Gastrointestinal Flashcards
What is the effect of increased parasympathetic tone on gastrointestinal contractions?
May cause segmental contractions which inhibit progressive motility.
Increase exocrine gland secretion.
How do you distinguish the small colon on palpation?
Presence of faecal balls and an antimesenteric band that is palpable along the length of this segment if it is impacted.
Which electrolytes are lost in large volumes of gastric reflux or diarrhoea?
Na, K, Ca, Mg and HCO3
What are the potential mechanisms for increased lactate concentration in cases of colic?
- Large colon ischaemia
- Reduced perfusion to peripheral tissue due to hypotensive shock
- Generalised intestinal ischaemia may result in absorption of lactate from the lumen
- Increased blood viscosity reduces perfusion of capillary beds, exacerbating ischaemia and tissue hypoxia.
If oesophageal rupture is suspected or aspiration is a possibility which contrast material should be used for a contrast oesophogram?
Iodinated organic compounds in an aqueous solution should be used instead of barium.
What are the sites for the FLASH U/S examination of the abdomen?
Ventral abdomen, gastric window, spleno-renal window, left middle third of the abdomen, duodenal window, right middle third of the abdomen and thoracic window.
For an oral glucose absorption test, how much glucose is given, at what time point and what level should the peak be in blood glucose be, and what are the different levels of malabsorption cut offs?
1g/kg of d-glucose as a 20% solution in water via NGT
Peak at >85% above baseline glucose between 90-120min
Complete malabsorption is a peak <15% above resting,
Partial malabsorption is between 15-85% above resting.
What are the benefits of a xylose absorption test over a glucose absorption test and how is the protocol different?
d-Xylose absorption is not confounded by hormonal effects of mucosal metabolism of glucose as the glucose absorption test is.
Protocol is: 0.5g/kg d-xylose as a 10% solution; peak is between 60-90min but is a concentration between 20-25mg/dl.
What effects do the normal diet have on results of an oral glucose absorption test or an oral xylose absorption test?
OGAT: higher peaks in horses eating grass/hay compared with concentrates and from those at pasture compared with stabled.
OXAT: higher peaks in horses fed low-energy diet such as alfalfa chaff than those fed high-energy diets such as oat chaff, oats and corn.
List tests for assessing gastric emptying
- Contrast radiography in foals
- Nuclear scintigraphy for liquid or solid phase emptying
- Acetaminophen absorption and measurement in serum
- 13C-octane acid breath test using a labelled test meal and detection of the novel isotope in breath.
List the intestinal barriers against pathological invasion at the varying cellular levels.
Epithelium: tight junctions and mucous layer
Macrophages: resident macrophages in the lamina propria, submucosa and intestinal lymphoid organs are among the first to respond to infection.
Describe the events that lead to intestinal inflammation with epithelial breach.
Breach of the mucosal barrier initiates an inflammatory response through synthesis of pro-inflammatory chemokines (IL8) and cytokine (TNFα, arachidonic acid metabolites) by epithelial cells which then trigger influx of neutrophils and other leucocytes into the tissue.
Mast cells are sentinel cells that sense microbial invasion and release TNFα.
Macrophages within the lamina propria, submucosa and intestinal lymphoid tissue activate CD14 TLR4 complex which initiates transcription of TNFα and IL1β which synergise with LPS to amplify the macrophage response.
Once initiated, TNFα, IL1β and other proinflammatory products of neutrophils, monocytes, mast cells and eithelial cells amplify the inflammatory response, in part through release of nitric oxide and other nitrogen radicals which are microbicidal but also vasoactive.
List the four important changes that occur in the intestinal vasculature in response to inflammation.
- Alteration of blood flow (initially increased, then decreased due to increased viscosity with fluid loss and oedema, increased leucocyte margination, platelet adhesion etc)
- Increased vascular permeability (due to histamine, leucotrienes, prostaglandins and other inflammatory mediators cause endothelial cell contraction, creating leaky gaps)
- Increased adhesiveness of endothelial cells, leucocytes and platelets (cytokines stimulate endothelial cells to express adhesion molecules that support adhesion of leucocytes and platelets.
- Exposure of the basement membrane and activation of the complement, contact and coagulation cascades. (adhesion to the exposed basement membrane enables exposure of neutrophils and platelets to mediators of inflammation which activates the cells to release oxidants and proteases that injure the endothelium and can cause irreparable harm to the microvasculature). Marginated neutrophils begin to transmigrate between endothelial cells and this, if not closely regulated can worsen vascular leakage.
Why is neutrophil depletion considered protective in some models of GIT inflammation?
During the acute response neutrophils are activated to release products that are not only lethal to pathogens and proinflammatory but are also damaging to host cells and tissues.
What are the most potent stimuli for neutrophil activation at the site of inflammation?
Complement (specially C5a), cytokines (TNFa and IL1B), platelet activating factor (PAF), immune complexes and bacterial products
What are the main regulators/stimulators of mast cells?
Complement fragments (C3a, C5a and C4a) Neural pathways which respond to enteric pathogen invasion
What are some important roles of mast cells during intestinal inflammation?
- First line defense at epithelial barriers
- When activated the release histamine, proteases, heparin and cytokines, as well as inflammatory mediators including prostaglandins, PAF and leucotrienes.
- On the vasculature they increase endothelial permeability and cause vasodilation
- Mast cell derived mediated enhance epithelial secretion, including the mast cell protease tryptase which regulates GIT physiologic responses during inflammation, including intercellular junction integrity, motility and pain responses.
- Mast cell products alter intestinal motility, generally increasing it to enable expulsion of intestinal contents.
- Mast cell derived leucotrienes and TNFa have a crucial role in host defence against bacterial pathogens, including neutrophil recruitment, regulating dendritic cells and adaptive immune responses.
- Mast cells are phagocytic and can act as antigen presenting cells.
What is the function of complement fragments?
During activation of the complement cascade, soluble fragments of C3, C5 and C4 (C3a, C5a and C4a) are liberated. These anaphylatoxins are chemotactic for neutrophils, and activate neutrophils and mase cell degranulation as well as stimulating ROS.
What is the basic mechanism behind ischaemia-reperfusion injury?
Reperfusion of ischaemic tissue is associated with platelet and neutrophil clumping in the small vessels of the mucosa which can impede blood flow. Platelets are activated and adhere to exposed basement membrane and activated endothelial cells and provide a surface for leucocyte adhesion. The accumulation of platelets and leucocytes reduces vessel diameter and blood flow while potentiating local coagulation and thrombus formation. Various factors (histamine, leucotrienes, prostaglandins, thromboxane etc) from the activated leucocytes have a role in regulating local perfusion during inflammation. In addition, nitric oxide is a potent regulator of blood flow. However, many of the mediators affecting perfusion also affect endothelial permeability, altering osmotic and hydrostatic balance and tissue oedema, so in extreme cases local and systemic coagulopathies initiated by the vascular injury and absorption of microbial products and inflammatory mediats induce a hypercoaguable state and exacerbate thrombus formation and tissue injury/infarction
How does neutrophil migration damage endothelial and epithelial barriers?
