hepatic dx Flashcards
Liver
Largest internal organ; located in the R upper quadrant
liver blood supply
➢ ~ 20 % Hepatic artery - oxygenated blood
➢ 80% Portal vein –nutrients
bile duct system
Common Hepatic Duct
- left and right hepatic ducts forms the common hepatic duct
- drains bile from the liver
- transports waste from the liver and aids in digestion by releasing bile
Common Bile Duct
- carries bile from the liver and the gallbladder through the pancreas and into the duodenum
- part of the biliary duct system; formed where the ducts from the liver and gallbladder are joined
Hepatic Veins
drain venous blood from liver to inferior vena cava and on to the right
Hepatic Artery
Hepatic Artery – provides oxygen and nutrition to liver tissues
Hepatic Portal Vein
delivers substances absorbed by the gastrointestinal tract (stomach, intestine, spleen and pancreas) for metabolic conversion and/or removal in the liver
hepatocytes proteins produced
- Immunoglobulins
- Albumin
- coagulation factors
- carrier proteins
- growth factors
- hormones
bilirubin
role of hepatocytes
➢ bilirubin is from breakdown of RBCs; bilirubin transported to liver by being bound to albumin (unconjugated form)
➢ Liver conjugates bilirubin by unbinding the protein binding it to glucose; this unconjugated form is in bile
➢ Produces bile for digestion
➢ Produces cholesterol for fat storage
Bilirubin levels escalate from:
➢ Blood disorders - hemolytic anemia, sickle cell anemia, inadequate transfusions
➢ **Chronic liver disease **
➢ Blockage of bile ducts in liver or gallbladder
➢ Viral hepatitis, EtOH induced hepatitis; drug induced hepatitis, cirrhosis, etc.
➢ Increased bilirubin –jaundice, fatigue, cutaneous itch, discolored urine, discolored feces (?)
nutritional function hepatocytes
➢ Regulates nutrients
- glucose
- glycogen
- lipids
- amino acids
excretion function hepatocytes
➢ Prepares drugs for excretion
➢ Responsible for drug conjugation and metabolism
oBilirubin conjugation
oPhase I –cytochrome P450; can produce toxic metabolites
oPhase II –conjugation (glucuronidation, sulfation, inactivation by glutathione, etc.)
forms of damage at liver
➢ Hepatocellular (inflammation and injury)
➢ Cholestatic (obstructive)
➢ Mixed
➢ Cirrhosis (fibrotic, end-stage); acute or chronic
➢ Neoplastic
general signs of liver dx
➢ skin?
➢ gut?
➢ swelling?
➢ bleed?
➢ urine?
➢ stool?
➢ Mental?
➢ eyes?
➢ Spider angiomas
➢ Palmar erythema
➢ nn?
➢ skin?
➢ Jaundice
➢ Ascites
➢ Edema
➢ GI bleed
➢ Dark urine
➢ Light stool
➢ Mental confusion
➢ Xanthelasma
➢ Spider angiomas
➢ Palmar erythema
➢ Asterixis
➢ Hyperpigmentation
symptoms liver dx
➢ Appetite loss ֎
➢ Bloating
➢ Nausea
➢ RUQ pain
➢ Fatigue
➢ Mental confusion
Xanthelasma
fatty chol deposits in occular area
spider angiomas
poor clotting factors= capillary fragibility
Asterixis
- a.k.a. flapping tremor
- classic sign in hepatic encephalopathy (HE)
- jerky movements when hands are extended at wrists.
