Gastrointestinal Flashcards
What is the effect of increased parasympathetic tone on gastrointestinal contractions?
May cause segmental contractions which inhibit progressive motility.
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 NGTPeak at >85% above baseline glucose between 90-120minComplete 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 layerMacrophages: 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 (TNFalpha, 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 TNFa. Macrophages within the lamina propria, submucosa and intestinal lymphoid tissue activate CD14 TLR4 complex which initiates transcription of TNFa and IL1B which synergise with LPS to amplify the macrophage response. Once initiated, TNFa, IL1B 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)2. Increased vascular permeability (due to histamine, leucotrienes, prostaglandins and other inflammatory mediators cause endothelial cell contraction, creating leaky gaps)3. Increased adhesiveness of endothelial cells, leucocytes and platelets (cytokines stimulate endothelial cells to express adhesion molecules that support adhesion of leucocytes and platelets. 4. 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, 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.
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 q24hAspirin 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 ulcerationSerosal 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 vasoactive intestinal peptide 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. 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 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 foodFeeds with high fibre but low bulkMay tolerate increased dietary fatSupplemental 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 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 status2. Depression, fever, anorexia and neutropenia without diarrhoea or colic3. Fulminant or peracute enterocolitis with diarrhoea4. 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 risticiiHigher 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 samplesCulture of the organism from blood is possible but difficultPCR 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-EType A: alpha toxin which interferes with glucose uptake and energy production and activates arachidonic acid metabolism and signalling pathways in enterocytesTypeA is the most common isolated from horses of all agesType B and C: beta toxin is a cytotoxin that causes enterocyte necrosis, ulceration and ultimately severe intestinal inflammation and haemorrhageEnterotoxin 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 morphologyToxin 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 tot he 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 migrationSegmental infarction secondary to thromboembolism and thrombus formation causing ischaemiaRelease 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 diarrhoeaAcute 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 diarrhoeaAnorexiaFeverDepressionPeripheral oedemaOral ulcerationColicHaematuria or oliguria with renal involvementHypoproteinaemia with hypoalbuminaemiaHyponatraemia, 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:DepressionSweatingIrritabilityAbdominal painElevated heart and respiratory ratesFeverPolyuria/polydipsiaProfuse diarrhoea (rarely haemorrhagic)Stranguria and pollakiuria is commonTremors and synchronous diaphragmatic flutter may occur due to hypocalcaemiaNeurologic 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 painSome horses die before diarrhoea developsWith 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 pressureDownside 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/antithromboticAspirin 10-30mg/kg POq12-48hCyathostomiasis: 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 equiStrep equi zooR. equiCorynebacterium pseudotuberculosisActinobacillus 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 germinativumBile 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: glutamineColonocytes: 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 nervesSympathetic supply is through postganglionic fibres of the cranial and caudal mesenteric plexuses. Excitatory neurotransmitter is acetylcholine through muscarinic type 2 receptors. Activation of alpha2 adrenergic receptors on cholinergic neurons within enteric ganglia inhibits release of acetycholine, reducing intestinal contraction. B1, B2 and B-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/kgNeostigmine: 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 habbits/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 diaphragmAcquired 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: guardedGrade 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 deteriorationSecondary 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. 2. Fungiform papillae are larger and easily seen at the rounded free end3. Vallate papillae are usually two or three in number and are found on the caudal portion of the dorsum of the tongue. 4. Foliate papillae are situated rostral to the palatoglossal arches of the soft palate on which they form rounded eminence about 2-3cm in lengthTypes 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 brainstemPeripheral nerves controlling prehensionCN V (sensory and motor)CN VIICN XIIPeripheral nerves transferring food bolus to pharynxCN V (sensory)CN XIIPeripheral nerves of swallowingCN IXCN 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 leguminicolaIt 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 nerveSmooth 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?
AcepromezineXylazine or detomidineOxytocin (limited evidence due to mixed effects)Instillation of lignocaineBuscopanIVFT
What are the likely systemic effects of prolonged choke?
HypovolaemiaElectrolyte 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 diseaseMotility disordersIncreased gastric volume from:Gastric outflow obstructionsGastric paresisIntestinal 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:EPMEHMIdiopathic vagal neuropathyEarly sign of dysautonomiaBotulism
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 submucosaMural structures - associated with muscular layers and adventitiaAnnular 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 wallTraction 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 berriesApolectolB vitaminsMagnesium hydroxide
List causes of primary and secondary gastric dilatation
Primary:Gastric impactionGrain engorgementExcessive water consumption post exerciseParasitismAerophagiaSecondary:Primary intestinal ileusSmall 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.
<p>adrenergic neurons are typically \_\_\_\_\_\_\_\_\_\_ to gut?</p>
<p>inhibit or stimulatory? Molecule?</p>
<p>Inhibitory: adrenaline/epinephrine</p>
<p>What is Aldosterone and where is it secreted?</p>
<p>Is a steroid hormone (mineralocorticoid) secreted by outer zone glomerulosa of adrenal cortex.</p>
<p>Secreted after low-salt diet, angiotensin, adrenocorticotropic hormone, or high potassium levels.</p>
<p>Aldosterone: function</p>
<p>act on distal convoluted tubules and collecting ducts of the kidney causing secretion of K+ and reabsorption of Na+ and H2O. </p>
<p>What is the GI function of Aldosterone?</p>
<p>It stimulates sodium and water reabsorption from the gut and salivary glands in exchange with K+ ions.</p>
<p>Species dependent: water and Na+ reabsorption in proximal colon and decrease absorption in distal colon.</p>
<p>Autocrine definition</p>
<p>secretions of a given cell modify or regulate functions of the same cell</p>
<p>By what process is water absorbed in the small intestine? </p>
<p>Entirely by diffusion</p>
<p>Where are the2CCK receptors located?</p>
<p>CCK-1 (CCKA) is primarily found in the GI tract. Its primary fnction is to stimulatebicarb secretion, gall bladder emptying and inhibiting gut motility.</p>
<p>CCK-2 (CCKB) is primarily found on CNS. Its primary function is to regulatenociception,anxiety,memoryandhunger.</p>
<p>Cholecystokinin: Action</p>
<p>Stimulates pancreatic enzyme secretion and gallbladder contractions; inhibits food intake and gastric emptying</p>
<p>Cholecystokinin: Production site</p>
<p>Duodenum, jejunum, ileum; endocrine I ("i") cells and enteric neurons of duodenum and jejunum</p>
<p>Cholecystokinin: Release stimulus</p>
<p>Fats and protein</p>
<p>Cholinergic neurons are typically \_\_\_\_\_\_\_\_\_ to gut? inhibit or stim? Molecule?</p>
<p>stimulatory, Acetycholine</p>
<p>Describe the basic electrical rhythm of the stomach. </p>
<p>Mixing waves = Slow waves (spontaneous) that result in mixing of the food (chyme), more intense at antrum</p>
<p>Discuss the blood flow in the salivary glands. </p>
<p>The salivary glands make kalikrein - which when secreted splits a-2 globulin into bradykinin = VASODILATION</p>
<p>Discuss the excretion of bilirubin. </p>
<p>1. RBCs are degraded by reticuloendothelial system (heme + globin)2. Via heme oxygenase = Biliverdin3. Unconjugated bilirbin (bound to albumin)4. In liver conguates with glucuronic acid = Bilirubin glucuronide (80%) and bilirbuin sulfate (10%) = Conjugated bilirubin5. Conjugated bilirubin is excreted in bile into intestesines6. In intestines - intestinal bacteria convert it into urobilinogen7. About 90% of urobilinogen is converted to stercobilinogen then converted to stercobilin and is excreted in feces8. About 10% of urobilinogen is absorbed into blood and is either recycled to bile (about 95%) or excreted by kidney (about 5%). When urobilinogen is exposure to air in the urine it is converted to urobilin</p>
