Where does blood flow after entering a liver lobule at the portal triad?
Blood flows through sinusoids from the portal-triad region toward the central vein.
Study 1 Liver Function and Injury Patterns with 12 free online flashcards. Review key terms, definitions, and concepts with this interactive flashcard deck.
Where does blood flow after entering a liver lobule at the portal triad?
Blood flows through sinusoids from the portal-triad region toward the central vein.
Which bilirubin form is water-soluble and may enter urine?
Conjugation makes bilirubin water-soluble; conjugated bilirubin can be excreted in urine.
What do elevated ALT and AST primarily indicate?
ALT and AST are released with cell injury; their levels do not, by themselves, measure how well the liver functions.
What enzyme pattern defines hepatocellular injury?
ALT and AST rise more prominently than ALP. Examples include viral hepatitis and ischemic injury.
How does the R value classify liver-injury patterns?
Calculate R=ALP ULNALPALT ULNALT using the same sample. R>5 is hepatocellular, R<2 cholestatic, and R=2–5 mixed; it classifies the pattern, not cause or severity.
In which direction does bile flow through a liver lobule?
Bile flows through canaliculi toward bile ducts, opposite to the direction of blood flow.
Which liver-lobule cells are relatively vulnerable to reduced oxygen delivery?
Cells near the central vein are relatively vulnerable because oxygen delivery is reduced there.
Why is unconjugated bilirubin not normally excreted in urine?
Unconjugated bilirubin is carried bound to albumin and is not normally excreted in urine.
How do ALT and AST differ in tissue specificity?
AST can rise with muscle or other tissue injury; ALT is more liver-specific.
How can GGT help interpret an elevated ALP?
A disproportionate ALP elevation may suggest cholestasis, but ALP also comes from bone and other tissues. GGT can support a liver or biliary source.
Why does low albumin alone not establish chronic liver dysfunction?
Low albumin can reflect chronic liver dysfunction, but also inflammation, malnutrition, kidney protein loss, or fluid overload. Its long half-life makes it less responsive to sudden changes.
What is an important limitation when interpreting PT/INR in liver disease?
A prolonged PT/INR may reflect impaired clotting-factor production, but other factors can affect it; in cirrhosis, INR alone is not a reliable measure of bleeding risk.
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