Equine Exam Flashcards by Ale Bostroem

The predilection site of OCD in the equine hock is

a. The central part of the distal intertarsal joint
b. The medial malleolus
c. The talocalcanei joint
d. Sustentaculum tali

b. The medial malleolus

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The proper name of the skyline-view for the examination of the equine carpus is

a. Dorsoproximal-dorsodistal oblique view
b. Dorsoproximal-palmarodistal oblique view
c. Caudoproximal-craniodistal oblique view
d. Palmarolateral view

a. Dorsoproximal-dorsodistal oblique view

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The exclaiming time needed to see an osteophyte formation on equine radiograph is

a. 1-2w
b. 2-3w
c. 3-5w
d. 4-7w

c. 3-5w

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The proper name of the “oxpring’ view for the examination of the navicular bone is:

a. Palmaroproximal-palmarodistal oblique view
b. Dorsoproximal-palmarodistal oblique view
c. Caudoproximal-craniodistal oblique view
d. Palmarolateral view

b. Dorsoproximal-palmarodistal oblique view

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The most common site of sub-chondral bone cyst in equine is:

a. Medial femoral condyle
b. Lateral femoral condyle
c. Medial trochlea
d. Lateral trochlea

a. Medial femoral condyle

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Where can a Birkenlund fracture be found in a horse?

a. In the dorsal recess of the fetlock joint
b. In the palmar/plantar recess of the fetlock joint
c. In the dorsal recess of the…

b. In the palmar/plantar recess of the fetlock joint

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OCD location in hock?

DIRT-distal intermediate ridge of the tibia dorsal in the talocrural joint

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Which statement is false?

a. Phenothiazines should be used with care in stallions
b. Phenothiazines are not usable in shock patients
c. Midazolam is an adequate drug to treat tetanus in horses
d. Phenothiazines are given most frequently to colic horse to reduce visceral pain

d. Phenothiazines are given most frequently to colic horse to reduce visceral pain

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Which is false?

a. Ketamine cannot be given to a standing horse to relieve pain
b. Lidocaine can be given to a standing horse to relieve pain
c. Lidocaine administered IV can have adverse effects on the CNS of a horse
d. Neuropathy can develop due to inadequate positioning during anaesthesia

a. Ketamine cannot be given to a standing horse to relieve pain

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Which is true?

a) Left laryngeal hemiplegia more common in ponies
b) Tracheal collapse is more common in thoroughbreds
c) Guttural pouch tympany typically affects older horses
d) Lymphoid hyperplasia typically affects young horses

d) Lymphoid hyperplasia typically affects young horses

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Which is false regarding the Winslow herniation (hernia foraminis omentalis) in horses?

a. Cribbing and aerophagia are predisposing factors
b. At late, intolerant stage of colic, the animal is apathic
c. Mostly the ileum or jejunum is involved
d. This kind of herniation is also called right dorsal displacement of the large colon

d. This kind of herniation is also called right dorsal displacement of the large colon

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In the colic horse surgery, the large colon enterotomy should be created to rinse out the content of the

a. Dorsal colon
b. Ventral colon
c. Pelvic flexure
d. Ligamentum caeco-colicum

c. Pelvic flexure

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The advised surgical method to treat upward fixation of the patella in horses is:

a. Lateral femoro-patellar ligament desmotomy
b. Medial femoro-patellar ligament desmotomy
c. Intermediate femoro-patellar ligament desmotomy

b. Medial femoro-patellar ligament desmotomy

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How do you suture the trachea of a horse?

a. Min 1 layer
b. Min 2 layers
c. Min 3 layers
d. Min 4 layers

b. Min 2 layers

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How can you perform a more or less “specific” anaesthesia of the origin of the suspensory ligament (m. interosseus medius) in the front limb?

a) High palmar nerve block
b) Lateral palmar nerve block
c) Carpometacarpal joint anaesthesia
d) N. medianus anaesthesia

b) Lateral palmar nerve block

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How can you anaesthetize the origin of the suspensory ligament (interosseus medius) on the hind leg?

a. With the abaxial sesamoidean block
b. With the low six point block – it will be anaesthetized within 30 min
c. With the deep branch anaesthesia of the lateral plantar nerve
d. With the high plantar nerve anaesthesia

c. With the deep branch anaesthesia of the lateral plantar nerve

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Intermittent lameness horse

a) Lameness occurring in comitions? because of the degeneration of the femoral muscles plus haemoglobinuria
b) Moving disability of the HLs occurring in loading disappearing at rest, with unknown origin
c) Lameness of sport horses receding for loading, caused by the thrombosis of the terminal aorta or iliac arteries

b) Moving disability of the HLs occurring in loading disappearing at rest, with unknown origin

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Intermittent lameness symptoms horse

a) Movement disorders in one of the HLs when loaded, disappearing after 20mins of resting
b) Feel wobbly when loaded, lameness of the HLs, disappearing after half an hour
c) Movement disorder of the FLs or in one of the HLs, when competing, disappearing after a short time of resting.

a) Movement disorders in one of the HLs when loaded, disappearing after 20mins of resting

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Osteoporosis horse

a) Thinning of the bone compacta due to the disturbance of Ca-metabolism
b) Hereditary, breed disposition, compacta incr / medullary cavity decr
c) Thickening of the tubular bones due to the disturbance of the mineral supply

a) Thinning of the bone compacta due to the disturbance of Ca-metabolism

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Osteoporosis CS horse

a) Thickening of the tubular bones, sensitivity to pressure, lameness
b) Genu valgum, locomotion disorder, exostoses on the leg bones
c) Retardation, spontaneous fractures, ruptures, not viable

c) Retardation, spontaneous fractures, ruptures, not viable

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Hyperplastic osteopathy (acropachia) horse

a) Symmetrical deformation of the distal leg bones, in connection with diseases of the digestive tract
b) Congenital acropachia, intensive pain to pressure, locomotion disorder  akinesia
c) Metabolic disturbance of the leg bones with pain of unknown origin, advance in application of glucocorticoids

a) Symmetrical deformation of the distal leg bones, in connection with diseases of the digestive tract

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Laminitis, diffuse aseptic/definition

a) Degeneration/necrosis of horny matter of the hoof due to circulatory disturbance, exungulation, deformation of the distal phalanx
b) Damage of the corium of the hoof, disconnection between corium and horny matter of the hoof due to circulatory disturbance, change in the structure of the hoof
c) Degeneration/necrosis of the horny matter of the hoof and distal phalanx, local circulatory disturbance

b) Damage of the corium of the hoof, disconnection between corium and horny matter of the hoof due to circulatory disturbance, change in the structure of the hoof

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Diffuse aseptic laminitis etiology

a) Overfeeding in fat animals, consequence of allergy/atopia, influence of burden
b) Malnutrition, complication of diseases, immune/autoimmune origin
c) Malnutrition, complication of diseases, in postparturient period, influence of burden

c) Malnutrition, complication of diseases, in postparturient period, influence of burden

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Diffuse aseptic laminitis nutritional origin

a) Carbohydrate and protein rich nutrition, fungus contaminated hay
b) Carbohydrate rich nutrition, low-protein/fibre rich nutrition, fungus contaminated corn fodder
c) Easy fermentation, carbohydrate and fiber rich nutrition, fungus contaminated corn fodder

b) Carbohydrate rich nutrition, low-protein/fibre rich nutrition, fungus contaminated corn fodder

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Diffuse aseptic laminitis complication of disease a) Diseases of stomach, enteritis, autoimmunopathies b) Gastroenteritis, inflammations – toxical enteropathies, hepatosis c) Serous-hemorrhagic gastritis, strangles, glomerulonephritis

b) Gastroenteritis, inflammations – toxical enteropathies, hepatosis

Diffuse aseptic laminitis symptoms a) Gradual deterioration in a week, pain during movement, horny matter of the hoof warm/intensive pain to pressure, oedema on the distal part of the legs b) Hoof warm/intensive pain to pressure, warm and painful edema on the leg, intermittent claudication c) Develops in 12-24h, general symptoms, waddling, locomotor disorder, lying position, warm and painful hoof, pulsation of the fetlock artery

c) Develops in 12-24h, general symptoms, waddling, locomotor disorder, lying position, warm and painful hoof, pulsation of the fetlock artery

Acute diffuse aseptic laminitis treatment a) Elimination of the causative, soft littering, complete rest, fixing of the hoof, plastering of the hoof, warm pack, hepatin, flunixin-meglumine b) Elimination of the causative, peat littering, complete rest, fixing of the hoof, ice pack, glucocorticoids c) Soft littering, only moderate movement, ice pack, strong analgesic, phenylbutazone, prednisolone

c) Soft littering, only moderate movement, ice pack, strong analgesic, phenylbutazone, prednisolone

Which is false regarding the Winslow herniation (hernia foraminis omentalis) in horses? a. Cribbing and aerophagia are predisposing factors b. At late, intolerant stage of colic, the animal is apathic c. Mostly the ileum or jejunum is involved d. This kind of herniation is also called right dorsal displacement of the large colon

d. This kind of herniation is also called right dorsal displacement of the large colon

Which statement(s) is/are typical of the strangulation obstruction of the SI in horses? a. There is secondary dehydration of the content in the large colon b. Secondary cecal impaction develops c. The stomach is dilated d. A and C are correct

d. A and C are correct

Which structure cannot be palpated certainly at rectal exam in the horse? a. Ventral taenia of caecum b. Duodenal ligament c. Ligamentum lati uteri d. Ligamentum renolienale

b. Duodenal ligament

Which is false concerning a colic horse? a. The degree of pain mostly correlates with the severity of the disease b. Dehydration can only be in the indolent phase c. Electolyte loss is significant

b. Dehydration can only be in the indolent phase

Which is not characteristic of the large colon obstipation in horses? a. Sometimes can cause severe colic signs b. The obstipation can always be treated conservatively c. Can be easily diagnosed via rectal exam

b. The obstipation can always be treated conservatively

In the colic horse surgery, the large colon enterotomy should be created to rinse out the content of the a. Dorsal colon b. Ventral colon c. Pelvic flexure d. Ligamentum caeco-colicum

c. Pelvic flexure

Which statement is true? a. In direct inguinal hernia, the SI escape into the SC space of the scrotum b. The indirect inguinal hernia is more common than the direct one c. Both d. None

b. The indirect inguinal hernia is more common than the direct one

Large colon impaction in adult horses is usually treated with a) IV neostigmine injections every 2h b) Lidocaine constant rate infusion c) Repeated nasogastric tubing with water and electrolytes d) Intramuscular metoclopramide injections every 12 hours

c) Repeated nasogastric tubing with water and electrolytes

On rectal examination, you palpate a segment of distended bowel without taeniae. The intestinal segment you are palpating is most likely: a) Small colon or small intestine b) Pelvic flexure or right ventral colon c) Base of caecum or right dorsal colon d) Pelvic flexure or small intestine

d) Pelvic flexure or small intestine

In which case is rectal admin. inappropriate? a. Dysphagia b. Lockjaw c. Reflux d. Diarrhea

d. Diarrhea

What is the location of the base of the caecum in a normal adult horse? a. Left paralumbar fossa b. Right paralumbar fossa c. Left ventral abdomen d. Right ventral abdomen

b. Right paralumbar fossa

During rectal examination of normal adult horses: a. The caudal pole of both kidneys can be palpated b. The caudal wall of the stomach can be palpated c. The ascending duodenum can be palpated d. The ventral taenia of the caeum can be palpated

d. The ventral taenia of the caeum can be palpated

When is rectal application NOT appropriate? a. Lock-jaw b. Diarrhea c. Dyspnea d. Reflux

b. Diarrhea

Rectal enema is used in case of obstruction of

Small colon

Colic (real) a) Pain syndromes because abdominal digestive organs hurt b) Abdominal disease c) Painful unrest syndrome in horses

a) Pain syndromes because abdominal digestive organs hurt

Colic-like symptoms causes a) Meningitis, COPD, estrus b) Rabies, urinary diseases, genital diseases c) Encephalon oedema, pneumonia, Lyme-disease

b) Rabies, urinary diseases, genital diseases

Predisposing factor for colic disease a) Slow motion of stomach, intestines predisposed to meteorism, innervation of digestive organs predisposed to spasms b) Undigested substance empty from stomach, small intestinal motility is strong, substance of large intestines quickly goes off with strong motility c) Cannot vomit, dislocation of intestines can easily evolve disposition to vagotony

c) Cannot vomit, dislocation of intestines can easily evolve disposition to vagotony

Parasitic cause of colic a) Toxocara equi, Bunostomumum magnum infection b) Strongylosis, Ascariosis c) Toxacariosis, Strongyloidosis

b) Strongylosis, Ascariosis

Viral and bacterial causes of colic a) Salmonellosis, Clostridiosis, Arteritis b) Anthrax, rabies, pyelonephritis c) Rabies, lyme disease, salmonellosis

a) Salmonellosis, Clostridiosis, Arteritis

Mechanical and physical causes of colic a) Bad teeth, oesophagus obturation, sand in stomach b) Tooth abrasion failure, pylorus obstruction, isthmus of intestines c) Chewing insufficiency, sand in intestines, strange object in intestinal system

c) Chewing insufficiency, sand in intestines, strange object in intestinal system

Colic disease pathological dislocations a) Internal hernias, torsion of small intestines, colon dislocation b) Stomach, small intestines, colon torsion c) Diaphragmatic hernia, duodenum torsion, ileum torsion

a) Internal hernias, torsion of small intestines, colon dislocation

Colic symptoms causing agents a) Atropine, clavulanic acid, diazepam b) Amitrase, arekolin c) Organophosphorous compounds, amitrase, chlorpromazine

c) Organophosphorous compounds, amitrase, chlorpromazine

Agents causing shock in the colic horse a) Pain, fluid loss, endotoxaemia b) Sympathetic nervous system activity, dislocation of intestines, septicaemia c) Rupture of stomach and intestine, spasm of intestines, dyspepsial digestion insufficiency

a) Pain, fluid loss, endotoxaemia

Reason for pain in the colic horse a) Development of shock, paralysis of intestines, dislocation of intestines b) Excitement of mechanoreceptors, release of mediators, local circulation insufficiency c) Stop of stomach function, dilatation of intestines, dyspepsial digestion insufficiency

b) Excitement of mechanoreceptors, release of mediators, local circulation insufficiency

Reason for hypovolaemia in the colic horse a) Rupture of the stomach/intestines, ileus, colon obstipation b) Stomach meteorism, small intestinal atonia, colon disposition c) Ileus, mucosa inflammation, pain

a) Rupture of the stomach/intestines, ileus, colon obstipation

Results of local circulation insufficiency in colic a) Accumulation of lactic acid, uremia extrarenale, liver insufficiency b) Metabolic acidosis, necrosis of intestines, shock c) Dominance of anaerobic oxidation, atonia of intestine, intestine displacement

b) Metabolic acidosis, necrosis of intestines, shock

Reasons for endotoxaemia in colic a) Increase of gr+ bact, circulation disorder of intestinal wall, typhlocolitis b) Bact incr/collapse, ischaemia of intestinal wall, ileus c) Collapse of gr- bact, incr of lipoproteins, disorder of intestinal absorption

c) Collapse of gr- bact, incr of lipoproteins, disorder of intestinal absorption

Results of endotoxaemia in colic a) Toxic effect to red/white blood cells, haemolysis, anaemia b) Toxic effect to intestinal cells, intestine motility incr, hypertension c) Vasoactive materials incr, toxic effects to blood cells, clotting tendency incr

c) Vasoactive materials incr, toxic effects to blood cells, clotting tendency incr

Main diagnostics of colic worrying a) How often, length of time, seriousness b) Seriousness, intermittent/permanent, freq of tenesmus c) Nature, seriousness, existence of diarrhea

a) How often, length of time, seriousness

Additional diagnostic exam in the colic horse a) Rectal exam, blood enzyme activity, exam of abd content b) Rectal exam, abd joggle, lab blood exam c) Rectal exam, exam abd content, exam bact culture of intestines

b) Rectal exam, abd joggle, lab blood exam

Colic horse blood exam in practical circumstances a) Qual blood count, Ht, TP b) RBC/WBC count, qual blood count c) Ht, TP, WBC count (hematocrit tube)

c) Ht, TP, WBC count (hematocrit tube)

Colic horse therapy a) Release of convulsions, naso-gastric tube, cecal puncture, liquid therapy b) Electrolyte therapy, gastric lavage w/ Marek pipe, purgative enema c) Abd centesis, cecal puncture, gastric lavage

a) Release of convulsions, naso-gastric tube, cecal puncture, liquid therapy

Reasons for referral to clinic for colic horse a) If the colic symptoms still exist after 1h, if infusion on spot not possible, pulse 40/min permanently b) Colic despite therapy/meteorism, clinical/rectal findings refer to a serious disease, pulse >50/min permanently, no good conditions for the therapy c) Active intestinal murmue/freq flatulation, colic worrying despite of negative rectal findings, and if you can’t use nasogastric tubing

b) Colic despite therapy/meteorism, clinical/rectal findings refer to a serious disease, pulse >50/min permanently, no good conditions for the therapy

Colic tx in hospital a) Part clinical/lab exams, spasmolytics, abdominocentesis b) Blood test, abd x-ray, US, bact coproscopy c) Emergency interventions, fluid and electrolyte replacement, laparotomy

c) Emergency interventions, fluid and electrolyte replacement, laparotomy

Laparotomy indications in colic a) Possibility of ileus in rectal findings, repetitive meteorismus despite puncture, severe alterations in clinical values b) CS of gastric-intestinal rupture, as long as clinical signs of ileus c) Gastric overload, irreversible shock status, peritonitis

a) Possibility of ileus in rectal findings, repetitive meteorismus despite puncture, severe alterations in clinical values

