexia cytootoic drugs Trauma infection temperature oxygen movement foreign bodies transformation into sarcoid. ```

Answer 127

Treat/prevent infection, prepare wound well at first visit, ensure all FB devitalised and tissue removed, remove all devitalised tendons bony sequestrae as soon as they become apparent, delayed primary closure, immobilise limb apply pressure to wound - badage, use a skin graft to promote epithelisation.

Answer 128

Tarsocrural joint - followed by fetlock, carpus, stifle and pastern.

Answer 129

Septic arthritis/tenosynovitis/bursitis results from the inoculation of microrganisms into a synovial structure resulting in an inflammatory response which fails to prevent proliferation of the micro organisms. A rapid influx of leucocytes occurs which are capable of phagocytosing bacteria and releasing destructive enymes. Disruption of the blood synovium barrier results in release of multiple inflammatory mediators into the joint. Leakage of fluid into the synoval coompartment results in joint or tendon sheath distension and increased intra articular pressure. this reduces blood flow to the synovium. Release of inflammatory mediatoors stimulates chondrocytes within the joint to release enzymes causing disruption of the prootoglycan hyaluronan complex in the articular cartilage. the protection of the articular cartilage is further compromised by changes in the synovial fluid due to changes in viscoosity, fibri and pus accumulation.

Answer 130

Gram positive isolates are more common in adults with staphylococcus aureus having the highest incidence and non haemolytic staph, b haemolytic and non b haemolytic strep, rhodococcus equi and corynebacterium have also been isolated. multiple and gram negative infections are more frequent in foals with E. coli being the most frequent isolate and pseudomonas, enterobacter, actinobacillus, proteus, klebsiella and salmonella have also been isolated.

Answer 131

Pain, heat and swelling, pyrexia often absent, pain may be sudden in onset and lameness almost Non WB. Synovial distension on palpation. Clear yellow viscous fluid exuding from a wound. May also be serum. Common signs: severe lameness, wound nearby, joint effuson. Not useful: pyrexia, local skin temperature, radiography

Answer 132

Significant changes occur within hours. collected in EDTA for cytology and a separate sample collected for aerobic and anaerobic culture. Gross changes indicate synovial fluid abnormality include turbidity,red or dark yellow colour, reduced viscoosity. total protein values >25g/l are indicative of synovitis, leukcyte counts in synovial fluid rise quickly most cases >30 x10^9 and most cases have >80% neutrophils. I

Answer 133

Syovial distension - of the joint or tendon sheath with sterile polyionic fluid from an aseptically prepared site may produce drainage through the wound ultrasonography - extremely useful to identify synovial distensions, increased thickness of synovial membrane, the presence of fibrin or pus in synovial fluid and changes to peripheral articular surfaces. Radioography - only become apparent after weeks.

Answer 134

Central 1/3 f frog carries highest risk of contaminating navicular bursa, coffin joint(DIPJ), flexor tendon sheath.

Answer 135

usually haematogenous in origin and should be considered as part of a more generalised disease eg septicaemia or failure of passive transfer of immunity. foals with rhodococcus equi can develop immune mediated synovitis or septic physitis.

Answer 136

Arthroscopic lavage - debridement followed by closed suction drainage. Improved drainage may be achieved by desomotomy of the palmar annular ligament which can be performed using an open or closed techinque. Lavage through needles is ineffective. Systemic antimicrobial therapy - gentamicin S.i.d. combined with sodium benzyl penicillin q.i.d. Intra articular medication - gentamicin, amikacin, cephazolin Regional limb perfusion - application of a tourniquet and administration of antibiotic into a peripheral vein. Antibiotic impregnated polymethylmethacrylate or gelatin sponges - PMMA beads impregnated with gentamycin and collagen spoonges. NSAIDS will mask lameness and may delay treatment. Withhold after arthroscopy as return of lameness is a Good indicator of recurrent sepsis.

Answer 137

Can be uniaxaial or biaxial, single or multi limb believed t be due to excessive exercise running after the mare. ommonly ocurs between 2 weeks and 2 months age, can be basilar or apex. commonly is comminuted.

Answer 138

characterised radiographicalyl by railucent areas oof bone often accompanied by a thn well demarcated rim of sclerotic bone. usually occur in the subchondral bone underlying a weight bearing surface of the articular cartilage e.g medial femoral condyle, phalanges. clinical signs include lameness &" joint effusion. lameness in young horses 1-3 years old usually occurs at onset of trainining.

Answer 139

Periarticular ligament laxity or hypoplasia f the cuboidal bones of the carpus or tarsus. malformation of the diaphysis of the long bones, intrauterine malpositioning, mare nurition.

Answer 140

Deviation due to growth asymmetry - partially restrict excercise, monitor diet too avoid overweight/rapid growth, check CU, ZN, CA,, P levels in the diet. check foor lameness. Use medial extension shoes for valgus deformities and lateral extension shoes for varus deformities. If does not respond to conservative management then surgical treatment is required - Growth acceleration via periosteal transection and elevation - performed on the short side of the bone. the periosteum is stripped from the physis on one side of the bone and then replaced. unsure of mechanism of growth acceleration. not possible to over correct the lesion using this method. Growth retardation via transphyseal bridging - surgical implants can be placed across the physis on the side that is growing too rapidly. used only in severe cases as it is possible to over correct.

Answer 141

oxytetracycline 2-4gms/foal IV in first 48 hours.

Answer 142

Usually develoops 6w-m, bxy upright foot, broken back hoof pastern axis, can develop very rapidly, type 1 dorsal hoof wall still slopes cranially, type 2 past the upright i.e slopes caudally. conservative management in mild cases including dietary restriction, nsaids, controlled exercise, rasp down heels and place toe extension. can try bandaging but usually Succesful in early cases only. surgical treatment in severe or progressive cases - either desmotomy of the ALDDFT, or deep digital flexor tenotomy.

Answer 143

Inflammation and disruption of growth in the physeal regions, caused by ooverload, over exercise, rapid grwht, firm often painful swelling of the physeal areas. Often in distal radius and tibia, also distal MT/C3. flaring oof the growth plates gives a hour glass shape. The outline of the bone is disrupted, with lipping and flaring of the physeal region. differentiate from septic physitis. most cases are self limiting. radographyically the physis is widened and irregular the outline of the bone is disrupted. Treatment is required if condition is painful or is suspected to be causing secondary growth disturbance leading to angular or flexural limb deformities. Exercise reduction is important. dietary intake should be reduced to slow growth.

Answer 144

Common seen in premature or dysmature foals, presenting clinically with various angular limb deformities following uneven loading of a dysmature skeleton. identified radiographically as incomplete ossification of the carpal or tarsal bones. if less than 30% of the cartilage skeleton has ossified then prognosis for athletic activity is hopeless.

Answer 145

It represents a disturbance in the process of endochondral ossification without a clearly understood aetiology. this can eventually lead to the formation of semi loose or completely loose fragments within a joint.

Answer 146

the process of transformation from the primordial cartilaginous skeleton into bone coupled with simultaneous growht. ossification of the primary centres of ossification in the diaphysis of the long bones occurs early in life however ossification of the secondary centres of ossification at the epiphysis continues after birth.

Answer 147

Biomechanical loading Failures of vascularisation of the blood supply - cartilage necrosis Exercise - steers the functional adaptation of cartilage to its topographically heterogenous character during the first year of life. Nutrition - hormonal factors and growth rate dietary copper is thought to have an effect on the final outcome of lesions as several studies have shown increased OC with low copper. Genetics - lesions rarely found in ponies and feral horses.

Answer 148

Distal intermediate ridge of the tibia, distal end of the lateral trochlear ridge of the talus, medial malleolus of the tibia, medial trochlear ridge of the talus.

Answer 149

Lateral trochlear ridge of the femur > medial trochlear ridge of femur, trochlear groove, distal end of the patella, subchondral bone cysts of the medial femoral condyle are also a manifestation of OC.

Answer 150

Dorsal edge of the sagittal ridge of the metacarpus.

