Jaundice and Liver Disease Flashcards

1
Q

jaundice

A

accumulation of bilirubin in circulation / skin

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2
Q

normal process of haem metabolism

A

heme converted to bilivredin then bilirubin
bilirubin passed from bloodstream to liver where it is conjugated
conjugated bilirubin then either passes to kidneys and is excreted in urine or to intestines to be excreted as stools or recirculated

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3
Q

what type of bilirubin can be excreted

A

only conjugated bilirubin can be excreted
gives excretions their colour
if bilirubin cant be excreted it builds up in blood first then the skin

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4
Q

pre hepatic jaundice

A

increased haem load meaning excess bilirubin in circulation as not all can be excreted
e.g mismatchednblood transfusion
excretions are of normal colour as conjugated bilirubin still being excreted

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5
Q

hepatic jaundice

A

liver cell failure e.g cirrhosis
bilirubin cant be conjugated therefore none excreted
excretions are pale in colour

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6
Q

post hepatic jaundice

A

caused by blockage in biliary tree e.g gallstones
conjugated bilirubin cant pass to intestines to be excreted in stools so excess passed to kidneys for excretion in urine
results in pale stools and dark urine

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7
Q

choleangiocarcinoma

A

cancer of bile ducts

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8
Q

kernicterus

A

brain damage from bilirubin
possible consequence of neonatal jaundice as blood brain barrier not fully established in neonates
managed vie blue light phototherapy

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9
Q

neonatal jaundice

A

increased haem load due to birth trauma / mother and fetal blood mixing on delivery
poorer liver function in neonate meaning less bilirubin can be conjugated and excreted so remains in bloodstream

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10
Q

encephalopathy

A

impairment of brain function caused by high levels of blood toxins

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11
Q

ascites

A

fluid accumulating in peritoneal area (abdomen)

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12
Q

oesophageal varices

A

portal system has no exit route as communicaion with hepatic vein lost due to cirrhosis
Blood accumulates in vessels at lower oesophagus making the veins dilate and protrude into oesophagus
these veins are at risk of rupture which could prove fatal

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13
Q

why are ascites and oedema sometimes seen in ptx with liver failure

A

less plasma proteins due to liver dysfunction so less oncotic pressure retaining water in vessels

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14
Q

what do high levels of the hepatic enzyes ALT and GGt suggest

A

these enzymes escape liver cells more easily when cells are damaged or inflmaed so high enzyme levels suggest damage

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15
Q

Why might an INR be used to test liver function

A

liver produces clotting factors and INR measures how long it takes for blood to clot

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16
Q

what are the dental considerations when treating a ptx with end stage liver disease

A

may need to reduce drug dose as no or little 1st pass metabolism
may bleed excessively if decreased clotting factors