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90 Cards in this Set

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What are the phases of deglutition?
oropharyngeal phase
-oral: prehension of food
-pharyngeal: bolus propelled from oropharynx to upper esophageal sphincter (UES) in laryngopharynx
-cricopharyngeal: UES relaxes to allow bolus to enter esophagus

esophageal phase
-food moved aborally via 1º (initiated by swallowing) & 2º (initiated by luminal distension) peristalsis
-dog’s esophagus is all striated muscle, while distal 1/3-1/2 of cat’s esophagus is smooth muscle

gastroesophageal phase: less important in dogs & cats
-relaxation of lower esophageal sphincter (LES) allows food to enter stomach
What are some breed predispositions to diseases assoc. w/ dysphagia or regurg?
boston terrier: hiatal hernia
bulldog: vascular ring anomaly, hiatal hernia, cleft palate
great dane: megaesophagus
shar-pei: hiatal hernia
What are some important hx points when working up dysphagia &/or regurg?
get a description of the act: regurg, vomiting, retching, gagging, or coughing?

if regurg, is it oropharyngeal or esophageal?

any trauma or caustic substance ingestion (foreign material, meds, plants)?
What are some important PE procedures when working up dysphagia &/or regurg?
observe the animal eating
thorough oropharyngeal exam: often requires general anesthesia
check for pain assoc. w/ mouth opening
palpate muscles of mastication, jaw, LN’s, salivary glands, retropharynx, neck
assess cranial nerves
evaluate resp. system for signs of aspiration pneumonia
How is oropharyngeal dysphagia differentiated from esophageal dysphagia?
oropharyngeal dysphagia: dysphagia common, +/- regurg (immediate), ptyalism, gagging, multiple swallowing attempts common, +/- poor drinking ability, +/- dropping food

esophageal dysphagia: +/- dysphagia*, regurg common, +/- ptyalism*, multiple swallowing attempts; gagging uncommon, normal drinking ability, no food dropping
How is regurgitation differentiated from vomiting?
regurg: no nausea, no abdominal effort, no retching, immediate to delayed expulsion of food (sec – hrs), typically undigested & bile free

vomiting: associated nausea (anxiety, lip smacking, drooling), **abdominal effort**, +/- retching, immediate to delayed expulsion of food (min - hrs), partially digested, bile stained, pH < 5
What are some ddx for dysphagia?
periodontal dz
stomatitis/gingivitis
mass lesions
-neoplasia: SCC, FSA, melanoma, epiludes, papillomas
-sialocele
trauma: bone fx, tooth fx, soft tissue laceration
neuromuscular dz
-CN V, VII neuropathy
-masticatory muscle myositis
What are some ddx for regurgitation?
megaesophagus
-congenital: idiopathic
-acquired: idiopathic, esophageal obstructive lesion, esophagitis, myasthenia gravis, Addison’s, hypothyroidism, lead toxicity, SLE

esophageal obstructive lesions
-foreign bodies
-benign stricture
-vascular ring anomaly
-hiatal hernia: brachycephalic breeds: lax LES --> reflux esophagitis

esophagitis: often 2º to reflux, hiatal hernia, FB, medications
What are some ddx for concurrent dysphagia AND regurgitation?
inflammatory or painful esophageal conditions: esophagitis, FBs, hiatal hernia
What is the diagnostic algorithm for working up oropharyngeal dysphagia?
R/O structural dz: oropharyngeal exam under anesthesia, +/- MDB (minimum database: CBC/Chem, U/A), FeLV/FIV (cat), cytology, bx, dental &/or skull films

work up functional dz: detailed neuro exam, MDB, fluouroscopic barium swallow, +/- AchR Ab, T4, extended neuro workup
What are some clinical signs assoc. w/ swallowing disorders?
painful swallowing (odynophagia), exaggerated swallowing & head movements, gagging, drooling, halitosis, dropping food, inappetance/anorexia, nasal d/c (ingesta regurgitated into nasopharynx), cough & dyspnea (d/t aspiration pneumonia)
What is the diagnostic algorithm for working up esophageal dysphagia?
R/O structural dz: chest & neck films, +/- static or dynamic barium swallow, esophagoscopy

work up functional dz: MDB, T4, AchR Ab, +/- ACTH stim, Pb level, ANA, extended neuro workup
What are some etiologies of esophagitis?
chemical injury: refluxed acid & bile, caustic substances

