Veterinary Medicine - Pancreas & Liver Diseases Flashcards
Pancreatitis - Etiologies
Primary hypertriglyceridemia (e.g. Familial hypertriglyceridemia of Miniature Schnauzers)
Secondary hypertriglyceridemia:
-High fat diet / Garbage eating
-Endocrinopathies: DM, Hypothyroidism, Cushing’s disease
-Hypercalcemia
-Ischemia (e.g. Dehydration, Shock, Anesthesia)
-Trauma (e.g. Iatrogenic)
-Drugs: TMS, Phenobarbital + KBR, Azathioprine, L-Asparaginase
-Toxins (e.g. Organic phosphates, Lilly flower in cats)
-Translocation of bacteria from the GI (Cats) -Idiopathic
Pancreatitis - Possible complications (Local, Systemic)
Local:
Peritonitis (Aseptic)
Necrosis
Cholestasis (Cats more than Dogs)
Gastritis
Enteritis
Colitis (Anatomical proximity)
Ileus
Systemic:
SIRS\MODS
ARDS\ALI
Pleural effusion
PTE
AKI
DIC
Arrhythmias
Chronic Pancreatitis - 3 Possible causes
Sequela to episodes of acute Pancreatitis
Immune-mediated
Repeat translocations of bacteria from the GI (Cats)
Chronic Pancreatitis - 2 Possible complications
Exocrine pancreatic insufficiency (EPI)
Diabetes mellitus (DM)
Acute Pancreatitis - US Sensitivity
70% (but dependent on the skill of the radiologist)
Pancreatitis - Possible CBC findings
Leukocytosis\Leukocytopenia
Anemia (e.g. GI Bleeding, Anemia of inflammation\neoplasia )
Thrombocytosis (Inflammation) \ Thrombocytopenia (e.g. Vasculitis ,DIC)
Pancreatitis - Possible panel findings and their respective explanations
-Hypoalbuminemia (Negative APP, GI bleeding) \ Hyperalbuminemia (e.g. Dehydration)
-Hypoproteinemia (GI bleeding)
-Hyperbilirubinemia (Cholestasis)
-Elevation of liver\bile enzymes (Cholestasis, Hepatic damage)
-Hyperamylasemia (Pancreatitis, GI damage, AKI)
-Hypercholesterolemia (Cholestasis)
-Hypertriglyceridemia (Lipolysis of peripancreatic\abdominal fat)
-Hypocalcemia (Saponification)
-Hypoglycemia (Destruction of beta-cells and release of Iinsulin) \ Hyperglycemia (depletion of beta cells)
-Azotemia: Dehydration, AKI, GI bleeding)
-Hyponatremia, Hypokalemia, Hypochloridemia (Diarrhea, vomiting)
Pancreatitis - Amylase - Why is it considered non-specific to pancreatitis? When can it be considered specific?
Elevation can also be secondary to: Damage to the duodenum, Decreased Renal GFR (e.g. AKI)
3x-4x the normal range - specific to pancreatitis
Pancreatitis - Specific enzymes - More useful for acute or chronic pancreatitis?
Acute Pancreatitis
General Lipase - Specific to pancreatitis? Why?
No
Many lipases in the body besides pancreatic lipase: Lipoprotein-lipase, Hormone-sensitive lipase, Stomach and liver.
Pancreatitis - Most sensitive test to diagnose pancreatitis
Snap PLI
Pancreatitis - Most specific test to diagnose pancreatitis
Spec PLI
Pancreatitis - Specific testing is more sensitive for cats or dogs?
Dogs > Cats
Pancreatitis - Snap PLI - More useful for confirming or rule out pancreatitis?
Rule-out (High sensitivity, low specificity)
Pancreatitis - DGGR Lipase - When ia it considered specific to pancreatitis?
3x Upper reference interval
Pancreatitis - What are the effects on coagulation? Explain the pathophysiology
First hypercoagulability and then Hypocoagulability and DIC
Release of proteases => Endothelial damage, Inflammation and consumption of anti-coagulants (e.g. AT-3, Alpha-2-macroglobulin, Alpha-1-proteinase) => Hypercoagulability => Consumption of pro-coagulation factors and platelets => Hypocoagulability and DIC
Pancreatitis - Diagnosis - Gold standard? When is it performed?