Answer 151

lameness and or synovial effusion usually in yearlings. less severe cases coincide with the onset of trainiing. lameness can vary frm subtle to obvious with owners smetimes reporting that the horse has difficulties getting up.

Answer 152

Radigraphy - DMPLOO and DP projections for DIRT lesions, lateral trochlear ridge, medial malloelus. Femeropatellar oc can be identified on the lateromedial and CaLCrMO prjections. ultrasound more sensitive for identifying less common OOC of the medial trohclear ride of the femur.

Answer 153

Non surgical management consists f rest, and controlled exercise. administration of NSAIDS and intra articular medications have not been shown too be of benefit for OC cases. Conservative management can only be expected to be successful in very young animals. Surgical management is the treatment of choice in most cases - arthroscopic fragment removal superier to arthrotomy as soft tissue trauma reduced.

Answer 154

Tarsoocrurual joint - prognosis for athletic function does not appear to be related to the lesion size for DIRt - 75-87% returning to athletic function post surgery. prognosis for effusion resolution is better for DIRT lesions (75%) than trochlear ridge (50%) or medial malleolar (50%). Femeropatellar joint - the prognosis does appear to be related to lesion size with 78% of horses with lesions 4cm only 54% returning to racig.

Answer 155

``` Carbohydrate overload Septicaemia/endotoxaemia Mechanical - excess weightbearing corticosteroid administration cushings disease, hypothyrooidism ```

Answer 156

Excess carbohydrate in caecum, increase in lactic acid producing bacteria, drop in caecal pH damages gram negative bacteria, endotoxin release into circulatin, peripheral vasoconstriction and activation of a-v shunts, decreases laminar perfusion, exacerbated by microthrombi. Laminar ischaemia causes necrosis and loss f pedal bone support. the dorsal laminae are vascularised last within the foot so they are most affected. once the laminae are damaged the pull of the DDFT is no longer resisted and the bone rotates. If all laminae are affected at the same time - then complete laminar separation may result and the pedal bone will sink ventrally without rotation, oor the whole hoof capsule can even be shed.

Answer 157

typical saw horse stance with fore feet placed forwards and the hind limbs under the body. front feet are painful - especially the toes. primarily affects the front feet. depressed, inappetant, increased HR & RR. markedly increased digital pulsation, heat in feet, painful across sole to pressure from hoof testers, coronary band depression.

Answer 158

Intermittent bouts of lameness. Flat or convex sole, seedy toe and abscesses common. prominent hoof wall rings, narrowing at dorsal hoof wall (ddx from nutritional rings).

Answer 159

remove the potential causes - placenta, pasture, give liquid paraffin if appropriate. support the feet by using styrofam support pads, very deep bedding, use glue on plastic shoes, analgesia, ACP QID iv or Im for vasodilation, feed hay only & methionine to promote hof growth. Use radiographs to establish severity of condition and provides a baseline for monitooring progress. lateromedial views with markers to indicate position of coronary band and point of frog. measure angle of rotation and founder distance (d distance) prognosis worse with increasing values as well with severity of lameness, solar prolapse and increasing number of feet affected. ski tip new bone formation at tip of pedal bone indicates previous bouts of laminitis.

Answer 160

Subsolar abscess/solar penetration, septic joint/bursa/sheath, severe tendon or ligament strain/rupture, subluxation/luxation, radial paralysis, upward fixation of the patella, cellulitis, rhabdomyolysis

Answer 161

Microcrack formation with fatigue - during process of remodelling, bone is weakened > microfractures occur. During fatigue, the muscles relax > tendons which provide support to the joints erlax, abormal range of movement, increased strains, microcracks caolesce > catastrophic fractures can occur.

Answer 162

How much weight does the bone normally bear? is it a joint invlved? degree of comminution and displacement, contaminatio, chronicity.

Answer 163

beware - lameness may improve within days if non displaced. treatment otions range from fixation using one or several lag screws to arthroscopic fragment removal or half limb cast. prognosis depends on fracture type and quality of repair but many horses will return to racing and repair is usually undertaken with that aim not just salvage. Prerequisite for successful surgical repair is at least one strut of bone which extends from fetlock to pastern.

Answer 164

Direct trauma - concussion i.e kicking a wall, landing on uneven surface or object, nail penetration through sole, fast work n hard tracks. less common - hyperextension of coffin joint, osteitis or laminitis.

Answer 165

acute severe lameness - may increase in the first 24 hours. increased digital pulsation. may have heat in foot, solar pain on hoof testers, pain on flexion, may have coffin joint effusion but only if fracture is articular. signs subside slowly - horses usually walk sound after 4-8 weeks, Take standard views of foot but may see some only on oblique views.

Answer 166

1 - non articular palmar /plantar process II - complete articular parasagital type II complete articular sagital Type IV - extensor process type V - comminuted type VI non articular solar margin Type VII - non articular palmar plantar eminences

Answer 167

type I - hoof immobilisation. healing time 11 months. good to excellent prognosis. Type II - conservative treatment, average healing time 12 months, 50% prognosis foor retur to soundness, worse prognosis for older horses. type III - surgical treatment or conservative as salvage for failure. type IV - lag screw fixation if large, arhtrocopy/arthrotomy for removal if smaller - prognosis guarded to fair. Type V - comminuted - poor prognosis , underlying pathology. type VI - solar margin fracture, often secondary to laminitis. other common cause is penetrating foreign body. conservative treatment unless infected. treat primary cause.

Answer 168

if distal oor non complicated proximal - conservative management, approx 76% return to exercise. if mid prtion - segmental ostectomy proximal intra articular and joint instability - interal fixatioon open fractures - treat as open wounds, systemic and regonal ab, chance for healing less successful. removal of distal 2/3 of split bone is safe. < Proximal 1/3 of the splint bone remaining > internal fixation. entire mt4 can be removed however surgical out come is only fair.

Answer 169

affected animals have characteristic dropped elbow due to disruption f stay apparatus. ddx from humerus fracture and radial paralysis.

Answer 170

You cannot obtain pus from the foot after 1-2 days of poulticing, horse is lame at the walk, there is obvious limb deviation, there is pain or oedema over a bone with or without a wound, there is a history of a kick or other severe trauma, it is a racehorse.

Answer 171

If the SDFT alone is fully transected then the metacarpophalangeal joint will be dropped when the limb is loaded. if the deep digital flexor tendon and SDFT are transected then the horse will knuckle the toe upwards, when the SDFT, DDFT and Sl are transected the horse has a platarograde stance and the metacarpphalangeal joint bears weight.

Answer 172

repetitive subthreshold mechanical overstimulation resulting in microdamage and activation of degradative enzymes and extracellular matrix destruction. Understimulation, loss of local homeostatic strain results in activation of degradative enzymes. Aberrant differentiation of resident progenitor cells to causing lipid cartilage or bone formation within the tendon and weakening mechanical properties.

Answer 173

Horses typically present acutely, severely lame with a soft painful bowed tendon in the mid canon region. When the limb is loaded the MCPJ can appear dropped if the SDFT injury is severe. Lameness often resolves quickly in non severe injuries. diagnosis is based on ultrasonography carried out 10-14 days after initial injury to confirm the extent of the fibre damage. A central core lesion is usually apparent area within hyperechoic, the length of damaged tendon, total cross ectional area and cross sectional area of fibre damage should be documented on the first ultrasound to allow monitoring.

Answer 174

In the inflammatory phase - strict box rest, cold hosing for 15- 20 minutes twice daily, supportive bandaging, non steroidal anti inflammatory medication with controlled walking exercise introduced as soon as the horse is sound at the walk.

Answer 175

1. Conservative management 12-18 months box rest and controlled exercise alone. Box rest and walking for 0-8 weeks, then trotting and walking 9-32 weeks, then 32-52 weeks can introduce canter work. from 52 months - full training/racing can commence. 2. Intralesional treatments with hyaluronan, BBAPTN, bone marrow derived mesenchymal stem cells, adipose derived stem cells, platelet rich plasma, bone marrow aspirate, insulin like growth factor 1, polysulphated glycosaminoglycans. 3. Surgery - desmotomy of the accesorry ligament of the SDFT.

Answer 176

DDFT is less common than injury to SDFT but can occur at several locations; within hoof capsule, within the digital flexor tendon sheath, within the tarsal sheath, within the carpal sheath, associated with desmitis of the accessory ligament of the DDFT.

Answer 177

Injury to the DDFT within the hoof capsule is most common in horses that jump. clinically cases present with sudden onset severe unilateral lameness that resolves and recurs when exercise is reintroduced. Lameness can usually be abolished by palmar digital analgesia just proximal to the collateral cartilages. Definitive diagnosis is made using MRI with the horse standing and sedated. Three types of lesions are described within the hoof capsule.

Answer 178

treatment is focussed on box rest, controlled exercise and corrective farriery. raising the heels reduces the tension on the DDFT but increases the tension on the SDFT and SL.

Answer 179

marginal tears of the DDFT present clinically with effusion of the DFTS and sudden onset lameness. the lameness usually is improved following intrathecal analgesia of the DFTS. these lesions are often missed during ultrasonography of the DFTS and definitive diagnosis is made tenescopically.

Answer 180

1. complete breakdown when both proximal sesamoid bones fracture in the racehorse. This is almost exclusively a condition of racehorses occuring predominantly in the forelimbs and more commonly in the USA. horses pull up non weight bearing lame with a dropped fetlock. Radiography can demonstrate bilateral PSB fracture. 2. Proximal suspensory desmitis in the forelimbs is different to PSD seen in the hind limbs. fore limb PSD usually presents as bilateral lameness with the lamer leg on the outside of the circle. lameness is alleviated by analgesia of the lateral palmar nerve, ultraonosgraphy can demonstrate heterogenous fibre pattern and increased depth of the ligament. 3. Mid body suspensory desmititis 4. Suspensory branch desmitis 5. Desmitis of the distal sesamoidean ligaments.

Answer 181

It presents clinically as acute onset moderate to severe lameness with swelling of the ALDDFT, possibly a higher incidence in ponies and horses that jump.

Answer 182

Recurrent forelimb lameness usually with no localising clinical signs. severe cases demonstrate palpable enlargement of the collateral ligament of the distal interphalangeal joint.

Answer 183

The osteoarthritic disease process can originate from various causes with trauma and synovitis being the most common as a result of overuse or poor conformation, leading to abnormal forces on normal cartilage. OR normal forces on abnormal cartilage resulting in OA. (e.g osteochondrosis)

Answer 184

Fibrillation of the articular surface, wear lines and erosion of the hyaline cartilage eventually down to subchondral bone in severe cases. microscopic changes to the articular cartilage include chondrocyte necrosis, chondrone formation, fibrillation, focal loss of safranin O staining and focal cell loss.

Answer 185

A progressive condition caused by gradual loss of articular cartilage usually with concomitant changes in the subchondral bone and synovium. OA is also known as degenerative joint disease and osteoarthrosis.

Answer 186

Once hyaline articular cartilage is damaged it is not capable of regeneration, deep cartilage lesions heal spontaneously by a progression from granulation to fibrous tissue that is remodelled to fibrocartilage.

Answer 187

