Liver Diseases High regenerative capacity; damage must be severe for signs to appear Drug/Toxin induced Liver Disease Acute liver failure requires >70%

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Presentation transcript:

Liver Diseases High regenerative capacity; damage must be severe for signs to appear Drug/Toxin induced Liver Disease Acute liver failure requires >70% of liver to be affected Susceptible to toxin ingestion (portal circulation) Some drugs have a Hx of liver toxicity Acetaminophen Phenobarbital The liver filters the blood coming from the digestive tract, before passing it to the rest of the body. The liver also detoxifies chemicals and metabolizes drugs Could be caused by medications animal has taken. It is important to run blood work often when an animal is on certain medications. The liver will rebuild itself so liver injury must be severe to show up on bloodwork. Portal system takes substance from digestive system to liver to be metabolized.

Drug/Toxin Induced Liver Disease Signs Anorexia vomiting/, diarrhea/constipation PU/PD Jaundice Melena, hematuria, or both CNS signs (depression, ataxia, dementia, coma, seizures) If the liver is damaged it can cause toxins to build up in the blood because p is not metabolizing the toxins. Could be due to an over dose of drugs or due to long term use of medications.

Drug/Toxin Induced Liver Disease Diagnosis Hx of drug administration Painful liver on palpation Chemistry panel ↑ liver enzymes Evidence of coagulopathy Liver biopsy Bleeding disorder because liver hold the clotting factors. If impaired p could have a clotting issue. Liver punch biopsy (DOVE ) 3 minutes

Drug/Toxin Induced Liver Disease Treatment Antidotes Induce vomiting Activated charcoal IV fluids Vit K for clotting Antibiotics Special diets (Hill’s L/d) Activated charcoal to prevent p from absorbing toxins that have built up. Antidote is a medication that counteracts toxins.

“Choose your friends carefully, your enemies will choose you.” SO TRUE “Choose your friends carefully, your enemies will choose you.” -Yassar Arafat

Portosystemic Shunt (PSS) Blood from GI tract bypasses liver, allows many toxins into systemic circulation CNS is most affected by the circulating toxins Bypasses hepatic detoxification: Toxins absorbed by the intestines skips over the liver and goes straight into the blood stream. The liver will appear small and atrophied (wasted away). This is because blood is not going to liver like it should. Ductus venosus: this is normal in a fetus while in the mother. It bypasses the liver (from the umbilical vein straight to the vena cava) due to the liver not being fully developed(only a small amount goes to the liver during this time). The fetus gets nutrients and stuff from the mother while in the womb. This should close after birth.

Skips the liver and goes straight to vena cava vein from the portal vein. Bypasses hepatic detoxification, leading to increase in systemic toxins. In the fetus, the ductus venosus shunts a portion of the umbilical vein blood flow directly to the vena cava. Thus, it allows oxygenated blood from the placenta to bypass the liver. With a shunt the ductus venosus does not close resulting in a congenital shunt.

Portosystemic Shunts Signs Dumb/numb, lethargic, depressed Ataxia, staggering Head-pressing compulsive circling, apparent blindness Seizures, coma Bizarre behavior Signs often more pronounced shortly after a meal After eating because body has started absorbing nutrients and then skips the liver. Ataxia/head pressing: toxins built up Start to show signs at 6 months of age

Portosystemic Shunts Diagnosis Chemistry panel Evidence of abnormal liver function X-rays Small liver (microhepatica) Contrast material By-passes liver The shunt will light up. They can use a CT to identify it.

Portosystemic Shunts Treatment Client info Medical management seldom very successful Low protein diet Surgery Ligation of shunt Total ligation often causes ↑ liver BP(portal hypertension) Partial ligation may be more practical Client info Prognosis often very good following ligation For best results, Surgery should be performed before 1 y old Total can lead to blood going through liver to quickly causing hypertension(remember this liver has not had blood flow in a while). This could lead to toxic shock, cardiovascular collapse, and abdominal pain. Partial, body could get used to it and then they could have a second surgery to finish closing the shunt. This allows the liver time to adjust to the increased blood flow. Partial: not fully tying off the shunt (Second surgery is usually done 1 month after first surgery)

Feline Hepatic Lipidosis Idiopathic – cause unknown Fatty liver disease Obese cats of any age, sex or breed Stress may trigger anorexia Diet change Boarding Illness Environmental change You never want a cat to stop eating. It can be very dangerous. 2 weeks without eating will result in lipid build up within the liver. If not treated it could lead to liver failure. Cause is unknown, but stress seems to be a trigger for this condition.