Histology\Cytology
Almost never, unless neoplasia is suspected
Acute Pancreatitis - Treatment (Dog)
Fluids, Electrolytes
Low fat diet: Enteral as soon as possible is preferred. Tube feeding if anorexic after a few days
GI support: Anti-emetics, GI protectants (if GI bleeding is suspected,) Appetite stimulants, Pro-motiles
Analgesia (e.g. Butorphanol/Buprenorphine/Fentanyl )
Antibiotics - not indicated in MOST cases of canine pancreatitis. Only if sepsis is suspected
*Plasma - Low AT-3/ suspected DIC - No proven efficacy
*Steroids - Last resort
Chronic pancreatitis - Treatment (Dog)
Low fat diet
Analgesia
Anti-emetics
*Immunosuppression - recurrent episodes of acute on chronic \ No response to therapy
Pancreatitis - Treatment - What’s different in cats (2 main differences)
Antibiotics - bacterial translocation more common than in dogs
Low fat diet - unless there is underlying hypertriglyceridemia - Not necessary
Pancreatitis - Prognosis
Depends:
1) Mild disease that passes with supportive treatment and dietary restriction (Low fat) for an indeterminate period (few weeks to life-long depending on the case) - good prognosis
2) Serious systemic disease that might require prolonged admission and with life threatening complications (SIRS, AKI, ALI/ARDS etc.) - fair to guarded
Pancreatitis - What are the top 3 associated disease with Pancreatitis In cats? (Concurrent together with Pancreatitis)
IBD
Cholangiohepatitis
Hepatic Lipidosis
What are the 2 most common sequelas of Pancreatitis?
DM
EPI
Exocrine pancreatic insufficiency (EPI) - Most common etiologies in both cats and dogs
Dogs: Sequela to chronic pancreatitis (50% of cases), Pancreatic acinar atrophy (Other 50% of cases)
Cats: Sequela to chronic pancreatitis (almost 100% of cases)
Exocrine pancreatic insufficiency (EPI) - Clinical signs
Common:
Weight loss
Polyphagia
Small intestine diarrhea (often with undigested food particles, Steatorrhea)
Possible additional signs (with prolonged disease):
Behavioral changes, Tremors
Seizures
Coma
Rare: Spontaneous bleeding
Exocrine pancreatic insufficiency (EPI) - Common bloodwork findings
Panel:
Hypocholesterolemia
Hypocalcemia (Total and ionized)
Hypophosphatemia (Rare)
Decreased B12, Increased Folate (less common)
Prolonged clotting times (Rare)
Exocrine pancreatic insufficiency (EPI) - Diagnosis (what is the gold standard)
Trypsin-like immunoreactivity (TLI)
Exocrine pancreatic insufficiency (EPI) - Treatment & Prognosis
Pancreatic enzyme extract - add with every meal\snack for life!
B12 Supplements (In case of deficiency)
Vitamin D analogs + Calcium supplements (in cases of clinical hypocalcemia) and taper off according to repeat blood tests
Excellent with normal life expectancy
Exocrine pancreatic insufficiency (EPI) - Reasons for treatment failure
Pancreatic extract ineffective\Poor quality\Owners fail to comply with giving extract according to instructions
B12 deficiency
Concurrent diseases: ARD, IBD, DM
How does dysbiosis affect bile acid metabolism? Specific treatments?
Dysbiosis can create secondary bile acids (which are harmless) into primary bile acids which are irritant to the GI - causing diarrhea
Colestid, Ursolit (Synthetic)
How would feces look like in cholestasis?
White (no stercobilirubin to give it color)
Clinical signs associated with liver disease - Causes for Hyperammonemia
Liver shunts (e.g. PSS, MVD)
Liver failure
B12 Deficiency
Arginine deficiency (Cat)
Congenital urea-cycle enzyme deficiency
Sepsis with urease positive urease-positive
Clinical signs associated with liver disease - For liver function to be affected - how much of the liver needs to be compromised?
70-80%
Clinical signs associated with liver disease - What causes vomiting in liver disease?
GI Ulcers caused by decreased metabolism of gastrin
Decreased detoxification activities
Hepatomegaly creating mechanical pressure on the GI
Portal hypertension
Clinical signs associated with liver disease - What causes Pu/Pd in liver disease
Decreased urea production
Hypercortisolemia
Due to behavioral changes (e.g. 2nd to hyperammonemia)
Clinical signs associated with liver disease - Hyperammonemia - Important clinical sign in cats
Hypersalivation
Clinical signs associated with liver disease - How can liver disease cause lower urinary tract signs (e.g. Pollakiuria, Stranguria, Hematuria)
Ammonium biurate crystals\uroliths
Clinical signs associated with liver disease - What causes Melena in liver disease
Hypergastrinemia
Coagulopathy
Portal hypertension
Clinical signs associated with liver disease - What causes white feces in liver disease
Cholestasis
Infectious diseases of the liver - DDs
Bacterial:
-Ascending infection from the GI (Cholangiohepatitis)
-Leptospirosis
-Mycobacteria
-Bartonellosis
Viral:
-Canine adenovirus
-FIP
Fungal:
-Aspergillosis
-Cryptococcosis
Parasitic:
-Leishmaniasis
-Neosporosis
-Toxoplasmosis.