<p>Do the slow waves in the GIT cause muscle contraction? </p>
<p>NO! Except in stomach. Provide electrical background to allow AP when excited by intermittent spike potentials (which excites muscle contractions)</p>
<p>Does the large intestinal have villi and Crypts of Lieberkuhn? </p>
<p>No villiYes - Crypts of Lieberkuhn</p>
<p>During fasting what type of gastric contraction periodically occurs? </p>
<p>Migrating myoelectric complexes = mediated by motiliin</p>
<p>Explain enterohepatic circulation of bile salts? </p>
<p>Bile salts are reabsorbed in SI (diffusion and active transport) → Portal blood → Liver venous sinusoids → Hepatocytes → BileAbout 94% of bile salts are recirculated (up to 17x)</p>
<p>Five Functions of the gut</p>
<p>motilitysecretiondigestionabsorptionstorage</p>
<p>Gastric inhibitory polypeptide: action</p>
<p>inhibits gastric secretions and emptying and stimulates insulin secretion. Slows movement of ingesta particularly from stomach to intestine.</p>
<p>Gastric inhibitory polypeptide: Production site</p>
<p>duodenum and jejunum</p>
<p>Gastric inhibitory polypeptide: release stimulus</p>
<p>fat and glucose (glu. in duodenum)</p>
<p>Gastrin &amp; histamine =?</p>
<p>Gastrin increases acid secretion indirectly by stimulation of histamine release from ECL which can activate H2 receptors on acid secreting gastric parietal cells.</p>
<p>Gastrin binds to \_\_\_\_\_\_\_\_\_\_\_\_</p>
<p>CCK-2 receptor, g-protein coupled receptor. Causes stimulation of gastric acid secretion and hyperplasia of enterochromaffin-like cells.</p>
<p>Gastrin forms</p>
<p>G-17 (90%) and G-34 (10%, duodenum)</p>
<p>Gastrin: Action</p>
<p>Stimulates acid secretion and growth of stomach epithelium (cancer marker)</p>
<p>Gastrin: prod. site</p>
<p>stomach (pylorus and antrum) and duodenum G cells</p>
<p>Gastrin: Release stimulus</p>
<p>Protein, increased high gastric acidity, gastric distention</p>
<p>How are bile salts made? </p>
<p>From cholesterol (diet or made in liver) → 1. cholic acid OR 2. Chenodeoxycholic acid → These combine with either 1. Glycine or 2. Taurine → Conjugated bile salts</p>
<p>How are pancreatic enzymes secreted? </p>
<p>Pancreatic enzymes are secreted as zymogens (INACTIVE form) - Such as trypsinogenOnce into the small intestine they are activated = Trypsin</p>
<p>How are the action potentials different in the GIT? </p>
<p>Calcium-sodium channels = Much slower to open/close = Longer duration of AP</p>
<p>How does parasympathetic stimulation affect the ENS? </p>
<p>Increases activity of ENSMainly vagus nn (some through pelvic nn)</p>
<p>How does sympathetic stimulation affect the ENS? </p>
<p>Inhibits GIT activity = From T5-L2 → sympathetic chains → celiac ganglion → mesenteric ganglia (postganglion neuron bodies) → Postganglic fibers to ENTIRE GIT → Secrete norepinephrine (small amounts of epinephrine)Inhibits intestinal smooth muscle, blocks/inhibits neurons in ENS</p>
<p>How dot he enterocytes of the Crypts of Lieberkuhn result in formation of a watery vehicle? </p>
<p>1. Active secretion of Cl-2. Active secretion of HCO3-Drags along Na+ and water</p>
<p>How is gastric secretion inhibited?</p>
<p>Food in SI1. Reverse enterogastric reflex (myeneteric NS, sympathetic NS, vagus n)2. Food in SI stimulates secretion of SECRETIN and 3 other inhibitors (gastric inhibitory peptide, somatostatin, vasoactive intestinal peptide)</p>
<p>How is pepsinogen activated? </p>
<p>Pepsinogen (inactive) is secreted by the peptic/chief cells in the gastric/oxyntic gland. This is converted to pepsin (ACTIVE = highly proteolytic at low pH) when HCl is present</p>
<p>How is urea formed in the urine? </p>
<p>Amino Acid + Keto acid (alpha keto-glutoric acid) gets transminated into keto acid + amino acid (glutamic acid)Via oxiative deamination glutamic acid is converted to keto acid + NH3 (ammonia)The ammonia combined with CO2 and creates urea!</p>
<p>In general what regulates stomach emptying? </p>
<p>Signals from stomach and duodenum (potent)</p>
<p>In the nerve fibers how are AP generated? </p>
<p>By rapid entry of Na into nerve through Na channels</p>
<p>Motilin: Action </p>
<p>induction/regulation of phase III of the MMC (migrating motor complex) during fasting (digestive state). Works on both muscles and nerves. Stimulates gastric emptying between meals and secretion of pepsinogen (protein digesting enzyme)</p>
<p>Motilin: Production site</p>
<p>M cells of duodenum and jejunum (jejunum lesser extent than duod.)</p>
<p>Motilin: Release stimulus</p>
<p>Acetylcholine</p>
<p>Name 1 thing that is stimulated and 2 things that are inhibited by gastric inhibitory peptide (GIP)? </p>
<p>Stimulates:1. Insulin releaseInhibits:1. Gastric motility (mild)2. Gastric Acid Secretion</p>
<p>Name 2 enzymes that aid in starch digestion that are not found in intestinal epithelium. </p>
<p>1. Salivary alpha amylase (Ptyalin)2. Pancreatic amylase</p>
<p>Name 2 mixing movements in the GIT? </p>
<p>1. Peristalsis again sphincter = churning of content2. Local intermittent constrictive contractions within gut wall (chopping and shearing contents)</p>
<p>Name 3 places that protein digestion occurs? </p>
<p>1. Stomach2. Duodenum/Upper jejunum (pancreatic secretions)3. Enterocytes (duodenum and jejunum)</p>
<p>Name 3 stimuli that result in secretion of cholecystokinin? </p>
<p>1. Protein2. Fat3. Acid</p>
<p>Name 3 stimuli that result in secretion of gastrin? </p>
<p>1. Protein2. Distension3. Nerve (gastrin releasing peptide from vagal stimulation)Acid = Inhibits release</p>
<p>Name 3 things that stimulate the secretion of motilin. </p>
<p>1. Fat2. Acid3. Nerve</p>
<p>Name 4 other functions of the liver in metabolism. </p>
<p>1. Stores Vitamins - A, D, B122. Blood coagulation - makes factors (needs Vit K)3. Storage of iron == Ferritin4. Metabolizes drugs, hormones, Ca2+, others</p>
<p>Name 4 things that are stimulated and 1 thing that is inhibited by secretin. </p>
<p>Stimulates:1. Pepsin secretion2. Pancreatic bicarbonate secretion!!! (neutralizes acidic contents)3. Biliary bicarbonate secretion4. Growth of exocrine pancreaseInhibits:1. Gastric Acid secretion</p>
<p>Name 6 roles of cholecytsokinin. </p>
<p>Stimulates:1. Pancreatic enzyme secretion2. Pancreatic bicarbonate secretion3. BG contraction4. Growth of exocrine pancreasInhibits:5. Gastric emptying (moderate - time for digestion)6. Appetite (sensory afferent in duodenum via vagus to appetite centers)</p>
<p>Name the 2 primary bile acids. </p>
<p>Cholic acid and chenodeoxycholic acid</p>
<p>Name the 4 fat soluble vitamins. </p>
<p>Vitamins A, D, E, K</p>
<p>Neurocrine definition</p>
<p>secretion by enteric neurons of neuromodulators or regulatory peptides that affect nearby muscle cells, glands, or blood vessels.</p>
<p>Paracrine definition</p>
<p>peptides secreted from cells with subsequent diffusion through the interstitial space to contact and affect other cells</p>
<p>Secretin: Action</p>
<p>stimulates HCO3- secretion and inhibits acid secretion (nature's anti-acid). Stimulates exocrine pancreatic and biliary secretions of water, bicarb. gastric mucus and pepsinogen; endocrine pancreatic secretions of insulin, glucagon, and somatostatin; and pancreatic growthInhibits gastric acid secretion, motility of intestine and gastric mucosal growth.</p>
<p>Secretin: production site</p>
<p>duodenum and upper jejunum; S cells</p>
<p>Secretin: Release stimulus</p>
<p>Gastric acid, fat, protein, bile acids, and herbal extractsControlled by action of hormones: CCK, hormonal-neuronal control (CCK-vagal) </p>
<p>What 3 locations do carbohydrate digestion occur? </p>
<p>1. Mouth2. Small intestine (pancreatic secretions)3. Villi (Brush border)</p>
<p>What 3 pancreatic enzymes are responsible for fat digestion? </p>
<p>Pancreatic lipase (fat into FA and monglycerides)Cholesterol esterase (hydrolysis of cholesterol)Phospholipase (FA splits from phospholipids)</p>
<p>What 3 pancreatic enzymes are responsible for protein digestion? </p>
<p>1. Trypsin!!!!2. Chymotrypsin3. Carboxypolypeptide (can release AA)</p>
<p>What 4 components are absorbed via micelles with bile salts? </p>
<p>1. Fatty Acids2. Monglycerides3. Cholesterol4. Other Lipids</p>
<p>What accounts for the huge regenerative capacity of the liver? </p>
<p>HGF (Heptocyte growth factor) produced by mesenchymal cells</p>
<p>What are 2 main things that are lost in diarrhea? </p>
<p>HCO3- and K+ = Hypercholermic metabolic acidosis</p>
<p>What are 2 stimuli for secretion of secretin? </p>
<p>1. Acid2. Fat</p>
<p>What are 3 stimuli for gastric inhibitory peptide (GIP) secretion? </p>
<p>1. Protein2. Fat3. Carbohydrates (less)</p>
<p>What are essential for emulsification of tryglycerides? </p>
<p>Bile salts and lecithin</p>
<p>What are hunger contractions? </p>
<p>When the stomach as been empty for hours - Rhythmic powerful contractions</p>
<p>What are slow waves in the GIT? </p>
<p>Rhythmic contractions - determine by frequency of slow waves (NOT AP but slow undulating changes in resting membrane potential)Varies along GIT</p>
<p>What are spike potentials in GIT? </p>
<p>True AP - Each time peaks of slow waves temporarily more + spike potentials = Peaks</p>
<p>What are the 2 actions of gastrin? </p>
