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Systemic Path-GI
Steinberg-systemic path-GI
| Question | Answer |
|---|---|
| Morphologic diagnosis should have 3 components | organ in question (liver:hepatitis), the process (pyogranulomatous), and a distribution (focal) |
| Congenital abnormalities | cleft palate, jaw (brachygnathia superior or inferior), teeth (enamel), esophagus (megaesophagus), stomach-pyloric stenosis, intestines (atresia) |
| Disturbances of blood flow | Obstructive diseases or vascular obstruction |
| Obstructive diseases | intussusception, intestinal torsion/displacement, hernation, lipoma |
| vascular obstruction | congestion and hemorrhage, equine verminous arteritis, lymphangiectasia |
| inflammation | structural/functional considerations, infectious (viral, bacterial, protozoal, fungal, or parasitic), toxic/chemical/metabolic/nutritional, or physical injury |
| Structural/functional inflammation | defense mechanisms, diarrhea, morphologic classification (oral, intestine) |
| Viral inflammation | rota, corona, parvo, flavi |
| Bacterial inflammation | peridontal dz, fusobacterium, actinobacillus, actinomyces, colibacillosis, salmonella, clostridium, serpelina, lawsonia, campylobacter, mycobacteria |
| protozoal | cryptosporidium, coccidiosis |
| Toxic/chemical/metabolic/nutritional | ruminal tympany, ruminal lactic acidosis, gastric dilatation, displaced abomasum, gastric ulcers |
| physical injury | esophagus, traumatic reticuloperitonitis |
| Pathology of oral cavity-clinical signs | inappetance, salivation, dysphagia, halitosis, hemoptysis, pain, failure of prehension, inability to nurse |
| cleft palate (palatoschisis) | failure of palatine arch to fuse on medial aspect-common in calves, can occur in all animals |
| brachygnathia superior | maxilla is too short-dogs, swine, cattle (sometimes sought after-pug, english bulldog) |
| brachygnathia inferior-micrognathia | mandible shortened-parrot mouth in horses-can be lethal esp. in sheep, cattle |
| Other congenital abnormalities of oral cavity | prognathia(lower jaw too large), agnathia(no jaws), epitheliogenesis imperfecta(congential absence of skin/mucosa) |
| Developmental anomalies of teeth | result from promary dysplasia of enamel organ, or secondary trauma, infection, toxicosis, or metabolic abnormalities |
| Adontia | absence of teeth |
| oligodontia | missing some teeth, fewer than normal number of teeth |
| polyodontia | presence of supernumerary teeth |
| heterotopic polydontia | extra teeth, or teeth outside the dental arcade; cattle, dogs, pigs, sheep, horses ("ear tooth") |
| Congenital disorder of teeth due to | rapidly dividing epithelial cells, rapidly growing |
| odontodystrophies-enamel doesn't cover external surface completely | abnormal growth of hard tissues in teeth resulting from nutritional, metabolic, and toxic insults |
| Enamel hypoplasia or Abnormal enamel | Causes-starvation, nutritional deficiencies, excess fluoride consumption, BVDV, K-9 distemper, placental problems |
| Esophagus congential abnormalities-clinical signs | inadequate growth rate, cachexia, ptyalism(drooling), dysphagia, regurgitation, vomition, and aspiration pheumonia |
| Esophageal anomilies are rare | megaesophagus |
| megaesophagus | infrequent disorder in dog, horse, cat, inbred strains of mice and rats |
| Clinical presentation of esophageal problems | oral or nasal regurgitation of food and water shortly, after a meal, coughing, dyspnea, and anorexia |
| Differentiate between congenital or acquired megaesophagus | what is the signalment? If VERY young then most likely congenital, if older may be acquired |
| Congenital megaesophagus | persistent right aortic arch obstructs esophagus preventing outflow |
| Sequelae of megaesophagus | esophagus occupies 33% of chest instead of 10% and compresses the lungs and causes collapse and atelectasis |
| acquired megaesophagus | idiopathic denervation, myasthenia gravis, polymyositis, lead toxicities |
| Stomach congenital | Pyloric stenosis-functional or anatomical; a congenital or acquired defect |
| Intestines congenital | segmental atresia, megacolon |
| Segmental atresia-anus or colon | Young animals, sporadically in pigs, calves, dogs, cats. |
| atresia ani | no anus, anus fails to develop so no normal patent opening |
| atresia recti | anus is patent and intact, but animal bloats and doesn't pass stool |
| Stenosis | failure of communication, narrowing |
| Age is extrememly important | is it atresia coli or is it chronic salmonellosis in a pig? If very young then likely atresia recti/coli |
| atresia of small intestine | reported calves, goats, cats, dogs, lambs. Most frequently in the jejunum of calves |
| Atresia of intestine | should be differentiated from intestinal stenosis which is an incomplete occlusion of the intestinal lumen |
| Atresia correction/treatment | Often NOT treatable or surgically correctable. And, if it is there are ethical considerations due to congential nature. |
| Megacolon | marked dilation of the colon occurs as a congenital or acquired condition |
| Congenital megacolon | hirschsprung's disease of people, identified in white paint and pinto foals that result from breeding overo horses, also pigs, dogs |
