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BDS2 BAMS Gastroenterology > Jaundice and liver failure > Flashcards

Jaundice and liver failure Flashcards

1
Q

What issues can you have with your liver?

A
  • viral liver disease
  • jaundice
  • cirrhosis
  • liver failure
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2
Q

How many lobes does the liver have? where is it?

A

3 lobes, can all function separately
separated from lungs from diaphragm
If you take a big breath in it becomes palpable

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3
Q

what is bilirubin

A

normal metabolic product from the break down of red blood cells, orange/yellow colour, passes through liver and is eventually excreted

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4
Q

If you have a high level of bilirubin where will it accumulate

A

in the skin (jaundice)

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5
Q

what makes you look yellow in jaundice

A

bilirubin

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6
Q

Where is it very easy to spot jaundice

A

whites of the eyes (sclera) turn yellow

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7
Q

where do we get bilirubin from

A

heme metabolism

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8
Q

what does the liver do to bilirubin? why?

A

conjugates it
helps it to be excreted

(heme released –> converted to bilirubin –> liver conjugates it)

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9
Q

What does bilirubin colour

A

stools and urinw

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10
Q

if someone has jaundice + normal stools and urine what does this mean

A

liver is doing it’s job

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11
Q

if someone has jaundice + abnormal coloured stools and urine what does this mean

A

problem with the liver

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12
Q

How many ways can you define jaundice

A

3

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13
Q

What are the 3 ways you can define jaundice

A
  1. Pre-hepatic (increased haem load, autoimmune, spleen, abnormal RBCs)
  2. Hepatic (liver cell failure, cirrhosis, hepatitis)
  3. Post-hepatic (biliary, gall bladder, pancreatic disease)
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14
Q

what is jaundice

A

excess bilirubin in the circulation

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15
Q

Describe normal bilirubin metabolism

A 
Blood = unconjugated bilirubin
Hepatocytes = endoplasmic reticulum
Canaliculus = conjugated bilirubin
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16
Q

What is pre-hepatic jaundice

A

jaundice due to factors before liver metabolism

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17
Q

What usually causes pre-hepatic jaundice? Give examples

A

usually excessive quantities of red blood cell breakdown products

e. g.
- haemolytic anaemia
- post transfusion (bad match)
- neonatal (maternal RBC induced)

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18
Q

Why does excessive quantities of RBC breakdown cause pre-hepatic jaundice

A
  1. increased bilirubin production beyond the liver’s capacity to conjugate it

or

  1. decreased bilirubin uptake by liver cells (Gilbert’s disease)
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19
Q

What is hepatic jaundice caused by? how can this happen?

A

liver failure

  • cirrhosis
  • drug induced liver dysfunction

prevents metabolism of RBC breakdown products

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20
Q

How can hepatic jaundice prevent metabolism of RBC breakdown products

A
  1. Impaired enzyme action (impaired bilirubin conjugation). Disease within cells themselves/too few to process

or

  1. Secretion failure (defective secretion of conjugated bilirubin from liver cells) - liver cell membrane impermeable
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21
Q

What is post-hepatic jaundice

A

obstruction to bile outflow

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22
Q

How does post-hepatic jaundice occur

A

Obstruction somewhere in the biliary network

  • Intrahepatic biliary system (primary biliary sclerosis)
  • Extrahepatic biliary system (gall bladder or common bile duct)
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23
Q

is conjugate or unconjugate bilirubin excreted in urine and faeces

A

conjugated

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24
Q

what does pale stool and dark urine suggest

A

post hepatic cause of jaundice (conjugated bilirubin causing jaundice)

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25
Q

should bilirubin in the bloodstream be conjugated or unconjugated

A

unconjugated

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26
Q

What does pale stools and pale urine suggest

A

problem with liver

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27
Q

What can happen in/to the gall bladder to cause obstructive jaundice

A
  1. gall stones
    - can block biliary tree
  2. acute cholecystits (inflammation of the gall bladder)
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28
Q

where do you feel pain if there is a problem with your gall bladder? why?

A

shoulder tip

gall bladder inflammation of surrounding tissues including diaphragm. Phrenic nerve (cervical 3,4,5) supplies diaphragm and shoulder tip

29
Q

when do you feel pain if there is a problem with your gall bladder, why?

A

brought on by eating fatty foods as stimulates bile release by contraction of gall bladder

30
Q

what usually causes gall bladder symptoms

A

gall stones (raresly cholangiocarcinoma - bile duct cancer)

31
Q

Who is high risk for gall stones

A
  • fair
  • fertile
  • female
  • fat
  • forty
32
Q

How can you investigate a (post hepatic) jaundiced patient

A
  1. ultrasound (break up gall stones?)
  2. plain radiographs
    3 Endoscopic Retrograde Cholangio Pancretography (ERCP)
33
Q

what is ERCP

A

Endoscopic Retrograde Cholangio Pancretography (ERCP)

  • inject dye into bile tree to see if there is a blockage
  • can use to put a stent in to stretch
34
Q

What disease management involves taking oral pancreatic enzyme supplements

A

cystic fibrosis

35
Q

what has an aetiological role which is linked to chronic pancreatitis

A

alcohol

maybe mumps virus?

