Equine GI Flashcards
1
Q
Which coagulation factor is stimulated by endotoxin to trigger intravascular coagulation by the intrinsic pathway?
- Heparin
- Factor II
- Factor X
- Factor XII
A
d. Factor XII
Factor XII (Hageman’s factor) is triggered by endotoxin, producing bradykinin and triggering intravascular coagulation
APTT (best for DIC) is specific for intrinsic pathway, very sensitive to collection. Independent of platelet function.
2
Q
Which drug is the best to enhance gastric emptying in foals with ulcerative duodenitis?
a. Lidocaine
b. Escopolamine
c. Erytromycin
d. Bethanecol
A
d. Bethanecol
3
Q
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
A
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.
4
Q
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
A
b. Diarrhea and antibiotic use
5
Q
What is the primary benefit for low molecular weight heparin over unfractioned heparin in treating horses with endotoxemia?
a. Decreased cost
b. Decreased toxicity
c. Decreased agglutination
d. Decreased fever
A
c. Decreased agglutination
LMHW is nonagglutinating and retains anticoagulant activity via inhibition of factor Xa.
**Remember to study the coagulation cascade**
6
Q
Main target cells of N. risticii
a. Monocytes, macrophages
b. Monocytes, mast cells
c. Submucosal lymphocytes
d. Submucosal neutrophils
A
a. Monocytes, macrophages
- Colonic and small intestinal epithelial cells
- Colon mast cells
7
Q
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
A
c. diaphragm
- Caudate process of the liver and caudal vena cava
- Pancreas, hepatoduodenal ligament, portal vein
???
8
Q
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
A
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
9
Q
Meckel diverticulum is a remnant of embryonic structure causing a blind pouch from which structure?
a. cecal base
b. duodenum
c. ileum
d. esophagus
A
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
10
Q
What are main risk factors for the developement of ESGUS and EGGUS respectively?
a. Race horse in competition eating a high concentrate/low roughage diet; stalled filly eating a mixture of oats, rice bran and cracked corn
b. Race horse in pasture supplemented with alfalfa based pellets; stalled colt eating alfalfa and commercial 12% grain
c. Pasture geriatric horse eating high concentrate/low roughage diet; pasture filly eating a mixture of oats, rice bran and cracked corn
d. Pasture yearling eating a low concentrate/high roughage diet; brood mare eating alfalfa and commercial 12% grain
A
a. Race horse in competition eating a high concentrate/low roughage diet; stalled filly eating a mixture of oats, rice bran and cracked corn
* ESGUS: mainly related to exercise intensity, also management changes – feeding: high-concentrate/low-roughage diets. EGGUS: in a study in thoroughbreds – gender (colts are at reduced risk, but not really sure why), trainer, no grass turnout, horses not fed haylage, feeding unprocessed grain, infrequently fed a complete diet, fast exercise in a short period of time (days_), horses that went swimming & that have been in direct contact with each other (???)._ So, diet is also a risk factor with EGGUS, but there appears to be NO direct correlation with exercise and intensity in this case.
11
Q
Describe treatment and prevention of PHF.
A
- Oxytet IV for 4d, can use doxy but absorption may be poor with GI dz; some horses replase 2-3 wks after initial resolution but ABs should eliminate infection. - IVFT. - +/- plasma. - Endemic areas vacc horses early Spring and early to mid-Summer –> dec severity of dz.
12
Q
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
A
c. Ingestion of aquatic insects or ingestion of infected fluke larvae
* Contaminated fluke is available from snail secretions
13
Q
What is the most predominant excitatory neurotransmitter in the gastrointestinal tract?
a. leptin
b. acetylcholine
c. norepinephrine
d. gastrin
e. cholecystokinin
A
b. acetylcholine
Mediates parasympathetic nervous system. Important for mechanism of action of prokinetics.
14
Q
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
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
15
Q
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
A
d. The vaccine fails due to the presence of different strains, and it is recommended only in endemic areas
* Failure up to 89%
16
Q
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
A
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.
17
Q
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
A
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
18
Q
Asign from the options below, the pathogen associated molecular pattern (PAMP) to the respective PRR (pathogen recognition receptor)
LPS from Gram neg bacteria –>
Lipoprotein and peptidoglycan –>
Flagellin –>
Options: TLR-11, TLR-5, TLR-2, TLR-4
A
- LPS –> TLR-4 –> monocytes
- Lipoprotein (RAGE) and peptidoglycan (Nod1/Nod2) –> TLR-2
- Flagellin –> TLR-5 –> neutrophils
19
Q
What is a ranula?
