clinical chem exam 1 liver funx

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clinical chem exam 1 liver funx
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2010-02-24 14:26:21
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clinical chem exam 1 liver
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  1. List important functions of the liver
    • a.
    • Liver produces bile from bile acids and salts,
    • cholesterol and biliruben pigment removed from the blood

    • b.
    • Bile stored in gallbladder

    • c.
    • Reabsorbs bile returned to live via portal vein

    • d.
    • Synthesize proteins- transport molecules mostly
    • (albumin, transferrin, ceruloplasmin)

    • e.
    • Syn glycogen- storage of glucose

    • f.
    • Syn lipids and lipoproteins- repackaging

    • g.
    • Syn Clotting factors- protein based

    • h.
    • Syn urea- N waste from the deamination of
    • proteins

    • i.
    • Storage of fat soluble vitamins (A,D,E,K, B12

    • j.
    • Key role in transport/storage/metabolism of
    • metals like iron

    • k.
    • Converts many noxious or insoluble chemicals
    • into other forms that are less toxic and more water soluble an therefore
    • excretable by the kidneys
  2. Bile
    • a.
    • Function- facilitates digestion and absorption
    • of lipids in small intestine

    • b.
    • Produced from bile acids and salts, cholesterol
    • and biliruben pigment removed from the blood

    • c.
    • Stored in gallbladder where it is concentrated
    • up to 10x


    • i. After
    • meal, gallbladder contracts and expels bile into intestine


    • ii. Bile
    • digests and facilitates lipid absorption


    • iii. Eventually
    • returned to liver via the portal vein
  3. Vitamins stored in the liver
    • a.
    • Fat soluble ones

    • b.
    • A, D, E, K, B12
  4. Detoxification role of liver
    • a.
    • Converts noxious or insoluble compounds into
    • other forms that are less toxic and more water soluble and therefore excretable
    • by the kidneys
  5. Formation of biliruben
    • a.
    • Formed from the breakdown of hemoglobin when
    • aged RBCs are removed from circulation

    • b.
    • Protein (globin) is reused

    • c.
    • Iron enters iron stores and is reused

    • d.
    • Porphyrin is broken down as a waste product and
    • is excreted


    • i. Action
    • of splitting the porphyrin ring and releasing the iron and globin forms
    • biliruben


    • ii. Biliruben
    • is transported to the liver bound to albumin and is taken up into the hepatic
    • cells


    • iii. Conjugated
    • by an enzyme within the hepatocyte


    • iv. Conjugated
    • bili passed along with other bile constituents to the gallbladder and
    • eventually the GI tract


    • v. Acted
    • upon by bacterial enzyme in GI tract producing urobilinogen


    • vi. Urobilinogen
    • is oxidized further to urobilin and excreted in the stool (pigment)
  6. Biliruben terminology
    • a.
    • Unconjugated biliruben (indirect)- form by
    • splitting of the porphyrin ring, and release of iron and globin. Transported by
    • albumin


    • i. Before
    • acted upon by enz in hepatocyte

    • b.
    • Conjugated biliruben (direct)- after acted upon
    • by enz in hepatocyte
  7. Jaundice
    • a.
    • Also called icterus

    • b.
    • Yellowish discoloration of the skin, fingernail
    • beds, and sclera due to the accumulation of bilirubin

    • c.
    • Causes kernicterus


    • i. Caused/associated
    • with jaundice


    • ii. Damage
    • to the brain of infants due to the build up of unconjugated bili
  8. Pre-hepatic hyperbilirubinemia causes
    • a.
    • Caused by the increased hemolysis and increased
    • degradation of hemoglobin

    • b.
    • Increase in unconjugated(indirect) bili (not
    • water soluble)

    • c.
    • Liver is functioning normally but is unable to
    • keep up with demand for conjugation

    • d.
    • Happens in certain anemias

    • e.
    • Normal enz with exception of LD & AST due to
    • their high concentrations in RBCs

    • f.
    • Very high LD concentrations are observed with
    • intravascular hemolysis
  9. Hepatic hyperbilirubinemia
    • a.
    • Causes


    • i. Generally
    • due to defective transport or defective bilirubin conjugation within the liver
    • itself


    • ii. Gilbert’s
    • disease

    • 1.
    • Conjugating fine but decreased bilirubin
    • transport into the hepatocyte

    • 2.
    • Hereditary

    • 3.
    • Causes an accumulation of indirect bili


    iii. Criger-Najjar

    • 1.
    • Hereditary deficiency in UDPG (necessary for
    • conjugation)

    • 2.
    • Fatal


    • iv. Hepatocyte
    • damage

    • 1.
    • Due to hepatitis, cirrhosis, toxins, etc.

