Equine GI 2 Flashcards by Mariano Mora

Which of the following forms of IBD is most likely to have an acute presentation with colic signs and normal plasma protein concentration?

a. Multisystemic eosinophilic epitheliotrophic disease (MEED)
b. Lymphocytic-plasmacytic enterocolitis
c. Idiopathic focal eosinophilic enteritis (IFEE)
d. Granulomatous enteritis

c. Idiopathic focal eosinophilic enteritis (IFEE)

Lesions –> intramural masses or cincunferential mural bands
Eosinophils and lymphocytes infiltrating all layers
Most likely a focal exacerbation of diffuse eosinophilic enteritis

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In horses with duodenitis-proximal jejunitis, which of the following is NOT a negative prognostic indicator?

a. Elevated serum GGT activity
b. Abdominal fluid protein concentration > 3.5 g/dL
c. Presence of hemorrhagic gastric reflux
d. Anion gap > 15 mEq/L

a. Elevated serum GGT activity

Horses with DPJ may also have increase in D-dimer
The increase in GGT activity can be also used to differentiate with SISO
Histopathologic evidence of liver pathology is a common feature in DPJ

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First target of salmonella once in the GI system

a. Crypt cells of distal ileum and cecum
b. Intestinal lymphoid tissue (M cells)
c. Peyer patches and submucosal cells
d. Kupffer cells for replication prior to colonization of enterocytes

b. Intestinal lymphoid tissue (M cells)

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Which of the following is the primary control for the inherent rhythmicity and primarily responsible for generation of slow waves within the intestine?

a. Vagus nerve
b. Sympathetic root
c. Interstitial cells of Cajal
d. Migrating motility complexes

c. Interstitial cells of Cajal

Responsible for generation and propagation of slow waves and pacemaker activity.

Reduction of ICC has been demonstrated in equine grass sickness

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Main target cells of N. risticii

a. Monocytes, macrophages
b. Monocytes, mast cells
c. Submucosal lymphocytes
d. Submucosal neutrophils

a. Monocytes, macrophages

Colonic and small intestinal epithelial cells
Colon mast cells

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Which of the following is NOT bordering the epipolic foramen?

a. caudate lobe of the liver
b. caudal vena cava
c. diaphragm
d. portal vein

c. diaphragm

Caudate process of the liver and caudal vena cava
Pancreas, hepatoduodenal ligament, portal vein

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What is the mechanism of action of bethanechol within the GI tract?

a. Ach receptor agonist –> binds to muscarinic receptors @ myenteric plexus + smooth muscle cells –> Promotility
b. Ach receptor agonist –> binds to adrenergic receptors @ myenteric plexus + smooth muscle cells –> Promotility
c. Ach receptor antagonist –> binds to muscarinic receptors @ myenteric plexus + smooth muscle cells –> Slows motility
d. Ach receptor antagonist –> binds to adrenergic receptors @ myenteric plexus + smooth muscle cells –> Slows motility

a. Ach receptor agonist –> binds to muscarinic receptors @ myenteric plexus + smooth muscle cells –> Promotility

> M3 receptors
Not degraded by anticholinestherase
Efffect throughout the GI tract

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What is the most important feature that differentiate DPJ from a strangulating intestinal obstruction?

a. Peritoneal fluid is turbid but not sanguineous
b. Disproportion of increase in TP compared to WBC in peritoneal fluid (increase TP relative to WBC)
c. Relative increase in peritoneal lactate is less than SIO
d. Peritoneal fluid glucose decrease is less sensitive than SIO

b. Disproportion of increase in TP compared to WBC in peritoneal fluid (increase TP relative to WBC)
* In strangulating lesion, peritoneal fluid WBC/TP is usually >3

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What is the best diagnostic test for Potomac Horse Fever?

a. Acute + convalescent samples for titers by ELISA
b. Acute + convalescent samples for titers by IFA
c. Fecal PCR + serum ELISA at presentation
d. Whole blood PCR at presentation

d. Whole blood PCR at presentation

Where do you expect to find the DNA?

Why not serology?

