biochem_mod4_ms1

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soren101
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52280
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biochem_mod4_ms1
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2010-12-04 21:20:33
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biochem mod4 ms1
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biochem mod4 GI
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  1. CELL CYCLE
    M - MITOSIS

    G0 - NONDIVIDING

    G1 - GROWTH, CYCLIN D, Cdks 4 & 6,

    S - DNA REPLICATION, CYCLIN E

    CYCLIN A, Cdk 2

    G2 - PREP FOR CELL DIVISION, CYCLIN B, Cdk 1
  2. HOW DO CYCLINS AND Cdks STIM DNA SYNTHESIS
    PROGRESSION THROUGH CELL CYCLE REQUIRES CYCLIN PROTEINS, OF WHICH THERE ARE AT LEAST 20 AND CLASSIFIED INTO A,B,D, OR E

    UNDERGO SEQUENTIAL BINDING TO A GROUP OF CYCLIN DEPENDENT KINASES (CDks) THROUGHOUT CELL CYCLE FORMING SPECIFIC CYCLIN-Cdk COMPLEXES

    CYCLIN-Cdk COMPLEXES PHOS A DNA BIND PROTEIN CALLED RETINOBLASTOMA GENE PRODUCT (pRb)

    PHOSED pRb RELEASES TRANSCRIPTION FACTOR (eg E2F

    E2F STIMS TRANSCRIPTION OF GENES ENCODING ENZYMES NEEDED FOR DNA SYNTH
  3. HOW DO GROWTH FACTORS ACTIVATE PHOS CASCADES
    BIND TO CELL SURFACE RECEPTORS

    STIM TYROSINE PHOSPHORYLATION AND ACTIVATING CELLULAR PHOS CASCADE
  4. WHAT IS ONGOGENE, HOW IS IT GENERATED, AND WHAT IS PROTO-ONCOGENE
    PROTO-ONCOGENES ARE GENES WHOSE PRODUCTS FUNCTION AS REGULATORS OF NORMAL CELL PROLIFERATION OR SURVIVAL

    MUTATIONS IN PROTO-ONCOs GIVE RISE TO ONCOGENES WHICH EXHIBIT INAPPROPRIATE ACTIVITIES

    PROTO-ONCOs CODE FOR WIDE VARIETY OF PROTEINS SUCH AS GROWTH FACTORS, GF RECEPTORS, HORMONE RECEPTORS, CELL SIGNALING MOLECULES, TRANSCRIPTION FACTORS, AND CELL CYCLE REGULATORS
  5. CLASSES OF PROTO-ONCOGENES
    GROWTH FACTORS (Sis)

    GROWTH FACTOR RECEPTORS (Erb-B2)

    HORMONE RECEPTORS (RARa)

    CELLULAR SIGNALING MOLECULES (Abl & Ras)

    TRANSCRIPTION FACTORS (Myc)

    CELL CYCLE REGULATORS (CYCLIN D, Cdk 4
  6. LIST PROTO-ONCO, ACTIVATION MECHANISM, AND DISEASE FOR GROWTH FACTOR
    PLATELET-DERIVED GROWTH FACTOR

    Sis

    OVER EXPRESSION

    • ASTROCYTOMA
    • OSTEOSARCOMA
  7. LIST PROTO-ONCO, ACTIVATION MECHANISM, AND DISEASE FOR GROWTH FACTOR RECEPTORS
    EPIDERMAL GROWTH FACTOR RECEPTOR

    Erb-B2

    AMPLIFICATION

    MULTIPLE CANCERS
  8. LIST PROTO-ONCO, ACTIVATION MECHANISM, AND DISEASE FOR HORMONE RECEPTORS
    RETINOID RECEPTOR

    RARa

    TRANSLOCATION

    ACUTE PROMYELOCYTIC LEUKEMIA (APL)
  9. LIST PROTO-ONCO, ACTIVATION MECHANISM, AND DISEASE FOR CELLULAR SIGNALING MOLECULES
    TYROSINE KINASES, Abl, TRANSLOCATION, CHRONIC MYELOID LEUKEMIA (CML) /

    GTP BINDING PROTEINS, Ras, POINT MUTATION, MULTIPLE CANCERS
  10. LIST PROTO-ONCO, ACTIVATION MECHANISM, AND DISEASE FOR TRANSCRIPTION FACTORS
    ...