To facilitate neutrophil migration to the site of inflammation they release serine proteases and metalloproteinases to liquefy tissue matrix proteins that make up intercellular junctions. These degradative enzymes are particularly damaging to basement membranes and the cellular barriers of the endothelium. However a similar effect occurs with the epithelium - TNFa and IFNy from activated neutrophils increases the permeability of tight junctions of enterocytes. Subepithelial accumulation of neutrophils can lead to deadhesion of the epithelial cells from the basement membrane and mild to severe ulceration. The end result is PLE and absorption of bacterial cell wall constituents.
What factors are thought to affect motility during diarrhoea?
- Invasive bacteria cause rapid bursts of motor activity in the colon that appear to decrease transit time through the large intestine.
- Absorption of endotoxin and release of inflammatory mediators such as prostaglandins disrupts the motility patterns of the large intestine, resulting in less coordinated contractions.
What are phagocyte derived reactive oxygen metabolites and what effects do they have on tissue?
Phagocytes produces superoxide radicals as a host defense mechanism to kill invading microorganisms. During inappropriate stimulation, as can occur with inflammation, trauma or ischaemia-reperfusion, increased levels of toxic oxygen species are produced causing marked tissue damage. Activated phagocytes secrete peroxidase enzymes into the extracellular space, which catalyse oxidation of Cl to yield HOCl which is 100-1000 times more toxic than O2- and is a non-specific oxidising and chlorinating agent that reacts with amines to form N-chloramines. The end result is marked tissue damage and altered permeability.
In what conditions is the GIT permeability to endotoxin/bacteria increased?
- Strangulating obstruction and bowel infarction
- Inflammation eg enteritis or colitis
- Bacterial overgrowth
- Intraluminal acidosis (eg grain poisoning/overload)
Which cytokines are of interest in the pathogenesis of endotoxaemia?
TNFa, the interleukins, chemokinse and growth factors such as granulocyte-monocyte colony stimulating factor.
What are the three conditions that occur when the pro- and anti-inflammatory responses are not balanced/controlled adequately?
- Predominance of proinflammatory response = SIRS
- Predominance of antiinflammatory response = CARS (compensatory antiinflammatory response syndrome)
- Combination = mixed antagonist response syndrome.
Which leucocyte is primarily responsible for endothelial cell damage?
Neutrophils - the damage is caused by oxygen-derived free radicals which are produced within endothelial cells through reactions involving neutrophil derived elastase and hydrogen peroxide molecules.
What is the primary cause of neutropenia in cases of endotoxaemia?
Neutrophil margination in the vasculature, especially of the lungs. This is facilitated by adhesion molecules on endothelial cells and leucocytes that interact and allow sticking of leucocytes to the endothelial lining of blood vessels.
What are the two manifestations of DIC?
A thrombotic syndrome leading to ischaemic organ failure or a fibrinolytic syndrome with uncontrolled haemorrhage; or a combination of the two.
Endotoxaemia activates which pathways of the coagulation cascade?
Intrinsic (via Factor XII); and
Extrinsic (via LPS-induced tissue factor expression and vascular injury).
What type of shock is associated with endotoxaemia?
Distributive shock (largely associated with vascular dysfunction in the periphery).
What is the pathogenesis of shock and organ failure with endotoxaemia?
Early in endotoxaemia there is widespread vasodilation leading to vascular pooling, decentralisation of flow, decreased pre-load and decreased effective circulating volume. The compensatory response is hyperdynamic with an initial phase of tachycardia, increased cardiac output and CVP, pulmmonary hypertension, peripheral vasoconstriction and increased peripheral vascular resistance. The decompensated stage involves progressive systemic hypotension, confounded by direct myocardial suppression via nitric oxide, increased vascular permeability, intravascular microthrombi and impaired tissue oxygen extraction leading to progressive metabolic acidosis and inhibition of normal cellular metabolism.
What are the external signs of hypodynamic shock?
Peripheral perfusion is compromised so MM become brick red or purple with a dark toxic line, capillary refill is prolonged, the extremities and skin become cold to the touch, the arterial pulse weakens and venous fill is decreased. With vascular endothelial damage and increased capillary permeability you get a muddy MM appearance and diffuse scleral redenning. Haemostatic abnormalities such as petechial haemorrhage may be seen.
What is the pathophysiology of renal failure secondary to endotoxaemia?
Ischaemic cortical necrosis and acute tubular necrosis occurs secondary to coagulopathy induced afferent arteriolar obstruction.
In addition to hypovolaemia, what is a common contributing factor to haemoconcentration and elevated total protein in cases of endotoxaemia?
Splenic contraction due to increased sympathetic stimulation, as well as influences from production of acute phase proteins and protein losses.
Alterations in which coagulation parameters might be seen with DIC?
- Prolonged prothrombin time (Factor VII consumption)
- Prolonged activated partial thromboplastin time (Factor VIII and IX consumption)
- Prolonged thrombin time
- Decreased antithrombin III activity
- Thrombocytopenia
- Decreased protein C and plasminogen activities.
In addition to anti-LPS antibodies in specifically formulated hyperimmune plasma, what other benefits does plasma have for horses with endotoxaemia and how much is required?
Manufacturers recommend a minimum dose of 1-2L for endotoxaemia, but a dose rate of 2-10mL/kg.
Additional active constituents that may be of benefit in patients with endotoxaemia induced coagulopathy include complement components, fibronectin, clotting factors, ATIII
What clinical/patient considerations should be made when administering polymixin B to ameliorate signs of endotoxaemia?
- Beneficial effects may be limited to the first 24-48hr after onset of endotoxaemia due to development of endotoxin tolerance
- Hypovolaemia and dehydration may exaccerbate toxic effects of polymixin B - attempts should be made to rehydrate or at a minimum improve peripheral tissue perfusion prior to administration
- If co-administration with other toxic products such as aminoglycosides rehydration is even more important, and close monitoring for side effects is important.
Why are NSAIDs effective in ameliorating the effects of endotoxin? And what dose is recommended?
Inhibition of COX inhibits prostanoid production; prostanoids have been identified as important mediators in inflammatory response.
Due to the findings that flunixin impairs recovery of intestinal barrier function and may increase mucosal permeability to LPS a reduced dose of 0.25mg/kg q6-8h has been recommended - at this dose flunixin inibits eicosanoid synthesis efficiently in a model of endotoxaemia.
co-administration of lidocaine (CRI) enhance recovery and decrease recovery time
What benefit may lidocaine be in cases of endotoxaemia?
