Learning Objectives Day 1-7 PDF

Day 1 Los Learning Objectives Dysphagia with Dr. Langlois Normal swallowing - Name and describe the various phases/stages of swallowing in the normal dog/cat. - Prehension is the handling of food in mouth - Mastication is the chewing of food via the masticatory muscles -...

Day 1 Los Learning Objectives Dysphagia with Dr. Langlois Normal swallowing - Name and describe the various phases/stages of swallowing in the normal dog/cat. - Prehension is the handling of food in mouth - Mastication is the chewing of food via the masticatory muscles - Lubrications via salvia - Manipulation is using the tongue to push the bolus to the back of the pharynx - Peristaltic contraction moves the bolus from the pharynx to the epiglottis - Closure of the epiglottis leads to inhibition of breathing - Relaxation of esophageal sphincter to promote acceptance of the bolus - Closure of the cricopharyneal and tyrodpharyeaus to inhibit retrograde of the bolus - Restoration of the epiglottis back to the relaxed position to promote breathing - Identify the major cranial nerves and muscles involved in the swallowing process. Here's an updated chart that includes both the cranial nerves and the muscles involved in the swallowing process for better clarity: **Cranial Nerve** **Key Function in Swallowing** **Muscles Involved** ------------------------------ ------------------------------------------------------- ------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------- **CN V (Trigeminal)** Mastication, oral cavity sensation **Masseter**, **Temporalis**, **Medial pterygoid**, **Lateral pterygoid**, **Mylohyoid**, **Anterior belly of digastric** **CN VII (Facial)** Lip closure, cheek tension, taste (anterior tongue) **Orbicularis oris**, **Buccinator**, **Platysma** **CN IX (Glossopharyngeal)** Pharynx elevation, posterior tongue sensation/taste **Stylopharyngeus** **CN X (Vagus)** Pharyngeal/laryngeal motor control, airway protection **Levator veli palatini**, **Palatoglossus**, **Palatopharyngeus**, **Pharyngeal constrictors (superior, middle, inferior)**, **Cricopharyngeus**, **Intrinsic laryngeal muscles** (e.g., **Thyroarytenoid**, **Lateral cricoarytenoid**) **CN XI (Accessory)** Assists with pharyngeal/laryngeal movements Works in conjunction with the vagus nerve to help elevate the larynx and pharynx; overlaps with CN X innervation. **CN XII (Hypoglossal)** Tongue movement **Genioglossus**, **Hyoglossus**, **Styloglossus**, **Intrinsic tongue muscles** (e.g., **Superior longitudinal**, **Inferior longitudinal**) Abnormal swallowing - Recognize the clinical signs that are suggestive of oropharyngeal dysphagia. - Overall CS are regurgitation, dropping food, repeated swallowing, gagging, nasal discharge, coughing, ect. - Oropharyngeal Dysphagia - Difficulty with prehension or transporting food with tongue - Pharyngeal Dysphagia - Inability to swallow or move food to back of mouth - CS: Abnormal Gag reflex, exaggerated chewing, flexing and extending neck - Cricopharyngeal Dysphagia - Unable to successfully swallow - CS: normal prehension and gag reflex - Use clinical features to further localize the type of oropharyngeal dysphagia present. - A white box with black text and blue text Description automatically generated - Explain the systemic consequences of pharyngeal and cricopharyngeal dysphagia. - Weight Loss - Aspiration Pneumonia - Esophagitis - Formulate a diagnostic plan for dogs presenting with oropharyngeal dysphagia. -  - Describe the major differences between pharyngeal and cricopharyngeal dysphagia. - The major differences between them is: - the reduction in the gag reflex - Location - Pharyngeal prevents bolus movement, while CPD is more UES dysfunction - Advise treatment plan for dogs or cats presenting with various forms of oropharyngeal dysphagia. - Pharyngeal Weakness - Nutritional Management of altered feeding strategies like with liquid diets, and feeding tubes - Treatment of underlying disease and secondary conditions like pneumonia - CPD: botulism injections, balloon dilations and surgical options  Equine Dentistry with Dr. Rapson-Strachota - Review from VM 525 Digestive System I. - Describe the normal dentition of adult horses. - Learning Center - How to properly care for your equine animal! - Differentiate between deciduous and permanent incisors in horses.  - Differentiate between a young (\ - Describe the components of a basic oral exam in the horse including normal periodontal probing depth, normal interdental spaces, and diastema. - Patient history - Full PE - Palpation of skull looking for swelling, atrophy, or enlarged lymph nodes - Quality oral examination under sedation - Standing sedation of an opioid and an alpha-2 agonist - Strachota likes Detomidine and butorphanol - 5 components include - External oral exam - Identification of swellings, enlarged lymph nodes, muscular and skeletal symmetry, and oral/nasal discharge - Oral soft tissue exam - Assessment of gingiva, mucosa, tongue, and palates - Observe pink color - Look for abrasions and ulcerations of mouth - Identify periodontal disease or oral neoplasia - Occlusion - Grinding function of teeth - ROM of jas - Looks for malocclusions and missing teeth - Check angle of cheek teeth - Endodontic exam - Assess integrity of crown, dentin, pulp chambers, cementin and infundibulum - Periodontal Exam - Determined by probing depth and radiographs - Normal is 2-5 mm - Describe proper charting of the equine dental exam findings. - Define malocclusions. - Overgrowth of single tooth - Treatment by removing tooth of only 5 mm - Wave Pattern - Reduce tooth by 5 mm and wait 3 months - Hooks and Ramps - Hooks on 06s - Ramps on 11s - Treat in one go or 5 mm and wait 3 months - Describe treatment planning and recognize when to refer to a dental specialist.  Small Animal Dentistry with Dr. Montgomery - Identify anatomy of the tooth and the surrounding structures. - Vet Tech Infographic: Anatomy of the Tooth - Learn the medical terms that are unique to dental application. - Rostral-Caudal - Medial - Distal - Vestibular (buccal or labial) - Lingual - Apical - Coronal - Learn the Modified triad system for dental nomenclature in the dog and cat. - Understand how to perform a proper evaluation of dentition on an awake/cooperative patient (dog/cat) and what issues can be evaluated. - Understand the temperament of the animal - Never attempt to do an oral exam when in danger - Use sedation and general anesthesia as normal -  - A cat with its mouth open Description automatically generated - What to look for: periodontal disease, missing teeth, tooth resorption sites, crown fractures, malocclusions, evidence of pulpitis - Identify normal radiographic positioning and be able to identify individual teeth from radiographs only. - Identify maxilla vs mandible - Place radiograph in proper real life orientation - Know tooth shapes, structures, and landmarks - Identify signs of periodontal disease on oral exam and radiographs.  Stage 1 Periodontal Disease Note that there is NO BONE Loss!! DO you See the build up Of tartar and the Slightly swollen and reddened --- this is the first Sign Of pain! Brushing the teeth now may be painful  - Identify tooth resorption on oral exam and radiographs and make treatment recommendations. - Recognize classes of malocclusion and indicated treatment recommendations. - Type 1: Tooth Position Related - Base narrow - Need to be extracted - Type 2: Lower Jaw too short (overbite) - Puppies should undergo extractions - Need to address jaw length as its genetic - Type 3: Underbite - Breed standard for brachys - Can cause issues and other abnormalities Day 2 Los Learning Objectives Equine Esophageal Obstruction with Dr. Munsterman - Understand the anatomic features of the equine esophagus, and how they affect approaches to treatment of esophageal diseases. - Esophagus is a long, tubular organ that is 125-200 cm long - Opens above the rima glottis - Comprised of majority striated muscle before transitioning to smooth muscle - Inter muscosal layers provide strength and the holding layers during surgery - Supplied by carotid and 9^th^ and 10^th^ CN - Identify common causes of esophageal obstruction. - Choke is the most common abnormality found in proximal esophagus - Caused by ingestion of non-feed material, poorly chewed food, poor dentition, not moistened feeds, dehydration, and eating under sedation - Common signalment: older horse, dental disease, over 10.5 years old, fresians - Common CS: saliva or feed muscous from nostils, tachypnea, tachycardia, anxious, stretching neck, gulp, cough and retch - Select the appropriate steps in the approach to diagnosis and treatment