physical injury: FB
What are some clinical & historical features of esophagitis?
hiatal hernia: brachycephalic dogs predisposed
-hole in diaphragm at point where esophagus goes thru --> cardia of stomach may be seen in thorax on rads

hx of recent anesthesia, vomiting, or FB/caustic ingestion
-recent anesthesia --> GE reflux --> esophagitis

regurgitation AND dysphagia common
esophagitis

a. dx
b. tx
c. px
a. barium swallow may be suggestive (regional hypomotility, irregular mucosa) & ID potential cause (GER, hiatal hernia)
-definitive dx: endoscopy +/- bx

b. remove insult (ex. FB, doxycycline)
-gastric acid inhibition (proton pump inhibitors or H2 blockers) --> ↓ acid injury to denuded mucosa
-prokinetics (Cisapride, Metoclopramide) --> ↓ gastric reflux by improving LES tone & gastric emptying
ABs: ↓ 2º bacterial involvement
+/- Sucralfate: binds to positively charged necrotic tissue
+/- esophageal rest & nutritional support: gastric feeding tube
c. guarded to excellent depending on severity & cause
-most common complications: stricture, aspiration
benign esophageal stricture (cicatrix)

a. etiology
b. clinical & historical features
a. inflammation extending to submucosa & muscularis layers --> fibrous CT formation
b. >60% of strictures occur post-anesthesia
-progressive regurgitation (solids, then liquids) +/- dysphagia if esophagitis
benign esophageal stricture (cicatrix)

a. dx
b. tx
c. px
a. barium swallow usually suggestive: regional narrowing
-definitive dx: esophagoscopy
b. bougienage (breaks stricture) or balloon dilation
-post dilation: gastric acid inhibition & prokinetics as for esophagitis
-intralesional or oral steroids: ↓ fibrous CT reformation
c. variable
-grave if perforation occurs: biggest complication (don’t overdilate)
-liquid diets usually well tolerated
-can be costly: avg. of 2-3 procedures required
What are the stimuli for vomiting?
vomiting center in brainstem receives input from:
peripheral receptors: inflammation, distention, hyperosmolality
-found in all abdominal visceral, esp. proximal GI tract
-heart in cats?

chemoreceptor trigger zone: blood borne (drugs, toxins, etc.)

higher centers: pain, fear, stress, CNS pressure/inflammation

vestibular system: inner ear dz, motion sickness
What are the 3 clinical phases of vomiting?
nausea: restlessness, anxiety, hiding, attention seeking, ptyalism, swallowing motions, lip licking, tachycardia
retching
expulsion of digesta
What are some breed predispositions & diseases assoc. w/ vomiting?
boxer: MCT
brachycephalic breeds: pyloric stenosis
great dane & other large dogs: GDV
miniature schnauzer: pancreatitis, HGE
acquired megaesophagus

a. primary etiologies in dogs
b. primary etiologies in cats
c. common clinical signs
a. idiopathic, or caused by a neuropathy, myopathy, or myasthenia gravis
b. gastroesophageal reflux, hiatal hernia
c. regurgitation, or cough w/ a little or no obvious regurg, +/- severe weight loss
acquired megaesophagus

a. dx
b. tx (for idiopathic megaesophagus)
a. plain or contrast rads: generalized esophageal dilation w/o evidence of obstruction
look for underlying cause: AchR test, ACTH stim, T4
b. dietary therapy: gruel from elevated platform, several small meals per day, +/- gastrostomy tube
cisapride: usually not helpful unless concurrent GE reflux
if asp. pneumonia: IV fluids, ABs
hiatal hernia

a. etiology
b. signs
c. dx
e. tx
a. diaphragmatic abnormality that allows part of stomach to prolapse into thoracic cavity
severe cases: lax lower esophageal sphincter --> GE reflux
may be congenital or acquired
b. regurg, may be asymptomatic
c. plain or contrast rads: herniation may be intermittent & hard to detect
occ. found on U/S
d. if symptomatic in young animal: sx more likely to be required to correct
older animals: aggressive medical therapy of GE reflux (cisapride, omeprazole) often sufficient
-if not, sx can be considered
What are some important history questions related to vomiting?
description of act & appearance of vomit
-confirm vomiting vs. regurg
-duration
-relationship to eating
* >10-12 hrs & vomiting food: abnormal motility or gastric outflow obstruction
* > 10-12 hrs & vomiting bile/saliva: may indicate reflux gastritis (bilious vomiting syndrome)
-severity
*blood
*projectile: suggests gastric outflow obstruction
*vomitus that looks/smells like feces: suggests intestinal obstruction
-diet & environment
*FB access
*dietary indiscretion
*potential for GI pathogens
-vaccination, deworming status
-medications
-systems check: PU/PD, C/S/V/D, appetite, wt. loss, attitude
*establish if primary GI vs. extra-GI dz
*severity & chronicity
What are some important parts of the PE for vomiting?
assess demeanor/posture
-hunched, tucked in abdomen may indicate back or abdominal pain
assess hydration & nutritional status
look for oral FB: cats
palpate thyroid: cats
examine abdomen in detail: pain masses, organomegaly, gut thickness, stool quality
always perform a rectal exam
What are some common causes of acute vomiting

