• hydrogen ions
• sodium
• potassium
• chloride
• water
• pepsinogen
• lipase
• mucus

• parietal
• CO2
• water
• bicarb
• in mucus layer protect mucosa from damage, with excess going into systemic circulation and excreted in urine

1. cephalic

2. gastric

3. intestinal

1. histamine
2. cholinergic vagal fibers
3. gastrin-secreting G cells in antrum

1. surface mucus
2. bicarb secreted by gastric epithelial cells
3. epithelial cell membranes
4. gastric mucosal blood flow
5. prolstaglandins and cytoprotection
6. basal membrane

caudal mesenteric vein, cranial mesenteric vein, splenic vein. also gastric veins

• signs are vague and nonspecific
• functional reserve and regenerative capabilities

• o   carb metab, glycogen storage, glycogenolysis, gluconeogenesis
• o   lipid metabolism 
• o   protein metabolism
• o   vitamin metabolism (fat soluble vitamin storage)
• o   immunologic function (Kupffer cells)
• o   detoxification and excretion
• o   digestive (bile acids)
• o  hematologic (factors I, II, V, VII, VIII, IX, X)

• bilirubiin
• steroids
• ammonia
• drugs

   symmetrical causes of hepatomegaly in cat:

• are associated with jaundice
•  lipidosis, cholangiohepatitis, lymphosarcoma

o   symmetrical causes of hepatomegaly in dog:

·         portal hypertension

·         hypoalbuminemia

which is liver specific, ALT or AST?

when is the greatest increases seen in these?

does the magnitude of increase correlate with severity of disease?

• ALT (AST also seen in muscle)
• necrosis
• no

dog presents ill. ALT 680 (10-100), ALKP 220 (10-100)?

a. hepatocellular

b. cholestatic

• albumin
• cholesterol
• BUN
• glucose
• bilirubin

• ammonia
• serum bile acids

PSS

hepatitis (acquired shunting)

·         marked increase in ALT

·         ALP much lower than ALT

·         bilirubin may be increased

o   persistent increases in ALT, ALP, (ALT>ALP)

o   decreased serum albumin

o   decreased urea nitrogen

o   bilirubinuria

o   abnormal bile acids

o   nonregen anemia

o   ↑↑↑ALP

o   ↑ or↑↑ ALT

o   ↑AST

o   normal or ↑GGT

• 1.      nausea-restless, sucking air, ptyalism, tachycardia, lip licking, decreased antral and duodenal tone
• 2.      retching-(min to hours after stage 1), sudden inspiratory movements against a closed glottis, relaxation of LES and retroperistalsis of jejunal and duodenal contents into stomach
• 3.      vomiting- repeated inspiration against closed glottis causes neg intrathoracic pressure. abdominal contractions force gastric and intestinal contents into esophagus. glottis protects airway

1. osmotic
2. secretory
3. exudative
4. disordered motility
5. mixed-usually this one

• o   unabsorbed fatty acids are hydroxylated by enteric bacteria
• o   change fluid and electrolyte movement
• o   ↑mucosal permeability
• o   ↓potential difference
• o   ↓mucosal cyclic AMP
• o   disrupt motor activity

• SI mucosal disease and EPI
•  severe villus atrophy in celiac sprue (gluten enteropathy)
•  severe canine IBD
• acute viral diseases (corona, rota, parvo)-crypt aplasia mucosal collapse
• acute bacterial and parasitic diseases (crypto, E. coli)

• usually secondary role, not the primary mechanism
• not enough time to absorb
• loperamide might trap the infective agent inside the GI tract and exacerbate 

• mediated by emetic center
• occurs when emetic center receives sufficient stim to reach threshold and initiate reflex
• reflex well developed in dogs and cats
• stim from highter brain centers (anxiety, anticipation)
• stim from cerebellum (motion)
• stim from viscera
• stim from extra-visceral sources
• effects of drugs/toxins on CRTZ (apomorphine, uremia, hepatotoxins, endotoxins, cardiac glycosides)

o   acute or chronic (~2 weeks)

o   relationship to eating

o   appearance (mucus, blood, food, grass, odor, hair)

o   diarrhea (before or after onset)

o   describe act (active or passive)

o   vomiting requires abdominal contractions, regurg is passive, effortless

o   vomiting features retching, premonitory signs, ptyalism, pacing, tachycardia, swallowing

o   regurg has few premonitory signs, but may have ptyalism in esophageal inflammation or obstructive disease

o   regurg may be semi-formed material, may smell fermented, contains mucus, never bile-stained.

