Liver 1

sihirlifil's version from 2018-03-14 21:10


Question Answer
How can a patient present for liver disease?Asymptomatic! :)
General malaise, GI signs
Hepatic encephalopathy (HE)
4 possible types of liver dz?Acute hepatic failure
Acute biliary obstruction
Chronic liver disease
End stage liver disease
Phases of liver disease: ACUTE = ?Inflammation, necrosis, recovery
Phases of liver disease: CHRONIC = ?inflammatory, fibrosis (irreversible)
Phases of liver disease: END STAGE = ?Cirrhosis, portal hypertension
Most COMMON patient presentation?Asymptomatic!
Best time to catch liver disease...when it's asymptomatic!!
What are the 2 enzyme patterns?Hepatocellular (leakage)
Cholestatic (inducible)
What do the liver enzymes tell you?Whether dz affects primarily hepatocytes vs. biliary tree. Wellness bloodwork helps the most
Name the enzyme pattern
Name the enzyme pattern
Name the enzyme pattern
If you have a MIXED enzyme pattern, how can you tell which one predominates?Check how many times above the highest reference interval the liver value is. E.g. ALT of 700 is 7x higher (RR 10-100U/L), while ALKP of 700 is only 4x higher than 155 (RR 23-155U/L). So more of a hepatocellular pattern in this case.
What GI signs might you see?ANY is possible?
Anorexia, vomiting, diarrhea
Melena: Portal hypertension (gastric blood flow disrupted), coagulopathy (not making clotting factors or recycling vit K)
Common presentation of liver disease in CATS?Triaditis! and general malaise
Ddx for acute liver failureToxin
Ddx for chronic liver diseaseInflammatory
Copper storage
Hepatic encephalopathy (HE): how does it present? (2)Mild: dull mentation, apathy, ataxia
Severe: Seizures, blindness, coma
Hepatic encephalopathy (HE): when can it happen? why?After a meal! Protein metab --> increased ammonia
Dogs with PSS: 2ry to gastric bleed
Special CS of HE in cats?Hypersalivation
(grading HE)
Ddx of HE: Intra-cranialVascular, inflam, infx, neoplasia, structural...
Ddx of HE: Extra-cranialToxin, metabolic, hepatic (acute liver failure, PSS vascular shunting), metastatic neoplasia, infx
PSS vascular shunting can cause neuro signs... 2 types of shunts?Acquired (end stage cirrhosis, portal hypertension)
How does icterus present?Subtle to obvious
May present for pigmenturia: dark brown to bright yellow urine
Icterus ddxPrehepatic, hepatic, post-hepatic!!!
How does ascites present?Enlarged abdomen --> fluid
Ascites: what kind of fluid?
(Ascites) Abdominocentesis --> Pure transudate ddx?Hypoalbuminemia (PLE, PLN, hepatic)
Portal hypertension (cirrhosis, liver failure)
(Ascites --> pure transudate) Liver diseases that lead to cirrhosis & portal hypertensionChronic liver disease --> end-stage liver failure
Congenital venous malformations: PSS, AV malformations
How does coagulopathy happen?Liver synthesizes coag factors I, II, V, VIII, IX, X, XI, XIII
Reduced clearance of activated coag factors
Biliary obstruction/stasis --> fat solube vitamins can't be absorbed (Vit K, factors II, VII, IX, X, Protein C, Protein S)
Coagulopathy: which branch of coag is affected?BOTH! PT & PTT prolonged
Hypocoagulability: what coag test would be abnormal?Only PT! ((Vit K dog: rodenticide, or biliary problem so not getting fat soluble vitamins in)
*Hypercoagulable state: how does it happen?Extra-hepatic biliary obstruction
(Coagulopathy) Ddx of cavity bleedRodenticide tox
Hepatic failure
Ruptured viscus/vessel
(Coagulopathy) Ddx of melenaGastric/duodenal ulcer
Inflam GI
Hepatic failure
Portal/renal hypertension
Liver dzs that lead to coagulopathyAcute liver failure
End stage liver failure
Biliary stasis: hepatic lipidosis, extrahepatic bile duct obstruciton, GB mucocele, obstructed GB/cystic duct