Idiopathic Hepatic Lipidosis Anorexia prolonged for 2 weeks causes imbalance between breakdown of peripheral lipids and lipid clearance within liver Lipids accumulate in liver Early diagnosis and aggressive treatment important 60-65% of cases have complete recovery

Idiopathic Hepatic Lipidosis Enlarged liver and hepatocytes.

Idiopathic Hepatic Lipidosis Clinical Signs Anorexia Obesity Wt loss (as much as 25% of body weight) Depression Sporadic vomiting Icterus Mild hepatomegaly +/- coagulopathies Could be bleeding tendencies.

Idiopathic Hepatic Lipidosis Diagnosis History of stress Chem panel Evidence of abnormal liver function CBC X-rays – mild hepatomegaly Liver biopsy Nonregenerative anemia, stress neutrophilia(increased release of neutrophils), lymphopenia. Elevated liver values.

Idiopathic Hepatic Lipidosis Treatment High protein, calorie dense diet Feeding tube usually required Nasogastric tube for short term liquid diets Esophagostomy tube Gastrostomy tube best Tubes can remain in place For up to 3-6 weeks Nasogastric tube: through nostril into stomach. Esophagostomy tube: placed through incision on neck, does not go into stomach. Cats don’t tolerate well. Gastrotomy tube: goes through abdominal wall into stomach. Best option if cat can handle anesthesia. Feeding tubes must be flushed before and after use.

Esophagostomy tube We actually used these tubes a lot in ICU. Nasogastric tube (DOVE) 10 minutes

Gastrostomy tube PEG tube placement (DOVE) 10 minutes (percutaneous endoscopic gastrostomy) They actually use an endoscope to place it

Idiopathic Hepatic Lipidosis Treatment IV fluids Metoclopramide SQ 15 min prior to feeding Monitor weekly Client Education Avoid stress in obese cats Any cat that stops eating is at risk Cats do not respond well to frequent diet changes Metoclopramide: helps with nausea. They are usually very nauseous. Can use Diazepam as an appetite stimulant. Recheck bloodwork every 2 weeks until liver values start to go down. Prognosis is guarded. 60-65% chance of a cure.

Pancreatic Dysfunction (Exocrine) Main function of Exocrine Pancreas → secretion of digestive enzymes (Amylase and lipase) into the small intestines Secretes bicarbonate to neutralize stomach acids Regulates blood glucose (secretes insulin) Located under the stomach and duodenum Digestive enzymes secreted in an inactive form to protect pancreas tissue Digestive enzymes, produced and stored within the pancreas, are released into the Sm. Intestines routinely. When stimulated by food, it secretes more enzymes. Inactive form meaning enzymes are activated after reaching the duodenum.

Pancreatic Dysfunction (Exocrine) When digestive enzymes are activated within gland → autodigestion Pancreatitis develops Inflammation of the pancreas More common in obese animal; high-fat diets may predispose animals to it Unpredictable results; some recover well, others worsen and may die Pancreatitis occurs when digestive enzymes are activated within the pancreas. Autodigestion develops resulting in an inflamed pancreas, resulting in tissue damage. Pancreatic enzymes are destroying its own tissue.

Pancreatitis Signs Older, obese dog or cat with history of recent high-fat meal anorexia, vomiting ± abdominal pain Shock, collapse may develop Often seen post-holiday Table scraps of ham, gravy, etc.

Pancreatitis Diagnosis Treatment CBC Chemistry panel Elevation of pancreatic enzymes Amylase and lipase Treatment IV fluids NPO 3-4 d Antibiotics Pain management Start back on low fat diet 1-2 days after vomiting stops Do not offer food for 48-72 hours – Pancreas needs to rest If the p smells food then the pancreas will produce more digestive enzymes. We want the pancreas to rest. The two enzymes. Amylase and lipase leak into the blood stream resulting in elevated values for both these enzymes.

Pancreatitis Client info Avoid obesity/overfeeding Feed low-fat treats Prognosis is difficult to assess Low fat diets are best because they are easily digested. This will help prevent other episodes.

Exocrine Pancreatic Insufficiency The pancreas stops making digestive enzymes May occur spontaneously or due to chronic pancreatitis Signs Wt. loss Polyphagia Coprophagia, pica Diarrhea, fatty stool Flatulence Coprophagia: eating stool. Polyphagia: always hungry. Pica: craving food Fatty stool: too much fat in stool, a sign that nutrients aren’t being absorbed properly

Exocrine Pancreatic Insufficiency Treatment Supplement pancreatic enzymes with each meal Pancrezyme Viokase-V Client info EPI is irreversible; life-long treatment Pancreatic enzyme replacement is expensive With enzyme replacement, dog will regain weight, diarrhea will stop Must be given with every meal