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My 2017 RUSVM SAM 2 > GI Dr. Niblett 2/17/17- > Flashcards

GI Dr. Niblett 2/17/17- Flashcards

1
Q

What are common presenting complaints in GI cases?

A

Dysphagia (difficulty swallowing), Halitosis (bad breath), Drooling (pseudoptyalism vs ptyalism), difficulty eating (dropping food)

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2
Q

What type of hx info would you start out gathering?

A

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)

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3
Q

How would you start the exam?

A

At the head! With an external exam & limited internal exam.
include:

  1. general PE - (thin BCS, unkempt coat)
  2. exam of face for symmetry, swelling, drainage
  3. initial oral exam: note calculus, missing/broken teeth, gingival inflammation
  4. sublingual evaluation: finger between mandibles pushing up while opening mouth
  5. palatal and pharyngeal inflammation (FB)
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4
Q

If there was dysphagia but no oral lesions/pain what might you consider putting on your DDx list

A

neuromuscular disease affecting the oral, pharyngeal or cricopharyngeal phases of swallowing

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5
Q

what are examples of neuromuscular dz affecting oral, pharyngeal or cricopharyngeal phases of swallowing

A

Myaesthenia gravis (MG)

cricopharyngeal achalasia

rabies

tetanus

botulism

idiopathic cranial n. dysfunction

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6
Q

Where might a lesion be localized to with:

halitosis, ptylism, difficulty prehending food

A

oral cavity

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7
Q

what if no oral disease is seen what should you consider?

what might also be seen?

A

neuromuscular dz

dysphagia

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8
Q

what are ddx for a feline where you find

jaw chattering

irregular surface

broken teeth

A

FORL’s

Feline Odontoclastic Resporptive Lesions

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9
Q

what is etiology of FORLs

tx?

A

idiopathic

  • based on radiographic type:*
  • restore, extract, crown amputation*
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10
Q

which xrays are predictive in cat FORLs

A

xrays of 407 & 307 predictive of whether full dental rads needed

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11
Q

What is this?

what spp seen in?

A

lymphocytic plasmacytic stomatitis

felines

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12
Q

What is seen in this cat?

A

feline periodontitis on canine tooth

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13
Q

although we call is idiopathic what is one thought as to etiology of lymphocytic plasmacytic stomatitis?

signalment seen?

hx?

A

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

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14
Q

PE findings with lymphocytic plasmacytic stomatitis

how dx

tx

A

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

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15
Q

What are the 3 types of FORL classification

A

Type 1: incr. periodontal space -> removal tx

Type 2: decr. periodontal space (ankylosed) -> crown amputation

Type 3: mixed

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16
Q

differences between vomition & regurgitation

A
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17
Q

what is regurgitation indicative of

A

esophageal dz

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18
Q

which spp don’t vomit

A

rabbits

horses

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19
Q

why does regurg happen

A

motility disorders

  • Obstructive
  • Weakness
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20
Q

what are the 2 types of regurgitaion

A

physiological

pathologic

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21
Q

what are the 2 types of pathologic regurgitation

A

Obstruction

Weakness

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22
Q

what types of etiologies (big picture) of both obstruction & weakness are seen in each

A

congenital & acquired

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23
Q

what are some obstructive regurg dz

A

congenital v acquired

PRAA - congenital

  • FB*
  • Cicatrix (strictures)*
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24
Q

what are some Ddx for seen in regurg due to weakness

A

Congenital v acquired

neuromuscular junctional dz: Myasthenia gravis

neuropathy

  • esophagitis*
  • hypo T4 (Addison’s?)*
  • lead toxicity*
  • idiopathic*
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25
Q

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?

A

megaesophagus

pneumonia (aspiration)

Myasthenia gravis (MG)

yes

yes confirmatory diagnostics for MG

the pneumonia

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26
Q

What is a simple test for MG that can be done during office visit to point you towards dx

A

palpebral reflex fatigues!

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27
Q

how is megaesophagus managed

A

Bailey chair
Small volume / high calorie meals
Work up/Treat underlying problem
Manage aspiration pneumonia / monitor for recurrence

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28
Q

what are CC/CS of esophageal disorders

A

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

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29
Q

ddx for congenital megaesophagus

A

vascular ring anomaly

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30
Q

congenital megaesophagus

etiology

signalment

Ddx

tx

A

abn innervation to esophagus

present from birth w/ CS starting at weaning (may be breed related)

vascular ring anomaly (PRAA)

supportive care

31
Q

acquired megaesophagus/ idiopathic

what is significance of the disorder being idiopathic?

A

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

32
Q

what can be seen in this image

etiology/ common locations seen

signalment

CS

Dx

Tx

Px

A

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.