    Myc

    TRANSLOCATION LEADING TO BURKITT LYMPHOMA

    AMPLIFICAITON LEADING TO NEUROBLASTOMA
  11. LIST PROTO-ONCO, ACTIVATION MECHANISM, AND DISEASE FOR CELL CYCLE REGULATORS
    ...

    CYCLIN D - TRANSLOCATION LEADING TO LYMPHOMA. AMPLIFICATION LEADING TO BREAST & LIVER CANCERS

    Cdk 4 - AMPLIFICATION LEADING TO GLIOBLASTOMA. POINT MUTATION LEADING TO MELANOMA
  12. HOW IS MUTATION OF Ras ONCOGENIC
    SIGNALING MOLECULE WHICH BINDS GTP

    NORMALLY REGULATED/INACTIVATED BY HYDROLYZING GTP TO GDP

    ACTIVE FORM STIMS PHOS OF SERIES OF CYTO AND NUC PROTEINS LEADING TO CELL PROLIFERATION

    MUTATION CAUSES PROLIFERATION EVEN IN ABSENSE OF GROWTH FACTORS (DESTRUCTION OF GTPase PRESENT IN Ras)

    MULTIPLE CANCERS SUCH AS COLON, LUNG, PANCREASE, THYROID AS WELL AS LEUKEMIAS

  13. HOW IS TRUNCATED EGF RECEPTOR ONCOGENIC
    ErbB ONCOGENE IN AVIAN LEUKEMIA VIRUS WHICH CODES FOR TRUNCATED VERSION OF EGF RECEPTOR

    LOSS OF EXTRACELLULAR LIGAN BINDING DOMAIN LEADS TO PERMINANT ACTIVATION IN THE ABSENCE OF EGF GROWTH FACTOR
  14. HOW ACTIVATING MUTATIONS OCCUR IN RETROVIRAL ONCOGENES
    ONCOGENE CARRIED WITHIN VIRAL GENOME

    VIRUS INSERTS NEXT TO CELLULAR PROTO-ONCOGENE LEADING TO UP OR DOWN REGULATION OF EXPRESSION

    eg TRUNCATED EGF RECEPTOR
  15. MECHANISM OF ACTION OF PRODUCTS OF TUMOR SUPPRESSOR GENES pRb AND p53
    RETINOBLASTOMA (pRb) BINDS EF2, KEEPING IT FROM STIMULATING TRANSCRIPTION OF GENES ENCODING ENZYMES NEEDED FOR DNA SYNTH

    p53 IS A TRANSCRIPTION FACTOR THAT CAUSES PRODUCTION OF PROTEINS THAT INHIBIT CELL CYCLE, STIM DNA REPAIR, AND CAUSE APOPTOSIS

    UPON DNA DAMAGE, p53 ACTIVATES p21 WHICH INHIBITS Cdks LEADING TO INHIBITION OF CELL CYCLE, INCREASED DNA REPAIR ENZYMES AND PROTEINS THAT PROMOTE APOPTOSIS

    CHEMO USING DNA DAMAGING AGENTS WORK BETTER IF p53 IS PRESENT
  16. WILM'S TUMOR
    TRANSCRIPTION FACTOR FROM TUMOR SUPPRESSING GENE

    WT-1 INHIBITS SYNTH OF GROWTH FACTOR OR GROWTH FACTOR RECEPTOR IS MUTATED
  17. ATAXIA TELANGIECTASIA
    PRODUCTS OF TUMOR SUPPRESSING GENES INVOLVED IN DNA REPAIR

    TUMOR SUPPRESSING GENE ATM IS DEFICIENT, THUS p53 NOT STIMULATED TO REPAIR DNA DAMAGE
  18. INKs
    INHIBITORS OF Cdks MADE FROM TUMOR SUPPRESSING GENES

    MANY CANCERS, INCLUDING MELANOMA, LUNG, AND PANC, INKs (eg INK 4) IS MISSING OR MUTATED

  19. WHAT GENES ARE ACTIVATED/INACTIVATED IN MOST COLON CANCERS
  20. WHERE IS GLYCOGEN STORED?
    MOSTLY IN LIVER AND MUSCLE

