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64 Cards in this Set

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Distinguish between dysphagia, regurgitation, and vomiting.
1. Dysphagia-Difficulty swallowing characterized by difficult prehension and swallowing, repeated swallowing, drooling. Localizes to the oral cavity and pharynx.
2. Regurgitation-Passive backward flow of food from the esophagus characterized by occurring soon after a meal, no prodrome of nausea or retching, food will be undigested. Localizes to the esophagus; no neural reflex involved.
3. Vomiting-Forceful expulsion of ingesta, fluid, bile or mucus, characterized by salivation, retching and abdominal contractions, has no temporal relation to eating. Localizes to the stomach, SI, LI (rare), or due to metabolic disease.
Common differentials for Oral dysphagia.
Idiopathic stomatitits-gingivitis
Periodontal disease
Foreign body in the mouth or pharynx
Ulcers-due to metabolic disease, immune-mediated disease, or eosinophilic granuloma complex of cats.
Hypoglossal nerve dysfunction
Oral dysphagia-Chronic gingivostomatitis of cats
Causes: Idiopathic, may be associated with feline calicivirus or immune-mediated response to oral microflora.
Diagnosis: Symmetrical proliferation of tissue, ulceration, and gingivostomatitis. Rule out all other possible causes-culture any abscesses or deep recesses; if lesions are asymmetrical, biopsy.
Treatment: Dental cleaning, then observe for improvement/recurrence; antibiotics, analgesics, immune-suppressive therapy (pred or cyclosporine). If medical therapy unsuccessful, consider laser thermoablation, or complete extraction of all molars and premolars.
Prognosis: Most require chronic therapy with glucocorticoids and antibiotics. May see complete resolution with full extraction.
Pharyngial dysphagia
Causes: Functional neuromuscular disease (myasthenia gravis or neuropathy), or morphologic disease (FB, neoplasia, trauma)
Diagnosis: Contrast fluoroscopy to localize to the pharynx; diagnostics for specific metabolic or neuromuscular causes.
Treatment: Fix underlying cause if identified. Symptomatic-elevated feeding, different food consistencies
Prognosis: Poor unless identifiable, treatable underlying condition. Most common complication is aspiration pneumonia.
Common differentials of regurgitation.
Motility disorders-Myesthenia gravis, hypoadrenocorticism
Obstructive lesions-Foreign bodies
Inflammatory-Esophagitis, gastroesophageal reflux
Idiopathic
Acquired megaesophagus
Causes: Idiopathic most common; Myasthenia gravis, systemic lupus, Addision's are most common identifiable causes.
Clinical presentation: Middle age and older dogs.
Diagnosis: Rule out underlying causes (MG testing, ACTH stim, etc). Chest radiographs, and contrast esophagram.
Treatment: Treat underlying disease if identifiable, may resolve. Feed in upright position, gastric feeding tube, small frequent meals. Promotility drugs have little benefit, and can worsen signs due to tightening of the lower esophageal sphincter.
Prognosis: Poor, most die from malnutrition or aspiration pneumonia.
Congenital megaesophagus
Cause: Probable defect in vagal afferent innervation.
Clinical presentation: <1 year of age, regurgitation usually first noted at time of weaning.
Diagnosis: Chest radiographs, contrast esophagram.
Treatment: Symptomatic
Prognosis: Guarded. Some cases may resolve as the animal ages. Early diagnosis and management to avoid aspiration pneumonia is key.
Esophagitis
Causes: persistent vomiting, gastroesophageal reflux, hiatal hernia, trauma, drug induced (specifically NSAIDs and doycycline).
Clinical presentation: depends on cause. Drug induced is most common in cats.
Diagnosis: Radiographs rule out strictures, megaesophagus, etc. Endoscopy.
Treatment: Prevention is best (chase pills with water or food, warm saline lavage and aspiration of esophagus if reflux during anesthesia). Medications: Sucralfate, corticosteroids, analgesics. Famotidine or Omeprazole may be used to prevent esophagitis from reflux. Metoclopramide helps by emptying gastric content and tightening the lower esophageal sphincter.
Prognosis: Good for mild to moderate. If severe, can lead to stricture.
Esophageal foreign body
TREAT AS AN EMERGENCY
Causes: bones, rawhides, fish hooks, hairballs, and greenies are most common.
Clinical presentation: Young and small breed dogs most commonly affected. Thoracic inlet, heart base, and diaphragmatic hiatus are most common locations.
