liver Flashcards
liver structure
-red brown color
-divided into lobes
-sharp edges (if soft edges something wrong
-composed of many hepatic lobules or acinus (same thing)
liver blood supply
- Dual blood supply:
1. Portal vein (drains blood from
spleen, intestine and
pancreas)
2. Hepatic artery - Portal vein and hepatic artery
both drain into hepatic
sinusoids - Blood leaves the liver via the
hepatic vein.
liver cell structure
-then layer of hepatocytes with hepatic and portal venule coming together and draining into sinusoids.
-sinusoids have holes which allow the interaction between liver and systemic circulation via the space of disse
-the space of disse: space between helatpcytes and sinusoids. contains stallate cells.
-liver filters blood
-in diseased cells the stellate cells with form firbous tissue. so fibrous tissue in space of disse so less blood filtering/ systemic circulation.
-any amount of liver firbosis is clinically relevent.
Space of Disse
- Space of Disse: Fluid filled space
between endothelial cells and
hepatocytes - Interface for interaction between
liver and blood. - Contain “Stellate cells” which:
1. Store vitamin A (normally).
2. Can synthesize collagen and thus
cause hepatic fibrosis (in
diseased liver).
Hepatic lobule (Hexagonal)
- Centre: Hepatic venule or
central venule - Periphery: Portal venule hepatic
arteriole bile duct, lymphatics,
nerves.
-least oxygenated in centerlobular area, and middle is midlobular area. most is periportal area
Hepatic acinus (diamond shaped)
- Centre: Terminal afferent branches of the portal venule and the hepatic arteriole
- Periphery: Hepatic venules
-zone 1 most oxygenated (closest to hepatic arteriol) , zone 2 middle, zone 3 less oxygenated
gallbladder
- Absent in horse, rat.
- Tubular organ
- Common bile duct empty into the
intestine
function of the liver: bilirubin metabolism
-bilirubin comes from RBC, where they are filtered by spleen (heme) is phagocytozed by macrophages in spleen. splits into heme + globin
-heme converted to bilirubim. (production)
-bilirubin leaves spleen binds albumin in blood, taken up by liver where it is conjugated. (uptake)
- excreted in bile ( intestines) and is absorbed again
high bilirubin 3 causes? and clinical
Jaundice = Icterus
Yellow Discoloration Of Tissues
3 types:
* Prehepatic Jaundice=
Cause: increase break down
of RBCs (liver can’t keep up!) lots of conjugated bilirubin.
* Hepatic Jaundice=
Cause: decreased uptake of
bilirubin due to liver disease
(bilirubin accumulates
because the liver is not
removing it from the blood)
* Post-hepatic Jaundice=
Cause: decreased hepatic
excretion of bilirubin with bile
(cholestasis)
common causes of jaundice in ruminants or horses
- In ruminants jaundice is most commonly prehepatic
(due to RBC hemolysis) - Icterus in other spps can occur to due prehepatic, hepatic, or post hepatic causes
- Horses develop physiologic icterus with starvation. NORMAL not disease.
Cause: Bilirubin uptake is energy dependent and is decreased during starvation. (This only occurs in
horses)
functions of the liver
1 bilirubin metabolism
2 bile acid metabolim
3 carb metabolism: (everything to do with glucose, storage, formation ect.)
4 lipid metabolism: production and degradation of plasma lipids.
5 protein synthesis: 15% of proteins (albumin, clotting factors) and site for ammonia metabolism.
-ammonia is a toxic product of protein catabolism (in intestines), converted into urea in liver through urea cycle.
Normal liver function
2. Bile acid metabolism
- Bile acids are major bile constituents
- Synthesized by the liver and secreted into the small intestine
- Most bile acids are reabsorbed by the intestine and taken up again by the liver (very efficient reabsorption and enterohepatic circulation)
- Usually only liver uptake of bile acids is reduced with hepatic disease (NOT production)
Responses of the liver to injury
What can happen to the liver?
- Degeneration, Necrosis and Apoptosis
- Disturbances of Bile Flow and Icterus
- Regeneration
- Fibrosis
- Bile Duct Hyperplasia
- End Stage Liver
- Liver Failure
Degeneration Necrosis and Apoptosis of liver 3 types
Patterns of distribution of degeneration and
necrosis:
1. Random= caused by bacteria or protozoa, brought from blood.
2. Zonal (5 types)
3. Massive
zonal pattern of necrosis: centrilobular
-Most common type of zonal
change
-Hepatocytes are least oxygentaed
i.e. Prone to necrosis
-Hepatocytes contain greatest conc. of detoxyfying enzymes, aka mixed function oxidases or Cytochrome P450 enzymes.