of esophageal obstruction. - First is to sedate the horse to prevent aspirations - Pass NG tube and get blocked by obstruction - Pass endoscope to assess trachea trauma - Give alpha 2 agonists to relax the esophagus - xylazine or butorphanol for dilation in thoracic inlet - Acepromazine is to NOT be given in hypovolemic animals - Buscopan eliminates swallowing reflex in distal esophagus - Ultrasound of thorax to determine severity of pneumonia - Esophagography for diverticulums or recurrent choke for surgical planning - Treat with gentle lavage and withhold feed for 1-2 days, and give antimicrobials like broad spectrum and tetanus toxoid - Recognize common complications of esophageal obstruction and management of these problems. - Mucosal Ulceration and Esophagitis - Can be longitudinal or circumferential - See with impactions, NSAID use, and reflux - Can see formation of strictures in 30 days and will continue up to 60 days but most will resolve without treatment - Rx: medical and dietary management for 2 months after choke - Esophageal Diverticula - - Provide recommendations to owners to prevent equine esophageal obstruction. - Feed appropriate and good quality feed - Prevent access to foreign objects, and provide adequate dental care Regurgitation with Dr. Cridge - Define the following terms: regurgitation, vomiting - Regurgitation is the passive "throwing up" of food from the esophagus - Vomiting is the active "throwing up" of food from the stomach and duodenum - Describe the clinical features of regurgitation and how they differ from vomiting. - Describe morphological differences between the canine and feline esophagus and why this may be important. - Dog has 100% skeletal muscle in the esophagus - Cats have both skeletal muscle and smooth muscle in the esophagus - UES is skeletal muscle - LES is made of smooth muscles and there is not a distinct muscle - Describe the neurological innervation of the esophagus. - Innervation is an involuntary reflex - Vagal afferent input goes to swallowing center in brain - Descending motor fibers from the vagus nerve cause contraction of esophageal musculature - List differential diagnoses for regurgitation. - Megaesophagus: Idiopathic vs congenital - Structural Disorders: FB, neoplasia, diverticulum, stricture, vascular ring - Neurological/Neuromuscular Disorder: CNS abnormality, peripheral neuropathy, autonomic dysfunction - Infectious Disorder: Spirocercosis, pythium isidiousm, neosporosis - Inflammatory Disease: Esophagitis - Describe the medical management of patients with megaesophagus and be able to recognize this condition on radiographs. - Characteristics: Focal or diffuse esophageal dilation and dysmotility - Most common form: Acquired - Causes: Myasthenia gravis, hypothyroid, Addison's - Diagnosis: radiographs, acetylcholine receptors for MG, thyroid and cortisol panels - Treatment: - Non-specific small meals, bailey chair, altered food consistency, maybe gastrotomy tube - Cats benefit from prokinetic drugs in the distal 1/3 of esophagus which is smooth muscle - Cisapride and metoclopramide increase LES tone - Dogs with congenital ME can benefit from sildenafil by decreasing LES tone - Can give antibiotics, treat for MG, and immunosuppressives - Prognosis: depends on etiology and complications and owner commitment - Describe the breed predispositions, clinical signs, diagnostic approach and treatment for a persistent right aortic arch (PRAA). - Most common in GSD and Irish setters - CS: regurg of food at time of weaning - Dx: radiographs, esophagram, esophagoscopy, CT - Tx: Surgical ligation and transections of ligamentum arterium - PX: may have hypomotility and regurg if surgery is delayed but most is corrective - Describe the terms esophagitis and esophageal stricture and the layers of the esophageal wall affected in each condition. - Esophagitis is an inflammatory condition of the mucosa involving the submucosa and muscularis - Strictures: Abnormal narrowing of lumen, damage to the muscularis layer with formation of fibrous leading to contraction and stricture formation - List potential causes of esophagitis / esophageal stricture formation. - Esophagitis: ingestion of caustic agents, chronic vomiting, FB, reflux, hiatal hernia, medication induced like with doxy and clindamycin - Strictures: reflux, chemical injury, FB, and