o   both regurg and vomiting: pH variable-unreliable. time after eating variable

painful or difficult defecation. vocalizing common. can be assoc with perianal

fistulas, foreign bodies, obstructing tumor

·         severe straining-distal alimentary or urogenital systems

·         history and phys findings usually indicate system involved

·         if alimentary, then distal colon, rectum, or anus involved

o   dietary and environmental, stress (esp in hospital)

o   painful defecation

o   obstruction (or orthopedic)

o   neuro (spinal cord disease)

o   endocrine and metabolic

o   drug-induced

• swallowed air as in brachycephalics
• bacterial degradation, esp. with soy

§  nutrient malabsorption-colonic bacterial degradation

§  dietary sensitivity

·         chemical poisoning

·         PSS in cats

·         oral disease (stomatitis in cats)

·         esophageal foreign body

·         nausea

·         direct oral (lingual) stim

·         bitter pills in cats (metronidazole)

·         esophagitis

·         topical flea treatment

o   decreased nutrient intake

o   maldigestion/malabsorption

o   malassimilation

o   excessive utilization

o   increased loss of nutrients

which are not a part of the GI microbiota?

bacteria, fungi, viruses, protozoa, archaea

• dyschezia is obviously painful, but can be productive or accompanied by tenesmus. dyschezia can indicate a perianal fistula, foreign body, or obstructing tumor.
• tenesmus is usually a non-productive straining. tenesmus can be due to urogenital or alimentary systems (in which case, caudal GI tract implicated)

only 5% are culturable because:

1. optimal growth conditions unknown or unobtainable

2. most are anaerobic

3. most require synergistic interactions with other microbes

real-time PCR, FISH

• great variability, but core microbiome is often fairly similar among individuals
• in cats there are higher duodenal counts and more anaerobic bacteria

·         gastric acid

·         bile (and bile salts and VFA's in colon) 

·         intestinal motility

·         intestinal mucus

·         immune response

·         bacteriocins produced by bacteria

• methanogens (archaea)- convert hydrogen to methane which interferes with fermentation
• sulfate-reducing bacteria (non-archaea)- convert hydrogen to hydrogen sulfite (damaging to intestinal epithelium)

·         chronic pancreatitis (dogs) and tumors of pancreas and bile duct (cat) are most common causes.

o   marked increase ALP (always higher than ALT)

§  star gazing, head pressing, seizures, behavior changes

intrahepatic-smaller dogs

extrahepatic-larger dogs

§  lo protein, hi qual diet

§  lactulose

§  +/-neomycin, amoxicillin

§  ameroid constrictor

§  cellophane banding

§  interventional

prebiotics: 

§  nondigestible dietary carbs

§  promote growth of good bacteria (Lacto and Bifido especially)

§  increased short chain fatty acids which provide energy for colonocytes

probiotics:

§  living microorg

§  survive gastric acid/bile

symbiotics: 

mixture of both

difficult or painful swallowing

·         oral disease-tooth root abscess, tongue, etc

·         pharyngeal disease-e.g. Labradors getting sticks stuck in the throat, masses, caustic burn

·         cricopharyngeal disease-e.g. muscle cannot relax

o   difficulty prehending food/chewing, gagging, coughing,   nasal discharge, aspiration pneumonia,  secondary pharyngitis/tonsillitis, and facial muscle atrophy can indicate what? 

1. treat underlying disease

2. treat cricopharyngeal achalasia (failure to relax)

myotomy or botox (not permanent, helps dx)

3. 3. PEG or E-tube

dog-entirely striated

cat-proximal 2/3 is striated, distal 1/3 smooth

o   primary peristaltic wave-carry-on of pharyngeal wave thru upper esophageal sphincter

o   secondary peristaltic wave-stimulated by stretch in esophagus (for residual material)

emetic center

CRTZ

the BBB is permeable at the CRTZ for emetic substances

K, Cl, Na

metabolic alkalosis due to loss of HCl, unless lots of duodenal fluid (hi in bicarb) is lost

3x

10x

20x

1. crypt- undifferentiated cells/secretory
2. maturation 
3. tip-absorptive

IgA

1. promote phagocytosis

2. activate alternative complement

3. prevent GI absorption of macomolecules

4. inhibit development of protozoal infection

1. mechanism responsible 

2. temporal (chronic vs acute)

3. anatomical location

4. functional (similar causes)

5. etiological (specific cause)

what is an example of each classification of diarrhea?

