allementry Flashcards
most important things to keep in mind about alimentary pathology
-normall mucosal and serosal surfaces should be smooth and shiny
-the quality and quantity of feces and vomit are good clinical signs of alimentary disfunction.
-anatomical location of organs and attachement
-need to know pathogens that affect different species and age groups and cause various
clinicopathological syndromes.
small vs large intestinal diarrea
small: liquidy
large: hemmoragic or mucoid
malfunction
-alterations in quallity and quantity of feces.
-diarrhea: increaed frequenxy and volume of discharged semisoild or fluid feces.
erosive/ ulcertive stomatitis causes
non infectious:
- forgion bodies (foxtails)
-uremic stomatitis
-Lymphoplasmacytic stomatitis in cats - idiopathic condition. or with calcivurus in cats with FeLV.
infectious:
-BVD
-bovine papular stomatitis
-malignant catarrhal fever (MLC
-blyetongue
-IBR in neonatal calves
-feline calicivirus
Uremic stomatitis
-Bucal and lingual erosions/ulcers often
occur adjacent to the openings of salivary ducts
-many causes, ammonia, uremic vasculitis and impaired microvascular perfusion, mechanical abrasions
Lymphoplasmacytic stomatitis
Idiopathic condition
hypothetically associated
with presence of bacteria
or calicivirus in cats
infected with FeLV and/or
FIV.
Proliferative (Parapox) stomatitis
-proliferative: bovine papular stomatitis: target lesion (looks like target) in oral, espohageal and ruminal mucosa.
-zoonosis are milkers nodules on humans fingers
Contagious ecthyma (orf, infectious pustular
dermatitis) in sheep and goats
- Proliferative crusting dermatitis of mucocutaneous
junction (lips commissure, eyelids, anus), udder,
teats, and coronary bands - High morbidity and low mortality
- Economic importance due to weight loss
- Zoonosis (orf)
Deep stomatitis (necrotizing)
- The end-stage of any forms of stomatitis when they are complicated by infection with Fusobacterium necrophorum that causes severe coagulation necrosis.
–Oral necrobacillosis (in calves which is
also laryngeal necrobacillosis)/
fibrinecrotis stomatits
-Actinobacillosis (“wooden tongue”)
caused by Actinobacillus lignieresii. Pyogranulomas resulting from infection with bacteria. inflammation and fibrosis-> wooden tongue.
-gangrenous stomatits (NOMA) human disease holes of mouth
o Eosinophilic stomatitis
- Oral eosinophilic granulomas or ulcers (“rodent ulcers”) occur frequently in cats
actinobacillosis causes
-wooden tongue
-granulomatous disease in soft tissue of tongue, makes granuloma in tongue.
-neutrophils lead to pus, multinucleated macrophages
-leads to fibrosis so hard wooden tongue
Gingival hyperplasia
o Simple overgrowth of gum tissue consisting of the fibrous submucosa lined by hyperplastic
gingival epithelium which is not driven by inflammatory process as in hyperplastic gingivitis.
Causes
* Idiopathic
* Breed predisposition
* Medications
Eosinophilic granuloma
-cats see nodules on tongue and mouth, granuloma stimulated by immune reaction
hyperplastic gingivitis
o Usually associated with periodontal disease and chronic irritation by plaque/tartar that initially
starts as inflammation (gingivitis) but can progress to severe hyperplastic gingivitis .
Gingival epulis
-(gingival mass/tumor)
-Fibromatous epulis - a begin tumor of dental mesenchyme.
with lymphoplasmacytic hyperplastic gingivitis
canine oral papillomatosis
It is a papillomavirus induced, transmissible and occurs in animals younger than 1 year.
o The lesions usually regress spontaneously and immunity is long-lasting.
oral melanoma
-kiss of death, poor prognosis has metatisis.
-black, dark melanoma
-malignant tumor
benign tumors of the mouth dog
-gingival hyperplasia
-firbomatous epulis
-locally invasive but begnin (acanthomatous ameloblastoma)
malignant tumors oral masses in dogs
-melanoma: locally invasive with metastiatic
-squamous cell carcinoma: LN metastisis
-fibrisarcoma: LN metastisis
-osetosarcoma
oral masses in cats mouth
-esonophilic granuloma: benign inflammatory always chronic.
-squamous cell carcinoma, firbosarcoma and lymphosarcoma: malignant, invasive, metastasis to LN.
diff between granulomatous vs abscess
Granulomatous: Always chronic.
Are inflammatory processes with macrophages and fibrous tissue. Ex johnes disease.
Purulent or suppurative: can have acute or chronic and can lead to abscess. Abscess are formed by pyogenic bacteria.