    • 2.
    • AST and ALT- liver enzymes that indicate
    • hepatocellular inflammation and damage often elevated

    • 3.
    • Bili results can vary depending on severity of
    • damage

    • b.
    • All enz can be increased, but AST & ALT
    • elevations are more pronounced
  10. Post-hepatic hyperbilirubinemia
    • a.
    • Causes


    • i. Generally
    • due to defect in transporting conjugated bili and bile out of the liver


    • ii. Often
    • called “obstructive jaundice” b/c can involve obstruction of the small
    • canaliculi within the liver, the hepatic bile duct, the common bile duct, or
    • gallbladder

    • 1.
    • Obstruction due to gallstones, scarring, nodules
    • from cirrhosis, or tumors

    • 2.
    • If stones not resolved, bacterial growth can
    • cause septicemia

    • b.
    • GGT and ALP- enz that indicate biliary cell
    • damage are often elevated

    • c.
    • Stools lose color, which is indicative of low
    • urobilinogen

    • d.
    • Pronounced elevations of ALP and GGT

    • e.
    • Normal to slightly increased AST & ALT
  11. Neonatal hyperbilirubinemia
    • a.
    • Causes


    • i. Not
    • always caused by liver function


    • ii. Most
    • commonly caused by a short-term in producing UDPG


    • iii. Also,
    • higher turnover of neonatal RBCs as fetal hemoglobin F is replaced by A


    • iv. Longer
    • more sustained hyperbili indicates serious condition such as

    • 1.
    • Hemolytic Disease of the Newborn (HDN)

    • a.
    • Presents as a pre-hepatic jaundice
    • (incompatibility btwn blood groups of mother an fetus)

    • 2.
    • Biliary atresia- anatomical obstruction of
    • biliary ducts


    • v. Other
    • factors such as progesterone or other hormones in breast milk my suppress
    • conjugation

    • b.
    • Phototherapy often treatment to prevent
    • kernicterus


    • i. UV
    • light converts bili to isomer which is water soluble and excretable

    • c.
    • Normally subsides in a few weeks
  12. Liver enzymes
    • a.
    • AST (aspartate amino transferase) (SGOT)

    • b.
    • ALT (alanine amino transferase) (SGPT)

    • c.
    • GGT (gamma glutamyl transferase)

    • d.
    • ALP (alkaline phosphatase)

    • e.
    • LD (lactate dehydrogenase)


    • i. AST,
    • ALT, & LD are mainly found in structural hepatic cells


    • ii. ALP
    • & GGT are more concentrated in the biliary ducts or canaliculi

    • f.
    • Measurement in enz aid in diagnosis and
    • treatment

    • g.
    • Enz are released into plasma at higher rate than
    • normal when cells become diseased

    • h.
    • Diff tissues can release diff enz depending on
    • location
  13. Isoenzymes
    • a.
    • Multiple forms of the same enz composed of diff
    • subunit strux and are distributed in diff types of tissues

    • b.
    • In addition to being found in the liver:


    i. AST: erythrocyte and muscle tissue


    • ii. LD:
    • erythrocyte and muscle tissue


    • iii. ALP:
    • osteoblast, intestinal mucosa, and placental tissue


    • iv. ALT:
    • only found in the liver, therefore most lliver specific
  14. Synthetic activities of the liver
    • a.
    • Protein synthesis


    • i. Liver
    • synthesizes majority of proteins in the plasma

    • 1.
    • Measurment can be indicative of liver function

    • 2.
    • Also indicative of malnutrition, renal loss, and
    • gastrointestinal loss



