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Systemic Path-GI

Steinberg-systemic path-GI

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
Created by: vermey



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