Equine 1 Flashcards by Laura O'Donoghue

Indirect causes of diarrhoea

NSAIDs, AB

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Increased borborygmi sound causes

Spasmodic colic

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Dereased borborygmi sound causes

Obstruction( displacements, strangulation , paralysis)

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Direction of colonic torsion

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

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Causes of colic in geriatric horses

Pendunculated lipoma, obstruation – bad dentition

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Drug for acting against endotoxins

Polymyxin-B, Flunixin meglumin

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Where would you look for sand impaction on an US?

Right dorsal (most common) / ventral colon

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Name 4 windows of US abdomen

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

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Duration of polyethylene catheter

up to 3 days

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% of thrombophlebitis

18.5%

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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)

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Liver enzyme parameter

GGT (SDH, AST, BA, GLDH)

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Most common physiological arrhythmia

2nd degree AVBlock

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Most common physiological arrhythmia

2nd degree AVBlock

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Which nerve is affected if the tongue is paralyzed

N.hypoglossus

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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

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Nerve block for cheek tooth 208? Extraction?

N. Maxillaris

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Non-musical adventitious resp sound

Non-musical rhonchi (crepitation, crackling or rattling sound)
* Sudden arising and stopping sounds
* These noises are generated at the beginning (larger bronchi >2mm) or end (smaller bronchi<2mm) of inspiration, sometimes continuing to the beginning of expiration. They occur in areas that are not adequately filled with respiratory gases but are infiltrated with fluid.
These sounds are caused by the abrupt opening of previously closed bronchi + vibration of the small bronchial wall
Early inspiratory or expiratory crepitation and crackling:
* obstruction of bronchi that are >2 mm in diameter (e.g. bronchopneumonia, COPD) Late inspiratory crepitation and crackling:
3
* compression of the bronchi <2 mm in diameter (pulmonary edema, interstitial pneumonia, neoplasms, pulmonary emphysema)

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Most important measurement technique during GA

Blood-gas

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Artery for taking pulse rate

A transversa faciei

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Respiratory rate physiological

8-16

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What to do with pelvic flexure Obstipation?

Nasogastric Tubing water and oil
Surgery: enterotomy

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Most distal perineural nerve block that blocks entire hoof

Abaxial sesamoid

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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)

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Ocular examination which drug dose and effect?

1% tropicamide sympathomimetic – local anaesthetic Atopine – mydriasis Opthalmoscope

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 Cranial distal aspect of the intermediate ridge of the tibia Medial Malleolus

What is the most common gastric disease in adult horses?

Gastric ulcer - EGUS

The predilection site of OCD in the equine hock is  The central part of the distal intertarsal joint  The medial malleolus  The talocalcanei joint  Sustentaculum tali

The medial malleolus

The predilection site of OCD in the equine hock is  The central part of the distal intertarsal joint  The medial malleolus  The talocalcanei joint  Sustentaculum tali

The medial malleolus

The proper name of the skyline-view for the examination of the equine carpus is  Dorsoproximal-dorsodistal oblique view  Dorsoproximal-palmarodistal oblique view  Caudoproximal-craniodistal oblique view  Palerolateral view

Dorsoproximal-dorsodistal oblique view

The exclaiming time needed to see an osteophyte formation on equine radiograph is  1-2w  2-3w  3-5w  4-7w

3-5W

The exclaiming time needed to see an osteophyte formation on equine radiograph is  1-2w  2-3w  3-5w  4-7w

3-5W

The proper name of the "oxpring' view for the examination of the navicular bone is:  Palmaroproximal-palmarodistal oblique view  Dorsoproximal-palmarodistal oblique view  Caudoproximal-craniodistal oblique view  Palmarolateral view

The most common site of sub-chondral bone cyst in equine is: 7  Medial femoral condyle  Lateral femoral condyle  Medial trochlea  Lateral trochlea

Where can a Birkenlund fracture be found in a horse?  In the dorsal recess of the fetlock joint  In the palmar/plantar recess of the fetlock joint  In the dorsal recess of the...

OCD location in hock?