Clinical pathology of the liver - CBC - Common findings
Non-regenerative anemia:
Anemia of inflammation\neoplasia
Regenerative anemia:
Bleeding (Coagulopathies, GI ulcers)
Hemolysis (e.g. Heinz-bodies)
Platelets:
Thrombocytopenia (Portal vein thrombosis, DIC)
Thrombocytopathy
Clinical pathology of the liver - Extra-hepatic causes for increase in liver enzymes
Reactive hepatopathy: Pancreatic\Biliary\GI Diseases
Muscle diseases (ALT from muscles)
Bone diseases
Growing animals (ALP) (B-ALP)
Drugs\Toxins (e.g. GC, Phenobarbital, Cycad)
Endocrinopathies (e.g. Cushing’s disease, Hypothyroidism, DM)
Vascular congestion (e.g. R-CHF)
Ischemia (e.g. Shock)
Cholestasis of sepsis (Cat).
Clinical pathology of the liver - What are the common patterns for muscle and liver damage using ALT,AST and CK?
Hepatic damage: ALT > AST
Muscle damage: AST,CK > ALT
Clinical pathology of the liver - ALP - Is a singular rise in ALP in a dog with no clinical signs or increase in additional liver enzymes requires further investigation? Why? and what about cats?
ALP Is non-specific and can increase from benign reasons: Hepatic nodular hyperplasia in older dogs, Overweight animals, Growing animals
In cats on the other hand - any increase in ALP is significant and is a marker for hepatic lipidosis
Clinical pathology of the liver - General patterns (ALP/ALT/AST/GGT) - Drugs
Corticosteroids - ALP (+++), GGT (++), ALT (+), AST (+)
Barbiturates: ALP (++), GGT (+), ALT (+), AST (+)
Clinical pathology of the liver - General patterns (ALP/ALT/AST/GGT) - DM, Cushings disease
DM: ALP > ALT
Cushing’s disease: ALP (+++), GGT (+), ALT (+), AST (+)
Clinical pathology of the liver - General patterns (ALP/ALT/AST/GGT) - Hypoxia
ALT (++), ALP (+), GGT (+), AST (+)
Clinical pathology of the liver - General patterns (ALP/ALT/AST/GGT) - Muscle damage
AST (++), CK (+), ALT (+)
Clinical pathology of the liver - General patterns (ALP/ALT/AST/GGT) - Hepatic lipidosis
ALP (+++), ALT (+), GGT (Normal)
Clinical pathology of the liver - General patterns (ALP/ALT/AST/GGT) - Chronic hepatitis
ALT (+++), ALP (+ or Normal)
Clinical pathology of the liver - General patterns (ALP/ALT/AST/GGT) - Cholangiohepatitis
GGT (+), ALT (+), ALP (+ or Normal)
Clinical pathology of the liver - What are the markers for liver function and how are they affected in liver failure?
Cholesterol - either hypercholesterolemia due to cholestasis, or hypocholesterolemia due to decreased production
Albumin - Hypoalbuminemia
Bilirubin - Hyperbilirubinemia
Glucose - Hypoglycemia
Urea - Decrease
Clinical pathology of the liver - What is the liver function that is usually affected last in liver failure?
Glucose
Clinical pathology of the liver - How is glucose affected in liver failure/PSS and what is the pathophysiology
Decrease (Hypoglycemia)
Liver failure - Decrease in gluconeogenesis, Increased insulin production
PSS - Glycogen storage decreases, response to glucagon decreases.
Clinical Pathology of the Liver - DDs For Hypoglycemia
Sepsis
Storage Diseases
Neoplastic
Addison’s disease
Polycythemia
Pancreatitis
Insulin overdose (e.g. for diabetics, Insulinoma)
Liver failure
Young - Fasting in puppies
Toy breeds
Xylitol
Tremors
Clinical pathology of the liver - Liver leakage enzymes (ALT/AST) are specific to liver damage in cats (as opposed to Extra-hepatic damage like Biliary tract/Pancreas/GI) - True/False
False
Because bile tract leakage enzymes in cats are not sensitive
Clinical pathology of the liver - Liver and biliary tract leakage enzymes are sensitive but not specific (True/False)
True
Clinical pathology of the liver - In clinically healthy dogs, a sole increase in ALT warrants further follow up but a sole increase In ALP doesn’t necessarily (True\False) - Why
True
ALT - Very specific to liver damage and could be an early sign for disease such as chronic hepatitis, neoplasia
Should invite for a follow up in a month for repeat bloodworks and possibly imaging
ALP - Not specific and can increase for many benign reasons, such as nodular hyperplasia, Growing animals, Steroids, Obesity etc.