    • a.
    • Liver also synthesizes carbs & lipids


    • i.
    • Glucose to glycogen


    • ii.
    • Gluconeogenesis from a.a., alcohols, and lipids

    • b.
    • Formation and metabolism of fat


    • i.
    • Chylomicrons removed


    • ii.
    • Conversion of acetyl CoA to fatty acids,
    • triglycerides, and cholesterol


    • iii.
    • VLDL, HDL


    • iv.
    • Repackages lipids
  15. what are proteins in aqueous solution
    Proteins are ampholytes in aqueous solution

    • May
    • have + or – charge

    • Property
    • exploited in electrophoresis
  16. Fiberous proteins
    • string like construction usually function as structural
    • components (fibrinogen, collagen, elastin)
  17. Spherical proteins
    • usually found in plasma and function as transporters, antigens, Ab’s,
    • hormones, enzymes, and clotting factors
  18. can liver produce both fibrous and spherical proteins
    liver capable of producing both types
  19. proteins found in protein measurement
    • i.
    • Protein measurement

    • a.
    • Albumin

    • b.
    • Globulins

    • five classes determined by
    • electrophoretic separation

    • ·
    • Albumin (half of total serum proteins)

    • ·
    • Alpha 1 globulins

    • ·
    • Alpha 2 globulins

    • ·
    • Beta globulins

    • ·
    • Gamma globulins (Ig, or Ab’s)
  20. Storage function of liver
    • a)
    • Stores all fat soluble vitamins and some water
    • soluble

    • b)
    • Converts carotene to Vit. A

    • c)
    • Clearinghouse for hormones

    • d)
    • Transport, storage, metabolism of iron

    • e)
    • Vit. K (part of coagulation mechanism)
  21. Detoxification reactions
    • a)
    • Ethanol- leading hepatic toxin

    • i)
    • Heavy consumption may lead to cirrhosis

    • ii)
    • Leading cause of morbidity and mortality in US

    • b)
    • Liver link between internal organs’ circulation
    • and systemic blood

    • c)
    • Protects body form potentially harmful
    • substances absorbed from the intestinal tract and toxic byproducts of
    • metabolism

    • i)
    • Ammonia converted to urea

    • ii)
    • Oxidation, reduction, hydrolysis, hydroxylation,
    • carboxylation, demethylation, conjugation

    • iii) Conversion
    • to water-soluble excretable compounds

    • (1) Glutamines,
    • glucuronic acid, acetate, etc combined with toxin so it can be excreted through
    • the kidneys
  22. Effects of acetaminophen
    • a)
    • Exhausts the liver’s normal route of metabolism

    • b)
    • Toxic metabolites kill the hepatocyte

    • i)
    • Necrosis, coma, death

    • c)
    • Half life of 4 hours, so can be used to
    • monitor/asses liver damage in other drug overdoses
  23. Cirrhosis
    • i)
    • Scarring of liver resulting in nodular
    • appearance

    • ii)
    • Result of chronic liver inflammation

    • iii) Synthetic
    • ability reduced = decreased proteins and clotting factors

    • iv) Portal
    • hypertension due to blood blockage by scarring

    • v)
    • Fluid accumulation (decreased albumin)

    vi) Causes


    • (1) Alcohol
    • abuse

    • (2) Iron
    • overload

    (3) Hepatitis


    (4) Autoimmune


    (5) Hemochromatosis
  24. Reye syndrome
    • i)
    • Hepatic destruction after viral infection such
    • as chicken pox or influenza

    • ii)
    • Abnormal liver funx but no increase in bili

    • iii) Increased
    • ammonia levels

    • iv) Neurological
    • complications first

    • v)
    • Primarily kids

    • vi) Linked
    • to aspirin therapy in these diseases

    • vii) Unknown
    • cause

    • viii)
    • Poor prognosis
  25. Tumors
    • i)
    • Hepatocellular

    • ii)
    • 2ndary to tumors from other sites (lungs,
    • pancrease, ovary)

    • iii) almost
    • always malignant

    • iv) usually
    • always linked to infection with hepatitis virus

    • v)
    • poor pronosis

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