In experimental models in rabbits lidocaine inhibited haemodynamic and cytokine responses to endotoxin if given immediately after LPS infusion. It also ameliorated the inhibitory effects of flunixin on recovery of mucosal barrier function following ischaemic injury in equine small intestine, hence it may have merit in endotoxaemic patients.
Because ATIII levels are frequently decreased in patients with coagulopathy (as can occur with endotoxaemia), addition of heparin to fresh frozen plasma can be effective, however has been associated with erythrocyte agglutination which can increase risk of microthrombosis. What is an alternate means of reducing the risk of coagulopathy?
Administration of low-molecular weight heparin at 50IU/kg SC q24h
Aspirin 10-20mg/kg q48h - irreversibly inhibits platelet COX activity to inhibit platelet aggregation and microthrombosis.
What are the gross findings with proximal enteritis?
Serosal surface may have varying degrees and distribution of bright red-dark red petechial and ecchymotic haemorrhages and yellow-white streaks.
The lumen is filled with malodorous red to brown-red fluid.
The mucosa surface is hyperaemic with varying degrees of petechiation and ulceration
Serosal fibrinopurulent exudate is a common finding in severe cases.
At a microscopic level, what are the findings with proximal enteritis?
Varying degrees of mucosal and submucosal hyperaemia and oedema, villous degeneration with necrosis and more severely, sloughing of villous epithelium. The lamina propria, mucosa and submucosa have varying degrees of granulocyte infiltration (mainly neutrophils) and the muscular layers and serosa may contain small haemorrhages.
Most severe lesions in the duodenum and proximal jejunum but may extend proximally to the gastric mucosa and aborally to the large colon.
What is the proposed eitiology of hepatic disease with proximal enteritis?
Ascending infection via the common bile duct, local absorption of endotoxin via the portal circulation, systemic consequences of endotoxin absorption, metabolic imbalances and hypoperfusion or hypovolaemia .
What are the two intracellular processes that control intestinal secretion and how do they do this?
Cyclic nucleotide (cAMP and cGMP) and calcium systems. cAMP can be induced by inflammatory mediators such as VIP and PGE2 and cGMP can be induced by bacterial enterotoxins. Increased intracellular Ca may be secondary to cyclic nucleotide-dependent release of stored Ca within the cell or from increased Ca entry across the cell membrane. The net effect is increased movement of Na and Cl into the mucosal cell from the interstitium, with secretion of Na and Cl into the intestinal lumen. Water follows the directional flux of Na and Cl.
In terms of acute abdominal discomfort, how can small intestinal obstruction be differentiated from proximal enteritis?
With small intestinal obstruction the signs of discomfort are typically consistent until correction. With proximal enteritis discomfort typically subsides after gastric decompression and volume replacement.
Why might metronidazole be indicated in cases of proximal enteritis?
Clostridium species have been suspected as a causative agent for proximal enteritis, hence metronidazole treatment may be appropriate. Penicillin has also been advocated although effects on dysbiosis may be more profound with penicillin.
Histologically what is the lesion seen with equine coronavirus?
Necrotising enteritis particularly of the jejunum and ileum with haemorrhage in the ventral colon in some cases.
What are the common clinicopathologic and diagnostic findings of alimentary lymphoma?
Anaemia, thrombocytopenia, neutrophilia or neutropenia, hypoalbuminaemia and hyperglobulinaemia.
Lymphocytosis is rare.
Enlarged mesenteric lymph nodes may be palpable.
Carbohydrate absorption tests usually reveal partial to total malabsorption indicative of a severely reduced surface area resulting from significant villous atrophy and extensive mucosal or transmural infiltration.
A biopsy is necessary for diagnosis.
What is the typical signalment for granulomatous enteritis and which breed seems predisposed?
Standardbreds are over represented.
Most horses are 2-3 yrs old and its possible there’s a genetic predisposition
The cause of granulomatous enteritis is unknown however a bacteria and a toxic agent have been implicated - what are they?
Mycobacterium avium and aluminium although the reliability of that case report is questioned.
What are the treatment options for granulomatous enteritis?
Long-term corticosteroids (often unrewarding)
Surgical resection of localised disease may be successful in some cases.
What are the clinical disorders associated with multisystemic eosinophilic epitheliotropic disease (MEED)?
Predominant eosinophilic infiltrate in the GIT, associated lymph nodes, liver, pancreas, skin and other structures accompanied by some degree of malabsorption and enteric protein loss.
What is the typical signalment of MEED affected horses and which breeds are over-represented?
Typically young horses aged 2-4yrs with SB and TB predominating.
What are the typical skin lesions with MEED?
Exudative dermatitis and ulcerative coronitis
Is systemic eosinophilia a common finding in MEED?
No, systemic eosinophilia is a rare finding despite extensive tissue eosinophilia.
What are the common haematological/clinical chemical abnormalities in cases of MEED?
Hypoalbuminaemia, elevations in GGT and ALP.
Which characteristics of the disease are typically associated with diarrhoea with MEED?
Segmental or multifocal granulomatous lesions with mucosal and transmural thickening and extensive ulceration
Is fibrosis a feature of affected tissue with MEED?
Yes
Where is Lawsonia intracellularis typically localised to in cases of proliferative enteropathy?
The cytoplasm of proliferative crypt epithelial cells of the jejunum and ileum. Preferentially infects proliferating cells, hence tropism for the crypt epithelium, and infection induces more rapid proliferation.
What is the incubation period for Lawsonia/proliferative enteropathy?
2-3 weeks.
What are the proposed risk factors for development of Lawsonia/proliferative enteropathy?
Weaning, transport, comingling/overcrowding, feed changes, antibiotics.
Which stain is required to detect Lawsonia intracellularis intracellularly?
Silver stain. Curved or comma shaped rods found clustered in the apical cytoplasm of hyperplastic crypt epithelium.
What biosecurity precautions should be taken in cases of Lawsonia intracellularis?
Affected animals should be isolated from unaffected animals for at least 1 week after institution of antimicrobial therapy to avoid shedding of organisms into the environment.
What are the general feeding recommendations for horses with chronic wasting disease and evidence of malabsorption?
Interval feeding small frequent meals of easily digestible food
Feeds with high fibre but low bulk
May tolerate increased dietary fat
Supplemental protein
Which is the most pathogenic serovar of Salmonella in horses?
Typhimurium
List risk factors for development of Salmonella
- High ambient temperatures (summer and fall)
- Transportation
- Antibiotic Tx
- Hospitalisation/prolonged hospital stay
- Dietary changes
- Immunosuppression
- Gastrointestinal disease (colic, diarrhoea etc)
- GIT or abdominal surgery
- General anaesthesia
- Leucopenia or laminitis during hospitalisation
Which factors of the host immune system are most effective at preventing infection with Salmonella?