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

Which statement is false?  Phenothiazines should be used with care in stallions  Phenothiazines are not usable in shock patients  Midazolam is an adequate drug to treat tetanus in horses  Phenothiazines are given most frequently to colic horse to reduce visceral pain

Which is false?  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 hrose  d. Neuropathy can develop due to inadequate positioning during anaesthesia

Which is true?  Left laryngeal hemiplegia more common in ponies  Tracheal collapse is more common in thoroughbreds  Guttural pouch tympany typically affects older horses  Lymphoid hyperplasia typically affects young horses

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

In the colic horse surgery the large colon enterotomy should be created to rinse out the content of the  Dorsal colon  Ventral colon  Pelvic flexure  Ligamentum caeco-colicum

The advised surgical method to treat upward fixation of the patella in horses is:  Lateral femoro-patellar ligament desmotomy  Medial femoro-patellar ligament desmotomy  Intermediate femoro-patellar ligament desmotomy

How do you suture the trachea of a horse?  Min 1 layer  Min 2 layers  Min 3 layers  Min 4 layers

How can you perform a more or less “specific” anaesthetise the origin of the suspensory ligament (m. interosseus medius) in the front limb?  High palmar nerve block  Lateral palmar nerve block  Carpometacarpal joint anaesthesia  N. medianus anaesthesia

How can you anaesthetize the origin of the suspensory ligament (interosseus medius) on the hind leg?  With the abaxial sesamoidean block  With the low six point block – it will be anaesthetized within 30 min  With the deep branch anest. Of the lat. Plantar nerve  With the high plantar nerve anaesthesia

Intermittent lameness horse  Lameness occurring in comitions because of the degeneration of the femoral muscles plus haemoglobinuria  Moving disability of the HLs occurring in loading disappearing at rest, with unknown origin  Lameness of sport horses receiding for loading, caused by the thrombosis of the terminal aorta or iliac arteries

Intermittent lameness symptoms horse? -Movement disorders in one of the HLs when loaded, disappearing after 20mins of resting  Feel wobbly when loaded, lameness of the HLs, disappearing after half an hour  Movement disorder of the FLs or in one of the HLs, when competing, disappearing after a short time of resting.

Osteoporosis horse  Thinning of the bone compacta due to the disturbance of Ca-metabolism  Hereditary, breed disposition, compacta incr / medullary cavity decr  Thickening of the tubular bones due to the disturbance of the mineral supply

Osteoporosis CS horse  Thickening of the tubular bones, sensitivity to pressure, lameness  Genu valgum, locomotion disorder, exostoses on the leg bones  Retardation, spontaneous fractures, ruptures, not viable

Hyperplastic osteopathy (acropachia) horse  Symmetrical deformation of the distal leg bones, in connection with diseases of the (GIT, Thoracic, UGT)  Congenital acropachia, intensive pain to pressure, locomotion disorderakinesia  Metabolic disturbance of the leg bones with pain of unknown origin, advance in application of glucocorticoids

Laminitis, diffuse aseptic/definition  Degeneration/necrosis of horny matter of the hoof due to circulatory disturbance, exungulation, deformation of the distal phalanx  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  Degeneration/necrosis of the horny matter of the hoof and distal phalanx, local circulatory disturbance

Diffuse aseptic laminitis etiology  Overfeeding in fat animals, consequence of allergy/atopia, influence of burden  Malnutrition, complication of diseases, immune/autoimmune origin  Malnutrition, complication of diseases, in postparturient period, influence of burden

Diffuse aseptic laminitis nutritional origin  Carbohydrate and protein rich nutrition, fungus contaminated hay  Carbohydrate rich nutrition, low-protein/fibre rich nutrition, fungus contaminated corn fodder  Easy fermentation, carbohydrate and fiber rich nutrition, fungus contaminated corn fodder

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

Diffuse aseptic laminitis symptoms  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  Hoof warm/intensive pain to pressure, warm and painful edema on the leg, intermittent claudication  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  Elimination of the causative, soft littering, complete rest, fixing of the hoof, plastering of the hoof, cool pack, hepatin, flunixin-meglumide  Elimination of the causative, peat littering, complete rest, fixing of the hoof, ice pack, glucocorticoids  Soft littering, only moderate movement, ice pack, strong analgesic, phenylbutazone, prednisolone

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

Which structure cannot be palpated certainly at rectal exam in the horse?  Ventral taenia of caecum  Duodenal ligament  Ligamentum lati uteri  Ligamentum renolienale

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

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

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

Which statement is true?  In direct inguinal hernia, the SI escape into the SC space of the scrotum  The indirect inguinar hernia is more common than the direct on  Both  None

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

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

In which case is rectal admin. inappropriate?  Dysphagia  Lockjaw  Reflux  Diarrhea

What is the location of the base of the caecum in a normal adult horse?  Left paralumbar fossa  Right paralumbar fossa  Left ventral abdomen  Right ventral abdomen

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

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

Colic-like symptoms causes  Meningitis, COPD, estrus  Rabies, urinary diseases, genital diseases  Encephalon oedema, pneumonia, Lyme-disease

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

Parasitic cause of colic  Toxocara equi, Bunostomumum magnum infection  Strongylosis, Ascariosis  Toxacariosis, Strongyloidosis

