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Medicine II > Gastro: Jaundice > Flashcards

Gastro: Jaundice Flashcards

1
Q

definition of jaundice

A

yellow discolouration of the skin, sclerae and other tissues due to excess circulating bilirubin

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2
Q

what is the clinical definition of jaundice?

A

conjugated/unconjugated concentration higher than 34umol/L

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3
Q

where is bilirubin metabolised?

A
  • red cell
  • plasma
  • hepatocyte
  • bile canaliculi
  • colonic bacterial gluronidases
  • intestine
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4
Q

what happens at the red cell?

A

haemoglobin is catabolised

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5
Q

what happens at the plasma?

A

unconjugated bilirubin bound to albumin, since this is lipid-soluble

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6
Q

what happens at the hepatocyte?

A

bilirubin conjugation - defective in Gilbert’s and Criggler Najjer

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7
Q

what happens at the bile canaliculi?

A

ATP-dependent biliary excretion of conjugated bilirubin; defective in Dubin-Johnson syndrome

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8
Q

what happens at colonic bacterial glucuronidases?

A

hydrolyse the conjugated bilirubin to form urobilinogen and urobilin which are excreted

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9
Q

what happens at the intestine?

A

absorption of urobilinogen which is re-excreted by liver and kidneys. renal component important in liver disease

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10
Q

how can you classify jaundice?

A
  • unconjugated

- conjugated

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11
Q

examples of conditions that cause unconjugated jaundice

A
  • haemolysis
  • gilbert’s
  • criggler najjar
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12
Q

what can cause conjugated jaundice?

A
  • hepatocyte failure

- cholestasis

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13
Q

things that can cause cholestasis

A
  • small duct disease
  • large duct obstruction
  • reduced canalicular excretion in hepatocytes
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14
Q

how can jaundice be classified by cause?

A
  • hepatic (prehepatic, hepatic, posthepatic)

- cholestatic

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15
Q

what is the problem in jaundice where the problem is cholestasis?

A

the conjugated bilirubin cannot be excreted

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16
Q

what can cause hepatocyte failure?

A
  • acute or chronic liver failure
  • viral
  • alcohol
  • drugs
  • autoimmune
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17
Q

clinical picture in haemolysis

A
  • increase bilirubin load
  • unconjugated hyperbilirubinaemia
  • normal liver enzymes
  • no bilirubinuria
  • check CBC and reticulocyte count
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18
Q

clinical picture in Gilbert’s syndrome

A
  • hereditary failure of bilirubin conjugation
  • isolated unconjugated hyperbilirubinaemia
  • normal liver enzymes
  • no bilirubinuria
  • bilirubin levels increase on fasting
  • no treatment required
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19
Q

clinical picture of Crigler-Najjer syndrome

A
  • hereditary failure of bilirubin conjugation
  • normal liver enzymes
  • phenobarbitone improve jaundice
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20
Q

2 types of Crigler-Najjer syndrome

A

Type 1: neonates die of kernicterus

Type 2: unconjugated hyperbilirubinaemia between Type 1 and Gilbert’s

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21
Q

what is kernicterus

A

brain damage found in newborns caused by jaundice

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22
Q

what is the cutoff between acute and chronic hepatic conditions?

A

6 months

23
Q

clinical picture in hepatic causes of jaundice?

A
  • prolonged INR
  • low albumin
  • conjugated hyperbilirubinaemia
  • maintained levels of uridine diphosphate glucuronosyl transferase
24
Q

causes of acute hepatitis causing liver failure

A
  • alcohol excess
  • drugs: NSAIDs, TB drugs, antiepileptics, paracetamol OD
  • infections: Hep viruses, EBV, toxoplasma, rickettsaie
  • autoimmune chronic active hepatitis
  • autoimmune diseases like SLE and RA
  • haemochromatosis
  • Wilson’s disease
  • liver infarction
25
Q

what do the criteria consider for the diagnosis of AICAH?

A
  • ANA
  • SMA
  • LKMA
  • SLA
  • IgG
  • liver histology
    score 6=probable AICAH
    score 7 or higher=definite
26
Q

treatment regiments for AICAH

A
  • prednisolone

- azathioprine

27
Q

what is cholestasis?

A

interference of bile flow or formation

28
Q

symptoms of cholestasis

A
  • jaundice
  • fatigue
  • pruritis
  • pale stools
  • dark urine
29
Q

how can you classify different types of cholestasis?