    MOST CONCENTRATED IN LIVER BUT MORE TOTAL IN MUSCLE
  21. SYNTHESIS OF GLYCOGEN
    REQUIRES UDP-GLUCOSE TO ADD GLUCOSE TO GROWING GLYCOGEN CHAIN

    • UDP-GLUCOSE PHOSPHORYLASE REACTION:
    • GLUCOSE 1-PHOS + UTP --> UDP-GLUCOSE

    GLUCOSE 1-PHOS GENERATED BY PHOS-GLUC-MUTASE FROM GLUC-6-PHOS
  22. GENERATION OF GLYCOGEN BRANCH POINTS
    NEED AT LEAST 11 LINEAR RESIDUES FIRST

    THEN BREAK AN a1,4 LINK AND TRANSFER TO A #6 INTERNAL C
  23. FATE OF GLUCOSE 1-PHOS AND GLUCOSE IN LIVER AND MUSCLE
    • LIVER
    • CONVERTS G-1-P TO G-6-P VIA PHOS-GLUC-MUTASE. THEN G-6-P TO GLUC VIA G-6-PHOSPHATASE FOR USE IN OTHER TISSUES

    • MUSCLE:
    • DOES NOT RELEASE GLUCOSE (LACKS G-6-PHOSPHATASE).
    • G-1-P TO G-6-P VIA PHOS-GLUC-MUTASE THEN GLYCOLYSIS
  24. ROLE OF GLYCOGENIN
    PROTEIN CORE OF GLYCOGEN POLYMER

    #1C OF FIRST GLUCOSE ATTACHED COVALENTLY TO HYDROXYL OF TYROSINE ON GLYCOGENIN. USES UDP-GLUCOSE

    GLYCOGEN SYNTHASE THEN TAKES OVER AFTER INITIAL RESIDUES ARE ADDED
  25. STEPS OF GLYCOGENOLYSIS
    GLYCOGEN PHOSPHORYLASE STOPS AT 4TH GLUCOSE FROM BRANCH POINT

    DEBRANCHING ENZYME TRANSFERASE REMOVES 3 GLUC FROM BRANCH AND MOVES TO MAIN STRAND

    a1,6-GLUCOSIDASE BREAKS THE 1 BRANCHING GLUCOSE
  26. GLYCOGENOLYSIS (GLYCOGEN BREAKDOWN)
    1) GLUCAGON & EPI INC cAMP, WHICH ACTIVATES PKA. PKA PHOSES GLYCOGEN PHOSPHORYLASE KINASE (ACTIVATION), WHICH PHOSES GLYCOGEN PHOSPHORYLASE (ACTIVATION).

    3) PKA ALSO INHIBITS PROTEIN PHOSPHORYLASE, KEEPING ENZYMES ACTIVE

    4) INSULIN INHIBITS GLYCOGEN PHOSPHORYLASE KINASE AND GLYCOGEN PHOSPHORYLASE BY ACTIVATING PROTEIN PHOSPHATASE

    • 5) LOCAL ALLOSTERIC CONTROL:
    • Ca++ ACTIVATES PHOSPHORYLASE KINASE
    • AMP ACTIVATES PHOSPHORYLASE
    • GLUCOSE INHIBITS PHOSPHORYLASE

    WHEN MUSCLES FIRST CONTRACT, INC Ca++ AND AMP SIGNAL NEED FOR ENERGY
  27. STEPS FOR GLYCOGEN SYNTHESIS
    1) GLUCAGON & EPI INHIBIT SYNTHESIS BY PHOS OF GLYCOGEN SYNTHASE

    2) Ca++ INHIBITS SYNTHESIS BY ACTIVATING CALMODULIN KINASE, WHICH PHOSES GLYCOGEN SYNTHASE

    3) INSULIN ACTIVATES PHOSPHOPROTEIN PHOSPHATASE WHICH INC GLYCOGEN SYNTHASE. INHIBITS GLYCOGEN SYNTHASE KINASE (GSK) --> INC GLYCOGEN SYNTHASE

    • 4) ALLOSTERIC CONTROL:
    • GLUC-6-PHOS INC GLYCOGEN SYNTHASE
  28. PKA IN GLYCOGEN SYNTHESIS
    PHOSES REGULATORY PROT G CAUSING PROT PHOSPHATASE TO DISSOCIATE FROM G AND LOSE ACTIVITY