(osmotic, secretory, exudative, disordered motility, mixed)

osmotic-EPI

secretory-E. coli

exudative-IBD, parasitic, bacterial, PLE, C. perfringens

disordered motility-no example given, usually secondary

mixed-TGE, parasitic, tumors, colitis

1. esophageal inflammatory disease
2. extraluminal esophageal compression
3. intraluminal esophageal obstruction
4. neuromuscular dysfunction

microbiota-all living microorganisms that inhavit the GI tract. (previously microflora)

microbiome-mutual interaction of microbiota with host cells

• bacteria communicat with host via TLR's and dendritic cells to stimulate a normal developed immune system. 
• participates in "colonization resistance" by competing for O2, nutrients, mucosal adhesion and creating a barrier against nonresident bacteria

1. antibiotics

2. rapid diet changes

3. dietary indiscretion

4. surgical intervention

5. EPI

pharyngeal and upper esophagus-dysphagia and regurgitation

esophageal body- regurgitation and ptyalism

distal esophagus-inappetence and ptyalism and regurgitation

1. inflammatory disease (esophagitis)
2. extra-luminal obstruction (PRAA)
3. intra-luminal obstruction (stricture, foreign body)
4. neuromuscular disease (megaesophagus)

• salivation, regurg, inappetence, dysphagia, repeated attempts at swallowing
• endoscopy

• o   resting? PEG tube
• o   sucralfate-orally to coat esophagus (can’t use with tube)
• o   increase LES tone (transition of skeletal to smooth muscle)-cisapride, metoclopramide
• o   reduce acid output- omeprazole
• o   pain meds-opioids, oral mouth rinses (lidocaine and bismuth)

• german shepherds, irish setters
• smaller than littermates
• regurg starts concurrent with intro of solid food (6-8 weeks)

• PRAA, thymoma, hilar lymphadenopathy, cervical masses, intrathoracic tumor
• survey thoracic radiographs with contrast, contrast CT helpful, endoscopy

·         foreign body, anesthesia, drugs, tumor, esophagitis

·         regurg, salivation, wt loss, inappetence, aspiration pneumonia

·         contrast esophagram or endoscopy

• o   balloon dilation-may need multiple times, not as reusable
• o   Bougienage-metal tubes that taper to a point, push in progressive sizes. reusable, cheaper
• o   stenting
• o   intralesional steroids
• o   mitomycin C
• o   omeprazole
• o   sucralfate
• o   can prevent worsening by treating immediately     

o   thoracic inlet

o   heart base

o   distal esophagus

• Great danes, german sheps, irish setters, mini schnauzers

·         toxicity: lead, organophosphate, hypoadrenocorticism, hypothyroidism ??

·         myasthenia gravis, polyneuritis, polymyositis

·         idiopathic

radiographs (esp. contrast), Ach receptor Ab test, CK, EMG, ACTH stim test

• ·         Tx: symptomatic and supportive
• ·         nutrition-feeding in elevated position
• ·         pyridostigmine gor myasthenia gravis
• ·         prednisone for myositis

1. acute gastritis
2. gastric foreign body
3. gastric dilatation volvulus

• anorexia, acute vomiting, polydipsia, lethargy, depression, food/bile-stained mucous vomit with hematemesis, dehydrated, abdominal pain or discomfort
• gastric foreign body, acute pancreatitis, hemorrhagic gastroenteritis, infectious diseases causing enteritis like distemper, toxin ingestion, drugs, intestinal foreign body, acute renal failure

·         most effective for acute self limiting vomiting is brief fasting. maropitant if continous vomiting

·         rest intestinal tract, protect mucosa, maintain hydration, bland diet (low fat, chicken/rice)

removal by endoscopy, exploratory laparotomy, gastrotomy

watch and supplement K to metabolic alkalotic patients

• o   lymphoplasmacytic (idiopathic)
• mostly idiopathic, similar to IBD
• may be assoc with food responsive 
• vomiting most consistent, hematemesis, appetite changes,  maybe some discomfort, maybe some wt loss
•  biopsy
• diet trial: hypoallergenic (hydrolyzed), bland diet
• Tx: omeprazole, pepcid in cats, cisapride/metoclopramide (prokinetics), immunomodulation in mod to severe disease (pred, azathioprine for dogs, clorambucil for cats)
•  
• o   eosinophilic
• §  unknown cause
• §  eosinophils infiltrate mucosa
• §  mucosa may be ulcerated
• position of relief
• §  Rotties predisposed
• §  treat by dietary manipulation (novel protein) and steroids
• 
  also granulomatous, atrophic