Clinical pathology of the liver - Common Urinalysis findings in dogs and cats in liver failure
Isosthenuria (USG between 1.008 - 1.012)
Ammonium biurate crystal\uroliths
Bilirubinuria
Clinical pathology of the liver - Coagulation-related findings in liver disease
Thrombocytopenia
Thrombocytopathy
Prolonged PT/PTT
Decreased AT-3
Decreased fibrinogen
TEG/\EM: Hepatic disease can cause either hypo or hypercoagulability.
Liver failure\DIC - How to differentiate
D-dimer - raises in DIC (and less affected in liver failure)
Thrombocytopenia, Prolonged PT/PTT and decreased AT-3 can be found in both instances
Clinical pathology of the liver - Ammonia challenge test - What to give? What’s the sensitivity for detecting PSS? For detecting parenchymatic disease?
High protein meal \ Ammonium chloride
Acquired PSS - 80%
Congenital PSS - 90%-100%
Parenchymatic liver disease - 50%
Clinical pathology of the liver - Ammonia challenge test - Possible complication
Causing\worsening hepatic encephalopathy
clinical pathology of the liver - Ammonia challenge test - What is the test most sensitive for?
PSS (congenital PSS the highest sensitivity)
Clinical pathology of the liver - Bile acids challenge test - Sensitivity to PSS? To parenchymatic disease?
PSS - 90%-100%
Parenchymatic disease - 50%-70%
Liver US - Highly sensitive and specific tool for detecting liver disease (True/False)
False
Liver US - High velocity portal vein blood flows can signify what?
Liver shunt
Liver US - low velocity portal vein blood flows can signify what??
Portal hypertension (e.g. due to decreased liver parenchyma in cirrhosis, Portal vein thrombosis)
Liver radiography - Useful for what disease? 2 Useful methods to perform it
PSS
Contrast injection US Guided to Splenic vein
Contrast injection to Cranial Mesenteric vein during a surgical operation
Liver US - What is it good for especially?
Detecting shunts
Detecting obstruction patterns
What is the best imaging modality for detecting liver shunts
Angio-CT
Liver FNA - What types of diseases is it most useful for?
Diffuse diseases: Such as vacuolar diseases (e.g. Hepatic Lipidosis), Diffuse neoplasia (Lymphoma)
Liver Biopsy - “Tru-Cut” - 2 Main Contraindications
Hypocoagulation (bleeding state)
Ascites
Liver biopsy through laparotomy - Main advantages as opposed to US-guided, and how to prepare for it, in terms of trying to prevent bleeding as much as possible
Better visualization
Larger samples
Larger quantity of samples
Samples from hard to reach location
Better control of bleeding
Vitamin K Supplementation, Plasma, Monitor PT/PTT
Treating hepatic diseases - Hepatic encephalopathy (and explain the reasoning behind each element)
Fluids (Correcting hypoglycemia, hypokalemia and alkalemia => in order to prevent a catabolic state and further translocation of ammonia from the intestine to the blood stream)
Low-medium protein Diet (e.g. K\d, L\d) (No aromatic AAs and short-chain FAs which can act as neurotransmitters)
Lactulose: Osmotic laxative which decreases overall bacterial load, Promotes growth of bacteria which prefer to metabolize carbohydrates, lowers colonic pH and promotes production of ammonium over ammonia
Antibiotics: Ampicillin and\or Metronidazole (To lower Intestinal bacterial load)
Flumazenil (In depressed animals) or Gabapentin (In hyper animals)
Additional supportive hepatic treatment if necessary (e.g. anti-oxidants, Ursolit, Vitamin K supplement, L-carnitine in cats with hepatic lipidosis)
Treating hepatic diseases - Portal hypertension
Low-sodium diet (to prevent systemic hypertension)
Diuretic: Spironolactone (First choice because of it being a K-sparing diuretic - not causing hypokalemia and potentially worsening hepatic encephalopathy
Furosemide (second choice)
Abdominocentesis (In case of ascites which leads to dyspnea).
Treating hepatic diseases - Cholestasis (Non-obstructive) - Treatment
Treat underlying cause
Ursolit
Treating hepatic diseases - Anti-oxident drugs
PO:
Alpha-tocopherol (vitamin E)
Thistle
SAMe
IV:
N-Acetylcysteine
Treating Hepatic Diseases - Important instructions to to tell the owners when administering SAMe
Give on an empty stomach
Treating hepatic diseases - Coagulopathy
Vitamin K supplements
Plasma\Full blood transfusion
Treating hepatic diseases - Coagulopathy - Why is it important to give vitamin K as soon as possible when suspecting bleeding tendencies?
It takes 24-36h before it takes effect so give it first so you can do FNA\Biopsy the next day without needing to wait longer than necessary
Treating Hepatic Diseases - Coagulopathy - Vitamin K toxicity is a danger in what animal and why?