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Toxic dose for cantharidin toxicity

a. < 0.5 mg/kg; 2 g of dead beetles (~50)
b. < 2 mg/kg; 8-10 g of dead beetles (~200)
c. <1 mg/kg; 4-6 g of dead beetles (~100)
d. >10 mg/kg; 45-50 g of dead beetles (~1,200)

c. <1 mg/kg; 4-6 g of dead beetles (~100)

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What is the causative agent and treatment of choice for atypical septic peritonitis that is markedly responsive to medical therapy and has 100% short-term survival?

a. Streptococcus equi - Penicillin
b. Actinobacillus equuli - Penicillin + gentamicin
c. Rhodococcus equi - Clarithromycin
d. Lawsonia intracellularis - Oxytetracycline

b. Actinobacillus equuli - Penicillin + gentamicin

Thought to be secondary to translocation of the bacteria from the GI tract or associated with Strongylus migration

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An owner wants you to vaccinate his horse for PHF. The horse lives in the SE, and you are hesitant to give the vaccine. How can you justify your position? I know you are stubborn, but the owner is even worse!

a. The vaccine is efficacious, but it is expensive and there is very low prevalence of the disease
b. The vaccine is efficacious, but the adverse effects in the face of a low prevalence justify not to use it
c. The vaccine fails due to the presence of different strains, which is higher in areas with low prevalence
d. The vaccine fails due to the presence of different strains, and it is recommended only in endemic areas

d. The vaccine fails due to the presence of different strains, and it is recommended only in endemic areas
* Failure up to 89%

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What is the optimal diagnostic testing plan in a foal suspected to have Lawsonia intracellularis?

a. Fecal PCR & Serum PCR
b. Fecal PCR & Serum serology (ELISA or IPMA)
c. Fecal ELISA & Serum PCR
d. Fecal PCR alone

b. Fecal PCR & Serum serology (ELISA or IPMA)

Both have high specificity but variable sensitivity
Negative PCR: previous ATB treatment or advanced disease
- Real-tiime PCR > sensitivity
Negative serology: early stage of disease
- IPMA has > sensitivity

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Which characteristic electrolyte derangement is associated with Cantharidin toxicity?

a. Hypocalcemia
b. Hypercalcemia
c. Hypokalemia
d. Hyperkalemia

a. Hypocalcemia

Both hypocalcemia and hypomagnesemia are common features
Synchronous diaphragmatic flutter is often observed

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Best disinfectant to kill the clostridium spores

a. Iodine
b. Sodium hypochlorite
c. Formalin
d. Hydrogen peroxide

b. Sodium hypochlorite

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What is the mechanism for heparin to prevent intra-abdominal adhesions?

a. Decrease fibrin formation by inhibiting thrombin
b. Decrease fibrin formation by promoting thrombin
c. Decrease fibrin formation by increasing endothelial tight junctions in capillaries
d. Increase fibrin formation by inhibiting thrombin

a. Decrease fibrin formation by inhibiting thrombin

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In foals, ulcerative duodenitis can produce clinical signs of fever, colic or diarrhea. Which clinical manifestation is highly suggestive of duodenal dysfunction?

a. Delayed gastric emptying (> 30 mins)
b. Irregular mucosal border of the stomach
c. Increase in duodeno-gastric reflux of bile through the pylorus
d. Decrease response of antiacid treatment

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c. Increase in duodeno-gastric reflux of bile through the pylorus
* Delayed gastric emptying is considered if > 2 hours

Which one is less likely a possible etiologic agent of DPJ in horses?

Clostridium perfringes
Clostridium dificile
Clostridium novyi
Salmonella
Fusarium moniliforme

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c. Clostridium novyi

All of the others are possible agents, but the disease is likely multifactorial.

In equine proliferative enteropathy, which is the most characteristic lesion?

a. Hyperplasia of the enterocytes of the distal duodenum
b. Proliferative adenomatosis of the distal jejunum and ileum
c. Increase mitosis of cells in the crypt cells of proximal duodenum
d. hyperplasia of the muscularis and lamina propria of the distal jejunum and ileum

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b. Proliferative adenomatosis of the distal jejunum and ileum

Invasion of proliferative crypt cells in the ileum → ↑ mitotic division → hyperplasia
Weight loss is usually the first sign observed

Meckel diverticulum is a remnant of embryonic structure causing a blind pouch from which structure?

a. cecal base
b. duodenum
c. ileum
d. esophagus

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c. ileum

It forms a blind pouch off the antimesenteric border of ileum that can sometimes attach to umbilicus, which can cause strangulating SI lesions

What is the most predominant excitatory neurotransmitter in the gastrointestinal tract?

a. leptin
b. acetylcholine
c. norepinephrine
d. gastrin
e. cholecystokinin

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b. acetylcholine

Mediates parasympathetic nervous system. Important for mechanism of action of prokinetics.