a. primary GI causes
b. extra GI causes
a. dietary factors/indiscretion: overeating, abrasive material, toxins, food sensitivity
-acute gastritis or gastroenteritis (ex. HGE, parvo, passing FB)
*most infectious diseases also have diarrhea
-obstructive lesions (ex. FB, GDV, intusussception)
-GI ulcers (ex. NSAIDs, MCT)
*more commonly cause chronic vomiting

b. acute pancreatitis
-Addison’s (dogs), hyperthyroidism (cats)
-acute liver failure, renal failure, prostatitis, pyometra, peritonitis
-septicemia
-drugs: chemo, ABs
-motion sickness, vestibular dz
What are some common causes of chronic vomiting

a. primary GI causes
b. extra GI causes
a. bilious vomiting syndrome
-IBD
-GI neoplasia
-partial/recurrent obstruction (ex. gastric FB, pyloric stenosis)
-GI ulcers
-GI parasitism, fungal infection, viral (FIV, FeLV, FIP)

b. chronic pancreatitis
-liver dz, renal failure, prostatitis
-Addison’s (dogs), hyperthyroidism (cats)
-heartworm dz (cats)
What are some common causes of hematemesis/melena?
coagulopathy: thrombocytopenia

swallowed blood

GI erosions/ulcers
-idiopathic chronic gastritis, IBD, hookworms, GI neoplasia, MCT, NSAIDs
-acute pancreatitis, Addison’s liver failure, renal failure
What is the symptomatic therapy for a well patient w/ acute vomiting?
-fast for 12-24 hrs
-introduce small frequent bland meals
+/- empirical deworming
+/- IV or SQ fluids
+/- mucosal/intestinal protectants (sucralfate, bismuth subsalicylate (Pepto Bismol): avoid in cats, kaopectate, zinc carnosine (Gastricalm): new)
bicarb, mucus, local PG secretion
+/- antiemetics: metoclopramide (not very effective for peripheral causes of vomiting), prochlorperazone, ondansetron (Zofran), maropitant (Cerenia): close to 100% ↓ in peripherally induced vomiting
*use when vomiting is persistent & adequately investigated
What is the diagnostic plan for a sick patient w/ acute vomiting?
CBC/Chem, U/A (& T4 in cats > 6 yo)
-ID extra-GI dz, assess hydration, acid-base status, electrolytes
-hypochloremic metabolic alkalosis: uncommon, but highly suggestive of GI obstruction
*indicates preferential vomiting of gastric contents
*vomiting dogs are usually acidotic
+/- fecal tests (float, direct smear, parvo & Giardia Ag): more important if concurrent diarrhea
abdominal rads: obstructive lesions, FB, perforation, peritonitis (R/O surgical abdomen)
+/- abdominal U/S, serum PLI, ACTH stim
What is the diagnostic plan for chronic vomiting?
food trial: elimination diet (often done 1st)
CBC/Chem, U/A, +/- T4 (older cats)
FeLV/FIV +/- HW test (cats)
fecal float/centrifugation: Physaloptera
+/- PLI
+/- cobalamin, folate
abdominal imaging
-rads &/or U/S: obstructive lesions, organ abnormalites, help w/ bx (U/S)
-contrast rads: more useful for acute vomiting
endoscopy or ex lap: GI ulcers, FB, masses, obtain bx
HGE

a. etiology
b. clinical signs
c. dx
d. tx
a. uncertain, possible intestinal anaphylaxis (gut is a shock organ in dogs), role of Clostridium toxin?
b. peracute onset of hematemesis +/- hematochezia (small dogs)
c. presumptive based on hx, PE, ↑ PCV w/ normal TP, response to fluid therapy
d. aggressive fluid therapy +/- ABs (ex. Clindamycin: anti-anaerobe effects for possible Clostridium)
IBD