Viral and bacterial causes of colic  Salmonellosis, Clostridiosis, Arteritis  Anthrax, rabies, pyelonephritis  Rabies, lyme disease, salmonellosis

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

Colic disease pathological dislocations  Internal hernias, torsion of small intestines, colon dislocation  Stomach, small intestines, colon torsion  Diaphragmatic hernia, duodenum torsion, ileum torsion

Colic symptoms causing agents  Atropine, clavulanic acid, diazepam  Amitrase, arekolin  Organophosphorous compounds, amitrase, chlorpromazine

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

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

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

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

Reasons for endotoxaemia in colic  Increase of gr+ bact, circulation disorder of intestinal wall, typhocolitis  Bact incr/collapse, ischaemia of intestinal wall, ileus  Collapse of gr- bact, incr of lipoproteins? LPS, disorder of intestinal absorption

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

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

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

Colic horse blood exam in practical circumstances  Qual blood count, Ht, TP  RBC/WBC count, qual blood count  Ht, TP, WBC count

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

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

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

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

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

Sedatives used in colic cases  Detomidine, medeteomidine  Detomidine, xylazine  Detomidine, flunixin-meglumide

Colic tx in case of endotoxaemia  Endotoxin antiserum, carbacol, detomidin  Endotoxin antiserum, medetomidine, metoclopramide  Polymixin-B sulphate, flunixin meglumide, pentoxifillin

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

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

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

Acute gastric dilatation Tx  Detomidine, xylazine, gastric lavage  Physostigmine, neostimin, flunixin meglumide  Noraminophenason, drotaverin, gastric lavage

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

Acute gastric dilatation complications  Gastric torsion, gastritis, infl of small int  Gastric meteorismus, gastric ulcers, gastritis  Laminitis, hemorrhagic gastritis, typhocolitis

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

Serous-hemorrhagic gastritis etiology  Feed w mycotoxins, lactic acid incr  Intake of immature maize, allergy  Mouldy hay, water with high nitrate

Serous-hemorrhagic gastritis CS (I don’t know what these words mean)  Serous gripes, “wineflake-like” gastric content, enteritis  Gripes perspiration, “wineflake like” gastric content, shock/death  Prostrate behaviour, “wineflake like” gastric content, laminitis

Acute gastritis CS (again.. what is going on here)  Anorexia, polydipsia, gape, breath smells sour-lushious, mild gripes  Gripes, stinky breach, retching, abd dilation  Freq gripes, stinky breath, regurgitation, left flank dilatation

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

Acute gastritis Tx  Fasting, laxation, bethanechol  Gastric lavage, laxation, physostigmine  Gastric lavage, fasting, linseed-slurry

Stomach parasite infection  Trichostrongylus, gasterophilus, habronematosis  Habronematosis, gasterophilus, parasoaridosis  Gasterophilus, habronematosis, strongylidosis

Signs of gastric parasite infestation in horse  Anaemia, fatigue, threadworm( not gastric) in feces  In colts, mild growth, irregular fur  Colic, slimming, diarrhea

Gasterophilosis  Gasterophilus, acute, gribes like gastritis, caused by gasterophilus larvae  Serous bloody gastritis caused by gasterophilus larvae, freq gribes  Gasterophilus caused by larva of equine gasterophilus causing chronic gastritis

Gastric ulcer etiology  Stress, NSAIDs, faulty nutrition  Stress, steroid anti-inflamm drugs, grazing  Fasting, NSAIDs, grazing

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

Catarrhal enteritis etiology  Vagotonia, cold water/food, meterorological front  Acute gastritis, int. obst., parasympathicotonia  Diathesis, larval migration, enteritis

C answer on slides = infectious/parasitic/canthardin toxicity – Inflammation- Increased secretion, mucosal and capillary permeability, decreased absorption - Intense peristalsis later ileus - Hemoconcentration, hypovolemia, tissue hypoperfusion, oliguria

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

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

C.......Also-reflux

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

Drugs to increase peristalsis in horses  Stigmosan, konstigmin  Neostigmine, flunixin-meglumide  Xylazine, neostigmine

Laxatives for horses  Mg sulfate, linseed mucin, detomidine inj  Paraffin, mg sulfate, stigmosan ing  Neostigmine, linseed mucin, drotaverin

Answer: b – linseed oil is also a laxative when fed in large quantities

Laxatives for horses  Mg sulfate, linseed mucin, detomidine inj  Paraffin, mg sulfate, stigmosan ing  Neostigmine, linseed mucin, drotaverin

Answer: b – linseed oil is also a laxative when fed in large quantities

Strongyloidosis horse  Bloody water like faeces, colic, weakness.  Occur inf, symptoms in case of impairment of resistance  In foals, resp symptoms, retarded growth

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

Removal of roundworm  Ivermectin, mebendazole, tetramizol  Fenbendazole, oxibendazole, ivermectin  Tiabendazole, mebendazole, tetramizol

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

Answer: c but also corona and adeno?