Diagnosis: Radiographs, esophagram
Treatment: attempt to pull out or push into stomach with an endoscope. Surgical removal best to avoid, but needed if necrosis, perforation, or if FB has sharp edges.
Prognosis: Guarded to good if removed within 24-48 hours.
Esophageal stricture
Causes: persistent vomiting, gastroesophageal reflux, hiatal hernia, trauma, drug induced.
Diagnosis: Thoracic radiographs, esophagram, esophageal endoscopy
Tratment: Balloon dilation, or stenting (if available).
Prognosis: Good to poor depending on severity and duration.
Vascular ring anomaly
Cause: Persistant right 4th aortic arch; esophagus is trapped in vascular ring that is formed.
Clinical presentation: identical to clinical megaesophagus.
Diagnosis: Radiographs, esophagram; dilation will be at the heart base.
Treatment: Surgical correction
Prognosis: Fair to good.
Summarize the process of emesis (pathways that stimulate it), and the mechanisms by which specific antiemetics work.
Ultimate stimulation of emesis comes from the Emetic Center, which receives input from four pathways.
1. CRTZ is sensitive to drugs, toxins, and metabolic derangement.
2. Vestibular system is responsible for motion sickness.
3. Visceral abdominal receptors are sensitive to distention or irritation of the GI and biliary tracts, peritoneum, and pharynx.
4. The cerebral cortex stimulates vomiting in response to anxiety, pain, or behavoir.
Antiemetics:
1. Maropitant (Cerenia)-blocks signals from the vestibular center and at the emetic center.
2. Dolasetron and ondansetron block signals from the CRTZ and at the emetic center.
3. Metoclopramide-blocks signals from visceral input, as well as from the CRTZ. Also has prokinetic effects.
4. Phenothiazines (chlorpromazine, prochlorperazine)-block signals from the CRTZ, and at the emetic center.
Formulate a differential diagnosis list for the acutely vomiting patient.
Non-GI:
1. Metabolic-Hypercalcemia, Hepatic, Renal, PANCREATIC, Endocrine.
2. Inflammation
3. Infection
4. Neoplasia
5. Neurologic
6. Pain
Primary GI:
1. Infectious-Parvo, Distemper, Infectious Hepatitis; also bacterial and parasitic (less common).
2. Inflammatory-Dietary indiscretion.
3. Nutritional-Food Allergy.
4. Obstructive-Foreign body, hairball (cats).
5. Toxic-NSAIDs, Antibiotics, Narcotics.
6. Neoplasia
7. Hypomotility-Outflow obstruction (FB, volvulus) more common than neurologic causes (ileus, dysautonomia).
Formulate a diagnostic plan for the vomiting patient.
1. History and PE!-Important to differentiate vomiting vs. regurgitation. Rectal exam and hydration status are most important. Characteristics of vomitus can give clues as to cause. (See chart on pg. 20)
2. Lab testing:
a. CBC-Chronic GI bleed looks like iron-deficiency anemia. Neutrophilia=bacterial. Eosinophilia=food allergy, parasites, or Addisions.
b. Chem-Abnormalities may indicate vomiting due to metabolic disease.
c. Urinalysis-rule out renal failure or ketoacidosis.
d. Fecal float-parasites.
e. Others-Parvo, ACTH stim, PLI/amylase/lipase, food trials.
3. Imaging-radiographs, contrast radiographs, ultrasound, and endoscopy are used to identify foreign bodies, masses, infiltrative disease, ulceration, decreased motility, delayed gastric emptying, and many other physical defects in the GI.
4. Exploratory laparatomy-must rule out metabolic disease before surgery, but exploratory is a good tool when imaging and other diagnostics fail to reveal a cause and animal does not respond to symptomatic treatment.
Formulate a theraputic plan for the vomiting patient.
1. NPO for 24-48 hours
2. Fluid therapy-may give SQ if mild dehydration; hospitalize and give IV if more severe. Saline and LRS are good initial options. Fluids may also be used to address electrolyte and acid/base imbalances.
Fluid rate=deficits+maintenance+ongoing losses.
3. Electrolytes-Potassium supplementation is the most common that will need to be ADDED to fluids (20 mEq/L is standard; 0.5mEq/kg/hr max if deficit is bad).
4. Antiemetics-Maropitant, dolasetron or ondansetron, metocloprimide, or phenothiazines depending on desired effect and cause of vomiting.
Gastroduodenal erosions/ulcers
Causes: Develop due to damage of the mucosal barrier. Primary causes include NSAID therapy, high dose glucocorticoid therapy, chronic liver disease, renal failure, Addison's disease, hypersecretory tumors, or tumors that disrupt the mucosa.