- Feed type associated with slaframine toxicity, causing hypersalivation
- Smooth, firm stone obstructing the parotid salivary duct
- Infection of the salivary gland, typically secondary to foreign bodies / G – bacteria
- Pocket of saliva and secretions secondary to ruptured sublingual salivary duct
A
d. Pocket of saliva and secretions secondary to ruptured sublingual salivary duct
a is clover, b is sialolith, c is sialoadenitis.
Ranula is specific type of salivary mucocoele
20
Q
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
A
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
21
Q
Describe the aetiologic agent of Potomac Horse Fever (PHF).
A
- Neorickestia risticii. - Obligate intracellular gram negative bacteria.
22
Q
The most important factor protecting the duodenal mucosa from gastric acid secretions are what?
- Absorption of the gastric acid and pepsin by small intestinal cells
- Sodium and Bicarb-rich secretions
- Potassium and peptic secretions
- Chloride secretion and pepsin absorption by small intestinal cells
A
b. Sodium and Bicarb-rich secretions
Sodium and bicarb rich secretions probably originating from the pancreas neutralize acid entering the duodenum from the stomach.
23
Q
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
A
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.
24
Q
At which region (by cervical vertebral number) can trauma readily result in esophageal perforation in the horse?
a. C2-C3
b. C4-C5
c. C6-C7
d. T1-T2
A
b. C4-C5
25
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
26
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
b. PCR of surfaces by using a wet gauze
27
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
c. Increase in duodeno-gastric reflux of bile through the pylorus
* Delayed gastric emptying is considered if \> 2 hours
28
What are the most important features of IL-6?
a. Pyrogenic, promotes function of C3, increase macrophage activity in tissues
b. Promotes function of C3 and C5, decrease monocyte diapedesis, pyrogenic
c. WBC activation, pyrogenic, production of acute phase proteins
d. Pyrogenic, production of acute phase proteins, anemia of chronic disease
c. WBC activation, **pyrogenic**, production of acute phase proteins
Major endogenous pyrogens
* IL-6
* IL-1
* TNF-a
* IFN
29
Best disinfectant to kill the clostridium spores
a. Iodine
b. Sodium hypochlorite
c. Formalin
d. Hydrogen peroxide
b. Sodium hypochlorite
30
When managing a septic horse, many factors come into play, however, from the list below, which one should be managed first for a better treatment success.
a. Remove the cause of sepsis
b. Inhibit pathogen-associated molecular pattern (PAMP)-induced inflammation
c. Neutralize circulating endotoxin and PAMPs
d. Cardiovascular resuscitation
e. Prevent laminitis.
d. Cardiovascular resuscitation
* 2. Prevent laminitis.
* 3. Remove the cause of sepsis
* 4. Neutralize circulating endotoxin and PAMPs
* 5. Inhibit pathogen-associated molecular pattern (PAMP)-induced inflammation
31
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.
32
What is the main reason for _treatment failure_ in cases of EGGUS?
a. The lack of use of mucosal protectants such as sucralfate or pectin-lecithin
b. Inadequate dosing of the PG analogue misoprostol
c. Fail to add antimicrobials to the therapy, for example doxycycline or TMS
d. Short treatment duration with omeprazole
d. Short treatment duration with omeprazole
EGGUS has an inferior response to tx. w/ omeprazole, needs longer tx. – generally, more than 28 days. Also, in refractory cases there might be a need to add ATB to tx. (Doxycycline) and also add mucosal protectants: sucralfate or pectin-lecithin complexes.
33
Which cellular signaling molecule is produced by macrophages after TLR 4 recognizes LPS, and is the central trigger for pathophysiology of septic shock?
1. IL-1
2. IL-6
3. Interferon gamma (IFN-γ)
4. Nuclear Factor K Beta (NF-KB)
Nuclear Factor K Beta (NF-KB)
NF-kB is a transcription factor that drives production of variety of pro-inflammatory mediators that wreak havoc and cause lots of bad things (see above). Macrophages produce IL-12 and IL-18, which make natural killer cells and T lymphocytes produce interferon, stimulating the cell-mediated immune response
34
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
35
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
36
What radiographic findings for a supernumerary incisor are used to differentiate it from a permanent incisor?
a. Longer reserve crown and uniform opacity
b. Shorter reserve crown and uniform opacity
c. Longer reserve crown and mature root
d. Shorter reserve crown and mature root
d. Shorter reserve crown and mature root It may be clinically difficult wheter an extra tooth is a retained deciduous or a supernumerary. It is important to compare with the adjacent permanent teeth.