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

a – not sure about the pancreatitis ?

Causes of acute proximal enteritis  Fungus toxin of feed, allergy  Unknown-idiopathic, w horse feed or fodder fed horses, inf cause = C.diff/ salmonella main  In foals, when fungus toxins in milk, fungus toxicosis

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

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

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

b fever+/-, tachycardia, laminits, illeus

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

Acute proximal enteritis tx  Gastric lavage antispasmodics, intense fluid and electrolyte therapy, flunixin meglumide  Antispasmodics, analgesic drugs w increase GI motility, sucralfate  Activated charcoal, paraffin, physostigmine inj

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

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

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

b?? bacterial infection (Salmonella and Clostridium species) prolonged antimicrobial therapy, non-steroidal anti-inflammatory drugs (NSAID) toxicity, and intestinal parasitism (Blood et al., 2000). Further sudden changes in feed or the ingestion of improperly balanced daily ration of feed can alter microbial flora of large intestine leading to bacterial overgrowth

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

cute typhlocolitis pathogenesis  Enteritis – intestinal peristalsis – severe colic – ileus – shock  Intestinal peristalsis incr – diarrhea – severe colic – necrosis – peritonitis – death  Prolif of toxin forming Clostridium, starvation – rising of intestinal pH, dysbiosis, endotoxaemia/ bactericemia, damage of mucosa, diarrhea, shock

c= I think-it’s the most right

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

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

Acute typhlocolitis lab features  Ht: 0.3-0.4, TPL 30-34g/L, leukocytes: 0.3g/L, lactate: 5.2mmol/L  Ht: 0.6-0.8, TP: 80-90g/L, leukocytes: 1.303g/L, lactate: 4mmol/L Tp will drop as the proteins begin to be lost but there is an initial increase due to the dehydration,  Ht: 0.65, TP: 35g/L, leukocytes: 8.2-5.1g/L, lactate: 20mmol/L

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

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

Acute typhlocolitis medical therapy  Inf against dehydration, lincomicin, probiotics  Treatment against dehydr, metronidazole, flunixin meglumide, probiotics  Treating shock and dehydr, OTC, artificial feeding

b prevention of further absorption of toxin to the circulation, neutralization of absorbed toxins, intravenous fluid, steroidal or non-steroidal anti inflammatory drugs and toxin binders.

Cause of mechanical ileus  Enterospasm, obstruction, intestinal paralysis  Obstruction, compression, intestinal dislocation, strangulation  Enterospasm, torsion of ileum, obturation of ileum

Cause of functional ileus  Disturbance of intestinal motility, spasmodic colic  Spasmodic colic, intestinal paralysis  Long lasting colic, intestinal paralysis

Cause of paralytic ileus  Enteritis, peritonitis, abd sx  Tetanus, botulism, enterotoxicosis  Stress, tetanus, sx

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

B Spastic contraction onto obstruction, gas and fluid accumulate proximal, dilation, compression of vessels, anerobic glycol, inlfam and oedema, and increased fluid influc, lots and lots of reflux.

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

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

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

SI strangulation ileus causes  Incarceration of internal hernia, intestinal retroflexion  Invagination of SI, strangulation of SI  Torsion of SI, strangulation of SI

SI dislocation ileus causes  Internal hernia, torsion of SI  Intestinal torsion, intestinal invagination, thromb-embolic intestinal disease  Diaphragmatic hernia, intestinal spasm, torsion of SI

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

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

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

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

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

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

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

A or B - often occurs after strangles?

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

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

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

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

Primary caecal meteorism symptoms  Heavy colic, drum like dilatation of right flank, dyspnea, rectal palp; dilated cecum  Heavy colic, heavy summetric dilatation of the abdomen, dyspnea, cyanosis, rectal palp; dilated cecum  Weak/average colic, dilated flanks, dyspnea, cyanosis, rectal palp; dilated cecum/colon

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

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

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

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

Answer: all wrongish! Starve, iv fluids, nasogast fluids, flunixin as analgesia laxatives. Often surgical to prevent rupture.

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

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

Colon impaction predilection sites  Ampulla of dorsal colon, colon transversum, caeco-colic opening  Caeco-colic opening, colon transversum, ampulla of dorsal colon  Flexura pelvina, ampulla of dorsal colon, colon transversum

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

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