``` Palliative drugs that reduce pain and inflammation or disease modifying osteoarthritis drugs that have a chondroprotective function in acting to slow the progression of the disease. NSAIDS INTRA Articular corticosteroids Hyaluronan Polysulphatedglycosaminoglycans Pentosan polysulphate Chondroitin sulphate and glucosamine Tiludronate Autologous conditioned serum ```

Answer 188

Pain relief is attribtued to inhibition of the prostaglandin synthesis specifically by inhibiting the enzyme phosphor lipase a2.

Answer 189

Triamcinolone and methyl prednisolone acetate MPA. Triamcinolone is less chondrocyte toxic than MPA therefore is recommended for use in high motion joints.

Answer 190

A large non sulphated glycosaminoglycan component of synovial fluid responsible for viscoelasticity, boundary, lubrication and steric hinderance. It is also an important component of proteoglycan in the cartilage matrix providing compressive stiffness. It is thought to reduce neutrophil chemotaxis and phagocytosis, reduce PGE, il1 and bradkinin production and scavenge free radicals.

Answer 191

PSGAGs have been shown to promote chondrocyte metabolic activity and inhibit the effects of cytokines and prostaglandins on cartilage and are therefore classed as DMOADs.

Answer 192

This is a PSGAG extracted from plants that is licensed for intra muscular use in horses and has been shown to achieve therapeutic levels in synovial fluid following IM injection.

Answer 193

Contain the component of cartilage and the precursor molecules chondroitin sulphate and glucosamine hydrochloride. there is still no conclusive data demonstrating absorption or bioavailability at the joint in the horse. excellent safety profile.

Answer 194

Tiludronate is a bisphosphonate that regulates bone remodelling through inhibition of bone resorption and it is therefore postulated that it should ameliorate the remodelling processes active in OA. one clinical study has shown efficacy of tiludronate in combination with a controlled exercise programme for the treatment of distal tarsal OA.

Answer 195

generated from the horses blood incubated overnight at 37C in a special syringe containing chromium coated glass spheres which stimulate white blood cells to produce anti inflammatory cytokines. the serum is aspirated the following day in an aseptic manner and stored in 2ml aliquots until used.

Answer 196

Arthroscopic debridement of meniscal or ligamentous injuries. Minimally invasive surgery. Exposure of collagen fibrils within the synovial environment is thought to potentiate inflammation and predispose to OA hence debridement and reduction of fibrillated ligament or meniscus is thought to be beneficial. Surgical arthrodesis - essentially facilitated ankylosis or fusing of the joint to obliterate any joint movement and therefore reduce pain. the low motion joints such as the proximal interphalangeal joint and the tarsometatarsal joint are amenable to surgical arthrodesis.High motion joints can be arthrodesed if the goal is pasture soundness.

Answer 197

Usually secondary to trauma. confirmation would require a positive intra articular block (difficult) and radiographic evidence of periarticular bone remodelling or acetabular rim fragments. standing radiographs are possible but often GA required.

Answer 198

Hip is usually displaced craniodorsally. limb is shortened and held in an outwardly rotated position. greater trochanter is very prominent and crepitus may be palpable. Can distinguish from fractured pelvis by rectal exam.

Answer 199

ilial wing or shaft - ilial wing fractures may be caused by a one off incident or result from stress remodelling in horses working at high speeds. tuber coxae fractures are usually due to hitting a fence post or stable door.

Answer 200

Usually a single traumatic incident but stress fractures of the ilial wing may have a history of recurrent and transient hindlimb lameness following fast work. tuber coxae fractures are usually due to hitting a fence post or stable door. tuber ischium fractures result from kick injuries or falling backwards while others are usually the result of a bad fall.

Answer 201

these depend on the site of the fracture e.g the involvement of the acetabulum and degree of fragment displacement and vary from moderate uni or bilateral hindlimb lameness to severe lameness or inability to rise with obvious crepitus. asymmetry of the tubera sacrale or coxae may be present and will be permanent. some cases may appear ataxic but have no neurological abnormalities when assessed. Chronic cases invariably have marked muscle wastage, most prominent in the gluteal region. A rare complication is damage to the iliac arteries caused by displaced bone fragments

Answer 202

Rectal palpation for pain, haematoma, displacement. Scintigraphy and ultrasonography are now the imaging modalities of choice for pelvic fractures. Radiography rarely performed as general anaesthesia is required for good quality images and recovery from anaesthesia may further displace a fracture.

Answer 203

Fragments of tuber ischii or tuber coxae may be surgically removed. for most other pelvic fractures, prolonged rest is the only treatment. euthanasia is indicated where lameness persists or the horse remains recumbent. Prognosis for fractures of ilial shaft, pubis or involving acetabulum = poor.