| Infarction-GI | occlusion of the arterial supply or the venous supply with inadequate collateral circulation leads to ischemic necrosis of the intestine within 18 hours |
| obstructive diseases-GI | intussusception, intestinal torsion and displacement, compression |
| intussusception | condition where one intestinal segment becomes telescoped into the immediately distal segment of intestine |
| Intussusception, contd | once trapped, invaginated segment propelled by peristalsis farther in to the distal segment and results of lumen obstruction |
| Intuss. causes | Nidus is often precipitating cause, peristalsis interrupted at one area, allows neighboring are to "suck in" to adjacent section |
| Intuss. nidus | polyp, worms, foreign body |
| Intuss. common sites | jejunum, proximal ileum, and ileum into the colon or cecum. Cecum sometimes invaginates into the colon, can occur terminally |
| intestinal torsion | volvulus, herniation, torsion |
| volvulus | twisting of the intestine upon mesentery |
| torsion | rotation of a tubular organ on its long axis |
| Consequences of volvulus or torsion | edema, congestion, hemorrhage, infarction, anoxia |
| Compression of blood flow | Venous is 1st to be cut off because they are more compressible-this cuts off the outflow of blood=congestion. Arterial can still pump in blood and you get diation, hyperemia, and edema. |
| mesenteric volvulus | dogs, calves, pigs, lambs, horses |
| cecal torsion | horses, cattle |
| large colon volvulus | common in horses |
| epiploic foramen | can get strangulated tissue here too |
| clinical signs of torsion or displacment | V, D, straining, hunching-over posture |
| Lipoma infarct due to torsion | you get a "rock" as the lipoma is mineralized |
| strangulating lipoma | very common cause of torsion or volvulus in horses |
| herniation | internal or external |
| internal hernia | common sites SI, horse-epiploic foramen, mesentery tears, volvulus can occur secondarily |
| external hernia | penetration of a hernial sac formed as a pouch of the parietal peritoneum through the abdominal wall and usually contains the small intestine |
| common sites of ext. hernia | umbilicus, ventral abdomen, inguinal canal, perineal area, femoral area, and diaphragmatic area |
| compression by external masses cause obstruction | strangulation of mesentery by pedunculated lipoma is common in the horse |
| vascular obstruction | congestion and hemorrhage, equine verminous arteritis, lymphangiectasia |
| congestion and hemorrhage | congestion-passive hemorrhage-in luminal surface, turn over and look at serosal surface you can see it |
| shock organ in the dog | intestine, results in hemorrhage in GI tract |
| Hemorrhage in GI-always include in Ddx | Clostridium |
| Equine verminous arteritis | due to strongid in cranial mesenteric artery, results in thrombosis in C. mesenteric a. where it comes off the aorta, will result in an embolus which breaks off and lodges in large colon |
| Endarteritis | inflammation within blood vessels |
| Size of embolus | determines where the embolus will lodge |
| color can be deceiving in: | GI and resp tract |
| ameloblastoma | tumor of enamel origin |
| compound odontoma | neoplastic growth of tooth-like structures-multiple denticles within the tumor |
| complex odontoma | cell of origin same as compound, but doesn't have tooth-like structures |
| gingival hyperplasia in a pigmented dog | can look like a malignant melanoma! |
| gastric adenoma in dog | often in lesser curvature-markedly expanded rugal folds-also an ulcer! Think gastric adnoma 1st |
| gastric adenoma in dog | you will also have sclerosising adenocarcinoma-neoplastic cells secrete cytokines to stimulate the non-neoplastic cells to proliferate |
| desmoplasia | normal response by normal tissue, but in response to an abnormal signal from neoplastic cells for example |
| lymphangiectasia-clinical signs | Diarrhea with steatorrhea, hypoproteinemia, edema and ascites, often lymphopenia |
| lymphangiectasia | most common cause of protein-losing enteropathy in the dog--common to see widespread edema due to decreased oncotic pressure, also ascites |
| forms of lymphangiectasia | congenital and acquired |
| congenital lymphangiectasia | malformation or neuropathy where there isn't proper innervation-often will manifest itself at an early age |
| acquired lymphangiectasia | usually going to be a reason-such as a lesion or obstruction. |
| lymphangiectasia | often this is idiopathic and we don't know cause, can have downstream inflammatory lesions that can obstruct downstream and cause back-up into intestinal lacteals |
| Defense mechanisms of the intestinal tract | non-immunologic or immunologic |
| non-immunologic defense of GI | indigenous microbial flora, secretions, gastric barrier, intestinal motility, epithelial turnover, bile salts inhibit growth of many microorganisms, liver (Kupffer cells-mac's of liver) |
| immunologic defense of GI | humoral-IgG, IgA Cellular-mac's limit the ability of toxin to gain access or lymphocytes in peyer's patch |
| Diarrhea | frequent passage of soft-unformed feces--clinical sign of intestinal dz |
| Diarrhea mechanisms | increased permeability of mucosal epithelium, hypersecretion, malabsorption/maldigestion |