Workup & Dx

Question Answer
Diagnostics depend on 3 things:Presentation, other ddx (e.g. icterus --> prehepatic, hepatic, post-hepatic)
Cholestatic vs. hepatocellular enzyme pattern
Acute, chronic, end-stage presentation CS
General workup: HepatocellularInfectious disease testing
Abdominal US
Chest radiographs
+/- liver FNA
+/- liver biopsy
+/- abdominocentesis
General workup: CholestaticAbdominal US (r/o obstruction)
Infectious disease (Lepto)
Cholecystocentesis cytology & culture (usually US-guided, get bile)
Chest rads
+/- abdominocentesis
+/- liver biopsy
General workup: Liver function failureBile acids
Ammonia +/- protein C
Abdominal US (find where to centesis)
Chest rads
+/- liver biopsy
+/- abdominocentesis
How is US for diagnosing types liver disease?NOT GOOD! Mass? 50/50. No mass? 50/50 (can see if cavitated)
What is ultrasound good for?Ruling out biliary obstruction & assessing other organs
What is CT good for?Hepatic parenchyma & biliary tree (can see neoplasia w/ metastasis)
Problem with CT?Availability
**The liver is highly regenerative... how can that mess with diagnostics?Scarring can look like a mass on US or CT!
Diagnosible by FNA:Hepatic lipidosis
Round cell neoplasia
Bacterial culture (liver & bile)
NOT diagnosible by FNAVascular diseases
Many infx
Many neoplasia
Metabolic dz (e.g. steroid hepatopathy)
Which liver sampling technique is least invasive? Most? what info do they give?
General dx plan for hepatocellularInfx dz test
Abd US
Chest rads
(+/- FNA, biopsy, abdcent)
General dx plan for cholestaticAbd US (r/o biliary obsx)
Infx dz (Lepto)
Chest rad met check
(Abdcent, biopsy)
General dx plan for function failureBile acids
Ammonia (+/- protein C)
Abd US
(+/- biopsy, abdcent)