-in abscess pyogenic bacteria are encapsulated by fibrous tissue.
salivary glands lesions
o Rabies virus causes microscopic inflammation of the salivary glands. = sialoadenitis
-ranula: saliva filled cysts/ duct
- Salivary mucocele is a pseudocyst (cavity not lined by epithelium) filled with saliva.
- It occurs secondary to leakage of saliva into surrounding soft tissue and forming cavity surrounded by reactive connective tissue.
o Salivary gland adenocarcinoma
megaesophagus
-is dilation of the esophagus because of bad/ uncoordinated peristalsis.
clinical signs: regurgitation after feeding, thin, aspiration pneumonia
causes:
-foreign bodies
-external pressure
-myasthenia gravis: either congenital or acquired due to autoimmune disease.
-lead poisoning
-due to persistent aortic arch
muscular hypertrophy of esophagus
-due to obstruction
-idiopathic seen in horses and pigs
-if foreign body can lead to necrosis no basement membrane no scaffold so you get necrosis and fibrous scaring
erosions and ulcers of esophagus (esophagitis)
-infectious erosive diseases
-BVD, stomatitis, foot & mouth
cats: calcicivirus
-reflux esophagitis
-improper use of stomach tubes
-foreign bodies
choke
o Choke is a clinical term referring to esophageal obstruction.
- Formation of strictures (if chronic), starvation and aspiration pneumonia: A foreign bodies lodged against the mucosa for longer than 2 days cause circumferential pressure necrosis of the esophageal mucosa (in part due to ischemia due to muscular constriction), which heals with fibrosis and cause strictures during healing
examination of ruminal contents
-dehydration= dry
-primary bloat= voluminous frothy
-urea toxicity= ammoniacidal odor and alkaline Ph
-organophophate toxicity=oder of cooked turnips
-grain overload=fermentative acidosis oder or ph less than 5
-lead toxicity= metalic lead, paint flakes or motor oil in rumen
bloat necropsy findings
-esophageal bloat line from pressure on thoracic inlet and jugular vein return is compromised.
-sinus hemorrhage
-cervical lymph node congestion: jugular vein compromised from bloat
-cranial congestion head and neck
-frothy ruminal contents
lymph edema in caudal portion
Bloat clinical signs and types
Primary (frothy) bloat: legume, frothy, due to diet.
* Secondary (free gas) bloat: caused by physical or functional defect in eructation of gas.
* Clinical signs of primary and secondary bloat are the same:
– Distended left paralumbar fossa and abdomen
– Increased respiratory and heart rates
– Decreased ruminal movements in late stages of disease
foreign bodies which can lead to bloat
- Trichobezoars (hair balls)
- Phytobezoars (plant balls)
- Nails and wire -> hardware disease
- Ingestion of lead plates from broken
batteries -> lead poisoning ->
polioencephalomalacia in cattle
-can lead to traumatic reticulitis which is firbinopurulent and constrictive pericarditus
Chemical rumenitis
- Sudden change to easily fermentable feed
- ↑ dissociated VFA
- Ruminal stasis
- Change in ruminal microflora
- ↑ [lactic acid]
- pH below 5
- Damaged epithelium -Superficial rumenitis
- Dehydration => acidosis => CV collapse
- Death due to dehydration and acidosis then circulatory collapse
Ruminal acidosis: Necropsy/Diagnosis
- Dehydrated carcass
- Grain/porridge-like, acidic watery content in rumen
- ↓ ruminal pH disappears after death (12 - 24hr)
- VENTRAL Ruminal mucosal epithelium is firmly attached
- Watery intestinal contents
- Microscopic confirmation of ‘chemical rumenitis’
– may be necessary in animals necropsied more than 12 hrs
after death - Surviving animals may develop ruminal necrobacillosis
and if survive stellate scars (healed ruminal ulcers)
chemical rumenitis causes of death and sequencally
-death is due to: dehydration, acidosis, eventually circulatory collapse
-if survives leads to ruminal necrobacillosis from fusobacterium or truperella pyogens causing ruminal necrobacillosis or in liver can cause caval syndrome. which will lead to stelate scar in rumen.
-mycotic rumenitis from fungal infection in blood vessels.
-ruminal fibropapillomas
post mortem examination of abomasum and stomach
-open along greater curvature
-sample from bottom of crypts in the fundus
-examine for blood.
-look at worm count, tie off pylorys and cardia and collect and count worms for haemonchosis
gastric dialation causes
-volvus-> due to no eruptation can lead to rupture or death. in animals which cant eructation or vomiting.
-dog dilation and volvulus is always counter clockways, fatal disease.
-dogs predisposing are large breeds, obstruction of cardia or pylorus and repeated dialation.