| Malabsorption/maldigestion | Diarrhea, weight loss, steatorrhea, +/- edema, and avitaminosis of fat-soluble vitamins (A,D,E,K) |
| Malabsorption/maldigestion | disturbances in one or more: digestion of nutrients into smaller, absorbable molecules, absorptive capacity of the bowel, transport of absorbed products |
| Maldigestion | defective intraluminal hydrolysis or solubility |
| Pancreatic hypoplasia | doesn't develop normally, smaller, congenital |
| pancreatic atrophy | secondary to chronic pancreatitis-fibrosis |
| malabsorption | reduction in mucosal surface area, infiltration of lamina propria, defective mucosal cells |
| viral enteritides with villus atrophy | viral enteritis-more commonly than bacteria--marked reduction in surface area |
| Lamina propria infiltration +/- epithelial changes | neoplastic infiltrate, interfere with absorption, protozoal diseases |
| Brush border enzyme or transport mechanism loss | biochemically affect absorption |
| lymphatic obstruction or other abnormality blocking normal transport of digested nutrients | neoplastic obstruction of lymphatics, obstructive lymphadenitis (inflammation of lymph node), lymphangiectasis (inflammation of lymph channel) |
| Vesicular stomatitis | viral-induced: Foot & Mouth Disease, vesicular stomatitis, Vesicular exanthema, swine vesicular disease, Herpes, calici Immune-mediated: pemphigus vulgaris, bullous pemphigoid |
| Erosions; ulcers | bovine viral diarrhea, bluetongue, rinderpest, malignant catarrhal fever, infectious bovine rhinnotracheitis, calicivirus, feline rhinotracheitits, chronic uremia, pemphigus vulgaris, herpes, eosinophilic granuloma complex, oral eosinophilic granuloma |
| Papular stomatides | bovine papular stomatitis(parapoxvirus), contagious ecthyma(poxvirus) |
| Necrotizing stomatides | fusobacterium, actinobacillus(wooden tongue), actinomyces(lumpy jaw), acute gangrenous stomatitis, aeromonas hydrophila (mouth rot in snakes, red mouth in salmonid) |
| Necrotizing stomatides | often will be a predisposing injury, animal chewing on rough straw, poked in mouth with something |
| Hemorrhagic enteritis | combination of severe vascular damage with epithelial injury, toxic(arsenic), bacterial(THINK CLOSTRIDIUM!, some e. coli), protozoal(acute coccidia), shock |
| Fibrinous, necrotic & Fibrinonecrotic enterocolitis | bacterial(salmonella-septic tank), viral and toxic diseases |
| ulcerative enterocolitis | sequella to focal or multifocal necrotizing or suppurative mucosal injury in a number of diseases |
| ulceration | raised leading edge-due to loss of basement membrane--any vascular lesion can result in an ulcer |
| hogcholera | button ulcers in proximal colon |
| suppurative or pyogranulomatous enterocolitis | fluctuant, squeezable, squirt in the face with pus |
| proliferative or hyperplastic enteritis | epithelial hyperplasia as an exaggerated response: some bacteria (lawsonia) and protozoa (cryptosporidia) |
| Granulomatous enterocolitis | Johne's-Mycobacterium paratuberculosis, bovine, macrophages in lamina propria |
| Viral infectious inflammation | young animals esp. calves and pigs, presented with signs referable to diarrhea: dehydration, fecal soiled perineal areas, diarrhea, and variable morbidity/mortality |
| Diagnosis at necropsy most effectively made with | adequate historical information, gross & microscopic examination and ancillary parasitologic, bacteriologic, virologic proceures |
| calves diarrhea | mixed infections are common: e. coli, rotavirus, coronavirus, and cryptosporidia |
| bovine viral enteric diseases | rotavirus, coronavirus, and BVD. Also, rinderpest and malignant catarrhal fever |
| major animal viruses | cornonavirus, parvovirus, and rotavirus relatively characteristic clinical signs and lesions in the SI |
| destruction of EITHER villar or crypt epithelium results in: | villus atrophy, broadening, and fusion of villi |
| rotavirus | attacks the tips, more common in younger calves |
| coronavirus | can attack anywhere along length of villus, older calves and winter dysentery in cattle |
| parvovirus | attacks rapidly dividing cells in the crypts |
| BVD | ulcer/erosion: palate, tongue, esophagus, peyer's patch necrosis, cerebellar hypoplasia |
| acute coccidiosis | hemorrhagic |
| chronic coccidiosis | proliferative |
| rotavirus | degeneration and necrosis villus tip mature epithelial cells, often hyperplasia of crypt epithelium |
| bovine rotavirus | young 3-8 days, mortality is not bad if there are no secondary complications, malabsorption, maldigestion |
| porcine rotavirus | older pigs, malabsorption and maldigestion |
| other rotavirus species | sheep, horse, similar disease and lesions in newborn |
| coronavirus | epithelial cell degeneration and necrosis in upper and middle portion of villus, spares crypt cells, often hyperplasia of crypt epithelium |
| bovine coronavirus | older cows, malabsorption and maldigestion |
| porcine coronavirus | transmissible gastroenteritis (TGE) less than 2 weeks of age, deadly, kills piglets, villus atrophy, diarrhea, malabsorption, maldigestion |
| canine coronavirus | produces similar diarrheal disease and lesions to those of coronavirus in other species |
| Parvovirus | necrotizing!! severe crypt epithelial necrosis |