•  reflux of bile into stomach is normal in the dog, cleared by peristalsis
• defect in pyloric function or a gastric motility defect allows prolonged contact of bile with mucosa
• bile is a detergent-damages cells! (fats)
•  characterized by chronic vomiting of bile-stained material after prolonged fast
• most often in early morning
• tx: increase feeding frequency (feed last thing at night, and early AM), feed low fat
• cisapride or metaclopramide
• H2 receptor antagonists
• §  cimetidine, ranitidine, famotidine
• §  ranitidine is prokinetic
• proton pump inhibitor
• §  omeprazole

what is diagnosed with Warthin-Starry stain in biopsy?

•  steroids and NSAIDS
•   liver diseasepancreatitis
• sepsis, DIC
• hypoadrenocorticism
•   tumors (mast cell, gastrinoma)
•  protein-calorie malnutrition
• uremia
•  stress

·         GDV

·         congenital stenosis

o   pyloric muscular hypertrophy

o   bostons, boxers, bulldogs, cats

o   signs start at weaning

·         acquired stenosis

o   antral pyloric mucosal hypertrophy

o   lhaso apso, pekingese, shih tzu

o   older male small breed

• foreign bodies

• vomiting past 12 hours after feeding, intermittent (projectile) vomiting
• hypoK, Cl, metabolic alkalosis 
• dx: signalment, survey rads (beak sign), endoscopy
• tx:  Y-U pyloroplasty or pyloromyotomy

   

• adenocarcinoma in dogs in antrum 
• lymphomas in cats
• sudden anorexia, anemia, diarrhea, hematemesis,  weight loss, middle-aged to older dog, inappetance, chronic vomiting

Physalloptera rara and Ollulanus tricuspis

pyrantel pamoate and fenbendazole respectively. 

self-resolving or life-threatening,

small intestine or large intestine

• §  helminthes
• ·         ascarids
• ·         hookworms-often worst signs
• ·         whipworms
• §  protozoa
• ·         coccidia-SI
• ·         giardia
• ·         cryptosporidium
• ·         tritrichomonas
• o   bacterial
• §  Clostridium-enterotoxin (perfringens and difficile)
• §  E. coli
• §  Salmonella
• §  Campylobacter-healthy animals have this too.
• o   viral
• §  parvovirus
• §  coronavirus

• type I-doesn’t cause enteric disease; abortion, not a big deal
• type II-  causes severe enteritis
• 2, 2a, 2b, 2c (more severe)
• o   related to feline panleukopenia
• o   resistant to Abx, freezing, heating, detergents
• o   need to bleach
• o   fecal-oral transmission
• o   incubation 3-7 days
• o   virus shed in feces (also in subclinical dogs)
• o   sub-clinical infections may occur
• o   oropharyngeal lymph node replication
• o   bone marrow-leukopenia (esp neutropenia)
• o   villi short, irregular, fused, blunted
• o   loss of villi, loss of neutrophils into lumen, exposed lamina propria

fluid and plasma(or albumin) replacement, prevention of hypokalemia, injectable antiemetics, and broad spectrum Abx. possible omega interferon, prokinetics and H2 receptor antagonists to prevent reflux esophagitis

Abx: SQ amikacin (keep hydrated bc kidney disease), enrofloxacin (in immature animals-cartilage damage)

• acute v/d progressing to dysentery
• cause unknown but possibly anaphylactic response to bacterial endotoxin
• usually 2-4 yrs old
• mini schnauzers susceptible
•  intravascular space dehydration (hypovolemia), so skin turgor is still normal, doesn’t look like classic dehydration

• o   PCV>60%, TP normal bc protein loss as well, thrombocytopenia, metabolic acidosis, shock, ↓BP

§  highly contagious

§  young, before vx or exposure

§  not vx’d a lot of times bc it’s in enviro, exposed to by mother.

§  highly variable

§  sudden onset of diarrhea,

§  less dramatic than parvo

§  dual infec with  parvo is possible, or alone.

