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JAUNDICE (ICTERUS)
YELLOWISH DISCOLORATION OF SKIN & MUCOUS MEMBRANES
EXCESS BILIRUBIN IN PLASMA.NORMAL RANGE 5-17 micromol/L (0.3 – 1.0mg/dl)LEVEL ABOUT 50 micromol/L (3mg/dl) →CLINICAL JAUNDICE(SCLERA,SKIN,PALATAL MUCOSA)
CONTD
DIAZO REAGENT(DIAZOTISEDSULPHANILIC ACID)→DEMONSTRATES + BILIRUBINSODIUM NITRITE +HCL →A RED COMPD. AZOBILIRUBINCONJUGATED BILIRUBIN →IMMEDIATE(POLAR MOLECULE) REACTION DIRECT van den Berg reactionUNCONJ.BILIRUBIN →NO REACTION until alc.is added(NONPOLAR) →INDIRECT van den Berg reaction
contd
UROBILINOGEN-CONSISTS OF UROBILINOGEN, MESOBILINOGEN, & STERCOBILINOGEN.Conj. B. (soluble in water)- excreted in urine.Unconj.B.(bound to albumin)- lipid soluble (does not enter
gl.filtrate) DANGER- binding capacity of albumin exhausted---
absorbed by lipid rich areas in Brain.Plasma level 340 micromol/l (20mg/dl)Basal ganglia deeply bile stained- irreparable damage to
neurons KERNICTERUS
TYPES OF JAUNDICE
HAEMOLYTIC.
OBSTRUCTIVE.&
HEPATOCELLULAR.
HAEMOLYTIC JAUNDICE
↑BILIRUBIN LOAD DUE TO- EXCESSIVE
BREAKDOWN OF RBCs.
-INEFFECTIVE
ERRYTHROPOIESIS (↑IN
THALASSEMIA,PERNICIOUS ANAEMIA)
CONDITIONS ARE THOSE ASSOC. WITH HAEMOLYTIC ANAEMIA.
UNCONJ. HYPERBILIRUBINAEMIA +HEPATIC DYSFUNCTION DUE TO ANAEMIA
CONTD.
BIOCHEM. MANIFESTATIONS
1. ↑ INDIRECTLY REACTING BILIRUBIN IN PLASMA.
2. ↑STERCOBILINOGEN IN FAECES
3. ↑UROBILINOGEN IN URINE.
4. ABSENCE OF BILIRUBIN IN URINE.
Jaundice not severe. seldom↑85micromol/l(5mg/dl) except
Rh haemolytic disease of newborn.
OBSTRUCTIVE JAUNDICE
OBSTRUCTION TO PASSAGE OF CONJ. BILIRUBIN FROM LIVER CELLS →INTESTINE.
CHOLESTASIS – EXTRAHEPATIC INTRAHEPATICEXTRAHEPATIC CHOLESTASIS( surgical jaundice) 1.Blockage of CBD by Gallstones. 2.Occlusion of Duct by Ca head of Pancrease 3.Pressure by enlarged L.nodes in Porta hepatis. 4.Ca. of Duct itself either at Ampulla of Vater or higher up.
Contd.
INTRAHEPATIC CHOLESTASISLESS OBVIOUSLY ASSOC. WITH MECH.
OBSTRUCTION.1.Sclerosing cholangitis cholangiography→ multiple areas of stenosis&
dilatations of intra & extra hepatic ducts.Pr.–85% assoc.with U. Colitis.Sec.– in pts.with AIDS &in those with untreated bile
duct stenosisAll varieties of sec. cholangitis progress to Cirrhosis.2.Pr. Biliary cirrhosis
contd
3.Rare compln.of last trimester of pregnancy(effect of oestrogen),oral contraceptives.4. Drugs(cholestatic drug jaundice) Chlorpromazine & other phenothiazines. Halothane,Steroids.BIOCHEMICAL MANIFESTATIONS 1.↑ Conjugated bilirubin in plasma. 2.↓ stercobilinogen in faeces. (pale, bulky, offensive)Bile salts excluded from bowel(absorption of fat)Long standing cases—Malabsorption syndrome, Fat soluble vitamins.↓Vit. K→bleedingHypovitaminosis D -Osteomalacia
Contd
3.Absence of urobilinogen in urine.4.Presence of bilirubin & bile salts in urine.5.↑ levels of Pl. alk.PO4ase&ץ glutamyl transferase.-- Pruritis (pl. bile salt concn.&unconj. bile salts in skin)-- Hypercholesterolaemia→cut. Xanthomas.-- ↑ in LDLs & ↓ in HDLs Abn.LDL-LipoproteinX(high proportion of unesterified cholesterol& phospholipid)--Hepatocellular damage--Cirrhosis
HEPATOCELLULAR JAUNDICE
DIRECT & INDIRECT reacting BILIRUBIN
---Failure of conjugating mechanism
---Obstruction to escape of cong. bilirubin
(from cells to canaliculi &from canaliculi)
intrahepatic cholestasis
contd
1.Enzyme deficiency.2.Intrahepatic cholestasis complicating liver cell
damage. a)Acute fatty liver-obstruction-pr. b)Severe neonatal jaundice –obstruction- inspissated bile in canaliculi.3.Cirrhosis-ac.exacerbation &terminally.4.Postop. Jaundice—hepatic necrosis(shock) ----hepatitis(drugs) ----red cell destruction(site,
haemolysis of transfused cells)
STEPS IN DIAGNOSIS OF JAUNDICED PATIENT
CLINICAL HISTORY &EXAMINATION.URINE,STOOLSERUM BIOCHEMICAL TESTS BILIRUBIN TRANSAMINASE(AST,SGOT) ALKALINE PHOSPHATASE, GAMMA GT. ALBUMINQUANTITATIVE IMMUNOGLOBULINS.HAEMATOLOGY-Hb,WBC,PLATELETSBLOOD FILMPROTHROMBIN TIME(before & after IM Vit.K)X’RAY CHEST
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