Path 1 - Hepatobiliary 1

drraythe's version from 2016-01-26 04:40

Liver & Intrahepatic Biliary System

Question Answer
What are the 2 types of necrosis the hepatocytes experience & what happens to them?(1) Coagulative Necrosis: Denaturation of hepatocytes, swollen hepatocytes
(2) Lytic Necrosis: Loss of hepatocytes
Random hepatocellular degeneration → What does this look like? What weird name for a liver fits this category?Single cell necrosis or Multifocal areas of necrotic hepatocytes. Sharply delineated from adjacent parenchyma. SAWDUST LIVER in cattle fits this
What type of hepatocellular degeneration does "SAWDUST LIVER" of cattle fall under?Random hepatocellular degeneration
Zonal hepatocellular degeneration and/or necrosis → what are the 5 locations/zones does this encompass?Periportal (Zone 1)
Midzonal (Zone 2)
Centrilobular (Zone 3)
Bridging necrosis
Explain where the "zones" are/ where the central vein/terminal hepatic venule isWhere 3 lobules come together, that is the portal tract, which has the hepatic artery, portal vein & bile duct in it. From the portal tract, the zones radiate outward → zone 1 is directly around the tract, zone 2 is around that & zone 3 is the farthest. Zone 3 is directly in contact w/ the central vein (aka terminal hepatic venule) which is in the CENTER of the hepatic lobule
What is the liver acini?It is the area which encompasses the 3 zones...instead of classifying the liver into lobules, which is anatomic, this is metabolic/blood flow based on the center being the portal tract & the edges being defined by the central/terminal hepatic venule
Zonal degen/necrosis → PERIPORTAL necrosis or degeneration occurs in what zone & is generally due to what?Zone 1, czd by Toxins that don’t require MOF(Mixed fxn oxidases → metabolism) activation
In terms of chemicals & biotransformation in the liver, where does biotransformation/metabolism of it take place?Drugs/chemicals arent usually metabolized until they reach zone 3
Zonal degen/necrosis → MIDZONAL necrosis or degeneration occurs in what zone & is generally due to what?Zone 2, czd by Aflatoxicosis (mycotoxins from aspergillus) (two aflack ducks))
Zonal degen/necrosis → CENTRILOBULAR necrosis or degeneration occurs in what zone & is generally due to what?Zone 3 & is czd by HYPOXIA (makes sense, by the time the blood gets here, it's the farthest zone from the hepatic artery, so there is the least amount of O2)
**TQ: WHAT CZS CENTRILOBULAR DEGEN?HYPOXIA (also the greatest enzymatic activity in zone 3, so most metabolized toxins end up there as well)
Zonal degen/necrosis → PARACENTRAL (PERIACINAR) necrosis or degeneration occurs where? & is usually due to what?Wedge around central vein (so, apex of triangular wedge is at central vein & base of wedge triangle at portal area) This is usually czd by a direct toxin(doesnt require biotransformation so damages through all the zones)
What is bridging necrosis?Where necrotic areas join
What is MASSIVE necrosis? What part of the liver is damaged?ENTIRE LOBULE is damages & there is scarring.
**TQ: What CZS MASSIVE necrosis?Selenium or Vit E deficiency!!!! Also TOXIC injury (mycotoxins, pyrrolizidine alkaloids) & CHEMICALS
What are the 2 situations where there is a disturbance of bile flow/icterus?(1) Overproduction of bilirubin due to hemolysis
(2) Reduced outflow of bile (cholestasis)
When in the liver is there regeneration, versus when is there scarring?If there is just damage to some hepatocytes w/in a lobule, there will be regeneration. If the WHOLE lobule is destroyed, then there is SCARRING.
What is the % or fractions of the liver which can be removed w/: no CS, hyperplasia+hypertrophy & what will keep the animal alive?(1) 2/3s or 66% of the liver can be removed w/ no signs of hepatic dysfxn
(2) If 70% of the liver is removed, you will see hyperplasia & hypertrophy
(3) You can remove 90% of the liver & the animal can still live
What CZS fibrosis(nodules)?REPEATED INJURY (CHRONIC)
What do Hepatic stellate cells (Ito cells) do? When would you see them, then?They synthesize collagen (I, III, IV) which leads to FIBROSIS! (Stellar fibers, man!)
Periportal (centroacinar) fibrosis from what 2 things?(1) Chronic inflammation
(2) Toxins (inflamed vessels in the portal area pressing on zone one/inflammatory mediators hit that part of the liver 1st? Chronically. makes sense. & of course toxins.)