-Both gastric and splenic
vein are compressed, resulting in a congested and edematous gastric wall (venous infarction
in later stages) and congested spleen, because the arterial blood supply remains patent longer
than venous drainage
gastric dilation cause of death and presisposing factors/ clinical
Predisposing factors:
* Hereditary predisposition – Large beeds
* Obstruction of the cardia that prevents eructation and emesis
* Obstruction of the pylorus that prevents passage of gastric contents
* Repeated episodes of gastric dilation, overfeeding,
Clinical consequences:
- Severe distention compromise respiration and cardiovascular function and electrolyte
balance
- Gastric rupture
Cause of death:
* Acid-base imbalance
* Increased intragastric pressure interferes with venous return from portal circulation
-decreased CO and shock
-pigs: gastric torsion is one of main causes of sudden death.
Gastric Dilation and Rupture
o Horses
- Acute gastric dilation and rupture in equids occurs most frequently as a terminal event in
small intestinal obstruction, ileus and displacement. - It can also be a result of the rapid ingestion of fermentable feeds or grain, a situation
analogous to grain overload with lactic acidosis in cattle
o Gastric/abomasal dilation in other animals is usually secondary to ulcer, pyloric stenosis,
overeating, gastritis/abomesitis, vagal indigestion etc.
Ante-mortem or postmortem gastric rupture:
The only reliable indicator of ante-mortem rupture of the stomach is the presence of hemorrhage along the margins and evidence of acute
inflammation (e.g. fibrin strands).
abomasum displacement cattle
-usually dairy cattle after parturition
-causes: abomasal atony due to heavy grain feeding, hypocalcemia.
-clinical: anorexia, dehydration, ketonuria.
-l sided most common not fatal, R sided 10-15% may progress to volvulus and be fatal.
volvus
-intestinal infarction/ twisting, torsion, counter clock wise. on its mesenteric axis
-should always be hemmorage, necrosis.
-has to be transmural to be volvus all levels will be effected not just mucosa.
-torsion: a rotation of abomasum. colon or cecum along its long axis.
hemmoragic abomastitis (braxy)
-caused by clostridium septcum.
-with submucosal emphysema in lambs and calves.
-caused by ingested of frozen feeds.
-death due to an exotoxemia endotoxin in blood.
-braxy effects only abomasum
gastritis in dogs
-acute: , more common in dogs due to ingestion of spoiled foods, toxins. ect. non fatal and transcient.
-canine hemmoragic gastroenteritis (fatal) will have clinical hematemesis.
-chronic:
-esoniophilic gastroenteritis, hyperplastic gastritis, uremic gastritis, lymphoplasmacytic gastritis, parasites
canine hemmoragic gastroenteritis
-smaller breeds
-hematemesis due to superficial hemmorahic necrosis
-die due to dehyrdation and cardio collapse, DIC
-could also be parvoviral enteritis (stomach and colon are not affected)
eosinophilic gastroenterocolitis
-parasites-> hypersensitivity reaction. skin disease. or food allergy.
-diagnosis by endoscopic biopsy of stomach duo and colon ALL THREE EFFECTED
hyperplastic gastritis
-focal: antral hyperplastic gastritis
-in older and small breeds
-clinical signs of upper GI obstrucyion and vomiting
-other diagnosis: pyloric obstruction due to pyloris muscular hypertrophy. (interfers with food ingestion leads to vommiting and aspiration)
-diffuse: chronic giant hypertrophic gastropathy is rare. weight loss, hypoprotenemia.
uremic gastritis
-caused by chronic renal disease/ failure
-gross: congestion and edema with ulceration (sometimes)
-caused by renal failure then injury to capillaries within the lamina propria.
-microscopic mineralizaition of gastric mucosa.
-can lead to renal fibrosis, erosive glossitis or stomatitis, mineralization of intercostal mucosa, uremic pneumonitis.
pars esophagea ulceration horses
gastric ulcers
-horses, very common with high workload.
-stress and NSAIDS if they are used predisposing to ulceration.
-can get gastric ulcer with exsanguination which is hemorrhagic ulcer
-perforating abscess CHRONIC -> leads to fibrous scar.
-if given PPI to horses which are dehydrated will destroy kidneys
gastric ulcer
o An ulcer is a mucosal defect in which the entire epithelial thickness with the basement
membrane was lost.
o Penetration through the remaining tissue layers to the peritoneal cavity is termed a perforating
ulcer.
o Partial-thickness epithelial loss is termed an erosion
o Chronic ulcers differ from acute ulcers by the presence of an indurated rim caused by fibrosis
and epithelial hyperplasia
gastric ulcer signs
-vommiting
-anorexia
-abdominal pain
-anemia
-excanguination-> death
-peritonitis and septicema
gastric ulcer path
-imbalance between acid sectrtion and mucosal protection
-high HCL: could be mast cell tumors in dogs/ cats. or gastronoma in dogs.