Diagnosis: Best detected with endoscopy
Treatment: Sucralfate, Misoprostol (best for NSAID induced, will prevent NSAID induced), antacids
Prognosis: Good
Physalloptera induced vomiting
Cause: Physalloptera nematodes
Diagnosis: routine fecal float or seeing worms during gastroscopy. Difficult to diagnose.
Treatment: Pyrantel pamoate, fenbendazole, or ivermectin.
Ollulanus tricuspis induced vomiting
Cause: Ollulanus tricuspis. Only occurs in cats!
Diagnosis: Microscopic exam of vomitus.
Treatment: Fenbendazole
Helicobacter associated vomiting
Cause: Helicobacter spp.
Diagnosis: Biopsy of GI mucosa in a clinical patient with no other determined cause of gastritis. This organism does occur in clinically normal animals.
Treatment: Amoxicillin (+/- metronidazole or clarithromycin), and antacids/GI protectants
Lymphocytic or lympholasmacytic gastritis
Causes: Idiopathic
Diagnosis: Biopsy of GI tract
Treatment: Best management is unknown.
Eosinophilic gastritis
Causes: Mast cell tumors, lymphoma; hypersensitivity to foods; migrating parasites
Diagnosis: Detection of masses, response to food elimination trials/hypoallergenic diet, response to deworming.
Treatment: Treat underlying cause. Corticosteroids may have some effect.
Delayed gastric emptying/gastric motility disorders
Causes: gastric-outlet obstruction such as mucosal hyperplasia, muscular hypertrophy, neoplasia, eosinophilic granuloma, mycoses, foreign bodies, and external lesions near the pylorus; or gastric motility disorders such as metabolic diseases, inflammatory diseases, electrolyte imbalances, neurologic disease, or drug therapy. Primary gastric motility disorders are rare.
Diagnosis: History of repetitive vomiting of large amounts of partially digested food several hours after eating. Exclusion of metabolic diseases with CBC/Chem/Lytes/UA, and parasites with fecal float. Survey radiographs, barium contrast studies, or other imaging.
Treatment: Surgical correction of antral pyloric hypertrophy, tumors, or polyps; removal of foreign bodies. Treatment of underlying cause if identifiable. Semi-liquid, fat and protein restricted diet. Prokinetics.
Define diarrhea.
Increase in one or more of the following: frequency, fluid content, or volume of the bowel movement.
Be able to distinguish between small and large bowel diarrhea.
Small: normal to increased volume, melena, normal to mild increase in frequency, weight loss, and possible vomiting.
Large: normal to decreased volume, mucus and hematochezia; weight loss and vomiting uncommon.
Basic diagnostic plan for the diarrhetic patient.
History and PE-characterize the diarrhea!
CBC/Chem/Lytes/UA
Fecal float, +/-parvo, giardia, etc.
Other tests: ACTH, cobalamine/folate, and PLI
Imaging
Biopsy
Trial therapy: Food, fenbendazole or metronidazole, antibiotics
Differential diagnosis list for small and large intestinal diseases.
Add me in when PPT is posted
Canine Parvovirus
Cause: Parvovirus. Occurs most commonly in puppies <6 months of age, most are unvaccinated. Spread by fomites. Viremia occurs 3-5 days after ingestion.
Clinical signs/characteristics: Malabsorptive diarrhea, protein-losing enteropathy, severe leukopenia. Anorexia, theargy, vomiting, profuse hemorrhagic diarrhea, dehydration. +/-Sepsis and DIC.
Diagnosis: Fecal ELISA, however only 40-50% sensitive. CBC/chem/lytes findings may increase suspicion. Rule out other causes.
Treatment: Aggressive fluid and antibiotic therapy! Give fluids IV, supplement dextrose, KCl, and vit B as needed. Use broad spectrum antibiotics. May also give antiemetics and gastroprotectants as needed.
Coronavirus
Causes: Canine Coronavirus
Clinical Signs: Mild, self-limiting diarrhea; anorexia, vomiting, lethargy
Diagnosis: Mostly based on clinical signs (definitive diagnosis requires electron microscopy)
Treatment: Withhold food for 24-48 hours, gradually reintroduce to low-fat diet, then transition back to normal. Fluid therapy if needed.
Feline parvovirus
Causes: Feline parvovirus
Clinical signs: Depression, fever, anorexia, abdominal pain, vomiting, bloody/watery diarrhea. Will cause PANLEUKOPENIA.