<p>Stimulates:1. Gastric acid secretion2. Growth of gastric mucosa</p>
<p>What are the 2 duodenal factor that control stomach emptying? </p>
<p>Inhibit Emptying1. Enterogastric Relfex (food in duodenum inhibit pyloric pump)2. Hormones = CCK (from jejunal cells that sense fat) = Blocks stomach motility (caused by gastrin)</p>
<p>What are the 2 gastric factors that control stomach emptying? </p>
<p>Promote emptying = increased pyloric pump1. Gastric food volume (stretch)2. Gastrin release</p>
<p>What are the 2 main blood supplies for the liver? </p>
<p>Portal vein and hepatic artery</p>
<p>What are the 2 main glands in the SI that result in secretions? </p>
<p>1. Brunner's glands = Mucus and bicarbonate2. Crypts of Lieberkuhn = Digestive Juices (mucus and watery vehicle)</p>
<p>What are the 2 main stimuli for secretion of pepsinogen from peptic/chief cells? </p>
<p>1. Acetylcholine (vagus n. and gastric enetric plexus)2. Acid in the stomach</p>
<p>What are the 2 main ways that proteins are absorbed in the SI? </p>
<p>Via Na+ co-transporter or less by facilitated diffusion</p>
<p>What are the 2 major movements in the SI? </p>
<p>1. Mixing contractions = segmentation contractions (from SI distension with chyme)2. Propulsive Movements = Perstaltic wavesStretch (chyme in duodenum), gastroenteric reflex, hormones (gastrin, CCK, insulin, motilin, serotonin)</p>
<p>What are the 2 major movements of the colon? </p>
<p>1. Mixing movements - large circular contractions2. Propulsion movements = MASS MOVEMENTS (dt gastrocolic and duodenocolic reflexes = distension)</p>
<p>What are the 2 reflexes that control defecation and which one is "stronger"? </p>
<p>1. Intrinsic Reflex (local ENS - myenteric plexus)2. Parasympathetic Defecation Relfex (via pelvic nn) = VERY POWERFUL peristalsis and inhibits internal anal sphincter?</p>
<p>What are the 2 types of movement in the GIT? </p>
<p>Propulsive movements (food to move to accommodate digestion/absorptive)2. Mixing movements (of contents)</p>
<p>What are the 2 types of peristalsis during the esophageal phase?</p>
<p>1. Primary peristalsis - continuous wave from pharynx</p>
<p>2. Secondary Peristalsis = from distension of esophagus (controlled by myenteric NS)</p>
<p>What are the 2 types of secretions from salivary glands? </p>
<p>1. Serous = Ptyalin (a-amylase) = Digest starch2. Mucus = Mucin = Lubrication</p>
<p>What are the 3 final monosaccharides? </p>
<p>1. Glucose2. Galatose3. Fructose</p>
<p>What are the 3 main actions that can result in depolarization of smooth muscle cells in GIT? </p>
<p>1. Stretching of muscle2. Stimulation by acetylcholine release from parasympathetic nn3. Stimulation by several specific GI hormones</p>
<p>What are the 3 main cell types that make of the gastric/oxyntic gland and what do they secrete? </p>
<p>1. Mucous Neck Cell = Mucus2. Oxyntic/Partiel Cells = HCl, intrinsic factor3. Peptic/Chief Cells = Pepsinogen</p>
<p>What are the 3 main functions of the liver in fat metabolism. </p>
<p>1. High rate of oxidation of fatty acids (fats → glycerol + FFA → Beta oxidation →Acetyl CoA→TCA Cycle or acretoacetic acid2. Synthesis cholesterol (for bile salts), phospholipids (cell membranes), lipoproteins3. Convert carbs and proteins into fat</p>
<p>What are the 3 main motor functions of the stomach? </p>
<p>1. Storage of food until into SI2. Mixing of food with gastroc secretions into chyme3. Slow empyting of chyme from sotmach into SI</p>
<p>What are the 3 main stimulators of H+ secretion on parietal cells and what are their receptors?</p>
<p>1. ACh (From Vagus n, M3 receptor)2. Gastrin (From G cells in antrum, CCKb receptor)3. Histamine (From ECL cells, H2 receptor)</p>
<p>What are the 3 main stimuli for HCl secretion and which cells do these substances stimulate? </p>
<p>1. Acetylcholine = All cells are stimulated2. Gastrin = Only parietal cells are stimulated3. Histamine = Only parietal cells are stimulated</p>
<p>What are the 3 main stimuli for pancreatic secretion? </p>
<p>1. Acetylcholine2. Cholecystokinin (CCK)3. Secretin</p>
<p>What are the 3 phases of gastric secretion and how much do they account for acid secretion? </p>
<p>1. Cephalic Phase = 30% acid production2. Gastric Phase = 60% acid production3. Intestinal Phase = 10% acid production</p>
<p>What are the 3 phases of pancreatic secretion? </p>
<p>Same as gastric secretion1. Cephalic = 20% pancreatic enzymes2. Gastric = 5-10% pancreatic enzymes3. Intestinal: LOTS of pancreatic fluid and bicarbonate (secretin); 70-80% pancreatic enzymes (CCK)</p>
<p>What are the 3 phases of swallowing? </p>
<p>1. Voluntary Stage (bolus into pharynx)2. Pharyngeal Stage (involuntary)3. Esophageal Stage (involuntary)</p>
<p>What are the 3 things in the portal triad?</p>
<p>1. Portal Vein2. Bile Duct3. Hepatic Artery</p>
<p>What are the 4 main functions of the liver in carbohydrate metabolism? </p>
<p>1. Store glycogen (glucose buffer)2. Convert galactose/fructose into glucose3. Gluconeogenesis</p>
<p>What are the 4 main functions of the liver in protein metabolism? </p>
<p>1. Deamination of AA2. Formation of urea3. Formation of plasma proteins (except Ig)4. Interconversion of AA</p>
<p>What are the 4 steps of Vitamin B12 absorption? </p>
<p>1. Dietary B12 released from pepsin (stomach)2. Free B12 binds to R protein (from saliva)3. Duodenum: Pancreatic proteases degrade R protein and Vit B12 transferred to intrinsic factor (prevented from degrading)4. Vit B12-Intrinsic Factor Complex - Ileum it is transported</p>
<p>What are the 6 magic properties of mucus? </p>
<p>1. Adheres tightly to food and spreads thin2. Sufficient body to coat GIT so that food rarely touches mucosa3. Causes formation of fecal balls4. Resistant to digestion by digestive enzymes5. Particles slide along it easily6. Amphoteric properties (can buffer acid or alkali)</p>
<p>What are the areas that lymph is created/filtrated in the liver lobules? </p>
<p>Within the Space of Disse</p>
<p>What are the basic steps in secretion from a glandular cell in the GIT?</p>
<p>1. Diffusion of substance from capillaries into glandular cell2. Secretory substance made in ER3. Formed by ribosomes and Golgi4. Stored Glogi vesicles5. Increased permeability = Increased intracellular Ca2+ = Vesicles fuse to apical membrane = Exocytosis</p>
<p>What are the Brunner's gland stimulated by in the SI? </p>
<p>Result in mucus and bicarbonate secretionStimulated by: food, vagal stimulation, secretinResult in protection of mucosa in duodenum</p>
<p>What are the effects of norepinephrine and epinephrine on GIT nerves (stimulation of smpathetic nn)? </p>
<p>More negative = Hyperpolarized (less excitable)</p>
<p>What are the enzymes in the duodenum/upper jejenum that aid in protein digestion? </p>
<p>Pancreatic enzymes: Trypsin. Chymotrypsin, carboxypolypeptidase, proelastase</p>
<p>What are the final products of carbodyhrate digestion? </p>
<p>Monosaccarides that are absorbed immediately into portal blood</p>
<p>What are the layers of the GI wall?</p>
<p>1. Serosa 2. Longitudinal smooth muscle layer 3. Circular smooth muscle layer 4. Submucosa 5. Mucosa (bundles of smooth muscle fibers)</p>
<p>What are the main villus enzymes? </p>
<p>1. Peptidase (peptides → AA)2. Sucrase, maltase, isomaltase, lactase (dissaccharides → monosaccharides)3. Intestinal lipase (fats → glycerol and FA)</p>
<p>What are the net results of gastric parietal cells? </p>
<p>Net secretion of HCl and net absorption of HCO3- (alkalaine tide that is seen after meals)</p>
<p>What are the steps in HCl secretion in a oxyntic/parietal cells? </p>
<p>1. Water dissociates into H+ and OH- in the cytoplasm2. H+/K+ ATPase allows H+ to be secreted into the canaliculi3. Potassium in brought into the cell on the basolateral membrane by a Na+/K+ ATPase pump, this makes low intracellular Na+, which brings Na+ into the cell from the canaliculus4. Pumping out of H+ allows formation of HCO3- since OH- is accumulating in the cell cytoplasm, this is mediated by carbonic anhydrase, this is then secreted in exchange for Cl-, which is sent out into the canaliculus to meet with H+ and make HCl5. Water passes into the canaliculus by osmosis</p>
<p>What are the steps in making bicarbonate in the pancreas?</p>
<p>1. CO2 diffuses into the cell from the blood, combines with water to form carbonic acid (H2CO3), dissociates into H+ and HCO3-2. H+ is traded in the blood for Na+, which is transported out of the cell with HCO3-3. This also pulls water by osmosis</p>
<p>What are the stimuli for propulsive movements = peristalsis in GIT? </p>
<p>Stimulus = Distenstion (stretching) caused by materialSome chemical and physical irritation, strong parasympathetic nervous signals</p>
<p>What are the two imperative steps in emptying the GB and what controls this? </p>
<p>Need contraction of GB and relaxation of Sphincter of Oddi (at exit of common bile duct into duodenum) This is stimulated by CCK that is released in response to a fatty meal in the duodenum</p>
<p>What are the two layers of muscles in the GIT? </p>
<p>1. Circular muscles2. Longitudinal muscles</p>
<p>What are the two main cells types of the Crypts of Lieberkuhn? </p>
<p>1. Goblet Cells = Mucus2. Enterocytes = Absorb and secrete water and electrolytes (PURE ECF, alkaline fluid)</p>
<p>What are the two main functions of pancreatic secretions? </p>
<p>1. Digestive enzymes2. Na bicarbonate</p>
<p>What are the two main roles of bile salts? </p>