Answer 204

may have concomitant uni or bilateral hindlimb lameness, shortened stride length affecting the hindlimbs , poor performance and deterioration in temperament or other behavioural signs such as bucking when riden. often veterinary attention is only sought at a late stage. There may be palpable focal enlargement of the supraspinsous ligament, the other ligaments can only be examined by ultrasound

Answer 205

dorsal impingement of the spinous processes - - causes thoracolumbar pain. the lumbar vertebral column narrows dorsally and the opposing bone surfaces remodel. AFfected horses usually resent flexion or extension of the back when manipulated. Radiography wil confirm impingement. Positive response to local anaesthesia is required for confirmation of diagnosis.

Answer 206

many horses wil recover with rest. local injections of steroid or surgical removal of the impinging processes are used as treatments. surgical treatment resulted in the return of around 80% of treated horses to their previous level of work after conservative treatment had failed. a novel surgery is less invasive - cutting of the interspinous ligament through small incisions. it is hoped that this will result in resolution of pain with a faster return to normal exercise than with removal of the spinous processes. t

Answer 207

Cyptroheptadine Carbamazepine avoidance of stimuli: masks, nets, lense, hoods sclerosis of posterior nasal nerve

Answer 208

37.8-38.9C

Answer 209

increased heat production, impairment of heat loss, CNS disorders disturbing hypothalamus, certain toxins, exercise, heat stroke, anhidrosis

Answer 210

PCR or Detection of pathognomoic histological inclusion bodies in the foals liver, lungs, and thymus.

Answer 211

``` RAO, SPAOPD Pleuropneumonia IAD acute <10days viral disease ```

Answer 212

At the site of injury, mediated by AA, PGs, LT, histmaine, nociceptors are rendered hyperresponsive.

Answer 213

Thoracic radiography, ultrasonography, tracheal aspirate culture. Hyperfibrinogenaemia, neutrophilia and thrombocytopenia are common but not specific. several serological tests are available but are not 100% accurate. prolonged treatment with rifampin and erythromycin are required.

Answer 214

cough, nasal discharge, slight submandibular lymph node enlargement, intermittent mild pyrexia. animals are not'sick

Answer 215

Influenza, EHV1, EHV4, RHinovirus, EVA, strangles. Less common : mycoplasma felis, equirhinis, bordetella, streptococcus, pasteurella, actinobacillus.

Answer 216

Nasopharyngeal swabs or guttoral pouch washes.

Answer 217

Culture of influenza and EHV from secretions takes several weeks so is more useful for disease epidemiology. influenza is detected rapidly by ELISA of secretions. paired serology takes 2-3 weeks.

Answer 218

occasionally respiratory disease but more commonly outbreaks of abortion and encephalomyelopathy.

Answer 219

Infections occur in conjunction with other infectious agents but generally do not case significant disease, it largely affects the URT.

Answer 220

respiratory disease, severe conjunctivitis, profound depression, periorbital oedema. it is venereal spread.

Answer 221

Pyrexia, bilateral purulent nasal discharge, dysphagia and marked swelling of submandibular and occasionally other head lymph nodes. atypical strangles cases have no lymph node abscessation and may be misclassified as viral respiratory disease unless culture/PCR is done.

Answer 222

A rare complication whereby abscessation occurs in other tissues including mediastinal and mesenteric lymph nodes and physes, affected horses present with fever, malaise, weight loss and signs related to local abscessation.

Answer 223

An immune mediated vasculitiis occuring 1-3 months after strangles infection. Signs include generalised oedema, petechiation, pyrexia, multi organ failure. treat with dexamethasone, penicillin and supportive care.

Answer 224

Endoscopy - incrased volumes of mucopus in thoracic trachea , tracheal aspirates have >20% neutrophils, BALF has >5% neutrophils. BAL involves lavage of the distal airways with 250-300 ml saline via an endoscope. Radiography and ultrasonography are of limited diagnostic value.

Answer 225

Chopped dried alfalfa, silage or complete cubed diets. feeding soaked hay is inefective.

Answer 226

environmental management. Bronchodilators - atropine, follow up with clenbuterol or salbutamol, inhaled beclomethasone or oral prednisolone, maintain hydration to avoid respiratory secretions becoming tenacious.

Answer 227

Severe and potentially fatal dyspnoea rather than coughing and nasal discharge

Answer 228

Syndrome characterised by coughing, exercise intolerance, increased volumes of neutrophilis mucopus within lower airways and occasionally nasal discharge. horses are not depressed sick or pyrexic and do not have overt airway obstruction that characterises RAO. all ages of horse may develop IAD> Commonly identified at the start of training. may self resolve. apears multifactorail - including bacterial infection and inhaled dust/endotoxin. oxytet, ceftiofur, tmps commonly used.

Answer 229

URT, cardiac failure, alveolitis/interstitial lung disease, smoke inhalation, neoplasia, plant and drug toxicity, immune mediated and volume overload.

Answer 230

Initially bacteria colonise lung causing localised pneumonia or pulmonary abscesses. Extension of inflammatory response to adjacent pleura. Extension of bacterial infection into pleura produces large volumes of infected purulent effusion which requires drainage. The organisation phase is characterised by significant fibrin deposition, resulting in a thick pleural peel which limits thoracic expansion.

Answer 231

epistaxis, poor performance, pulling up and very rarely death, excessive coughing is not a feature of EIPH. diagnosis by ronchoscopy.

Answer 232

``` Musculoskeletal problems respiratory tract lack of fitness unrealistic expections of ability inappropriate training cardiovascular abnormalities (<2% of cases) Others - medical , neurological ```

Answer 233

A reentrant rhythmn initiated by a premature atrial contraction and maintained as a result of the horses large atrial mass and high vagal tone. it may be caused by atrial dilatation secondary to valvular dysfunction or there may be no obvious underlying pathology. large horses are predisposed due to their large atrial size. May also be associated with administration of alpha 2 agonist drugs or electrolyte abnormalities.

Answer 234

The loss of atrial contraction has little effect on Qt. During excercise any decrease in Qt caused by the decrease stroke volume is offset by slight elevations in heart rate, however heart rate maximum will be attained at a lower exercise intensity and they will fatigue sooner.

Answer 235

Auscultation - long pauses greater than 2 preceding cardiac cycles with occasional beats occuring earlier than normal. ECG - irregularly irregular rhthmn, no p waves, fluctuating isoelectric line, f waves which may be coarse or fine, QRS morphology is normal unless fibrillation is due to underlying heart disease.

Answer 236

Quinidine sulphate - via nasogastric tube every 2 hours until sinus rhythm is restored. Electric defibrillation or cardioversion - application of a direct current shock under GA to stop the atrial fibrillation . it requires right heart catheterisation via the jugular vein to allo electrodes to be placed in the pulmonary artery and right atrium.

Answer 237

May be atrial or ventricular in origin. may be associated with hypoxia, myocardial disease, electrolyte and metabolic disturbances, elevated sympathetic tone fever and toxaemia. atrial premature systoles are detected fairly frequently in horses in training and affect performance only if they produce excessive heart rates during exercise. more commonly the premature excitatory focus is over ridden as sinus nodal rate increases and the extrasystoles diappear.

Answer 238

The ecg trace shows P waves which occur earlier than expected rfrom the underlying P - P interval. If the P wave occurs after refractory period - then a normal QRS complex follows. If P wave occurs during refractory period P wave is not conducted

Answer 239

Wide bizare configuration as ventricular depolarisation does not follow the normal conduction pathways. If the premature QRS complex occurs during the preceding T wave the vulnerable period of cells, this may result in the development of ventricular fibrillation.

Answer 240

Usually no specific anti arrhythmic treatement is indicated as the premature beats are usually too infrequent to significantly affect cardiac output at rest. it is important to establish what happens during exercise . in many cases with atrial premature complexes when sinus rate exceeds the ectopic firing rate cardiac rhythm and rate become normal. If premature ventricular complexes are identified during exercise the horse should be retired from riden ork.

