GI Dr. Niblett 2/17/17- Flashcards
What are common presenting complaints in GI cases?
Dysphagia (difficulty swallowing), Halitosis (bad breath), Drooling (pseudoptyalism vs ptyalism), difficulty eating (dropping food)
What type of hx info would you start out gathering?
previous treatments for dental problems (including dental prophylaxis and home care)
as well as behaviors that put them at risk for dental disease (chewing tennis balls, rocks, cage bars, or coprophagia)
How would you start the exam?
At the head! With an external exam & limited internal exam.
include:
- general PE - (thin BCS, unkempt coat)
- exam of face for symmetry, swelling, drainage
- initial oral exam: note calculus, missing/broken teeth, gingival inflammation
- sublingual evaluation: finger between mandibles pushing up while opening mouth
- palatal and pharyngeal inflammation (FB)
If there was dysphagia but no oral lesions/pain what might you consider putting on your DDx list
neuromuscular disease affecting the oral, pharyngeal or cricopharyngeal phases of swallowing
what are examples of neuromuscular dz affecting oral, pharyngeal or cricopharyngeal phases of swallowing
Myaesthenia gravis (MG)
cricopharyngeal achalasia
rabies
tetanus
botulism
idiopathic cranial n. dysfunction
Where might a lesion be localized to with:
halitosis, ptylism, difficulty prehending food
oral cavity
what if no oral disease is seen what should you consider?
what might also be seen?
neuromuscular dz
dysphagia
what are ddx for a feline where you find
jaw chattering
irregular surface
broken teeth
FORL’s
Feline Odontoclastic Resporptive Lesions
what is etiology of FORLs
tx?
idiopathic
- based on radiographic type:*
- restore, extract, crown amputation*
which xrays are predictive in cat FORLs
xrays of 407 & 307 predictive of whether full dental rads needed
What is this?
what spp seen in?
lymphocytic plasmacytic stomatitis
felines
What is seen in this cat?
feline periodontitis on canine tooth
although we call is idiopathic what is one thought as to etiology of lymphocytic plasmacytic stomatitis?
signalment seen?
hx?
thought to be related to an excessive host response to oral flora
possibility of an infectious agent (calici virus) has not been ruled out
mature cats
chronic condition where weight loss and anorexia may be noted due to difficulty / pain associated with prehending food. Mild improvement with but recurrence following dental cleaning
PE findings with lymphocytic plasmacytic stomatitis
how dx
tx
gingival erythema, swelling, bleeding, all of which may be severe. submandibular ln may be enlarged
histopathology of biopsy
extraction of all teeth as bacteria adhere to the teeth. Cats can typically keep the canines and incisors. Refractory cases may respond to intermittent systemic antibiotics, gold salts therapy, steroids or even Ovaban
What are the 3 types of FORL classification
Type 1: incr. periodontal space -> removal tx
Type 2: decr. periodontal space (ankylosed) -> crown amputation
Type 3: mixed
differences between vomition & regurgitation
what is regurgitation indicative of
esophageal dz
which spp don’t vomit
rabbits
horses
why does regurg happen
motility disorders
- Obstructive
- Weakness
what are the 2 types of regurgitaion
physiological
pathologic
what are the 2 types of pathologic regurgitation
Obstruction
Weakness
what types of etiologies (big picture) of both obstruction & weakness are seen in each
congenital & acquired
what are some obstructive regurg dz
congenital v acquired
PRAA - congenital
- FB*
- Cicatrix (strictures)*
what are some Ddx for seen in regurg due to weakness
Congenital v acquired
neuromuscular junctional dz: Myasthenia gravis
neuropathy
- esophagitis*
- hypo T4 (Addison’s?)*
- lead toxicity*
- idiopathic*
what is 1o lesion seen in this radiograph
what is 2o lesion seen
probable etiology
related?
more diagnostics needed?
what will this dog die from more likely?
megaesophagus
pneumonia (aspiration)
Myasthenia gravis (MG)
yes
yes confirmatory diagnostics for MG
the pneumonia
What is a simple test for MG that can be done during office visit to point you towards dx
palpebral reflex fatigues!
how is megaesophagus managed
Bailey chair
Small volume / high calorie meals
Work up/Treat underlying problem
Manage aspiration pneumonia / monitor for recurrence
what are CC/CS of esophageal disorders
Regurgitation, dysphagia, odynophagia, repeated swallowing attempts and salivation
Weight loss may occur
Nasal discharge may result from nasopharyngeal reflux
Cough / lower respiratory tract signs may occur due to pneumonia secondary to aspiration during regurgitation / dysphagia
ddx for congenital megaesophagus
vascular ring anomaly
congenital megaesophagus
etiology
signalment
Ddx
tx
abn innervation to esophagus
present from birth w/ CS starting at weaning (may be breed related)
vascular ring anomaly (PRAA)
supportive care
acquired megaesophagus/ idiopathic
what is significance of the disorder being idiopathic?