<p>1. Emulsifying or detergent function (decrease surface tension, allows GIT to break down fats)2. Absorption of micelles into blood (MAJOR effect! = fatty acids, monoglycerides, cholesterol, other lipids)</p>
<p>What are the two main roles of bile? </p>
<p>1. Fat digestion and absorption (based on bile acids/salts that aid in emulsifying and absorbing fats)2. Excretion of waste (including bilirubin and cholesterol)</p>
<p>What are the two major glands in the stomach and what do each of them secrete? </p>
<p>1. Oxyntic Gland (Gastric Gland) = HCl, Pepsinogen, intrinsic factor, mucus2. Pyloric Gland = Mucus, Gastrin</p>
<p>What are the two major plexus and what do they control? </p>
<p>1. Myenteric Plexus (Auerbach's): Outer plexus twn longitudinal and circular muscle layers - mainly control GI movements2. Submucosal Plexus (Meissner's): Inner plexus - controls mainly GI secretions and local blood flow</p>
<p>What are the two stages of bile secretion? </p>
<p>1. Bile is secreted by hepatocytes into bile canaliculi2. Bile flows through ducts to the hepatic duct → common bile duct → duodenum OR cystic duct to GallbladderAlong the way in the ductules/ducts watery Na+ and HCO3- solution secreted by secretory epithelial cells (stimulated by secretin)</p>
<p>What are tonic contractions in the GIT? </p>
<p>Continuous (not associated with slow waves) - can last mins to hoursThese are in addition or instead of rhythmical contractions</p>
<p>What causes Ca to enter the muscle fiber to result in a contraction? </p>
<p>Slow waves do NOT cause Ca to enter (ONLY Na), thus no muscle contraction aloneDuring a spike potential (generated by slow waves) = Large amount of Ca enters = muscle contraction</p>
<p>What cells are consider the electrical pacemakers for smooth muscle cells? </p>
<p>Interstitial cells of Cajal - Undergo cyclic change in membrane potentialUnique ion channels that periodically open = inward pacemarkers currents</p>
<p>What cells secrete gastric inhibitory peptide (GIP)? </p>
<p>K cells of duodenum and jejunum</p>
<p>What components are in salivary to attack bacteria? </p>
<p>1. Thiocyanate ions2. Lysozyme3. Ig</p>
<p>What controls stomach emptying? </p>
<p>"Pyloric pump" - intense peristaltic wave in the antrum, pyloric sphincter also controls this</p>
<p>What controls the cephalic phase of gastric secretion? </p>
<p>Sight, smell, taste of food → HCl + pepsin releaseControlled by: Cerebral cortex (appetite center amygdala and hypothalamus) → Vagus n. → Stomach via AcetylchoineG cells →Gastrin Releasing peptide = GASTRIN release</p>
<p>What controls the cephalic phase of pancreatic secretion? </p>
<p>Acetylcholine (vagal n.) = 20% pancreatic enzymes (BUT NO fluid)</p>
<p>What controls the gastric phase of gastric secretion? </p>
<p>Food in stomach (stretch) = HCl releaseControlled by:Long vagovagal reflex = acetylcholineLocal enteric reflex Peptides and AA → G cells → GASTRIN</p>
<p>What controls the gastric phase of pancreatic secretion?</p>
<p>Acetylcholine (vagal n.) = 5-10% pancreatic enzymes (BUT NO fluid)</p>
<p>What controls the intestinal phase of gastric secretion? </p>
<p>Food in duodenumControlled by:Enterooxyntic (not gastrin per CVT??)</p>
<p>What controls the intestinal phase of pancreatic secretion? </p>
<p>1. Chyme in SI (acid) → Secretin (from S cells in duodenum) → Lots of pancreatic fluid and bicarbonate2. Food in SI (peptides/fat) → CCK (from I cells in duodenum and upper jejunum) → 70-80% pancreatic enzymes</p>
<p>What determines the rate and action potentials and contractions in various segments of GIT? </p>
<p>The frequency of slow waves which is controlled by pacemaker = Interstital cells of Cajal</p>
<p>What do neural and hormonal input influence in GIT? </p>
<p>Neural input and hormonal input DO NOT influence the frequency of slow waves, they do influence the frequency of action potentials</p>
<p>What do the ECL cells secrete that results in the parietal cells secreting HCl and what controls this process?</p>
<p>Rate and amount of HCL produced is directly related to histamine from ECL cells, which is controlled by GASTRIN</p>
<p>What does ECL cells stand for? </p>
<p>Enterochromaffin-Like cell (ECL cell)</p>
<p>What does lactase do? </p>
<p>Splits Lactose into galactose and glucose</p>
<p>What does maltose and other 3-9 glucose polymers split into? </p>
<p>Glucose by maltase and alpha-dextinase</p>
<p>What does motilin do in GIT? </p>
<p>Stimulates gastric and intestinal motility (cyclic release = waves → interdigestive myoelectrical complexes</p>
<p>What does sucrose do? </p>
<p>Splits sucrose into fructose and glucose</p>
<p>What enzyme is made in pancreatic acini that helps to prevent autodigestions and were is it present? </p>
<p>Trypsin InhibitorPrevents activation of zymogens in pancreas or ducts or intracellular</p>
<p>What enzymes and where are disacchardies hydrolyzed into monosaccharides? </p>
<p>Intestinal Epithelial Enzymes - Within villi in the brush border1. Maltase2. Alpha-Dextrinase3. Lactase4. Sucrase</p>
<p>What happens in the stomach glands between meals? </p>
<p>They make mucus, almost NO acid!</p>
<p>What happens to bile when it is stored in the GB? </p>
<p>The bile is concentrated (Water, Na+, Cl- are absorbed through the wall of the GB) - via active transport of Na+ and passive movement of others = Concentration of bile salts, cholesterol. Lecithin, bilirubin</p>
<p>What is a reflex that comes from the GIT to spinal cord/brain and then back to GIT? </p>
<p>Defecation reflexes = from colon/rectum to spinal cords and back to produce powerful colon, rectal, and abdominal contractions = Defecation</p>
<p>What is a unique feature of the electrical activity of GIT smooth muscle? </p>
<p>Slow waves = Not AP but oscillating depolarization and repolarization</p>
<p>What is another name for gastric inhibitory peptide (GIP)? </p>
<p>Glucose-dependent insulinotrophic peptide</p>
<p>What is another name for pits? </p>
<p>Crypts of Lieberkuhn = Secretory cells in GIT</p>
<p>What is another name for the Na+/glucose cotransporter in the SI? </p>
<p>SGLT 1</p>
<p>What is important about the 3 stimuli that result in pancreatic secretions? </p>
<p>The stimuli potentate each other, meaning that pancreatic secretion is greatest with the combined stimuli as compared to single stimuli</p>
<p>What is mucus made of? </p>
<p>Water, electrolytes, glycoproteins</p>
<p>What is ptyalin? </p>
<p>a-Amylase to digest starches, found in salivary secretions are part of serous secretion</p>
<p>What is renointestinal reflex and vesicointestinal reflex? </p>
<p>Inhibits intestinal activity due to kidney or bladder irritation</p>
<p>What is splanchnic circulation? </p>
<p>• Blood flow in gut, spleen, pancreas → liver (via portal vein) → hepatic sinusoids (reticuloendothelial cells to remove bacteria, carbs and proteins absorbed) → hepatic veins → vena cava</p>
<p>What is the "law" of the gut? </p>
<p>Peristaltic reflex = gut reflexes to result in receptive relaxation (easier propulsion) - Perstaltic waves to the anus</p>
<p>What is the accessory pancreatic duct and which species have it? </p>
<p>Opens into duodenum at minor duodenal papillaDogs = ALWAYS!Cats = Occasionally</p>
<p>What is the action potential in GIT dependent on? </p>
<p>Action potentials in GIT cannot occur unless the slow wave brings the membrane potential to threshold</p>
<p>What is the colonoileal reflex? </p>
<p>Reflexes from colon to inhibit emptying of ileal contents into colon (reflex from gut to prevertebral sympathetic ganglia back to GIT)</p>
<p>What is the driving force behind secretion of HCl from the oxyntic/parietal cells? </p>
<p>H+/K+ ATPase pump on the apical membrane that results in secretion of H+ intot he canaliculus</p>
<p>What is the enterogastric reflex? </p>
<p>Signals from colon/small intestines to inhibit stomach motility and secretions (reflex from gut to prevertebral sympathetic ganglia back to GIT)</p>
<p>What is the enzyme in the enterocytes that aids in final polypeptide and amino acid digestion? </p>
<p>Peptidases (aminopolypeptidase, dipeptidase)</p>
<p>What is the enzyme in the stomach that aid in protein digestion? </p>
<p>Pepsin</p>
<p>What is the final composition of saliva and where do these changes take place? </p>
<p>Within the salivary ducts = HIGH K+ and HCO3- (little Na and Cl)1. K+ active secretion2. HCO3- secretion3. Na active absorption4. Cl- passive absorption (follows Na)</p>
<p>What is the final product of fat digestion? </p>
<p>Fatty acids and 2-monoglycerides</p>
<p>What is the final product of protein digestion? </p>
<p>Amino Acids</p>
<p>What is the function of the myenteric plexus in peristalsis? </p>
<p>If no myenterix plexus (congenital) peristalsis will NOT occurBlock it with atropine (affecting cholinergic nn in myenteric plexus)</p>
<p>What is the gastrocolic reflex? </p>
<p>Signals from stomach to cause evacuation of colon (reflex from gut to prevertebral sympathetic ganglia back to GIT)</p>
<p>What is the gastroielal reflex? </p>
<p>After a meal = increased peristalsis in ileum = emptying</p>
<p>What is the main difference btwn the myenteric and submucosal plexuese? </p>
<p>Myenteric Plexus = Linear chain of interconnected neurons that run the length of GIT - Control muscle activity along length of gutSubmucosal Plexus = Functions within the inner wall of each segment of intestine, sensory signal from epithelium integrate at submucosal plexus to help control intestinal secretions, local absorption, location contraction of submucosal muscle</p>