Diagnosis: Primarily based on clinical signs. Canine parvo snap test will detect some cases (better for rule out; neg is neg).
Treatment: Same as canine parvo virus-fluids, antibiotics, antiemetics and other supportive therapies.
Campylobacter spp
Causes: C. jejuni is most common.
Clinical signs: Symptoms occur most often in young, parasitized, or immunocompromised animals. Watery, mucoid, or hemorrhagic diarrhea; vomiting, tenesmus, pyrexia, and anorexia.
Diagnosis: Culture or PCR of fresh feces.
Treatment: Abx-erythromycin or fluoroquinolones for patients with hemorrhagic mucoid diarrhea AND signs of systemic disease.
Note: ZOONOTIC
Salmonella spp
Causes: Any salmonella spp.
Clinical signs: Hemorrhagic gastroenteritis (SI, LI or mixed); fever, neutropenia, sepsis. Cats may present with fever only.
Diagnosis: Isolation from feces, or blood in septic patients.
Treatment: Antibiotics; not recommended to treat healthy animals or animals with stable acute diarrhea.
Clostridium perfringens or C. difficile
Causes: Clostridium perfringens, C. difficile
Clinical signs: Large bowel diarrhea; vomiting, fever, weight loss, systemic signs.
Diagnosis: Culture or PCR combined with toxin assay. Must rule out other causes of diarrhea.
Treatment: May be self-limiting. Metronidazole
Hemorrhagic gastroenteritis of dogs (HGE)
Causes: Unknown, hypersensitivity or clostridium toxin suspect.
Clinical signs: Necrotizing, hemorrhagic enteritis-vomiting, bloody diarrhea, rapid dehydration, shock. Occurs most often in young, small breed dogs.
Diagnosis: Presumptive based on PCV of >55% with no other detected causes.
Treatment: Fluid therapy +/-colloidal therapy, antibiotics.
Dysbiosis
Causes: alteration in the population of GI microflora.
Clinical signs: Associated with a variety of chronic GI conditions.
Antibiotic responsive diarrhea
Causes: Specific unknown; IgA deficiency, host-bacteria interaction, barrier dysfunction, excess immune response, diffuse mucosal disease, dysbiosis, folate/cobalamine deficiency.
Clinical signs: Chronic or recurrent small bowel diarrhea (rarely will be large bowel). Occurs most often in young, large breed dogs (GSD, goldens); rare in cats.
Diagnosis: Clinical signs and response to treatment.
Treatment: Antibiotics-tylosin, amoxicillin, and metronidazole most common; treat for 4-6 weeks. Supplement cobalamine.
Trichomonad-related diarrhea of cats
Causes: Tritrichomonas foetus
Clinical signs: Chronic large bowel diarrhea
Diagnosis: fresh fecal smear; fecal culture or PCR.
Treatment: Ronidazole current recommended treatment. Usually self-limiting, but takes 6-36 months to clear!
Pythiosis
Causes: Pythium insidiosium (aquatic oomycete)
Clinical signs: GI tract disease, varies by location of infection-thickens bowel wall. May also see ocular or skin involvement. Occurs mostly in the gulf coast region; young, male, large breed dogs most affected; rare in cats.
Diagnosis: Abdominal ultrasound-thickening/destruction of normal architecture and enlarged lymphnodes. Biopsy, ELISA or PCR.
Treatment: Aggressive surgical resection of affected areas; hard to achieve full cure.
Histoplasma capsulatum
Causes: Histoplasma capsulatum (dimorphic fungi)-GI signs occur with disseminated disease
Clinical signs: Mixed bowel diarrhea, malabsorption, PLE; lethargy, fever, anorexia.
Diagnosis: Biopsy. May find organism in cytologic or hstopathologic samples.
Treatment: Itraconazole; amphotericin B in severe cases or if also neurologic involvement.
Food reactions
Causes: Intolerance or allergy
Clinical signs: diarrhea. If intolerance, may only occur in response to a particular preparation (ie. brand of food); if allergy, will occur in response to any preparation.
Diagnosis: Biopsy-chronic eosinophilic infiltration. Response to food trial-should see improvement within 3 weeks.
Treatment: Food trial-hypoallergenic, novel protein, or "intestinal diet". +/- added fiber if large bowel diarrhea.
Inflammatory bowel disease
Causes: Idiopathic mucosal inflammation in the absence of detectable disease.
Clinical signs: Vomiting, diarrhea, hyporexia, weight loss. Intermittent and mild signs. Vomiting may be the only sign in cats.