-ex (nutmeg liver)
Common causes:
1. Toxins requiring metabolic
activation
2. Passive congestion in the liver
zonal pattern of necrosis paracentral
- Involves only a wedge around
central vein (only one acinus is
affected)
-happens with severe acute anemia or hemorrhage (blood loss), loss of BS to liver
Zonal pattern
3. Periportal (least common) 4 midzonal both rare
- Closest to blood supply
- Have high oxygen tension
- Affected first by toxins that
do not require activation - Have limited mixed function
oxidase enzymes i.e
generally, it is affected by
toxins that do NOT require
activation - Uncommon ex. Phosphorus
toxicity
Zonal pattern
5. Bridging necrosis
- May link centrilobular
areas (central bridging) or
centrilobular areas to
periportal areas
massive necrosis of liver
-The term describes
necrosis of an entire
hepatic lobule or
contiguous lobules
Disturbances of bile flow =(cholestasis)-Two types
-Intrahepatic & Extrahepatic
-intrahepatic Cholestasis:
Affects bile caniliculi or
ductules within the liver
Causes:
- Liver injury (fibrosis)
- Inherited abnormality of
bile synthesis and secretion
-Extrahepatic Cholestasis:
Affects extrahepatic bile duct
Causes:
-obstruction due to a mass within or outside the lumen. Will lead to
intrahepatic cholestasis
-If prolonged leads to fibrosis &
bile duct proliferation in the liver
liver regeneration
-Depends on the extent of damage
- If small: local proliferation of adjacent hepatocytes
- If extensive loss of hepatocytes and loss of extracellular matrix scaffold (basement membrane) (reticulin) occur:
You see regenerative nodules, disorganized regeneration.
-they don’t restroy hepatic function completely due to BF and bile flow is abnormal from firbosis.
fibrosis due to liver injury
-reduced interaction from liver and systemic circulation
-examples: long standing R sided H failure, lack of flow causes liver firbosis
- Random areas of fibrosis are see when parasites migrate through the hepatic parenchyma.
-“Bridging fibrosis” indicates that
the fibrosis extends from one portal area to another or to
centrilobular area
-liver with firbosis will have irregular surface, pale & firm from collagen. mishaped (shrink)
End Stage Liver (Cirrhosis)
3 processes all happening at same time:
-Degeneration and necrosis
-Regeneration,
-Fibrosis
These processes must be present almost diffusely throughout the liver to call it an end stage liver
hepatic failure definition
“loss of adequate hepatic function as a consequence of either acute or chronic hepatic damage”.
Consequences of hepatic failure
hepatic encephalopathy
- Hepatic encephalopathy:
-Accumulation of ammonia due to reduced uptake by the liver
-Ammonia is toxic to the brain
-Leads to abnormal neurotransmission in the CNS
and the neuromuscular system
Consequences of hepatic failure
2. Metabolic abnormalities
a. Bleeding tendencies due to:
Decreased synthesis of coagulation factors
b. Decreased albumin synthesis edema, low albumin means liver is fried.
Consequences of hepatic failure
3. Vascular and Hemodynamic alterations
Example: Acquired portosystemic shunt
-An abnormal vascular communication between
the portal vein and the systemic circulation, firboris leads to PORTAL HYPERTENSION. and ascites.
-fibrosis reroutes blood flow: leads to serum bile acid and ammonia increases, get ammonia bicurate crystals (bladder/ urine), hepatic enephalopathy.
extrahepatic shunt in liver failure
-Blood coming to liver by portal vein, if we have hepatic fibrosis we have Uncomplient liver so increase hydrostatic pressure in portal vein–> ascites. Lots of tension in portal vein so portal hypertension. Forms new portal to the vena cava=
Extrahepatic shunt. So blood is being shunted away from the liver and not being filtered and instead
Going back into systemic circulation.
You can also have an intrahepatic shunt in the liver.
-these are acquired portosystemic shunts.
Consequences of hepatic failure
4. Cutaneous Manifestations
A. Superficial necrolytic dermatistis DOGS ONLY rare.
- crusting and ulceration of the epidermis
- muzzle, mucocutaneous areas of the face, footpads,
and pressure points of the skin in some dogs
- Unknown mechanism
- Also occurs with diabetes
Consequences of hepatic failure
4. Cutaneous Manifestations:
B. Photosenstization
B. this is secondary Photosenstization secondary to hepatic dysfunction
-ruminants
-they eat plants (chlorophyl) which is converted into phE absorbed in liver and excreted in bile. if you have liver failure phE will accumulate into skin and absord UV light and lead to photosensitization. (oxidative damage and necrosis)
cytsts in liver 2 causes
Congenital biliary cysts=
- Single or few cysts can be found
as an incidental finding, not significant.
Polycystic disease=
- Rare occurrence
- Reported in Cairn Terriers, West
Highland white Terriers and
Persian cats pigs and goats
- Extensive cysts within the liver,
kidney and pancreas
- Can be fatal