<p>What is the main electrolyte that is secreted by enterocytes? </p>
<p>Cl- (based on increased cAMP). Na+ and water follow = secretion</p>
<p>What is the main mechanism of ion absorption in SI? </p>
<p>Active transport of Na+Na+ is actively transported from basolateral membrane into interstitial space Low intracellular conc of Na → electrochemical gradient → therefore more Na moves from chyme into enterocyte</p>
<p>What is the major component of the Crypts of Lieberkuhn in the large intestine? </p>
<p>MUCUS (some bicarbonate) - Lubrication and hold feces together</p>
<p>What is the major site of Na+ absorption in the SI? </p>
<p>Jejunum</p>
<p>What is the MOA of PPI, omeprazole? </p>
<p>Inhibit the H+/K+ ATPase on the apical membrane of the gastric parietal cell</p>
<p>What is the most important enzyme of fat digestion? </p>
<p>Pancreatic lipase (little by enteric lipase)</p>
<p>What is the most important function of pepsin? </p>
<p>Digestion of collagen (to allow digestion of other cellular proteins)</p>
<p>What is the name of gastrin secreting tumors? </p>
<p>Zollinger-Ellison Syndrome within the pancreas</p>
<p>What is the name of the reticuloendothelial cells in the liver? </p>
<p>Kupffer cells</p>
<p>What is the nervous system that is within the wall of the gut? </p>
<p>Enteric Nervous System</p>
<p>What is the neurotransmitters that results in excitation in GIT? </p>
<p>Acetylcholine</p>
<p>What is the neurotransmitters that results in inhibition in GIT? </p>
<p>Norepinephrine</p>
<p>What is the pancreatic duct and which species have it? </p>
<p>Opens within bile duct at major duodenal papillaDogs = Usually (smaller, but can be absent)Cats = ALWAYS!</p>
<p>What is the peritoneointstinal reflex? </p>
<p>irritation of peritonenum = intestinal paralysis</p>
<p>What is the primary nerous control of saliva? </p>
<p>Parasympathetic = 2 salivary nuclei in brainstemStimulated by high centers (appetite) or something on tongue</p>
<p>What is the primary secretion from salivary glands? </p>
<p>Either ptyalin or muscus with same electrolyte composition as ECF</p>
<p>What is the primary secretion in the esophagus? </p>
<p>MUCUS for Lubrication (simple and compound mucous glands)</p>
<p>What occurs in the colonocytes for Na and K? </p>
<p>Na+ absorption (+++aldosterone)K+ secretion</p>
<p>What pancreatic enzyme is responsible for carbohydrate digestion? </p>
<p>Pancreatic amylase (starch into disaccharides and trisaccharides)</p>
<p>What results in relaxation of stomach during the storage function of the stomach? </p>
<p>Distension with food → “vasovagal reflex” to brain stem → relaxes stomach wall (to accommodate more food)</p>
<p>What stimulates the conversion of pepsinogen into pepsin? </p>
<p>HCl</p>
<p>What stimulates the release of acetylcholine that results in pancreatic secretions? </p>
<p>Vagus n. and ENS stimulation</p>
<p>What stimulates the release of cholecytskinin (CCK) that results in pancreatic secretions? </p>
<p>Released from duodenum and upper jejunum from I cells in response to protein or AA in the lumen</p>
<p>What stimulates the release of secretin that results in pancreatic secretions? </p>
<p>Released from duodenum and jejunum in response to acidic content of chyme in the lumen</p>
<p>What type of channels control the depolarization and repolarization of the slow waves in GIT? </p>
<p>Ca 2+ open resulting in Ca2+ entering cell = DepolarizationK+ open resulting in K+ OUT of cell = Repolarization</p>
<p>What would you expect with bilirubin in Cholestasis? </p>
<p>Conjugated bilirubin high</p>
<p>What would you expect with bilirubin in hemolysis? </p>
<p>Unconjugated bilirubin high</p>
<p>What would you expect with bilirubin in total EHBDO? </p>
<p>NO bilirbin in feces (since no stercobilin stool is light), no urobilin in urine</p>
<p>When the G cells in the pyloric glands sense that there is a protein rich meal what occurs? </p>
<p>G cells are stimulated by protein to release GASTRIN into the blood to reach the ECL cells, which when stimulated by gastrin will release HISTAMINE which results in HCL release from the parietal cells</p>
<p>Where is cholecystokinin secreted? </p>
<p>I cells of duodenum, jejunum, and ileum</p>
<p>Where is gastrin produced? </p>
<p>G cells from antrum, duodenum, jejunum</p>
<p>Where is secretin secreted from? </p>
<p>S cells from duodenum, jejunum, ileum</p>
<p>Which anal sphincter is under voluntary control? </p>
<p>External anal sphincter</p>
<p>Which cell type does the parietal cells in the gastric glands work closely with?</p>
<p>ECL cells</p>
<p>Which cell type secretes HCl? </p>
<p>Oxyntic/parietal cells (part of gastric/oxyntic gland)</p>
<p>Which cell type secretes intrinsic factor (dog)? </p>
<p>Oxyntic/parietal cells (part of gastric/oxyntic gland)</p>
<p>Which cell type secretes pepsinogen? </p>
<p>Peptic/Chief cells (part of gastric/oxyntic gland)</p>
<p>Which cells in the pancreas make bicarbonate? </p>
<p>Epithelial cells that line the ductules and ductsRole of bicarbonate is to neutralize acid from stomach chyme</p>
<p>Which cells make gastrin?</p>
<p>G cells in the pyloric glands in the distal end of the stomach</p>
<p>Which cells secrete motilin? </p>
<p>M cells of stomach, duodenum, jejunum</p>
<p>Which enzyme in the brush border in the SI converts trypsinogen into trypsin? </p>
<p>Enterokinase</p>
<p>Which hormones control release of pancreatic digestive enzymes? </p>
<p>Vagal stimulation (acetylcholine)Cholecystokinin (CCK)</p>
<p>Which hormones control release of pancreatic fluid and bicarbonate? </p>
<p>Secretin</p>
<p>Which hormones decreased motility in SI? </p>
<p>Secretin and glucagon</p>
<p>Which hormones increased motility in SI? </p>
<p>gastrin, CCK, insulin, motilin, serotonin</p>
<p>Which hormones results in secretion of watery Na+ and HCO3- solution from secretory epithelial cells during the second stage of bile secretion? </p>
<p>Secretin!! Which is stimulated by presence of acid within the duodenum</p>
<p>Which nerves control the parasympathetic defecation reflex? </p>
<p>Pelvic nn</p>
<p>Which nutrient is NOT carried in portal blood and why? </p>
<p>o Fats absorbed from GIT (not carried in portal blood) into intestinal lymphatics to thoracic duct to systemic circulation</p>
<p>Which pancreatic enzyme can activate all the other pancreatic enzymes? </p>
<p>Trypsin</p>
<p>Which plexus in GIT controls GI movements? </p>
<p>Myenteric Plexus (Auerbach's)</p>
<p>Which plexus in GIT controls GI secretions and local blood flow? </p>
<p>Submucosal Plexus (Meissner's)</p>
<p>Which secretagogue is the most important in gastric acid secretion? </p>
<p>Histamine!</p>
<p>Which transporter is located on the basolateral surface to transport glucose, galactose, and fructose into the blood? </p>
<p>GLUT 2</p>
<p>Which transporter on the apical surface allows for facilitated diffusion of fructose? </p>
<p>GLUT 5</p>
<p>Why are the directional movements of peristalic waves to the anus? </p>
<p>Can occur in either direction, but orad dies out = likely related to polarization of myenteric plexus</p>
<p>Why is neural stimulation of the salivary glands unique? </p>
<p>They are controlled by both parasympathetic and sympathetic NS</p>
<p>Why is saliva hypotonic? </p>
<p>Active net solute absorption and salivary ducts are impermeable to water</p>
<p>Ptyalin in the saliva hydrolyzes starch into which disaccharide?A. FructoseB. GlucoseC. LactoseD. MaltoseE. Sucrose</p>
<p>D. Maltose Ref: Guyton, Ch.66 pg. 834</p>
<p>Which of the following pancreatic enzymes leads to digestion of proteins into individual amino acids?A. TrypsinB. CarboxypolypeptidaseC. ChymotrypsinD. Aminopolypeptidase</p>
<p>B.Ref: Guyton p 835</p>
<p>Which of the following is not a potential stimulus for gastric acid secretion?a. Norepinephrine secretion resulting from stimulation of sympathetic nerves.b. Vagal nerve activity resulting from the sight of food.c. The presence of undigested protein in the pyloric antrum.d. Acetylcholine release stimulated by gastric stretch receptors acting on nerves of the ENS.e. Histamine release from cells in the gastric mucosa.</p>
<p>ACunningham Ch. 29</p>
<p>Which gastrointestinal hormone is released in response to digestive products in the intestines and causes gallbladder contraction and release of bile, inhibits stomach contraction, and inhibits appetite?a. Gastric inhibitory peptideb. Cholecystokininc. Gastrind. Secretin</p>
<p>b. Cholecystokinin</p>
<p>Which of the following is true regarding hydrochloric acid secretion in the parietal cells?a. H+ is secreted from the apical membrane of the parietal cell via facilitated diffusionb. H+-K+ ATPase works at the basolateral membrane to load the parietal cell with hydrogen ionsc. Bicarbonate is formed by carbonic anhydrase and transported out of the parietal cell by the bicarbonate chloride cotransporterd. H+ is pumped into the lumen by active transport from a H+-K+ ATPase at the apical membrane of the parietal cell</p>
<p>d. H+ is pumped into the lumen by active transport from a H+-K+ ATPase at the apical membrane of the parietal cell</p>
<p>Saliva contains high concentrations of which two ions?a. bicarbonate and sodium b. sodium and chloride c. chloride and bicarbonate d. bicarbonate and potassium </p>
<p>d. bicarbonate and potassium </p>