hepatic encehpalopathy
Asterixis pathogenesis
common blood tests
*Complete Blood Count (CBC)
*Comprehensive Metabolic Panel (CMP)
*Multiple others available for specific patient evaluations
Complete Blood Count (CBC)
- evaluate the cells that circulate in blood: red blood cells (RBCs), white blood cells (WBCs), platelets (PLTs)
- indicator of overall health
- may detect a variety of diseases and conditions
Comprehensive Metabolic Panel (CMP)
- aka chemical screen or, SMAC 14 (Sequential Multiple Analysis –Computer)
- consists of 14 blood tests which serves as an initial broad medical screening tool
- Includes
- General tests
- Kidney function assessment
- Electrolytes
- Protein tests
- Liver function assessment
- there are also SMAC 8, 12, 16 and 20 variants
Liver Function Tests
*Bilirubin
*Alkaline phosphatase (ALP)
*Transaminases
- Aspartate amino transferase (AST)
- Alanine amino transferase (ALT)
- Gama-Glutamyl Transferase (GGT)
*Albumin
*Globulin
high bilirubin levels
oProduct of heme breakdown
oIncreased total bilirubin, increased severity of liver injury
measured in congugated and unconguated forms
uncongugated bilirubin
oUnconjugated (indirect)
❖Insoluble, bound to albumin, not filtered by kidney
❖Increased SERUM not really indicative of liver disease,
❖indicates hemolysis, ineffective erythropoiesis (thalassemia,
vitamin B deficiency, Gilbert syndrome)
congugated bilirubin
oConjugated bilirubin (direct)
❖Increased SERUM indicative of liver disease
❖Water-soluble, excreted by kidney
❖All URINE bilirubin is conjugated
➢ Alkaline phosphatase (high)
oaltered in myriad of diseases especially bone neoplasms
onot specific to liver disease,
omay indicate cholestatic disease
➢Transaminases are elevated
AST, ALT, and GGT
elevated AST
- AST - Aspartate Aminotransferase (SGOT)–a.k.a. Serum Glutamic-Oxaloacetic Transaminase-
–related to glutamic oxalate metabolic pathways
elevated ALT
- ALT - Alanine Aminotransferase (SGPT) –a.k.a. Serum Glutamic-Pyruvic Transaminase-
–part of pyruvate pathway in cell metabolism
elevated GGT
- Gama-Glutamyl Transferase (GGT)- needed for protein synthesis
- useful to detect alcohol-induced liver cell injury and chronic alcoholics
- can detect the slightest degree of cholestasis
- sensitive to biliary obstruction, cholangitis, and cholecystitis
- good marker for pancreatic cancer, prostatic carcinoma, and liver cell
high transaminases
indicates? individually? level? important ratio?
o Indicates damage to hepatocytes from hepatocellular disease
o Not individually proportionally reflective of severity of liver damage
o Up to 300 UI/L –> non-specific
o AST:ALT ratios more informative
- the lower the ratio, the more specific an indicator of hepatic disease
o GGT more indicative of cholestatic disease and alcoholic liver disease
albumin levels
synthesized by?
half life?
more indicative of?
specific?
➢ Albumin (low)
oSynthesized “exclusively by hepatocytes”
oHalf-life: 18-20 days
❖More indicative of chronic liver disease
❖Not specific to liver disease:
✓ Malnutrition
✓ Chronic infection
✓ Gut disease
PT time
oLiver produces all coagulation factors except?
oPT measures factors:
oVitamin K dependent coagulation factors:
Prothrombin time (extrinsic and common pathway)
oLiver produces all coagulation factors except VIII (vascular endothelial cells)
oPT measures factors I, II, V, VII, X
oVitamin K dependent coagulation factors: II, VII, IX, X
oINR is actually PT-INR
Viral Hepatitis
➢ All viral hepatitis are RNA virus, except for Hep B (HBV) which is enveloped DNA virus
how can Hep damage liver
➢ Hepatocellular damage –> host immune response to viral antigens rather than direct cytopathic effect from virus
oCytotoxic T-cells
oProinflammatory cytokines
oNatural killer cell response
oAntibody-dependent cellular cytotoxicity
how can hep infection present?
o Chronic hepatitis can lead to:
➢ Infection may be asymptomatic/symptomatic and acute/chronic
o Patient may clear the virus or virus may become inactive
o Reactivation may occur
o Chronic hepatitis can lead to:
❖ Cirrhosis
❖ Liver failure
❖ Hepatocellular carcinoma.\
❖ Risk factor for immunosuppression
o Chronic hepatitis can lead to:
❖ Carrier state (low levels)
Hepatitis B (Hep B; HBV)
on surfaces? incubation period? chronic in dif demos? vax? reactivation?
➢ Virus can last for up to 7 days on an infected surface
➢ Incubation period: 90 days average
➢ Chronicity:
o90% for infants
o25-50% in children (1-5)
o<5% in adults
➢ Vaccination
o3 doses (initial, 1 month, 6 months)
oSeroconversion necessary
➢ Reactivation
hep b tx
➢ Peg- interferon or antivirals such as entecavir and tenofovir
acute hep b infection with recovery serology