surgeries or mass lesions - Describe treatment options for esophagitis and esophageal strictures. - Esophagitis: can feed smaller less-fat meals, PPI, sucralfate, prokinetics - Strictures: Ballon dilation    Vomiting and Supportive Care with Dr. Cridge - Define the term vomiting and describe why the vomiting reflex evolved - Evolved as a protective mechanism against toxic or other substances ingestion - List potential consequences of severe or prolonged vomiting - Volume depletion - Acid-base and electrolyte derangement - Aspiration pneumonia - Esophagitis - Describe the humoral and neural pathways of vomiting - Focus on the emetic center reflex within the brainstem where there are serotonergic and adrenergic receptos - Humoral: - CRTZ is activated by bloodborne substances - Located outside of BBB which allows exposure to drugs, toxins, and other things - Neural: - Activated by vagal and sympathetic afferents of the emetic center to trigger vomiting - Associations with anxiety or anticipation is via the neural pathways - Associations with vestibular diseases is via the neural pathways - Describe differential diagnoses for vomiting in dog and cat patients - Describe the management of acute and chronic vomiting - Identify a patient's level of dehydration based on physical examination findings and be able to calculate fluid rates for clinical patients - List and describe the mechanism of action, uses and contra-indications of commonly used anti-emetic drugs Classification/ Name Mechanism Metabolism Best-Use Contraindications ---------------------- ----------------- ------------------ --------------------------------------------------------------- ------------------------------------------------------------- Maropitant NK1 antagonist Liver Broad spectrum motion sickness GI obstruction, can cause SQ administration discomfort Ondansetron 5HT3 antagonist Liver and kidney Nausea, cats GI obstruction, hypotension, hepatic dysfunction, MDR1 gene Metoclopramide D2 antagonist Renal Ileus, anti-emetic, increase in LES, continuous infusion rate Obstruction, movement disorders, and extrapyramidal signs - List and describe the mechanism of action and uses of commonly used pro-kinetic drugs Name Mechanism Best-Use Contraindications ---------------- ------------------------------ --------------------------------------------------------------------------------------------------------------- -------------------------------------------------------- Metoclopramide 5HT3 and 5HT4 Delayed gastric emptying, reflux, hypomotility, CRTZ induced emesis Distal small intestine less effective, striated muscle Cisapride 5HT3 and 5HT4 Contraction of distal esophageal SM (cats), increase LES, decrease pyloric tone, and contraction of GI tracts Dogs with idiopathic megaesophagus Erythromycin Mimicking effects of motilin Increases LES, reflux, and gastric emptying, SI contractions Ranitine H2 anatgonist Gastric emptying Bethanechol Esophageal contractions in idiopathic megasophagus - List and describe the mechanism of action(s) and uses of commonly used mucosal cytoprotectants - Prostaglandins - Increase blood flow, mucus secretion, stabilizing cells, and decrease acid secretion - Sucralfate: forms stable complexes with protein in damaged muscosa - Describe indications for acid-suppression - Gastroduodenal ulcerations and erosions - Hepatic disease - Reflux esophagitis - List and describe the mechanism of action, comparative efficacy and onset of action of commonly used acid-suppressant medications - Proton Pump Inhibitors: omeprazole, any of the -zoles - Irreversibly bind to cystines on H-K ATPase to cause enzyme inactivation - More effective in decreasing pH and healing acid related injuries - H2 Receptor Antagonists -- some of the tidiness - Block H2 receptors on parietal cells - Inferior to PPI, but can cause upregulation of gastrin - List four potential appetite stimulants used in companion animal species - Diazepam, cyproheptadine, mirtazapine, capromorelin - List medications that can be used to induce emesis and describe why there are species differences in efficacy - Dogs: - Apomorphine as it is for dopamine receptors which dogs are rich in - Ropinirole is the dopamine receptors - Cats: - Xylazine or Dexmedetomidine: Rich in Alpha 2 agonists in emetic center - Hydrogen peroxide is not recommended in cats