Diagnosis: Presumptive-must rule out any and all other causes of inflammation. Biopsy-characterize inflammation as plasmacytic-lymphocytic, eosinophilic, neutrophilic, or mixed. Should also assess cobalamine/folate.
Treatment: Diet change, antibiotics, and immunosuppressive therapy or chemotheraputic agents.
Megacolon
Causes: May be primary/congenital, or acquired from any disease that causes obstruction of the normal passage of feces. Idiopathic is most common in cats!
Clinical signs: Recurrent episodes of constipation, inappetence, vomiting, and weight loss.
Diagnosis: Palpable firm, distended colon. Radiographs-colonic dilation and impaction (diameter will be larger than L7).
Treatment: Step 1) Fluid therapy, enemas and deobstipation; Step 2) Lactulose and cisapride to promote frequent and softer stools; low-residue, high fiber, highly digestible diet; maximize hydration; frequent litter box cleaning; Step 3) Surgical intervention-subtotal colectomy.
Understand the relationship between exocrine pancreatic function and the clinical manifestation of pancreatic disease.
Pancrease produces digestive enzymes:
1. Overproduction/blocked release->activation of enzymes->autodigestion of tissue->swelling, inflammation, edema; vasculitis, hemorrhage, DIC, other systemic complications.
2. Underproduction->maldigestion. 90% of pancreas must be lost before function is lost.
Acute pancreatitis
Causes:
1. Dogs-being fat, eating fatty diets, dietary indiscretion, diabetes, hypertriglyceridemia, being a Schnauzer.
2. Cats-Unknown. Obesity does not predispose.
Clinical signs: Vomiting, anorexia, dehydration, abdominal pain, fever; shock/collapse, peritonitis, secondary sepsis, petechiae, dyspnea, icterus. CATS: often only present with lethargy, anorexia, and dehydration.
Diagnosis: Chem abnormalities, Increased amylase/lipase, PLI (lab test of choice), Rads-R cranial quadrant density, Ultrasound-enlarged pancrease, hyperechoic fat.
Treatment: Fluid therapy (may require colloids), correct acid/base and electrolyte abnormalities, provide adequate (calculated) nutrition-IV or orally/nasogastric tube, analgesia, anti-emetics
Chronic pancreatitis
Cause: Poorly understood. Clinical significance unknown.
Clinical signs: waxing and waning subtle GI signs and anorexia.
Diagnosis: PLI? Biopsy if in the abdomen for other reasons?
Treatment: Not known; treat other associated illnesses (Diabetes, hyperlipidemia).
Exocrine pancreatic insufficiency
Causes: Progressive, immune-mediated disease. May be secondary to recurrent episodes of pancreatitis (more common in middle-age/older cats).
Clinical signs: German shepards predisposed, signs develop before 4 yrs of age. Rare in cats. Discolored feces, increased fecal volume, weight loss, polyphagia, flatulence, thin body condition.
Diagnosis: cTLI-decreased; Abdominal ultrasound-pancrease difficult to visualize.
Treatment: Digestive enzyme supplementation-powder works better than tablets(even crushed). May cause digestion of mucus membranes
Prognosis good, but 20% of dogs do not respond.
Pancreatic neoplasia
It's bad, mkay!
Which breed is primarily predisposed to portosystemic shunt? Copper toxicity? Idiopathic chronic hepatitis? Hepatic amyloidosis?
PSS-Yorkies
Copper toxicity-Bedlington terriers
Idiopathic chronic hepatitis-Doberman pinchers
Hepatic amyloidosis-Shar Pei
What are the common clinical signs of hepatobiliary disease?
1. Hepatic encephalopathy-increased circulating ammonia is neurotoxic.
2. Jaundice, bilirubinuria-cholestasis, back up of bile->increased circulating bilirubin
3. Abdominal Effusion-Pure transudate from hypoproteinemia, modified transudate from portal hypertension.
4. Stranguria, pollakiuria, and hematuria-Ammonia biurate stones.
5. Coagulopathies-dec clotting factor synthesis (dec function), dec vit K (cholestasis), DIC if septic.
6. PU/PD-mechanism unknown.
7. Bacterial infection/sepsis-cholestasis->decreased clearance of bacteria from bile.
8. GI ulceration-hypergastrinemia, portal hypertension, decreased mucosal turnover.
Briefly review the changes on a Chem panel that reflect decreased liver function, cholestasis, and hepatocellular damage.
Dec function-increased bilirubin, ammonia, and bile acids; decreased BUN, glucose, cholesterol, albumin; increased clotting times.