Cats (Can cause Heinz-bodies anemia)
Treating hepatic diseases - Cirrhosis/ Hepatic fibrosis - What is the most effective treatment? Why?
Find and treat the underlying issue causing the fibrosis (If possible)
Liver might still be able to regenerate
Treating hepatic diseases - Copper storage disease - treatment options
Low copper diet (L\d)
D-Penicillamine (chelation
Zinc in diet (Competes with copper absorption)
What is the most common liver disease in cats?
Neutrophilic cholangiohepatitis
Neutrophilic cholangitis/cholangiohepatitis - Signalment, Possible cause, Clinical signs
Middle aged-old cats
Translocation of bacteria from the GI
Lethargy, Anorexia
Fever
Vomiting
Diarrhea
Jaundice
Neutrophilic cholangitis/cholangiohepatitis - Classic CBC, Panel, US findings
Neutrophilia
Increased GGT
Increased ALT+-AST
Increased ALP
Hypercholesterolemia
Hyperbilirubinemia
Thickening of extra-hepatic biliary tract walls, Widening of biliary tract, thickening of gall bladder wall, Pus +- calculi in biliary tract
Neutrophilic cholangitis/cholangiohepatitis - Cytology and biopsy findings, Treatment, Prognosis
Neutrophils + Bacteria (Send to C&S)
Antibiotics (4-6 Weeks. Treat for 1 week after enzymes normalize)
Anti-oxidants (e.g. NAC, SAMe)
Ursodiol
Anti-emetics
Appetite stimulant
Analgesia
Good. Recurrence is possible. Worse in case of gall bladder stones
Lymphocytic cholangitis/cholangiohepatitis - Signalment, Possible Cause, Clinical Signs, Jaundice?
Middle age - old cats
Immune-mediated
Anorexia, Lethargy
Weight loss
Vomiting
Diarrhea
Jaundice
Less common: Ascites, lymphadenopathy, Hepatomegaly
Lymphocytic cholangitis/cholangiohepatitis - CBC, Panel findings
Lymphopenia
Possible neutrophilia
Increased GGT
Increased ALT+-AST
Increased ALP
Hypercholesterolemia
Hyperbilirubinemia.
Lymphocytic cholangitis/cholangiohepatitis - Biopsy, Treatment, Prognosis
Lymphocytic infiltrate (Mainly around portal zone)
Immunosuppression (GC +- additional Immunosuppression)
Anti-oxidants
Ursolit
GI support
Analgesia
Guarded
Dogs/Cats - Which tend to have cholangitis (+/- hepatitis) and which tends to have hepatitis?
Dogs - Hepatitis
Cats - Cholangitis
Chronic hepatitis in dogs - What is the best marker?
ALT
Chronic hepatitis (Dog) - What is the gold standard for diagnosis
Histology
How do you differentiate between a primary copper-associated chronic hepatitis and secondary copper-related hepatitis (Due to cholestasis, inflammation etc.)
Primary: Copper staining on histology revels aggregates of copper in the centrilobular area
Secondary: Aggregates are in the peri-portal area
Copper-related chronic hepatitis - What are some common poster breeds of the disease?
Bedlington terrier, Labrador retriever, Dalmatian, WHWT
Chronic hepatitis - Clinical signs
Lethargy, Anorexia
Weight loss
Vomiting , Diarrhea, Melena\Hematochezia\ Hematemesis
Pu/Pd
Jaundice
Ascites\Pleural effusion\Peripheral edema
Spontaneous bleeding
Hepatic encephalopathy
Hemolysis (Copper-associated chronic hepatitis)
Copper-related chronic hepatitis - How soon to screen for the disease in a Bedlington Terrier
1 Year of age
Copper-Related Chronic Hepatitis - 2 important diagnostic tests - for achieving diagnosis of copper storage disease and prognosis
Copper staining (Qualitative assessment)
Copper quantification (Achieved with biopsy taken through laparotomy)
Breed-associated/Idiopathic chronic hepatitis - What are the 2 main processes going on in the liver?
Inflammation
Fibrosis
Breed-associated/Idiopathic chronic hepatitis - 3 possible histological findings?
1) Moderate to severe lymphocytic infiltrate +- fibrosis. Eventually can progress to cirrhosis
2) Lobular dissecting hepatitis - Severe fibrosis cutting through the lobules with little to no inflammation
3) Reactive hepatopathy - Mild portal inflammation. Secondary process Indicative of an extra-hepatic pathology (e.g. Pancreatitis, Cholangitis, Enteritis)
Breed-associated/Idiopathic chronic hepatitis - Signalment
Young-young adult dogs
Breed-associated\Idiopathic chronic hepatitis - Diagnosis, Treatment
Biopsy (Also rule out infection, toxins, copper-storage disease)
If inflammation is present on histology - worth trying GC +- 2nd Immunosuppression (e.g. Cyclosporine, Azathioprine, Cellcept)
Diet for liver disease (e.g. L\d)
Hepatic support:
Anti-oxidants
Ursodiol
Vitamin K supplements
GI support (e.g. anti-emetics, PPI, appetite stimulant)
Treat complications: Hepatic encephalopathy, Portal hypertension.