<p>The extrinsic innervation of the gut consists of:a. The enteric nervous system.b. The myenteric and submucosal plexuses.c. Sympathetic (splanchnic) and parasympathetic (vagus) nerves.d. Sympathetic (vagus) and parasympathetic (splanchnic) nerves.e. The pelvic nerve</p>
<p>CCunningham Ch. 27</p>
<p>What are the anatomical differences between the esophagus of dogs, cats and horses? </p>
<p>Dogs, cattle and sheep, its entire length is striated muscleCats, horses and humans, the proximal esophagus has striated muscle and the distal esophagus smooth muscle.</p>
<p>Which of the following hormones stimulates insulin release?A. GastrinB. CCKC. Gastric Inhibitory PeptideD. Motilin</p>
<p>C. Now known as glucose dependent insulinotrophic peptideRef. Guyton 802</p>
<p>Which of the following are effects of the gastric hormone secretin?a.Stimulation of mucosal endothelial growthb.Promotion of insulin secretionc.Promotion of bicarbonate secretiond.Stimulate gastric acid secretion </p>
<p>c. Promotion of bicarbonate secretion</p>
<p>Intrinsic factor must be present in gastric secretions to allow for adequate absorption of vitamin \_\_\_\_ in the ileum. Without intrinsic factor, pernicious anemia can occur. A. B6B. B12C. CD. DE. E</p>
<p>B. B12Ref: Guyton, Ch. 67 pg. 844</p>
<p>Inhibition of the enzyme carbonic anhydrase is likely to have what effect on gastric pH?a. Decrease gastric pHb. Increase gastric pHc. Have no effect on gastric pH</p>
<p>BCunningham Ch. 29</p>
<p>3. The term slow waves as applied to the gut refers to:a. Slowly moving fronts of electrical activity that are propagated down the enteric nervous system.b. Slowly moving fronts of electrical activity that result from coordinated changes in cell membrane potential occurring throughout the smooth muscle of the intestinal wall.c. Slowly moving fronts of ingesta that proceed down the intestine in response to peristaltic movement.d. Slowly moving fronts of action potentials that are constantly passing over the gut smooth muscle.e. Slowly moving fronts of peristaltic contractions that pass uniformly over the entire small intestine during the digestiveperiod.</p>
<p>BCunningham Ch. 28</p>
<p>The \_\_\_\_\_\_\_\_\_\_\_\_ reflex occurs as a result of distension of the stomach and duodenum after a meal and is transmitted by way of the autonomic nervous system. a. Defecationb. Enterogastricc. Gastrocolicd. Gastroileal</p>
<p>c. Gastrocolic</p>
<p>What factor does not contribute to depolarization of intestinal smooth muscle?a. Stretching of the muscleb. Sympathetic stimulation by norepinephrine releasec. Stimulation by several gastrointestinal hormonesd. Parasympathetic stimulation by acetylcholine</p>
<p>b. Sympathetic stimulation by norepinephrine release</p>
<p>Which of the following causes decreased blood flow to the gastrointestinal tract? A. CCKB. BradykininC. AdenosineD. Sympathetic stimulation </p>
<p>D. sympathetic stimulationRef. 805</p>
<p>Which of the following hormones inhibits small intestinal peristalsis? A. GastrinB. CCKC. InsulinD. SecretinE. Motilin F. Serotonin</p>
<p>D. Secretin Glucagon can also inhibit motility in small intestineGuyton 13th ed Ch. 64</p>
<p>Irritation of the peritoneum results in which of the following neurologic reflexes?a. peritoneointestinal reflex – the strong inhibition of excitatory enteric nerves resulting in intestinal paralysisb. peritoneoenteritis reflex - the strong inhibition of excitatory enteric nerves resulting in intestinal paralysisc. peritoneointestinal reflex – the strong excitation of the enteric nervous system inducing hypermotilityd. renointestinal reflex - the moderate inhibition of excitatory enteric nerves resulting in intestinal paralysis</p>
<p>a. peritoneointestinal reflex – the strong inhibition of excitatory enteric nerves resulting in intestinal paralysis</p>
<p>The enteric nervous system is composed mainly of two plexuses. Which one controls mainly gastrointestinal secretion and local blood flow?a. Myenteric plexusb. Mucosal plexusc. Submucosal plexusd. Parasympathetic plexus</p>
<p>Answer: cGuyton (12th ed.) p. 755</p>
<p>List the steps in HCL production by the parietal cell</p>
<p>1. H2O + CO2 + carbonic anhydrase = H2CO3 (carbonic acid)2. Carbonic acid dissociates into: a. H+ - active transport in the apical membrane into the lumen b. Bicarb - exchanged with Cl in the basolateral membrane 3. Cl diffuses through the apical membrane into the lumen 4. In the lumen H+ + Cl- = HCl </p>
<p>Which of the following hormones stimulates gastric acid secretion?A. GastrinB. CCKC. SecretinD. Motilin</p>
<p>A. GastrinRef. Guyton 802</p>
<p>An animal is presented to you with aspiration pneumonia (the result of food material entering the lower respiratory tract). Which of the following lesions would be a likely cause?a. Loss of myenteric plexus function in the pharynx and upper esophagusb. Loss of slow-wave activity in the pharynx and upper esophagusc. A lesion in the brainstemd. A lesion in the tracheae. None of the above</p>
<p>CCunningham Ch. 28</p>
<p>What is the source of the most important signal that regulates gastric emptying?A. StomachB. DuodenumC. IleumD. Colon</p>
<p>B. Duodenum Guyton 13th ed p. 811</p>
<p>Which of the following is required for normal absorption of cobalamin in the ilium?a) enterokinaseb) glucose-dependent insulinotropic peptidec) intrinsic factord) pepsinogen</p>
<p>Answer CGuyton pg. 844</p>
<p>Damage to which of these neurologic structures can result in paralysis of the swallowing mechanism?A. CN V, IX, X, &amp; swallowing center of the brainstemB. CN V, IX, &amp; XC. CN V, VII, &amp; XIID. CN V, IX, X, XII, &amp; swallowing center of the brainstem</p>
<p>Answer DV - trigeminal - sensory to face and motor to m of masticationIX - glossopharyngeal - muscles of swallowing X - vagus - efferentXII - hypoglossal - motor to tongue efferent nerve fibers from swallowing center in the brainstem travel in the facial, vagus, hypoglossal and glossopharyngeal nerves and motor branch of trigeminalCunningham p 276</p>
<p>Which of the following is the most important enzyme for starch digestion? a) Ptyalinb) Pancreatic Amylasec) a-dextrinased) maltase</p>
<p>B. pancreatic amylase Ptyalin - (also an amylase but just in saliva)Alpha dextrinase - disaccharides Maltase - maltose Guyton pg. 834</p>
<p>The myenteric plexus is inhibited by which of the following hormones? A. GastrinB. CCKC. SecretinD. VIP - vasoactive inhibitory peptide</p>
<p>D. VIP (thought to be but not for sure)Ref. Guyton 800</p>
<p>Which cell in the pyloric glands is responsible for secreting histamine in response to stimulation by gastrin?a. Parietal cellsb. Chief cellsc. Enterochromaffin-like cellsd. Goblet cells</p>
<p>c. Enterochromaffin-like cells</p>
<p>Which of the following aspects of colon physiology is common to many species, irrespective of interspecies anatomicaldifferences in colon structure?a. Rapid flow of ingestab. Adaptive relaxationc. Retropulsion, or antiperistalsisd. Haustra formation</p>
<p>CCunningham Ch. 28</p>
<p>Which of the following is characteristic of the inter digestive phase of small intestinal motility?a. Migrating motility complexes consisting of waves of peristaltic contractions that pass over the entire length of the small intestineb. Rhythmic segmentationc. Short waves of peristalsis that die out after a few centimetersd. Complete relaxation of small intestinal smooth muscle</p>
<p>ACunningham Ch. 28</p>
<p>This reflex results when food stretches the stomach allowing for the stomach reducing the tone of the muscular walla. Vasovagal reflexb. Gastrocolic reflexc. Gastroenteric reflexd. Gastroesophageal reflex</p>
<p>a. Vasovagal reflex</p>
<p>Most proteins are absorbed through intestinal epithelial cells in the form of dipeptides, tripeptides, and a few free amino acids. By what mechanism are most absorbed?A. Co-transportB. Facilitated diffusionC. Simple diffusionD. Primary active transport</p>
<p>Answer A. Co-transportGuyton Pg 841</p>
<p>Action potentials in the GI smooth muscle are potentiated by the influx of which ion? A. Cl- B. NaC. CaD. K</p>
<p>C. Ref. 799</p>
<p>Parietal cells within the gastric glands release \_\_\_\_\_\_\_\_\_\_, which is needed for absorption of vitamin B12 in the ileum.a. Intrinsic factorb. Hydrochloric acidc. Cortisold. Histamine</p>
<p>a. Intrinsic factor</p>
<p>Which of the following best describes the motility of the proximal region of the monogastric stomach?a. Rhythmic segmentationb. Peristalsisc. Retropulsiond. Adaptive relaxation</p>
<p>DCunningham Ch. 28 </p>
<p>Which of the following ions has higher concentrations in saliva compared to plasma?a. Calciumb. Chloridec. Potassiumd. Sodium</p>
<p>c. Potassium</p>
<p>What factor within the duodenum cannot initiate enterogastric inhibitory reflexes?a. Distension of the duodenumb. Irritation in the duodenal mucosac. Alkalitity of the duodenal chymed. Osmolality of the chyme</p>
<p>c. Alkalitity of the duodenal chyme</p>
<p>Which one of the following hormones is secreted by K cells?a. Cholecystokininb. Secretinc. Motilind. Gastric inhibitory peptide</p>
<p>d. Gastric inhibitory peptide</p>
<p>Which nerve controls the external anal sphincter?a. Pelvic nervesb. Pudendal nervec. Myenteric plexusd. Obturator nerve</p>
<p>b. Pudendal nerve</p>