a. etiology
b. clinical signs
c. dx
d. tx
a. uncertain, immune mediated mechanisms involved (food, bacterial & endogenous epithelial Ags), abnormal microbial pop’ns (people & cats w/ IBD have ↑ # of harmful bacteria)
b. chronic vomiting, diarrhea, wt. loss, inappetance
c. intestinal bx: non-specific mucosal inflammation
R/O infectious & neoplastic causes of inflammation
d. elimination diet: start w/ this unless severe IBD
ABs: Metronidazole, Tylosin (R/O AB responsive enteropathy)
immunosuppressive therapy: Pred, azathioprine, chlorambucil
other: omega 3 FAs, prebiotics (ex. fiber), probiotics, cobalamin supplementation
pancreatitis

a. risk factors
b. dx
c. tx
a. dietary indiscretion, hyperlipidemia (ex. Miniature schnauzers), any endocrine dz w/ hypercholesterolemia (DM, Cushing’s, hypothyroidism)
b. definitive: serum PLI
Chem: inc. amylase/lipase (dogs), pre-renal azotemia, modest hyperglycemia, hypocalcemia, inc. ALP, ALT, moderate hyperbilirubinemia, hypercholesterolemia, hypoalbuminemia
abdominal rads, abdominal U/S
c. remove inciting cause
NPO +/- J tube
IV fluids
anti-emetics
analgesics
+/- broad spectrum ABs
+/- heparin
bilious vomiting syndrome

a. etiology
b. clinical signs
c. dx
d. tx
a. may be caused by GE reflux that occurs when dog’s stomach is empty for long periods (ex. during an overnight fast)
b. pet vomits saliva + bile stained fluid SID, usually late at night or in morning just before eating
c. suggestive hx; R/O obstruction, GI inflammation, extra-GI dz
d. feed dog an extra meal late at night to prevent stomach from being empty for long periods
-if vomiting persists, gastric prokinetic may be given late at night to prevent reflux
parvoviral enteritis

a. pathogenesis
b. clinical signs
c. dx
d. tx
a. preferentially invades & destroys rapidly dividing cells: BM progenitors, intestinal crypt epithelium
b. diarrhea, vomiting, intestinal bleeding, subsequent bacterial invasion
c. hx, PE findings, neutropenia, fecal Ag ELISA
d. fluids + KCl +/- colloids
analgesics
broad spectrum ABs: ampicillin + amikacin
anti-emetics
gastric foreign bodies/obstruction

a. etiology
b. clinical signs
c. dx
d. tx
a. vomiting may result from gastric outflow obstruction, gastric distension, or irritation
b. vomiting, anorexia, or asymptomatic
c. abdominal palpation, abdominal rads, contrast rads, endoscopy, hyokalemic hypochloremic metabolic alkalosis consistent w/ gastric outflow obstruction
d. induce vomiting if safe else sx or endoscope removal of object
What are the 4 mechanisms of diarrhea?
inc. osmolality: osmotically active unabsorbed substrates in intestinal lumen (malassimilation) --> intraluminal water retention

inc. secretion: crypt cell secretion exceeds villus absorption

inc. mucosal permeability: gut mucosal barrier disruption or ↑ hydrostatic pressure --> loss of plasma proteins & fluids into intestinal lumen

deranged motility: more rapid gut transit time
What are some important hx questions for patients w/ diarrhea?
get a stool description
-duration, severity, progression, painful?
-differentiate small bowel from large bowel diarrhea
diet & environment
vaccination, deworming status
medications
systems check: PU/PD, C/S/V/D, appetite, wt. loss, attitude
-establish if primary vs. extra-GI dz (often small bowel diarrhea)
What are some important parts of the PE for patients w/ diarrhea?
demeanor/posture, hydration/nutrition, thyroid palpation (cats), abdomen palpation in detail, rectal exam
How can small bowel & large bowel diarrhea be differentiated?
small bowel: ↑↑ volume,
normal frequency to ↑ frequency (2-4x/day),
color change, melena, steatorrhea, foul odor common,
no tenesmus/dyschezia,
vomiting, wt. loss, polyphagia, flatus/borborygmus common

large bowel: normal to ↑ volume, ↑↑ frequency ( > 4x/day), mucus, hematochezia common, tenesmus/dyschezia common, +/- vomiting
What are some common causes of acute diarrhea