Answer 241

As a response to training induced eccentric hypertrophy and increased blood volume. Also in response to thickening and fibrosis of the valve leaflets (progressive but slowly), Mitral regurgitation will also develop as a result of rupture of one or more chordae tendinae, or secondary to any other condition that causes dilation of the valve annulus e.g secondary to dilated cardiomyopathy, may also occur as a result of congenital dysplasia of the mitral valve apparatus, infective endocarditis (rare)

Answer 242

Further diagnostic tests - echocardiography. Gives baseline information against which future progression can be assessed. Would likely be excluded from loss of use insurance policies as MR cause atrial enlargement, predispose to atrial fibrillation or may progress to cause cardiac failure. mitral regurgitation would not increase the risk of sudden cardiac death so this should not be an exclusion criterion.

Answer 243

Is not associated with thickening of valve leaflets tends not to progress and if mild/moderate will not affect racing performance. tricuspid regurg does not normally result in cardiac failure although very occasionally primary right sided cardiac failure can occur. May also develop as a result of pulmonary hypertension caused by left ventricular failure. If not associated with thickening of leaflets - unlikely to progress or affect performance. if has a high grade band shaped murmur the very rare possibility of valvular disease cannot be ruled out - must do echocardiography. would be excluded from loss of use insurance as may cause atrial enlargement and predispose to atrial fib. Would not increase risk of sudden cardiac death so this should not be an exclusion criterion.

Answer 244

This is a progressive disease associated wth thickening and fibrosis of the aortic valve leaflets, more common in horses over 10yo, tends to progress slowly and rarely affects performance in older horses. it causes volume overload and left ventricle resulting in dilatation. this occurs gradually and may result to mitral regurgitation. MR then result in cardiac failure. If present in a young horse it is likely to be due to dilatation of the aortic root or another cause of early degeneration eg congenital abnormality of the valve and these cases may progress more rapidly.. Aortic insufficiency also causes decreased coronary perfusion due to reduced diastolic aortic pressure and oxygen delivery to the myocardium is compromised. increased oxygen demand and reduced coronary reserve increases susceptibility to ventricular arrhythmias that can result in sudden death. Affected horses must be monitored regularly so that they can be retired from work before severe ventricular dilatation develops. The progression is difficult to predict in young horses therefore most cannot be considered suitable for ridden work. horses with dilated ventricles are at increased risk of sudden cardiac death. horses will require regular expensive monitoring if they are to be kept in work. insurance companies are likely to exclude the heart from both loss of use and sudden death. In old horses the progression is usually slow. so could be suitable for purchase in some cases. further tests needed.

Answer 245

Significance depends on size of defect. Usually located in the membranous septum below the aortic and tricuspid valves. this is usually in shetland and welsh mountain ponies. Less commonly defects are located in the muscular part of the septum - usually in arabian or Tb breeds. Valid insurance exclusions include any liability from atrial fibrillation and congestive heart failure but should not include sudden cardiac death.

Answer 246

Salmonella, clostridium difficile and perfringens, cyathostomiasis, NSAIDS, antibiotic associated, carbohydrate overload.

Answer 247

Chronic salmonellosis, chronic cyathostomiasis, lawsonia intracellularis, sand NSAID toxicity, granulomatous enteritis, lymphocytic plasmacytic enteritis, multisystemic eosinophilic epitheliotropic disease, dietary, liver, congestive heart failure, renal disease.

Answer 248

PCV, WBC, Serum protein concentration (consider protein loss in face of dehydration), Acid base status (acute colitis), electrolyte abnormalities (hyponatraemia, hypochloraemia, hypokalaemia, (serum BUN - may have pre renal azotaemia), gross appearance of faces, bacterial culture of faeces, toxin analysis, faecal PCR, rectal examination

Answer 249

Anterior enteritis, colitis, peritonitis and intestinal abscessation

Answer 250

Coupled with weak rapid pulse indicates shock,

Answer 251

Abdominal auscultation\Rectal examination Passage of a nasogastric tube - reflux/gas >2 l considered abnormal., abdominal paracentesis - protein and fibrinogen increases, Leukocyte counts increase - acute ischaemia is characterised by a neutrophilia and an increased erythrocytes, gross appearance of fluid, protein >25g/l, cells >5x10^9, cytology, bacteriology culture. Acid base balance, serum electrolytes, plasma fibrinogen, faecul occult blood assay.

Answer 252

Severe, continuous pain showing no or only short duration improvement with analgesia, pulse >60 progressively rising and weakening, progressive cardiovascular collapse, PCV >55 injected or cyanotic mms despite fluids, rectal findings positive for acute abdominal disease, progressive reduction in intestinal motility or continual gastric reflux, increasing abdominal distension, serosanguinous peritoneal fluid with protein >25g/l and WBCs >10x10^9.

Answer 253

Liquid paraffin - common initial treatment of choice for treating simple impactions. \Dicotyl sodium sulfosuccinate - anionic wetting agent with lubricant properties. do not administer with liquid paraffin as systemic absorption of the liquid paraffin may occur. Oral magnesium sulphate - cathartic laxative and acts as an osmotic agent to draw water into the intestine.

Answer 254

polyionic fluids, most practical and cost effective. Isotonic glucose saline - can be used to replace second 50% of a deficit. 8.4% sodium bicarbonate - only if you can assess acid base balance accurately, best to rehydrate with a polyionic solution first, the improved circulation will often correct the acid base deficits without the need for bicarbonate. Hypertonic 7.2% saline - 2 litres of hypertonic saline to temporarily improve circulating volume in cases of ensuing shock, acts by osmotically drawing interstitial fluid into IV space, interstitial deficit that is created must then be corrected by subsequent and immediate IV infusion of large volumes of isotonic fluid.

Answer 255

GLDH - liver specific, peak 1-2 days, AST non liver specific, GGT - liver specific very sensitive for biliary tract disease, AP - non liver specific. Bile acids - to determine if associated with liver function -9% restricted to enterohepatic circulation, increase in serum levels indicates loss of approx >70% hepatic function. Values <20umol rule out livver failure.

Answer 256

Increased NH3 and other false neurotransmitters- results in dull vacant expression, yawning, ataxia, tremors, circling, head pressing, aggression, coagulopathy, petechiae, bilateral laryngeal paralysis.

Answer 257

1. Head. - tone, sensation, symmetry, nasal septum response, forebrain sensation, tongue paresis, pupillary light reflex, swinging light reflex, menace response, palpebral response, nystagmus. 2. Neck & trunk - thoracolaryngeal reflex, local cervical and cervicofacial reflexes, cutaneous trunci refex 3. Perineum - tail tone, anal tone, hypalgesia/hypreflexia of perineal region, tail anus and degrees of urinary bladder paresis and rectal and anal dilatation. 4. Gait and posture - gait and posture, walk down a slope, swing horse around. 5. Autonomous zones. 6. Ancillary aids.

Answer 258

Cervical vertebral malformation, trauma, EHV1 myeloencephalopathy, EPM, west nile virus

Answer 259

type 1 - large, younger horses, various manifestations of developmental orthopaedic disease, vertebral canal stenosis/wedging/angular fixation, often C3-C4 Type 2 - large, older horses, arthritis of caudal cervical vertebrae, compression of spinal cord by bone and soft tissues, grave prognosis

Answer 260

often acute onset symmetrical ataxia & paresis, signs progress rapidly for about 2 days then stabilise. pelvic limbs > thoracic limbs. ataxia & cauda equina syndrome. CSF often xanthocrhomic.

Answer 261

often abortion outbreaks and respiratory disease. Infection of respiratory epithelium causes cell associated viraemia > endothelial infection and ischaemia of CNS microvasculature.

Answer 262

d752 nucleotide polymorphism is significantly associated with outbreaks in which neurological signs are seen. They cause higher levels of viraemia and preferentially infect cd4 lymphocytes > virus transfer to endothelia > relatively uninhibited by virus neutralizing antibodies. Inflammation causes vasculitis of arterioles int he brain and spinal cord and multifocal haemorrhagic myeloencephalopathy.