<p>Which of the following accurately describes forward movement of a food bolus through the gastrointestinal tract?A. The swallowing center is located in the medulla and pons of the CNS.B. The movement of a food bolus through the esophagus is passive and only performed by smooth muscle.C. The stomach processes food and has no storage capacity. D. Having hunger pangs (I.e. being "hangry") does not exist, and the stomach does not contract strongly with prolonged emptying.</p>
<p>A. The swallowing center is located in the medulla and pons of the CNS.</p>
<p>Which of the following gasses are formed from bacteria in the large intestine?A. Methane, nitrogen, carbon dioxideB. Oxygen, carbon monoxide, methaneC. Hydrogen, methane, and carbon dioxideD. Carbon monoxide, methane, hydrogen</p>
<p>Answer C. Hydrogen, methane, and carbon dioxideGuyton Pg 849</p>
<p>Which one of the following electrolytes has the highest concentration in bile secreted from the gallbladder?a. Nab. Kc. Cad. Cl</p>
<p>a. Na</p>
<p>The main driving force for hydrochloric acid secretion by the parietal cells is…a. H-K ATPaseb. Cl-HCO3 antiporterc. Na-K ATPased. Cl diffusion</p>
<p>a. H-K ATPase</p>
<p>Which of the following is most responsible for creating an action potential in gastrointestinal smooth muscle and accounts for the long duration of action potential seen? a. Chloride channels b. Calcium-sodium channels c. Fast sodium channels d. Potassium channels</p>
<p> b. Calcium-sodium channels</p>
<p>Which of the following is not a natural ligand for receptors in the pancreas?a. Cholecystokininb. Acetylcholinec. Gastrind. Secretin</p>
<p>CCunningham Ch. 29</p>
<p>Chloride is absorbed in which primary locations in the gastrointestinal tract?A. proximal small intestine &amp; ileumB. duodenumC. ileumD. colon</p>
<p>Answer Apg. 839</p>
<p>Which of the following cells are considered the pacemakers of the GIT?A. G cells B. Cells of Cajal C. I cells D. K cells </p>
<p>B. Ref. 798</p>
<p>Which of the following hormones inhibits gastric acid secretion?A. GastrinB. CCKC. SecretinD. Motilin</p>
<p>C. Ref. Guyton 802</p>
<p>Which of the following causes the GI smooth muscle hyperpolarization? A. StretchB. Acetylcholine C. Hormones D. Norepinephrine </p>
<p>D. NorepiRef. Guyton 799</p>
<p>The rectosphincteric reflex is integrated in the:a. Brainstem.b. ENS.c. Lumbar spinal cord.d. Sacral spinal cord</p>
<p>DCunningham Ch. 28</p>
<p>Pepsin becomes inactivated and has no proteolytic activity above:a. pH 3b. pH 5c. pH 7d. pH 9</p>
<p>b. pH 5</p>
<p>Bile salts have two primary actions, what are they?a. (1) act as a detergent or emulsifying agent to decrease surface tension and (2) facilitate absorption from the intestinal tractb. (1) act as a detergent to increase surface tension and (2) facilitate absorption from the intestinal tractc. (1) induce absorption of food from the gastrointestinal tract and (2) induce digestion of chylomicrons within the lymphatic systemd. (1) regulate electrolyte absorption and secretion within the intestinal tract and (2) digest fatty acids</p>
<p>a. (1) act as a detergent or emulsifying agent to decrease surface tension and (2) facilitate absorption from the intestinal tract</p>
<p>Glucose is transported into the cell via: A. Facilitated diffusionB. Primary active transport C. Secondary active co - transport D. Secondary active counter transport </p>
<p>C. Secondary active co transport occurs more commonly in GI and renal cells, in all other cells glucose enters the cell via facilitated diffusion. Ref: Guyton p 840</p>
<p>Which factor(s) stimulate pepsinogen secretion by the peptic cells?a. Acetycholine onlyb. Acetylcholine and gastrinc. Acetylcholine and secretind. Cholecystokinin only</p>
<p>Answer: aGuyton (12th ed.) p. 779</p>
<p>The normal resting membrane potential of gastrointestinal smooth muscle cells is:a. -80 to -90 mV b. -105 to -110 mV c. -50 to -60 mV d. -30 to -40 mV </p>
<p>c. -50 to -60 mV </p>
<p>Which of the following can occur as complications to chronic gastritis?I. AchlorhydriaII. Ulcerative colitisIII. Peptic ulcerIV. Pernicious anemiaa) III, IVb) I, IVc) I, III, IVd) I-IV</p>
<p>Answer: c Source: Guyton ed 13, Ch 67, page 844</p>
<p>The control of glandular secretion is mostly due to local stimulation in which of the following locations?a. Jejunumb. Salivaryc. Rectumd. Pancreas</p>
<p>a. Jejunum</p>
<p>1. A unique feature of gastrointestinal (GI) smooth muscle cells is that:a. Their resting transcellular electrical potential has the positive pole on the outside surface of the cell membrane.b. Action potentials, or spikes of membrane depolarization, are not associated with muscle contractions.c. Muscle contractions are stimulated by partial depolarization of the membrane.d. There are spontaneous, rhythmical undulations in the electrical potential across the cell membrane.e. Contraction of the muscles is never influenced by nervous activity.</p>
<p>DCunningham Ch. 28</p>
<p>Which hormone is released from the G cells, stimulating mucosal growth? a. Gastrinb. CCKc. Secretind. GIP</p>
<p>a. Gastrin</p>
<p>Conditions in the duodenum, such as low pH or high fat concentration, can reflexively inhibit gastric emptying. Which reflex arc is involved in this inhibition?a. Parasympathetic nervous systemb. GI enteric nervous systemc. GI endocrine systemd. All the above</p>
<p>DCunningham Ch. 28</p>
<p>The neurotransmitters in the gut are:a. NO and Ach as excitatory, and substance P and VIP as inhibitory.b. NO and Ach as inhibitory, and VIP and substance P as inhibitory.c. NO and VIP as excitatory, and Ach and substance P as inhibitory.d. NO and VIP as inhibitory, and Ach and substance P as excitatory.e. NO and substance P as inhibitory, and Ach and VIP as excitatory. </p>
<p>DCunningham Ch. 27</p>
<p>Which of the following hormones stimulates gastric motility?A. GastrinB. CCKC. SecretinD. Motilin</p>
<p>D. MotilinRef. Guyton 802</p>
<p>Secretion of gastric inhibitory peptide from the K cells of the duodenum and jejunum is stimulated by protein, fat, and carbohydrates. What does secretion of gastric inhibitory peptide stimulate?a. Insulin releaseb. Gastric acid secretionc. Pepsin secretiond. Biliary bicarbonate secretion</p>
<p>a. Insulin release</p>
<p>Which of the following is secreted by activated salivary cells and is important in enzymatic formation of bradykinin?a. cAMPb. Kallikreinc. Secretind. Pepsin</p>
<p>b. Kallikrein</p>
<p>In what specific location in the gastrointestinal tract is the intestinal phase of gastric secretion initiated?a. Stomachb. Duodenumc. Ileumd. Jejunum</p>
<p>b. Duodenum</p>
<p>Cholecystokinin and gastrin:a. Share all of the same receptors.b. Share CCK1 receptors.c. Share CCK2 receptors.d. Share gastrin I receptors.e. Share gastrin II receptors</p>
<p>CCunningham Ch. 27</p>
<p>Which of the following correctly describes the secretion or action of secretin?a. Secretion is mainly stimulated by the presence of carbohydrates in the duodenumb. Secreted from the stomachc. Decreases stomach acid production d. Secretin’s main effect is increasing intestinal motility</p>
<p>c. Decreases stomach acid production </p>
<p>Which of the following hormones stimulates insulin release?a. Cholecystokininb. Gastrinc. Gastric Inhibitory Peptide d. Motilin </p>
<p>c. Gastric Inhibitory Peptide </p>
<p>2. The interstitial cells of Cajal are:a. Modified neurons capable of generating contraction.b. Modified neurons capable of generating only action potentials.c. Modified neurons capable of generating only slow waves.d. Modified smooth muscle cells capable of generating only slow waves.e. Modified smooth muscle cells capable of generating only action potentials.</p>
<p>DCunningham Ch. 28</p>
<p>Colonic “pacemakers”:a. Are anatomically distinct structures composed of specialized smooth muscle cells.b. Shift in their sites under the influence of the ENS.c. Are involved in segmentation, but not peristalsis.d. Control defecation.</p>
<p>BCunningham Ch. 28</p>
<p>The cholera toxin specifically targets which area of the gastrointestinal tract?a. duodenum b. duodenum, jejunum, and ileum c. distal ileum and colon d. colon only </p>
<p>C. Distal Ileum and Colon (location of crypts of liberkun)The enterocytes in these crypts are responsible for water secretion toxin --> increase cAMP --> Cl channels open --> Cl loss activates Na pump--> Na into lumen --> H2O follows Na --> excess water loss --> diarrheaGuyton p. 846</p>
<p>Which of the following hormones stimulates gallbladder contraction?A. GastrinB. CCKC. SecretinD. Motilin</p>
<p>B. CCKRef. Guyton 802</p>
<p>Which of the following reflexes occurs as a result of chyme entering the duodenum?a. gastroileal reflexb. gastroenteric reflexc. mienteric reflexd. viscointestinal reflex</p>
<p>b. gastroenteric reflex </p>
<p>Which enzyme is most active at a pH of 2.0 to 3.0 and plays an important role in digesting collagen? a. Alpha dextrinase b. Amylase c. Pepsin d. Elastase</p>
<p>Answer: C.Reference: Guyton Ch. 66 Pg. 835</p>
<p>3. Which of the following reactions in the liver could be expected to occur during both the digestive phase and a prolonged fast?a. Glycogen synthesisb. Fatty acid synthesisc. Ketone body synthesisd. Ketone body oxidatione. Triglyceride synthesis from fatty acids</p>
<p>ECunningham Ch 32</p>
<p>Lower esophageal achalasia is secondary to damage of:A. Myenteric plexus B. Lower esophageal sphincterC. Cranial nerve X D. Meissner’s plexus </p>
<p>A. The myenteric plexus aka auerbach's plexus is located in between the longitudinal and circular muscle layers and control movement through the entire GIT. The submucosal aka meissner's plexus controls local secretion and blood flowRef: Guyton p 843</p>