a. primary GI
b. extra GI
a. dietary factors/indiscretion
inflammatory/infectious: HGE, parasites, bacterial (Campylobacter, Salmonella, Clostridium, E. coli), parvo, coronavirus, FeLV/FIV
b. fairly uncommon to have acute diarrhea only
acute pancreatitis (colitis), Addison's, sepsis/toxemia, drugs
What are some common causes of chronic small bowel diarrhea

a. primary GI
b. extra GI
a. dietary, idiopathic (food responsive, AB responsive, IBD), lymphangiectasia, neoplasia
b. EPI, liver failure, renal failure, Addison's, hyperthyroidism
What are some common causes of chronic large diarrhea

a. primary GI
b. extra GI
a. dietary (fiber responsive), idiopathic (food responsive, AB responsive, IBD), infectious (histiocytic colitis: boxers, whips, T. fetus, C. perfringens), neoplasia
b. renal failure (uremic colitis), pancreatitis (colitis)
What is the tx plan for a well patient w/ acute diarrhea?
fast 12-24 hrs
small frequent “bland” meals: nonabrasive, highly digestible, fat restricted (dogs)
empirical deworming
+/- fluid therapy
+/- intestinal protectants
+/- motility modifiers
What is the diagnostic plan for a sick patient w/ acute diarrhea?
CBC/Chem, U/A
fecal tests: direct smear, float/centrifugation, +/- sedimentation, parvo or Giardia ELISA
other fecal tests: rectal/fecal cytology, fecal culture, InPouch TF (cats)
What is the diagnostic plan for a patient w/ chronic diarrhea?
CBC/Chem, U/A
T4, FeLV/FIV: cats
+/- TLI
+/- cobalamin, folate
fecal tests: direct, float, Giardia ELISA, InPouch TF (cats), +/- rectal cytology, +/- fecal α-1 protease inhibitor
abdominal imaging: rads, U/S, +/- contrast
endoscopy vs. ex lap: GI bx
What is the symptomatic therapy for chronic diarrhea?
empirical deworming: Fenbendazole SID x 3 d.
fiber response trial: fiber supplementation (ex. Metamucil), esp. for chronic large bowel diarrhea
elimination diet trial
AB response trial: Metronidazole, Tylosin
other: omega 3 FAs, probiotics
EPI

a. common cause in dogs
b. common cause in cats
a. pancreatic acinar cell atrophy (immune mediated?)
b. chronic pancreatitis --> progressive destruction of acinar tissue (often have concurrent DM)
EPI

a. clinical signs
b. dx
c. tx
a. predominant signs are wt. loss +/- small bowel diarrhea
may have pica, coprophagia, rarely steatorrhea
feces often look just like food
b. ↓ TLI (<2.5 ug/dl in dogs is diagnostic)
c. pancreatic enzyme supplementation
+/- parenteral cobalamin (esp. cats)
+/- ABs if poor response (possible SIBO): Metronidazole, Tylosin
ddx for weight loss despite a good appetite
malabsorption/maldigestion: chronic small intestinal dz, EPI
endocrinopathies (excessive catabolism): DM, hyperadrenocorticism, hyperthyroidism
PLE
PLE

a. ddx
b. clinical signs
c. dx
a. IBD, intestinal neoplasia (esp. LSA), lymphangiectasia
b. effusions (pleural &/or peritoneal), small bowel diarrhea, wt. loss
-however, stools can be normal
c. panhypoproteinemia, hypocholesterolemia, & lymphopenia
-differentiate from poor liver function: ↓ albumin & cholesterol only (not globulin)
extensive GI workup including gut bx
fecal α-1 protease inhibitor used for early detection
PLE