§  orange, malodorous rarely hemorrhagic diarrhea

§  no fever, leukopenia

§  spontaneous resolution 8-10days

fill out the following chart:

1. duration
2. diet
3. progression
4. appetite
5. weight loss
6. appearance of feces
7. frequency of defecation
8. vomiting
9. tenesmus
10. environment
11. breed

• cbc/chem panel,
• small intestine diarrhea: TLI, abdominal imaging, folic (low in malabsorptive dz), cobalamin (low in SIBO or mucosal dz), biopsy, response to therapy
• large intestine diarrhea:  Trichuris (whipworm), Tritrichomonas, diet change, rationaly therapy (metronidazole or sulfasalazine), colonoscopy, referral 

• low albumin<2à protein loss enteropathy à intestinal biopsy
• normal albuminà non-protein loss enteropathyà do a serum TLI

what is most important for conducting a diet trial? 

only parts you can reach, and not full thickness, and not jejunum

·         idiopathic

·         stomach, SI, LI or combo

·         infiltration of lamina propria

o   lymphs, neuts, eos, plasma cells

·         loss of tolerance to bacteria or food antigens

o   TLR’s

o   alterations in T reg lymphs

·         clinical signs due to mucosal cell infiltrates AND inflam mediators

·         release of complement, prostanoids, leukotrienes, pro-inflam cytokines, NO, free radicals

·         german sheps, lundehund, basenji, irish setter, soft coated wheaten terriers,

·         stress in cats

o   vomiting most freq sign

o   retching, fluid, non-assoc with feeding times, rare hematemesis

o   intermittent or continuous (maybe stress related)

o   acute or chronic

o   role of stress

o   abdominal pain

o   diarrhea-usually small bowel

o   triaditis: IBD, chronic pancreatitis, and cholangiohepatitis

o   possibly due to bile and pancreatic duct merging (more chance of reflux of pancreatic juices up with bacteria

o   lethargy

o   changes in appetite ↑ or ↓

o   loss of BW and condition

o   hairball accumulation

mesenteric LN↑↑

o   diarrhea

o   large, small, or both bowels

o   vomiting may be present

o   borborygmus and flatus

o   halitosis

o   abdominal pain

o   pica, polyphagia

o   NOT: IBS is human dz

o   edema/ascites (not in cats!)

o   mesenteric LN↑ (less than cats)

• dogs have more diarrhea, cats vomit more
• dogs have ascites/edema
• cats get more mesenteric lymph node enlargement
• dogs can get polyphagia, cats have variable appetite changes

what is key to diagnosing IBD?

how should the report be handled?

what microscopic signs should one look for?

• biopsy any obvious lesions, then go systematically down the GI tract surgically (except the colon still endoscopically).
• MUST EXCLUDE OTHER CAUSES OF INFLAMMATION
• get the report to interpret degree of inflammation
• look for crypt abscesses, mucosal atrophy, villous atrophy/fusion, fibrosis, epithelial erosion, lymphangiectasia, bacteria

o   mild to mod dz in SI

§  diet

§  pred (immunosuppressive, then taper down)

§  metronidazole

o   severe dz in SI

§  azathioprine for dogs

§  chlorambucil for cats

§  cyclosporine

o   mild dz in LI

§  diet

o   moderate to severe dz in LI

§  sulfasalazine

§  prednisone

o   BOXERS, other breeds

o   LI diarrhea

o   poorly responsive to immunosuppressants

o   enrofloxacin seems to work

§  remember chondro effects of fluoroquinolones

o   probably more infectious than IBD,

o   invasive E. coli. 

o   causes PLE

o   most are secondary

o   predominant in Yorkshires

o   chronic, intermittent diarrhea

o   wt loss, edema, pleural effusion, ascites

o   hypoproteinemia, lymphopenia, hypocholesterolemia, hypocalcemia, hypomagnesemia (in yorkies)

o   dx: intestinal biopsy

o   tx: treat underlying disease!