- Mucosal antibody secretion and enterocyte-derived cationic peptides prevent colonisation of the mucosa
- Opsonising antibodies and activation of the complement cascade are important for fighting systemic invasion by S. enterica by increasing efficacy of phagocytosis and by direct bactericidal activity.
- Humoral immunity is often ineffective in preventing disease and dissemination once invasion occurs intracellularly.
- S. enterica is capable of surviving and multiplying within macrophages, rendering the humoral immune system ineffective.
How does Salmonella invade intestinal cells?
Invasion occurs through specialised enterocytes called M cells through self-induced uptake (type III secretory system) via the apical membrane of the M cell, often killing the cell in the process.
It then invades neighboring cells via the basolateral membrane eventually spreading the destruction of the epithelium beyond the principle area of attack
What is the effect of S. enterica enterotoxin on the development of inflammation and diarrhoea?
The enterotoxin induces secretion of Cl and water by colonic mucosal cells, triggers an inflammatory reaction in intestinal tissues including stimulation of chemokine and cytokine production resulting in recruitment of leucocytes and activation of resident mast cells and macrophages. In addition the enteric nervous system inhibits sodium and water absorption, causes motility disturbances and potentiates tissue injury. All of these contribute to enhanced pathogenicity and dissemination of S. enterica and pathogenesis of diarrhoea.
What are the 4 clinical syndromes of Salmonella?
- Inapparent infection with latent or active carrier status
- Depression, fever, anorexia and neutropenia without diarrhoea or colic
- Fulminant or peracute enterocolitis with diarrhoea
- Septicaemia (enteric fever) with or without diarrhoea
What are the gross changes seen with acute enterocolitis due to Salmonellosis?
Severe fibrinonecrotic typhlocolitis with interstitial oedema and variable degrees of intramural vascular thrombosis that may progress to infarction. Severe ulceration of the large intestinal mucosa may occur with serosal ecchymoses and congestion.
What do increased numbers of leucocytes in the faeces indicate and are they specific for any one pathogen?
Suggest an invasive process in the colon but are not pathogen specific.
What is the causative agent, common geographic distribution and seasonality associated with potomac horse fever?
Neorickettsia risticii
Higher incidence of cases along waterways and rivers (likely due to intermediate host being operculate freshwater snails which then transmit to aquatic insects than infect horses)
Most common from late summer to early fall
Which cells does N. risticii infect? And what is the target organ?
Monocytes and monocyte-derived leucocytes (survives by inhibiting production of reactive oxygen intermediates and avoiding lysosomal digestion by blocking phagosome-lysosome fusion). Target organ is gastrointestinal mucosa.
What are the gross and histologic changes seen in cases of N. risticii infection?
Fibrinous necrotising typhlocolitis with severe mucosal ulceration and inflammation of the lamina propria later in disease. Vasculitis and intravascular coagulation are consistent features in the large intestine with perivascular oedema.
What is the typical case progression from infection with N. risticii?
Biphasic fever (second phase 6-7 days after first) with diarrhoea typically occurring 2 days after the second febrile episode. Ileus may develop at any stage resulting in colic. Diarrhoea can be moderate-severe and signs of endotoxaemia, shock and peripheral oedema may occur. Abortion may occur. Laminitis may occur in 20-30% of cases and is typically severe. Renal failure may also occur. Coagulopathies and DIC are common with N. risticii.
What diagnostic tests are available for N. risticii? And what preventive measures are possible?
Serological evidence of infection with paired samples
Culture of the organism from blood is possible but difficult
PCR tests are rapid and highly sensitive - can be applied to blood or faeces.
A killed vaccine is available and experimentally it prevents clinical illness but may be of limited benefit for preventing natural infection.
What are the five types of C. perfringens, based on the exotoxins they produced? And which ones are associated with different disease presentations?
Types A-E
Type A: alpha toxin which interferes with glucose uptake and energy production and activates arachidonic acid metabolism and signalling pathways in enterocytes
TypeA is the most common isolated from horses of all ages
Type B and C: beta toxin is a cytotoxin that causes enterocyte necrosis, ulceration and ultimately severe intestinal inflammation and haemorrhage
Enterotoxin may be produced by virulent strains of A and C and inserts into cell membranes to form pores which alter permeability to water and macromolecules and ultimately leads to cellular necrosis and massive desquamation of the intestinal mucosa.
Types A, B, C and D have all been associated with haemorrhagic enteritis in foals <10days
What are the two main C. difficile toxins and what are their respective roles in disease?
Toxin B: potent cytotoxin but its role in enterocolitis is unclear. It does not induce fluid secretion, inflammation or characteristic alterations in intestinal morphology
Toxin A: an enterotoxin that induces an inflammatory response with hypersecretory diarrhoea, neutrophil influx, mast cell degranulation and secretion of prostaglandins, histamine, cytokines and 5-HT by activated leucocytes, and it also triggers the enteric nervous system which further induces intestinal inflammation and mucosal secretion.
Which larval stage of S. vulgaris causes migratory damage in the GIT and what is the typical damage seen?
4th stage larvae migrate through the mucosa and submucosa into the arterioles of the intestine causing verminous arteritis consisting of mural oedema, haemorrhage and infiltration of inflammatory cells. Interstitial oedema and damage to the interstitial matrix and mucosa may occur as a result of inflammation and migration, causing increased secretion of fluid and albumin loss.
What are the likely contributors to diarrhoea in cases of S. vulgaris?
Abnormal GIT motility secondary to the inflammatory effects of migration
Segmental infarction secondary to thromboembolism and thrombus formation causing ischaemia
Release of vasoconstrictive inflammatory mediators as well as elaboration of parasitic antigens or toxins further exacerbate ischaemia and alter secretion, absorption and motility, leading to diarrhoea.
Disrupted motility secondary to ischaemia likely contributes to diarrhoea
Acute infarction and mucosal ulceration causes severe diarrhoea.
What trans-rectal palpation finding might make you suspicious of S. vulgaris infestation?
Thickening and fremitus in the cranial mesenteric artery
Aberrations in which clinicopathologic marker might help to differentiate S. vulgaris from cyathostomin infestation?
Serum IgG(T) concentration is usually normal with cyathostomes and elevated with S. vulgaris (along with serum alpha and beta globulins).
Which two groups of bacteria have a strong influence on colonisation resistance in the GIT and can be depleted by antibiotic treatment?
Obligate anaerobes and streptococci
Anaerobic bacteria produce short chain fatty acids (SCFA) and other metabolites that are toxic to facultative anaerobic bacteria; antibiotic induced depletion of these bacteria results in reduced SCFA - in addition to enabling overgrowth of potentially pathogenic anaerobes, what other effect does reduced SCFA have?