| feline parvovirus (panleukopenia) | systemic disease, affects cats of all ages |
| FPV | viremia following ingestion, lodge in mitotically active cells, decreased WBC, diarrhea, dehydration, elctrolyte imbalance, anemic, febrile, vomiting |
| FPV | villus blunting, fusion, collapse and crypts are destroyed |
| FPV | dilated crypts with necrotic debris/abscesses distinct grossly, intestine of cat should coil normally and when it is flaccid it is parvo, also segmental reddening |
| canine parvovirus | segmental enteritis, characteristic smell (only smells like that in dogs, not cats) |
| Bovine viral diarrhea virus | persistently infected animals can spread to other, can have teratogenic effects=cerebellar aplasia |
| BVDV | acute disease-oral cavity with irregular punctate, erosions and/or ulcers. Epithelium is the target |
| BVDV | acute=contact exposure, viremia, hemorrhage, necrosis, ulcers |
| BVDV | GI-ulcer/erosive esophagitis, rumenitis, reticulitis, omasitis, enteritis, colitis Lymphoid tissue=peyer's patch necrosis |
| BVDV | skins and conjunctiva=necrotizing dermatitis and conjunctivitis repiratory and kidney=viral replication |
| BVDV sequella to acute infection | chronic infection, immunosuppression, fetal infection in pregnant animals |
| BVDV fetal infection | route of exposure: viremia or viral persistence in dam-transplacental, widespread fetal tissue infection |
| BVDV fetal | response determined by gestational age |
| persistent infection with BVDV | already infected with BVDV and gets infected a second time this animal will break into the mucosal disease |
| peridontal disease | inflammation of the periodontal ligament, occurs most commonly as extension of gingivitis |
| periodontal dz occurence | very common in sheep, dogs, cats, horses |
| periodontal dz | wide variety of bacteria that live in the mouth, gingivitis followed by peridontitis, loss of peridontal ligament, recession of bone, loss of teeth |
| gingivitis is the first problem, then peridontitis | can have osteomyelitis if persistent and really bad |
| Fusobacterium necrophorum | common in oral cavity and intestinal tract, cattle, sheep, pigs others secondarily invade mucosal defects to produce coagulative necrosis |
| oral necrobacillosis | bacterial infection often secondary to any type of injury infectious or physical can lead to infection with Fusobacterium |
| oral necrobacillosis lesions | fibrin, hemorrhage, necrotizing tissue damage |
| bacterial rumenitis/ruminal necrobacillosis | Abscess complex forms from initial infection with the fusobacterium and leads to liver abscesses |
| bacterial rumenitis | separate from oral lesion, so injury to rumen such as rumenal lactic acidosis |
| bac. rumenitis | areas of almost full thickness necrosis in rumen and multiofocal necrotizing hepatitis, inner seeding from rumenitis--liver takes most of blood from GI and filters |
| bac. rumenitis | sequella-an abscess can rot thru the blood vessel into the lumen, portal vein is usually what it invades. then it breaks through and you can get abscess in liver, heart and lungs. Also, can have hemorrhage. |
| actinobacillosis | Wooden tongue-cattle, small ruminants, horses and pigs |
| wooden tongue | very firm tongue, necrotizing glossitis, opportunistic infection of tongue secondary to some sort of injury |
| DDX for wooden tongue | fusobacterium, actinobacillus |
| actinomycosis | lumpy jaw-actinomycosis bovis |
| lumpy jaw | traumatic lesion or peridontitis, no bone left-large yellowish areas of necrosis. sulfur granules |
| Lumpy jaw-sulfur granules | looks like sulfur granules, reaction with inflammatory cells and bacteria in necrotic foci |
| enteric diseases caused by E. coli (newborn calves, pigs, foals, lambs) | septicemic colibacillosis, enterotoxigenic, enteroinvasive, enteropathogenic, enterotoxemic |
| septicemic colibacillosis (e. coli) | endotoxin-bacterial cell wall-interstinal lesions and diarrhea are NOT always present-so in very acute cases you may not see anything-if you do it will be petechia |
| enterotoxigenic | enterotoxin-adhere and cytotoxin intestinal cell specific-surface adhesion with enterotoxin production (cAMP/cGMP) |
| enteroinvasive | invade-toxin related and necrosis. invade epithelial cells, via shiga-toxin=necrosis |
| enteropathogenic | attach and efface microvilli via shiga-toxin |
| enterotoxemic | exotoxin-extracellular toxin-edema |
| salmonellosis | irregular areas of redness in small intestine-no plication, hyperemia in lumen transmurally, redness on serosa that you see transmurally on mucosal surface, when you open you see fibrinonecrotic exudate |
| salmonellosis | septic tank smell |
| Peracute septicemia-salmonella-calves, foals, pigs | animal dies right away, may see nothing or fibrinous response or can have athritis, synovitis |
| acute enterocolitis-salmonella-cattle, pigs, horses, cat, dog | lesions in peyer's patches=necrosis, lot's of fibrin, pseudomembrane can be peeled off. |
| chronic enterocolitis-salmonella-pigs, less frequent in cattle, horses | increased thickness, irregular areas of necrosis and redness |