a. tx
b. px
a. varies w/ cause
for lymphangiectasia & IBD:
-ultra low fat diet (↓ lacteal engorgement), elimination diet
-prednisone +/- other immunosuppressants
b. may or may not be able to have complete resolution
potential complications warrant immediate workup
ex. thromboembolic dz: panhypoproteinemia --> hypercoaguable state
What are some important hx questions in patients w/ dyschezia/constipation?
get a description of defecation & stool
-straining to defecate vs. urinate (esp. in cats)
normal posture, normal stool, pain?
diet & environment: foreign material, poor quality diet?
trauma: old pelvic fx
scooting or licking anus?: signs of anal irritation
systemic questions
What are some important parts of the PE in patients w/ dyschezia/constipation?
evaluate posture/gait: orthopedic pain?
-ex. lumbosacral dz, severe OA
palpate caudal abdomen carefully: colon contents, bladder, prostate, masses
examine perineum, anus, & rectum in detail (+/- sedation)
-ex. perineal hernia, anal dz, prostate or rectal masses, medial iliac ln’s
neurological function: anal tone, perineal sensation, tail function, hind limb proprioception
What are some common causes of constipation & dyschezia?
painful/inflammatory lesions: colitis/proctitis, prostatitis, anal sacculitis, perinanal fistula
obstructive causes: perineal hernia, prostatomegaly
motility disorders: idiopathic megacolon
misc: dehydration, dietary (ex. bones)
What diagnostic tests can be used for patients w/ dyschezia/constipation?
CBC/Chem, U/A
-R/O metabolic dz --> ↓ colonic motility
-ID sepsis: “toxic colon”
T4 (dog): hypothyroidism is a rare cause of constipation
survey abdominal films: R/O fx, masses, FB
U/S not very helpful: can’t see back in pelvic canal
rectal exam & enema +/- sedation
+/- colonoscopy or barium enema: obstructive lesions (stricture, colonic/rectal mass)
idiopathic megacolon

a. etiology
b. clinical signs
c. dx
d. tx
a. unknown, but generalized colonic smooth muscle disturbance (vs. neurologic cause) is suspected
b. infrequent defecation, straining to defecate, inappetance/anorexia, vomiting, poor body condition
c. PE, R/O other obstructive or functional causes of constipation (dietary, behavioral, metabolic, & anatomic causes)
-massively dilated colon on palpation or abdominal rads
d.
medical
-remove impacted feces: multiple warm water retention & cleansing enemas over 2-4 days
-fluid therapy +/- ABs if depressed/anorexic
-fecal softeners (fiber supplementation, DSS) or osmotic laxatives (lactulose, miralax)
-prokinetics: cisapride (has a colonic effect)

if medical therapy fails, subtotal colectomy is indicated
What are some important hx questions in patients w/ suspected hepatobiliary dz?
any behavioral/neurologic signs?
-worst postprandially (esp. after high protein meal)?
diet/environment
vaccine, deworming status
medications, incl. past anesthetic recovery
systems questions: abnormalities common
What are some important parts of the PE in patients w/ suspected hepatobiliary dz?
assess body stature, demeanor, gait
examine mm, sclera, skin for icterus, bleeding tendencies, hepatocutaneous syndrome
assess hydration & nutritional status
examine abdomen in detail: pain, masses, hepatomegaly, fluid
perform rectal exam: melena, acholic feces
- ~90% of patients w/ liver failure have GI ulceration  +/- melena
What are some non-specific clinical signs of hepatobiliary dz?
nausea, vomiting, diarrhea
anorexia, wt. loss
lethargy, depression
small body stature: PSS
may be a normal animal w/ ↑ liver enzymes
What are some more specific clinical signs of hepatobiliary dz?
icterus
abdominal enlargement: ascites
hepatomegaly
PU/PD (dogs)
acholic feces
coagulopathy
CNS dysfunction: hepatic encephalopathy (HE)
urinary tract signs (urate stones): PSS
hepatic encepalopathy

a. mechanism
b. signs
a. reversible neurologic syndrome: NT dysfunction d/t NH3 accumulation
b. behavioral abnormalities: personality change (aggression), mental dullness
staggering, ataxia, circling, head pressing
seizures (cats > dogs)
coma
ptyalism (cats)
ddx for hepatomegaly

a. generalized
b. focal/asymmetric
a.
infiltrative
-neoplasia: primary or metastatic
-lipid: hepatic lipidosis
-glycogen: Cushing's, glucocorticoids
-reticuloendothelial hyperplasia: common w/ any chronic inflammatory dz
passive congestion: RHF, pericardial dz
b. neoplasia, nodular hyperplasia
ddx for icterus

a. prehepatic
b. hepatic
c. posthepatic
d. misc
a. hemolysis
b. hepatic lipidosis, chronic hepatitis or cholangiohepatitis, generalized neoplasia, drug or toxin induced injury, infectious (lepto, infectious canine hepatitis, FIP, Histoplasmosis, toxo)
c. pancreatitis
cholangitis or cholecystitis
neoplasia: pancreatic, biliary, duodenal
bile duct rupture
d. sepsis
ddx for ascites
hypoproteinemia: liver, gut, or renal origin

portal hypertension (PH): ↑ hydrostatic pressure in portal system
-prehepatic PH: obstruction of v. before liver (uncommon); portal v. hypoplasia, portal v. thrombus, hepatic AV fistula
-intrahepatic PH: end stage liver dz (most common); hepatic or biliary cirrhosis, hepatic neoplasia
posthepatic PH: R heart failure: ↑ in pressure in caudal vena cava --> back up in pressure to portal system; pericardial dz, caudal vena cava obstruction (HW dz, neoplasia)