Colic direct emergency interventions a) Gastric lavage, spasmolytics, shock therapy b) Gastric lavage, cecal puncture, hypovolaemic chock prevention c) Gastric overload therapy w/ physostigmin, meteorismus tx w/ rectal puncture, shock therapy

b) Gastric lavage, cecal puncture, hypovolaemic chock prevention

Sedatives used in colic cases a) Detomidine, medeteomidine b) Detomidine, xylazine c) Detomidine, flunixin-meglumine

b) Detomidine, xylazine

Colic tx in case of endotoxaemia a) Endotoxin antiserum, carbacol, detomidin b) Endotoxin antiserum, medetomidine, metoclopramide c) Polymixin-B sulphate, flunixin meglumine, pentoxifillin

c) Polymixin-B sulphate, flunixin meglumine, pentoxifillin

Acute gastric dilatation pathogenesis a) High firm feed  pyloric spasm  dilatation  rupture b) Great amount of feed  motility decr  colic  vomiting  metabolic alkalosis c) Gastric content firm  dilution, lactic consistence  dilatation  regurgitation

a) High firm feed  pyloric spasm  dilatation  rupture

Acute gastric dilatation etiology a) Difficulty to digest feed + lack of water b) Highly fermentable feed + hard working after feeding c) Overfeeding + weather change

b) Highly fermentable feed + hard working after feeding

Acute gastric dilatation CS a) Severe colic, highly tense abd, rectal finding: gastric dilatation b) Sudden onset, severe colic, neg rectal finding, regurgitation c) Recurrent colic, strong int sounds, rectal grinding: dilated stomach

b) Sudden onset, severe colic, neg rectal finding, regurgitation

Acute gastric dilatation Tx a) Detomidine, xylazine, gastric lavage b) Physostigmine, neostimin, flunixin meglumide c) Noraminophenason, drotaverin, gastric lavage

c) Noraminophenason, drotaverin, gastric lavage

Gastric rupture CS a) Colic decr, shock, sweating in spots, typical abdominocentesis b) Signs of severe abd pan, fever, bloody abd puncture c) “Sitting dog posture”, regurgitation, bloody disturbed abd puncture

a) Colic decr, shock, sweating in spots, typical abdominocentesis

Acute gastric dilatation complications a) Gastric torsion, gastritis, infl of small int b) Gastric meteorismus, gastric ulcers, gastritis c) Laminitis, hemorrhagic gastritis, typhocolitis

b) Gastric meteorismus, gastric ulcers, gastritis

Acute gastritis etiology a) Gasterophilus, allergy, toxication by Datura Stramonium b) Parascariosis, Stachybotris atra toxicosis, gastric overload, FB c) Bad dentition, strongylosis, aflatoxins, allergy

a) Gasterophilus, allergy, toxication by Datura Stramonium

Serous-hemorrhagic gastritis etiology a) Feed w mycotoxins, lactic acid incr b) Intake of immature maize, allergy c) Mouldy hay, water with high nitrate cc

b) Intake of immature maize, allergy

Serous-hemorrhagic gastritis CS a) Serous gripes, “wineflake-like” gastric content, enteritis b) Gripes perspiration, “wineflake like” gastric content, shock/death c) Prostrate behaviour, “wineflake like” gastric content, laminitis

a) Serous gripes, “wineflake-like” gastric content, enteritis

Acute gastritis CS a) Anorexia, polydipsia, gape, breath smells sour-lushious, mild gripes b) Gripes, stinky breach, retching, abd dilation c) Freq gripes, stinky breath, regurgitation, left flank dilatation

a) Anorexia, polydipsia, gape, breath smells sour-lushious, mild gripes

Chronic gastritis etiology a) Mastication disorder, after acute gastritis, mainly colts b) Bad dentition, air-swallow, after acute gastritis c) Fault in feeding, incr prod of gastric acid, mainly cold blooded horses

c) Fault in feeding, incr prod of gastric acid, mainly cold blooded horses

Acute gastritis Tx a) Fasting, laxation, bethanechol b) Gastric lavage, laxation, physostigmine c) Gastric lavage, fasting, linseed-slurry

c) Gastric lavage, fasting, linseed-slurry

Stomach parasite infection a) Trichostrongylus, gasterophilus, habronematosis b) Habronematosis, gasterophilus, parasoaridosis c) Gasterophilus, habronematosis, strongylidosis

a) Trichostrongylus, gasterophilus, habronematosis

Signs of gastric parasite infestation in horse a) Anaemia, fatigue, threadworm in feces b) In colts, mild growth, irregular fur c) Colic, slimming, diarrhea

c) Colic, slimming, diarrhea

Gasterophilosis a) Gasterophilus, acute, gribes like gastritis, caused by gasterophilus larvae b) Serous bloody gastritis caused by gasterophilus larvae, freq gribes c) Gasterophilus caused by larva of equine gasterophilus causing chronic gastritis

c) Gasterophilus caused by larva of equine gasterophilus causing chronic gastritis

Gastric ulcer etiology a) Stress, NSAIDs, faulty nutrition b) Stress, steroid anti-inflamm drugs, grazing c) Fasting, NSAIDs, grazing

a) Stress, NSAIDs, faulty nutrition

Gastric ulcers symptoms a) Anorexia, weight loss, laying much, mild-moderate colic symptoms b) Wight loss in spite of good appetite, anaemia c) Anorexia, serious colic symptoms, anaemia

a) Anorexia, weight loss, laying much, mild-moderate colic symptoms

Catarrhal enteritis etiology a) Vagotonia, cold water/food, meterological front b) Acute gastritis, int. obst., parasympathicotonia c) Diathesis, larval migration, enteritis

c) Diathesis, larval migration, enteritis

Colic important lab exams a) Ht, total plasma protein, plasma electrolytes, acid-base, peritoneal fluid b) Ht, qual hemogram, composition of blood protein, plasma Ca/P c) Hgb/Ht, quan hemogram, plasma crea/urea, urine density, urine protein

a) Ht, total plasma protein, plasma electrolytes, acid-base, peritoneal fluid

Catarrhal enteritis therapy a) Walking, No-spa inj, sigmosain IV b) Neostigmine, walking, use of laxative c) Anticonvulsive drug IV, enema w tepid water, warm stable

b) Neostigmine, walking, use of laxative

Catarrhal enteritis symptoms a) Serious colic/struggling, stomach rupture, high mortality rate b) Serious/moderate colic in seizures, fast process, advantageous prognosis c) Mild/moderate, recurrent colic, diarrhea, lasts for 2-3d

c) Mild/moderate, recurrent colic, diarrhea, lasts for 2-3d

Drugs to increase peristalsis in horses a) Stigmosan, konstigmin b) Neostigmine, flunixin-meglumine c) Xylazine, neostigmine

a) Stigmosan, konstigmin

Laxatives for horses a) Mg sulfate, linseed mucin, detomidine inj b) Paraffin, mg sulfate, stigmosan ing c) Neostigmine, linseed mucin, drotaverin

b) Paraffin, mg sulfate, stigmosan ing

Strongyloidosis horse a) Bloody water like faeces, colic, weakness b) Occult inf, symptoms in case of impairment of resistance c) In foals, resp symptoms, retarded growth

a) Bloody water like faeces, colic, weakness

Parascariosis a) In intestines of suckling foals, catarrhal enteritis, small intestinal obturation, wasting/cachexia b) In stomach, SI, occult inf in adult horses c) Enteritis in foals, ileus, larval migration/hepatic trauma

a) In intestines of suckling foals, catarrhal enteritis, small intestinal obturation, wasting/cachexia

Removal of roundworm a) Ivermectin, mebendazole, tetramizol b) Fenbendazole, oxibendazole, ivermectin c) Tiabendazole, mebendazole, tetramizol

b) Fenbendazole, oxibendazole, ivermectin

Viral enteritis of foals a) Adenovirus, coronavirus, in sep foals, melena, dehydr, poor health b) Adenovirus, coronavirus, enteralgia, 3-6m old foals c) Rotavirus + resistance decr at 1-2m

c) Rotavirus + resistance decr at 1-2m

Typical of acute proximal enteritis a) In older horses, sudden medium (average)/serious colic, duodenojejunitis + gastritis, pancreatitis b) Young foals after separation, infl of SI, melena for days c) Suckling foals, in studs in larger nr mortality

a) In older horses, sudden medium (average)/serious colic, duodenojejunitis + gastritis, pancreatitis

Causes of acute proximal enteritis a) Fungus toxin of feed, allergy b) Unknown, w horse feed or fodder fed horses, inf cause c) In foals, when fungus toxins in milk, fungus toxicosis

b) Unknown, w horse feed or fodder fed horses, inf cause

Pathogenesis of acute proximal enteritis a) GI motility incr  melena  dehyr  die in 3-4d b) Enteritis hemorrhagica, melena, recovery after tx c) GI motility  GI paralysis  ileus, enteritis, enterotoxaemia, often bad outcome

c) GI motility  GI paralysis  ileus, enteritis, enterotoxaemia, often bad outcome

Acute proximal enteritis a) Paralysis of intestines  reflux  gastric dilatation  nasogastric reflux  loss of fluid and electrolytes, enterotoxaemia, shock b) Diarrhea  hypovolaemia  shock, endotoxaemia c) Enteritis  diarrhea  lactacidaemia  metabolic acidosis  death

a) Paralysis of intestines  reflux  gastric dilatation  nasogastric reflux  loss of fluid and electrolytes, enterotoxaemia, shock

Acute proximal enteritis CS a) Colic, powerful GI sounds, sunken abdomen, diarrhea, exsiccation b) Fever colic – depression, poor health, cyanosis, round abd, regurgitation, gastric lavage: weak yellowish stinking content c) Average/serious colic, meteorismus, melena, dehydr, shock

b) Fever colic – depression, poor health, cyanosis, round abd, regurgitation, gastric lavage: weak yellowish stinking content

Lab results of acute proximal enteritis a) Ht 0.3-0.4, TPP 30-34g/L, leukocytes <3.0g/L, lactacid >5.2mmol/L b) Ht 0.6-0.8, leukocytes: leukopenia, lactacidaemia: metabolic acidosis c) Ht 0.6-0.8, neutropenia: neutrophilia, hypochloremia, metabolic alkalosis – acidosis

c) Ht 0.6-0.8, neutropenia: neutrophilia, hypochloremia, metabolic alkalosis – acidosis

Acute proximal enteritis tx a) Gastric lavage, antispasmodics, intense fluid and electrolyte therapy, flunixin meglumine b) Antispasmodics, analgesic drugs w increase GI motility, sucralfate c) Activated charcoal, paraffin, physostigmine inj

a) Gastric lavage, antispasmodics, intense fluid and electrolyte therapy, flunixin meglumine

Ddx of acute proximal enteritis from other diseases of SI a) Colic in the beginning, then apathic, the abdominal probe is open (opaque?), yellowish w high leukocyte content b) Slight/average colic symptoms permanently, abd probe is translucent, yellowish w low leukocyte conent c) Apathic, abd probe is opaque, yellowish w low leukocyte content and high erythrocyte content

a) Colic in the beginning, then apathic, the abdominal probe is open (opaque?), yellowish w high leukocyte content

Acute typhlocolitis features a) Sudden appearance of colic accompanied by writhing, meteorism, death within 12-24h b) Sudden appearance of appenditis, colicitis, endotoxaemic shock, high mortality c) Sudden appearance of colic in horses kept on pasture, paralytic ileus, meteorism

a) Sudden appearance of colic accompanied by writhing, meteorism, death within 12-24h b) Sudden appearance of appenditis, colicitis, endotoxaemic shock, high mortality

Acute typhlocolitis incidence and predisposing factors a) Springtime grazing, driving into rich pastures, forage liveration of scatol, stress b) Hospitalization, abd surgery, fasting, stress, ABs c) During transport of horses kept in stable, stress, fumonisin intake

b) Hospitalization, abd surgery, fasting, stress, ABs

Acute typhlocolitis study of origin a) Bacterial/virus inf of unknown origin, mycotoxins, stress b) Unknown (colitis x), multicause, Cl difficile inf/prop, dysbacteriosis, salmonellosis, endotoxin prolif, stress, NSAIDs c) Chlamydophila inf – lib of endotoxins, feeding alfalfa without transition, feeding new corn

b) Unknown (colitis x), multicause, Cl difficile inf/prop, dysbacteriosis, salmonellosis, endotoxin prolif, stress, NSAIDs

Acute typhlocolitis pathogenesis a) Enteritis – intestinal peristalsis – severe colic – ileus – shock b) Intestinal peristalsis incr – diarrhea – severe colic – necrosis – peritonitis – death c) Prolif of toxin forming Clostridium, starvation – rising of intestinal pH, dysbiosis, endotoxaemia/bacteremia, damage of mucosa, diarrhea, shock

c) Prolif of toxin forming Clostridium, starvation – rising of intestinal pH, dysbiosis, endotoxaemia/bacteremia, damage of mucosa, diarrhea, shock

Acute typhlocolitis consequences a) Fever, endotoxaemia, dehydration, hypovolaemia, metabolic acidosis, shock b) Writhing, watery/bloody diarrhea, state of shock c) Writhing, ileus – meteorismus, dyspnea, blood circulation insufficiency

a) Fever, endotoxaemia, dehydration, hypovolaemia, metabolic acidosis, shock

Acute typhlocolitis symptoms a) Anorexia, fever, colic – languor, profuse diarrhea, meteorismus, intestinal sounds incr – intestinal atonia, shock b) Writhing, profound colic, sweating, chronic diarrhea, recovery after AB tx c) Chronic colic, hemorrhagic inf of int/diarrhea, sunken flanks, uptight abdomen, intestinal peristalsis, hypovolaemic shock

a) Anorexia, fever, colic – languor, profuse diarrhea, meteorismus, intestinal sounds incr – intestinal atonia, shock

Acute typhlocolitis lab features a) Ht: 0.3-0.4, TPL 30-34g/L, leukocytes: 0.3g/L, lactate: 5.2mmol/L b) Ht: 0.6-0.8, TP: 80-90g/L, leukocytes: 1.303g/L, lactate: 4mmol/L c) Ht: 0.65, TP: 35g/L, leukocytes: 8.2-5.1g/L, lactate: 20mmol/L

b) Ht: 0.6-0.8, TP: 80-90g/L, leukocytes: 1.303g/L, lactate: 4mmol/L

Acute typhlocolitis adverse outcome a) CRT: 3-4s, pulse: 40-52/min, red conjunctiva, resp: 18-20/min, leukocyte: 2g/L, lactate: 20mmol/L b) CRT: 6s, pulse: 60/min, cyanosis, tachypnoe, leukocyte: 2g/L, lactate: 15-20mmol/L c) CRT: 6s, pulse: 80/min, cyanosis, tachypnoe, leukocyte: 1g/L, lctate: 20mmol/

c) CRT: 6s, pulse: 80/min, cyanosis, tachypnoe, leukocyte: 1g/L, lctate: 20mmol/?