| Clostridial enteritis and enterotoxemia-can look like parvo, or colibacillosis | Clostridium perfringens type C: Hemorrhagic enteritis with necrosis in young farm animals generally seen in the first several weeks of life. Toxins induce the massive D. More common cause of hemorrhagic diarrhea in younger animals. |
| Cl. perfringens type B: | similar, milder, newborn lambs & calves |
| Brachyspyra (Serpolina or Treponema) hyodysenteriae [Swine dysentery] | massive diarrhea, poor weight gain, blood and fibrin, sloughing tissue in feces, colitis ONLY, death common due to hemorrhagic diarrhea |
| swine dysentery | LIMITED to large intestine-necrosis of the epithelium. Characteristic limitation to the large intestine and if you do a silver stain you will see the spirochetes in the crypts. |
| Lawsonia intercellularis enterocolitis | porliferative hemorrhagic enterocolitis, feels ropey and thicker due to proliferation of mucosa, may see fibrinonecrotic tissue as well |
| Lawsonia | see in pocket pets and horses and pigs, campylobacter good ddx, adenomatosis, normal response to abnormal signal to proliferate |
| Campylobacter enterocolitis | "Wet tail" and transmissible ileal hyperplasia in hamsters, Proliferative enteritis in ferrets |
| Mycobacterial enterocolitis | Caused by a variety of organisms in mammals:Mycobacterium paratuberculosis-Johne's disease, M. tuberculosis and M. bovis intestinal tuberculosis, M. paratuberculosis avium histiocytic or granulomatous enteritis in macaques, horses, birds |
| Paratuberculosis [M. paratuberculosis Johne's disease] | affects cattle, sheep and goats, looks like lawsonia in that you have proliferation but you have dilated lymph channels!! Granulomatous!!!! Macrophages in lamina propria and makes it palpate firm and thick |
| Johne's disease | Diarrhea, wasting away of animal, still good appetite, protein-losing enteropathy, enlarged lymph nodes, obligate intracellular parasite, replicates in macrophages |
| Johne's disease | Histo is millions of macrophages=Granulomatous!! Swollen lymph is lymphangiectasia |
| When you see mass lesions think of these three things | neoplasia, granuloma, abscess |
| . Mycotic Esophagitis Candidiasis (Candida albicans) | white, green fuzzy think Fungus!! mycotic stomatitis can extend down esophagus, usually a precipitating problem that suppresses the immune system |
| Mycotic esophagitis | prone: diabetes, immunodeficiency, antibiotic therapy |
| mycotic rumenitis-forestomachitits or abomasitis | Needs to be a primary insult. Secondary to some other injury. Lactic acidosis is a common precursor. Or, lacerations due to rough grass or other ingesta. |
| mycotic rumenitis | Characteristic lesion is a geometric shape with target appearance. Targetoid lesions think fungal 1st, 2nd, and think bacterial 3rd. Circular, targetoid think fungal FIRST!! Need special stains to visualize the fungal hyphae like a silver stain. |
| Cryptosporidiosis (Cryptosporidium parvum) | most common in calves, look for it in feces, blunted, collapsed villi, can cause villus atrophy and diarrhea, ZOONOTIC, think of this 4th year!! |
| Crytosporidiosis | Will see dilated lacteals, tons of nuclei in the lamina propria mostly lymphocytes occasional plasma cell. Non-suppurative, non-proliferative enteritis, with lymphangectasia. |
| Crypto | little blue dots at brush border of enterocytes, non-suppurative, lymphoplasmacytic enteritis w/ protozoa |
| coccidiosis | acute vs. chronic hemorrhagic enteritis, most common in sheep and goats, acute disease similar to clostridium=hemorrhagic |
| coccidiosis | chronic disease-will have nodular coalescing foci, on histo you see the coccidia |
| coccidia | . More common in younger animals. So, young animals with D think Crypto and Coccidia. But, remember that the diseases can look quite different depending on what stage of the dz. |
| Parasites in cows | Ostertagia ostertagia (Morroccan leather)-hypoproteinemic due to malabsortption, Trichostrongylus axei, Haemonchus placei and H. similis |
| parasites in sheep | Trichostrongyloidosis: Haemonchus contortus (“bottle jaw”)-lesion is similar to Ostertagia but they also are blood-suckers so you will see anemia, Ostertagia circumcincta, O. trifurcata, Trichostrongylusaxei. |
| parasites in horses | Horses: Gastrophilus sp. (Gastric bots) Draschia megastoma (Habronemiasis): Trichostrongylus axei |
| parasites in pigs | Hyostrongylus rubidus |
| Ruminal Tympany (Bloat): over distension of the rumen and reticulum with gases of fermentation. Two major forms: | primary tympany (frothy bloat) and Secondary Tympany-physical or functional defects |
| Primary bloat-frothy | grossly the rumen is distended, material should be compact, looks frothy and like spinach souffle, airy, frothy, greenish, over-filling prevents normal motility, 1-2 hours or days to develop |
| Primary bloat-frothy | immature legumes and grains can cause a "stable" foam in the rumen, feed concentrates with less than 10% of roughage, soluble protein which is fermented and lowers pH |
| primary bloat-frothy | at lower pH there is a flora change, slime bacteria love lower pH and contribute to the foam with methane production |
| primary bloat-frothy | Bloated rumen completely expanded. Trouble breathing is a complication. Cause of death will be constriction of heart as diaphragm is pushed forward and compression of the vena cava. Big, bloated esp. on left side, heart rate increased. |