37
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
38
Outline diagnosis of PHF.
- Serum IFA or ELISA: 4 fold inc b/w acute and convalescent samples confirms infection, but negative does not rule it out b/c CSx can be delayed up to 14d post-infection. - qPCR of N. risticcii in leukocytes (whole blood) appears to be sensitive and specific in horses w supportive CSx.
39
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
40
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
a & c????
41
What is the most common adverse effect associated with the use of metoclopramide as a prokinetic agent in the horse?
1. Gastroesophageal reflux
2. Diarrhea
3. Hindlimb paresis
4. Extrapyramidal neurologic signs
d. Extrapyramidal neurologic signs
Metoclopramide can cause extrapyramidal neuro signs in horses- can reduce risk by using CRI instead of intermittent boluses.
42
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?
43
Transection of which nerve results in reduced febrile response to intraperitoneal LPS administration?
a. Phrenic nerve
b. Myenteric plexus
c. Vagus nerve
d. Splanchnic nerve
c. Vagus nerve --\> Local production of cytokines stimulate vagal receptors, releasing noradrenaline at the brainstem. This induces production of PGE2 and fever.
44
Describe the proposed pathophysiology of PHF.
- Intracellular parasite; infects peripheral monocytes and macrophages, SI epithelial cells and large colon mast cells. - Incompletely understood; horses appear to develop CSx and complications similar to Salmonellosis. - Experimental infection --\> fever in 2-4d and GI signs in 10-14d. - CSx of sepsis incl fever, leukopaenia, MM congestion, hypercoagulability. - Magnitude of intestinal inflammation less than Salmonella, but hypoproteinaemia can be severe through GI loss.
45
Some gastroprotectants like ranitidine and cimetidine work by competing at the level of the histamine receptors, thus inhibiting the release of **_histamine_**, which is considered the **main stimulus for HCl secretion**. In which specific cells of the gastric mucosa does histamine inhibitors work?
a. Zymogen cells
b. Parietal cells
c. Chief cells
d. Enterochromaffin-like cells
b. Parietal cells
* Zymogen cells --\> pepsinogen
* Chief cells --\> pepsinogen
* Enterochromaffin-like cells --\> Histamine, serotonine
46
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
47
Which is the most likely electrolyte and acid-base status after chronic esophageal obstruction?
1. Low Na, Low Cl, Low K, Metabolic acidosis
2. Low Na, Low Cl, High K, Metabolic acidosis
3. Low Na, Low Cl, Low K, Metabolic alkalosis
4. Low Na, Low Cl, High K, Metabolic alkalosis
c. Low Na, Low Cl, Low K, Metabolic alkalosis
* Acutely lose Na, Cl, K, Bicarb in saliva.
* After some time, even lower K due to lack of feed and renal compensation for low Cl makes them have metabolic alkalosis
48
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.
49
What is the main stimulus for HCl secretion in the stomach?
a. Gastrin
b. Histamine
c. Somatostatin
d. Pepsinogen
b. Histamine
The parietal cells, mostly located in the gastric fundus, have abundant H2 receptors. These receptors once activated will initiate the production of HCl.
50
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?
51
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
52
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)
53
Which one is less likely a possible etiologic agent of DPJ in horses?
1. Clostridium perfringes
2. Clostridium dificile
3. Clostridium novyi
4. Salmonella
5. Fusarium moniliforme
c. Clostridium novyi
All of the others are possible agents, but the disease is likely multifactorial.
54
List clinical signs of PHF.
- Anorexia, lethargy, fever, depression, inappetence. - GI signs from mild colic and soft faeces to severe dxa. - Congested MMs. - Laminitis in up to 30% horses w PHF (w or w/out dxa).
55
Which intracellular process is triggered within enterocytes after bacterial infection in enteritis, causing hypersecretion and diarrhea?