Biliary Diseases

Question Answer
How does patient present for biliary disease?Icterus
Abdominal pain
CATS: general malaise, GI
OR asymptomatic, chronic elevation of cholestatic enzymes
Origins of biliary dz (4)Hepatocyte-level (obstruction of canaliculi & hepatic ducts
Cystic duct
Common bile duct (pancreas, duodenum)
**Which biliary dz is hardest to dx?
Hepatocyte-level (hepatic lipidosis can cause cholestasis here)
Biliary disease origins: diagnosis?GB, cystic duct, & common bile duct level biliary dz are easier to dx with ultrasound
Causes of biliary tract obstruction?Mucocele
Infection/inflam debris
CS of biliary obstructionSAME regardless of location or cause!!
**Painful abdomen 1st dx?Abdominal rads! R/o sx emergency
Diagnostics: what ddx is r/o with abdominal radiographs?Sx emergency! find out this before the cause of CS
Diagnostics: what ddx is r/o with CBC/CHem/UA?Prehepatic vs. Hepatic vs. Post-hepatic
Diagnostics: what ddx is r/o with Abdominal ultrasound?Post-hepatic (good for biliary tree!)
Diagnostics: what ddx is r/o with chest radiographs?Belly full of fluid, perforation, ruptured abscess
What's this?
Distended GB (L), with solid blob at neck (R)
What is a GB mucocele?Solidified bile + mucus
Why does a GB mucocele form?Dysmotility? Excess mucus? dyslipidemia? steroids?
Endocrine diseases (hypoT4, cushings)
How does GB mucocele present?From incidental to life-threatening emergency
What's this?
GB mucocele
What happens with GB/Common bile duct obstruction?From ANY cause --> rupture --> Bile peritonitis, effusion, surgical emergency
How does cytology of a ruptured GB/common bile duct look?
How is the mortality of ruptured GB/CBD obstruction surgery?40%! So if you find mucocele as incidental finding... can tell owner what to monitor as emergent sign, can recommend sx too. depends
Choleliths: happen in who? how?Uncommon in dogs (Mini Schnauzers, mini poodles), rare in cats
May be associated with infection or dysmotility. May be incidental, or cause obstruction
Cholelith: if INCIDENTAL?Stay tuned!
Non-obstructive biliary diseases (6)Dysmotility
Abnormal bile
Early mucocele formation
Inflammatory dz
Infection ascending from GIT
How do non-obstructive biliary diseases & mucocele/cholelith formation relate?All (dysmotility, abnorm bile, hyperlipidemia, inflam dz, ascending GIT infxn) are theoretically causes of mucocele/cholelith formation. Often a combination of factors, can lead to obstructive biliary dz
How does non-obstructive biliary disease present?Asymptomatic (incidental, chronic elevations of cholestatic enzymes)
General malaise, GI
Dx plan for non-obstructive biliary dzAssess for dysmotility (hardest, dx of exclusion), abnormal bile, hyperlipidemia (TG & chol lvls +/- endocrine), inflam dz, ascending GIT infection
How do you assess hyperlipidemia?Triglycerides & cholesterol levels
+/- endocrine testing
Function of bile?Helps digest lipids & fats. Bile contents messed up --> inappropriate metab --> abnormal lvls of triglycerides in blood (except familial form which is other way around)
Cholecystocentesis: how is it done?US-guided, stick needle & collect bile, do cytology & culture (aerobic and anaerobic)
Treat if you see bacteria on culture OR cytology!
Risk of cholecystocentesis? can it be prevented?Small risk of bile leakage. Can put needle through liver side, so if some bile leaks it goes into the liver where the cannaliculi pick it up
Common type of non-obstructive biliary disease in cats:Feline cholangitis
Feline cholangitis: inflammatory form (4 combos)?Triaditis: Cholangitis + pancreatitis + IBD
Cholangitis + IBD
Pancreatitis + IBD
Cholangitis + pancreatitis
Feline cholangitis: infections form?Ascending from GIT
Suspected secondary to IBD or other intestinal diseases that mess up GI flora (no sphincter in duct + gut microflora out of whack = setup for infxn)
What's the arrow pointing at?
(Feline liver) Can see bile duct! Normal finding
Canine cholangitis: which type is more common?Infectious >>> inflammatory
Canine cholangitis: how does it happen?2ry to ANY 1ry liver or GB disease
Canine cholangitis: Which dx do you ALWAYS want to do?Take a culture! Bile, GB wall, stone (Infections is most common cause)
Monitoring non-obstructive dz: inform owners...Obstruction can occur, and CS they would see if it does
Monitoring non-obstructive dz: which tests?Ultrasound (look at GB & biliary tree)
Triglycerides, cholesterol, bloodwork
Tx of cholestasis/abnormal GB contents: 3 main pointsLow fat diet
Tx: Diet?Low fat
Treatment of concurrent hyperlipidemia, endocrinopathy
Tx: If bacteria cultured from bile OR cytology...Antibiotics 4-6 weeks
Poor penetration (usually abscess) so need long course. Use bloodwork & US
Tx: What is Ursodiol? how does it work?Ursodeoxycholic acid: hydrophilic bile salt
Give in pill form, goes into GB, sucks water in, helps content go through biliary system
Has anti-apoptotic properties to protect hepatocytes from killing themselves
Neutraceutical (low risk of SEffx)
If a patient presents, looks, and has bloodwork like a cholestatic patient but you can't see an obstruction on US, think...Hepatocyte-level cholestasis
Causes of cholestasis at the hepatocytes/canaliculi?Feline cholangitis (infx or inflam) (previously cholangiohepatitis)
Many hepatocellular dz --> swelling of hepatocytes --> physical obstruction of canaliculi (E.g. Feline hepatic lipidosis)
Cholestasis --> hepatocyte damage
Vicious cycle of cholestasis (pic)
Cornerstones for tx of many types of liver/biliary diseasesUrsodiol
Antioxidants: SAM-e, Milk thistle/silymarin, Denamarin (combo of SAM-e & milk thistle), Vit E
**Something to note about Denamarin?In most patients, silymarin is the less necessary part of Denamarin (just an antidote for cetrain toxins e.g. mushrooms). So can give SAM-e by itself and dose appropriately