↑ vascular permeability/lymphatic obstruction: hepatobiliary & intra-abdominal neoplasia, pancreatitis
What are some common CBC findings assoc. w/ hepatobiliary dz?
microcytosis: PSS
poikilcytosis: d/t alterations in lipoprotein metabolism
evidence of sepsis: liver failure
What are some differences in interpretation of ALP in cats vs. dogs?
any increase is significant in cats d/t short T1/2
not induced by drugs
What are the 5 serum biochem markers of poor liver function?
dec. BUN, cholesterol, albumin, glucose
inc. bilirubin
What are some liver function tests?
serum bile acids: NOT useful if hyperbilirubinemic: can't distinguish b'twn hepatic & post-hepatic icterus
fasting plasma NH3 &/or NH3 tolerance test: NOT affected by causes of post-hepatic icterus
coag profile: recommended prior to liver bx
What types of abdominal imaging can be used in patients w/ hepatobiliary dz?
surveys rads: evaluate liver size, fluid, masses
U/S: differentiate hepatic vs. post-hepatic icterus, guide FNA & tru-cut bx
colorectal scintigraphy or portal venography or CT: PSS
What are some hepatic sampling procedures?
FNA (cytology): most useful for detecting vacuolar hepatopathies (lipid, glycogen) or LSA
tru-cut bx: small sample --> questionable diagnostic accuracy
laparascopic or surgical bx: sx preferred if therapeutic correction of condition possible
portosystemic shunt

a. etiology
b. dx
c. tx
a. congenital: usually single vessel, normal portal pressure
acquired: multiple vessels, high portal pressure --> shunt development
b. microcytosis, biurate crystals, inc. bile acids often > 100 (caution w/ Maltese), resting NH3 +/- NH3 tolerance test (not if signs of HE), abdominal imaging (U/S to detect shunt vessels), +/- colorectal scintigraphy
c.
surgical ligation: 80% success rate
medical therapy: control signs of HE
-reduced protein diet
-dec absorption of NH3: lactulose, ABs (Metronidazole or neomycin)
What are some clinical differences b'twn congenital & acquired PSS?
congenital: young age, small body stature, no icterus, HE present, no ascites, no hepatomegaly, +/- uroliths

acquired: normal body stature, +/- icterus, HE, ascites, hepatomegaly, uroliths rare
What are some etiologies of canine chronic hepatitis?
familial
drug associated: phenobarb
infectious: ICH, lepto?
idiopathic
canine chronic hepatitis

a. signs
b. clin path data
c. dx
d. tx
a. icterus, V/D, wt. loss, ascites
b. persistently inc. ALT +/- inc. ALP, GGP, +/- abnormal liver function tests
c. liver bx AND R/O infectious or drug induced causes
d. remove insult
high quality protein diet
dec. pathologicc processes based on liver bx:
-dec. Cu accumulation: zinc, d-penicillamine
-dec. inflammation & fibrosis: glucocorticoids +/- colchicine
-antioxidants: vit. E, SAM-e, ursodiol, silymarin
What are some causes of extrahepatic bile duct obstruction d/t:

a. intraluminal obstruction
b. extraluminal compression
a. cholelithiasis, inspissated bile, flukes (cats)
b. pancreatitis, neoplasia, stricture
What are some complications of hepatobiliary dz that require medical intervention?
HE: diet, lactulose, metronidazole or neomycin
ascites: diet, diuretics, abdominocentesis
GI ulcers: acid suppression
coagulopathy: vitamin K, plasma, heparin
sepsis: ABs
hepatic lipidosis

a. etiology
b. clinical signs
a. idiopathic: usually obese cat that becomes anorexic d/t some stressful event
secondary: cat becomes anorectic d/t another illness (top 3: pancreatitis, cholangiohepatitis, IBD)
b. icterus, intermittent vomiting, dehydration, anorexia, HE (depression, ptyalism)
hepatic lipidosis