1. Upregulation of cyclic nucelotides (cAMP + cGMP) --\> Secrete Cl into the crypt --\> water follows
2. Downregulation of cyclic nucelotides (cAMP + cGMP) --\> Secrete Cl into the crypt --\> water follows
3. Upregulation of cyclic nucelotides (cAMP + cGMP) --\> secrete albumin into lumen --\> water follows
4. Downregulation of cyclic nucelotides (cAMP + cGMP) --\> Secrete albumin into lumen --\> water follows
a. Upregulation of cyclic nucelotides (cAMP + cGMP) --\> Secrete Cl into the crypt --\> water follows
Neutrophils + other inflammatory cells interact with apical membrane, triggers intracellular pathway by making 5’-AMP --\> upregulates cAMP + cGMP --\> activates protein kinases – in absorptive cells, it blocks the Na + Cl absorption from the lumen, and in secretory cells, it promotes secretion of Cl into the lumen, and water follows that through the paracellular route (made more leaky by TNF-alpha) --\> diarrhea.
56
Gastrin is produced by the G-cells in the gastric antrum. If you suspect an increase in gastrin production, how can you manage this better? There is not a lot of money for fancy medications...
a. Increase digestible fiber in diet at the same time as protein so a ratio 1:1 is achieved
b. Decrease dietary protein to the minimum and balance appropriately the amount of fats and carbohydrates
c. Increase the fiber to produce increase in saliva
d. Prevent stress to decrease cholinergic stimulus to the G-cells
b. Decrease dietary protein to the minimum and balance appropriately the amount of fats and carbohydrates
Proteins in the food that is being digested is the main stimulus for gastrin secretion
57
What is the most consistent finding of clinical equine proliferative enteropathy (EPE)?
a. hyperlactatemia
b. hyponatremia, hypochloremia
c. hyperglobulinemia, hyperfibrinogenemia
d. hypoalbuminemia
d. hypoalbuminemia
58
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
59
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
60
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)
61
Lolita is an 8-year-old Colombian Paso Fino mare that was imported to the United States 1 month ago and has been in training since. She has been experiencing acute abdominal pain episodes after each meal. The owners also reported that they have noticed mild weight loss in the face of the "amazing" sweet feed diet the mare is receiving.
You're very smart indeed, therefore you suspect poor Lolita has gastric ulcers and refer her for gastroscopy. With the clinical signs mentioned, what grade of squamous ulceration are you suspecting?
At least a grade III-IV/IV
Many horses with grades I-II/IV are subclinical.
62
You present with a horse that has mild inttermitent colic and decreased fecal output. It is summer and the owners don't check the water that often, the horse is kind of an "easy keeper"; you also notice that the grass in the pasture is quite dry. There is only a shed to protect from the sun but no natural shade from trees.
On rectal exam you can feel on the left side, with just the tip of your fingers a hard viscous, you are thinking that maybe is a cow and not a horse! On ultrasound the stomach reaches the 17th ICS. What is the most appropriate diagnosis?
a. Left dorsal displacement and impaction of the large colon
b. A type III gastric impaction and a pelvic flexure impaction
c. A type II gastric impaction most likely due to an underlying motility disorder
d. A type I gastric impaction secondary to persimmon ingestion
c. A type II gastric impaction most likely due to an underlying motility disorder
There are 3 types of gastric impactions
* **Type I**: is when there´s feed material impacted & the size of the stomach is NOT increased.
* **Type II**: it´s also feed material impacted BUT compared to Type I, the size of the stomach is much increased & possibly there´s an underlying motility disorder.
* **Type III**: happens with presence of a phytobezoar secondary to Persimmon seed ingestion
63
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
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
64
Which of the following congenital abnormalities is associated with esophageal obstruction?
a. wry nose (campylorrhinus lateralis)
b. patent ductus arteriosus
c. persistent right aortic arch
d. pyloric stenosis
c. Persistent right aortic arch
65
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
66
It is well known that PGE2 is fundamental to maintain the integrity of the stomach glandular mucosa. What are the main mechanisms of this?
a. Local vasodilation leading to mucus redistribution, HCO3 secretion and HCl clearance
b. increase mucosal blood flow, which contributes to HCO3 secretion, mucus production and supress HCl
c. increase mucosal blood flow, which contributes to HCl neutralization and mucus stability
d. decrease mucosal blood flow, decreasing HCO3 clearance and mucus breakdown
b. increase mucosal blood flow, which contributes to HCO3 secretion, mucus production and supress HCl
* **EGGUS**: ulcers result from break down of the normal defense mechanisms that protect the mucosa from acidic gastric contents. This in humans is related to bacteria *(Helicobacter pylori*) and NSAIDs, in horses we don´t really know yet.