Breed-associated/Idiopathic chronic hepatitis - Prognosis
If there is still inflammation on biopsy - Regeneration might be possible and worth a try
In general: MST of 1.5-2 years from diagnosis.
-Cirrhosis on histology: MST of 1 month
-Ascites: MST of 1 month
-Lobular dissecting hepatitis: MST of 1 month
Idiopathic canine acute hepatitis - What is the main cell infiltrate and what is the treatment
Neutrophils
Hepatic and GI support + Antibiotics
Vascular anomalies of the liver - Congenital Porto-systemic shunts - What is common in what breed sizes: Extra/Intra-hepatic shunts, Large/Small breeds dogs
Small breeds - Extra hepatic
Large breed - Intra hepatic
Vascular anomalies of the liver - Congenital Porto-systemic shunts - Classic history & clinical signs. Also what is the typical onset of clinical signs
Growth retardation (smaller than expected/littermates)
Pu\Pd - due to decreased urea production, Hypercortisolemia, Psychogenic polydipsia due to hepatic encephalopathy
Intolerance to anesthesia (e.g. Long recovery period post neutering) - decreased hepatic metabolism of anesthetic drugs
Neurological signs (e.g. Behavioral changes, Star-gazing, Head pressing) - due to hepatic encephalopathy
Pollakiuria\Stranguria\Hematuria - due to ammonium biuate stones
Onset - usually up to 6 months of age
Vascular anomalies of the liver - Congenital Porto-systemic shunts - Common complications include ascites and portal hypertension (True/False)
False
PSS leads to increased blood velocity through the portal vein, as opposed to other hepatic diseases (e.g. cirrhosis, NCPH)
Vascular anomalies of the liver - Congenital Porto-systemic shunts - Common lab findings
Mild non-regenerative anemia
Normal to mild increase in liver enzymes
Hypocholesterolemia
Hypoalbuminemia
Hypoglycemia
Low urea
Increased bile acids
Hyperammonemia
Vascular anomalies of the liver - Congenital Porto-systemic shunts - Definitive diagnosis
US (80-100% Sensitivity)
Contrast X-ray
Angio-CT (Gold standard)
Vascular anomalies of the liver - Congenital Porto-systemic shunts - Treatment
Medical:
Low protein diet (e.g. L\d or k\d)
Lactulose
Antibiotics
Anti-oxidants (SAMe)
Surgical:
Closer of the shunt with:
Surgical knot \ Cellophane \ Stent (Mainly for intra-hepatic shunts) \ Ameroid constrictor)
**It is recommended to first stabilize the animal with medical treatment for 2-3 weeks and then perform surgery.
Vascular anomalies of the liver - Congenital Porto-systemic shunts - Surgical procedure success rate and possible complications
65-85% (Better in extra-hepatic shunts)
Complications:
-Acute portal hypertension post-surgery
-Seizures
-Incomplete closure of the shunt
-Hepatic encephalopathy
Vascular anomalies of the liver - Multiple acquired shunts - Signalment, Clinical signs, Diagnosis
Older dogs.
GI signs
CNS signs (Hepatic encephalopathy)
Ascites (Portal hypertension)
Jaundice
Pu\Pd
Abdominal US
Vascular anomalies of the liver - Multiple acquired shunts - Treatment
Treat primary hepatic disease if possible
Medical supportive treatment only:
GI support
Livet diet
Anti-oxidant
Ursodiol
Treat hepatic encephalopathy (i.e. lactulose, Antibiotics)
Treat portal hypertension (i.e. Spironolactone
Cannot be fixed surgically
Vascular anomalies of the liver - Multiple acquired shunts - Cause
Severe chronic liver disease which leads to portal hypertension (e.g. NCPH, Arteriovenous malformation, Idiopathic chronic hepatitis)
Portal vein hypoplasia without portal hypertension (Hepatic microvascular dysplasia) - Pre-sinusoidal/Sinusoidal/Post-sinusoidal anomaly
Pre-sinusoidal\Sinusoidal
Portal vein hypoplasia without portal hypertension (Hepatic microvascular dysplasia) - Signalment
Small breed dogs & Cats
Portal vein hypoplasia without portal hypertension (Hepatic microvascular dysplasia) - Diagnosis
History and clinical signs indicative of shunting (GI signs, CNS signs, Dysuria, Pu\Pd)
Can be milder to-non clinical as opposed to cPSS. Also with no signs of portal hypertension!