Centrilobular (periacinar) fibrosis from what 2 things?(1) Chronic toxic injury (metabolism of toxins in this area, chronic!)
(2) Long standing right heart failure (which czs hypoxia)
Biliary hyperplasia → what is happening here? What is going on?when new biliary ducts form. It is nonspecific, idiopathic pathogenesis, and/or longstanding hepatic injury
**TQ: If you see cirrhosis, how long has this been going on?CHRONIC PROBLEM
What is the typical presentation of a cirrhotic liver?Diffuse FIBROSIS (multiple nodules), liver ATROPHY (it will be FIRM to the touch) & there will be INFLAMMATION
What is the atypical presentation of a cirrhotic liver? when might this occur?E.g. Lobular dissecting hepatitis: young dogs.... liver will be smooth & small
What are some czs of liver cirrhosis?CHRONIC STUFF → chronic toxicity, chronic cholangitis and/or obstruction, chronic congestion (right side heart failure), Inherited disorders of metal metabolism (copper or iron), chronic hepatitis, idiopathic
What is the vicious cycle pathogenesis of cirrhosisHepatic injury → necrosis → regen → fibrosis → CHRONIC insult czs self-perpetuating damage, which leads you back to hepatic injury
**HOBNAIL LIVER: aka? what does it look like? What czs it & what are the results?PORTAL CIRRHOSIS! Distorted lobules /irregular nodules. It is from ACUTE TOXIC hepatitis & there is periportal fibrosis (Toxic=periportal fibrosis, remember?)
4 patterns of cirrhosis are?Portal, biliary, post-necrotic, cardiac
Biliary cirrhosis is difficult to distinguish from?Portal (hobnail) cirrhosis. Which I assume means that biliary also looks like Distorted lobules /irregular nodules
**TQ: When do you see microhepatica?In Post-necrotic cirrhosis!
Post-necrotic cirrhosis → what does this LOOK LIKE?**Microhepatica**: liver is SMALL, firm/hard w/ irregular large nodules
**When do you see NUTMEG LIVER?In Cardiac cirrhosis (nutmeg is good for your heart)
Cardiac cirrhosis → what is going on where? What does it look like?Chronic passive liver congestion → scarring around central veins & “nutmeg liver” (Essential feature of cirrhosis usually absent)
What are the 2 major sequale to liver cirrhosis?(1) Profound Vascular abnormalities (anastomosis & venous shunts)
(2) Liver failure (loss of fxn)
Hepatic failure leads to what 6 sequale?Icterus, Hepatic encephalopathy (portosystemic encephalopathy), Metabolic disturbances, Vascular & hemodynamic alterations, Cutaneous manifestations, Immunologic manifestations
Hepatic encephalopathy (portosystemic encephalopathy) → what is the common cz of this? uncommon?(COMMON) Ammonia not metabolized by liver. (UNCOMMON) imbalance of AA neurotransmitters
What are the 2 Metabolic disturbances of hepatic failure?(1) Bleeding tendencies (hemorrhagic diathesis
(2) Hypoalbuminemia (↓ production & loss in ascites)
What are the Vascular & hemodynamic alterations of hepatic failure?Portosystemic shunts, Ascites (modified transudate)
What are the 2 major Cutaneous manifestations of hepatic failure?(1) Hepatocutaneous syndrome
(2) Photosensitization
Hepatocutaneous syndrome → AKA? what happens in this syndrome?AKA: necrolytic migratory erythema, superficial necrolytic dermatitis, “French flag lesion”. w/ chronic hepatic injury there is abnormal metabolism & you will see CRUSTING & Parakeratosis (keratinization w/ retained nuclei)
**TQ: What is FRENCH FLAG lesion? (whats happening, why?)It is a Hepatocutaneous syndrome from liver failure! Abnormal metabolism leads to crusting & Parakeratosis (keratinization w/ retained nuclei) of the skin
Photosensitization → What is happening in 1° photosensitization?Ingestion of 1°/preformed photodynamic agent
Photosensitization → What is happening in 2° photo-sensitization?Hepatic dysfxn or biliary obstruction → Can’t breakdown or excrete Phyloerythrin(in plant chlorophyll)
Photosensitization → Congenital porphyria. What kinda disorder is this? what happens?Metabolic disorder, where abnormal heme metabolism + abnormal excretion + accumulation of porphyrins
What are some immunologic manifestations of liver failure?Endotoxemia
↓ synthesis of ɑ & β globulins
Look over portals of entryNot highlighted, so I'm not making cards
Look over defense mechanismsNot highlighted, so I'm not making cards
Mechanisms of liver injury → how can bioactivation cz liver injury?Metabolic bioactivation of chemicals via cytochrome P450 to reactive species
Mechanisms of liver injury → how can calcium relate to this?Disruption of calcium homeostasis leading to cell surface blebbing & lysis
Mechanisms of liver injury → Canalicular (tiny ducts collecting bile formed by hepatocytes) injury czs what?Cholestasis


Question Answer
What are 3 incidental findings you might find in the liver?Tension lipidosis (steatosis), capsular fibrosis, postmortem changes
Tension lipidosis (steatosis) → who does this happen in? what happens & what are the lesions like? how important is this?Happens in HORSES & CATTLE (big things w/ big heavy livers). Ligament attachment TENSION → impeded blood supply → hypoxia → lipidosis. You will see discrete PALE areas at liver MARGINS. They are of NO FXNAL SIGNIFICANCE!