* PGE2 --\> Promotes mucosal blood supply, maintain intercel tight junct, + secr HCO3 and mucus, supress secr HCl
67
Is the following statement true or false?
Abnormalities that involve dental development can involve tooth number, morphology, or position in the dental arcades. When talking about enamel hypoplasia, even though an association with certain drugs/ chemicals administered to the dam during gestation has not been confirmed, an underlying cause is identified in all cases.
**FALSE**. It CAN be idiopathic in origin, and it is believed that can be related to some drugs administered to the dam during gestation.
68
Described the epidemiology of PHF.
- Association between affected horse and proximity within 5 miles of a river is strong. - Trematode stages have been found in aquatic snails (Pleurocerdia, Juga spp, Acanthatrium spp, Lecithodendrium spp) and aquatic insects (cadis flies). - Suggested route of transmission is ingestion of aquatic insects or trematode stages release by snails into water.
69
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)
70
What are the major intrinsic factors promoting ulcer formation in the stomach?
- hydrochloric acid (predominant factor) - bile acids - pepsin (pepsinogen secreted by chief cells - converted to pepsin in an acidic environment pH \< 3)
71
What are the intrinsic factors protecting against ulcer formation in the stomach?
- mucus-bicarbonate layer - maintenance of adequate mucosal blood flow - mucosal prostaglandin E2 - epidermal growth factor production - gastroduodenal motility
72
What is the normal pH of equine gastric contents?
- variable from \< 2 to \> 6 - dependent on dietary state (fasted vs fed)
73
What are the predominant stimuli to hydrochloric acid secretion in the stomach?
- gastrin (released by G cells in antral mucosa; release controlled by gastrin-releasing peptide which is stimulated by gastric distension and increased luminal pH) - histamine (released by mast cells and ECL cells in the gastric gland) - acetylcholine via the vagus nerve
74
What are the factors that inhibit gastric acid secretion in the stomach?
- somatostatin (released by fundic and antral D cells) - epidermal growth factor (EGF), a peptide produced in saliva
75
What is the predominant mechanism responsible for squamous mucosal ulceration?
- excessive acid exposure
76
What is the prevalence of ESGD and EGGD?
- prevalence varies with breed, use, level of training as well as between ESGD and EGGD - highest prevalence of ESGD occurs in TB racehorses; 37% untrained, increasing to 80-100% within 2-3 months of training - prevalence of EGGD less well understood
77
Where are the majority of EGGD lesions located?
pyloric antrum
78
Are breed, age or sex associated with the presence of ulceration?
- other factors such as intensity or duration of exercise outweigh any potential age or sex effect - breed effect may be present with TBs predisposed to ESGD
79
What are the nutritional risk factors associated with ulceration?
- forage type - increased starch/grain intake - increased time between forage feeds (\>6h) compared with more frequent forage feeding (\<6h) increases the likelihood of ESGD - intermittent access to water - intermittent starvation causes and increases the severity of ESGD - NB. fasting model poorly reflects multifactorial nature of gastric disease
80
List the main clinical signs associated with EGUS
- colic (postprandial; possibly due to altered GIT motility) - reduced appetite (mild to severe) - poor body condition - behavioural effects (inconsistently reported) - poor performance - direct consequence of gastric pain?; other factors need to be considered - differences in clinical signs between ESGD and EGGD unknown - NB. wide variety of clinical signs may be present but they are nonspecific and poorly associated with presence of EGUS
81
Which age group is more commonly affected by gastroduodenal ulcer disease (GDUD)
- suckling and early weaning foals
82
What are the potential complications of GDUD?
- gastric or duodenal rupture - pyloric or duodenal stricture - ascending cholangitis - severe squamous and oesophageal ulceration and aspiration pneumonia can occur secondary to gastro-oesophageal reflux
83
List the causes of primary gastric dilation
- gastric impaction - grain engorgement - excessive water intake after exercise - aerophagia - parastism
84
List the causes of secondary gastric dilation
- (more common than primary dilation) - primary intestinal ileus small or large intestinal obstruction
85
Describe the common location and features of gastric rupture
- usually along greater curvature - if resulting from gastric dilation, tears in seromuscular layer frequently larger than corresponding tears in mucosal layer - if secondary to gastric ulceration, usually full-thickness tears of equal sizes in all layers
86
List the causes of acquired megaoesophagus
- chronic/recurrent oesophageal obstruction - extra-oesophageal obstruction eg. tumours, abscesses, pleuropneumonia, vascular ring anomalies - neurologic disorders eg. diseases that cause vagal neuropathy (EPM, EHV myeloencephalitis, idiopathic vagal neuropathy) - neuromuscular disorders eg. equine dysautonomia (botulism) - alpha-2 agonists (detmoidine) - transient and reversible - genetic predisposition eg. Friesians (recessive inheritance) - reflux oesophagitis (cause or effect?)