Blood results that might suggest shunting (previously discussed, such as hypocholesterolemia, Hypoalbuminemia, decreased urea, Hyperammonemia) - usually to a milder degree than those found in cPSS
Gold standard - a combination of the following:
1) No evidence of shunts on US \ angio-CT
2) Histology - Underdeveloped portal veins + abundance of portal arterioles
Portal vein hypoplasia without portal hypertension (Hepatic microvascular dysplasia) - Pathogenesis
Microscopic intra-hepatic connections between portal veins and systemic circulation
Portal vein hypoplasia without portal hypertension (Hepatic microvascular dysplasia) - Treatment
Main treatment - Low protein diet
GI\Hepatic encephalopathy medical treatment if further indicated
Portal vein hypoplasia with portal hypertension (Non-cirrhotic portal hypertension) - Pathogenesis
Hypoplasia of the portal system, but as opposed to HMD - Does cause portal hypertension - leading to both HE and ascites
No evident fibrosis/cirrhosis
Portal vein hypoplasia with portal hypertension (Non-cirrhotic portal hypertension) - 2 main clinical signs
CNS signs (hepatic encephalopathy)
Ascites
Portal vein hypoplasia with portal hypertension (Non-cirrhotic portal hypertension) - Treatment, Prognosis
Supportive:
Treat HE (i.e. Lactulose, Antibiotics, Low-protein diet +- Gabapentin/Flumazenil)
Treat ascites (Low sodium diet, Spironolactone, Abdominocentesis if indicated)
Prognosis: Poor - MST 2 years
Post-sinusoidal diseases - Arteriovenous malformation - Pathology
Fistula between hepatic artery and portal vein
How can you differentiate between pre and post-sinusoidal portal hypertension based on the abdominal effusion
Based on the TS of the effusion:
Pre-sinusoidal: Transudate (<3 g\dL)
Post-sinusoidal - Modified transudate (~3 gr/dL)
Post-sinusoidal diseases - Arteriovenous malformation - Diagnosis
Angio-CT
Post-sinusoidal portal hypertension - Etiologies
Arteriovenous malformation
R-CHF
Tamponade
Budd-Chiari syndrome
Thrombus in the Vena Cava
Post-sinusoidal diseases - Best diagnostic tools
CT
R-CHF \ Cardiac Tamponade - US
Vacuolar hepatopathy - Common etiologies
Hypothyroidism
Cushing’s disease
DM
Tetracycline
Obesity
Hepatic lipidosis (Cat) - Signalment, Classic history
Middle-aged-old cats
Overweight cat that hasn’t eaten for a few days (2-7 days) or lost weight lately
Hepatic lipidosis (Cat) - Pathogenesis
Cats are obligatory carnivores and when they become anorexic, they stop getting essential amino acids and fatty which are necessary for fat metabolism:
-L-Carnitine deficiency: responsible for transporting fatty acids to the mitochondria for beta-oxidation and transport from the hepatocytes to the blood stream
-Apoprotein deficiency: VLDL production decreases - reducing transport of fat from the liver to the blood stream
Overweight cats: abundant amount of fat that can be transported to the liver (Main reason for the classic signalment of the disease
Diabetogenic hormones increase and insulin secretion decreases
HSL levels Increase and LPL levels Decreases
Hepatic lipidosis (Cat) - Clinical signs
Anorexia, Lethargy, GI signs (e.g. Vomiting, Diarrhea), CNS signs (e.g. Aimless walking, Star gazing, Seizures), Jaundice
Hepatic lipidosis (Cat) - Classic bloodwork findings
Mild non-regenerative anemia
ALP (+++), ALT (++). GGT Normal
Hypocholesterolemia (Liver failure) or hypercholesterolemia (Cholestasis)
Hypoalbuminemia
Hyperbilirubinemia
Decreased urea
Hyperglycemia (Hypoglycemia less common)
High ammonia levels
Low B12
Hepatic lipidosis (Cat) - Diagnosis (Gold standard)
FNA of the liver showing hepatocytes with vacuolar changes
Hepatic lipidosis (Cat) - Treatment, Prognosis
Treat underlying cause (i.e. Pancreatitis, Cholangiohepatitis)
Feeding (The most crucial principal). Mostly done through an esophageal tube. High protein diet (Some protein might be necessary in cases of hepatic encephalopathy)
Liver support:
L-Carnitine supplement
Anti-oxidant
Vitamin B1 supplement (Thiamine)
Vitamin K supplement
Vitamin B12 supplement
*Ursodiol is contraindicated
GI support (e.g. anti-emetics, Pro-motile, Appetite stimulant)
Treat hepatic encephalopathy if present (e.g. Lactulose, Antibiotics, Gabapentin/Flumazenil)
65-90% - depending on the primary cause. First 24-48h after feeding has started is the most crucial due to refeeding syndrome
Hepatic lipidosis (Cat) - Possible life threatening complication when starting to treat hepatic lipidosis
Refeeding syndrome:
Hypokalemia
Hypomagnesemia
Hypophosphatemia
Hypoglycemia
Low Thiamine levels
Can cause GI signs, CNS signs, Arrhythmias and can lead to death
Give examples for drugs that can cause hepatotoxicity (6)
Acetaminophen
Carprofen (Idiosyncratic)
Phenobarbital
Tetracyclines
Ketoconazole
TMS
Mucocoele - Predisposing diseases\etiologies
Hypothyroidism
Cushing’s disease
Hypertriglyceridemia
Mucocoele - Treatment
2 Approaches:
Surgical - Cholecystectomy (Removal of the gallbladder) - Considered the preferred approach in order to avoid risk of bile peritonitis
Medical - Ursodiol, Anti-oxidant, GI support and analgesia if indicated
Antibiotics if indicated.