Most cases of acquired megaesophagus are idiopathic (>70%).
Dz is seen primarily in middle age to older lg breed dogs
Idiopathic = dx of exclusion = must rule out all of the following causes of megaesophagus:
Myasthenia gravis (2nd most common cause of acq. megaesophagus), Hypoadrenocorticism, Hypothyroidism, Dysautonomia, Esophagitis, Spirocerca lupi, SLE, lead, chagas…all of which may be associated with neuropathy or myopathy
what can be seen in this image
etiology/ common locations seen
signalment
CS
Dx
Tx
Px
Objects with sharp points are most common (bones/fish hooks)
@ thoracic inlet, base of heart and caudal esophagus
Dogs >>>Cats
Regurgitation and anorexia - acute onset - systemic signs with perforation - partial to complete obstruction - potential to impinge on airways.
Radiographs (look close for chicken bones and evidence of perforation as indicated by air in SQ) +/- contrast. Esophagoscopy can be used for both dx and also tx
Esophagoscopy using forceps or snare to remove FB unless perforation or esophagoscopy fails, then thoracotomy. Usually the FB removed via oral cavity but if not possible, consider push to stomach (then gastrotomy).
No apparent injury or mild: NPO and antacids (liquid sucralfate).
Mild to moderate trauma: add bigger or more antacids (liquid sucralfate and omeprazole) and maybe prokinetics.
Moderate to severe injury: consider gastrostomy feeding tube.
Good with no perforation but watch for cicatrix formation esp. w/ mucosal damage.
esophageal cicatrix
signalment
CS
Dx
Tx
Px
A stricture that may result from esophageal mucosal injury.
dogs and cats
regurgitation
Contrast esophagram or esophagoscopy
balloon dilation or bougienage followed by intralesional / systemic corticosteroids. Referral.
Prevent - early recognition of and appropriate tx for esophagitis
depends on the length of esophagus involved and duration of lesions
what is a leading cause for esophageal cicatrix in felines
oral doxycycline admin
make sure capsule moves through to stomach!
esophagitis
etiology
Dx
Tx
Caused by gastroesophageal reflux, persistent vomiting, esophageal foreign bodies and caustic agents.
iatrogenic cause possible! post anesthetic or post pill (doxycycline)
Hx of meds or, anes and vomiting, followed by vomiting and regurgitation all suggestive of
Esophagoscopy w or w/o bx
Decr gastric acidity: Proton pump inhibitor (omeprazole)
Decr reflux: cisapride
mucosal protectant : sucralfate (liquid)
By-pass esophagus: gastrostomy tube
Abx: only if submucosal injury. broad spectrum (incr anaerobes)
name most common type of vascular ring anomaly that leads to obstructive esophageal dz
Tx
persistant right aortic arch
Sx
With stomach disorders…
Why is it important to distinguish obstructive versus non-obstructive?
Is there one particularly powerful test to aid in distinguishing the them?
type of tx preferred: surgical v medical, how long to dx (emergent v non emergent: GDV vs ADR)
imaging! either radiographs or u/s
what are 3 types of non-obstructive gastropathies
- acute* gastritis
- hemorrhagic gastroenteritis*
- chronic* gastritis
when thinking about chronic gastritis what should you think more about & why
that it is more typically a chronic gastroenteritis not just gastritis as there are not many chronic gastropathies that only involve the stomach w/o intestines also!
what are 2 medically managed obstructive gastropathies
idiopathic gastric hypomotility
bilious vomiting syndrome
what are 3 specific infiltrative gastropathies
Neoplasia
Pythiosis
Inflammatory Bowel Dz (really a gastroenteropathy!)
what are 5 categories of gastropathies (problems) that can be specific to stomach
Acute gastritis
Chronic gastritis
Gastric outflow problems
Gastric ulceration
Infiltrative gastric dz
What are DDx specific to stomach for acute gastritis problem
Bad food/rich food
FB
toxins
drugs
What are DDX specific to stomach for chronic gastritis problem
IBD
helicobacter
physalopter
ollulanus
What are DDx speccific to stomach for gastric outflow problems
idiopathic hypomotility
bilious vomiting syndrome
What are DDx specific to stomach for gastric ulceration problem
shock
drugs
gastrinoma/MCT
helicobacter
IBD
local tumor
pythiosis
what are DDX specific to stomach for infiltrative gastric disease problems
IBD
neoplasia
pythiosis
Tx for acute gastritis
supportive care of parenteral fluids as needed
and withholding food for 12-24hrs
Refeeding initially sm amts of H2O followed by sm freq meals of bland diet.