Answer 263

Early dexamethasone useful. oral antiviral drugS: acyclovir poor bioavailability, pro drugs may be better, prognosis good if horse able to stand throughout disease, improvement within a few days.

Answer 264

Supported by ruling out other conditions, demonstrating xanthochroma, elevated EHV1 protein concentration, identifying or isolating EHV1 from the respiratory tract, buffy coat or CSF, demonstrating a 4 fold increase in serum antibodies.

Answer 265

Equine protozoal myeloencephalitis - Caused by sarcocystic neurona, definitive host is the north american opossum, intermediate hosts - racoon , armadillo. can cause huge variety of CNS signs, focal spinal cord signs are most common.

Answer 266

CSF or serum immunoblot test for antibodies.. Treatment: inhibit enzymes which catalyze reduction of folic acid: sulfonamides & pyremithamine.

Answer 267

Vaccination history, clinical signs, CSF mononuclear plecytosis, serology (IgM antibody capture ELISA), PRNT neutralizing IgG antibody, post mortem immunohistochemistry.

Answer 268

paresis, ataxia, abnormal mentation, fasciculations, increased body temperature, anorexia, may have cranial nerve deficits

Answer 269

Trauma, viral disease, meningitis in foals, hepatic encephalopathy, neonatal hypxoa, leukoencephalomalacia, intracarotid injections, hydrocephalus, epilepsy (rare), neoplasia (rare)

Answer 270

Failure of passive transfer,gram negative organisms, forebrain signs/head held lowered in rigid extension, often not pyrexic, CSF cloudy with low glucose, grave outlook.

Answer 271

response to multiple toxic breakdown products from intestinal degradation including ammonia, amino acids, shortchain fatty acids, mercaptans, imbalance of GABA and glutamate (disrupted glutamate transporter and receptor function).

Answer 272

Rare, caused by fusarium spp mycotoxicosis, usually in mouldy feed, acute forebrain necrosis. very grave outlook.

Answer 273

Almost all recover when water soluble agents are used eg romifidine, but outlook is bad with oil based drugs and suspensions, typically forebrain signs seen.

Answer 274

Polyneuritis equi - chronic granulomatous inflammation of the extradural nerve roots of many peripheral nerves. PNE can present first with cranial nerve signs. disease is progressive and early euthanasia should be considered. Sacral trauma is far more likely. Life may be proloned by use of supportive measures including manual evacuation of the rectum, catheterisation of the bladder.

Answer 275

Rectal examination, abdominal paracentesis (not always that useufl), faecal analysis, haematology (with neoplasia/inflammatory disease - neutrophilia) biochemistry - proteins, fibrinogen, alkaline phosphatase (present in intstinal brush border), liver screen - GLDH and GGT

Answer 276

Serum electrophoresis, oral glucose absorption test (normal result is doubling of glucose then return to baseline by 4-6 hours) , less than 15% absorption is strongly suggestive of Severe SI pathology. Rectal biopsy - a standard uterine cervical biopsy is suitable, abdominal ultrasound - transrectal and trans abdominal, faecal occult blood, nuclear scintigraphy, laroscopy or exploratory laparotomy.

Answer 277

In cases where there is a high suspiscion of cyathostome infestation, then using either a single dose of moxidectin or the older regime of repeating 5 day fenbendazole followed by ivermectin on day 6 at ten day intervals for three treatments. may also be prudent to administer steroids concurrently to minimise inflammation associated with any worm death/emergence.

Answer 278

1. Fasting glucose and insulin levels 2. oral glucose tolerance test (starved of concentrates for 12 hours, water removed 1 hour prior to test, glucose administered, blood glucose levels and insulin tested prior to and after administration at various increments - should double within two hours and reduce to normal levels within 6). 3. combined intravenous glucose and insulin tolerance test

Answer 279

Control calories. judicious exercise. treat underlying cause eg ECD with pergolide. Feed with low glycaemic index should be used. complete starvation should be avoided. Care re risk of hyperlipaemia. Rich grass should be avoided. restricted grazing and exercise. grass hay good but may be variable in carbohydrate/sugar content therefore best to have it analysed. soaking hay may also reduce soluble CHO as it gets trapped in the water. If further feeding is required then use other low GI foods eg sugar beet, alfalfa chaff, short chopper alfalfa. Antioxidant therapies eg Vit e, Vit C. Excercise may improve insulin sensitivity. Can be difficult if active laminitis. placing an animal out to grass in theory is beneficial but can be difficult at high risk times of year. grazing muzzles possible. night grazing may be an option.

Answer 280

Primary /psychogenic polydipsia, ECD, primary renal disease

Answer 281

Urinalysis. USG - 1.020-1.050 normal. Isothenuric 1.009-1.014. Hyposthenuric 75% tubular function loss. protein levels: albumin may decrease with glomerular diseases or tubular diseases. Electrolytes following may indicate renal disease; sodium decrease, chloride decrease, calcium increase, potassium increase, phosphate decrease.

Answer 282

Sodium decrease, chloride decrease, phosphate decrease, calcium increase, potassium increase.

Answer 283

Rectal examination, evaluate size of kidneys and presence of pain on palpation. Ultrasonography: evaluate size and echogenicity of kidneys, fractional excretion of electrolytes eg to demonstrate increased sodium loss, renal biopsy.

Answer 284

water deprivation tests - normal horse should concentrate urine >1.025 within 12-24 hours. stop test if >5% loss of body weight. Some horses with prolonged PD will have medullary washout. ADH stimulation test - animals which fail to concentrate after both WDTS possibly have diabetes insipidus. use adh analogue to distinguish between central and nephrogenic (desmopressin)

Answer 285

Due to the overproduction of propriomelanocortin peptides from pars intermedia. the resultant increase in adrenocorticotrophin levels, coupled with the possible potentiating efects of other POMC peptides on ACTH causes dysregulated cortisol secretion.

Answer 286

Hirsutism, Hyperhidrosis, laminitis, lethargy, fat redistribution, predisposition to infections, weight loss, PU PD - hyperglycaemia, polyphagia, blindness, seizures.

Answer 287

Observing hirsuitism. Basal glucose, Basal insulin. Basal ACTH - sensitivity 82-100% specificity 78%. Seasonal variation. DST - administer dexamethasone. 50-100% sensitivity and specificity. TRH response test - sample basal cortisol, inject TRH, cortisol sample at 30 mins post injection. +ve if >66% increase at 30 minutes. DST/TRH combined response test - +ve if >66% at 30 mins post TRH.

Answer 288

Seasonal effect - due to photoperiod. false positives. higher levels in september. (especially post DST and basal ACTH)

Answer 289

good attention should be paid to feeding, dentistry, anthelmintic regimes and the early detection of clinical abnormalities, clipping the excesively long haircoat may be advantageous, regular farriery, continued exercise if no orthopaedic disease, treat with PERGOLIDE - 85% efficacy. Cyproheptadine and trilostaine - very poor efficacy.

Answer 290

Reflex / upper motor neurone bladder e.g EHV, EPM. Paralytic lower motor neuron bladder e.g polyneuritis equi, EHV1 , trauma, non neurogenic - inflammatory eg cystitis, detrusor atony, neoplasia, ectopic ureter, breeding trauma.

Answer 291

Acute tubular necrosis, toxicity due to drugs, aminoglycosides, NSaids, polymixin B, Hb, Mb, vitamins, Heavy metals, aconrs

Answer 292

Immune mediated e.g purpura haemorrhagica, bacterial mediated e.g strep E coli.

Answer 293

ultrasonography to evaluate size appearance and echogenicity of kidneys, fractional excretion of electrolytes - Increased Na and Po4 common with ART, must be carried out before fluids initiated or results are invalid. measure GFR - excellent measure of renal function, measure endogenous or exogenous compounds. Biopsy - more use in chronic RF.

Answer 294

Fluid therapy - balanced fluids with regular monitoring of electrolyte status, care regarding overhydration and oedema formation, monitor urination. Ideally creatinine should be decreased by atleast 30% in the first 24 hours. may need continued electrolyte supplementation at least in short term.