33
Q

esophageal cicatrix

signalment

CS

Dx

Tx

Px

A

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

34
Q

what is a leading cause for esophageal cicatrix in felines

A

oral doxycycline admin

make sure capsule moves through to stomach!

35
Q

esophagitis

etiology

Dx

Tx

A

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)

36
Q

name most common type of vascular ring anomaly that leads to obstructive esophageal dz

Tx

A

persistant right aortic arch

Sx

37
Q

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?

A

type of tx preferred: surgical v medical, how long to dx (emergent v non emergent: GDV vs ADR)

imaging! either radiographs or u/s

38
Q

what are 3 types of non-obstructive gastropathies

A
  • acute* gastritis
  • hemorrhagic gastroenteritis*
  • chronic* gastritis
39
Q

when thinking about chronic gastritis what should you think more about & why

A

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!

40
Q

what are 2 medically managed obstructive gastropathies

A

idiopathic gastric hypomotility

bilious vomiting syndrome

41
Q

what are 3 specific infiltrative gastropathies

A

Neoplasia

Pythiosis

Inflammatory Bowel Dz (really a gastroenteropathy!)

42
Q

what are 5 categories of gastropathies (problems) that can be specific to stomach

A

Acute gastritis

Chronic gastritis

Gastric outflow problems

Gastric ulceration

Infiltrative gastric dz

43
Q

What are DDx specific to stomach for acute gastritis problem

A

Bad food/rich food

FB

toxins

drugs

44
Q

What are DDX specific to stomach for chronic gastritis problem

A

IBD

helicobacter

physalopter

ollulanus

45
Q

What are DDx speccific to stomach for gastric outflow problems

A

idiopathic hypomotility

bilious vomiting syndrome

46
Q

What are DDx specific to stomach for gastric ulceration problem

A

shock

drugs

gastrinoma/MCT

helicobacter

IBD

local tumor

pythiosis

47
Q

what are DDX specific to stomach for infiltrative gastric disease problems

A

IBD

neoplasia

pythiosis

48
Q

Tx for acute gastritis

A

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

49
Q

risk factors for GI ulceration

how prevent

tx

A

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

50
Q

CC is acute onset vomiting a/o diarrhea, what type of problem might you call it

DDx

A

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

51
Q

dx of acute diarrhea

tx

A

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

52
Q

categories of dz assoc. w/ chronic diarrhea (chronic enteropathies or gastroenteropathies)

A

maldigestive/malabsorptive disease

chronic obstructive disease

neoplasia

functional intestinal disease (irritable bowel disease)

53
Q

what are maldigestive dx

A

Exocrine pancreatic insufficiency (EPI)

54
Q

what are ddx for malabsorptive dz

A

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

55
Q

how is EPI dx

tx

A

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.
56
Q

dx of IBD

A

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

57
Q

tx plan for IBD

A

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**
58
Q

etiology of intestinal lymphangiectasia

A

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).

59
Q

clinical presentation of intestinal lymphangiectasia

A

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.

60
Q

signalment, PE findings & tx of perianal fistulae

A

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-

  1. 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
  2. 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.
  3. Antibiotics /local cleaning for 2o infection for first 2 weeks
  4. Hypoallergenic diet frequently used as well and when $ issues make cyclosporine/ tacrolimus not possible, use prednisone
  5. Neuter
  6. 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
61
Q

tx of anal sac dz

impaction, sacculitis, abscessation & fistulation

A
  • 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.
62
Q

causes of constipation

A

Pain (perianal disease or impaction with inappropriate foods), obstruction (stricture or pelvic fracture) or colonic weakness can cause constipation

63
Q

etiology of megacolon

short & long term mgmt

A

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

64
Q

presentation of pancreatitis in dog vs cat

A

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

65
Q

mild v severe pancreatitis mgmt

A

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

66
Q

what about plasma is useful in pancratitis

A

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).

67
Q

what are some drugs that incr risk of pancreatitis

A

thiazide diuretics

furosemide

azathioprine

L-asparaginase

corticosteroids

sulfonamides and tetracycline

68
Q

when should you start enteral feeding in a pancreatitis case

A

as soon as the pt can tolerate (vomiting controlled)

concept of feeding through pancreatitis is becoming more widely accepted

69
Q

how is chronic pancreatitis managed in the cat

A

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

70
Q

mgmt of pancreatitis in dog & cat

A

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

71
Q

what is the most common hepatopathy of cats?

why does it occur?

mgmt?

Px?

A

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

72
Q

what clinical pathology findings tell you re liver function

A

ALT

ALP

73
Q

how to obtain a liver biopsy, risk factors & quality of the sample

A

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

My 2017 RUSVM SAM 2 (8 decks)

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