What is the first step in the response to local inflammation in the equine peritoneum?

a. Peritoneal mast cells + macrophages release histamine + serotonin –> Chemotaxis of neutrophils from capillaries into peritoneal fluid
b. Peritoneal mast cells + macrophages release histamine + serotonin –> Vasodilation + vascular permeability causes leakage of plasma into peritoneal fluid
c. Chemotaxis of neutrophils from capillaries into peritoneal fluid –> Peritoneal mast cells + macrophages release histamine + serotonin
d. Chemotaxis of neutrophils from capillaries into peritoneal fluid –> Vasodilation + vascular permeability causes leakage of plasma into peritoneal fluid

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b. Peritoneal mast cells + macrophages release histamine + serotonin –> Vasodilation + vascular permeability causes leakage of plasma into peritoneal fluid

Remember that mesothelial cells release TPA
- If they are damaged –> decrease TPA and increase thromboplastin –> fibrin formation

What is the best test to declare a stall free of salmonella (biosecurity purposes)

a. 5 cultures, 1 day apart of surface swabs
b. PCR of surfaces by using a wet gauze
c. Hose the stall first and 3 cultures of the fluid drained
d. Hose the stall and 2 PCRs of the drained fluid

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b. PCR of surfaces by using a wet gauze

How can a horse acquire PHF?

a. Contact of infected fluke larvae with open wound
b. Ingestion of N. risticii carried in houseflies secretions
c. Ingestion of aquatic insects or ingestion of infected fluke larvae
d. Ingestion of contaminated deer feces or ingestion of aquatic insects

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c. Ingestion of aquatic insects or ingestion of infected fluke larvae
* Contaminated fluke is available from snail secretions

What is the pathologic lesion in lethal overo white syndrome? a. Blind-ended, non-continuous segment of large colon, from mutation in endothelin receptor type B gene b. Blind-ended, non-continuous segment of large colon, from ischemic vascular event during embronic development c. Continuous intestinal tract with myenteric aganglionosis, from mutation in endothelin receptor type B gene c. Continuous intestinal tract with myenteric aganglionosis, from ischemic vascular event during embronic development

c. Continuous intestinal tract with myenteric aganglionosis, from mutation in endothelin receptor type B gene * What is the mutation trait? * Which phenotype of mare and sire is at higher risk?

Which drug is the best to enhance gastric emptying in foals with ulcerative duodenitis? a. Lidocaine b. Escopolamine c. Erytromycin d. Bethanecol

d. Bethanecol

The most important factor protecting the duodenal mucosa from gastric acid secretions are what? 1. Absorption of the gastric acid and pepsin by small intestinal cells 2. Sodium and Bicarb-rich secretions 3. Potassium and peptic secretions 4. Chloride secretion and pepsin absorption by small intestinal cells

b. Sodium and Bicarb-rich secretions Sodium and bicarb rich secretions probably originating from the pancreas neutralize acid entering the duodenum from the stomach.

Which of the following adhesion mechanisms has had the most dramatic impact on adhesion formation? a. carboxymethylcellulose b. simple lavage (no additives) c. heparin in lavage d. recombinant tPA e. sodium hyaluronate

The incidence of duodenal ulcer disease is greater in foals \<1 yo and it’s believe to be associated with rotavirus infection and/or H. Pylori infection. a. True b. False

False. In the 80’s it was thought to be associated with rotavirus infections however it has been proven that most foals with duodenal ulcer disease are not infected with rotavirus. Also, the relation to H. pylori infection it’s in humans but has not been proven in equines.

In weanlings infected with L. Intracellularis, the mechanism of enteritis involves: a. There’s severe edema of the small intestines and secondary hypoalbuminemia due to protein loss via the gastrointestinal tract. b. Invasion of the proliferating crypt cells in the ileum by the bacteria causes excessive mitotic division and severe hyperplasia, which leads to limited brush border development and decrease absorptive capacity. c. The main differential diagnosis is salmonellosis as it can also cause ulceration in the areas of the Peter patches throughout the small intestine, cecum and colon.

b. Invasion of the proliferating crypt cells in the ileum by the bacteria causes excessive mitotic division and severe hyperplasia, which leads to limited brush border development and decrease absorptive capacity. The crypts are elongated and tortuous with marked proliferation of enterocytes and occasionally goblet cells

What is the most sensitive testing protocol for Lawsonia? a. IPMA serology alone b. fecal PCR alone c. fecal PCR + IgM titer ELISA d. fecal PCR + IPMA serology

d. fecal PCR + IPMA serology Best to do molecular AND serology to increase sensitivity (increased chances of detection)- fecal shedding low after treatment or in late-stage disease, and serology low early in disease. Immune peroxidase monolayer assay works better than ELISA in horses.

