Test 2: 12 liver 1 Flashcards
liver gets blood from
Portal Circulation
hepatic artery
red?
centriloblar lobule- zone 3
midzonal lobule- zone 2
periportal lobule- zone 1
blood flows from portal triad to the central vein
portal triad includes
portal venule
hepatic arteriole
bile ductule
kupffer cells (macrophages of liver)
stellate cells
leakage enzymes such as — live — in the hepatocytes
ALT- Alanine Aminotransferase
AST- Aspartate Aminotransferase
SDH- Sorbitol Dehydrogenase
cytoplasm
if there is damage to hepatocyte, you will find these in the blood
induced enzymes such as — are found where in the hepatocyte
Alkaline Phosphatase- ALP
Gammaglutamyl Transpeptide –GGT
membrane bound- seen with increased stress on hepatocyte- increased metabolic activity
Macrophages within sinusoids/space of Disse
kupffer cells
kupffer cells eat —
RBC and bacteria, immune complex and endotoxins
kupffer cells will accumulate —
iron, ceroid /lipofuscin/lipid
from eating RBC, bacteria and old cells
Stellate cells are involved in — metabolism
vit A
found in space of Disse
stellate cells are also called
Ito cells or hepatic lipocytes
stellate cells may transform to —
myofibroblasts and contribute to
fibrosis, along with other fibroblasts
what proteins does the liver make
Albumin
Fibrinogen
Clotting factors
Globulin
primary Photosensitization
is caused by
Liver incapable of excreting photodynamic compound
Ingestion of St. John’s wort (Hypericum perforatum)
secondary photosensitization (hepatogenous) is caused by
damage to liver
eat food with cholestasis, can’t break down Phylloerythrin (catabolite of chlorophyll) or other
photodynamic compounds
these accumulate in the skin and cause severe sun burn
type 2 Photosensitization
congenital porphyria
hereditary defect in heme metabolism
hemoglobin break down
kupffer cells with eat iron
bilirubin metabolism
RBC breaksdown in spleen, gets attached to albumin complex
unconjugated bilirubin: albumin enters liver
hepatocyte conjugates bilirubin making it water soluble
excreted in bile into the intestine
some reuptake
most degraded to urobilinogen by bacteria and excreted in poop
bile in liver flows
in canaliculi opposite direction of blood
will flow toward the portal triad
another name for jaundice
icterus
hyperbilirubinemia
prehepatic icterus is caused by
massive breakdown of RBC
leading to large amounts of unconjugated bilirubin
hepatic icterus is caused by
liver issue- unable to uptake and/or excrete bilirubin
leads to Increased conjugated and unconjugated bilirubin
posthepatic icterus is caused by
Bile duct obstruction
Increased conjugated bilirubin
Hepatoencephalopathy can be caused by —
portosystemic shunt
blood skips liver- cause too much ammonia in the blood leading to neuro issues
3 types of reversible injury to liver
also called vacuolar hepatopathy
Hepatocellular swelling *Glycogen accumulation *Hepatic lipidosis
hepatocellular swelling is caused by —. and looks —
cells accumulate water due to inability to maintain
ionic and fluid homeostasis
issue with sodium pump
marked swelling with
very pale staining cytoplasm
hepatocellular swelling is reversible or irreversible
reversible but can lead to necrosis if not resolved
glycogen accumulation is caused by
glycogen accumulation without displacement of
the nucleus from the center
usually midzonal, but can be diffuse, zonal, or
involve individual cells
glycogen accumulation in dogs is caused by
Steroid Hepatopathy
glucocorticoids (endogenous or exogenous)
* may be seen with stress or other drugs
glycogen accumulation
glycogen accumulation is reversible or irreversible
reversible; usually NOT associated with necrosis
hepatic lipidosis cause — in the cytoplasm of the hepatocytes
vacuoles of lipid
hepatic lipidosis is reversible or irreversible
reversible form of cellular injury; but may lead to necrosis
another name for hepatic lipidosis
fatty change or steatosis
5 ways fat can accumulate in the liver
A. Excessive entry of FAs due to — (most
common)
B. Excessive FA synthesis and TG formation due to excessive intake of —
C. Decreased — of FAs due to hepatocyte dysfunction
D. Decreased — with subsequent decreased export of lipoproteins
E. Impaired secretion of — (often due to hepatocyte dysfunction)
excessive dietary intake or increased mobilization
carbohydrates
oxidation
apoprotein synthesis
lipoprotein
tension lipidosis
ligaments pull on edge of liver causing decreased blood flow and fat accumulation
Feline Fatty Liver Syndrome
storage disorder in the liver are accumulations in hepatocytes and — due to inherited metabolic disorders
Kupffer cells
Common findings include clear vacuoles, vacuoles with granular or hyaline material, or cytoplasmic yellow brown material
what causes canine copper-associated hepatopathy
not really sure
might be chronic active hepatitis
Cu accumulates in centrilobular hepatocytes → progressive → hepatocellular necrosis and inflammation with copper-laden hepatocytes and macrophages → chronic hepatitis and cirrhosis
what type of dogs have genetic mutation in copper transport proteins
Bedlington terrier
what type of dog has familial association for copper-associated hepatopathy
West Highland white terrier, Dalmatian
what type of dog has breed predisposition for copper-associated hepatopathy
Doberman pinschers, Labrador retrievers, and cocker spaniels
Multifocal Random necrosis is caused by
Infectious agents (virus, protozoa, bacteria)
massive necrosis is caused by
Toxic and nutritional
zonal necrosis is caused by
toxic or hypoxia (zone 3)
Centrilobular (periacinar / zone 3)
Midzonal (midacinar / zone 2) - rare
Periportal (centroacinar / zone 1)
inflammation of the liver parenchyma
Hepatitis
inflammation of the bile ducts
Cholangitis
inflammation of the bile ducts with extension into the liver parenchyma
Cholangiohepatitis:
inflammation of the gall bladder
Cholecystitis
inflammation of the bile ducts
Choledochitis
Bile stasis is also called
cholestasis
cholestasis is caused by
toxins, inflammation, duct
obstruction
cholestasis will cause increased — in circulation
inducible enzymes
Alkaline Phosphatase- ALP-dogs and cats
Gammaglutamyl Transpeptide –GGT-Liver and Biliary-All Species
— is severe diffuse (bridging) hepatic
fibrosis with nodular regeneration and bile duct hyperplasia
cirrhosis
necrosis and inflammation in the liver can lead to
Regeneration
Fibrosis
Bile Duct Hyperplasia
Cirrhosis
liver
Fibrosis and Nodular Regeneration
Cirrhosis
severe diffuse (bridging)
hepatic fibrosis with nodular regeneration and bile duct hyperplasia
cirrhosis leads to
portal hypertension→ multiple acquired
portosystemic shunts, ascites
Loss of hepatic function →insufficiency →
failure
Coagulopathies
Hyperbilirubinemia
Hepatoencephalopathy
Edema, Ascites (hypoproteinemia)
Photosensitization