87
List the causes of oesophageal stricture
- pressure necrosis from oesophageal impactions that induce circumferential erosion or ulceration of the oesophageal mucosa - oesophageal injury caused by oral administration of corrosive medicinal agents - trauma to the neck - congenital
88
List the types of oesophageal stricture
- Oesophageal web or ring: stricture caused by mucosal and submucosal trauma - Mural stricture: originating in muscular layers and adventitia of the oesophagus - Annular stenosis: stricture originating in all layers of the oesophagus
89
How are oesophageal strictures diagnosed?
- Endoscopy can be used to detect oesophageal webs or rings - Identification of mural strictures or annular stenosis may require a double-contrast oesophagram
90
What is the treatment for oesophageal strictures
- Conservative management - slurry diet, anti-inflammatories, antimicrobials; allow 60 days - bougienage and balloon dilation - surgery: resection and anastomosis, temporary oesophagostomy with fenestration of the stricture, oesophagomyotomy (for strictures of muscularis and adventitia), patch grafting with local musculature ----\> high complication rates with surgery.
91
Describe the two types of oesophageal diverticula
- Traction (true) diverticula: result from wounding and subsequent contraction of perioesophageal tissues with resulting tenting of the wall of the oesophagus; appear as dilation with a broad neck on contrast oesophagography; usually asymptomatic - Pulsion (false) diverticula: arise from protrusion of oesophageal mucosa through defects in the muscular wall; usually result from trauma or acute changes in intraluminal pressure; flask shape with a small neck on an oesophagram; can fill with feed material, ultimately leading to oesophageal obstruction and rupture; can be corrected surgically by inverting or resecting prolapsed mucosa and closing defect in wall
92
List congenital disorders of the oesophagus
- congenital stenosis - persistent right aortic arch and other vascular anomalies - oesophageal duplication cysts - intramural inclusion cysts - idiopathic megaoesophagus
93
Describe the muscle types in the oesophagus and their innervation
- a transition occurs in the muscle type composing the tunica muscularis: proximal two thirds = striated skeletal muscle; motor innervation includes pharyngeal and oesophageal branches of vagus n. distal third = smooth muscle; parasympathetic fibres of the vagus n. supply the smooth muscle - sympathetic innervation of the oesophagus is minimal
94
Describe the function of the lower oesophageal sphincter
- relaxation of the lower oesophageal sphincter permits passage of ingested material from oesophagus to stomach - distension of stomach with ingesta mechanically constricts lower oesophageal sphincter - gastric distension also triggers a vagal reflex that increases lower oesophageal sphincter tone, a safety mechanism against gastro-oesophageal reflux - the mechanical and vagal mechanisms that promote lower oesophageal sphincter tone prevent spontaneous decompression of the stomach, which, along with lack of vomiting reflex in the horse, increases the risk of gastric rupture during episdoes of severe distension
95
List the causes of primary oesophageal obstruction
- impactions of roughage - prior oesophageal trauma or poor mastication (dental abnormalities) - wolfing or gulping food; if exhausted or mildly dehydrated after long ride or weakened from chronic debilitation
96
List the causes of secondary oesophageal impaction
- disorders that physically impede passage of food material and fluid by narrowing luminal diameter, reduce the compliance of the oesophageal wall or alter conformation of oesophageal wall (food material may accumulate in pocket or diverticulum) - foreign bodies - intramural (tumours esp SCC, strictures, diverticula, cysts) or extramural (mediastinal or cervical masses) masses - acquired or congential anomalies
97
List the clinical signs of oesophageal obstruction
- related to dysphagia - anxious, stand with neck extended - gagging or retching - bilateral frothy nasal discharge containing saliva, water, food - coughing - odynophagia - ptyalism - other signs include dehydration, electrolyte or acid-base imbalances, weight loss, aspiration pneumonia
98
Where are the most common locations for oesophageal obstruction?