Reduced absorption of Na and H2O as this is stimulated by absorption of SCFA.
What are the roles of prostaglandins, specifically PGE2 and PGI2 in maintaining mucosal function/integrity?
PGE2 increases mucosal blood flow, increases secretion of mucous, water and bicarbonate, increases mucosal cell turnover rate and migration and stimulates adenyl cyclase activity; in addition, and importantly, it has a role in maintaining epithelial tight junction integrity.
PGI2 also has a role in maintaining epithelial tight junction integrity.
List clinical signs of NSAID toxicity
Mild diarrhoea with no clinical signs through to severe dehydrating diarrhoea
Anorexia
Fever
Depression
Peripheral oedema
Oral ulceration
Colic
Haematuria or oliguria with renal involvement
Hypoproteinaemia with hypoalbuminaemia
Hyponatraemia, hypocalcaemia, hypokalaemia, hypochloraemia, metabolic acidosis and elevated hepatocellular enzymes all might be seen.
At a cellular level what are the effects of cantharidin from Blister beetles?
It is a potent irritant causing acantholysis and vesicle formation. It is thought to disrupt the oxidative metabolism in the mitochondria, causing mitochondrial swelling, plasma membrane damage, and changes in membrane permeability. Cell swelling and necrosis occur, resulting in mucosal ulceration.
What are the clinical findings with cantharidin toxicity?
Oral, oesophageal , gastric, small intestinal and large intestinal ulceration with fibrinous to pseudomembraneous inflammation and submucosal oedema of the intestine. Cystitis and myocarditis also occur, along with renal pathology, likely associated with excretion of the toxin renally.
List clinical signs of cantharidin toxicity
Varies from mild depression and abdominal discomfort through to fulminant signs of toxaemia and rapid death. Commonly: Depression Sweating Irritability Abdominal pain Elevated heart and respiratory rates Fever Polyuria/polydipsia Profuse diarrhoea (rarely haemorrhagic) Stranguria and pollakiuria is common Tremors and synchronous diaphragmatic flutter may occur due to hypocalcaemia Neurologic signs can include head pressing, swaying and disorientation
What is the pathogenesis of arsenic toxicosis?
Arsenite uncouples oxidative phosphorylation leading to breakdown of energy metabolism in the cells of many tissues, causing widespread cellular injury and death hence multiorgan failure. Damage to the large intestine is likely in part by direct cellular toxicity and corrosion. Acute haemorrhagic colitis with severe mural oedema and mucosal ulceration occurs in horses; vasculitis is a feature in humans.
What clinical signs may be seen with arsenic toxicosis?
Haemorrhagic diarrhoea, weakness and abdominal pain
Some horses die before diarrhoea develops
With progression, cardiac arrhythmias, pulmonary oedema, acute renal failure and neurologic deficits may develop.
May see isosthenuric urine with haematuria, cylinduria and preteinuria.
What type of reaction is associated with severe intestinal anaphylaxis?
IgE-mediated type I hypersensitivity or can be an IgE independent anaphylactoid reaction
What is the pathogenesis of severe intestinal anaphylaxis?
Exposure to an allergen (food, environmental, drug) results in mast cell degranulation, secretion of inflammatory mediators and activation of enteric neural reflexes in the intestine that cause profound alteration in blood flow, increased vascular permeability and interstitial oedema, recruitment of neutrophils, altered motility, mucosal injury, absorption of microbial products and mucosal hypersecretion. The end result is multiorgan failure resulting from DIC and peracute death.
What is the pathogenesis of colitis from carbohydrate overload?
Rapid fermentation by gram-positive lactic-acid producing bacteria and a sudden increase in organic acid production in the large colon rapidly decreases caecal pH. The organic acid production overwhelms the buffering capacity of the large intestine and lactic acid producing bacteria overgrow while gram-ve bacteria such as Enterobacteriacea are killed, releasing large quantities of endotoxin. The osmotic load from lactic acid facilitates development of diarrhoea and the contents of the GIT are toxic to the mucosa causing necrosis. Mucosal ulceration enables absorption of large quantities of endotoxin and lactic acid.
In addition to volume replacement/expansion, what other benefit do colloids have in cases of diarrhoea and what are the risks of prolonged use?
Also helps to maintain plasma oncotic pressure
Downside is that prolonged use of Na containing fluids can promote diuresis and renal water loss
NSAIDs can be beneficial in horses with colitis due to antisecretory effects on the inflamed GIT however there is evidence that they impede mucosal healing and repair. What are the advantages and disadvantages of using COX-2 selective NSAIDs with this in mind?
Advantages: they don’t inhibit prostaglandins such as PGI2 and PGE2 which have a cytoprotective effect on GIT mucosa and are important for mucosal repair.
Disadvantages: COX-2 selective drugs can be prothrombotic so should be used with cuation in patients with systemic inflammation at risk of thrombosis.
What are the proposed benefits and adverse effects of misoprostol?
As a PGE analogue it is proposed to enhance mucosal healing and promote recovery (does this in colitis models) but it is unproved in equine colitis.
Adverse effects includ abdominal cramping, diarrhoea, sweating and abortion.
What are the proposed benefits of addition of Psyllium mucilloid to the diet of horses with diarrhoea?
Increases production of short chain fatty acids which are a major energy source for colonocytes, hastens epithelial maturation and stimulates Na and fluid absorption hence improves the clinical course of ulcerative colitis and hastenss colon healing.
Under which circumstances would antimicrobial treatment be indicated with colitis?
If N. risticii is suspected (lipid soluble choices as these are intracellular pathogens)
If Lawsonia is suspected (lipid soluble for above reason)
If Clostridial species are confirmed treatment with metronidazole is recommended.
What dietary manipulations should be made for horses with colitis?
- Avoid grains due to delivery of highly fermentable carbohydrate to the colon
- Avoid long-stem roughage
- Feed a complete pelleted diet (minimum 30% dietary fibre) to reduce mechanical and physiologic load on the colon
- Provide frequent meals (4-6 times daily)
- Addition of corn oil to increase caloric intake
- High quality grass hay can be provided if a pelleted diet is refused
- Enteral or parenteral nutrition may need to be considered.
What are the treatment recommendations for Strongylosis and cyathostomiasis?
Strongylosis: fenbendazole 10mg/kg PO q24h for 3-5 days or ivermectin 200mg/kg PO.
Heparin therapy (20-80iu IV/SC q6-12h as an anticoagulant/antithrombotic
Aspirin 10-30mg/kg POq12-48h
Cyathostomiasis: Fenbendazole 10mg/kg PO q24h for 5 days then ivermectin 200mg/kg PO on the 6th day or moxidectin 400ug/kg PO. Pretreatment with dex or pred is recommended if heavy larval loads are suspected
What is the innervation and vascular supply to the parietal and visceral peritoneum?