§  lo fat diet

§  anti-inflams

o   increased bacteria and abnormal host response

o   german shepherds

o   tylosin, amoxicillin, metronidazole/enrofloxacin can be helpful

o   these may have to be longterm therapy

acinar cells: NaCl, water, digestive enzymes and cofactors

duct cells: NaHCO3, water

what is the function of PSTI?

turns off trypsin

• enzymes sep from lysosomes
• proteases formed and secreted as zymogens
• PSTI secreted in parallel with trypsinogen
• enterokinase is extrapancreatic 
• low intracellular calcium

• indiscriminant eating, obesity, hi fat diet, malnutrition, hypertriglyceridemia, drugs, toxins, hypercalcemia, duct obstruction, duodenal reflex, pancreatic trauma, parasites, pancreatic ischemia
• middle-aged to older, mini schnauzers, yorkshire, silky terriers, miniature poodles. siamese cats

• acute gastroenteritis, (HGE)
• exacerbations of IBD
• gastric or intestinal foreign body
• peritonitis
• acute renal failure
• hemorrhagic gastroenteritis
• gastric ulcer

• dog: neutrophilia and left shift, thrombocytopenia, maybe anemia
• cat: anemia, hemoconc, leukocytosis, leukopenia
• azotemia, hypoalbuminemia, hyperglycemia, hypocalcemia, hyperlipidemia, hyperbilirubinemia, increase liver enzyme activity

what is the treatment for pancreatitis?

·         fluid replacement with potassium if needed

·         rest pancreas. nutrition is important. E/NE tubes within 24-48 hours recover quicker. early enteral nutrition. j tubes? no difference

·         TPN

·         parenteral Abx-usually not needed. bac translocation or true infection.

·         analgesics- important! opioids- buprenorphine, oxymorphone, fentanyl patch, epidural

o   lidocaine, ketamine CRI, or epidural catheter

·         blood, plasma, or plasma expander-----maybe

·         surgical exploration-not anymore

·         low fat diet with clinical improvement and gradual. moderate fiber

• lack of pancreatic enzymes
• dogs, degenerative atrophy
• German sheps and assoc breeds
• cat-chronic pancreatitis
• polyphagia with concurrent weight loss and steatorrhea
• voluminous soft stool
• dx: TLI test
• tx: powdered enzymes (viokase, pancreazyme)
• oral Abx for SIBO
• Cobalamin

• waxing/waning and vague
• decreased appetite
• lethargy
• swollen abdomen (ascites/hepatomegaly)
• jaundice
• ptyalism
• vomiting
• neurologic signs (enceophalopathy)
• weight loss

o   neutrophilic form

§  acute or chronic

§  ascending E. coli infection?

§  not necessarily middle age to older cats

§  anorexia, fever, vomiting, jaundice

§  +/- abdominal pain

§  chronic disease is milder

o   lymphocytic form

§  immune-mediated?

§  triaditis

§  not more common in younger cats

§  Persians

§  jaundice, ascites, wt loss, hepatomegaly

§  obesity

§  disease-induced weight change

§  pancreatitis, stress, boarding, weight reduction, FLUTD

§  rapid weight loss in short time

§  decreased caloric intake

·         negative nitrogen balance

o   anorexia with weight loss in obese cats, but fat pads intact

o   1-3 week duration

o   jaundice

o   hepatomegaly

o   hepatic encephalopathy

o   marked muscle wasting

o   rads: enlarged liver

§  tx underlying

§  nutritional support (60-90kcal/kg/d)

·         NE, E, or G tubes

·         hi protein diet (restrict carbs?)

·         Vit E, K

§  appetite stimulant

·         oxazepam

·         valium (not generic diazepam?)cats-idiosyncratic hepatic necrosis. anecdotally, is generic, not injectable. 

·         cyprohepatadine

·         mirtazapine

§  general supportive therapy

§  depends on biopsy

§  neutrophilic

·         fluoroquinolone, metronidazole

·         potentiated penicillin

o   clavamox

§  lymphocytic form

·         prednisone 2mg/kg/d

·         ursodeoxycholic acid

·         Vit E, SAMe

·         chlorambucil

• ·         fibrosis makes liver stiff, can’t distend to accept fluid. fluid pushed back into portal vein, hypertension into splancnic system.
• ·         reach for Lasix? --> metabolic alkalosis and hypokalemia can worsen hepatic encephalopathy. spironolactone is a better choice. 

What could the following indicate?

o   persistent increases in ALT, ALP, (ALT>ALP)

o   decreased serum albumin

o   decreased urea nitrogen

o   bilirubinuria

o   abnormal bile acids

history: waxing and waning recurrent, nonspecific ADR

• toxins-xylitol, acetaminophen, sago palms
• infections-lepto
• drugs-methimazole in cat, anticonvulsants, immunosuppressants
• idiopathic

what does the following suggest?

acute symptoms

o   marked increase in ALT

o   ALP much lower than ALT

o   bilirubin may be increased