Answer 295

Fluid therapy for 24-48 hours, identify any primary abnormalities e.g urinary stones, pyelonephritis, correct any electrolyte or acid base abnormalities, small frequent and varied meals encourage appetite, avoid high calcium foodstuffs e.g alfalfa, calcium is excreted from the kidney in the horse, poor renal function leads to hypercalcaemia, increase CHO intake e.g using oils but maintain adequate protein, anabolic steroids may stimulate appetite.

Answer 296

Urethral tears, cystitits/UTI/urolithiasis, idiopathic renal haematuria (arabs), neoplasia eg bladder urethra, penis sheat, NSAIDS, vaginal varicosities in mares, exercise induced haematuria, non urinary systemic disease - haemolysis, acute myopathies, coagulopathies.

Answer 297

Throughout urinartion: kidney, ureters, bladder beginning of urination: distal urethra End of urination: proximal urethra and bladder neck Hburia and Mburia differentiation requires special techniques.

Answer 298

Pyrethrins or pyrethroid shampoos/sprays/powders, two applications at 14 day intervals

Answer 299

coat brushings, hair pluck/skin scrape, swabs, fungal culture, aspirates, impression smears, biopsy/punch biopsy, allergy testing - intra dermal, serum, photographs.

Answer 300

A seasonal dermatitis caused by onchcerca cervicalis microfilaria. parasite transmitetd by culicoides sp and other biting insects. type 1 and 3 hypersensitivity reactions.

Answer 301

Management of skin lessions, corticosteroids, immunotherapy/desensitisation treatment offered by a number of labs, fly repellents (permethrin), preventing midges biting, oil based liquids eg benzyl benzoate, stabling at dusk and dawn/rugs hoods , insect proof stables with meshes, fans/wing prevent midges landing, avoid rivers/water/woodland

Answer 302

An autoimmune disease characterised by an exfoliative dermatitis, results from a type 2 hypersensitivity du to autoantibodies directed against the cell membrane of epidermal cells. inflammation around the chestnut, ergot and coronary band is common. biopsy required.

Answer 303

Dermatophilus congolensis.

Answer 304

An ulcerating cutaneous granulating nodule or wound caused by the larvae of habronema muscae, habronema majus. Disease has several forms; opthalmic habronemiasis, cutaneous habronemiasis - larvae penetrate wet areas of the face. Diagnosis made on impression smears and washes. Topical /oral ivermectin. control of muscid flies.

Answer 305

skin condition of the unpigmented distal limb. aetiopathogenesis uncertain but IgG and C3 portion of complement have been detected by direct immunoflueorescence in vessel walls. unpigmented skin involvement suggests role of UV light although this condition is not thought to be a true photosensitisation. clinical signs include erythema, oozing and crusting of the white areas of the distal limbs, can appear very similar to mud fever. Biopsies reveal leucocytoclastic vasculitis, vessel wall necrosis and thrombosis.

Answer 306

lymphangitis - inflammation of cutaneous lymphatics usually but not always secondary to a bacterial infection obtained via a small cut/abrasion. Cellulitis - wound infection that rapidly spreads along tissue planes, caused by a number of bacteria, commonly affects the limbs. Vasculitis - inflammatory reaction involving the blood vessel walls, commonly immune mediated involving type 1 and type 3 reactions. Purpura haemorrhagica - an immune mediated vasculitis associated with recovery of an upper respiratory tract infection most commonly caused by M protein antigen of strep equi equi. immune complexes deposited in the walls of peripheral blood vessels increase vascular permeability and cause oedema, primarily of the limbs.

Answer 307

Surface of clitoris, with single central fossa. can harbour CEM (taylorella equigenitalis), klebsiella pneumoniae and pseudomonas aeruginosa.

Answer 308

Beta haemolytic streptococci, E coli, other enterobacter. Less common : pseudomonas, klebsiella.

Answer 309

Culture. Cytology - using a uterine flush or double guarded swab and stain with diff quick - presence of neutrophils >1/10 epithelial cells indicates endometritis. Endometrial biopsy - often performed if other tests inconclusive - use endometrial or rectal forceps, easiest to perform in oestrus but easier to interpret during dioestrus, can diagnose endometritis, periglandular fibrosis, cystic glandular distension

Answer 310

Progesterone: dioestrus/pregnancy Anti mullerian hormone: GCT Testosterone/inhibin: raised in 50% of GCT chromosomal karyotyping

Answer 311

Pregnancy!, silent heat - cycle progresses as normal but mare does not show signs of oestrus, failure of luteal regression: PGF2a from uterus fails to cause luteolysis at day 15, early embryonic loss: mare conceives but embryo lost before first scan takes place, dioestrus ovulation: occasionally ovulation takes place in mid dioestrus, CL formed too late to be lysed at day 15.

Answer 312

endometrial transluminal adhesions endometrial cysts endometrosis- non inflammatory chronic pathology endometritis - either veneral disease, chronic uterine infection or persistent mating induced endometritis

Answer 313

Uterine infusion for several days with antibiotics, topical wash of clitoral fossa wth 2% chlorhexidine, pack external genitals with nitrofurazone or chlorhexidine ointment. clitoral infections can be hard to treat, consider clitorectomy /sinusectomy inv ery difficult cases.

Answer 314

``` pneumovagina urovagina parturition copulation veterinary procedures. ```

Answer 315

Short cycle mare with PGF2 to bring into oestrus. Administer Oxytocin IV or IM. lavage uterus with sterile hartmanns solution. infuse uterus with appropriate antibiotics such as neomycin or penicillin, repeat treatment for 3-5 days. correct any predisposing conformational abnormalities, maintain good hygiene.

Answer 316

Free intra uterine fluid accumulates and clinical signs and diagnosis are as for CUI. reatment involves oxytocin, flushing and antibioticcs but must be started after sperm have reached oviduct and before the fertilized ovum descends into the uterus (4 hours and 5 days respectively)

Answer 317

Artificial control of photoperiod start at december to initiate transitional period by end of february - provide natural or artificial light from 8am to 10pm. Onset of normal cyclicity during the transitional breeding season can be hastened by - altrenogest (progesterone) orally for 10-15 days, HCG iv, Exoggenous GnRH - deslorelin implant or twice daily injections of buserelin.

Answer 318

Interovulatory interval of 18-24 days, oestrus lasts 3-8 days, dioestrus 14-18 days, follicles grow during oestrus. usualy one follicle will become dominant and ovulate >40mms. There is also a smaller mid dioestrus wave of follicle growth. PGF@a is released by endometrium at about day 15 if no embryo is detected. day - ovulation, CH forms day 5 - fully functional CL day 15 - CL lysed by PGF2a one or two dominant follicles develop day 18 standing oestrus begins day 0 ovulation

Answer 319

Progestogens - oestrus occurs 4-5 days after withdrawal. Prostaglandin F2 - used to lyse a CL and allow mare to return to oestrus, must be between 5 and 14 days to respond. OEstradiol - not available in UK HcH - LH like activity, can hasten ovulation of a mature follicle, GnRH - given to cause ovulation of a mature follicle, use IM 6 hours before service, ovulation is expected within 24 hours.

Answer 320

primary - head/acrosome defects, bent mid pieces, proximal cytoplasmic droplets, tail stump defects. associated with spermatogenesis. secondary - acquired in duct system- distal cytoplasmic droplets/kinked tails, tertiary - in vitro damage - detached heads, kinked tails

Answer 321

Scan mare daily until dominant follicle reaches 35-40mm, EO grade 3 or 4, cervix fully relaxed, no free fluid in uterus, give induction agent hcg or deslorelin, order semen for arrival following day. scan mare to check not ovulated, inseminate semen, save a few drops for examination.

Answer 322

Exmaine mare daily as for chilled AI but use deslorelin implant as induction agent to give a shorter likely ovulation interval. if implanted at 6pm , should ovulate the next but one day between 8am and 12pm but ideally keep scanning in the meaintime to monitor progress. inseminate within 6 hours of ovulation before or after is fine but because predicting ovulation time is difficult, insemination usually takes place when CH seen. may consider fixed time AI at 36 and 48 hours post deslorelin if two doses semen available at no extra cost.

Answer 323

Equine viral rhinopneumonitis (EHV1) - transmitted via respiratory tract. usually occurs between 5 months and term. fresh foetus often with placental membrnes. Equine viral arteritis - severe systemic illness in dam which may be followed by abortion 7-10 days later. fever, lethargy, depression, conjunctivitis, oedema. respiratory or venereal spread. Bacterial Fungal - small and emcaited, mycotic placentitis foals can survive. aspergillus. Twinning - responsible for 6%.prevalent 8-10 months. Placental insufficiency - endometrial fibrosis/scarring in older mares. hypoxia. umbilical cord defects - such as torsion. most common cause of abortion.

Answer 324

Treat if retained more than 3 hours. use Oxytocin IV or IM every 15 minutes, usually expelled within 30 mins. If retention is >8 hours - beware of the sequelae: laminitis and endometritis. use more aggressive therapy including anti inflammatories, broad spec antibiotics, exercise. th allantochorionic space may be infused with 10-12 L dilute povidone iodine solution or saline. this stimulates uterine contractions.

Answer 325