<p>Which cell type acts as the electrical pacemaker for the smooth muscle of the gastrointestinal tract?a. Epithelial cells of Cajalb. Enteric nervous plexusc. Enteric purkinje fibersd. Interstitial cells of Cajal</p>
<p>d. Interstitial cells of Cajal</p>
<p>The functions of the GI tract are mainly controlled by:a. The central nervous system.b. The enteric nervous system.c. The endocrine system.d. The enterochromaffin system.e. The hormonal and central nervous systems.</p>
<p>BCunningham Ch.27</p>
<p>In the small intestine, sodium is mainly reabsorbed in the APICAL border of epithelial cells by which protein?a) Na+/K+ ATPase pumpb) Na+ and substrate co-transportersc) Na+ leak channeld) Na+/Cl- antiporter</p>
<p>B. Na and substrate co-transporters ie. aa, glucose vs the basolateral membranes in which Na/K pump regulates Na transport. Source: Guyton ed 13, Ch 66, page 838</p>
<p>How long does it take for aldosterone to take effect and increase sodium absorption in the intestine?A. 1-3 hoursB. 3-6 hoursC. 6-9 hoursD. 9-12 hours</p>
<p>Answer A. 1-3 hoursCl and H2O follow Na Guyton Pg 839</p>
<p>At the level of the salivary gland, what happens with the following ions?A. Sodium is passively absorbed, chloride is actively absorbed, potassium is actively secreted, and bicarbonate is secreted.B. Sodium is actively secreted, chloride is passively secreted, potassium is actively absorbed, and bicarbonate is secreted.C. Sodium is actively absorbed, chloride is passively absorbed, potassium is actively secreted, and bicarbonate is secreted.D. Sodium is actively secreted, chloride is passively secreted, potassium is passively secreted, and bicarbonate is absorbed.</p>
<p>C. Sodium is actively absorbed, chloride is passively absorbed, potassium is actively secreted, and bicarbonate is secreted.</p>
<p>The term cephalic phase is used in reference to a number of activities occurring in the GI tract. In general, the term means:a. The early phases of digestion, when food is nearest the head.b. Any actions stimulated directly by the presence of food in the stomach.c. Any actions stimulated directly by the presence of food in the mouth.d. Digestive events stimulated by the presence of food in the GI tract, but requiring reflexes integrated in the CNSe. Digestive events that occur before the ingestion of food and in response to central nervous system stimulation that is brought on by the anticipation of eating.</p>
<p>ECunningham Ch. 28</p>
<p>Which of the following does not play a role in regulating pancreatic secretions? A. SecretinB. CCKC. AchD. Pepsinogen</p>
<p>D. Pepsinogen (stimulates acid secretion in the stomach)Secretin - stimulates bicarb secretion by pancreas in response to acid in SI CCK - stimulate bicarb and pancreatic enzyme in response to food in SI Ach - excitatory neurotransmitter Guyton 13th ed. p 826</p>
<p>At which site in the gastrointestinal tract do peptic ulcers most commonly occur? a. Lesser curvature b. Greater curvature c. Gastric cardia d. Pylorus</p>
<p>Answer: D.Reference: Guyton Ch. 67 Pg. 844; Fig 67-1</p>
<p>Which of the following is an important action of cholecystokinin? a. Inhibit gastric acid secretionb. Mucosal growthc. Intestinal motilityd. Stimulate pancreatic enzyme secretion</p>
<p>d. Stimulate pancreatic enzyme secretion</p>
<p>In monogastric animals, saliva produced during periods of rapid secretion has a higher electrolyte concentration than saliva produced during periods of slow salivary secretion. From your understanding of salivary gland physiology, which appears to be the most likely explanation?a. During periods of slow salivary secretion, the acinar cells are inactive, and low-electrolyte saliva is secreted by the duct cells.b. Parasympathetic stimulation of the acinar cells results in the elaboration of a more electrolyte-rich saliva.c. Gastrin stimulation increases the electrolyte concentration of saliva.d. During rapid secretion, fluid produced by the acinar cells is exposed to the actions of the duct cells for a shorter time than during slow rates of secretion.e. Different cell types within the acinus are responsible for salivary production, depending on the type of stimulus.</p>
<p>D Cunningham Ch. 29</p>
<p>Which of the following factors inhibit gastric emptying by initiating enterogastric inhibitory reflexes?a. Increased pH of the chymeb. Irritation of the duodenal mucosac. Stretching of the stomach walld. Decreased filling of the duodenum</p>
<p>Answer: bGuyton (12th ed.) p. 767</p>
<p>The arrangement of smooth muscle fibers in the muscular layer of the intestinal wall is best described as:a. inner longitudinal and outer circular smooth muscle layers b. inner circular and outer longitudinal smooth muscle layers c. single layer of circular smooth muscle d. two layers of circular smooth muscle, separated by a nerve plexus </p>
<p>b. inner circular and outer longitudinal smooth muscle layers </p>
<p>Small intestinal motility is inhibited by which hormone?a. Secretinb. Motilinc. CCKd. Serotonin</p>
<p>a. Secretin</p>
<p>The pathophysiologic basis of which of the following conditions is associated with damage to the myenteric plexus?A. Pancreatitis B. Achlasia C. AchlorydiaD. Gastritis </p>
<p>B. Achalasia is a condition in which the lower esophageal sphincter fails to relax during swallowing. Pathophysiological studies have shown damage in the neural network of the myenteric plexus of the lower two thirds of the esophagus, which causes spasticity of the musculature of the lower esophagus. As a result, the lower portion of the esophagus fails to undergo receptive relaxation as the bolus of food approaches this area after swallowing. pp. 845-846</p>
<p>In achalasia, damage to which structure in the lower esophagus results in failure of the gastroesophageal sphincter to relax during swallowing ?A. Myenteric plexus B. Submucosal plexus C. Esophageal mucosaD. Esophageal musculature</p>
<p>Answer AGuyton (12th ed.) p. 799</p>
<p>During sodium absorption by glucose co-transport:a. Chloride is absorbed by the paracellular route.b. Chloride absorption is not affected.c. Chloride is absorbed in exchange for bicarbonate.d. Chloride absorption is coupled with potassium absorption.e. Chloride is absorbed in exchange for hydrogen ion</p>
<p>ACunningham Ch 30</p>
<p>Entry of food into the small intestine leads to secretion of which of the following substances important for stimulating pancreatic secretion?a. Cholecystokininb. Vasoactive intestinal peptidec. Acetylcholined. Secretin</p>
<p>a. Cholecystokinin</p>
<p>Rate of digestion is dependent upon which one of the following?a. Total surface area available to digestive enzymesb. Increased sympathetic nervous system stimulationc. Total volume of bile secreted into the proximal duodenumd. Diameter of the pyloric sphincter</p>
<p>a. Total surface area available to digestive enzymes</p>
<p>From luminal to serosal layers, which of the following is the appropriate order in which the layers of the gastointestinal tract occur?A. Epithelium --> mucosa --> mucosal muscle --> sub mucosa --> longitudinal muscle -> circular muscle -> serosaB. Mucosa --> epithelium --> mucosal muscle --> sub mucosa --> circular muscle -> longitudinal muscle -> serosa C. Epithelium --> mucosa --> submucosa --> mucosal muscle --> circular muscle -> longitudinal muscle -> serosa D. Epithelium --> mucosa --> mucosal muscle --> sub mucosa --> circular muscle -> longitudinal muscle -> serosa </p>
<p>D. Epithelium --> mucosa --> mucosal muscle --> sub mucosa --> circular muscle -> longitudinal muscle -> serosa </p>
<p>Which coagulation factor is stimulated by endotoxin to trigger intravascular coagulation by the intrinsic pathway?</p>
<ol> <li>Heparin</li> <li>Factor II</li> <li>Factor X</li> <li>Factor XII</li></ol>
<p>d. Factor XII</p>
<p>Factor XII (Hageman’s factor) is triggered by endotoxin, producing bradykinin and triggering intravascular coagulation</p>
<p>APTT (best for DIC) is specific for intrinsic pathway, very sensitive to collection. Independent of platelet function.</p>
<p>Which drug is the best to enhance gastric emptying in foals with ulcerative duodenitis?</p>
<p>a. Lidocaine</p>
<p>b. Escopolamine</p>
<p>c. Erytromycin</p>
<p>d. Bethanecol</p>
<p>d. Bethanecol</p>
<p>You aretreating peritonitis in a 15 year old QHgeldingwith broad spectrum ABX therapy and choose a beta lactam (penicillin) + a gram negative drug (eitheraminoglycoside (gent) or enro), but you leave out metronidazole due to concerns about destroyingGI flora-what important and frequently culturedanaerobe does this combination not cover?<br></br><br></br>a. Clostridium<br></br>b. Bacteroides fragilis<br></br>c. Actinobacillus<br></br>d. Rhodococcus</p>
<p>b. Bacteroides fragilis</p>
<p>Bacteroides fragilis is most commonly ID'ed anaerobe cultured from peritonitis in horses.</p>
<p>A is an anaerobe but should be covered by penicillin.</p>
<p>C + D are aerobic bugs- <strong>Actinobacillus should respond to pen</strong>/gen, and rhodococcus is unlikely in an older horse.</p>
<p>Which one is NOT a risk factor for shedding of salmonella in hospitalized horses?</p>
<p>a. Horses admitted for colic</p>
<p>b. Diarrhea and antibiotic use</p>
<p>c. Presence of reflux</p>
<p>d. Severe GI disease</p>
<p>b. Diarrhea and antibiotic use</p>
<p></p>