Anti-emetics maybe
In non responsive cases to conservative therapy, the dx likely not correct.
Pursue further diagnostics
risk factors for GI ulceration
how prevent
tx
variable – shock, NSAIDs (especially with corticosteroids), high dose steroids, MCT, gastrinomas (APUDomas), Helicobacter, renal and hepatic failure, IBD, neoplasia, pythiosis
Misoprostol is used to prevent NSAID induced ulcers in high risk patients, none of other tx have shown clinical efficacy in ulcer prevention
depends on the cause:
Symptomatic therapy with antacids, H2-blockers, proton pump inhibitors or sucralfate (later two most effective and sucralfate has benefit of coating duodenal ulcers) combo w/ parenteral fluids, withholding food and parenteral nutrition is often successful
CC is acute onset vomiting a/o diarrhea, what type of problem might you call it
DDx
1o Acute Gastroenterits (AGE)
dietary: indiscretion, intolerance, sudden change, food poisoning, toxin/drug ingestion
infectious: parvo, salmonella, campy, salmon poisoning, helminths, Giardia
intestinal obstruction: FB, intestinal accidents
dx of acute diarrhea
tx
hx, PE & fecal
Other diagnostics TBD by severity of CS and possibility of contagious disease. (Emergency panel, Parvo-cite, abdominal radiographs/ultrasound, complete blood count, serum biochemistry and electrolytes, urinalysis…)
Symptomatic.
Many disorders are self limiting. Appropriate fluid therapy, abx in shock/neutropenic/febrile patients, anti-emetics, withhold food? (feeding enterocytes may be important to faster recovery), small meals of easily digested food provided frequently
categories of dz assoc. w/ chronic diarrhea (chronic enteropathies or gastroenteropathies)
maldigestive/malabsorptive disease
chronic obstructive disease
neoplasia
functional intestinal disease (irritable bowel disease)
what are maldigestive dx
Exocrine pancreatic insufficiency (EPI)
what are ddx for malabsorptive dz
Inflammatory Bowel Disease, food intolerance/allergy, parasitism (rounds, hooks, Giardia causing small bowel disease, and whips, Tritrichomas causing large bowel disease), infectious (Salmonella, Clostridium) antibiotic responsive enteropathy, neoplasia, pythiosis, histoplasmosis, lymphangiectasia, chronic intussusceptions
how is EPI dx
tx
Etiology: caused by pancreatic acinar atrophy
Signalment: Dogs with German Shepherd Dogs over represented. 1-5 years of age. Possible history of recurrent pancreatitis
Clinical features: Weight loss with good appetite. Chronic small bowel diarrhea
- *once parasitic and dietary causes are eliminated, measure trypsin-like immunoreactivity (TLI). It is low in affected dogs.**
- Pancreatic enzyme supplementation with a low fat diet (<15%), forever.* Response seen in stool consistency w/i one week. If not responding, consider concurrent antibiotic responsive diarrhea or use of H2 blocker to decrease stomach acidity which may be inactivating the enzyme supplement.
dx of IBD
Elimination of known causes of small bowel diarrhea (includes therapeutic trials) combined with histologic examination of intestinal biopsy is required for a dx
abn inflammatory cell infiltrate found on histopath that may be predominated by particular cell type such as lymphoplasmacytic (most common), eosinophilic, or granulocytic least common).
Full thickness (ie. surgical) bx are gold standard. N.B. What is seen grossly on endoscopy does not correlate with what is seen on histopathology
tx plan for IBD
Prior to biopsy, provided the patients were not hypoproteinemic, deworming protocol
elimination diet (single unique protein and carbohydrate, ideally home cooked for 2-4 weeks)
antibiotic trial (tetracycline, tylosin or amoxicillin 2-4 weeks) are all explored, often serially **With histopath supporting IBD, a strict hypoallergenic diet combined with immunosuppressive therapy and possible antibiotic therapy is indicated**
etiology of intestinal lymphangiectasia
Intestinal lymphatic obstruction leading to dilation, subsequent rupture of lacteals and resultant loss of protein, lymphocytes and chylomicrons at the same time as granulomas occur
cause of lymphatic obstruction is usually idiopathic, may be congenital or acquired (pericarditis, infiltrative mesenteric lymph node disease, infiltrative intestinal mucosal disease or congenital malformation).
clinical presentation of intestinal lymphangiectasia
diarrhea but not uncommon to have no hx of diarrhea and present for ascites. This disease has a high likelihood for protein losing enteropathy.