``` Rhabdomyolysis botulism equine motor neurone disease hyperkalaemic periodic paralysis hypocalcaemia myasthenia gravis ```

Answer 326

rhabdomyolysis, tetanus, hypocalcaemia, shivering and stiff horse syndrome.

Answer 327

toxicoinfectious botulism. intiaily they appear alert, then progression is associated with paresis, stilted gait and most prominent and generalised muscle trembling, ptosis and decreased tail tone is frequently evident, dysphagia is present despite a normal appetite, may show slow PLr, ileus, constipation and urine retention, death is caused by respiratory paralysis or complications such as pneumonia.

Answer 328

Acetylpromazine, sodium benzylpenicillin, procaine penicillin, antitoxin, hydrogen peroxide in wound.

Answer 329

Blood biochemistry - muscle enzyme levels, electrolyte levels, vitamin E and selenium levels, genetic testing for type I PSSM, electromyography, fractional excretion of electrolytes

Answer 330

EXcessive glycogen > lactic acid & o2 produced > coagulative necrosis > futher muscle hypoxia > presevents muscular relaxation. excessive glycogen > lactic acid and O2 radicals > coagulative necrosis of Muscle.

Answer 331

Elevations in the serum levels of enzymes creatinine kinase, aspartate aminotransferase and lactate dehydrogenase. the degree of increase reflects the degree of muscular damage but not the degree of clinical signs. CK is most specific for skeletal muscle damge. CK rises first and disappears first followed by LDH, then AST. CK peaks at 2-12 hours after onset and may reach 100,00IU/L or more. LDH peaks at approx 15 hours and may reach several thousand. AST peaks at 24 hours and may reach many thosuand.

Answer 332

often treated with a combination of topical washing with pevidine followed by drying and packing the penis with gentamicin cream (klebsiella) or 1% silver nitrate (pseudomonas) daily for 1-2 weeks. Taylorella - wash penis daily for 2-5 days with chlorhexidine followed by topical application of nitrufurazone or penicillin ointment.

Answer 333

Signs may vary from none at all to severe systemic illness including fever, depression, filling of the lower limbs, conjunctivitis with periorbital oedema, nasal discharge, urticarial rashes, and oedematous plaques and ventral oedema. Infected mares may abort 7-10 days later. Infection is via the respiratory or venereal route. virus localises in the accessory sex glands of stallions . shedder stallions are always seropositive but not all seropositive stallions are shedders. Diagnosis by virus detection in nasopharyngeal swabs, heparinised blood, semen and posibly urine.

Answer 334

Increased PCV/normal plasma protein + dehydration and protein loss. hypnatraemia - may occur if voluntarily drinking - relative water excess. Hypokalaemia - depleted K stores through diarrhoea. Metabolic acidosis - decreased Hco3= Hypoglycaemia in endotoxaemia Hyperfibrinogenamia - acute inflammatory protein Colitis - neutropaenia, also in endoxotaemia lymphopaenia in endotoxaemia

Answer 335

Measure fasting insulin and glucose (Increased insulin - IR, increase glucosed - IR/type 2DM.) Oral glucose tolerance test - should double within two hours, and reduce to normal levels within six hours). I:G ratio 0.03:0.5 - IR Combined IV glucose & insulin tolerance test For ECD - dexamethasone suppression test TRH response test, BASAL ACTH.

Answer 336

azotaemia, hyperkalaemia, hyponatraemia, hypochloraemia and metabolic acidosis

Answer 337

Equine influenza - from 4-6 months of age for first, then 2nd 4-6 weeks later, then 3rd 5 months later. Equine herpes virus - EHv1 and EHV4, initial course 4 weeks apart and boosters every 6 months. Tetanus - all horses should be vaccinated for tetanus - 2 vaccines 1 month apart then boosters every 2 -3 year. Equine viral arteritis Streptococcus equi - 2 vaccines 4 weeks apart. booster every 3-6 months. reduces signs only.

Answer 338

Biological transmission via culicoides sp of the african horse sickness virus (orbivirus) -. Extension of range of known vectors, importation of animals incubating disease, batton effect from C imicola to C putans., increased activity and number offvectors, facilitation of viral replication within vector. Pulmonary form - most likely to occur in the UK - pyrexia, acute severe dyspnoea, death within a few hours of clinical signs. Cardiac form - pyrexia, subcutaneous oedema of head and neck, death within 4-8 hours of pyrexia. Mixed form - cardiac form progresses to pulmonary form or vice versa. Horse sickness fever - often subclinical , low mortality. Diagnosis by ELISA PCR. Notifiable

Answer 339

A flavivirus - primary transmission cycle between wild birds and culex sp mosquitoes, horses are dead end hosts. Signs: pyrexia, behavioural changes, cranial nerve deficits, impaired vision, ataxia , muscle fasciculations, can progress to complete paralysis of one or more limbs, rapid improvement within first week. diagnosis by serology, PCr, immunohistochemistry. Notifiable.

Answer 340

it is a lentivirus - mechanical transmission between horse by transfer of infected blood or blood products. insct vectors eg biting flies and very rarely mosquitoes, infected blood products, contaminated equipment eg veterinary, dental. clinical signs = recurrent pyrexia, inappetance, depression, ventral oedema, anemia, thrombocytopaenia, petechiation. Diagnosis by coggins agar test, elisa.

Answer 341

Powerful blepharospasm produced by contraction of orbicularis muscle may be overcome using a palpebral nerve block. proxymetacaine squirted onto the cornea will effectively anaesthetise the ocular surface should this be required. the supraorbital or frontal nerve may be blocked at thesupraorbital foramen. This removes sensation from the medial 2/3 of the upper lid allowing easier opthalmic exam as the horse cannot feel the lid being manipulated.

Answer 342

Primary uterine inertia - usually due to voluntary suppression caused by disturbance. Secondary uterine inertia, usually caused by foetal malpresentation. Failure of abdominal expulsive effort obstruction of the birth canal Fetopelvic disproportion is rarely a problem in mares.

Answer 343

Transverse presentation, uterine torsion malposture of living foetus which cannot be corrected rapidly, oversized foetus, maternal pelvic deformities.

Answer 344

not recommended unless the mare has a life threatening injury or illness and is unable to carry the foal to term. induction pf parturition is associated with a very poor prognosis for survival of the foal and significantly increased risk of complications in the mare. Assess concentrations of electrolytes in the milk - Ca, Na, K+. Use oxytocin.

Answer 345

Pre exercise should have CK <100iu/l, no more than doubling of CK at 2-6 hours, return to baseline of CK at 24 hours, no more than 50% increase in AST at any point, no clinical signs of stiffness.

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