Parietal peritoneum: vascular supply from branches of the intercostal, lumbar and iliac arteries; innervation from the phrenic and intercostal nerves.
Visceral peritoneum: vascular supply from the splanchnic vessels and innervation from visceral autonomic nerves.
What is the lymphatic drainage of the peritoneal space?
Lymphatic drainage through subendothelial pores for small molecular weight substances and though the diaphragmatic stomata and subsequent entry into the thoracic duct for larger molecular weight substances (>40,000mw eg bacteria)
What are the commonly reported monomicrobial causes of peritonitis?
Strep equi equi Strep equi zoo R. equi Corynebacterium pseudotuberculosis Actinobacillus equuli
Contamination or injury to the peritoneal lining or space results in what biologic or cellular cascade that can ultimately result in peritonitis?
Release of catecholamines from peritoneal mast cells, vasodilation and hyperaemia, increased peritoneal vascular permeability, secretion of protein rich fluid into the peritoneum, transformation of mesothelial cells into macrophages, influx of polymorphonuclear cells, humoral opsonins, natural antibodies and serum complement.
In addition, depression of the peritoneal fibrinolytic activity results in fibrin deposition on the peritoneal surface and inflammatory mediated and sympathetic mediated ileus.
What are the different stages of peritonitis and how do these occur from a time-frame perspective?
- The contamination stage lasts 3-6 hours and involves introduction of bacteria and subsequent initiation of the acute inflammatory resposne
- Diffuse peritonitis develops if the organisms are not eliminated in the first stage, and this occurs within several hours and lasts up to 5 days.
- As the inflammatory response persists it escalates with continued exudation of fluid and protein and influx of inflammatory cells. If infection is still not eliminated disease enters the transitional stage or acute adhesive stage that occurs 4-10 days after the initial insult. At this pint organisation of fibrin proceeds and organisms become isolated from host defences.
- At this point the disease process etners the stage of chronic abscessation - can occur as early as 8 days after inoculation and persist indefinitely.
How quickly does the peritoneal white blood cell count return to normal after uncomplicated procedures such as enterocentesis or enterotomy during celiotomy?
Within 5-7 days
What is the main difference between the tight junctions/resistance of the paracellular space between different segments of intestine?
Tight junctions in the intestinal glandular structures/crypts are leakier than those in the surface epithelium. This correlates with the absorptive capacity of the epithelium and secretory function of the crypts.
Tight junctions are less leaky in the ilium than the jejunum but less leaky again in the colon which is in keeping with the largely absorptive role of the colon and is advantageous given the hostile microbial environment of the colon
List the primary mechanisms of mucosal barrier function in the stomach
- The stratified squamous epithelium of the stomach is exceptionally impermeable due to tight junctions and muco-substances secreted by the stratum spinosum
- The gastric mucosa secretes both mucous and bicarbonate that forms a mucous layer. In addition, if mucous back-diffuses towards the epithelium there are Na/H exchangers that can expel the H if the pH reaches a critical point. Trefoil peptides interact with this mucous layer, possibly contributing to the barrier properties of mucous and repairing injured mucosa.
- Prostaglandins appear to be cytoprotective in the stomach at doses less than those used to inhibit gastric acid.
- In addition, the pace with which mucosa can repair is another protective mechanism (also the case in the duodenum.
What role do short chain fatty acids and bile salts on gastric mucosal injury?
SCFAs are weak acids that are present as a result of microbial fermentation, and can penetrate the squamous mucosa and damage Na transport activity principally located in the stratum germinativum
Bile salts may be present as a result of duodenal reflux. Despite their high pH, bile salts can adhere to stratified squamous epithelium, becoming lipid soluble and triggering damage once the pH falls below 4.
What are the regulatory mechanisms behind gastric acid secretion?
Parietal cell secretion of acid is almost continuous but regulated by enterochromaffin like (ECL) cells within the proper gastric mucosa and G and D cells, which are present within the pyloric mucosa. Acid secretion is amplified by ECL-released histamine (H2 receptors) and G cells which secrete pro-secretory hormone gastrin whereas D cells are sensitive to an acidic environment and release somatostatin which inhibits gastric acid secretion.
Which segment of the small intestinal mucosa is most susceptible to hypoxia and why?
The villus tip - largely because of the counter current exchange (of O2) mechanism of blood flow in the small intestinal villus, which renders the villus tip in a state of relative hypoxia even under normal circumstances. However when blood flow is reduced, the counter-current exchange of O2 is enhanced and the tip becomes absolutely hypoxic.
In general why is the intestinal mucosal epithelium so susceptible to hypoxia?
Because of the relatively high level of energy required to fuel the Na/K ATPase that directly or indirectly regulates ion and nutrient flux.
The first biochemical event to occur during hypoxia is loss of oxidative phosphorylation, the result of which is diminished ATP and failure of the energy dependent Na/K ATPase and accumulation of Na and subsequently H2O.
The cascade that follows which involves lactic acidosis, falling pH and damage to cellular membranes allows accumulation of high concentrations of Ca in the cytosol, activating Ca-dependent degredative enzymes and apoptosis, and epithelial sloughing starting from the villus tip down to the crypt as the last place (due to a separate blood supply to the crypt).
What role do prostaglandins have in intestinal mucosal repair and what influence do NSAIDs have on this?
Prostaglandins are thought to mediate closure of tight junctions during epithelial restitution to restore barrier function. Hence treatment of post-ischaemia injured horses with NSAIDs may be detrimental to this function due to ongoing increased intestinal permeability.
What is the role of polyamines in intestinal repair?
Polyamines appear to stimulate enhanced proliferation and cytoskeletal cellular migration by increasing expression of protooncogenes which control the cell cycle. They are produced by fully differentiated enterocytes at the villus tipe and reach the crypt either within sloughed luminal epithelium or via local villus circulation.
Why are trefoil peptides so important for mucosal repair?
They are the most potent stimulators of epithelial migration and have the ability to induce their own expression, further amplifying the level of reparative factors at site of mucosal repair.
What are the respective principle metabolic fuels of enterocytes and colonocytes?
Enterocytes: glutamine
Colonocytes: butyrate
How is the enteric nervous system involved in modulation of motility?
ENS is involved either directly via neurotransmitters, or indirectly via interstitial cells of cajal (ICC) or immune or endocrine regulation.
ICC: These cells are electrically coupled to myocytes and are responsible for generating the slow-wave activity (pacemakers of the intestine). Central and autonomic innervation influence events but neural input is not required for contraction.
What is the nervous supply to the intestinal tract?
