small animal GI Flashcards
sailocele
accumulation of saliva in SQ tissue due to salivary duct obstruction/rupture
just open and drain mass then remove salivary gland
no biggie
what breeds are likely to have sialadenosis (inflammation of salivary gland)
GSD
small terriers
clinical features of sialadenosis
- painless
- mandibular most common!
- episodic ptyalism
- dysphagia
- regurge/vomiting
dx and tx of sialadenosis
dx: via exclusion
treat it like a seizure (for w/e reason): phenobarbital
3 different type of epulides and their characteristics
- fibromatous: seen in boxers
- ossifying more aggressive; includes bone
- acanthomatous - benign but is very locally invasive
what breeds are predisposed to eosinophilic granulomas
huskies
cavalier king charles spaniel
cats are most likely to get what kind of oral neoplasia?
SCC
feline eosinophilic granuloma
CS
diagnosis
CS: presence of ulcerated mass on base of tongue, hard palate, etc., may have concurrent cutaneous lesions
dx: deep biopsy
feline eosinophilic granuloma
Tx
px
Tx: prednisolone, cyclosporine, chorambucil
px: young cats have better prognosis
stomatitis
etiology
CS
etiology: inflammation of mucus lining of any structures of the mouth. can cause renal failure or immune mediated disease if left untreated
CS: thick saliva, halitosis and suuuper painful
stomatitis
dx
tx
dx: biopsy/histopath
tx: symptomatic - abx, analgesics, oral rinses, etc. salvage procedure is to take out all the teeth
feline lymphocytic-plasmacytic stomatitis
CS
Dx
Tx
CS: most common = anorexia/painful, halitosis and dental neck lesions
dx: biopsy!
tx: teeth extraction - remove all of them! does better
cleft palate
classification: primary vs. secondary
CS
tx
primary: cleft lip (hare lip)
secondary: roof of mouth (hard/soft palate)
CS: cant suck or nurse, aspiration pneumonia
tx: wait until 3 -4 months then surgery
masticatory muscle myositis
etiology
acute CS vs chronic CS
immune mediated - circulating antibodies (IgG) to type 2M myofibers
CS: young-middle aged dogs - large breed
acute: painful swelling of temporalis/masseter muscles, exophthalmus, pyrexia, pain on palpation of muscles and trying to open mouth
chronic: more common - severe atrophy of temporalis/masseter muscles, difficulting opening mouth
masticatory muscle myositis
dx
tx
dx: elevated CK, AST, globulin
tx: pred!
cricopharyngeal achlasia dysfunction
incoordination between cricophyarngeus m. and swallowing reflex
seen in young dogs; congenital
dx via barium study
tx: surgery - cut the cricopharyngeal muscle
pharyngeal dysphagia/dysfunction etiology CS dx tx
etiology: acquired - inability to form food bolus at base of tonge and propel down esophagus (CN 9 & 10)
CS: seen in older animals, regurgitation during swallowing
dx: barium study
tx: treat underlying myasthenia gravis
what is an important factor in determining location of esophageal weakness?
the presence or absence of dysphagia with regurgitation.
if there is dysphagia - that localizes the dysfunction to the level of the oral, pharyngeal or cricophyarngeal region
if there is NO dysphagia, that localizes the issue to general esophageal dysfunction (obstruction or muscle weakness)
what treatment is available for congenital esophgeal weakness and megaesophagus?
there is no definitive treatment but supportive care includes:
- dietary modification: small and frequent meals
- elevated feeding
- gastrotomy tubes
what are the clincal signs of acquired esophgeal weakness and megaesophagus?
CS: regurgitation, cough, weight loss, excessive drooling
how do you dx acquired esophgeal weakness and megaesophagus?
- thoracic rads
- confirm megaesophagus via ACh receptor antibody titer
- hypothyroidism and addison’s can also be uncommon causes
pathophys of myasthenia gravis
Ab to nicotinic Ach receptors bind at the NMJ and prevent activation of skeletal muscle.
how can you diagnose acquired myasthenia gravis?
tensilon test - give endrophonium and they will be able to move normally for like 10 seconds
how do you treat myasthenia gravis?
pyridostigmine and neostigmine
what meds can cause esophagitis in cats?
doxy and tetracycline
what is the etiology and clinical features of esophagitis?
how do you dx it?
reflux, persistent vomiting, regurge, drooling
dx = esophagoscopy
how do you treat esophagitis?