A
  • intrahepatic (hepatocyte/cholangiocyte or small duct disease)
  • extrahepatic (dilatation of the bile ducts)
30
Q

causes of bile duct dilatation

A
  • obstruction

- no obstruction

31
Q

obstructive causes of bile duct dilatation

A
  • strictures

- stones

32
Q

causes of strictures within the bile duct system

A
  • neoplasms (cholangiocarcinoma, gallbladder adenocarcinoma, pancreatic adenocarcinoma)
  • postinflammatory (pancreatitis, post-radio/chemotherapy)
  • inflammatory (AIDS cholangiopathy, biliary parasites, primary sclerosing cholangitis)
33
Q

non-obstructive causes of bile duct dilatation

A
  • caroli disease
  • choledochal cyst
  • recurrent pyogenic cholangitis
  • primary sclerosing cholangitis
34
Q

investigations in large duct obstruction

A
  • trans-thoracic US
  • cross sectional imaging (CT/MRCP)
  • endoscopic US
  • ERCP and brush cytology (this is more therapeutic rather than diagnostic)
35
Q

management of a patient with biliary dilatation, obstruction and is septic?

A

emergency ERCP and stenting

36
Q

management of a patient with no obstruction

A

CS imaging and follow up

37
Q

classify according to the liver biopsy

A
  • disorder of the bile ducts
  • disorders with spare the bile ducts
  • no disorders
38
Q

conditions that can cause bile duct involvement

A
  • AMA negative PBC
  • primart/secondary sclerosing cholangitis
  • congenital disorders
  • sarcoidosis
  • idiopathic ductopenia
  • prolonged drug induced cholestasis
  • developmental abnormalities
  • cholangitis associated with malignancies
  • IgG4 associated cholangitis (autoimmune disease)
  • cystic fibrosis
  • graft vs host disease
39
Q

histological features of PBC

A
  • granulomatous changes
  • dense lymphocytic infiltrate
  • ruptured interlobular bile duct
  • epitheloid granuloma
  • FLORID DUCT LESION (focal duct obliteration with granuloma formation)
40
Q

treatment of PBC

A
  • ursodeoxycholic acid
41
Q

how does ursodeoxycholic acid work in PBC?

A

protects injured cholangiocytes from toxic bile acids in the early stages; stimulates secretion from impaired hepatocytes in advanced cholestasis

42
Q

things to note about ursodeoxycholic acid

A
  • does not have an effect on pruritis or fatigue

- improves bilirubin levels, enzyme levels and IgM levels

43
Q

histological features of PSC

A
  • moderately dense inflammatory infiltrate

- onion skin fibrosis

44
Q

which dose of UDCA has been shown to have benefits?

A

15-20mg/kg/day

45
Q

what kind of benefits does UDCA have

A
  • improves LFTs

- improves histological findings

46
Q

interventional treatment for PSC

A
  • ERCP (balloon dilatation, stenting)

- liver tranplantation

47
Q

surgical interventions for PSC

A
  • resection of the extrahepatic biliary tree

- Roux-en-Y choledochojejunostomy (indicated in advanced cirrhosis, failed ERCP stricture management)

48
Q

which are abnormalities causing jaundice which do not involve the bile ducts?

A
  • malignant infiltration
  • benign infiltration (amyloidosis/sarcoidosis)
  • peliosis hepatis
  • cirrhosis
  • congenital hepatic fibrosis
  • sinusoidal dilatation: Budd Chiari, veno-occlusive disease, congestive heart failure
49
Q

what is peliosis hepatis?

A
  • large blood filled spaces which may not be lined with sinusoidal cells
  • associated with drugs such as tamoxifen, OCP, androgenic steroids, danazol
  • seen in renal transplant recipients
50
Q

what is sinusoidal dilatation associated with?

A

acute right heart failure

51
Q

what is benign recurrent intrahepatic cholestasis

A
  • inherited condition
  • presents in adolescents/adults
  • acute episodes of cholestasis with jaundice and pruritis
  • can resolve in weeks/months but they may recur after
  • BRIC 1 - pancreatitis
  • BRIC-2 - gall stones
  • may have liver fibrosis
52
Q

drug treatment for pruritis

A
  • UDCA
  • cholestryramine
  • rifampicin
  • naltrexone
  • sertraline
53
Q

which drugs are not recommended for treating pruritis

A
  • anti-histamines
  • ondansetron
  • phenobarbitone
54
Q

supportive care

A
  • pruritis
  • fatigue
  • fat-soluble vitamins
  • osteoporosis

Medicine II (16 decks)

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