pathophysiology of obstructive jaundice
TRANSCRIPT
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PATHOPHYSIOLOGY OF OBSTRUCTIVE
JAUNDICE
DR. VIGNESH KUMARAMBEDKAR HOSPITAL
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ContentsMetabolismEffect on systemsSymptomatology The why behind it
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Jaundice “jaune” in french = yellowNormal bile secretion 600-
1200ml/dayBilirubin 250-350mg/dayTypes of jaundiceVan der Bergh test /
PhotospectrometryScleral icterus is evident at
2.5mg/dl, and cutaneous/mucous membrane icterus at 6mg/dl
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Hemoglobin catabolism
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Bilirubin metabolism
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Bile salt metabolism
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Systemic effectsHepatobiliary
◦ Normal biliary pressures 7-14 cm H₂O◦ As the pressure in the biliary tree increase,
the cholangiolymphatic reflux and cholangiovenous reflux come into play l/t systemic toxicity
◦ As biliary pressure increases (30 cm H₂O), the bile secretion completely stops
◦ Reflux into space of disse and hepatic sinusoids resulting in an inflammatory response followed by increased fibrogenesis
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Greenfield's surgery
Cholangiolymphatic and cholangiovenous reflux
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Systemic effectsCardiovascular
◦decreased cardiac contractility; reduced left ventricular pressures; impaired response to β- agonistic drugs; decreased peripheral vascular resistance
Renal ◦depressed cardiac function;
hypovolemia; endotoxemia may l/t renal impairment
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Systemic effectsImmunity
◦increased bacterial translocation from the gut in the setting of bile duct obstruction
Wound healing◦Delayed wound healing and a high
incidence of wound dehiscence and incisional hernia have been observed in patients undergoing surgery to relieve obstructive jaundice
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Symptomatology PruritisClay coloured
stoolsHigh coloured
urineRUQ painIcterus Steatorrhoea Bleeding
tendencyf/o fat soluble
vitamin deficiency
AnorexiaFeverNausea /
vomitingHigh grade fever
with chillsWeight lossSystemic
endotoxemiaf/o liver cell
failure
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The why behind it allPruritis
◦Bile salts reflux back into plasma, l/t mast cell degranulation in the skin
Clay coloured stools◦Conjugated bilirubin does not reach
the gut, no sterco/urobilin, stools devoid of yellow colour
High coloured urine◦Conjugated bilirubin (soluble) diffuses
into plasma, is filtered by kidney
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The why behind it all (cont.)RUQ pain and tenderness
◦ Stasis of bile in ducts l/t inflammatory response causing pain
◦ Elicited as tenderness (irritation of parietal peritoneum) and palpable lump (omentum)
Biliary colic◦ A misnomer as CBD in most individuals
does not contain muscle layers◦ Stasis leads to release of inflammatory
mediators (phospholipase A₂ and prostaglandins)
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The why behind it all (cont.)Steatorrhoea
◦Fat does not get absorbed without bile salt (micelle formation)
Bleeding tendency◦Vitamin K deficiency l/t prolonged PT
Deficiency of fat soluble vitamins◦Deficiency of vitamins A,D,E,K and
their manifestations
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The why behind it all (cont.)Icterus
◦Bilirubin has a high affinity for elastin that is abundant in sclera and skin
Fever◦Release of TNF alpha and IL-1d/t
inflammatory response ◦Local PG activity in anterior
hypothalamusNausea / Vomiting
◦Gut irritation and vagal stimulation d/t pain
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The why behind it all (cont.)Anorexia
◦IL-1 effects on satiety centreWeight loss
◦IL-1 increases production of IL-2 and TH-2 cells, l/t skeletal muscle proteolysis and thereby weight loss
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The why behind it all (cont.)High grade fever with chills
◦Stasis leads to ascending bile infection
Systemic endotoxemia◦elevated intraductal pressure in the
bile duct allows translocation of bacteria or endotoxin into the vascular and lymphatic system (cholangio-venous/lymphatic reflux)
Courvoisier’s law
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The why behind it all (cont.)Features of liver cell failure
◦Portal hypertension◦Ascitis◦Gynaecomastia ◦Vascular spider naevi◦Palmar erythema◦Testicular atrophy◦Dupuytrens contracture◦KF ring◦Flapping tremors◦Fetor hepaticus◦Hepatic encephalopathy
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