Acute typhlocolitis prevention a) Hospital/general hygiene, only short term food withdrawal before surgery, stress tolerance, giving lincomicin, oxitetracyclin prohibited, probiotics b) AB therapy preventing Clostridium, thorough fasting prior to sx, medical attendance after sx c) Laxatives/fasting before sx, preventing AB therapy before sx, medical attendance after sx

a) Hospital/general hygiene, only short term food withdrawal before surgery, stress tolerance, giving lincomicin, oxitetracyclin prohibited, probiotics

Acute typhlocolitis medical therapy a) Inf against dehydration, lincomicin, probiotics b) Treatment against dehydr, metronidazole, flunixin meglumine, probiotics c) Treating shock and dehydr, OTC, artificial feeding

b) Treatment against dehydr, metronidazole, flunixin meglumine, probiotics (but would not use metronidazole, not needed, use of NSAIDs are controversial, can weaken the mm, can cause colitis itself)

Cause of mechanical ileus a) Enterospasm, obstruction, intestinal paralysis b) Obstruction, compression, intestinal dislocation, strangulation c) Enterospasm, torsion of ileum, obturation of ileum

b) Obstruction, compression, intestinal dislocation, strangulation

Cause of functional ileus a) Disturbance of intestinal motility, spasmodic colic b) Spasmodic colic, intestinal paralysis c) Long lasting colic, intestinal paralysis

b) Spasmodic colic, intestinal paralysis

Cause of paralytic ileus a) Enteritis, peritonitis, abd sx b) Tetanus, botulism, enterotoxicosis c) Stress, tetanus, sx

a) Enteritis, peritonitis, abd sx

SI obstruction pathogenesis a) Gas and fluid accumulate cranially, intestinal paralysis, protein and fluid loss, int necrosis at place of ileus – peritonitis b) Spastic contraction of intestinal + fluid penetration, meteorism, reflux – gastric dilatation, shock + electrolyte turnover dysfunction c) Bacterial invasions of the place of obstruction – peritonitis, severe colic/rolling – gastric and intestinal rupture

b) Spastic contraction of intestinal + fluid penetration, meteorism, reflux – gastric dilatation, shock + electrolyte turnover dysfunction

SI obstruction CS a) Violent long lasting colic, rectal finding; obstruction, strong intestinal sounds, sunken lumbar region, peritonitis pointing punctuation b) Alternative intestinal colic, negative rectal finding, mild meteorism, diarrhea c) Medium/strong colic, sec gastric contents by nasogastric tube, regurgitation, bicycle inner tube intact at rectal palpation

c) Medium/strong colic, sec gastric contents by nasogastric tube, regurgitation, bicycle inner tube intact at rectal palpation

SI obstruction outcome a) Surgery, spasmolytic in case of obturation, poor prognosis, death in next 48h b) Strong painkiller, spasmolytics, doubtful prognosis, after 3-4d w/out progress – death c) Lg amount of physostigmine in case of obstruction, repeated application, fast recovery after solving the obturation

a) Surgery, spasmolytic in case of obturation, poor prognosis, death in next 48h b) Strong painkiller, spasmolytics, doubtful prognosis, after 3-4d w/out progress – death

Dislocation and strangulation of ileus pathogenesis a) Intestinal motility decr, int secretion incr – fluid/gas incr – circulatory and resp disturbances – dies within 24h b) Compression of vessels – infarct of intestinal wall – damage intestinal wall + pain + hypovolaemia + endotoxaemia – shock c) Compression of arteries in intestinal wall – impairment of supply of int wall – necrosis – toxaemia/bacteraemia – endotoxic shock

b) Compression of vessels – infarct of intestinal wall – damage intestinal wall + pain + hypovolaemia + endotoxaemia – shock c) Compression of arteries in intestinal wall – impairment of supply of int wall – necrosis – toxaemia/bacteraemia – endotoxic shock

SI strangulation ileus causes a) Incarceration of internal hernia, intestinal retroflexion b) Invagination of SI, strangulation of SI c) Torsion of SI, strangulation of SI

c) Torsion of SI, strangulation of SI

SI dislocation ileus causes a) Internal hernia, torsion of SI b) Intestinal torsion, intestinal invagination, thromb-embolic intestinal disease c) Diaphragmatic hernia, intestinal spasm, torsion of SI

a) Internal hernia, torsion of SI

SI torsion causes a) Unequal content of int, colon reflux, disposition because of anatomy b) Int motility incr, colic rolling, disposition because of anatomy c) Forage intake – lactic acid incr – colic rolling – sI torsion

b) Int motility incr, colic rolling, disposition because of anatomy

SI torsion CS a) Weakness, int motility incr, colic, rectal findings; SI strangulation b) Colic/weakness left flank dilatation, rectal findings; place of basic disease c) Severe colic, int sounds decr, reflux, rectal findings; SI like bicycle tube

c) Severe colic, int sounds decr, reflux, rectal findings; SI like bicycle tube

SI torsion outcome a) Sx/ maybe, poor prognosis, death in 24-36h b) Neostigmine, doubtful prognosis, improvement after 24h not expected c) Physostigmine/torsion might resolve as a result of walking, doubtful prognosis, significant mortality

a) Sx/ maybe, poor prognosis, death in 24-36h

SI invagination reasons a) As a result of enteritis, int motility incr, depending on basis of disease/poor prognosis b) Foals have unequal peristalsis + ascariosis, acute/subacute course of disease, doubtful prognosis c) Race horses/sport horses, result of stress, short/favourable course of disease

b) Foals have unequal peristalsis + ascariosis, acute/subacute course of disease, doubtful prognosis

SI invagination CS a) Severe colic, weakness, left flank dilatation, rectal findings; flatulent SI b) Progressive colic, sitting dog posture, rectal findings; flatulent SI c) Mild/mediocre colic, int sounds incr – decr, rectal findings; tense intestines

c) Mild/mediocre colic, int sounds incr – decr, rectal findings; tense intestines

Intestinal stenosis CS a) Periodic colic, subileus, mending/aggravation dyspepsia b) SI obturation, ileus, quick/slow progression c) Occasionally colic/dyspepsia, improving after purgative, recurring diarrhea

a) Periodic colic, subileus, mending/aggravation dyspepsia

Mesenteric abscess a) Foals after strangles, colic of variable intensity, dyspepsia, rectal findings, mostly neg b) Recurrent/mediocre colic, relapse/emaciation, rectal findings; round, size of fist or head, tuberity formula c) Colic in foal after strangles/failure, rectal findings; in pelvis, formula w fluctuating palpation on the right side

a) Foals after strangles, colic of variable intensity, dyspepsia, rectal findings, mostly neg b) Recurrent/mediocre colic, relapse/emaciation, rectal findings; round, size of fist or head, tuberity formula

Grass sickness a) Dyspepsia during pasture, cachexia, disappearing after housing b) Pasturage/after being fed with harshly cut grass, mostly in foal recently separate dfrom mother, encephalo and soinal consequences c) Neurotoxin – GI myoparalysis, pastured horse

c) Neurotoxin – GI myoparalysis, pastured horse

Acute form of grass sickness symptoms a) Gastric dilatation/reflux, paralytic ileus, dysphagia, lameness b) Alimentary symptoms, colic, heavy diarrhea, dehydration c) Fever, intestinal motility incr, diarrhea, colic, dehydration  shock

a) Gastric dilatation/reflux, paralytic ileus, dysphagia, lameness

Primary caecal meteorism etiology a) Feeding with Lucerne – lactic acid incr – paralysis of cecal musculature – gas accumulation b) Feeding huge amount of papilionaceae without gradation, fermentation incr, seasonal c) Feeding w forage – VFA/lactic acid incr – gas production incr

b) Feeding huge amount of papilionaceae without gradation, fermentation incr, seasonal

Primary caecal meteorism pathogenesis a) Gas acc – intestinal dilatation – int paralysis – int rupture b) Fermentation of CH/cecum – lactic acid + gas prod incr – int paralysis + int dilatation – shock c) Cecal dilatation – spastic pain – atonia – fluid entrance – dyspnea – shock

b) Fermentation of CH/cecum – lactic acid + gas prod incr – int paralysis + int dilatation – shock

Primary caecal meteorism symptoms a) Heavy solid, drum like dilatation of right flank, dyspnea, rectal palp; dilated cecum b) Heavy colic, heavy symmetric dilatation of the abdomen, dyspnea, cyanosis, rectal palp; dilated cecum c) Weak/average colic, dilated flanks, dyspnea, cyanosis, rectal palp; dilated cecum/colon

a) Heavy solid, drum like dilatation of right flank, dyspnea, rectal palp; dilated cecum

Primary cecal meteorism outcome, method of tx a) Paracentesis just farthest case, physostigmine gives good result in high doses, antichock if therapy, outcome: generally good b) Cecal paracentesis, without this, danger of death is very high (trocarisation?) c) Physosyigmine + Nospa inj, walking, fasting, reacts quickly to therapy

b) Cecal paracentesis, without this, danger of death is very high (trocarisation?)

Chronic caecal impaction causes and pathogenesis a) Old horses, rough fibre feed, intestinal peristalsis decr, stasis/impaction of int content, endotoxamia, peritonitis, int rupture b) Rough fibre feed, chewing disorder, older age, int peristalsis decr, stasis/impaction of int content – colic – wasting, int rupture c) Fibery/chopped hay – VFA incr – intestinal atony – intestinal content compaction – colic – wasting

b) Rough fibre feed, chewing disorder, older age, int peristalsis decr, stasis/impaction of int content – colic – wasting, int rupture

Caecal impaction symptoms a) Medium/recurring colic, anorexia, failure, rectal palp; hard resistance at right upper region of abdomen b) Colic nervousness, no defecation, wrong general health, rectal palp; faeces filled resistance at left upper 3rd of abdomen c) Weak/constant colic, small berrylike feces, or no defecation, rectal palp; hard, feces filled resistance at right middle region of abdomen

a) Medium/recurring colic, anorexia, failure, rectal palp; hard resistance at right upper region of abdomen

Caecal impaction tx and outcome a) Starving, cachectic, enema, good recover change b) Inf therapy, spasmolytics, deep enema, yeast mash through centesis, result; doubtful, danger of rupture c) Physostigmine inj many repeats, enemas, mechanical removal of feces, recover in days after tx

b) Inf therapy, spasmolytics, deep enema, yeast mash through centesis, result; doubtful, danger of rupture??

Colon impaction causes a) Rough fibre feed, bad teeth, old horses b) Rough fiber feed, overfeeding, chewing disorder c) Eating of litter, milling industry by-product, intestinal atony, intestinal paralysis, old horses

a) Rough fibre feed, bad teeth, old horses

Colon impaction pathogenesis a) Intestinal paralysis – int content impaction/stasis, dehydr – hypovolemic shock b) Int motility decr – disturb of int content passage/stasis, int atrophy c) Hardening/acc of int content, ileus – colic/dehydr – shock

c) Hardening/acc of int content, ileus – colic/dehydr – shoc

Colon impaction predilection sites a) Ampulla of dorsal colon, colon transversum, caeco-colic opening b) Caeco-colic opening, colon transversum, ampulla of dorsal colon c) Flexura pelvina, ampulla of dorsal colon, colon transversum

c) Flexura pelvina, ampulla of dorsal colon, colon transversum

Colon impaction CS a) Constant/mediocre colic, “rocking horse” bearing, apathy, “seize up” faeces, rectal palp; hard faeces filled intestinal parts b) Fluctuating power colic, “dog-like sitting”, rare defecation of hard balls, rectal palp; faeces filled intestinal parts c) Medium/stronger colic from time to time, fast pulse rate, dilated abdomen, rectal palp; faeces filled colon

a) Constant/mediocre colic, “rocking horse” bearing, apathy, “seize up” faeces, rectal palp; hard faeces filled intestinal parts

Colon impaction outcome, prognosis a) Impaction of ampulla of dorsal colon: fast recover, colon transversum: doubtful, intestinal rupture is unfavourable b) Good results with early recognition, advanced stage; doubtful, intestinal atrophy, infaust c) Good rxn to proper tx, the ampulla of the dorsal colon is susceptible to pressure necrosis

b) Good results with early recognition, advanced stage; doubtful, intestinal atrophy, infaust

Large colon obstipation tx a) Paraffin oil poured into horse mouth, enema, neostigmine b) MgSO4 poured into horse mouth, repeated neostigmine inj c) Flunixin-meglumine to treat endotoxaemia, fluid therapy, paraffin oil, istizin

c) Flunixin-meglumine to treat endotoxaemia, fluid therapy, paraffin oil, istizin

Small colon obstipation causes a) Small rough plant parts get into small colon – convulsions, intestinal passage stops b) Many rough plantal fibres get into small colon – intestinal atony – thickening of int content c) Small colon fills with thickened content – int dilatation/atony – int passage stops

c) Small colon fills with thickened content – int dilatation/atony – int passage stops

Small colon obstipation CS a) Slight/serious colic, faintness/lack of appetite, defecation faiure, rectal findings; hard deces balls in small colon b) Slight colic, few hard faecal balls, rectal findings; hard, thickened faeces in small colon c) Permanent colic changing in its intensity, total lack of food uptake/faintness, no defecation, rectal findings; hard fecal balls in small colon

c) Permanent colic changing in its intensity, total lack of food uptake/faintness, no defecation, rectal findings; hard fecal balls in small colon

Small colon obstipation tx a) Intestinal tamponade, laxative oil/salts, mechanical removal b) Enema, repeated IM physostigmine inj, walk c) Fasting, sucralfate inj, intestinal tamponade, istizin

a) Intestinal tamponade, laxative oil/salts, mechanical removal

Meconium colic a) Intestinal obturation in newborn foal caused by chorion b) Meconium accumulation in small colon of newborn foals c) Convulsion/obstipation caused by meconium in the newborn foal

b) Meconium accumulation in small colon of newborn foals

Meconium colic causes a) Lengthened gravidity, lg amount of meconium, difficult birth b) Retained placenta, lack of colostrum, premature birth c) Lack of colostrum, lengthened gravidity, tight pelvis

c) Lack of colostrum, lengthened gravidity, tight pelvis

Meconium colic symptoms a) Defecation attempts, bad general state b) Hard/pitch like feces, permanent colic, anuria c) Pitch-like feces, colic, faintness

a) Defecation attempts, bad general state

Meconium colic tx a) Enema, istizin, im physostigmine inj b) Mechanical removal of meconium, enema, paraffin oil given through nasal tube c) Enema, laxative oil/salt poured into foals mouth, mechanical removal of meconium

b) Mechanical removal of meconium, enema, paraffin oil given through nasal tube

Mechanical ileus of large colon causes a) Intestinal obturative ileus b) FB gets into int / spastic ileus c) Conglobatum, enteroliths, phytotrichobezoars/obturative ileus

c) Conglobatum, enteroliths, phytotrichobezoars/obturative ileus

Mechanical ileus of large colon CS a) Long lasting course, colic, intestinal sounds incr, defecation decr, coprological investigation, loosened colon b) Course lasts 1-2d, colic, int paralysis, meteorism, rectal findings; int wall oedema, causing thing is touchable c) Fatal fast course, colic, meteorism, shock, rectal findings; oedematous colon filled by gas

b) Course lasts 1-2d, colic, int paralysis, meteorism, rectal findings; int wall oedema, causing thing is touchable

Forms of large colon dislocation ileus a) Torsion, thrombo-embolic enteropathy, angle refraction b) Angle refraction/retroflexion, torsion, large intestinal exclusion caused by spleen-kidney ligament c) Retroflexion, torsion, intestinal obturation/compression

b) Angle refraction/retroflexion, torsion, large intestinal exclusion caused by spleen-kidney ligament

Large colon dislocation etiology a) Motility of large colon incr because of enteritis, rolling, anatomic disposition b) LI/meteorismus, irritation of int wall – int motility incr, suddenly moving c) Unequal fullness of large colon, suddenly powerful moving (plica colica) anatomical disposition

c) Unequal fullness of large colon, suddenly powerful moving (plica colica) anatomical disposition

Large colon torsion pathogenesis a) Compression of int veins – circ decr in lg areas – hypovolaemic + endotoxaemic shock b) Int motility incr – diarrhea – fluid loss – hypovolaemic shock c) Torsion/compression of vessels – local circulation insuff – int necrosis – endotoxaemia/bacteraemia

a) Compression of int veins – circ decr in lg areas – hypovolaemic + endotoxaemic shock

Large colon torsion CS a) Powerful colic, hard intestinal sounds, bad general health, rectal findings; place of torsion can be tangled as a gross band b) Continuous colic thrashing, bloat, alarming general health, rectal finding; oedema infiltration of int wall is typical c) Hard colic + int motility incr, bloat, bad general health, rectal finding; torsion is tangled

b) Continuous colic thrashing, bloat, alarming general health, rectal finding; oedema infiltration of int wall is typical

Large colon torsion outcome a) Cannot solve with surgery, mortality within 1d b) Sx rarely successful, physostigmine inj can help, mortality within 2-3d c) Sx can be successful within 8h, otherwise death within 1d

c) Sx can be successful within 8h, otherwise death within 1d

Thrombo-embolic intestinal disease a) A thrombosis/embolism in wall of colon/mesenterium caused by strongylus vulgaris larvae b) Colic disease caused by Strongylus vulgris roundworm c) Hypermotility – large intestine displacement colic caused by roundworm larvae

a) A thrombosis/embolism in wall of colon/mesenterium caused by strongylus vulgaris larvae

Thrombo-embolic intestinal disease etiology a) Roundworm migration in intestinal wall – blood supply decr – intestinal wall oedema/necrosis – peritonitis/shock b) Embolism in intestinal artery – blood supply decr – colic, int wall oedema/necrosis – peritonitis/shock c) Strongylus vulgaris infection – intestinal vessel thrombosis – intestinal paralysis – paralytic ileus – shock

b) Embolism in intestinal artery – blood supply decr – colic, int wall oedema/necrosis – peritonitis/shock

Thrombo-embolic intestinal disease CS and outcome a) Colic, meteorismus, paralytic ileus, roundworms in feces, rectal findings; LI bloating, physostigmine inj, prognosis doubtful b) Light/medium colic, meteorismus/diarrhea, rectal findings; LI filled w gas, strongylus eggs in feces, surgery, prognosis doubtful c) Sudden serious colic, bloat, paralytic ileus symptoms, rectal findings; not typical, tx palliative, mortality within 1d

c) Sudden serious colic, bloat, paralytic ileus symptoms, rectal findings; not typical, tx palliative, mortality within 1d

Rectum rupture etiology a) Amateur rectal finding/covering b) Rectal finding, obstipation c) Amateur covering/colic tx, intestinal torsion

a) Amateur rectal finding/covering

Rectum rupture/intestinal wall rupture consequences a) Hard colic, paralytic ileus, blood flow from the rectum, peritonitis, sx ineffective, death within 2-5d b) Painful worrying, blood from rectum, septicaemia/endotoxaemia, death within 2-3h in case of perforation c) Colic worrying, blood from rectum, defecation disorder, injury can be successfully treated even in case of perforation

b) Painful worrying, blood from rectum, septicaemia/endotoxaemia, death within 2-3h in case of perforation

Rupture of rectum / mucosal injury effects a) Colic restlessness, fatigue/weakness, bleeding from rectum, surgery useless, death in 2-3d b) Defecation painful, feces covered with blood, worsening condition, untreatable c) Bleeding during rectal palpation, pain, wound has to be stitched, prognosis good/unstable

b) Defecation painful, feces covered with blood, worsening condition, untreatable c) Bleeding during rectal palpation, pain, wound has to be stitched, prognosis good/unstable