    PKA ALSO PHOSES INHIBITOR PROT I CAUSING IT TO BIND AND FULLY INACTIVATE PHOSPHATASE

    INSULIN REVERSES BY CAUSING DEPHOS OF G CAUSING REJOINING OF G AND ACTIVATION
  29. TYPE I GLYCOGEN STORAGE DISEASE
    HYPOGLYCEMIA - LIVER/KIDNEYS CAN'T RELEASE GLUCOSE

    HYPERLIPEMIA AND KETOSIS - FATTY ACID MET IS INCREASED

    BLOOD PYRUVATE AND LACTATE INC BECAUSE FLOOD GLYCOLYSIS WITH GLUC-6-PHOS

    NEED TO PROVIDE GLUC
  30. TYPE II GLYCOGEN STORAGE DISEASE
    CERTAIN AMOUNT OF GLYCOGEN GETS INTO LYSOSOMES

    NORMALLY a1,4 GLUCOSIDASE DEGRADES

    IF DEFICIENT, LYSOSOME BECOMES ENGORGED WITH GLYCOGEN RESULTING IN TOXICITY
  31. TYPE III & IV GLYCOGEN STORAGE DISEASES
    • III
    • DEBRANCHING ENZYME DEFICIENCY, THE GLUCOSIDASE

    CANNOT FULLY MET GLYCOGEN

    • IV
    • BRANCHING ENZYME DEFECT. GENERATION OF LONG GLYCOGEN POLYMERS DAMAGE HEPATOCYTES
  32. TYPE V & VI GLYCOGEN STORAGE DISEASES
    PHOSPHORYLASE DEFECTS

    McARDLE'S - INITIAL EXERCISE IS INHIBITED, INDICATED BY HIGH MUSCLE ADP (CAN'T GENERATE ATP EFFICIENTLY). DEMONSTRATES REQUIREMENT OF MUSCLE GLYCOGEN AT BEGINNING OF EXERCISE. BODY ADJUSTS THROUGH BLOOD-BORNE GLUCOSE RELEASE
  33. HEME SYNTHESIS FROM BEGINNING TO RING FORMATION (1-4)
    • 1) SUCC-CoA + GLYCINE + ALA SYNTHASE --> ALA ACID
    • MITOCHONDRIA AND RATE LIMITING STEP

    • 2) 2 ALA ACIDS + ALA DEHYDROGENASE --> PORPHOBILINOGEN (CONTAINS PYRROLE RING)
    • CYTOSOL

    3) 4 PORPHOBILINOGEN + UROPORPHYRINOGEN I SYNTHASE --> HYDROXYMETHYLBILANE. BREAKS DOWN TO TOXIC UROPORPH I. MUST FURTHER CONVERT

    4) HYDROXYMETHYLBILANE + UROPORPHYRINOGEN III COSYNTHASE --> UROPORPHYRINOGEN III. FLIPPING ONE PYRROLE RING DURING CYCLIZATION MAKES URO III INSTEAD OF URO I
  34. LAST STEPS OF HEME SYNTHESIS FROM CYCLIZATION (5-8)
    • 5) URO III + URO DECARB --> COPROPORPHYRINOGEN III.
    • ALL ACETYL GROUPS DECARBED INTO METHYL GROUPS. COPROPOR MOVES INTO MITOCHONDRIA

    • 6) COPROPOR III + COPROPOR OXIDASE --> PROTOPORPHYRINOGEN IX.
    • 2 PROPIONYLS CONVERTED TO VINYL (CH=CH2)

    • 7) PROTOPORPHYRINOGEN IX + PROTOPOR OXIDASE --> PROTOPORPHYRIN IX.
    • DOUBLE BONDS IN RINGS MOVE BETWEEN SIDE CHAINS.