What is the most common GI lesion in rhodococcus enteritis? a. ischemic lesion to the small intestine secondary to abscessation at the cranial mesenteric artery b. multifocal ulcerative enteritis in peyers patches of ileum, +/- mesenteric abscesses c. caseous lesions of small intestine with discrete yellow foci (kunkers) d. multifocal ulcerations and strictures in the proximal duodenum

b. multifocal ulcerative enteritis in peyers patches of ileum, +/- mesenteric abscesses This is the pathologic lesion for rhodococcus, similar to lawsonia (with less corrugation to ileum than lawsonia). A is strongylus vulgaris lesion, C is pythium, D is ulcerative duodenitis

What is the most sensitive test for Potomac Horse fever in the desert of west Texas (non endemic location)? a. paired acute + convalescent IFA for 4X increase in titer b. paired acute + convalescent ELISA for 4X increase in titer c. fecal PCR for N. risticii d. whole blood PCR for N. risticii in WBC

d. whole blood PCR for N. risticii in WBC Best to look for intracellular N. risticii where it lives during active disease (circulating WBC). Titers hard to interpret because "acute" sample at time of diz onset is usually 14 days post exposure so they will have already seroconverted at time of c/s. Also vax + prior exposure w/o diz affects titer. IFA has lots of false positives so not recommended in non-endemic areas.

Species of animals that can be infected and serve as potential hosts of Lawsonia intracellularis include: 1. Horses, pigs, dogs, cats, rabbits, opossums, skunks, mice, rats, and coyotes 2. Horses, dogs, opossums, squirrels, rats, snakes, birds 3. Pigs, dogs, rabbits, opossums, skunks, coyotes 4. Only horses, pigs, and mice

1. Horses, pigs, dogs, cats, rabbits, opossums, skunks, mice, rats, and coyotes Horses, pigs, dogs, cats, rabbits, opossums, skunks, mice, rats, and coyotes. The VNTR profiles of pig and equine isolates differ greatly, thus it is believed to show host specificity.

What role does Sacharomyces boulardii have in the treatment of clostridial diarrhea? a. Produces DTO smectite, which binds C. diff toxins A+B b. Produces proteases, which bind C. diff toxins A+B c. Produces DTO smectite, which degrades C. diff toxins A+B d. Produces proteases, which degrade C. diff toxins A+B

d. Produces proteases, which degrade C. diff toxins A+B

Which one is NOT a risk factor for shedding of salmonella in hospitalized horses? a. Horses admitted for colic b. Diarrhea and antibiotic use c. Presence of reflux d. Severe GI disease

b. Diarrhea and antibiotic use

There are several serologic assays that have been validated to dx. Infection of L. Intracellularis in pigs, including: IFAT, ELISA and IPMA. It’s also essential to combine both molecular and serological assays. Which serologic test is the most specific to determine presence of anti-L. Intracellularis antibodies in equines? a. IFAT b. ELISA c. IPMA d. Real time PCR

c. IPMA

What is the most consistent finding of clinical equine proliferative enteropathy (EPE)? a. hyperlactatemia b. hyponatremia, hypochloremia c. hyperglobulinemia, hyperfibrinogenemia d. hypoalbuminemia

d. hypoalbuminemia

You are treating peritonitis in a 15 year old QH gelding with broad spectrum ABX therapy and choose a beta lactam (penicillin) + a gram negative drug (either aminoglycoside (gent) or enro), but you leave out metronidazole due to concerns about destroying GI flora- what important and frequently cultured anaerobe does this combination not cover? a. Clostridium b. Bacteroides fragilis c. Actinobacillus d. Rhodococcus

b. Bacteroides fragilis Bacteroides fragilis is most commonly ID'ed anaerobe cultured from peritonitis in horses. A is an anaerobe but should be covered by penicillin. C + D are aerobic bugs- **Actinobacillus should respond to pen**/gen, and rhodococcus is unlikely in an older horse.

The horse from the picture has a history of weight loss and intermittent diarrhea. The owner is worried about sand enteropathy, however no sand is seen on radiographs. What is the most likely cause of the horse's condition? a. Parasitemia due to small strongyles b. Lymphocytic-plasmacytic enterocolitis c. Pemphigos foliaceous d. Multisystemic eosinophilic epitheliotropic disease (MEED) Which other tests might be useful to support your diagnosis?

d. Multisystemic eosinophilic epitheliotropic disease (MEED) * Liver enzymes (GGT) * Abdominocentesis (↑TP ↑WBC) * +/- glucose absorption test (LI\>SI)

Equine GI 2 Flashcards

(40 cards)