Mechanisms of Diarrhea with Dr. Watson - Describe the four major mechanisms of diarrhea. - Define and identify hematochezia. - Bright red undigested blood - Colitis or damaged muscosa of colon - Define and identify melena. - Dark tarry stool, digest blood - Mucosa damage in stomach or SI - Differentiate small bowel diarrhea from large bowel diarrhea in small animals. - Describe mechanisms by which microbes cause diarrheal disease. - Compare the characteristics of diarrhea unique to patients infected with enterotoxigenic *E. coli* (ETEC), enteropathogenic *E. coli* (EPEC), or enterohemorrhagic *E. coli* (EHEC). **Characteristic** **ETEC** **EPEC** **EHEC** ------------------------------- ------------------------------------------------------------------------------------------------------------------------ ------------------------------------------------------------------------------------------------------------------------------------------------------- ------------------------------------------------------------------------------------------------------------------- **Mechanism of Pathogenesis** Produces heat-labile (LT) and/or heat-stable (ST) enterotoxins that cause increased fluid secretion in the intestines. Adheres to intestinal epithelial cells via a type III secretion system, causing disruption of microvilli (effacement) and loss of absorptive surface. Produces Shiga toxin, which damages endothelial cells, leading to inflammation and potential systemic effects. **Onset** Impacts calves 1-7 days old, 4-5 days old average Gradual onset, typically 1-2 days after exposure. Usually within 2-5 days after ingestion. **Type of Diarrhea** Watery diarrhea, often profuse and non-bloody. Malabsorptive, Watery diarrhea, but less profuse than ETEC. Can occasionally progress to persistent diarrhea. Starts as watery diarrhea and progresses to **bloody diarrhea** (hemorrhagic colitis) in many cases. **Diagnosis** Detection of LT/ST toxins or ETEC-specific genes in stool via PCR Identified via stool culture and tests for EPEC adherence factors (e.g., intimin), PCR for virulence genes Stool culture with detection of Shiga toxin or genes (e.g., stx1, stx2). PCR for shiga toxins **Treatment** Rehydration therapy; antibiotics (e.g., fluoroquinolones) may be considered in severe cases. Rehydration; supportive care. Antibiotics not commonly recommended. Supportive care; **antibiotics are contraindicated** due to risk of exacerbating toxin release and worsening HUS. **Key Distinctions:** 1. **ETEC**: Primarily causes profuse, watery diarrhea with no systemic complications. 2. **EPEC**: Mainly affects infants and causes watery diarrhea due to epithelial cell damage. 3. **EHEC**: Causes bloody diarrhea and systemic complications like HUS due to Shiga toxin production. - Describe the pathophysiologic mechanisms involved in diarrhea caused by ETEC, EPEC, and EHEC. - Explain how ETEC, EPEC, and EHEC are diagnosed. Day 3 Los Learning Objectives Viral Causes of Diarrhea with Dr. Maes et al - Describe the characteristics of parvovirus, panleukopenia virus, rotavirus, coronavirus. - Connect the virus to the important viral proteins that lead to pathogenesis and/or immune response. - Describe the pathogenesis of disease due to enteric viruses. - Explain how the lesions are produced in animals infected with enteric viruses. - Define hyperemia, petechia, intussusception, crypt necrosis, villous blunting. - Explain how clinical signs are produced in animals infected with enteric viruses. - Describe how to obtain samples, which samples are needed, and which diagnostics tests are performed to diagnose enteric virus infection(s). - Describe major principles of prevention against enteric viruses.     Bacterial Enteropathogens with Dr. Dirita et al - Describe the mechanisms by which microbes cause gastrointestinal disease, giving specific examples of each, and correlate these mechanisms with clinical signs observed. - Describe the pathophysiologic mechanisms involved in gastrointestinal diseases caused by Clostridial bacteria (e.g., *Clostridioides difficile*, *Clostridium perfringens*) including target cells and pathologic changes. - Identify and describe the different toxins produced and their mechanisms of action on intestinal epithelial cells and inflammatory cells. Focus on alpha toxin, beta toxin, enterotoxin, and NetF.  - Describe how toxins are exploited for therapeutics against *C. perfringens* - Describe the pathophysiologic mechanisms involved in gastrointestinal diseases caused by *Salmonella s*pp* *including target cells and pathologic changes. - Describe the pathophysiologic mechanisms involved in gastrointestinal diseases caused by *Mycobacterium avium* subspecies *paratuberculosis* (Johne\'s/MAP) including effects on inflammatory cells. - Define the stages of Johne\'s in cattle. - List the common patient signalment and clinical signs caused by *Salmonella*, *C. perfringens*, *C. septicum*, *C. difficile*, MAP, and *Campylobacter.* - Define the importance of colostrum (passive transfer) in immune response/prevention of enteropathogens. Day 4 Los Learning Objectives Anti-Parasitic Drug Classes and Strategic Control with Dr. Mansfield - For the Pre-class prep material on anti-parasitic drug classes, please recall the scientific names for the seven major drug classes used to treat parasite infections in animals. - Inspect and compare the modes of action for these compounds. - Recall the spectrum of activity of the seven major drug classes used to treat parasite infections in animals. - Recall any special concerns for toxicity of these compounds that are mentioned in this unit. - Recall the best practices for using these drugs and the accompanying control strategies. Diarrhea Cases in Small Animals with Dr. Mansfield (Hours 2 and 3) - **[If needed]**, you can review in prep the GI Parasites of Dogs and Cats PowerPoint. - Use the information from the Pre-Class prep on Anti-Parasitic Drug Classes and In-Class Strategic Control units for today on small animals to solve the case exercises in Articulate. - Recall the scientific and common names of the nematodes that live in the GI tract and/or migrate through the body in small animals. - Sketch the lifecycle of the small animal nematodes and protozoa from memory identifying the interactions of each parasitic stage with the tissues of the host listing important time frames of infection. - Inspect and compare the pathologic lesions of small animal nematodes and protozoa in dogs and cats. - Compare the epidemiology, clinical signs, diagnosis and treatment of small animal nematodes and protozoa in dogs and cats. Diarrhea case in Large Animals with Dr. Mansfield (Hour 4) - Use the information from the Pre-Class prep on Anti-Parasitic Drug Classes and In-Class Strategic Control units for today to solve the case exercise in Articulate. - Recall the scientific and common names of the nematodes that live in the GI tract and/or migrate through the body in large animals. - Sketch the lifecycle of the large animal nematodes from memory identifying the interactions of each parasitic stage with the tissues of the host listing important time frames of infection. - Inspect and compare the pathologic lesions of large animal nematodes in ruminants and horses. - Compare the epidemiology, clinical signs, diagnosis, and treatment of large animal nematodes in ruminants and horses. Day 5 Los Learning Objectives Approach to Chronic Enteropathy with Dr. Langlois - Explain the value of bloodwork in pets with chronic diarrhea.  - Identify labwork abnormalities that could be a consequence of severe intestinal disease.  - List differentials for chronic intestinal disease in dogs/cats, and be able to prioritize differentials given signalment, history, and physical exam.  - Be able to develop a diagnostic plan for a dog/cat with chronic diarrhea.  - List the benefits and limitations of diagnostic imaging and endoscopy for assessing chronic intestinal disease in dogs/cats.  - Be able to design an empiric treatment protocol for a dog/cat with chronic diarrhea.  - Select appropriate diets for pets with chronic enteropathies.  - Be able to explain how a diagnosis of "IBD" or steroid responsive chronic enteropathy is obtained.    Colic Diagnosis and Common Causes of the Equine Acute Abdomen with Dr. Munsterman - Define colic and causes of abdominal pain. - Understand the unique indicators of the presence and severity of abdominal pain in horses with colic.   - Construct a clear and concise list of questions for the owner that can help lead to the diagnosis of acute colic.   - Identify the characteristics of normal and abnormal borborygmi in the horse.  - Understand the need for nasogastric intubation and interpret the meaning of net reflux. - Identify which normal structures can be palpated rectally in the horse. - Describe the role of ancillary diagnostics, including ultrasonographic examination, fecal evaluation, radiography, and abdominocentesis in horses with colic. - Localize the gastrointestinal lesion in the horse based clinical exam and diagnostic tests.  - Identify key clinical findings in the history and initial examination that would indicate the need for referral for intensive medical or surgical treatment.   - Identify the two most common causes of colic in horses.  - Differentiate common causes of gastrointestinal disease in the small intestine, cecum, large and small colon of the horse based clinical exam findings and diagnostic tests. - List the 2 key clinical findings that indicate a small intestinal lesion. - Differentiate between the three most common causes of small intestinal diseases based on clinical exam and diagnostic procedures. - Differentiate between the three most common causes of large intestinal diseases based on clinical exam and diagnostic procedures. - Understand the pathogenesis and prevention of large intestinal disorders. - Describe the two types of cecal impaction and the risk factors for cecal impactions. - Know the unique clinical findings that may help identify cecal impactions. - List causes for small colon impaction and predisposing factors that may increase risk of impaction. - Understand which diagnoses may prompt referral for medical or surgical management. - Provide a treatment plan for the management of vagotonia and large colon impactions. - Compose a fluid therapy plan to address losses, maintenance and therapeutic treatment of a colicky horse.  - Define cathartics and describe their use in equine large colon impactions. - Differentiate between a positive response to therapy and a lack of response to treatment for colic. - Describe adjective therapies that may be useful to treat displacement of the large colon. - Understand the risks and benefits for medical and surgical treatment of cecal impactions. - Understand the need for prompt identification and referral of small intestinal diseases. - Identify findings on clinical exam that would prompt referral for intensive therapy or surgical intervention. - Be able to provide a prognosis for treatment of common equine gastrointestinal diseases. - Provide recommendations for horse owners to prevent or reduce the risk of colic.  Day 6 Los Learning Objectives Pathology and Diagnostic Procedures with Dr. Gerras and Dr. Watson - Recognize pathologic appearance of mucosal ulcers in gastrointestinal tract.   - Recognize common postmortem lesions of the Gastrointestinal tract and develop morphologic diagnoses for specimens discussed in Pathology Station in Lab.  - Identify which samples are needed for tests for common infectious causes of diarrhea.   Parasitology and Anthelminthic Resistance with Drs. Mansfield and Satti    - Recall the major risk factors for development of anthelminthic resistance.   - Inspect and compare the factors that can modulate development of anthelminthic resistance.   - Review and recall the control and management methods for preventing anthelminthic resistance.   - Use the anthelminthic resistance concept map to practice developing control and management practices in the cases provided for sustainable anthelminthic use.  - Recall the scientific and common names of the nematodes that live in the GI tract and/or migrate through the body in horses.​  - Recall and perform the main diagnostic test(s) for horse nematodes.    Equine Colic Lab with Dr. Munsterman, et al   - Review Colic Diagnosis and Procedures lecture with Dr. Munsterman:  - Construct a clear and concise list of questions for the owner that can help lead to the diagnosis of acute colic.    - Identify the characteristics of normal and abnormal borborygmi in the horse.   - Understand the need for nasogastric intubation and interpret the meaning of net reflux.  - Identify which normal structures can be palpated rectally in the horse.  - Describe the role of ancillary diagnostics, including ultrasonographic examination, fecal evaluation and abdominocentesis in horses with colic.  - Localize the gastrointestinal lesion in the horse based clinical exam and diagnostic tests.