36
Q

what is a consequence of chronic pancreatic disease

A

diabetes

37
Q

what is the general prognosis for pancreatic malignancy

A

poor

38
Q

How do you manage pre-hepatic jaundice

A

identify and treat the cause

39
Q

How do you manage post-hepatic jaundice

A

remove obstruction

  • gall stones via ERCP
  • gall stones via lithotripsy (ultrasound)
  • force open channel with a stent

prevent gall stone recurrent

40
Q

How can you prevent gall stone recurrence?

A
  • remove gall bladder (cholecystectomy)
  • prevent build up of bile acid (uresodeoxycholic acid, low calorie and low cholesterol diet)
  • prevent bile acid reabsorbtion from the GIT (colestyramine)
41
Q

How can neonatal jaundice occur

A

increased haem breakdown

  • birth trauma
  • ABO and Rh incompatibility

poor liver function in neonate (especially if premature)

42
Q

what does neonatal jaundice give a risk of

A

kernicterus

- brain damage from bilirubin

43
Q

what is brain damage from bilirubin in a neonate called

A

kernicterus

44
Q

How do you treat kernicterus

A

phototherapy (put baby in blue light)

45
Q

How can acute liver failure occur

A
  • paracetamol poisoning (very slow death as need to use up clotting factors first)
  • other drug reaction
46
Q

What happens during acute liver failure

A
  • sudden loss of liver function

- rapid death (bleeding as can’t produce clotting factors, encephalopathy- damage to brain because of toxic materials)

47
Q

How can chronic liver failure occur

A
  • cirrhosis
  • primary liver cancer
  • secondary liver cancer (metastases)
48
Q

what is cirrhosis

A

combination of healing and scarring, eventually more damaged than functioning liver

49
Q

what causes cirrhosis

A
  • alcohol
  • primary biliary cirrhosis
  • hep b and c (chronic active hepatitis)
  • autoimmune chronic hepatitis
  • haemachromatosis
  • excessive iron storage in liver
  • cystic fibrosis

(often due to a combination of causes and even though can regenerate it’s often not in the right architecture)

50
Q

What is a common way to get liver cancer

A

following on from hep infection

51
Q

Signs and symptoms of cirrhosis

A
  • None!
  • acute bleed (portal hypertension)
  • jaundice
  • oedema and ascites (abdominal fluid)
  • encephalopathy
  • spider naevi, palmar erythema (high oestrogen levels from reduced metabolism)
52
Q

How does ascites occur

A

major sign of liver failure

  • high portal venous pressure
  • low plasma protein synthesis (low oncotic pressure)
53
Q

How does oesophageal varices occur? what is it a sign of

A

liver failure

- acute bleed (portal hypertension)

54
Q

What are the functions of the liver? i.e. what do you loose when it fails

A

SYNTHETIC function

  • plasma proteins
  • clotting factors

METABOLIC function

  • drug metabolism
  • detoxification
  • conjugation of RBC breakdown products
55
Q

How can you test the function of the liver

A
  • traditionally use hepatic cell enzyme levels (raised in inflammation, proportional to the number of hepatic cells
  • International normalised ratio (INR) useful
56
Q

What does INR test do

A

measures PROTHROMBIN time against a control

prothrombin –> thrombin

57
Q

what is a normal INR value

A

1.0

58
Q

if on warfarin what is the therapeutic INR range

A

2.0-4.0

59
Q

If not on warfarin and INR is not 1.0, what might that indicate

A

significant liver synthetic dysfunction (i.e. not enough clotting factors)

60
Q

What effects on the body does liver failure have

A
  • fluid retention (ascites)
  • raised INR and prolonged bleeding
  • portal hypertension
  • inability to remove ‘waste’
  • build up of haem breakdown products (jaundice)
61
Q

What is the treatment for liver failiure

A

Supportive

  • end stage disease
  • acute failure - recovery lively

“artificial liver”
- experimental

Transplantation
- only ‘cure’ possible

62
Q

what effect does alcohol cessation have on liver failure

A

greatly improved 5 year survival expectation

63
Q

What is relevant to dentists for hepatic disease

A
  • what do ‘liver function tests’ mean
  • end stage liver disease
  • liase with the physician
  • metabolic consequences
  • synthetic consequences
  • no problem with LA
64
Q

what do dentists need to know about end stage liver disease

A
  • clotting disorders

- abnormal drug metabolism

65
Q

what do dentsits need to liase with physicians about with hepatic disease

A
  • INR test

- platelets (make sure they are normal)

66
Q

What metabolic consequences in hepatic disease do dentists need to know about

A
  • Prolonged effect of senatives
  • Reduce drug doses? Care with antifugals
  • suitable analgesics? (paracetamol probably safest but ask)
67
Q

What synthetic consequences in hepatic disease do dentists need to know about?

A
  • reduced clotting factor synthesis (bleeding tendency, work with haematologist)
  • reduced plasma transport protein synthesis (drug binding reduced, dose may need reduced)
  • reduced ‘gamma globulin’ synthesis (more prone to infections?)
68
Q

Why is giving LA not a problem for people with hepatic disease

A

it’s metabolised in the plasma, not the liver

BDS2 BAMS Gastroenterology (5 decks)

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