Rupture of rectal wall tx a) Conservative therapy in simple cases, sx + conservative therapy in more complicated cases, untreatable in case of perforation b) Always sx, can help even in case of complete rupture of rectal wall c) Conservative tx is long, but useful except if complete perforation, in that case prognosis is uncertain

a) Conservative therapy in simple cases, sx + conservative therapy in more complicated cases, untreatable in case of perforation

Chronic enteritis, cyathostomiasis tx a) Fenbendazole, moxidectin b) Ivermextin, moxidectin c) Mebendazole, ivermectin

a) Fenbendazole, moxidectin

Chronic enteritis etiology a) Granulomatous enteritis appears usually in horse older than 15y b) Multisystemic eosinophil epitheliotrop disease causing lesions in gut mucosa and skin c) Proliferative enteropathy caused by Lawsonia intracellularis and appears in horses older than 15y

b) Multisystemic eosinophil epitheliotrop disease causing lesions in gut mucosa and skin

Pathomechanism of colic. What is not typical? a) Hypovolaemia b) Hyperthermia c) Endotoxaemia d) Disseminated intravascular coagulopathy

b) Hyperthermia

Causative agent of equine proliferative enteropathy? a) E. coli b) Lawsonia intracellularis c) Clostridium difficile d) Clostridium perfringens D

b) Lawsonia intracellularis

Aetiology of acute gastric dilation in horses? a) Poorly digestible feed + lack of water b) Highly fermentable feed + hard work after feeding c) Overfeeding with hay + weather front changes d) Sand-containing food + weather front changes

b) Highly fermentable feed + hard work after feeding

Acute primary gastric dilation/treatment/horse? a) Gastric lavage by tubing, spamolytics, iv. Fluid and electrolyte replacement, flunixin meglumine (analgesia) b) Analgesics, mobilisers, sucralfate, iv. Fluid and electrolyte replacement c) Mineral oil, activated charcoal, sennoside, iv. Fluid and electrolyte replacement d) Diet coke, lidocaine, acepromazine

a) Gastric lavage by tubing, spamolytics, iv. Fluid and electrolyte replacement, flunixin meglumine (analgesia)

Large colon torsion/outcome? a) Can't be solved by surgery, always fatal outcome within one day b) Operation rarely successful, physostigmine inj. otherwise death within 2-3 days c) Operation can be successful within 8 hours, without surgery: death d) Specific body rotation in general anaesthesia can be solution

c) Operation can be successful within 8 hours, without surgery: death

Dysphagia/causes/horse? a) E.g. blister beetle toxicosis, mandibular trauma, cyst of the soft palate b) E.g. guttural pouch mycosis, retropharyngeal abscess, cleft palate c) E.g. Dorsal displacement of soft palate, sinusitis, hypertriglyceridemia d) Equine motor neuron disease, herpesvirus infection, West Nile virus infection

b) E.g. guttural pouch mycosis, retropharyngeal abscess, cleft palate

Cause of paralytic ileus? a) Enteritis, peritonitis, abdominal surgery (postoperative stage) b) Tetanus, botulism, enterotoxicosis, herpes c) Stress, organic phosphorous ester toxicosis d) Intestinal intussusception, chantaridin toxicosis

a) Enteritis, peritonitis, abdominal surgery (postoperative stage)

Clinical signs of acute proximal enteritis/horse? a) Colic, strong GI sounds, sunken abdomen, diarrhoea, dehydration b) Colic depression, poor general status, reflux, distended small intestinal loops on US c) Mild/moderate colic, meteorism, melaena, dehydration, shock d) Loss of appetite, weight loss, recurrent fever

b) Colic depression, poor general status, reflux, distended small intestinal loops on US

Oesophageal obturation/treatment/horse? a) Trocarisation of the caecum if necessary, dipyrone, xylazine b) Dipyrone, xylazine, trying to remove the solid food by hand if it is located behind the pharynx c) Oxytocin, butylscopolamine, xylazine, oesophagostomy if other methods of removal fail d) Neostigmine, lidocaine, liquid paraffin

c) Oxytocin, butylscopolamine, xylazine, oesophagostomy if other methods of removal fail

Grass sickness/horse/cause? a) Salmonella sp. b) Cl. tetani c) Cl. botulinum d) Groundsel

c) Cl. botulinum

Grass sickness/horse/clinical signs? a) Obstipation, nasogastric reflux, ptosis, muscle fasciculations b) Diarrhoea, reflux, miosis c) Reflux, nystagmus, muscle fasciculations d) Obstipation, nystagmus, dysphagia

a) Obstipation, nasogastric reflux, ptosis, muscle fasciculations

Spasmodic colic/symptoms? a) Severe colic/rolling, danger of gastric rupture, high mortality rate b) Mild/moderate colic in attacks, negative rectal findings, fast course, favourable outcome c) Mild/moderate, recurrent colic, diarrhoea, rectal finding: distended intestines d) Poor performance, recurrent

b) Mild/moderate colic in attacks, negative rectal findings, fast course, favourable outcome?

Esophageal obturation in horses/etiology: a) Dry chopped feed b) Solid pieces of feed (apple, potato, sugar beet) c) Abnormal position of the ligamentum botalli d) Most commonly secondary to other problems

b) Solid pieces of feed (apple, potato, sugar beet)

Esophageal obturation/symptoms/horse: a) Dysphagia due to secondary pharyngeal paralysis, regurgitation, colic b) Esophageal spasm, retching, regurgitation, aspiration pneumonia c) Inability to swallow, esophageal paralysis, secondary laryngeal paralysis d) Swollen neck, ptyalism

b) Esophageal spasm, retching, regurgitation, aspiration pneumonia

Mycotic stomatitis of horses/aetiology? a) Fusariosis, actinomycosis b) Cryptococcosis, aflatoxicosis c) Candidiasis, satratoxicosis d) Aspergillosis, trichomoniasis

c) Candidiasis, satratoxicosis

Grading of gastric ulcers/horse: a) 0-4 b) 0-5 c) 0-10 d) a-d

a) 0-4

Stomatitis of horses/viral and fungal origin/causes? a) Vesiculovirus, candidiasis, satratoxicosis b) Aphtovirus, herpesvirus, candidiasis c) Vesiculovirus, satratoxicosis, crptococcus neoformans d) Herpesvirus, rotavirus, adenovirus

a) Vesiculovirus, candidiasis, satratoxicosis

Laxatives for horses? a) Magnesium sulfate, neostigmine, sennoside b) Mineral oil, magnesium sulfate, sodium sulphate (Na) c) Mineral oil, magnesium sulfate, carbachol d) Diet coke, charcoal

b) Mineral oil, magnesium sulfate, sodium sulphate (Na)

Cleft palate in horses? a) Signs: dysphagia, nasal discharge with food particles b) Complications: decreased weight, diarrhoea, aspiration pneumonia c) Diagnosis: radiography d) Treatment: none

a) Signs: dysphagia, nasal discharge with food particles

Oesophageal obturation/prognosis/horse? a) Mostly unfavourable b) Mostly favourable c) Always fatal outcome d) Poor prognosis

b) Mostly favourable

Real colic is? a) A painful syndrome of the abdominal digestive organs b) All diseases causing abdominal pain c) A syndrome in horses characterised by pain and unrest d) A painful syndrome of the digestive organs

a) A painful syndrome of the abdominal digestive organs

Esophageal obturation/etiology/horse: a) Primary; dry, chopped food, secondary; other esophageal diseases b) Primary; sharp metallic objects, secondary;primary gastric obturation c) Primary; foreign bodies, poor dentition, secondary; mycotic innervation disorder due to inflammation of guttural pouch d) Primary; esophageal paralysis, secondary; reflux due to gastric ulcer

a) Primary; dry, chopped food, secondary; other esophageal diseases

Colitis aetiology/horse? a) Lawsonia intracellularis, Salmonella, E. coli b) Metronidazole, lincomycin, Streptococcus zooepidemicus c) E. coli, salmonella, carbohydrate overload, Aspergillus, microsporon d) Salmonella, certain antibiotics, blister beetle

c) E. coli, salmonella, carbohydrate overload, Aspergillus, microsporon

Stomatitis of horses/viral and fungal origin/which statement it NOT true? a) Can be caused by vesiculovirus, Candida albicans b) Can be caused by aphtovirus, herpesvirus, Trichophyton mentagrophytes c) Can be caused by vesiculovirus, Stachybotris atra d) Can be caused by vesiculovirus, candidiasis, stachybotryotoxicosis

b) Can be caused by aphtovirus, herpesvirus, Trichophyton mentagrophytes

Oesophageal obturation/most common complication/horse? a) Angina pharynges b) Secondary gastric dilation c) Pharyngeal paralysis d) Aspiration pneumonia

d) Aspiration pneumonia

Equine gastric ulcer/treatment/horse? a) Spasmolytic, flunixin meglumine b) H2 antagonist, proton pump inhibitor, sucralfate c) Mineral oil, proton pump inhibitors, NSAID, H2 antagonist d) Phenylbutazone, sucralfate, aluminium hydroxide

b) H2 antagonist, proton pump inhibitor, sucralfate

A physiological arrhythmia in horses is a) 2nd degree AV block b) 3rd degree AV block c) Atrial premature complex d) Ventricular premature complex

a) 2nd degree AV block

In a normal ECG, P-wave is followed by: a) T wave b) R wave c) Q wave d) S wave

c) Q wave

Normal in horses: a. Atrial fibrillation b. Ventricular fibrillation c. 2nd degree AV block d. Arrhythmia

c. 2nd degree AV block

The cardiovascular system can’t be examined with: a. ECG b. Ultrasound c. Phonocardiography d. Endoscopy

d. Endoscopy

Point of maximum intensity for mitral valve a. Right ICS 6 b. Left ICS 6 c. Left ICS 5 d. Left ICS 4

c. Left ICS 5

Point of maximum intensity of aortic valve? a. Right ICS 3 b. Right ICS 4 c. Left ICS 4 d. Left ICS 7

b. Right ICS 4

Heart murmur grading: a. 1-6 scale b. 1-4 scale

a. 1-6 scale

Common cardiac malformations in horses a) Persistent ductus Botalli b) Tricuspid valve deformity c) Interventricular septal defect

c) Interventricular septal defect

Bacterial endocarditis locations in horse a) Mostly the pulmonary orifice b) Mostly the tricuspid valve c) Mostly the aorta- and mitral valve

c) Mostly the aorta- and mitral valve

Bacterial endocarditis symptoms horse a) Fever, weariness, pulse rate incr, holodiastolic noise in the orifice of the aorta, decrescendo b) Fever, poor health, cardiac dullness enlarged, strong systolic noise, oedema in the abdominal skin c) Weariness, anorexia, rapid/weak pulse, cardiac dullness increased, holosystolic heart noises, oedema on foot

a) Fever, weariness, pulse rate incr, holodiastolic noise in the orifice of the aorta, decrescendo

Bacterial endocarditis treatment horse a) AB cure for 1-2w, bronchodilators, secretolyics b) AB cure for 4-6w, sensitivity test, penicillin, gentamycin, cephalosporin, therapy of the congestive heart failure c) AB cure for 4-6 days, penicillin, streptomycin, lincomicin, clindamycin

b) AB cure for 4-6w, sensitivity test, penicillin, gentamycin, cephalosporin, therapy of the congestive heart failure

Aortic insufficiency horse a) Strong systolic heart noise in the left 4 ICS, rapid pulse, frequent in older horses b) Strong holodiastolic heart noise in the left 5-6 ICS, bumping pulse c) Strong holodiastolic heart noise, bumping pulse, frequent in older horses

c) Strong holodiastolic heart noise, bumping pulse, frequent in older horses

Mitral insufficiency horse a) Holosystolic heart noise, tachypnoe, congestion in the pulmonary circulation b) In the left 3 ICS strong pandiastolic heart noise, tachypnoe, dyspnoe, decline of performance, frequent c) In the right 3 ICS strong pandiastolic heart noise, tachypnoe, dyspnoe, decline of performance, very rare

a) Holosystolic heart noise, tachypnoe, congestion in the pulmonary circulation

Tricuspid insufficiency horse a) Pansystolic noise on the area of the left cardiac dullness, right heart insufficiency, high/rapid pulse, strong venous pulse on the jugular fossa, frequent in sport horses b) Systolic noise in the puctum maximum of the tricuspidal valve, right heart insufficiency, wide v. jugularis, positive vein pulse, rare c) Holodiastolic heart noise on the area of the right relative cardiac dullness, strong venous pulse on the right jugular fossa, frequent in old horses

b) Systolic noise in the puctum maximum of the tricuspidal valve, right heart insufficiency, wide v. jugularis, positive vein pulse, rare

Diagnosis of the valve diseases with echocardiography in horse a) One dimension: valve problems, two dimensions: changes of the size of the heart ventricles, fractional shortening, Doppler: the imstakes of the heart’s blood supply b) One dimension: fractional shortening, two dimensions: valve problems, Doppler: abnormal blood flowing round the valves. c) One dimension: size changes of the heart chambers, fractional shortening, two dimensions: morphological abnormalities of the valves, Doppler: abnormal blood flowing in the chambers of the heart.

b) One dimension: fractional shortening, two dimensions: valve problems, Doppler: abnormal blood flowing round the valves.

Myocardiopathies/causes/horse a) Rhinopneumonitis, Equine influenza, septicaemia, Strongylus-larves, aflatoxin poisoning b) Equine influenza, Equine Infectious Anaemia, strangles, dirofilariosis, mebendazol toxiosis c) Rhinopneumonitis, Equine influenza, Equine Infectious Anaemia, stranglesr, Strongylus-larves, monenzin toxicosis

c) Rhinopneumonitis, Equine influenza, Equine Infectious Anaemia, stranglesr, Strongylus-larves, monenzin toxicosis

Heart rhythm disorders/reasons of the medical treatment/horse a) Decline of performance, heart frequency during endurance test >200, in rest >90/minute, ventricle extrasystoles/tachyarrhythmias b) Decline of performance, heart frequency during endurance test >120, in rest >40/minute, auricle extrasystoles, in case of ventricle tachyarrhythmias c) Poor health, heart frequency during endurance test >200, in rest >90/minute, atrioventricular heart block

a) Decline of performance, heart frequency during endurance test >200, in rest >90/minute, ventricle extrasystoles/tachyarrhythmias

Intermission cordis causes and background information in horse a) Vagotonia, 2nd degree AV block b) Heart muscle damage, ectopic centre c) Stimulus generalisation deficiency, failing of 1-1 heart cycle

a) Vagotonia, 2nd degree AV block

Ventricular tachycardia features in horse a) Heartbeat dropout in serious cardiac muscle lesion, sequence of ventricle escape beat b) Dropout heart contractions, sequence of extrasystoles, intermittent IV leveled AV-block c) Sequence of ventricular extrasystoles, in serious cardiac muscle lesion

c) Sequence of ventricular extrasystoles, in serious cardiac muscle lesion

Pericarditis sicca symptoms in horse a) Pain in cardiac area, soft heartsounds, scratching murmurs: increasing when the nose is occluded b) Cardiac friction sounds, cardiac dullness incr, heartbeats almost silent: increasing/disappearing when the nose is occluded c) Cardiac pain, enlargement of the cardiac dullness, far heartsounds, friction sounds: disappearing when the nose is occluded

a) Pain in cardiac area, soft heartsounds, scratching murmurs: increasing when the nose is occluded

In the course of Valsalva test a) Increasing of pericardial friction sound, pleuropleural murmurs disappeared b) Pericardiac murmurs disappeared c) Pleurocardiac murmurs increased

a) Increasing of pericardial friction sound, pleuropleural murmurs disappeared

Exsudative pericarditis symptoms horse a) Cardiac dullness enlargement, far heartsounds, endocardial cardial murmus, positive vein pulse, underbelly oedema b) Cardial dullness enlargement, heartsounds sub-, non-audible, swelling of the jugular vein, underbelly oedema, abdominal punction: exsudation c) Cardiac dullness incr, friction sounds, Valsalva test +

a) Cardiac dullness enlargement, far heartsounds, endocardial cardial murmus, positive vein pulse, underbelly oedema

Intracardiac shunt detection horse? a) Doppler echocardiography b) Scintigraphy, X-ray examination c) Measurement of the intracardiac blood pressure d) Contrast angiocardiography

a) Doppler echocardiography

Bacterial endocarditis in horses/complication: a) Purulent meningoencephalitis of hematogenous origin b) Disseminated, multifocal, purulent nephritis with renal infarcts c) Acute, immune-mediated glomerulonephritis d) Pneumonia, polyarthritis, enteritis v

b) Disseminated, multifocal, purulent nephritis with renal infarcts

The aortic insufficiency of the horse is characterised by? a) Strong diastolic cardiac murmur at the left, 4th intercostal space, rapid pulse, frequent in younger b) Strong holodiastolic cardiac murmur on the left 5-6th intercostal space, slow pulse c) Strong machinery murmur on the left 5-6th intercostal space, water-hammer pulse d) Strong holodiastolic cardiac murmur, in the left, 4th intercostal space, bumping pulse, rather in adult horses

d) Strong holodiastolic cardiac murmur, in the left, 4th intercostal space, bumping pulse, rather in adult horses