- sites of natural narrowing of oesophageal lumen eg. cervical oesophagus, thoracic inlet, base of the heart or terminal oesophagus
99
List the diagnostic techniques for oesophageal obstruction
- endoscopy is most direct method for diagnosis and also useful for critical diagnostic and prognostic information after resolution (ulceration, rupture, masses, strictures, diverticula, signs of functional abnormalities) - passage of NGT - ultrasonography - radiography +/- air or barium contrast studies for evaluation after relief of obstruction if stricture is suspected
100
List the important sequelae to oesophageal obstruction that may predispose to re-obstruction
- dilation proximal to site of obstruction - mucosal injury from trauma - stricture formation - formation of a diverticulum - megaoesophagus - oesophagitis - underlying functional or morphological abnormalities much more likely in recurrent cases
101
Aspiration pneumonia is a potential complication in every case of oesophageal obstruction. What is a good predictor of pneumonia?
- duration of obstruction before presentation - endoscopic evidence of tracheal food contamination is NOT a good predictor
102
What are the major protective mechanisms of the oesophageal mucosa?
- salivary and food material buffers - normal peristaltic motility - barrier formed by gastro-oesophageal sphincter
103
List the causes of oesophagitis in horses.
1) reflux oesophagitis (repeated episodes of gastric fluid regurgitation into the distal oesophagus and subsequent chemical injury to mucosa): - gastric ulcer disease - motility disorders - increased gastric volume from gastric outflow obstructions - gastic - intestinal ileus - impaired lower oesophageal sphincter function 2) other causes of oesophagitis: - trauma (foreign bodies, food impactions, NGT) - infection (mural abscess) - chemical injury (pharmaceuticals, cantharidin)
104
Effects of stalling in horses
Decrease fecal output
105
E.TEC toxin is a:
Heat ST toxin A
106
Downside of ELISA for antibody detection for PHF
* Failure to seroconvert does not rule out infection
* Frequent false +
107
Asymptomatic esophageal diverticula
Traction (true)
Dilation with broad neck
108
Source of infection in Lawsonia?
Not determined in horses
109
Duration of quarantine of equine coronavirus
? 21?
110
Current standard for diagnosis of PHF
PCR in whole blood (DNA in leukocytes)
111
Receptor for LPS?
TLR 4
112
Increase risk for salmonella
Antibiotic treatment and colic
113
Type of rotavirus in foals
Group A
114
Treatment of choice for PHF
Oxytetracycline
Horses do not remain carriers of N. risticii
115
Pathogenesis of PHF
1. Ingestion of aquatic insect containing metacercariae or cercariae from environment
2. Replicates in colon epithelial cells, tissue macrophages, mast cells and blood monocytes
116
Sensitivity of salmonella fecal culture with 5 collections
97%
117
Lawsonia causes
Increased mitosis in ileum crypt cells, Hyperplasia
118
Lesion of lawsonia
Adenomatosis of the ileum (hyperplasia)
119
Clostridium difficile in foals can be pathogenic or non-pathogenic?
Toxin A more important in pathogenesis and severity of disease; both nontoxigenic and toxigenic strains can be found
120
Salmonella that is potentially zoonotic
S. newport
121
Reason for high vaccine failure for PHF
Different circulating strains
122
Why is the vaccine for Potomac horse fever not 100% effective?
Multiple strains
123
Predictors for lower survival in PHF
* Electrolyte loss (Na and Cl)
* Hemoconcentration
* Prerenal azotemia
124
Clinical pathology findings in case of MEED
Anemia
Eosinophilia)
↑GGT
125
Potomac horse fever, infection
Horse eats aquatic insects
126
Mare with suspected stomach ulcer, dx test at farm
Sucrose absorption test
127
Neorickettsia risticii, transmission
trematode –snail
128
Foal 21 days febrile, icteric mucous membranes and with high liver enzymes
Clostridium pilosum
129
Blood smear for Neorickettsia
Rarely find intracytoplasm granules in monocytes
130
What is the best to prevent rotaviral diarrhea in edemic farms?
Vaccine for pregnant mares (3 doses: 8, 9 and 10 months gest)→ ↓clinical signs, mild form (not prevent)
131
Which cells are target for N. risticii?
1. Monocytes/Macrophages
2. Colonic and small intestinal epithelial cells
3. Colon mast cells
132
Site of infection of Lawsonia intracellularis
Proliferative crypt cells in the ileum → ↑ mitotic division → hyperplasia
133
Foal 7 months, losing weight, ventral edema, hypoalbuminemia, fibrinogen high, leukocytosis. What do you expect to find in the biopsy or necropsy?