| primary bloat-frothy | HR increased to move blood against compression of large rumen, cervical esophagus is blanched and thoracic esophagus is hyperemic |
| primary and secondary bloat look similar | can distinguish because the frothy contents do not go away quickly and will remain frothy vs. secondary with normal looking contents and just gas build up |
| secondary bloat | The gas is an artifact of death, but the contents will look normal. Normal amount of fluid and normal compacted contents. |
| secondary tympany | functional or physical obstruction |
| secondary tympany | esophageal lesion preventing eructation, tumors, abscess, vagal nerve problems |
| secondary tymapny | no frothy contents in rumen, just gas, no esophageal bloat-line |
| ruminal lactic acidosis-causes | grain overload, rumen overload, overeating disease, and acute carbohydrate engorgement |
| ruminal lactic acidosis-causes | carb overload, anywhere in forestomach, usually in intensive beef and dairy production, in dairy seen after cow breaks loose |
| ruminal lactic acidosis-causes | feed lot beef fed lot of grain, easily fermentable grains, brewers yeast, apples, need gradual change in diet to prevent |
| ruminal lactic acidosis-clinical signs | decreased production, anuric, elevation in electolytes and other enzymes |
| ruminal lactic acidosis-clinical signs | rapid transition to different flora, lowers pH drastically, acid-burn mucosa, acid pH further damages rumen normal flora, dehydration |
| ruminal lactic acidosis | Death? Due to circulatory collapse related to the dehydration. Case mortality level can vary greatly depending on the circumstances |
| ruminal lactic acidosis-necropsy | may not see anything, submerge in water and see decreased surface area, superficial necrosis, if sudden huge hit can have lots of necrosis even loss of omasal leafs |
| sequellae of ruminal lactic acidosis | FATAL-secondary bacterial infection (fusobacterium), secondary mycotic, abscessation in liver, erosion through vena cava and explosion and septicemia NON-FATAL-complete recovery with only residual scars |
| Gas dilatation of stomach-clinical signs | abdominal distension, discomfort, anxious, whining, panting, pacing in some species, repeatedly getting up and lying down in others, attempted vomiting, salivation,saw horse stance, and prostration. abdominal guarding |
| gas dilatation of stomach-pathogenesis | not able to vomit due to gas obstruction, gorging on something not supposed to, clostridium type A, most important factor is whether stomach will twist=then surgical emergency |
| gas dilatation of stomach-twisting | surgical emergency, stomach can explode, can have massive effects of cardiovascular system, usually consumption of a large meal followed |
| canine acute gastric dilatation | Giant breed dog, eats large meal, exercise leads to twisting |
| canine gastric dilatation | when twisted it is a physical obstruction, prevents sphincter from opening, compression on vena cava, respiratory/cardiovascular shock and collapse |
| canine gastric dilatation | barrel swelling abdomen, tap abdomen and it sounds like a bass drum |
| canine gastric dilatation-complications | massive distension of stomach due to physical obstruction of esophagus by twisting, venous outflow obstructed, arterial still patenet so congested/engorged spleen and stomach, acid-base abnormalities |
| cardiac manifestations | Electrolyte abnormalities and shock. Myocardial problems, release of myocardial depression factors released from the pancreas which also has disrupted blood flow |
| left displaced abomasum-clinical signs | anorexia, weight loss, decreased production, dehydration, scanty feces and ketonuria, auscult high-pitched ping over abomasum (L or R) |
| Left displaced abomasum-signalment | barrel shaped, often highly/intensively managed, can be 1-2 months post-partem, seen more in winter and spring, usually a predisposing factor or additional problem |
| Left displaced abomasum-signalment | Predisposing factors: ketotic from lactation or parturition, metritis, mastitis,etc. dehydration, abrupt decrease in production |
| canine acute gastric dilatation | Giant breed dog, eats large meal, exercise leads to twisting |
| canine gastric dilatation | when twisted it is a physical obstruction, prevents sphincter from opening, compression on vena cava, respiratory/cardiovascular shock and collapse |
| canine gastric dilatation | barrel swelling abdomen, tap abdomen and it sounds like a bass drum |
| canine gastric dilatation-complications | massive distension of stomach due to physical obstruction of esophagus by twisting, venous outflow obstructed, arterial still patenet so congested/engorged spleen and stomach, acid-base abnormalities |
| cardiac manifestations | Electrolyte abnormalities and shock. Myocardial problems, release of myocardial depression factors released from the pancreas which also has disrupted blood flow |
| left displaced abomasum-clinical signs | anorexia, weight loss, decreased production, dehydration, scanty feces and ketonuria, auscult high-pitched ping over abomasum (L or R) |
