Liver Function (Anatomy and Physiology) Flashcards
Largest and complex organ responsible for major metabolic functions in the body
Liver
Primary organ that can ONLY EXHIBIT KETOGENESIS
Liver
Liver is found at the
Right upper quadrant of abdomen
Liver has abundant blood supply approximately
1500 ML/MIN
Two major vessels of liver (2)
Hepatic Artery
Hepatic Portal Vein
Branch of aorta that provides most of the oxygen requirement; contributes 20% blood supply
Hepatic Artery
Drains the gastrointestinal tract and Spleen, Transports most of the recently absorbed materials from the intestines to the liver
Hepatic Portal Vein
Metabolic Activity of liver takes place within the___ ; constitutes 80% of organ mass
Parenchymal Cells
Aside from Parenchymal cells, liver also contains cells like (2)
Kupffer Cells
Stellate cells (major cell type responsible for Fibrosis)
Six-sided functional unit of Liver
Liver Lobule
Branches of Hepatic Artery and portal vein
Central Vein
Sinusoids
Hepatocytes and Kupffer cells
Bile canaliculi
Bile ducts
Component of Liver Lobule
Bile ducts
Hepatic Portal Vein
Hepatic Artery
Portal Triad
It is responsible for METABOLIC, SYNTHETIC, SECRETORY, EXCRETORY FUNCTION
Liver
First-Pass
Phagocytosis by KUPFFER CELLS
Metabolism and excretion of drugs
Production of Urea
Detoxification
Synthesis of Bile acids and Bile salts
Excretory System/Biliary System
Loss of functioning hepatocytes
Cirrhosis and Hepatitis
Decreased Levels (bile acids)
Regurgitation from hepatocytes
Biliary Obstruction and Hepatocellular Disease
Increased Levels (Bile acids)
Secretion Function
heme waste products (Bilirubin and Porphyrin)
Bile pigments
Bilirubin
Ammonia
Lipids
Bile salts
Drug Metabolism
Metabolic
Drug Metabolism is tested using
Cytochrome p450
- measure after 1hr
- Cynthelation Counter
Serum Total Protein
Albumin
AAT
Ceruloplasmin
Coagulation Factors
Synthetic Function
Except:
FVIII - produced in Endothelial Cells
FVII - First factor to be increased in Liver disease
Transaminases (AST and ALT)
Biliary Epithelium (ALP, 5-NT, GGT)
Hepatic Injury
Carbohydrates
Fats
Lipoproteins
Ketone bodies
Proteins
Hormones ( Somatomedin and Angiotensinogen)
Synthesis or Metabolism Function
Fat Soluble and water-soluble vitamins, Glycogen, Iron
Storage
B1 —-> B2 reactions is catalyzed by enzyme
UDPGT
Uridyl diphosphate Glycuronyltransferase
Structure: Bilirubin
Bound to protein: Yes (albumin)
Type of Compound: Non-Polar
Soluble in water: No
Present in Urine: No
Reaction with Diazotized Sulfanilic Acid: Indirect (Requires accelerator)
Affinity for Brain Tissue: High
Unconjugted Bilirubin
Structure: B1, B2, Delta Bilirubin
Bound to protein: No (Except for Delta Bili)
Type of Compound: Polar
Soluble in water: Yes
Present in Urine: Yes
Reaction with Diazotized Sulfanilic Acid: Direct (no accelerator)
Affinity for Brain Tissue: Low
Conjugated Bilirubin
Laboratory Assays to Assess Liver Disease:
Hepatocellular damage
AST
ALT
Laboratory Assays to Assess Liver Disease:
Cholestasis
ALP (inc. period of growths)
GGT (small liver insults)
5-NT (Specific for hepatobiliary disease)
Laboratory Assays to Assess Liver Disease:
Liver Excretory Function
Serum Bilirubin
Urine Bilirubin
Blood Ammonia
Laboratory Assays to Assess Liver Disease:
Assays of biosynthetic function
Total Protein, Albumin, Globulins
Coagulation factors
Hemolysis
Hereditary Erythrocytes Enzymopathies
Bilirubin
Bone cancer, Pregnancy
ALP
Muscle Damage, Cancer, Pancreatitis, Renal Disease
ALT
Myocardial Infarction, Skeletal Muscle damage
AST
Myocardial Infarction, Skeletal Muscle damage, renal disease, cancer
LDH
Pesticide Poisoning
DECREASE CHOLINESTERASE
LIVER DISORDERS:
may be acute or chronic or combination of both; damage to and destruction of liver cells
Hepatitis
LIVER DISORDERS:
regeneration leads to fibrosis, scarring, and destruction of normal liver architecture
Cirrhosis
destruction of intrahepatic bile ducts; presence of ANTI-MITOCHONDRIAL ANTIBODIES
Primary Biliary Cirrhosis
LIVER DISORDERS:
Both primary, more frequently secondary to cancer of bowel, stomach, and bronchus
Tumors
ASMA-CAH
Anti-Smooth Muscle Antibody
Chronic Active Hepatitis
STAGES OF ALCOHOLIC LIVER DISEASE:
Ethanol in lipid metabolism; decreasing fatty acid oxidation and increasing formation/deposits of TRY in liver
Steatosis (1st stage) / Alcoholic Fatty Liver
STAGES OF ALCOHOLIC LIVER DISEASE:
Takes place with INFLAMMATION and development of fibrosis or necrosis
Steatonecrosis (2nd stage)
STAGES OF ALCOHOLIC LIVER DISEASE:
EXTENSIVE development of fibrosis, hepatocelullar carcinoma
Alcoholic Cirrhosis
yellowish pigmentation of the skin, mucous membrane, and sclera of eyes due to hyperbilirubinemia
Jaundice/Icterus
Bilirubin exceeds 3.0-5.0
Overt Jaundice
CLASSES OF JAUNDICE:
Known as Hemolytic or Retention Jaundice
Pre-Hepatic
CLASSES OF JAUNDICE:
Excessive destruction of RBC
HDN, Erythroblastosis fetalis, Malaria
Hepatic Uptake DECREASED: Prolonged fasting and intake of drugs
Pre-Hepatic Jaundice
CLASSES OF JAUNDICE:
Also known as Infectious Jaundice
Hepatic Jaundice
CLASSES OF JAUNDICE:
- Damage to hepatocytes due to microorganisms or ALCOHOL
- Starvation and Certain Medications
- Hepatitis and Cirrhosis
- Parasitism (FASCIOLA HEPATICA)
Hepatic Jaundice
HEPATIC JAUNDICE:
Physiologic neonatal jaundice
Gilbert’s disease
Crigler-Najjar Syndrome I and II
Lucey-Driscoll Syndrome
Bilirubin Conjugation Decreased
Bilirubin Conjugation Decreased:
UDPGT is 30% functional
Defect in Transport protein LIGANDIN
Benign
Gilbert’s Disease
Bilirubin Conjugation Decreased:
UDPGT deficiency - Conjugation Deficiency
Crigler-Najjar Syndrome
Bilirubin Conjugation Decreased:
UDPGT deficiency - Conjugation Deficiency
Complete Absence of UDPGT
Criggler-Najjar Syndrome I
Bilirubin Conjugation Decreased:
UDPGT deficiency - Conjugation Deficiency
Partial Absence of UDPGT
Criggler-Najjar Syndrome II
Bilirubin Conjugation Decreased:
Circulating inhibitor of conjugation
Lucey-driscoll syndrome
Bilirubin Conjugation Decreased:
Defect in Chromosome 2
Gilbert’s Syndrome
Criggler Syndrome
Impairment of Hepatic Excretion:
Dubin Johnsons Syndrome
Rotor Syndrome
Impairment of Hepatic Excretion:
Presence of DELTA bilirubin; dark stained granules (Lipofuscin) in liver biopsy
Dubin Johnsons Syndrome
Impairment of Hepatic Excretion:
Reduced/Defective ligandin; UPTAKE/TRANSPORT DEFICIT
Rotor Syndrome
Also known as Regurgitive, Obstructive, Cholestic Jaundice
Post-Hepatic Jaundice
Obstruction of Biliary Flow
Post-Hepatic Jaundice
Intra-hepatic cholestasis
Obstruction of Extra-hepatic biliary Tree
Cholethiasis or Gallstones
Strictures, Spasms, artresia, and Microorganisms
Cancer of Pancreas
ASCARIS LUMBRICOIDES
Post-Hepatic Jaundice
TB: Increased
B1: Increased
B2: Normal
Urine Bil: Normal
Urine urobilinogen: INCREASED
Stool: Dark Brown
Pre-Hepatic
TB: Increased
B1: Increased
B2: Increased/Normal
Urine Bil: Variable
Urine urobilinogen: Normal
Stool: Pale/Brown
Hepatic
TB: Increased
B1: Normal
B2: Increased/Normal
Urine Bil: Positive
Urine urobilinogen: Normal
Stool: Clay
Post-Hepatic
Buildup of unconjugated bilirubin
2-3 days of neonatal life
Most common cause is HDN
Neonatal Jaundice
Poorly developed blood brain barrier allowing B1 to cause damage to central nervous system
B1 > 20 mg/dL
Kernicterus
Treatment for Neonatal Jaundice
Phototherapy
SUMMARY OF LIVER DISORDERS :
AST/ALT 10-110 x ULN
Acute Viral Hepatitis
SUMMARY OF LIVER DISORDERS :
AST/ALT: Slight persistent elevation
Total Protein: Decreased
Chronic Hepatitis
SUMMARY OF LIVER DISORDERS :
GGT 2-3 x ULN
Lipid: Elevated
Alcoholic Liver Disease
SUMMARY OF LIVER DISORDERS :
Albumin, Cholesterol: Decreased
PT: Prolonged
Cirrhosis
SUMMARY OF LIVER DISORDERS :
Total bilirubin and B1: Elevated
Primary Biliary Cirrhosis
SUMMARY OF LIVER DISORDERS :
GGT up to 20 x ULN
ALP: elevated
Hepatic Tumors
SUMMARY OF LIVER DISORDERS :
GGT and ALP markedly Elevated
Cholestasis
recovery from viral infection and aspirin ingestion in children, neurologic abnormalities, accumulation of ammonia in CNS
Reye’s Syndrome