-infection: helicobacter
-stress induced disturbance in BF (shock)
-NSAIDs depressing prostaglandin formation, decreasing HC03 and blood perfusion. directly toxic to vascular endothelium
-local trauma to mucosa, bile salts from dueodenum, lipid solvents such as alcohol.
gastric ulcer in pigs
-affecting pars esophagea
-from finley grown grain, ingredients in diet (whey), and stress
-mortality due to esanguination.
gastric ulcer in cattle
-subclinical to fatal
-in calves its mechanical irritation by roughage
-in dairy: heavy grain feeding (LA)leads to mycotic infection
-displacement of abomasum
-BVD and bovine leukosis
Mycotic rumenitis
-occurs secondary to the damage to the ruminal mucosa caused by
lactic acidosis or secondary to administration of antibiotics, which disturb the normal flora
and allow fungi (Aspergillus, Mucor etc) to proliferate.
- Ruminal lesions are generally red circular and well delineated, because they are caused by
infarction from thrombosis secondary to fungal vasculitis
Bots equine
-gasterophilus intestinalis and G. nasalis.
-not deworming properly
-if bots in stomach no significance
-larve lay eggs on horse very annoying
haemonchus contortus
-sheep and goats
-clinical signs (blood eaters blood loss), count worms in abomasum, severe anemia (pale mucus membranes), bottle jaw (hypoprotenemia), weight loss.
-haemonchus paeci affects calves
-barber pole worms, red look like candy canes, mucosa is thickened and edema and black.
ostertagia ostertagi
-o,ostertagi BOVINE
-o. circumcinta OVINE
-ingestion of larve, destroys glands in mucosa and destroys partial and cheif cells. (metaplasia as they are replaced by mucus cells) and hypoplasia.
-type I larve develop into adults summer or type II are dormant winter.
-clinical signs: inappetence, diarrhea, wasting, edema
-diagnosis: morocco leather abomasum. generalized edema from hypoprotenemia. proper worm count.
gastric / abomasul neoplasia
horses: squamous cell carcinoma of pars esophagia
cattle: lymphoma from BLV
dogs and cats: gastric adenocarcinoma is locally invasive and metastatic
Ileus
- Non-mechanical hypomotility resulting in a functional obstruction of the bowel
- Causes:
– Post-surgical - bowel manipulation
– Peritonitis
– Severe abdominal pain
– Electrolyte imbalances (especially hypokalemia) - There are no gross lesions other than atonic dilation of the intestine.
intestinal strictures
causes:
-failure of regeneration
-postenterotony healing-> firbosis-> stricture
rectal stricutres
-causes:
-Recurrent rectal prolapse -> circumferential
necrosis -> fibrosis -> stricture, from high perastalis leads to constricting and circumferential necrosis.
-Salmonellosis -> thrombosis of hemorrhoidal artery -> necrosis -> circumferential fibrosis -> stricture.
salmonella causes erosive ulcerative enterocolotis.
Terminal or post-mortem invagination
versus antemortem intususeption
post mortom:
* easily reduced
* there is no vascular compromise (edema, congestion, hemorrhage)
* no fibrin or adhesions (peritoneal surfaces is smooth and glistening)
* no necrosis
hernias
o Internal herniations are displacements of intestine through a normal or pathologic foramen in the abdominal cavity
-horses: herniation through mesenteric tears and through the epiploic foramen
.o External hernias are formed when a hernial sac, formed by a pouch of parietal peritoneum,
penetrates outside the abdominal cavity. Types of external herniation include umbilical,
diaphragmatic, hiatal, inguinal,
Intestinal venous infarction
- Blood is pumped into the twisted segment but cannot drain due to occlusion of veins
- Transmural congestion, edema, hemorrhage, venous infarction
- Dark red intestine is distended with gas and hemorrhagic fluid
- Sharp line of demarcation between he affected and normal intestine
- During surgery, important to determine the viability of the bowel after reduction of a volvulus
- If reduction of a volvulus results in re-established circulation, reperfusion injury may occur.
cranial mesenteric artiritis and thrombosis leading to intermittend colic ? cause
Horses recover: not as distinct demarcations than a torsion. More multifocal, can be caused by strongyles vugaris. Confirm by cranial mesenteric artery with thrmbosis and firborisis. Thromb travel down to intestines cause intermittent colic.
intestinal lymphanigiectasia in dog
- Most common protein-losing enteropathy in
dogs, dialation of lymphatics - Clinical signs:
– Diarrhea
– Steatorrhea
– Hypoproteinemia -> ascites - Causes:
– Acquired (lymph vessel obstruction)
– Congenital (disorder of the lymphatic vessels
diarrhea
-increase in feces with fluid consistency or increased defecation or both
-leads to dehydration, lactic acid build up leads to acidosis. decreased perfusion, losing electrolytes, hypovolemia leads to hypovolemic shock. tissue isn’t perfused properly.