a. dx
b. tx
a. definitve: liver FNA or bx (lipid vacuolation in hepatocytes)
Chem: hyperbilirubinemia, ↑ ALT, ↑ ALP
•GGT normal or only slightly ↑ as would be expected w/ other cholestatic hepatobiliary dz
abdominal rads: hepatomegaly
abdominal U/S: generalized hyperechoic liver
additional tests to look for concurrent illnesses
b. complete nutritional support: goal is to feed w/in 24 hrs
•can try appetite stimulants (ex. diazepam, cyproheptadine) w/ cats that are minimally affected
•IV fluids
•nasoesophageal tube: give liquid enteral diet
•when stable, can place a more permanent feeding system (esophagostomy, gastrostomy tube) under general anesthesia
+/- vitamin K supplementation (liver dz)
+/- antiemetics, gastric acid inhibitors
treat known concurrent & possibly precipitating illnesses
acute abdomen

a. concerns w/ penetrating abdominal trauma
b. concerns w/ blunt abdominal trauma
a. size of external injury bears NO relation to extent of internal injury
only takes 1 hole in bowel or gallbladder to cause peritonitis & death
if instrument of injury entered abdomen, abdomen should be explored ASAP
b. usual surgical injuries include significant hemorrhage, ruptured urinary tract, hernias
What is a quick approach to a patient w/ acute abdomen of unknown cause?
quick hx
use signalment to point you in right direction
PE: concentrate on location of abdominal pain, presence of masses, dilation of bowel, presence of fluid, & integrity of abdominal wall
assess CV status of patient & start treating immediately
proceed to imaging, aspiration, lavage
decide if patient needs further stabilization or immediate sx
What are some common PE findings in animals w/ acute abdomen?
attempt to localize pain & determine if PE findings suggesting cause of pain are present
common findings: ↑ or ↓ borborygmus, gas or fluid filled bowel, abdominal masses, abdominal fluid, inability to palpate normal abdominal structures, organomegaly
signs of shock: pale mm, rapid thready pulse, cold extremities, slow CRT
What are some major categories of conditions of organ systems that require surgical correction in patients w/ acute abdomen?
•organ is losing its blood supply & becoming necrotic
•organ is malpositioned
•organ is leaking into peritoneal cavity --> peritonitis
•organ is obstructed
•organ is infected & needs to be removed or drained
•there is bleeding that must be stopped
What are signs of sepsis on CBC/Chem?
neutrophilic leukocytosis w/ L shift +/- monocytosis
↑ ALP
↓ albumin: vessels get leaky
↓ glucose: consumed by bacteria
toxic neutrophils
inappropriate release of nRBCs: BM cranking out WBCs, sometimes nRBCs get out
What are some abdominal radiographic findings in patients w/ acute abdomen that suggest the need for sx?
•free gas in abdomen: leakage from GI tract
•free peritoneal fluid: easier to see on U/S
•obvious organ enlargement or displacement: ex. GDV, pyometra, splenic torsion
•intestinal obstructive pattern or obvious FB
•bunching of intestines: linear FB
•loss of diaphragmatic detail: diaphragmatic hernia
What are some U/S findings in patients w/ acute abdomen that suggest that sx is needed?
•hypoechoic areas: suspected abscesses or hematomas
•free peritoneal fluid
•obvious organ enlargement or displacement
•loss of blood flow to an organ
What is the definitive test as to whether sx is needed in a patient w/ acute abdomen?
abdominocentesis

U/S guided or peritoneal lavage
What abdominocentesis findings in a patient w/ acute abdomen suggest that sx is needed?
creatinine in abdominal fluid > serum creatinine: probable urine leakage
green staining of fluid: bile leakage
PCV in abdominal fluid similar to blood PCV in animal that is not stable: indicates active bleeding
vegetable fibers in fluid: bowel leakage
bacteria in fluid or glucose < 50 mg/dl: presence of infection (may not work in cats)
-BFG: blood/fluid glucose difference
> 2000 WBC/µL or > 500 degenerative neutrophils/ µL: severe peritoneal irritation
lactate > 5.5 mmol/L (dogs): d/t anaerobic metabolism by bacteria
-BFL: blood/fluid lactate difference
high amylase/lipase: pancreatitis likely (NOT a surgical dz)
feline cholangitis

a. etiology
b. dx
c. tx
a. unknown: immune mediated
often accompanied by IBD (80%), pancreatitis (50%)
b. ↑ ALP, ↑ ALT
U/S: distended bile ducts & gallbladder, inspissated bile
bile culture +/- liver bx
c. acute cholangiohepatitis: ABs for 4-6 wks
lymphocytic cholangitis: long term corticosteroids
ursodiol: avoid if bile duct obstruction
nutritional support