Common physiological arrhythmia in horses? a) Second degree atrioventricular block b) Premature ventricular extrasystole c) WPW syndrome d) Sinus pause

a) Second degree atrioventricular block

Mitral insufficiency/symptoms/horse? a) Holosystolic cardiac murmur in left 5th IC space, tachypnoea, dyspnoea, left-heart failure b) Strong pansystolic cardiac murmur in left 3rd Ic space, tachypnea, dyspnoea, exercise intolerance c) Holodiastolic cardiac murmur in left 4th intercostal space, tachypnoea, dyspnoea, left-heart failure d) II/VI-V/VI diastolic cardiac murmur in the left 4th IC space

a) Holosystolic cardiac murmur in left 5th IC space, tachypnoea, dyspnoea, left-heart failure

The aortic insufficiency of the horse is characterised by? a) Strong systolic cardiac murmur left, 4th intercostal space, rapid pulse, frequent in older horses b) Strong holodiastolic cardiac murmur on left 5-6th intercostal space, bumping pulse c) Strong holodiastolic cardiac murmur, in left, 4th intercostal space, bumping pulse, rather in adult horses d) Common in the first 2 weeks of life holodiastolic cardiac murmur on the right side

c) Strong holodiastolic cardiac murmur, in left, 4th intercostal space, bumping pulse, rather in adult horses

Common complication of bacterial endocarditis in horses? a) Meningoencephalitis b) Disseminated purulent nephritis c) Thromboembolism of the iliac arteries d) Rupture of the dilated left atrium

b) Disseminated purulent nephritis

The most specific plasma biochemical parameter to evaluate the biliary tract in horses is a) Glutamate dehydrogenase b) Lactate dehydrogenase c) Aspartate dehydrogenase d) Gamma-glutamyl transferase

d) Gamma-glutamyl transferase

How do we take blood if we try to get pH and PaCO2 from arterial blood? a. 5 ml syringe, 12 G needle b. After sampling, take the syringe and cover the tip immediately with a small piece of rubber c. Not necessarily cool, the sample can be tested tomorrow d. Without boditus from the metatarsal dorsalis, the wine is cut with a sterile scalpel above the artery

b. After sampling, take the syringe and cover the tip immediately with a small piece of rubber

For further evaluation of a suspected liver disease in horses, we can measure plasma concentration of a. Glutamate dehydrogenase b. Amylase c. Creatinine d. Creatinine kinase

a. Glutamate dehydrogenase

Which statement is correct for normal urine sample (SG=specific gravity) a. pH 8, SG 1014, mild proteinuria b. pH 8, SG 1028, glycosuria + with reagent strips c. pH 5, SG 1028, calcium carbonate crystals d. pH 8, SG 1028, calcium carbonate crystals

d. pH 8, SG 1028, calcium carbonate crystals

When serum parameters would be increased in this foal with Se- Vitamin -E deficiency? a) AST, CK, LDH b) GGT, AST, ALT c) CK, SDH, GLDH d) Creatinine, ALT, CK

a) AST, CK, LDH

Laboratory findings of a hepatopathy in horses? a) ALT ↑, AST ↓, SDH ↑, total protein ↑, blood anaemia ↓ b) Erythrocyte count ↓, left shift of the granulocytes, bilirubin ↑, bile acids ↓ c) Bilirubin ↑, bile acids ↑, AST ↑, GGT ↑, GLDH ↑, SDH ↑ d) BUN ↑, ammonia ↑, total protein ↑, creatinine ↑

c) Bilirubin ↑, bile acids ↑, AST ↑, GGT ↑, GLDH ↑, SDH ↑

Physiological values of serum sodium in horses? a) 55-100 mmol/l b) 100-135 mmol/l c) 135-155 mmol/l d) 155-175 mmol/l

c) 135-155 mmol/l

Physiological upper limit of blood urea in horses? a) 5 mikromol/liter b) 5 mmol/liter c) 20 mmol/liter d) 10 mmol/liter

d) 10 mmol/liter

The upper physiological value of coagulation time in horse: a) <15 min b) <25 min c) <5 min d) <35 min

a) <15 min

PPID diagnosis: a) Measuring GGI, LDH, CK b) Measuring ACTH, dexamethasone suppression test c) Thyroid profile tests d) Measuring TRH and insulin

b) Measuring ACTH, dexamethasone suppression test

The upper physiological value of prothrombin time in horses? a) < 10 sec b) < 20 sec c) < 30 sec d) < 40 sec

b) < 20 sec

Normal values of blood glucose in horses? a) 3-5 mmol/l b) 8-10 mmol/l c) 2-3 mmol/l d) 6-8 mmol/l

a) 3-5 mmol/l

Physiological values of blood bicarbonate in horses a) 25-30 mmol/l b) 20-25 mmol/l c) 15-20 mmol/l d) 5-10 mmol/l

b) 20-25 mmol/l

Approximate normal value of hematocrit in horses: a) 0.55 b) 0.40 c) 0.30 d) 0.25

b) 0.40

The upper limit of serum potassium in the horse? a) 7 mmol/l b) 15 mmol/l c) 3 mmol/l d) 5 mmol/l

d) 5 mmol/l

What midriatics would you use to dilate the pupil in the ophthalmic examination? a) 2% atropine b) 1% tropicamide c) 2% lidocaine d) 1% pilocarpine

b) 1% tropicamide

What is a subpalpebral lavage catheter used for? a) To anaesthetize the ocular surface b) To provide long-term frequent topical treatment c) To check intraocular pressure d) To check nasolacrimal drainage patency

b) To provide long-term frequent topical treatment

How do you remove cheek teeth in horses in most cases? a) In the standing horse – oral extraction b) In general anaesthesia – repulsion c) In general anaesthesia – oral extraction d) In the standing horse – repulsion

a) In the standing horse – oral extraction

Dental diseases in horses/signs? a) Riding difficulties, decreased appetite, weight loss, diarrhoea b) Riding difficulties, decreased appetite, weight loss, nasal discharge c) Dysphagia, nasal discharge, head tilt d) Dysphagia, diarrhoea, nasogastric reflux

b) Riding difficulties, decreased appetite, weight loss, nasal discharge

What is the most important monitoring during GA in horses? a) Blood gas control b) Palpation of the pulse c) Auscultation of the thorax d) Direct blood pressure measurement

a) Blood gas control | d) Direct blood pressure measurement ??

Which drug is used for premedication for general anaesthesia? a) Propionil promazine b) Ketamine c) Acepromazine d) Dobutamine

c) Acepromazine

Which is the most often used inhalational anaesthetic in horse? a. Desfluran b. Halothan c. Isofluran d. Enfluran

c. Isofluran

Which drug is used for induction in GA? a. Xylazine b. Ketamine c. Acepromazine d. Dobutamine

b. Ketamine

The pulse in normal horses can be palpated on the a) Coccygeal artery b) Femoral artery c) Brachial artery d) Transverse facial artery

d) Transverse facial artery

The following intravenous fluids are crystalloids, except: a) Normal saline b) 5% glucose solution c) Hetastarch d) Ringer’s solution

c) Hetastarch

Which of the following is true regarding the placement of an intravenous cannula a. In horses, primarily the transversa facial vein is used for catheterization b. It is not necessary to scrape the cannula inserted into the lo wine, usually a cover c. When one jugular vein jugular vein is obstructed, it is usually cannulated with one of the thoracic external veins d. There is no need for sterile preparation at cannula preparation

c. When one jugular vein jugular vein is obstructed, it is usually cannulated with one of the thoracic external veins

Which muscle is used for IM drug admin. in horses? a. M. quadriceps femoris b. M. gluteus c. M. Triceps brachii d. M. Supraspinatus

b. M. gluteus

Which option is not true for intravenous drug delivery? a. The sharp point must be closed with the ven (approx. 45 degrees) b. Paravenous administration of thipental and phenylbutazone causes skin necrosis c. Inflammation of the jugular vein exterior does not (or does?) have long-lasting, severe consequences d. The jugular vein in the upper third of the neck is the most suitable for suction

d. The jugular vein in the upper third of the neck is the most suitable for suction

The pulse in normal adult horses can be palpated on the a. Coccygeal artery b. Femoral artery c. Brachial artery d. Transverse facial artery

d. Transverse facial artery

In a healthy horse, it is possible to palpate a) Mandibular LN b) Retropharyngeal LN c) Prescapular LN d) Iliosacral LN

a) Mandibular LN

How to withdraw if you want arterial blood ph and PaCO2?

Should be processed immediately or it can be placed on ice. Samples analysed for pH and PaCO2 determination are fairly stable and can be held at room temperature for up to 1h. Arterial samples for determination of PaO2 are less stable and must be collected in glass syringes and stored on ice (for up to 2h) if not immediately processed.

IM injection in horses location

- Neck: above the cervical vertebrae, below the nuchal ligament and in front of the scapula - Lower half of semitendinosus and semimembranosus muscles - Pectoral muscles - Gluteal muscles

What is NOT true about abdominocentesis

Decision CANNOT be made b/w medical or surgical treatment of colic

Which of the following statements is correct about taking a urine sample from horses? a. It is only possible under sedation b. Transrectal aspiration from the urinary bladder is acceptable under general anaesthesia c. It is possibly only after administering furosemide d. Placing the horse on fresh bedding may induce spontaneous urination

d. Placing the horse on fresh bedding may induce spontaneous urination

Which of the following is the sign of incorrect placement of the needle when giving intraperitoneal injections? a. A hiss of air when puncturing the abdominal wall b. Haemorrhage from needle c. Free movement of needle in the abdominal cavity d. No resistance when administering the solution

b. Haemorrhage from needle

What would cause central distension of the jugular vein in the horse? a) Thrombophlebitis b) Pericardial effusion or tricuspid insufficiency c) Cor pulmonale d) AO insufficiency

a) Thrombophlebitis

Which nerve is affected when the tongue is paralyzed in a horse? a) Median nerve b) Hypoglossal nerve c) Vagal nerve d) Maxillary nerve

b) Hypoglossal nerve

Cerebrospinal fluid can be collected from the a) Atlantoaxial space b) Thoracolumbar space c) Lumbosacral space d) Sacrococcygeal space

c) Lumbosacral space

Cerebrospinal fluid can be collected from: a. The lumbosacral region b. The sacrococcygeal space c. Between any two vertebrae d. Between C7 and Th1

a. The lumbosacral region

Cerebellar hypotrophia (inherited abiotrophy) a) Esp in arab foals, cerebellum cortical, congenital, purkinje fibres degeneration, symptoms after 6m age, head tremor, spastic ataxia, dysmetria (high steps) b) Hereditary cerebellar disease of English thoroughbreds, cerebellum atrophy, symptoms start in one month old foals, ataxia, rotary motion, disorder of balance, weakness c) Hereditary in pony foals, cerebellar disease, cortex degeneration, symptoms after 3m age, unsteady movements, foals suck only with help, ataxia, retarded growth

a) Esp in arab foals, cerebellum cortical, congenital, purkinje fibres degeneration, symptoms after 6m age, head tremor, spastic ataxia, dysmetria (high steps)

Hydrocephalus in adult horse etiology and pathogenesis a) Liquor flow block – aqueduct of mesencephalon is obturated – cerebral edema – cerebral ventricle dilaration – pressure atrophy of cerebral ventricles peripheral neurons b) Block of liquor flow because of stricture of aqueduct of mesencephalon – cerebral oedema – protrusion – compression of aqueduct of mesencephalon – cerebral ventricle dilatation – cortex atrophy c) Incr liquor prod – liquor stagnation – cerebral oedema – cerebral ventricle dilatation – destruction of brain stem neurons

b) Block of liquor flow because of stricture of aqueduct of mesencephalon – cerebral oedema – protrusion – compression of aqueduct of mesencephalon – cerebral ventricle dilatation – cortex atrophy

Hydrocephalus in adult horse CS a) Skull hypertrophy, dumbing, deafness, blindness, mutation of cerebral neurons, strabismus, eyelids-ear dangling, paralysis of tongue b) Dumbed countenance, spasms of temporal muscles, strabismus, nystagmus, imbalance, consciousness disorder c) Gradually deteriorate cortical outages, disorder of feeding and drinking, dumbing, moving disorder, disorder of proprioception

c) Gradually deteriorate cortical outages, disorder of feeding and drinking, dumbing, moving disorder, disorder of proprioception

Heat stroke in horses a) In working horse in vapoured hot summer, languor weakness, tachycardia – pulmonary oedema – cerebral oedema, 41-43⁰ b) Horse kept in warm stable, strong sweating, languor, excitement of vasomotoric centrum, high mortality, high mortality, 39.5-40⁰ c) Hot summer, colic-like restlessness, later weakness, spasms, loss of consciousness, high mortality, >42⁰

a) In working horse in vapoured hot summer, languor weakness, tachycardia – pulmonary oedema – cerebral oedema, 41-43⁰

Cholesterol granuloma horse a) Cholesterol cessation in cerebral ventricles – cerebral ventricle dilatation – pressure atrophy of cortex b) Granuloma formation of cerebral ventricles – liquor circulatory disorder – hydrocephalus c) Brain stem granulomatosis – lesion of nucleus of V, Vii, IX cerebral neurons, strabismus, face paralysis, pharynx paralysis

b) Granuloma formation of cerebral ventricles – liquor circulatory disorder – hydrocephalus

Narcolepsia, cataplexia in horse a) Appears in attacks, falling asleep voluntarily, gradually deteriorate attacks until collapse, clonic convulsions, coma – death b) Sleepiness/collapse, senseless status, generalized atonia, areflexia c) Hereditary, nervous system complient, temporal loss of consciousness, behaviour disorder in the breaks of the attacks, irritability

b) Sleepiness/collapse, senseless status, generalized atonia, areflexia

Rabies etiology and pathogenesis a) Arbovirus, bites from rabid dogs, stabled horse, haematogenous virus prop, penetration into cerebrum only in case of immune def b) Virus inf from bites of rabid dogs, virus prop along nerves, replication in synapses, encephalomyelitis c) Lentivirus, nucleate encephalomyelitis, prop by bites of rabid foxes, penetration through a wound, penetration by lymph vessels

b) Virus inf from bites of rabid dogs, virus prop along nerves, replication in synapses, encephalomyelitis

Rabies CS a) Within 1-3d after inf, behaviour disorder, anorexia, involuntary movement, high fever, loss of consciousness, spasms, death within 1-2d b) 1-3d after inf, langor, weakness, paralysis of cerebral nerves, gradually deteriorating status, 3-4w disease progression c) Estrus like behaviour or emergence of penis, colic like restlessness, disorder of feed, water uptake, salivation, spasms, seizures, consciousness disorder, usually 2-6d lethal ending disease progression

c) Estrus like behaviour or emergence of penis, colic like restlessness, disorder of feed, water uptake, salivation, spasms, seizures, consciousness disorder, usually 2-6d lethal ending disease progression

Malformation and malarticulation of cervical vertebrae CS a) Locomotion disorder in ½ - 3y old foals, often HLs, ataxia, paresis, cervical pain, appearing suddenly, deteriorative, then stabilized process b) Imbalance esp in racehorses, stumbling, dangling head, painful when moving neck, paraparesis, slowly deteriorative progression c) Painful neck in 6m old English thoroughbred foals, dangling neck and head, later deterioration locomotion disorder, rotary motion, intermittent lameness, feeling wobbly, then tetraparesis

a) Locomotion disorder in ½ - 3y old foals, often HLs, ataxia, paresis, cervical pain, appearing suddenly, deteriorative, then stabilized process

Malformation and malarticulation of cervical vertebrae diagnosis a) Cervical x-ray in extended and flexed position, myelography b) Liquor sampling, CT exam c) Myelography, CT exam

a) Cervical x-ray in extended and flexed position, myelography

Myeloencephalomalacia caused by Herpesvirus a) Serious resp symptoms, after 6-8d NS CS, convulsions, paralysis of cranial nerves and skeletal muscles b) Pneumonia, after 3-4w paraparesis, paresthesia in gluteal region, paralysis of caudal/anal muscles, limbs, unconsciousness in more serious cases c) Resp symptoms, paraparesis, ataxia, sitting dog position, recumbency

c) Resp symptoms, paraparesis, ataxia, sitting dog position, recumbency

Myeloencephalomalacia caused by Herpesvirus a) Horses previously immunized never show CNS CS b) CNS CS are usually detected in young 1-2y old horses, most cases fatal c) CNS CS usually appear after resp CS and at the same time with epidemic abortion in the herd

b) CNS CS are usually detected in young 1-2y old horses, most cases fatal

Therapy of myeloencephalomalacia caused by Herpesvirus a) Diuretics, NSAIDs, manual removing of urine and feces if necessary, lifting cradle b) Manual removing of urine and feces if necessary, lifting cradle, ABs, penicillins, vitamin C c) NSAIDs, DMSO infusion, manual removing of urine and feces if necessary, lifting cradle

c) NSAIDs, DMSO infusion, manual removing of urine and feces if necessary, lifting cradle

Borna disease a) ssRNA virus inf – slow degeneration of neurons – meningoencephalomyelitis, abnormal behavious, apathy, ataxia, compulsive movements, course takes 2-6w, fatal disease b) Herpesvirus inf – encephalomyelitis, paralysis, convulsions, “pushing syndrome”, slow course leading to death c) Arbovirus infection – perineural spreading to CNS – encephalomyelitis, confusion, apathy, convulsions, ataxia, compulsive movement, course takes 2-6w, fatal disease

a) ssRNA virus inf – slow degeneration of neurons – meningoencephalomyelitis, abnormal behavious, apathy, ataxia, compulsive movements, course takes 2-6w, fatal disease