Parasympathetic supply is via the vagus and pelvic nerves
Sympathetic supply is through postganglionic fibres of the cranial and caudal mesenteric plexuses.
Excitatory neurotransmitter is acetylcholine through muscarinic type 2 receptors.
Activation of α2 adrenergic receptors on cholinergic neurons within enteric ganglia inhibits release of acetycholine, reducing intestinal contraction. β1, β2 and β-atypical receptors are directly inhibitory to intestinal smooth muscle.
List risk factors for development of POI
- Duration of surgery
- Jejuno-caecostomy more commonly results in POI than other small intestinal resection and anastomosis procedures
- Age >10yrs is associated with increased risk
- Arabians are at higher risk than other breeds
- Pelvic flexure enterotomy & intraoperative lidocaine may be protective.
What is the main implication of intestinal inflammation post surgery with respect to efficacy of prokinetic drugs?
Most prokinetic drugs require a healthy gut wall to enhance intestinal contraction, and downregulation of motilin receptors has been demonstrated in the inflamed equine jejunum.
What is the MOA and efficacy of cholinomimetics such as bethanechol and neostigmine?
Bethanechol: parasympathomimetic agent that acts on muscarinic receptors. It has efficacy in increasing gastric emptying, reducing small intestinal transit time, increases the strength and duration of wall contractions in the caecum and right ventral colon. Adverse effects are abdominal discomfort, sweating and salivation but these are minimal at 0.025mg/kg
Neostigmine: increases receptor concentration of acetylcholine by inhibiting cholinesterase. It promotes caecal and colonic contractile activity and hastens emptying of radiolabeled markers from the caecum. May be delayed gastric emptying.
What is the MOA and efficacy of benzamides and dopamine antagonists susch as metoclopramide and cisapride?
Metoclopramide: acts as a 5HT-4 agonist and 5HT-3 receptor antagonist, as well as dopamine receptor antagonist. Crosses the BBB so can cause extrapyramidal signs including seizure. It increases contractility of muscle strips in vitro in the pyloric antrum, proximal duodenum and mid jejunum.
Cisapride is a second generation benzamide that acts as a 5HT-4 agonist and 5HT-3 antagonist but without anti-dopaminergic activity. Supposedly leads to resolution of persistent large colon impaction and prevention of POI after SI surgery. Has the potential to cause adverse cardiac effects including lengthening of the QT interval and development of torsdes de pointes.
What is the MOA of lignocaine as a prokinetic?
Proposed to be due to suppressing primary afferent neurons, limiting reflex efferent inhibition of motility, in addition to antiinflammatory properties through NF-kB signalling or improving mucosal repair. Also has analgesic effects although may alter somatic but not visceral antinociception.
What are the boundary/landmarks for the epiploic foramen and how does intestine enter?
Caudate process of the liver (dorsal border)
Caudal vena cava (dorsally)
Pancreas (ventrally)
Hepatoduodenal ligament (ventrally)
Portal vein (ventrally).
Intestine can enter from the visceral surface of the liver toward the right body wall or the opposite direction.
What event is proposed to put foals at increased risk for small intestinal volvulus?
Changing feed habits/adaptation to bulkier diets
Which segment of small intestine is most commonly involved in volvulus in adults?
The distal jejunum and ileum because of their relatively longer mesenteries.
Which breeds are predisposed to inguinal hernias and why?
Standardbreds and Tennessee Walking horses sue to large inguinal canals
What is the difference between a direct and an indirect inguinal hernia?
Indirect hernias remain within the parietal vaginal tunic and hence technically within the peritoneal cavity.
Direct hernias rupture through the parietal vaginal tunic and occupy a SC location - even in neonates these should be surgically corrected.
Why should stallions be castrated on the side affected by inguinal herniation?
Vascular compromise within the spermatic cord is likely to have occurred resulting in congestion of the testicle and although it may remain viable it is likely not to and may cause subsequent problems.
What are the most common type of intussusception in horses?
Ileocaecal (typically young horses)
What are the more common locations for acquired versus congenital diaphragmatic hernias?
Large congenital hernias: most common ventralmost aspect of the diaphragm
Acquired hernias: at the junction of the muscular and tendinous portion of the diaphram
What is the mechanism behind a low-normal heart rate in horses with volvulus of the large colon?
Increased vagal tone
What are indicators of viability after correction of colon volvulus?
- Bleeding at the enterotomy site
- Palpation of a pulse in the colonic arteries
- Serosal colour
- Appearance of colonic motility
What are the grades of rectal prolapse?
Grade 1: Prolapse of rectal mucosa; prognosis: good (most common type)
Grade 2: Prolapse of full-thickness rectum; prognosis: fair.
Grade 3: Grade 2 prolapse with additional protrusion of small colon; prognosis: guarded
Grade 4: Intussusception of rectum and small colon through the anus; prognosis: poor.
What makes Grade 4 rectal prolapse almost always fatal?
Stretching and tearing of mesenteric vasculature often results in infarction of affected bowel
What is a common predisposing factor to ileal impactions?
Tapeworm infection (evidence in approximately 80% of cases in one study)
What is ileal hypertrophy?
Idiopathic hypertrophy of the circular and longitudinal muscle layers that is proposed to be associated from parasympathetic neural dysfunction resulting in chronically increased muscle tone and subsequent hypertrophy (possibly associated with parasite migration) or chronic increases in muscle tone of the ileocaecal valve leading to muscular hypertrophy of the ileum as it contracts against a partially occluded ileocaecal valve.
What are the clinical signs of ileal hypertrophy?
Chronic intermittent colic, partial anorexia and chronic weight loss.
If a Meckels diverticulum is identified, what additional congenital abnormality should be ruled out?
Mesodiverticular band that can course from the diverticulum to the umbilical remnant or from the embryonic ventral mesentery to the ante-mesenteric surface of the bowel.
Differentiate primary from secondary caecal impactions
Primary caecal impactions result from excessive accumulation of ingesta which is typically dry and hard. Onset is usually gradul over a couple of days and they may rupture before the development of severe abdominal pain or systemic deterioration
Secondary caecal impactions develop while a horse is being treated for a separate condition and the contents is typically fluidy. Often secondary to post-operative pain (eg orthopaedic surgery). These may be difficult to detect as depression and reduce faecal output may be attributed to the operative procedure rather than colic. Again these are at risk of rupture.
What are dietary risk factors for development of enteroliths?
Feeding of lucerne hay, decreased dietary proportions of grass and pasture hay are risk factors. The diet is usually high in magnesium and protein - high protein increases the ammonia nitrogen load in the large intestine and may contribute to calculus formation.
What are the 4 types of papillae on the tongue?
- Filiform papillae are fine threadlike projections across the dorsum of the tongue.
- Fungiform papillae are larger and easily seen at the rounded free end
- Vallate papillae are usually two or three in number and are found on the caudal portion of the dorsum of the tongue.