| Left displaced abomasum-signalment | barrel shaped, often highly/intensively managed, can be 1-2 months post-partem, seen more in winter and spring, usually a predisposing factor or additional problem |
| Left displaced abomasum-signalment | Predisposing factors: ketotic from lactation or parturition, metritis, mastitis,etc. dehydration, abrupt decrease in production |
| Acute displacement to the right | progress to a volvulus, distension, hyperemia, obstruction of outflow, metabolic alkalosis due to HCl not able to leave abomsum, since it can't pass into small intestine, it can't be absorbed, Surgical issue |
| Acute displaced abomasum-right | surgical repair, need to tack, more life threatening than left, edema and hemorrhage |
| acute displaced abomasum-right | anorexia, restlessness, rapid HR, grunting and groaning, teeth grinding, abnormal posture, kicking at belly, get up/lie down, decreased rumen sounds, distension of right flank, scanty diarrhea |
| gastric ulcers | significant economic concern for pigs and cattle |
| abomasul ulcers in cattle | in mature cattle or calves, young calves due to ingestion of foreign body, trichobezoar, dietary indiscretion, feedlot cattle during winter fattening, dairy is after parturition |
| abomasal ulcer in cattle | Is there increased thickness or not? If no increased thickness then just an ulcer due to stress, feed change, etc. If it is thickened then it IS malignant lymphoma!! |
| Theories of pathogenesis of abomasal ulcer in cattle | local mucosal barrier, increased gastric HCl secretion, local blood flow disturbances, some drugs, exogenous or endogenous steroids. |
| lesions most commonly along greater curvature in fundic and pyloric regions | epithelial loss, covered with digested blood, serosal view of worst case scenario is full thickness ulcer and peritonitis, bovine very good at walling off into abscess |
| abomasal ulcer lesions | may have local abscess, may be incidental finding at necropsy, acute or chronic inflammation |
| abomasal ulcer due to lymphoma | abomasal folds look very lumpy bumpy with lymphoma |
| Pars esophagea ulcer in pigs | crowded animals who are fed high grain diets to fatten, may not see clinical signs, may just see white, anemic, or dead pig, ulcer erodes through blood vessels and acute bleed out |
| pig pars esophagea ulcer | at pars esophagea, may have melena, blood clot filling stomach, apple or vinegar smell indicates bleeding |
| stress ulcers | commonly found in young animals, calves and foals. In fundus or body, may be associated with crowding or feed changes |
| gastric ulcers of horses | Can have localized ulcers at margo plicatus. Seen at junction between the squamous and glandular portion. More frequently seen in the squamous portion, but can see in glandular portion. Can be incidental finding and may not have ANY clinical signs. |
| esophageal obstruction, stenosis or perforation | choke in horse can cause this. Problems with teeth leads to ingestion of too large food. Corn cob for ex causes damage and then heals by fibrosis |
| esophageal obstruction, etc. | can have physical barrier at esophagela inlet/cardia, can perforate, in bovine with obstruction they can bloat, dogs ingesting FB that can't pass, |
| traumatic reticuloperitonitis/pericarditis | hardware dz, eats something which perfs, straight wire goes into peritoneum, j or c shaped goes into pericardium |
| sequela of hardware dz | acute/chronic peritonitis/pericarditis, abscess in abdomen with adhesion, tear in diaphragm, perforate liver/liver abscess, fibrinous inflammation around heart |
| sequela of harware dz | compression on heart, gastric epiploic actery can be lacerated, 8) Secondary septicemia, endocarditis, pericarditis. Peritonitis, septic arthritis after seeding into the joint capsules Can be a HUGE problem or can just be an incidental finding. |
| most common oral neoplasm in the dog | : periodontal fibromatous epulis(tumor but not considered a neoplasia) > malignant melanoma-most common malignancy > squamous cell carcinoma > fibrosarcoma (FSA)(mesenchymal tumor) > oral papilloma |
| cat oral neoplasm | squamous cell carcinoma is the most common oral!!! |
| squamous cell carcinoma | raised white plaques or ulcerated lesions, think SCC 1st, 2nd, and 3rd in cats!! local areas of destruction include mandible or maxilla, can also have in tonsil |
| SCC | common in oropharynx of cat and dog, spordadic in horse, cattle and sheep |
| malignant melanoma | most clinically important in the dog, very rare in cats and other species. most are pigmented, not all. |
| malignant melanoma | older dogs, males more than females, some breed predisposition, 90% are malignant, usually metastasize |
| Fibrosarcoma | most common oral canince sarcoma,Middle age; Male slightly > female; No breed predilection |
| Fibrosarcoma | locally invasive into bone, rapid growth, frequent recurrence, infrequent metastsis (LN and lung if it does) |
| malignant melanoma gross appearance | black or amelanotic plaque, mass or crater |
| fibrosarcoma gross appearance | firm, smooth, sometimes nodular that becomes ulcerated |
| canine oral papillomas | benign neoplasm of papovirus etiology, young, no breed or sex predilection |
| canine oral papilloma | host and tissue specificity, transmissible, spontaneous regression, immunity following recovery, potential to undergo transformation to malignant SCC |