Bacterial meningitis horse a) Caused by septicaemia in foals, atypic symptoms, aggressive behaviour, paraparesis – paraplegia, fast progression of CNS symptoms b) Septicaemia in foals, abnormal behaviour and movement, paraesthesia, disorder of cranial nerve, recumbency – death c) In adult, atypic symptoms, general spastic paresis, normal consciousness

b) Septicaemia in foals, abnormal behaviour and movement, paraesthesia, disorder of cranial nerve, recumbency – death

Bacterial meningitis tx a) Trimethoprim, sulphonamides, amoxicillin, ketaprofen b) K-penicillin, gentamicin, enrofloxacin c) Ampicillin, tylosin, virginiamycin

a) Trimethoprim, sulphonamides, amoxicillin, ketaprofen b) K-penicillin, gentamicin, enrofloxacin check doc

Equine leukoencephalomalacia (ELE) a) Mycotoxin uptake from rotten silage – encephalomalacia – convulsions, laryngoparesis b) Hepatic failure – toxins to brain – encephalomalacia – usually confusion, dementia, coma c) Food infected by moulds – fumonisin B1 toxins, encephalomalacia – dysphagia, dyskinesis – recumbency

c) Food infected by moulds – fumonisin B1 toxins, encephalomalacia – dysphagia, dyskinesis – recumbency

Botulism in horse a) Animal corpse, rotten food, infected wounds – botulotoxin – weakness, paralysis, laryngoparalysis, mydriasis, normal consciousness, recumbency b) Animal corpse, rotten food, infected wounds – botulotoxin – encephalomalacia – confusion, general weakness and paralysis – recumbency c) Botulotoxin uptake with contaminated food – encephalomalacia and hepatosis – jaundice, confusion, dysphagia – death in 7d

a) Animal corpse, rotten food, infected wounds – botulotoxin – weakness, paralysis, laryngoparalysis, mydriasis, normal consciousness, recumbency

Tetanic convulsions of mare a) Decr blood Ca, because of malnutrition of endocrine malfunction. Around parturition, epileptiform convulsions with consciousness. b) Epileptiform convulsions in mares, around estrus on genetic base c) In sensitive thoroughbred mare, mainly after races. Some minut-long convulsions because of the decr of blood Ca

c) In sensitive thoroughbred mare, mainly after races. Some minut-long convulsions because of the decr of blood Ca

Tetanus CS a) Flag like tail, muscular rigidity, ptosis, lock jaw, salivation b) Heperreflexia, muscular rigidity, general muscular rigidity (esp ear, tail), lock jaw c) Hyperreflexia, rigidity of the neck, confusion, contorted facial expression

b) Heperreflexia, muscular rigidity, general muscular rigidity (esp ear, tail), lock jaw

Tetanus outcome a) In treated cases recover after 4-5d b) Course takes 10-14d, outcome adverse c) Short course – death in days, if 10-12d survival – possible to recover

c) Short course – death in days, if 10-12d survival – possible to recover

Tetanus tx a) Provide suitable place, diazepam, treat the wound, liquid nutrient supplement, muscle relaxants b) Major tranquilizers, muscle relaxants, infusions, serum therapy, drinking from the ground, provide good hay, walking twice a day c) Xylazine, narcotics, microlaxants (?), provide suitable place, infusions, ABs, easily chewable feed

a) Provide suitable place, diazepam, treat the wound, liquid nutrient supplement, muscle relaxants

Unilateral facial nerve paralysis in horse a) Floppy ear, palpebral paralysis, face deform on the sick side, trismus b) Deformed face, floppy ears, ptosis, paralytic nose and lips c) Nose, lips hanging flagily, horse cannot close its mouth, tongue hangs out

b) Deformed face, floppy ears, ptosis, paralytic nose and lips

Neuritis caudae equinae a) Spastic paralytic flagging tail, skin hyperaesthesia near tail, closing m of rectum shrinking crampingly b) Muscles of tail shrinking crampingly, strong skin pain around tail, difficult to defecate and urinate c) Anaesthesia by anus, hyperaesthesia, tail paralysis, rectum paralysis

a) Spastic paralytic flagging tail, skin hyperaesthesia near tail, closing m of rectum shrinking crampingly

Neuritis caudae equinae a) Another name is polyneuritis equi and degenerative disease of peripheral nerve system b) Another name is equine motor neuron disease and is caued by def in vit E c) Polyneuritis and equine motor neuron disease are caused by peripheral nerve system and the def of vit E

a) Another name is polyneuritis equi and degenerative disease of peripheral nerve system

Equine motor neuron disease/cause? a) Selenium toxicity b) Vitamin E deficiency c) Vitamin B1 deficiency d) Unidentified clostridium strain

b) Vitamin E deficiency

Dysphagia/causes/horse? a) Disorders of the V, VII, IX, X, XII cranial nerves b) Disorders of the V, VI, IX, X, XI cranial nerves c) Disorders of the IV, IX, XII cranial nerves d) Disorders of the III, VII, X, XI, XII cranial nerves

a) Disorders of the V, VII, IX, X, XII cranial nerves

Grass sickness/horse/characteristics? a) Draft horses on pasture, myopathy b) Young horses on pasture, myopathy c) Older horses on pasture, dermatologic disease d) Young horses on pasture, neurologic disease

d) Young horses on pasture, neurologic disease

Definitive diagnosis of equine leukoencephalomalacia? a) Elevated liver and kidney parameters b) Feed analysis and histopathology (brain, liver) c) Clinical signs are definitive d) Elevated liver parameters and glucosuria

b) Feed analysis and histopathology (brain, liver)

Thromboembolic meningoencephalitis (TEME)/prognosis and treatment: a) Sulphonamides, antibiotics might help in early stage b) Always fatal outcome, affected animals should be slaughtered c) Only symptomatic treatment is possible, sometimes improvement might occur d) Only symptomatic treatment is possible, with poor prognosis

a) Sulphonamides, antibiotics might help in early stage

Botulism Aetiology Horse a) Cl. botulinum + botulinum toxin contaminated carrion remnant in the feed e.g. rotten silage, exceptionally Cl. botulinum infected wounds or gastrointestinal tract b) Cl. botulinum -> per os uptake of bacterium contaminated carrion in the feed or rotten silage -> Cl. botulinum septicaemia c) Spreading of Cl. botulinum in anaerobe wounds; exceptionally per os uptake of botulinum toxin contaminated carrion remnants with the feed d) Spreading of Cl. botulisnum in the gut, bacteraemia

a) Cl. botulinum + botulinum toxin contaminated carrion remnant in the feed e.g. rotten silage, exceptionally Cl. botulinum infected wounds or gastrointestinal tract

Herpesvirus myeloencephalopathy clinical signs/horse a) Epileptiform convulsions, cranial nerve paralysis, then severe resp. signs within 6-8 days b) Pneumonia, followed by facial and trigeminal paralysis within 3-4 weeks, unconscious c) Asymmetric gluteal muscle atrophy d) Resp. signs, followed by paraparesis, ataxia, dog sitting position, recumbency

d) Resp. signs, followed by paraparesis, ataxia, dog sitting position, recumbency

Polyneuritis/aetiology/horse? a) EHV-2, adenovirus, Rhodococcus equi b) EHV-1 adenovirus, Streptococcus c) EHV-1, fumonizin, Actinobacillus equuli d) Clostritidium botulinum C

b) EHV-1 adenovirus, Streptococcus

What are the causes of pyrrolizidine-toxicosis in horses? a) Senecio, Crotalaria-sp. b) Insecticides with organophosphates c) Anti-parasitic agents containing pyrrolizidine d) Accumulation of toxic metabolites in hepatic fibrosis

a) Senecio, Crotalaria-sp.

Which disease is abbreviated with ELE(M) and what is its cause? a) Equine leukoencephalomyelitis, togavirus b) Equine leukoencephalomalacia, fumonisin-B1 toxin c) Equine lekoencepahlomacia and myelosis, satratoxin d) Equine lymphocytic encephalitis viral infection

b) Equine leukoencephalomalacia, fumonisin-B1 toxin

Cerebral commotion in horses/treatment? a) General anaesthesia b) DMSO infusion c) 0.45% NaCl solution d) Pentoxiphylline

b) DMSO infusion

Causes and features of Tyzzer-disease in horses? a) Listeria monocytogenes-caused meningoenphalitis b) Actinobacillus equulis infection, septicaemia in foals c) Clostridium piliforme acute hepatitis in foals d) Clostridium botulinum, hepatocencephalopathy in foals

c) Clostridium piliforme acute hepatitis in foals

Neurophysiologic background of botulism? a) Paralysis of the striated muscles due to inhibited released of GABA at the presynaptic motor nerve endings b) Paralysis of the striated muscles due to inhibited release of acetylcholine at the presynaptic motor nerve endings c) General muscular paralysis due to inhibited release of acetylcholine at the presynaptic motor nerve endings d) Paralysis of striated muscles due to inhibited release of GABA at postsynaptic motor n. endings

b) Paralysis of the striated muscles due to inhibited release of acetylcholine at the presynaptic motor nerve endings

Features of equine herpesvirus myeloencephalopathy? a) Horses previously immunised never show CNS signs b) CNS signs usually appear in 1-2 years old, before respiratory signs, and in most cases are fatal c) CNS signs usually appear in adult horses after the respiratory signs d) Horses with herpes myeloencephalopathy have grave prognosis

c) CNS signs usually appear in adult horses after the respiratory signs

Cerebral commotion in horses/consequences? a) Long-lasting loss of consciousness, recumbency, convulsions b) Temporary loss of consciousness, disorders of locomotion c) Recumbency, bleeding from the nostrils and from the ears d) Bilateral facial paralysis

c) Recumbency, bleeding from the nostrils and from the ears

Facial paralysis/aetiology/horse? a) Guttural pouch mycosis, otitis media b) Basilar skull fracture, hydrocephalus c) Stachybotriotoxicosis, wobbler syndrome d) Fracture of the basisphenoid bone, leukoencephalomyelitis

a) Guttural pouch mycosis, otitis media

Characteristics of equine leukoencephalomalacia (ELE)? a) Mycotoxin uptake from rotten silage -> encephalomalacia -> convulsion, laryngoparalysis b) Hepatic failure -> toxins into the brain -> encephalomalacia -> usually confusion, dementia, coma c) Food contaminated with moulds -> fumonisn-B1 toxin: encephalomalacia -> dysphagia, dyskinesis -> recumbency d) Pirrolizidine toxicosis -> encephalomalacia -> dementia

c) Food contaminated with moulds -> fumonisn-B1 toxin: encephalomalacia -> dysphagia, dyskinesis -> recumbency

Cerebral commotion (concussion) in horses/prognosis? a) Favourable in young individuals, poor in older horses b) Usually favourable c) Depends on region of the skull injured d) Usually unfavourable

b) Usually favourable

Equine herpesvirus myeloencephalopathy. Which statement is not true? a) It is caused by EHV-2, on immuno-mediated basis, due to type 3 hypersensibilization b) It is caused by EHV-1, or sometimes by EHV-4, on an immune-mediated basis, due to type 3 hypersensibilization c) The symptoms can be seen in horses vaccinated against EHV because of immuno-complex based vasculitis d) In foals neurologic signs are less frequent

a) It is caused by EHV-2, on immuno-mediated basis, due to type 3 hypersensibilization

Which disease most resembles rabies in horses? a) Tetanus b) Botulismus c) Equine Leukoencephalomalacia ELE d) Equine Meningoencephalitis THEME caused by Heamophilus somnus

c) Equine Leukoencephalomalacia ELE

Equine laryngeal hemiplegia/diagnosis? a) Grade 1: obvious asymmetry at test, no movements b) Grade 3: asynchronous movement, no complete opening c) Grade 1: asynchronicity, tremor, weak movements, complete open with nasal occlusion d) Grade 3: synchronicity, complete closure and opening

b) Grade 3: asynchronous movement, no complete opening

COPD(RAO) a) Allergic disease b) Chronic fungal infection c) Chronic bacterial infection d) Chronic viral infection

a) Allergic disease

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

c) Epistaxis, nasal discharge, dysphagia, laryngeal paralysis, Horner syndrome

Resp rate of normal adult horse is: a. 10-18 bpm b. 20-28 bpm c. 30-38 bpm d. 40-48 bpm

a. 10-18 bpm

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

c. Aspiration through the accessory channel of the endoscope

A tracheal wash sample is suitable: a. Culture b. Cytology c. Antibody sensitivity test d. All three

d. All three

Thoracocentesis possible side effect:

Pneumothorax

Thoracocentesis location

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

Nose bleed in racehorse a) Consequence of competition’s trauma b) Consequence of incidence of lung-bleeding c) Consequence of dope-using

b) Consequence of incidence of lung-bleeding

Nose bleed in racehorse reasons a) Trauma, haemorrhagic purpura, pharyngitis b) Nasal-tumor, dominant successions, coagulopathy c) Trauma, recessive thoroughbred-sick, guttural pouch mycosis

c) Trauma, recessive thoroughbred-sick, guttural pouch mycosis

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

a) Strangles, satratoxicosis, smoke-, dust inhalation

Ethmoid haematoma a) Haematoma in region of nose or ethmoid, slow progression, nasal stridor, angiomatic tissue growth b) Haematoma in sphenoid bone, unilateral nasal discharge, nervous symptoms c) Haematoma in sphenoid bone, bilateral purulent nasal discharge, progressing in weeks

a) Haematoma in region of nose or ethmoid, slow progression, nasal stridor, angiomatic tissue growth

Maxillary sinusitis reasons in horse a) Rhinitis, trauma, sedentation of parasitic larvae b) Strangles, purulent periodontitis, rhinitis c) Infectious arthritis, gasterophilus, strangles

b) Strangles, purulent periodontitis, rhinitis

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

c) Single side nasal discharge, region of maxillary pain, deformation

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

a) Congenital, a plica salingopharyngea hypertrophy, air-outflow blocked

Guttural pouch tympany symptoms a) Ballooning/pain of region of guttural pouches, dyspnea, regurgitation b) Ballooning, of region of guttural pouches, tympanic percussion sound, paroxysmal cough c) Ballooning/palpation sensitivity of region of guttural pouches, incomplete dullness percussion sound, dysphagia

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

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

c) Infection through Eustachion tube, or with spread over, caused by bacteria or mycotic disease

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

a) During lowering of head purulent nasal discharge, ballooning of region of parotis, complications of nervous system

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

c) Cause exercise intolerance, sounds during expiration, diagnose in submaximal load via endoscope

Tracheal collapse a) Disease of ponies b) Congenital disease c) In big horses

a) Disease of ponies

Laryngeal hemiplegia causes a) Idiopathic, common in carthorse, frequent occurrence in pharyngo-laryngitis b) Hereditary, in rhinopneumonitis, idiopathic, distal axonopathy c) Hereditary in Arabian horses, n. vagus nucleus trauma, idiopathic

b) Hereditary, in rhinopneumonitis, idiopathic, distal axonopathy

Laryngeal hemiplegia symptoms a) During inspiration beep sound-rattle, dyspnea, swallowing disorder b) During expiration beep sound-rattle, expiration dyspnea, sore swelling of muscles of larynx c) During inspiration stridor laryngis, fremitus laryngitis, barren larynx

c) During inspiration stridor laryngis, fremitus laryngitis, barren larynx

Laryngeal hemiplegia diagnosis a) Endurance test, endoscope, “slap” test b) Keeping horse stopped, US exam, endoscope c) Endurance test, larynx x-ray, “slap” test

a) Endurance test, endoscope, “slap” test

Laryngeal oedema causes a) Allergy, pneumonia, bee-sting b) Laryngitis, hemorrhagic purpura, insect-sting c) Hemorrhagic purpura, laryngeal paralysis, lead poisoning

b) Laryngitis, hemorrhagic purpura, insect-sting

Laryngeal oedema treatment a) Prednisolone, laryngotomy, metronidazole b) Laryngotomy, prednisolone, bromhexine inj c) Prednisolone, tracheotomy, antihistamines

c) Prednisolone, tracheotomy, antihistamines

COPD diagnosis, complementary examination a) TTL, atropine test, resp function exam, thorax x-ray b) BAL-neutrophil %, atropine test, resp function exam, endoscopy c) BAL and TTL-eosinophil %, thorax supersonic wave, lobelin test

b) BAL-neutrophil %, atropine test, resp function exam, endoscopy

COPD incidence a) In older, stalled horses, giving mouldy hay b) In free keeping horses, in hard working horses c) In hereditary dispositional foals or horses

a) In older, stalled horses, giving mouldy hay

COPD etiology a) Hereditary disposition, bacterial, viral bronchitis, race b) Inspiration allergen (Micropolyspora faeni, Aspergillus spore), genetic predisposition c) Allergic or bacterial resp disease hyperactivity

b) Inspiration allergen (Micropolyspora faeni, Aspergillus spore), genetic predisposition

COPD pathogenesis a) Bronchitis  pneumonia  emphysema pulmonis b) Rhinitis  laryngitis  bronchitis  allergen inspiration  emphysema pulmonis c) Hypersensitivity  neutrophils accumulating intraluminal  intraluminal fibrosis  emphysema

c) Hypersensitivity  neutrophils accumulating intraluminal  intraluminal fibrosis  emphysema