Diagnosis: Clinical path findings of hypoalbuminemia, hypocholesterolemia (+/- lymphopenia) are classic but not specific. Endoscopic appearance of snowball that leak chyle following biopsy is highly suspect but dx confirmed by histopathology. Full thickness bx may be particularly helpful with this dz.
signalment, PE findings & tx of perianal fistulae
Signalment- GSD most commonly affected breed (esp. mature intact male)
Clinical findings- constipation, odor, rectal pain/discharge
Dx- draining tracts typically present around anus or may palpate granulomas/abscesses rectally
Treatment-
- Cyclosporine (Neoral or Atopica) for 16 weeks or until 2 weeks past remission then taper to every other day and discontinue to use lowest effective dose to maintain remission
- Tacrolimus topical once daily for 16 weeks or until 2 weeks past remission then taper and discontinue or use lowest effective dose to maintain remission. Can use cyclosporine to induce partial remission then add tacrolimus when they are less painful/more tolerant of topical medication. . Most dogs will need tacrolimus EOD or 2x/week to maintain remission.
- Antibiotics /local cleaning for 2o infection for first 2 weeks
- Hypoallergenic diet frequently used as well and when $ issues make cyclosporine/ tacrolimus not possible, use prednisone
- Neuter
-
Surgery- only with failed medical therapy: surgical removal of draining tracts (incontinence risk), amputate tail, deroofing & fulguration using surgery/cryo/laser.
* Px: guarded* but can achieve remission and taper to lowest effective dose and potentially d/c meds. Continue hypoallergenic diet
tx of anal sac dz
impaction, sacculitis, abscessation & fistulation
- impaction*: periodic expression, local infusion of anti-inflammatory drugs, abx topical preparations, & high fiber diet.
- Infection:* systemic antibiotics, sac expression, lavage, infusion of antibiotic cream, & dietary change.
- *Failure of medical therapy (recurrence of the problem, or no improvement with therapy) is an indication for anal sacculectomy**. Usually both sacs are removed even if only one is involved. Treat infection, and control inflammation in local tissue before surgery to reduce hemorrhage and infection complications. Be sure to warn owners about the possibility of incontinence, fistulation, and infection before surgery.
causes of constipation
Pain (perianal disease or impaction with inappropriate foods), obstruction (stricture or pelvic fracture) or colonic weakness can cause constipation
etiology of megacolon
short & long term mgmt
Etiology: often idiopathic. It is thought that there may be abnormal colonic neurotransmitters.
Signalment: principally in cats
Treatment:
Acute care: de-obstipation with fluids, enemas and/or oral/rectal PEG solutions. Do not use phosphate containing enemas or detergent in the cat.
Chronic care: altered fibre of low or high, stool softeners (lactulose) and motility modifier (cisapride). A clean litterbox must be provided.
Surgical: Subtotal colectomy is a last resort
presentation of pancreatitis in dog vs cat
The cause of acute pancreatitis in dogs & cats is usually unk.
In cats, pancreatitis may be a single dz but may also be assoc w/ cholangiohepatitis, & IBD (then called triaditis) or assoc w/ either hepatic lipidosis (HL secondary to pancreatitis), diabetes (secondary to pancreatitis and hard to control when pancreatitis continues), or pulmonary thrombosis (sequelae to pancreatitis).
No pathognomonic signs of pancreatitis: Dogs most commonly have an acute pancreatitis with the following clinical signs commonly present: anorexia, lethargy, vomiting, fever, and abdominal pain (each of variable severity) (icterus, dyspnea, and diarrhea less common).
DDx will often include: AGE, IBD, gastrointestinal obstruction, peritonitis & acute renal failure
mild v severe pancreatitis mgmt
SUPPORTIVE CARE for severely affected cases: IV crystalloid fluid therapy, Potassium supplementation, Fresh frozen plasma transfusion, Colloids may be indicated, antiemetics, gastroprotectancts, Prophylactic broad-spectrum antibiotics (e.g., amoxicillin ± enrofloxacin depending on severity), Analgesia is an important aspect of caring for animals with pancreatitis, NPO until the parameters used to make a diagnosis return to normal? (classically 3-5 days in moderately affected dogs). In cats, we are more reluctant to keep NPO for prolonged intervals (hepatic lipidosis) and will feed via a nasoesophageal tube a liquid diet (Clinicare) to achieve at least partial daily caloric intake, Total or partial parenteral nutrition may be necessary if unable to feed enterally for a prolonged time (beyond 3 or 5 days??