Proliferative enteritis
134
Horse with ulcerative coronitis, hypoproteinemia, weight loss and anemia
MEED
135
Neoricketssia risticii best for diagnosis
PCR blood, feces
136
Difference of peritoneal fluid between DPJ and strangulation
DPJ: Yellow turbid (serosang), ↑↑PT 3.5, ↑WBC 11
Strangulation: Serosanguineous, ↑↑TP 4.5, ↑↑WBC 20-50
137
When is the seasonal ocurrence of Potomac Horse Fever?
May- November
Peak occurrence July-August
138
Type III gastric impaction
Phytobezoar secondary to Persimmon ingestion
139
Diagnosis of cantharidin toxicity
Urine early in process about 500ml urine or 200g gastric content
* Demonstration toxin via GC-MS
140
Which inflammatory cytokines does Salmonella upregulate?
IL-1B
TNF-a
141
Sucralfate interferes with absorption of other drugs, which group is parrticularly important?
Fluoroquinolones
142
What is a PAMP?
Lipoteichoic acid TLR pathogen
143
What is the main factor for treatment failure with omeprazole in cases of EGUS?
Location of the ulcers
144
Who first activate macrophages in MAP infection?
Macrophages activated by Th1 cytokines (IFN-g) are able to limit proliferation
145
How to decrease incidence of C. perfringens type C enteritis in foals?
Feeding of smaller amounts of grain prepartum
Antitoxin to mares and foals
146
Consistent necropsy finding in cases of DPJ
Serositis
147
Horse with lesion in skin, also chronic weight loss
MEED
148
Vector and intermediate host por N. risticii
* Vector: Trematode
* Intermediate host: aquatic insects, operculated snails
149
Main clinical pathoogy finding in lawsonia cases
Albumin → \< 2 g/dl
150
Best diagnostic test for L. intracellularis
Combine both serology and fecal PCR
151
Abortions, oral lesions, ptyalism in sheep
Bluetongue?
152
Why are neonates predisposed to necrotic enteritis due to C. perfringens type C?
Trypsin inhibitors in colostrum Trypsin → proteolytic enzyme that can destroy beta-toxin
153
Horse with peritonitis, response to penicillin. Most probable organism cultured?
Actinobacillus equuli: Gram neg rod (rapid response to atb pen/gent)
154
Necropsy diagnosis for L. intracellularis
Silver staining with Warthin Starry stain → bacilli in the apical zone of the crypt epithelial cells
155
Causative agent of equine enterotoxemia
C. perfringens Type A
156
Mule with clinical signs of dysautonomia, what diagnostic test would have to be performed
Intestinal biopsy (decrease of Cajal cells)
157
C. difficile toxins
A: Secretory and cytotoxic effects → Activates inflammatory cells → release proinflammatory cytokines and vasoactive mediators → Induction of substance P (neurotransmissor) ▪ Dependence on substance P for expression of pathologic effects B: Enterotoxygenic (secretory), and cytotoxic → unknown role in animals
158
C. perfringens toxins
• Types → A and C ○ A → most frequent → enterotoxin Foals \<10d (Type C: alpha and beta) Exotoxin Effect Alpha\* Phospholipase Beta-2 Necrotizing cytotoxic Epsilon Iota Theta Hemolytic
159
Correlation of glucose with septic peritonitis
Serum-to-PF glucose conc difference \> 50 g/dl → septic peritonitis
Glucose \<30 mg/dL
160
How does salmonella reaches the intestinal mucosa?
Through invasion of M cells (intestinal lymphoid tissue)
161
Gold standard diagnosis of clostridial diarrhea
Cell cytotoxic assay\*
Immunoassay: ELISA --\> reliable and rapid
162
Which cell salmonella uses for dissemination?
Macrophages
163
PG that is gastroprotectant
PGE
164
What is the effect of sucralfate in cases of esophagitis?
Uncertain efficacy since needs a low pH to attach to the ulcers
165
Which drug can be used to enhance gastric emptying in foals with ulcerative duodenitis?
Bethanechol
166
What are the 4 syndromes of gastric ulceration in foals?
Subclinical, clinical, perforating, pyloric stricture
167
TP/WBC in DPJ vs strangulation
**DPJ:** Disprop↑PT/normal WBC (no leukotactic stim)
**Strangulation:** WBC/TP \>3
168
Which group of salmonella is more common in horses?
Group B
169
What is associated with mortality in equine coronavirus
Hyperammonemia?