COPD 3rd grade CS a) Frequent, light cough, dyspnea, border of lings shifting 1-2 ICS b) Humid cough, broken-wind groove, border of lungs shifting ½ ICS c) Paroxysmal cough, doubled expiration, border of lungs shifting 1 ICS

a) Frequent, light cough, dyspnea, border of lings shifting 1-2 ICS

COPD 4th grade CS a) Frequent paroxysmal cough, severe dyspnea, suffocating enlarged cardiac dullness b) Frequent light cough, doubled expiration/broken-wing groove, border of lungs shifting back 2 ICS c) Frequent aching cough, inspirational dyspnea

b) Frequent light cough, doubled expiration/broken-wing groove, border of lungs shifting back 2 ICS

COPD tx with glucocorticoids a) Inspiration glucocorticoids dispose to pododermatitis b) The best is prednisolone PO c) It is contraindicated to give them with bronchodilators

b) The best is prednisolone PO

Bronchodilators in horse a) Clenbuterol, salmeterol, albuterol b) Albuterol, atropine, bromhexine c) Clenbuterol, acetylcysteine, dembrexine

a) Clenbuterol, salmeterol, albuterol

Mucolytics for horses a) Atropine, terbutaline, dembrexine b) Acetylcysteine, bromhexine, dembrexine c) Terbutaline, celbuterol, dexamethasone

b) Acetylcysteine, bromhexine, dembrexine

Acute alveolar pulmonary emphysema causes a) Allergic rxn, heavy physical strain, glechoma hederacea (ground ivy) poisoning b) Autoimmune rxn, pulmonary aspiration, threadworm larvae c) Trichostrongylosis, allergy, aflatoxin poisoning

a) Allergic rxn, heavy physical strain, glechoma hederacea (ground ivy) poisoning

Acute alveolar pulmonary emphysema signs a) Incr resp effort, caudal shift of lung border, dull-tympanic percussion sound b) Serious dyspnea, 1-3 rib spaces shift of the lung border, cyanosis c) Quick fatigue, epistaxis, tympanic percussion sound

b) Serious dyspnea, 1-3 rib spaces shift of the lung border, cyanosis

Exercise induced pulmonary hemorrhage a) Epistaxis in English thoroughbreds, frequently returns, causes anaemia b) Pulmonary hemorrhage in racehorses, caseous necrosis of the lung’s lobe, exercise intolerance c) Pulmonary hemorrhage after competition, recidivism, bleeding spontaneously stops

c) Pulmonary hemorrhage after competition, recidivism, bleeding spontaneously stops

Bronchitis-pneumonia origin of viral infection a) EHV-1, equine influenza virus A, rhinovirus 2 b) Adenovirus A, equine reovirus A, equine arbovirus 1 and 2 c) Equine influenza virus 1 and 3, equine adenovirus, PI-B

a) EHV-1, equine influenza virus A, rhinovirus 2

Bacterial bronchitis pneumonia origin a) Bordetella pneumoniae equi, Streptococcus pneumoniae equi, Chlamydia bronchiseptica b) Streptococcus equi, Rhodococcus equi, Bordetella bronchiseptica c) Mycoplasma hyopneumoniae equi, Chlamydophila equi, Corynebacterium pyogenes

b) Streptococcus equi, Rhodococcus equi, Bordetella bronchiseptica

Mycotic bronchitis pneumonia origin a) Pneumocystic carinii, Aspergillus species, Histoplasma equi b) Coccidiodes equi, Pneumocystis carinii, Actinobaculum equi c) Histoplasma capsulatum, Rhinosporidium seeberi, Coccidiodes immitis

c) Histoplasma capsulatum, Rhinosporidium seeberi, Coccidiodes immitis

Bronchopneumonia characteristics a) Catarrhal style, bacterial origin, lobular extent b) Catarrhal-purulent, bacterial origin, interstitial c) Effusion, bacterial origin, interstitial

a) Catarrhal style, bacterial origin, lobular extent

Viral pneumonia characteristics a) Lobular  interstitial, hepatic character, becoming chronic b) Interstitial fibrosis and/or secondary bacterial infection  hypoxia, acidosis c) Purulent-necrotic outcome, purulent metastases, fast course

b) Interstitial fibrosis and/or secondary bacterial infection  hypoxia, acidosis

Croupous pneumonia stages a) Yellow hepatisation  grey hepatisation  resolution b) Fibrinous  haemorrhagic  hepatisation  crisis c) Hyperaemia  hepatisation  resolution

c) Hyperaemia  hepatisation  resolution

Gangrenous pneumonia pathogenesis a) Aspiration, putrid bronchitis  lung cavities  septicaemia b) Pneumonia crouposa, exudate  putrid bacteria c) Metastasis or transmission; purulent localization in the lungs  infection with protease bacteria

a) Aspiration, putrid bronchitis  lung cavities  septicaemia

Purulent pneumonia CS a) Languor, serous-purulent nasal discharge, dullness with horizontal upper border by percussion, dyspnea b) Weakness, purulent nasal discharge, dyspnea, whistling-wheezing resp sounds c) Fever, bloody-frothy nasal discharge, dyspnea, dry cough, wide dullness

b) Weakness, purulent nasal discharge, dyspnea, whistling-wheezing resp sounds

Croupous pneumonia CS a) Peracute, racking cough, by mobbing stronger dyspnea, dullness with horizontal upper border, course within 1w b) Course in 2-3w, freq becomes chronic, serous nasal discharge, dullness, catarrhal resp sounds c) Acute course: 2w, high fever, serosanguinous nasal discharge, wide dullness, dyspnea/cyanosis

c) Acute course: 2w, high fever, serosanguinous nasal discharge, wide dullness, dyspnea/cyanosis

Gangrenous pneumonia CS a) Within days fast general health decay  death, malodorous-putrid breath, smelly nasal discharge, dyspnea b) Course in 1-2w  freq death, bloody-purulent nasal discharge, rapid, often cough, splashing sounds in the dullness area c) Typically insp dyspnea, wide dullness, catarrhal resp sounds, long recovery

a) Within days fast general health decay  death, malodorous-putrid breath, smelly nasal discharge, dyspnea

Aspiration pneumonia – localization of the dullness and resp sounds a) Lower third of the chest, region of the cardiac basis b) Caudal third of lungs, where the ventilation is bad c) Craniodorsal part of the lungs

a) Lower third of the chest, region of the cardiac basis

Pneumonia treatment – antibacterial agents a) Ampicillin, lincomycin, ticarcillin, metronidazole b) Amoxicillin, gentamycin, tilozin, cephalexin c) Cephalexin, clindamycin, metronidazole, neomycin

b) Amoxicillin, gentamycin, tilozin, cephalexin

Pleuropneumonia aerobic bacteria a) Streptococcus pleuropneumoniae, Mycoplasma equi, Actinobacilus multiformis b) Bacteroides fragilis, Klebsiella pneumonia, fusobacterium c) Streptococcus equi, pasteurella, Actinobacillus equi

c) Streptococcus equi, pasteurella, Actinobacillus equi

Pleuropneumonia anaerobic bacteria a) Bacteroides fragilis, Clostridium sp., fusobacterium b) Klebsiella equi, Fusobacterium virilise, Mycoplasma felis c) Actinobacillus pneumonia, Clostridium multifactoralis, Bacteroides pleuropneumoniae

a) Bacteroides fragilis, Clostridium sp., fusobacterium

Pleuropneumonia CS a) Whistling and wheezing resp sounds, cardiac dullness, discharge of transudate b) Dullness with horizontal uppor border by percussion, no respiration, by puncture: exudation c) Discharge of inflammatory exudate, loud catarrhal resp sounds, chest oedema

b) Dullness with horizontal uppor border by percussion, no respiration, by puncture: exudation

Pleuropneumonia treatment a) Thoracocentesis, dexamethasone, sulfadimidine, aminophylline b) Thoracocentesis, bromhexine, prednisolone, gentamicin c) Antimicrobial therapy, flunixin-meglumine, lowering of the pleural exudate

c) Antimicrobial therapy, flunixin-meglumine, lowering of the pleural exudate

COPD (RAO)/ Bronchoalveolar lavage sample a) Neutrophils <2%, eosinophils >2% b) Mast cells >20% c) Eosinophils >2%, neutrophils >5% d) Neutrophils >20%

d) Neutrophils >20%

Equine pneumonia/treatment/antibacterial drugs? a) Ampicillin, lincomycin, metronidazole b) Amoxicillin, gentamicin, metronidazole c) Clindamycin, metronidazole, neomycin d) Erythromycin, clarithromycin, amphotericin

b) Amoxicillin, gentamicin, metronidazole

Equine laryngeal hemiplegia/ Diagnosis a) Auscultation, "slap" test b) Occlusion of the nostrils; US exam of the larynx; radiographic examination of the larynx c) Endoscopy, palpation, "slap" test d) Computed tomography, endoscopy

c) Endoscopy, palpation, "slap" test

COPD(RAO)/Which statement is NOT true/horse? a) Occasionally mild radiographic changes in the lungs: interstitial, bronchial, peribronchial pattern b) Usually severe radiographic changes in the lungs: fibrosis, chronic oedema c) Thoracic radiography mainly serves for differential diagnostic purposes d) Bronchectasia and increased air content sometimes visible on chest x-ray

b) Usually severe radiographic changes in the lungs: fibrosis, chronic oedema

Tracheal collapse in horses/occurrence a) English thoroughbred horses b) Large, jumping horses c) Ponies, miniature horses d) Large, draft horses

c) Ponies, miniature horses

Aspiration pneumonia/localisation of dullness and abnormal respiratory sounds/horse? a) Lower third of the thorax, over the heart base b) The caudal third of the lungs, because of poor ventilation in this region c) Craniodorsal part of the lungs d) Caudodorsal lung quadrant

a) Lower third of the thorax, over the heart base

How can we treat pleuropneumonia in horses? a) Thoracocentesis, dexamethasone, sulfadimidin, aminophylline b) Thoracocentesis, bromhexine, prednisolone, gentamycin c) Antimicrobial therapy, flunixin-meglumine, thoracic drainage d) Thoracotomy, dexamethasone, bromhexine

c) Antimicrobial therapy, flunixin-meglumine, thoracic drainage

COPD (RAO)/Drugs/Horse? a) Clenbuterol, atropine, fluticazon b) Albuterol, ipratropium, trilostane c) Salmeterol, aminofillin, edrophonium d) Antihistamines, aspirin

a) Clenbuterol, atropine, fluticazon

Caudal shift of the caudal lung border. It is characteristic for? a) EGME b) RAO c) ELE(M) d) FLUTD

b) RAO

Bronchitis-pneumonia/Etiology/Obligate pathogenic viruses/Horse a) Equine herpesvirus-1 and 4, equine influenza virus-A, african horse sickness virus b) Equine adenovirus, equine reovirus-1 and 3, african horse sickness virus c) Equine herpesvirus-2, equine adenovirus, parainfluenza virus-3 d) Rhinovirus, herpesvirus, coronavirus

a) Equine herpesvirus-1 and 4, equine influenza virus-A, african horse sickness virus

COPD (RAO) common occurrence: a) In older horses kept in stables and getting mouldy hay b) In horses kept on pasture and in horses performing hard exercise c) In young foals after chronic respiratory infection d) Most common in thoroughbreds, trotters and younger sport horses

a) In older horses kept in stables and getting mouldy hay

Bronchodilators for horses a) Loperamide, albuterol, aminophylline (teophylline) b) Albuterol, dimethyl-sulfoxide, bromhexine c) Salbutamol, acetylcysteine, dembrexine d) Clenbuterol, albuterol, aminophylline (theophylline)

d) Clenbuterol, albuterol, aminophylline (theophylline)

Rhabdomyolytic myoglobinuria in horses a) Disease with paralysis like locomotion disorder and myoglobinuria of untrained cold-blooded due to an extremely heavy work b) Disease with paralysis like locomotion disorder and myoglobinuria of continuously working cold-blooded horse c) Disease with paralysis like locomotion disorder and myoglobinuria of untrained racer due to an extremely heavy and uncommon exercise

b) Disease with paralysis like locomotion disorder and myoglobinuria of continuously working cold-blooded horse

Muscular degeneration myoglobin-micturition pathogenesis a) 2-3d rest in strong well-fed horses, then hard work within transition b) 1 week rest in well-fed horses, then hard work within transition c) In undernourished, yoke horses, for the sake of grim-hard work

a) 2-3d rest in strong well-fed horses, then hard work within transition

Muscular degeneration myoglobin-micturition pathogenesis a) Muscular-glycogen incr  local lactic acid incr + hypoxemia  muscular contraction incr  zenker muscular paralysis + myoglobinuria b) Hypoxia  muscular glycogen decoupling incr  local lactic acid incr  Zenker-muscular necrosis  paralysis + myoglobinuria c) Muscular glycogen synthesis incr  lactic acid decoupling incr + hypoxemia  muscular contraction decr  muscular bulge  Zenker muscular paralysis + myoglobinuria

b) Hypoxia  muscular glycogen decoupling incr  local lactic acid incr  Zenker-muscular necrosis  paralysis + myoglobinuria

Muscular degeneration myoglobin-micturition symptoms a) After the first interception within 2-3h: lameness, wobbly, drop down, rump muscular bulge, saw-horse position, brown-ruddy urine b) After the first interception within 2-3h: serious lameness, wobbly, downfall, rump muscular bulge, pasty delicate muscular, brown ruddy urine c) Normal walk, wobbly, downfall, rump muscular bulge, compact rubber delicate muscle, brown-ruddy urine

c) Normal walk, wobbly, downfall, rump muscular bulge, compact rubber delicate muscle, brown-ruddy urine

Muscular degeneration myoglobin-micturition effects a) Muscular atrophy, lameness, recumbency  death b) Claudication, debilitation, renal failure c) Atrophic muscular slow degeneration, claudication, myocardosis

a) Muscular atrophy, lameness, recumbency  death

Muscular degeneration myoglobin-micturition prevention a) During rest days be aware of changing the feed, ensure the calm of the resting horse, gradual increase of the forage portion b) Half forage portion under rest days, ducting, after first interception humane loading c) During rest days vitamin B supplement, be aware that the horses are under calm condition in their equerry, they have limitations under hard work in the first day

c) During rest days vitamin B supplement, be aware that the horses are under calm condition in their equerry, they have limitations under hard work in the first day

Muscular degeneration myoglobin-micturition what to do a) Try to rig up the recumbent horse to put up to walk, give it vitamin B, blood-letting b) Transfer the recumbent horse to its equerry and place it to a hammock, abet the healing with blood-letting and vit B inj c) Immediately terminate the work, grooming, give it NaHCO3, flunixin-meglumine, if a horse cannot stand up, it has a big change to die

c) Immediately terminate the work, grooming, give it NaHCO3, flunixin-meglumine, if a horse cannot stand up, it has a big change to die

Muscular degeneration (myalgia) incidence in horse a) Racehorse under hard/drastic load, stress, individual sensibility b) Racehorses with hard loading without training, after transport, inherited individual sensibility c) Syndrome under horse transportation or racing, it’s familiar in studs, the individual sensibility has a big lead in it

a) Racehorse under hard/drastic load, stress, individual sensibility

Muscular degeneration (myalgia) symptoms in horse a) Claudication, drop with comedown, hobbyhorse attitude b) Racehorses with hard loading without training, after transport, inherited individual sensibility c) Breast-, loins-, thigh muscular to be swollen and to be stiff, serious and irreversible lameness, renal failure

b) Racehorses with hard loading without training, after transport, inherited individual sensibility? maybe a is better ?

Pathophysiology of post-exercise myopathy (myoglobinuria paralytica)/Horse? a) Muscular-glycogen ↑ -> local lactic acid ↑ -> vasoconstriction due to hypoxaemia -> Zenker type myopathy -> muscular-paralysis + myoglobinuria b) Hypoxia -> anaerobe glycolysis ↑-> local lactic acid ↑ -> myonecrosis -> + myoglobinuria + tubulonephrosis c) Hypoxia -> anaerobe glycolysis ↑ -> local lactic acid ↑ -> Zenker type myopathy -> + myoglobinuria + immune-mediated glomerulonephritis

b) Hypoxia -> anaerobe glycolysis ↑-> local lactic acid ↑ -> myonecrosis -> + myoglobinuria + tubulonephrosis

Physical properties of horse urine a) Mucous containing mucin, muddy, rich in Ca-carbonate b) Streams easily, contains mucin, translucid, contains Mg-P c) Streams with difficulty, contains protein, translucid, contains Ca-Oxalate

a) Mucous containing mucin, muddy, rich in Ca-carbonate

Cause of renal infarction a) Large necrosis, hemophilic area in cortex of kidney, embolia renalis, migration of Strongylus vulgaris 0 thrombosis – embolia b) Circumscribed infarct with hemorrhagic area in kidney, embola in arteria renalis, migration of Strongylus vulgaris – thrombosis – embolia

b) Circumscribed infarct with hemorrhagic area in kidney, embola in arteria renalis, migration of Strongylus vulgaris – thrombosis – embolia

Renal infarct CS a) Deterioration of hematuria, colic, renal failure b) Serious hematuria – shock – bleeding out c) Sudden occurrence of large amount of urine, enlarged kidneys

c) Sudden occurrence of large amount of urine, enlarged kidneys

Causes of nephrotoxicosis from drugs or chemicals a) Gentamicin, hemoglobin/myoglobin, heavy metals b) Aminoglycosides, glucocorticoids, Pb, Hg, Se c) Cephalosporins, NSAID’s, aflatoxin

a) Gentamicin, hemoglobin/myoglobin, heavy metals ?