SUPPORTIVE CARE for mildly affected cases 1) Keep NPO for at least 12 hours and then begin with oral alimentation as previously described.
2) Use subcutaneous fluids until vomiting ceases for 12 hours.
3) Re-assess often to decide if more aggressive supportive care (as noted previously) is required.
4) Analgesia: See above
what about plasma is useful in pancratitis
Fresh frozen plasma transfusion may be beneficial in cases that are deteriorating or in cases that have hypoalbuminemia or a coagulopathy like disseminated intravascular coagulation. It restores a more normal protease-antiprotease balance (alpha 2-macroglobulins).
what are some drugs that incr risk of pancreatitis
thiazide diuretics
furosemide
azathioprine
L-asparaginase
corticosteroids
sulfonamides and tetracycline
when should you start enteral feeding in a pancreatitis case
as soon as the pt can tolerate (vomiting controlled)
concept of feeding through pancreatitis is becoming more widely accepted
how is chronic pancreatitis managed in the cat
Chronic pancreatitis may result in exocrine pancreatic insufficiency (esp cats)
Cats are more likely to have difficult to diagnose low grade smoldering pancreatitis than dogs (this lesion is found commonly on post mortems) and may develop exocrine pancreatic insufficiency. In addition pancreatitis is a likely a common reason for hepatic lipidosis
Subclinical
Diagnostic dilemma –fPLI?
Treatment dilemma –must feed them!! Add Vitamin K. pancreazyme?
Only way they get EPI
Risk of DM
mgmt of pancreatitis in dog & cat
SUPPORTIVE CARE for severely affected cases: IV crystalloid fluid therapy, Potassium supplementation, Fresh frozen plasma transfusion, Colloids may be indicated, antiemetics, gastroprotectancts, Prophylactic broad-spectrum antibiotics (e.g., amoxicillin ± enrofloxacin depending on severity), Analgesia is an important aspect of caring for animals with pancreatitis, NPO until the parameters used to make a diagnosis return to normal? (classically 3-5 days in moderately affected dogs). In cats, we are more reluctant to keep NPO for prolonged intervals (hepatic lipidosis) and will feed via a nasoesophageal tube a liquid diet (Clinicare) to achieve at least partial daily caloric intake, Total or partial parenteral nutrition may be necessary if unable to feed enterally for a prolonged time (beyond 3 or 5 days??
SUPPORTIVE CARE for mildly affected cases 1) Keep NPO for at least 12 hours and then begin with oral alimentation as previously described.
2) Use subcutaneous fluids until vomiting ceases for 12 hours.
3) Re-assess often to decide if more aggressive supportive care (as noted previously) is required.
4) Analgesia: See above
what is the most common hepatopathy of cats?
why does it occur?
mgmt?
Px?
hepatic lipidosis (fatty liver)
may occur in association with underlying disease such a pancreatitis, neoplasia, small intestinal disease, or idiopathic
Obesity appears to be a predisposing factor and anorexia an inciting cause of hepatic lipidosis.
Tx:
Stabilization for 24 hrs prior to anesthesia for placement of feeding tube +/- liver aspirate/biopsy:
Fluids: replacement with appropriate potassium supplementation
Antiemetics if needed
Nasoesophageal feeding of liquid diet (Clinicare) at 1/3 to ½ of resting energy requirements once emesis under control
Vitamin K1
Place esophageal feeding tube or gastrostomy tube
Other therapies: S-Adenosylmethionine, L-carnitine, Vitamin E are not much proven benefit at this time.
Monitor for refeeding syndrome where phosphorus drops precipitously and a hemolytic crisis is induced
Px: Usually achieve complete resolution in the suppurative cholangitis/cholangiohepatitis cases while the chronic non-suppurative cases will likely continue to wax and wane despite tx though are unlikely to go on to die from the disease
what clinical pathology findings tell you re liver function
ALT
ALP
how to obtain a liver biopsy, risk factors & quality of the sample
Needle aspirate is quickest method requiring no sedation, but results are often very limited in the amount of information produced
Percutaneous needle biopsy requires sedation, special needles. Only a small blind sample is obtained and thus the area of pathology could be missed. ultrasound guidance is generally used to choose the site more specifically. There is danger of uncontrolled bleeding
Laparoscopic needle biopsy requires anesthesia and proper equipment. The laproscope can be used to examine color, texture of the liver
Surgical biopsy via exploratory laparotomy is the most effective method for producing a biopsy. A larger specimen can be obtained & surgical remedy could be done if warranted, relatively safe w/ exp surgeon