    8) PROTOPORPHYRIN IX + FERROCHELATASE --> HEME. Fe ADDED TO RING
  35. ALA SYNTHASE 1 vs. 2
    1 FOUND IN NON-ERYTHROID CELLS

    2 IN ERYTHROIDS
  36. REGULATION OF HEME IN ERYTHROID CELLS
    A) Fe INDUCES HEME SYNTHESIS. 5'UTR OF mRNA FOR ALA 2 HAS SEGMENT WHICH BINDS Fe-BINDING PROTEIN (STABILIZES), BUT ONLY WHEN Fe IS PRESENT

    B) EXCESS HEME INHIBITS Fe UPTAKE. DIETARY Fe TRANSPORTED IN BLOOD BY TRANSFERRIN (LIGAND FOR RECEPTOR LETTING Fe INTO CELL). HEME INHIBITS (A)

    C) HEME AND GLOBIN ARE BALANCED. HEME INHIBITS A KINASE THAT ACTS ON eIF2. eIF2 THUS UNPHOSED AND INC GLOBIN SYNTH.

    GLOBIN COMBINES WITH HEME, SO HEME [] DROPS, THUS PHOSING eIF2 AND INHIBITING GLOBIN SYNTH
  37. REGULATION OF HEME IN NON-ERYTHROID CELLS
    A) HEME INHIBITS TRANSPORT OF ALA SYNTHASE 1 INTO MITOCHONDRIA (MAJOR CAUSE)

    B) HEME INHIBITS SYNTH OF ALA SYNTHASE 1

    C) HEME ALLOSTERICALLY INHIBITS ALA (NOT PHYSIOLOGICALLY IMPORTANT...?) SYNTHASE 1
  38. RETICULOENDOTHELIAL (RE) SYSTEM
    HEME DEGRADATION AND IMMUNE SYSTEM

    MACROPHAGES, MONOCYTES, AND KUPFFER CELLS IN LIVER

    RE ISOZYME OF HEME OXIGENASE INDUCED BY HEME, TIN, COBALT, OR STRESS

    ASIDE FROM RE ISOZYME, 2 OTHERS IN BRAIN AND TESTES

    C0 AS BYPRODUCT
  39. WHAT IS PORPHYRIA
    FAMILY OF DISEASES WHICH ARISE FROM LESIONS IN HEME BIOSYNTH PATHWAY

    CAUSED BY ACCUMULATION OF INTERMEDIATES

    NO PORPHYRIAS CAUSED BY DEFECT IN ALA SYNTHASE GENE
  40. X-LINKED ANEMIA
    ALA SYNTHASE PORPHYRIA

    RARE

    LESIONS IN ALA SYNTHASE

    NOT ENOUGH HEME --> LESS HEME FEEDBACK CONTROL OF ALA SYNTHASE --> HIGH ALA SYNTHASE
  41. ALA DEHYDROGENASE PORPHYRIA
    VERY RARE

    ABDOMINAL AND NEUROLOGICAL

    BUILD-UP OF dALA

    VERY SUSCEPTIBLE TO LEAD POISONING
  42. ACUTE INTERMITTEN PORPHYRIA
    PORPHOBILINOGEN DEAMINASE

    ONE OF MOST FREQUENT

    LESSENED ACTIVITY OF PB DEAMINASE RESULTING IN INC PB AND dALA

    ABDOMINAL AND NEUROLOGICAL

    SOME PSYCHOSIS
  43. CONGENITAL ERYTHROPOIETIC PORPHYRIA
    UROPOR-GEN III COSYNTHASE

    VERY RARE

    ACCUMULATION OF UROPOR-GEN I, UROPORPHYRIN I, COPOR-GEN I, AND COPROPORPHYRIN I

    PHOTOSENSITIVITY, DISCOLORED URINE, PIGMENTS IN TEETH
  44. PORPHYRIA CUTANEA TARDA
    UROPORPHYR-GEN DECARB

    MOST COMMON

    ACCUMULATION OF UROPORPHYRIN III

    SYMPTOMS LARGELY IN SKIN

    MAY BE INDUCED BY HEXACHLOROBENZENE

    TREAT WITH CHLOROQUIN AND PHLEBOTOMY
  45. HEREDITARY COPROPORPHYRIA
    COPROPOR-GEN OXIDASE

    RARE

    ACCUMULATION OF COPROPORPHYRIN III

    NEUROLOGICAL AND ABDOMINAL

    SOMETIMES INVOLVES SKIN
  46. VARIEGATE PORPHYRIA
    PROTOPORPHYRINOGEN OXIDASE

    ACCUMULATION OF SEVERAL PORPHYRINS

    SKIN LESSIONS

    SOME ABDOMINAL AND NEUROLOGICAL
  47. ERYTHROPOIETIC PROTOPORPHYRIA
    FERROCHELATASE

    PHOTOSENSITIVITY

    ACCUMULATION OF PORPHYRINS IN SKIN
  48. LEAD POISONING
    SOME SYMPTOMS OF PORPHYRIA

    SOME ENZYMES IN HEME SYTH INHIBITED BY LEAD (dALADEHYDE AND FERROCHELATASE)