Cholestasis-increased ALP, bilirubin, and cholesterol
Hepatocellular damage-increased ALT and AST.
What are the most common etiologies of acute liver conditions? Chronic liver conditions?
Acute-Toxic, inflammatory, infectious, ischemic, and traumatic.
Chronic-Metabolic, vascular, genetic, neoplastic, degenerative, infection, and immune-mediated.
Differentiate between intrinsic hepatotoxicity and idiosyncratic hepatotoxicity.
Intrinsic-direct action of the toxin or it's metabolite on the hepatocyte.
Idiosyncratic-drug reaction that is most likely immune-mediated and initiated by cell surface receptors.
Which drugs are common liver toxins?
Phenobarbitol-intrinsic
Carprofen-idiosyncratic
Acetominophen-intrinsic, CATS! One of the few toxins with a specific treatment (N-acetylcystein, or S-adenosylmethionine)
Diazepam-idiosyncratic
General treatment for acute hepatic disease
If less than 8 hours-emesis, gastric lavage, activated charcoal, and high cleansing enema.
Antioxidant therapy-SAMe, milk thistle, vit E.
If infection is suspected, Abx.
Fluid support, correction of electrolytes and acid/base imbalance.
May need to supplement vit K or give plasma if coagulopathy develops.
Monitor for other organ dysfunctions, DIC, and hepatic encephalopathies.
Copper associated hepatitis
Cause: metabolic defect impairing biliary excretion of Cu. Genetic in Bedlingtons and other terriers.
Diagnosis: Liver biopsy and copper levels. If Cu>2000, copper associated hepatitis; if >400 but <1000, Cu accumulation is secondary to another hepatic disease process.
Idiopathic chronic hepatitis
Cause: Suspected to be immune dysregulation from a previous subclinical hepatic insult. Occurs in middle-aged dogs; females>males; often asymptomatic until very progressed.
Diagnosis: Biopsy-periportal inflammation and fibrosis.
Neutrophilic Cholangitis (in cats)
Acute-ascending bacterial infections of GI origin; occurs in young to middle age cats. Treat with Abx based on gall bladder aspirate and culture.
Chronic-long term bacterial infection, occurs in middle aged to older cats. Biopsy-mixed inflammation of portal areas, +/-fibrosis. Treat with abx and steroids.
Lymphocytic cholangitis
Cause: Immune-mediated inflammation. Occurs in middle aged to older cats.
Treat with steroids, plus abx in culture positive cases.
Hepatic Lipidosis
Accumulation of fat in the liver.
Causes: Can be secondary to other metabolic disease; most cases are idiopathic. Occurs in young to middle age obese cats after episodes of anorexia.
Clinical signs: Anorexia, depression, vomiting, muscle wasting, hepatomegaly
Diagnosis: Definitive diagnosis by liver biopsy or FNA. Chem-inc ALP, ALT, bilirubin, ammonia/bile acids.
Treatment: Aggressive nutritional and fluid support. Do not force feed! Place nasoesophageal, esophagostomy or gastrotomy tube if patient is not eating. Use fluid therapy to correct acid/base and electrolyte imbalances. Antibiotics, antiemetics, antioxidants, treatment for hepatic encephalopathy, and vit K may be necessary if indicated by appropriate complications.
General treatment for Copper Hepatopathy
Dietary management-Low copper diet such as Hills u/d or l/d
Decrease absorption-Zinc. Must monitor PCV, can cause hemolytic anemia.
Increase excretion-Penicillamine. Copper chelating agent, requires long term therapy.
Affects of Ursidiol in treating chronic hepatic disease
Increases water content of bile-promotes movement of bile.
Displaces accumulated toxic bile acids.
Decreases hepatic inflammatory responses.
Drugs to manage inflammation/fibrosis associated with chronic hepatic disease
Corticosteroids
Azathioprine
Cyclosporine
Colchecine
+/-Ursudiol, Silymarin
Indications: Chronic hepatitis or cholangitis
Drugs to prevent oxidative damage from chronic hepatic disease
Vitamin E
S-Adenosyl-L-Methionine (Denosyl/SAMe)
Silymarin (Marin)
Indications: Inflammatory, infectious, necrosis, cholestasis, or ischemic liver diseases
Drugs that promote bile flow
Ursudiol
Silymarin
Antibiotics used for bacterial hepatitis/hepatic encephalopathy
Metronidazole
Amoxy
Based on culture/sensitivity, want a drug that is secreted in bile.