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 etiology
-non infectious: forgion bodies (foxtails or porcupine quils)
-uremic stomatitis
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)
–Oral necrobacillosis
–Noma
-laryngeal necrobacillosis
-fibrinecrotis stomatitis
-gangrenous stomatits (NOMA) human disease holes of mouth
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
Causes
* Idiopathic
* Breed predisposition
* Medications
Eosinophilic granuloma
-cats see nodules on tongue and mouth, granuloma stimulated by immune reaction
gingival hyperplasia
Causes
* Idiopathic
* Breed predisposition
* Medications
Gingival epulis
-(gingival mass/tumor)
-Fibromatous epulis:
with lymphoplasmacytic hyperplastic gingivitis
oral melanoma
-kiss of death, poor prognosis in moth
-black, dark melanoma
-malignant tumor
benign tumors of the mouth
-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
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.
ranula dog
-saliva filled cysts/ duct
megaesophagus
clinical signs: regurgitation after feeding, thin, aspiration pneumonia
causes:
-foreign bodies
-external pressure
-myasthenia gravis
-lead poisoning
-due to persistent aortic arch
muscular hypertrophy of esophagus
-due to obstruction
-idiopathic
-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
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
* Secondary (free gas) bloat
* 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
Ruminal acidosis: Necropsy/Diagnosis
- Dehydrated carcass
- Grain/porridge-like, acidic watery content in rumen
- ↓ ruminal pH disappears after death (12 - 24hr)
- 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.
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
-should always be hemmorage, necrosis.
-has to be transmural to be volvus all levels will be effected not just mucosa.
abomastitis
-inflammation of abomasum
-mycotic: from ruminal acidosis mitotic lesions.
-clostridium septicum: hemmoragic abomastitis (braxy) with submucosal emphysema in lambs and calves.
-caused by ingested of frozen feeds.
-death due to an exotoxemia endotoxin in blood.
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)
-chronic: esoniophilic gastroenteritis, hyperplastic gastritis, uremic gastritis, lymphoplasmacytic gastritis
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
-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 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
gasterophilasis 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 right away type II are dormant
-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
- easily reduced
- there is no vascular compromise (edema,
congestion, hemorrhage) - no fibrin or adhesions (peritoneal surfaces is
smooth and glistening) - no necrosis
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.
intermitent colic
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