    ENZYMES HAVE SULFHYDRYL GROUPS THAT REACT WITH HEAVY METALS
  49. ETIOLOGY OF PORPHYRIA SYMPTOMS (4)
    ABDOMINAL - BUILD-UP OF TOXIC INTERMEDIATES AND BY-PRODUCTS IN LIVER CAUSE PAIN

    NEUROLOGICAL - BUILD-UP IN BRAIN CAUSES PSYCH BEHAVIOR AND/OR NEURO SYMPTOMS

    SKIN - BUILD-UP IN SKIN, REACTIONS WITH ULTRA-VIOLET LIGHT MAKE FREE RADICALS

    TEETH - BUILD-UP CAUSES DISCOLORATION AND BRITTLE TEETH
  50. DRUG INTERACTION IN PORPHYRIAS
    CERTAIN TYPES AGGRAVATED BY CERTAIN DRUGS SUCH AS PHENOBARBITAL

    INDUCE LIVER TO MAKE CYTOCHROME P450 WHICH CONTAINS HEME, AND MAKE HEME ITSELF

    ACCUMULATION OF TOXIC INTERMEDIATES

    MUST PROPERLY DIAGNOSE PATIENT BEFORE TREATMENT
  51. PUBERTY AND PORPHYRIA
    SYMPTOMS DUE NOT APPEAR UNTIL PUBERTY

    INC SEX HORMONES AND INCREASE ACTIVITY/AMOUNT OF ENZYMES (CYTOCHROME P450)

    PUBERTY INDUCES HEME SYNTH WHICH CAUSES ACCUMULATION IN THOSE WITH LESIONS IN HEME SYNTH PATHWAYS
  52. HEMOLYTIC JAUNDICE
    EXCESS ERYTH DESTRUCTION

    HIGH BIL-ALB, HIGH EXCRETION
  53. CIRRHOSIS, INFECTIOUS HEP (JAUNDICE)
    LIVER DAMAGE SO LESS REACTION OF BILIRUBIN WITH GLUCURONOSIDE

    HIGH BIL-ALB, LOW BIL EXCRETION, LOW BIL-GLUCURONIDE
  54. NEONATAL JAUNDICE
    IMMATURE LIVER

    SIMILAR BILIRUBIN METABOLISM TO CIRRHOSIS AND HEP

    TEMPORARY

    TREAT WITH UV RAD TO DESTROY EXCESS BIL

    HIGH BIL-ALB, LOW EXCRETION
  55. CRIGLER-NIJJAR SYNDROME TYPE I
    RARE JAUNDICE

    COMPLETE LOSS OF UDP-GLUCUNOSYLTRANSFERASE ACTIVITY

    BIL DISTRIBUTION SIMILAR TO CIRRHOSIS AND HEP, BUT MORE EXTREME

    FATAL IF LEFT UNTREATED

    UV RAD FOR TREATMENT OR LIVER TRANSPLANT

    HIGH BIL-ALB, LOW EXCRETION
  56. CRIGLER-NAJJAR SYNDROME TYPE 2
    JAUNDICE

    UDP-GLURUNOSYLTRANSFERASE ACTIVITY DOWN 90%

    ENCEPHALOPATHY IF UNTREATED

    TREAT WITH PHENOBARBITAL - INDUCES UDP-GLURUNOSYLTRANSFERASE SYNTHESIS
  57. GILBERT SYNDROME
    JAUNDICE

    UDP-GLURUN-ASE ACTIVITY IS DOWN 50%

    BEGNIGN CONDITION & IN 10% OF POPULATION

    TREAT WITH PHENOBARBITAL
  58. OBSTRUCTIVE JAUNDICE
    JAUNDICE

    OBSTRUCTION PREVENTS BILE FROM REACHING INTESTINE

    BIL-GLUCURONOSIDE IS HIGH, BIL-ALB NORM, EXCRETION LOW

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