| canine oral papilloma-gross | multiple, develop as single, smooth, papular lesions, progress to multiple, proliferative, cauliflower-like lesions |
| Oral papillomas-other | due to bovine papillomavirus type 4 |
| epulis-non-specific growth on gingiva | periodontal origin, common in dog, occasional in cat, soft, nodular mass covered with epithelium near tooth |
| epulis | all share periodontal ligament stroma, dense fibrillar collagen |
| fibromatous epulis of periodoontal ligament origin | most common oral neoplasm in dog, behave benignly |
| tumors of enamel origin | most are rare, nonmalignant, infiltrative, expansive, destruction of bone, complete excision is difficult |
| ameloblastoma | odontogenic epithelium, common in mandible, more common in dogs and cattle, less in horses and cats |
| ameloblastic fibroma | rare, in calves and maxilla of young cats, odontogenic epithelium and mesenchyme |
| ameloblastic firboodontoma | rare, found in immature animals, dog, sheep horse, cattle, rat and primate |
| Acanthomatous ameloblastoma – odontogenic epithelial origin,mesenchyme seen only in early cases | The major importance must be differentiated from more invasive and life threatening oral neoplasms: squamous cell carcinoma, fibrosarcoma, & malignant amelanotic melanoma |
| odontoma | tumor of enamel origin contain dentin and enamel, usually found in young animals |
| complex odontoma | completely disorganized, no normal tooth structure |
| compund odontoma | neoplastic components arranged in orderly fashion, forms small tooth-like structure |
| pseudoneoplastic lesions | hyperplastic/hypertrophic gingiva commonly seen in old dogs |
| esophagus-rare neoplasm | SCC in cat, horse, dog, sheep and cattle(assoc with bracken fern), canine leiomyoma often eso-stomach junction, bovine papillomas |
| tumors in GI | less likely to see tumors in esophagus, are much more common in stomach or intestines |
| gastric adenocarcinoma | pyloric antrum, extends into body, lesser curvature more common than greater |
| Carcinoma | can metastasize and seed |
| gastric lymphosarcoma | seen in cattle abomasum and cats, lymphoma in very rare instances in a cat can seed. can have ulcers with either lymphosarcoma or adenocarcinoma |
| squamous cell carcinoma | in horse squamous portion of stomach, non-glandular |
| leiomyoma | old dog stomach at necropsy, indicidental finding, at esophagus-gastric junction, bulging, firm, rubbery, tan mass. benign smooth muscle tumor. often clinically silent, deep to mucosa |
| adenomatous polyps | incidental finding at necropsy unless result in clinical signs=become nidus, dogs in rectum |
| benign neoplasm | leiomyoma-infrequent in intestine, lipoma-uncommon, hemangioma-uncommon |
| intestinal adenocarcinoma | dogs, cat, sheep. rare in cattle and swine. most frequent in dogs, small intestine and rectum-can palpate the desmoplasia due to neoplastic cells causing increased proliferation of fibroblast |
| intestinal adenocarcinoma | gross lesion-napkin ring stenosis, annular thickening, growth and metastasis usually by time of clinical presentation |
| carcinomatosis | seeding though peritoneal cavity and lymph nodes |
| intestinal adenocarcinoma | second most common cause in cats-SI, can also see in dog large intestine, can feel a thickening and also could be malignant lymphoma |
| intestinal adenocarcinoma | also common in sheep, in jejunum and ileum |
| sarcomas | fibrosarcoma and leiomyosarcomas infrequently in the intestine |
| lymphosarcoma | increased thickness, ropey mets through intestine, can also involve liver and spleen in cat. Weight loss is biggest clinical sign!! |
| lymphosarcoma | diffuse infiltration results in malabsortption vs. adenocarcinoma where you get wt. loss, D, melena, hematochezia |
| intestinal mast cell tumors | mostly in cats |
| carcinoid tumors-argentaffin carcinomas | rarely dog, cat, cattle |
| 3 causes of hypoalbuminemia (protein losing enteropathy) | Johne's, lymphangiectasia, Ostertagia ostertagia |
| causes of esophageal obstruction and possible sequelae | choke in horse, labs ingesting foreign bodies, ulceration can heal by fibrosis, neoplasia, abscess--sequelae-aspiration pneumonia, cow with bloat, increased pressure leads to ischemia, perforation |
| oral necrobacillosis-fusobacterium necrophorum | occurs secondary to an inciting lesion-viral, traumatic, physical or foreign body-causes toxin-induced coagulative necrosis |
| melanoma most common | lip, cheek, pharynx, and palate |
| malignant melanoma | most clinically important in the dog, common sites-gum, lip, cheek |
| fibrosarcoma | most common oral sarcoma in the dog |
| tumor of odontogenic origin | most are rare, non-malignant, infiltrative or expansive |
| 3 types of odotogenic tumors | ameloblastoma-only epithelium amyloid-producing odontogenic-epithelium and amyloid Canine acanthomatous ameloblastoma |
| fibromatous epulis | common in dogs of any age |
| pseudoneoplastic | gingival hyperplasia |
| abomasal displaement | more common to left-85% vs. right only-15% |
| haemonchus in sheep | bottle jaw from edema-anemia from blood sucking |
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