- Foliate papillae are situated rostral to the palatoglossal arches of the soft palate on which they form rounded eminence about 2-3cm in length
Types 2-4 are covered in taste buds and secondary papillae.
What is the sensory and motor innervation to the mouth?
Sensory: trigeminal (CNV)
Motor: facial (CNVII)
What is the innervation of the tongue?
Motor: hypoglossal (CNXII)
Sensory: lingual and glossopharyngeal (CNIX)
What is the normal age of tooth eruption?
First incisor present at birth; second erupts 4-6wk; 3rd 6-9mo. Permanent incisors erupt at 2.5yr, 3.5yr and 4.5yr, canine tooth 4-5yr.
First pre-molar (wolf tooth) 5-6mo, 2nd PM 2.5yr, 3rd PM 3yr, 4th PM 4yr.
Molars: 10-12mo, 2nd molar 2yrs; 3rd molar 3.5-4yr.
List the neural sites and nerves that could be associated with dysphagia.
Forebrain and brainstem Peripheral nerves controlling prehension CN V (sensory and motor) CN VII CN XII Peripheral nerves transferring food bolus to pharynx CN V (sensory) CN XII Peripheral nerves of swallowing CN IX CN X
What electrolytes are likely to be lost in saliva?
Na, K and Cl.
What is the origin of subepiglottic cysts in foals?
Cystic distortion of the remnants of the thyroglossal duct.
What are the clinical signs of sialolithiasis and what fluid characteristics could differentiate this from other swellings?
Fluid swelling in the form of a mucocele proximal to the stone and occasionally inflammation of the parotid gland.
Measurement of electrolytes in fluid aspirates may help differentiate - salivary K and Ca concentrations are higher than plasma.
What is an example of a toxic cause of hypersalivation?
Slaframine from the fungus Rhizoctonia leguminicola
It is a parasympathomimetic that stimulates exocrine secretion in the parotid gland.
What are the muscle types of the tunica muscularis of the oesophagus, where do they transition and what is there innervation?
Striated muscle in the proximal 2/3, innervation from the pharyngeal and oesophageal branhces of the vagus nerve
Smooth muscle in the distal third; innervation from the parasympathetic fibres of the vagus nerve.
Sympathetic innervation of the oesophagus is minimal.
Within the smooth muscle layer of the distal oesophagus the outer layer becomes more longitudinal whereas the inner layer thickens and becomes circular.
What are common sites of oesophageal obstruction?
Sites of natural narrowing such as the cervical oesophagus, the thoracic inlet, base of the heart or the terminal oesophagus.
What therapeutics may be useful in management of choke?
Acepromezine Xylazine or detomidine Oxytocin (limited evidence due to mixed effects) Instillation of lignocaine Buscopan IVFT
What are the likely systemic effects of prolonged choke?
Hypovolaemia
Electrolyte derangements (hyponatraemia, hypochloraemia, metabolic alkalosis)
Aspiration pneumonia?
Hypertriglyceridaemia
How long should food be withheld after resolution of oesophageal obstruction?
24-48 hours after which assessment of the mucosal integrity is warranted. Treatment with oral sucralfate during this period may be of benefit.
Under which circumstances/concurrent with which conditions does reflux oesophagitis usually occur?
Gastric ulcer disease Motility disorders Increased gastric volume from: Gastric outflow obstructions Gastric paresis Intestinal ileus Impaired lower oesophageal sphincter function.
What are the treatment options for reflux oesophagitis?
Proton pump inhibitors or H2 receptor antagonists to reduce the gastric acidity are important for repair.
If primary gastric outflow obstruction is present surgical intervention is warranted.
If delayed gastric outflow in the absence of obstruction metoclopramide or bethanechol may be indicated.
List neurological cause of megaoesophagus,
Any condition causing vagal neuropathy: EPM EHM Idiopathic vagal neuropathy Early sign of dysautonomia Botulism
Which breed are predisposed to oesophageal diseases such as meaoesophagus, oesophaglea diverticulum and oesophageal rupture?
Friesians.
What are the different types of oesophageal stricture?
Webs or rings - associated with the mucosa or submucosa
Mural structures - associated with muscular layers and adventitia
Annular stenosis - associated with all of the layers of the oesophagus.
What is the main limitation to anastomosis of the oesophagus?
It lacks a serosal layer and does not form a fibrin seal so anastomoses tend to leak.
What are the two types of oesophageal diverticula?
Pulsion divertical is protrusion of oesophageal mucosa through a defect in the muscular wall
Traction diverticular occur secondary to wounding and subsequent contraction with resultant tenting of the wall of the oesophagus.
List some potential complications of gastro-duodenal ulcer syndrome in foals.
Gastric or duodenal rupture, pyloric or duodenal stricture, ascending cholangitis, reflux oesophagitis and potential aspiration pneumonia if reflux is severe.
List the MOA of H2 antagonists and proton pump inhibitors.
H2 Antagonists suppress HCl secretion through competitive inhibition of the parietal cell histamine receptor. This can be partially overcome with exogenous pentagastrin.
PPI block secretion of H at the parietal cell membrane by irrreversibly binding to the H/K ATPase proton pump.
Which neutraceuticals have shown some promise in prevention of EGUS?
Sea buckthorn berries
Apolectol
B vitamins
Magnesium hydroxide
List causes of primary and secondary gastric dilatation
Primary: Gastric impaction Grain engorgement Excessive water consumption post exercise Parasitism Aerophagia Secondary: Primary intestinal ileus Small or large intestinal obstruction
Where in the stomach does gastric rupture usually occur and in what breed is it predisposed?
Greater curvature. With rupture from gastric dilatation tears in the seromuscular layer are frequently larger than the corresponding tears in the mucosal layer, indicating that the seromuscularis weakens and tears before the mucosa.
Friesians
What percentage of horses with chronic colic had neoplasia as a cause?
4%
What is the most common tumour of the proximal GIT?
Squamous cell carcinoma
In which segment of the GIT does adenocarcinoma most frequently occur, and what other tissues may be involved?
Most frequently in the small intestine (specifically arises from the glandular crypts) but can be found int he caecum and large colon too with metastasis to the liver, lymph nodes and lungs.
Leiomyosarcoma and leiomyoma have been reported to affect the small intestine, stomach and small colon/rectum. In which gastrointestinal tissue layer does this neoplasm arise?
Smooth muscle.
Ameloblastoma occurs most commonly in the mandible, while ameloblastic odontoma typically occurs in the maxilla. They are both benign. How can they be differentiated?
Radiographically - ameloblastoma is a radiolucent lesion while ameloblastic odontoma is a radiolucent lesion with partially mineralised density. Tx for both is resection and or radiation therapy.