Mucocoele - Possible complications
Cholangitis
Gallbladder rupture and bile peritonitis
Copper-related chronic hepatitis - Age of onset
Bedlington Terrier - as soon as 1 year of age
Other breeds - middle-age adults
Vascular anomalies of the liver - Congenital Porto-systemic shunts - commonly causes hyperbilirubinemia (True\False)
False
PSS does not cause cholestasis and therefore does not cause hyperbilirubinemia
When is it indicated to perform a Bile Acid test? When is it indicated to perform a Post-Prandial Bild Acid test? What result is considered abnormal\elevated?
Animal with GI signs and decreased liver functions +- elevated liver enzymes that is not Icteric!
If fasting bile acids levels are normal
> 25 micromol\L for both tests
Mucocele - Treatment
Conservative:
Low fat diet
Ursodiol
Antioxidants (e.g. SAMe / Thistle)
Antibiotics
Surgical: Cholecystectomy
GGT Elevation - Which organs should Be suspected to be involved?
Biliary tract
Pancreas
Small Intestine
What is the mean age for copper-associated chronic hepatitis in Labradors?
7 Years
Copper-associated chronic hepatitis - common breeds (5)
Bedlington terrier, Labrador retriever, WHWT, Doberman Pinscher, Dalmatian
Chronic hepatitis - diagnosis
Signalment & Clinical signs
Blood works (Most common - elevation in ALT, other liver & bile enzyme elevations possible, Changes in Liver functions (Chol, Alb, Bili, Glu, Urea, Bile Acids, Ammonia, Coagulation factors)
Urinalysis (Isosthenuric USG, evidence of ammonium biurate crystals)
Abdominal US (Liver size, shape, echogenicity, Evidence of Portal hypertension)
Screening for infectious diseases (e.g. Leptospira, Leishmaniasis, Toxoplasmosis, Bartonella, Mycobacterium, Aspergillosis)
Liver biopsy, copper staining & Quantification
Culture and sensitivity for bacteria and mycology.
Copper-associated chronic hepatitis - Treatment
D-Penicillamine
Zinc supplementation
Low copper diet
Anti-oxidants
Chronic Hepatitis - Common Breeds (5)
Labradors, Doberman, Dalmatian, Cocker Spaniel, WHWT
Chronic hepatitis - Treatment
Treat underlying causes
Supportive treatment (e.g. GI Protectants, anti-emetics, Apatite stimulant)
Liver diet
Anti-oxidant
Ursodiol
Ascites => Abdominocentesis, Spironolactone, Low sodium diet
Hepatic encephalopathy => AB + Lactulose
Prednisone +- Immunosuppressant (If indication of active inflammation on histology)
Treat for copper-accumulation (if indicated)
In which species (Dog/Cat) Is GGT elevation more specific to biliary tract disease
Cats
Neutrophilic Cholangitis - Treatment
Treat underlying cause
Supportive treatment
ABs (C&S Preferred) for a period of 4-6 weeks
Ursodiol
Anti-oxidants
If recurrent episodes and Lympho-plasmacytic cholangitis suspected - consider glucocorticoids\Immunosuppressant.
Destructive cholangitis - Common histological findings (3)
Ductopenia
T-Cell Predominate - Infiltrate to duct walls
Lipograuloma
What is the algorithm of analyzing cytologic samples?
1) Is the cellularity low\moderate\high
2) Is the slide Inflammatory?
3) What is the dominant cell type - Epithelial \ Mesenchymal \ Round Cell
4) What is the morphology of the cells - Hypercellularity\Anisocytosis\Anisokaryosis || Prominent Nucleoli\Multiple Nucleoli\Vacuolation\Basophilic Staining\Mitosis\Cytophagia (Not Macrophages)\Cells in wrong location\Nuclear molding
EPI - Most dogs have TLI levels of…?
> 2.5microgram\L