- decrease acidity of stomch: famotidine (H2 antagonist) and omeprazole
- prevent reflux: metoclopramide (increases LES tone), cisapride
- esophageal protectants: sucralfate
- Abx for anaerobes: amoxicillin, clindamycin
etiology of hiatal hernia: sliding and peri-esophageal
sliding: cranial displacement of esophagus and stomach into mediastinum thru hiatus
hiatal hernia: CS, dx and tx
CS: intermittent reflux esophagitis (regurge, vomiting, ptyalism)
dx: rads while placing pressure on abdomen
tx: medical: famotidine (H2 antagonist to decrease acidity), sucralfate (mucosal protectant), cisapride/metoclopramide (increase LES tone).
tx: sx: diaphragmatic crural apposition, esophagopexy, gastropexy
vascular ring anomalies:
etiology
CS
- congenital defect - PRAA most common
CS: regurge is most common sign. signs begin after switching to solid food
vascular ring dx and tx
dx: rads - will see esophgeal dilation cranial to herat. contrast esophagram is definitive diagnosis.
sx: resection of anomalous vessel
foreign body in esophagus: what are the 3 most common locations
- thoracic inlet
- base of heart - the worst
- immediately cranial to diaphragm
esophageal stricture
etiology and CS
etiology: can be caused by esophgagitis or FB or reflux while under anesthesia
CS: regurge, reflux during anesthesia, anorexia
esophogeal stricture dx and tx
dx: contrast esophgrams, esophagoscopy
tx: esophageal ballooning (may require multiple procedures), esophagitis therapy: omeprazole and sucralfate
what esophgeal neoplasia is most common in cats?
SCC!
what esophgeal neoplasia is most common in dogs? what is special about it?
leiomyoma/leiomyosarcoma at the LES
it is curative!!
hemorrhagic gastroenteritis signalment CS dx tx
- small dogs more common
- CS: hemmorhagic diarrhea, hematochezia (fresh blood in stool rasperry jam appearance), hematoemesis
- dx: presumptive: increased PCV, normal TS
- tx: IV fluids, NPO, antiemetics, PPI, fenbendazole
chronic gastritis
etiology
CS
- etiology: lymphocytic/plasmacytic = most common - an initial defect in mucosal barrier followed by immune mediated inflammatory reaction (antigen)
- CS: anorexia, chronic vomiting, weight loss, melena
chronic gastritis
dx
tx
dx: histopath is required!
tx before biopsy: dietary therapy low fat, low fiber, novel protein, H2 receptor anatogonists (famotidine)
tx after biopsy: corticosteroids, immuno-suppressants (cyclosporine, azathioprine)
px of chronic gastritis for cats and dogs
cats: lymphocytic gastritis will progress to LSA
dogs: good for lymphocytic/plasmacytic gastritis and eosinophilic gastritis
helicobacter associated disease
a spirochete bacteria gram (-)
- usually asymotomatic (sometimes have signs of gastritis)
- dx via giemsa stain
- tx w/ metronidazole, omeprazole, amoxicillin
usually respond well
what breeds are susceptible to chronic hypertrophic pyloric gastropathy (aka pyloric stenosis)
congenital: brachycephalic breeds and siamese cats
acquired: lhasa apso, shih tzu, pekingese, poodle
signs and dx of chronic hypertrophic pyloric gastropathy
CS: chronic VOMITING shortly after eating (not regurge!)
dx: hypoCl, hypoK, metabolic alkalosis, imaging to show obstruction, histopath to rule out infiltrative dz like neoplasia
tx of chronic hypertrophic pyloric gastropathy
surgery - pyloroplasty
how do you dx GDV?
hypothermia
VPCs, v-tach
rads (R lateral)
hypoK, high lactate
what is an underlying etiology of GI ulceration erosion other than NSAIDs and how do you dx it?
addisons (hypoadrenocorticism) - check Na:K ratio <20 = diagnostic