Causes of vitamin nephropathy a) Calciferol, riboflavine, menadion, nikotinacid b) Menadion-natrium, ergocalciferol, cholecalciferol c) Tocoferol, menadion-natrium, calciferol

b) Menadion-natrium, ergocalciferol, cholecalciferol

Plants and drugs causing nephrosis acuta a) Aflatoxin, ochratoxin, tetracyclines, gentamicin, levamisole b) Fumonisin, aflatoxin, plants rich in oxalate, aminoglycosides, cephalosporins c) Mycotoxins, plants rich in oxalate aminoglycosides, monensin

c) Mycotoxins, plants rich in oxalate aminoglycosides, monensin

Severe acute nephrosis/combined aetiology/horse? a) Endotoxaemia + repeated flunixin meglumine + dehydration b) Endotoxaemia + repeated flunixin meglumine + overdosed HAES-infusion c) Repeated flunixin meglumine + NSAID + cephalosporins d) Clostridium botulinum toxin + repeated furosemide infections

a) Endotoxaemia + repeated flunixin meglumine + dehydration

Characteristics of urticaria in horses? a) Can be caused by inhaled allergens (fungi), rounded wheals on the skin within minutes or hours. Usually fast healing, but it might reoccur b) Can be caused by inhaled allergens (dust), rounded wheals on the skin within days. Always fast healing c) Can be caused by fodder (e.g. oat), rounded wheals on the skin always together with small bleedings of mucosa membranes (nose, mouth) d) Caused by nettle plant, allergic reaction with pruritus and alopecia, rapid regeneration

a) Can be caused by inhaled allergens (fungi), rounded wheals on the skin within minutes or hours. Usually fast healing, but it might reoccur

Etiology of secondary photodermatitis in horses? a) Uptake of photosensibilizing plants b) Accumulation of phylloerythrin (from chlorophyll) caused by hepatic insufficiency c) Retention of photosensibilizing substances because of renal failure d) Contact dermatitis caused by pasture plants phylloerythrin

b) Accumulation of phylloerythrin (from chlorophyll) caused by hepatic insufficiency

Photosensitisation/which statement is not true? a) Hypericum perforation (st. johns wort) causes primary photosensitization b) Fagopyrum esculentum & lupinus albus cause secondary photosensitisation c) Hepatogenous photosensitisation is characterised by phylloerythrin accumulation d) The colchicine does not cause photosensitization

b) Fagopyrum esculentum & lupinus albus cause secondary photosensitisation

Secretolytics for horses? a) Atropine, terbutaline, dembrexine b) Acetylcysteine, bromhexine, dembrexine c) Terbutaline, clenbuterol, dexamethasone d) Clenbuterol, albuterol, dembrexine

b) Acetylcysteine, bromhexine, dembrexine

Atrial fibrillation in horses treatment: a) Quinidine sulphate b) Procainamide c) Lidocaine

a) Quinidine sulphate

Atropine toxicosis/horse/treatment? a) Pilocarpine b) Physostigmine c) Metoclopramide d) Lidocaine

b) Physostigmine

Intestinal motilisers for horses (prokinetics) a) Flunixin meglumine, metoclopromaide b) Neostigmine, lidocaine c) Xylazine, neostigmine d) Morphine, neostigmine, lidocaine

b) Neostigmine, lidocaine?

EIPH/ horse/ therapy a) Furosemide b) Antibiotics c) Non-steroid anti-inflammatory drugs d) Glucocorticoids e) Vitamin C

a) Furosemide

COPD (RAO)/Drugs/Horse? a) Clenbuterol, atropine, fluticazon b) Albuterol, ipratropium, trilostane c) Salmeterol, aminofillin, edrophonium d) Antihistamines, aspirin

a) Clenbuterol, atropine, fluticazon

Secretolytics for horses? a) Atropine, terbutaline, dembrexine b) Terbutaline, imodium c) Terbutaline, clenbuterol d) Acetylcysteine, bromhexine

d) Acetylcysteine, bromhexine

Glucocorticoids for horses (in RAO/COPD)? a) Beclometazon, triameinolone, fluticazon b) Bromhexine, dembrexine, dobutrex c) Albuterol, clenbuterol, salmeterol d) Atropine, ipratropium bromide, scopolamine bromide

a) Beclometazon, triameinolone, fluticazon

Neonatal pharyngeal weakness/foal? a) Clinical signs: milky nasal discharge, bruxism, fever b) Physiologic up to 2-4 weeks of age c) Treatment with calcium d) Treatment with antibiotics and NSAIDs

b) Physiologic up to 2-4 weeks of age

EGUS/clinical signs/foals/NOT true? a) Diarrhoea b) Salivation c) Colic d) Fever

d) Fever

General therapy in equine hepatitis diseases? a) Diet low in carbohydrates, vitamin B, folic acid, lactulose b) Diet restricted in protein, glucose iv., insulin, B-vitamins, antioxidants c) Diet low in lipids, insulin, heparin d) Diet high in lipids, vitamin E

b) Diet restricted in protein, glucose iv., insulin, B-vitamins, antioxidants

Causes and features of Tyzzer-disease in horses? a) Listeria monocytogenes-caused meningoencephalitis b) Actinobacillus equulis infection, septicaemia in foals c) Clostridium piliforme acute hepatitis in foals d) Clostridium botulinum, hepatocencephalopathy in foals

c) Clostridium piliforme acute hepatitis in foals

General therapy in equine hepatic diseases? a) Diet low in carbohydrates, vitamin B6, folic acid, lactulose b) Diet restricted in protein, glucose iv, insulin, B-vitamins, antioxidants c) Diet low in lipids, insulin, heparin d) Diet high in lipids, vitamin E

b) Diet restricted in protein, glucose iv, insulin, B-vitamins, antioxidants

Additional diagnostic methods in Equine hepatic diseases: a) Ultrasound examination, Ultrasound guided biopsy b) Ultrasound examination, ultrasound guided liver biopsy c) Doppler ultrasound, radiography, diagnostic laparotomy d) Creatinine clearance test, Bromsulphthalein, clearance test

a) Ultrasound examination, Ultrasound guided biopsy

Large strongyles may cause? a) Thromboembolism b) Chronic diarrhoea c) Intussusceptions d) Gastric ulceration

a) Thromboembolism

Chorioptes mange affects horses'? a) Head b) Limbs c) Mane d) Ventral abdomen

b) Limbs

Blood-sucking lice in horses: a) Haematopinus asini can cause anaemia in foals b) Linognathus vituli causing anaemia and weakness c) Hippobosca equienea; can cause anaemia in adult horses

a) Haematopinus asini can cause anaemia in foals

Blister beetle causes? a) Intussusception, anaemia, hypokalaemia b) Diarrhoea, haematuria, hypomagnesemia, hypocalcaemia c) Diarrhoea, myocardial necrosis, hypochloraemia, hypermagnesemia d) Gastric ulceration, oliguria, invagination

b) Diarrhoea, haematuria, hypomagnesemia, hypocalcaemia

Ethmoid hematoma/cause? a) Traumatic injury of the ethmoid region (e.g. nasogastric tubing) b) Secondary to hemostatic problems c) Angiomatous tissue overgrowth d) Neoplastic origin

c) Angiomatous tissue overgrowth

Curative treatment of hypovolaemic shock in horses a) Perfusion, isotonic infusion 10-20 ml/ttkg/24h, dextran b) 40-50ml hypertonic infusion/24h, perfusion c) 40-60 ml/ttkg Ringer-liquor; fast infusion, dextran-liquor, plasma inf.

c) 40-60 ml/ttkg Ringer-liquor; fast infusion, dextran-liquor, plasma inf.

Haemolytic anaemia causes in horses a) Infectious anaemia, babesiosis, leptospirosis, immune-/autoimmune processes b) Infectious anaemia, leptospirosis, listeriosis, immune-/autoimmune processes c) Infectious anaemia, horse plague, strangles, immune processes

a) Infectious anaemia, babesiosis, leptospirosis, immune-/autoimmune processes

Haemolytic syndrome of foals a) Destruction of the equine foetus, in 1-w postprandially weakness, haemolyticus icterus  death b) Immunogenetic origin, after colostral uptake, 1/2-3d postprandially, haemolysis, icterus c) Blood type incompatibility  destruction of the fetus in the uterus, icterus at birth, haemoglobinuria, unviability

b) Immunogenetic origin, after colostral uptake, 1/2-3d postprandially, haemolysis, icterus

Congenital coagulopathies in horses a) Haemophilia-A and –B, in stallions; von Willebrand disease: recessive inheritance, in mares b) Haemophilia B: Belgian horses and ponies; von Willebrand disease: symptoms in elderly horses c) Haemophilia-A: recessively inherited in stallions; von Willebrand-disease: recessively inherited, independent from sex

c) Haemophilia-A: recessively inherited in stallions; von Willebrand-disease: recessively inherited, independent from sex

Haemorrhagic purpura causes a) Immune complex production in chronic purulent processes  immune-originated vasculitis  plasma and blood outflow b) Immune disease in horses after viral infections immune complex forming  immune-originated vasculitis  plasma and blood outflow c) Autoimmune disease, immune complex formation  vasculitis of autoimmune origin  plasma and blood outflow

a) Immune complex production in chronic purulent processes  immune-originated vasculitis  plasma and blood outflow

Haemorrhagic purpura symptoms a) Haemorrhages, haematomas, “elephant leg”, “hippo head”, hypovolaemia b) Haemorrhages in the mucous membranes, skin oedema, oedema of the head, leg, ventral abdominal hypoproteinemia c) Urticaria, haemorrhages, exudation under the skin and in coelomae?, hypovolaemic shock

b) Haemorrhages in the mucous membranes, skin oedema, oedema of the head, leg, ventral abdominal hypoproteinemia

First symptoms of haemorrhagic purpura, localisation a) Glottis, conjunctiva b) Internal nasal wings, lips c) Mucosa of the preputium, outer genital organs

b) Internal nasal wings, lips

Haemorrhagic purpura treatment a) NSAID treatment, transfusion, isotonic infusion, ABs b) Glucocorticoid treatment, transfusion, infusion of glucose, heparin c) Treatment of purulent process (abscess), dexamethasone, blood plasma IV, ABs to treat the original matter

c) Treatment of purulent process (abscess), dexamethasone, blood plasma IV, ABs to treat the original matter

Thrombophlebitis therapy in horse a) Locally: ice packing, parenteral: prednisolone, ABs, operation: phlebotomy b) Locally: iodine paste, parenteral: NSAID-drugs, ABs, operation, phlebotomy c) Locally: prednisolone-paste, parenteral: heparin, ABs, operation: phlebotomy, transplantation from v. femoralis

c) Locally: prednisolone-paste, parenteral: heparin, ABs, operation: phlebotomy, transplantation from v. femoralis

Thrombophlebitis prevention in horse a) In case of several IV injections rotating, using correct IV catheter, heparin flush through the catheter b) Compliance with the regulation of IV application, catheter sterilization/heparin, we do not ive tissue-irritant materials IV c) Keep the asepsis, applicating tissue irritant material to the vein is allowed only when also use heparin, use vein needle as thin as possible

a) In case of several IV injections rotating, using correct IV catheter, heparin flush through the catheter

Hyperlipaemia of mares occurrence a) Lipemic blood plasma is a symptom characteristic of a metabolic disease of Arabian mares, which occurs often after exercise b) In this serious metabolic disease, that occurs mainly in mares before parturition, hyperlipaemia is the main symptom, blood triglyceride >5-6mmol/L c) The around parturition often occurring lipidaemia is a symptom suggesting hepatopathy

b) In this serious metabolic disease, that occurs mainly in mares before parturition, hyperlipaemia is the main symptom, blood triglyceride >5-6mmol/L

Hyperlipaemia of mares pathogenesis a) In draft mares, pregnancy, physical overload, malnutrition b) Idiopathic disposition, low energy nutrition, in the last trimester of pregnancy, wasting disease c) Breed disposition, pregnancy, obesity, stress, anorexia

c) Breed disposition, pregnancy, obesity, stress, anorexia

Hyperlipaemia of mares symptoms a) Colic  weakness, hepatocerebral syndrome, lipaemic plasma b) Colic, fever, icterus, weakness, disturbed plasma c) Lack of appetite, diarrhea, icterus, nervous signs, bloody-disturbed plasma

a) Colic  weakness, hepatocerebral syndrome, lipaemic plasma

Hyperlipaemia of mares treatment a) Antispasmodic/sedatives, in case of colic: walking, high energy nutrition, infusion several times b) Stall rest, 4h long drip infusion/Ringer solution + glucose, artificial nutrition, liver protective therapy c) Gentle treatment, regular walking, glucose infusion several times, insulin, heparin

b) Stall rest, 4h long drip infusion/Ringer solution + glucose, artificial nutrition, liver protective therapy

Hyperlipaemia of mares prevention and prognosis a) Suitable management and nutrition, avoid exercise during pregnancy. Reacts good to therapy. b) Good nutrition during pregnancy, vitamin supplementation. It is mostly favourable without treatment. c) Avoid fattening during pregnancy, avoid stress and predisposing diseases. Therapy is often ineffective, high death risk.

c) Avoid fattening during pregnancy, avoid stress and predisposing diseases. Therapy is often ineffective, high death risk.

Yellow fat disease and steatosis horse a) Fat tissue discoloration, degeneration, and steatitis mainly in pony foals b) Yellow discoloration of SC fat tissue in overfed horses. Icterus, swelling in the fat tissue. c) In lg breed, fat horses. Yellow swellings in the skin, formation of increments, icterus

a) Fat tissue discoloration, degeneration, and steatitis mainly in pony foals

Yellow fat disease and steatosis pathogenesis a) Fat degeneration and steatitis because of Fe- and E-vitamin deficiency, Fe- and/or Se- deficient nutrition, formation of glutathione-peroxidase decr b) Lesions of adipocytes because of fatty acid peroxidases at the embryonic stage, Se or E-vitamin deficiency, food rich in peroxidases c) In areas lacking Se, without Fe-replacement in case of dominance of oxiperoxidases: adipocytes degeneration and necrosis

b) Lesions of adipocytes because of fatty acid peroxidases at the embryonic stage, Se or E-vitamin deficiency, food rich in peroxidases

Yellow fat disease and steatosis symptoms a) Muscle weakness, gradually slowing movement, SC oedema, painful movement of neck. b) Skin discoloured into yellow; yellow, palpable, sensitive swellings on the head + neck c) Muscle weakness, foal paralysis, painful movement of the head and neck, painful swellings on the neck

c) Muscle weakness, foal paralysis, painful movement of the head and neck, painful swellings on the neck

Yellow fat disease and steatosis treatment and prevention a) High energy/carbohydrate food, Se and E-vitamin replacement, analgesics b) Liver protective therapy, glucose infusions, analgesics c) Food rich in fibre, analgesics, spasmolytics, physiotherapy

a) High energy/carbohydrate food, Se and E-vitamin replacement, analgesics

Indirect causes of diarrhoea

NSAIDs, AB

Increased borborygmi sound causes

Spasmodic colic

Dereased borborygmi sound causes

Obstruction( displacements, strangulation , paralysis)

Direction of colonic torsion

>90 most of the time (270- 720, medially & dorsally)

Causes of colic in geriatric horses

Pendunculated lipoma, obstruation – bad dentition

Drug for acting against endotoxins

Polymyxin-B, Flunixin meglumin

Faeces with red worms, what parasite?

Cyanthostoma (small strongyles )

Where would you look for sand impaction on an US?

Right dorsal (most common) / ventral colon

Name 4 windows of US abdomen

Stomach: left 10 –(12th) - 15th | Spleen & left kidney: left 16th IC space

% of thrombophlebitis

18.5%

Duration of polyethylene catheter

up to 3 days

Treatment of proximal enteritis

removal of gastric reflux, intravenous administration of balanced electrolyte solutions, lidocaine as a continuous intravenous infusion, drugs designed to combat the ill effects of endotoxemia ( Flunixin)

Liver enzyme parameter

GGT (SDH, AST, BA, GLDH)

Most common physiological arrhythmia

2nd degree AVBlock

Which nerve is affected if the tongue is paralyzed

N.hypoglossus

What is isosthenuria and how to dx it

Normal: SG >1.020, Isothenuria SG<1.020 • Causes: AKD, CKD – glomerulonephritis – PLN • EIA, lepto, EHV • TX: fluid therapy, inc. CHO dec. protein, glucocorticoids, plasma

Nerve block for cheek tooth 208? Extraction?

N. Maxillaris

Non-musical adventitious resp sound

crepitation, crackling or rattling sound

Most important measurement technique during GA

Blood-gas

Artery for taking pulse rate

A transversa faciei

Respiratory rate physiological

8-16

What to do with pelvic flexure Obstipation

Nasogastric Tubing water and oil |  Surgery: enterotomy

Most distal perineural nerve block that blocks entire hoof

Abaxial sesamoid

Which tooth is most commonly affected in 10 year old horses

2/3rd mandibular cheek teeth 407/408 or 307/308 | 3/4th maxillary teeth( 4th maxillary molar – oldest) (108/109 or 208/209)

Ocular examination which drug dose and effect?

1% tropicamide sympathomimetic – local anaesthetic Atopine – mydriasis Ophthalmoscope

Induction of anaesthesia

Ketamine

Most common skin tumors

Sarcoid

What is the most common side for ocd lesions in horses with exact description of place and joint?

DIRT- distal intermediate ridge of the tibia dorsal In the talocrural joint

What is the most common gastric disease in adult horses?

Gastric ulcer - EGUS

Equine Exam Flashcards

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