Who do you see capsular fibrosis in?Horses
Post mortem changes of liver → who does this happen most quickly in? What are the color changes you'd see?Happens quickest in FAT animals. GIT bacteria → degradation → formation of hydrogen sulfide (green-blue). The Imbibition of bile (yellow-green)
Acute hepatitis → characterized by what 3 things? CZD by what 3 things?Inflammation, apoptosis, necrosis. Czd by viruses (non-supperative, (mononuclear cells, lymphocytes) ), Bacteria (supperative, neutrophils), or fungi
**TQ~: CHRONIC hepatitis can be czd by WHAT 3 THINGS & what LESIONS result from this?(1) Virus → Multifocal Necrosis → Fibrosis
(2) Bacteria → Focal necrosis → Abscess
(3) Fungus → Granulomatous (tan-yellow, caseous)
Nonspecific reactive hepatitis → usually a response to what? describe its characteristicsResponse to systemic illness (usually GIT). There is MILD inflammation, NO NECROSIS, acute will show neutrophils & chronic will show mononuclear cells: lymphocytes, plasma cells, Kupffer cells
What is Cholangitis?Inflammation of the bile duct
What are the 3 types of cholangitis?Lymphocytic, Neutrophilic & Destructive
What does Lymphocytic cholangitis look like?Periphery of ducts → Fibrosis, intrahepatic cholestasis
What does Neutrophilic cholangitis look like? what does it imply?BACTERIAL infxn → abscess. Can happen in lumen or epithelium.
What does destructive cholangitis look like?Epithelial Necrosis from Chemicals (e.g. Trimethoprim sulfa)
What is Cholangiohepatitis?Inflammation of cholangio-bile duct & hepatic-liver parenchyma
Disturbance of OUTFLOW → chronic passive congestion leads to what?NUTMEG LIVER
Hepatic veno-occlusive Dz happens bc of what? What is the result? What are 2 czs?Thickening of CENTRAL VEIN leads to FIBROSIS. This can be from Hepatotoxicity: pyrrolizidine alkaloids, or Vitamin A overdose
ANEMIA results in what type of degeneration/necrosis of the liver?CENTRILOBULAR (zone 3)
What are the 2 Congenital portosystemic SHUNTS? what vessel czs each one?(1) Intrahepatic: ductus venosus
(2) Extrahepatic: portal vein
Portal HYPERTENSION leads to what?→ splanchnic vein → ASCITES
PREHEPATIC portal hypertension can happen bc of what?(1) Portal vein thrombosis
(2) Hypercoagulability
(3) Tumor
(4) Infxn
(5) ↑ Splenic flow
HEPATIC portal hypertension can be czd by what 2 things?(1) Cirrhosis (↑ resistance in sinusoids)
(2) Fibrosis
POSTHEPATIC portal hypertension can be czd by what?(1) Hepatic vein thrombosis
(2) Vena-caval obstruction
(3) Chronic passive congestion
What are 2 vascular anomalies which can cz portal hypertension?(1) Intrahepatic arteriovenous shunts (anastomoses)
(2) Portal vein hypoplasia (microvascular dysplasia, noncirrhotic portal hypertension)
**TQ: WHAT IS Telangiectasis? What does it look like? Who is it common in? What is its clinical sig?Dilation of sinusoids where hepatocytes have been lost. Dark red-purple pinpoints-cm (variably sized). Common in CATTLE w/ no clinical sig.