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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
should bilirubin in the bloodstream be conjugated or unconjugated
unconjugated
26
What does pale stools and pale urine suggest
problem with liver
27
What can happen in/to the gall bladder to cause obstructive jaundice
1. gall stones - can block biliary tree 2. acute cholecystits (inflammation of the gall bladder)
28
where do you feel pain if there is a problem with your gall bladder? why?
shoulder tip gall bladder inflammation of surrounding tissues including diaphragm. Phrenic nerve (cervical 3,4,5) supplies diaphragm and shoulder tip
29
when do you feel pain if there is a problem with your gall bladder, why?
brought on by eating fatty foods as stimulates bile release by contraction of gall bladder
30
what usually causes gall bladder symptoms
gall stones (raresly cholangiocarcinoma - bile duct cancer)
31
Who is high risk for gall stones
- fair - fertile - female - fat - forty
32
How can you investigate a (post hepatic) jaundiced patient
1. ultrasound (break up gall stones?) 2. plain radiographs 3 Endoscopic Retrograde Cholangio Pancretography (ERCP)
33
what is ERCP
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
What disease management involves taking oral pancreatic enzyme supplements
cystic fibrosis
35
what has an aetiological role which is linked to chronic pancreatitis
alcohol | maybe mumps virus?
36
what is a consequence of chronic pancreatic disease
diabetes
37
what is the general prognosis for pancreatic malignancy
poor
38
How do you manage pre-hepatic jaundice
identify and treat the cause
39
How do you manage post-hepatic jaundice
remove obstruction - gall stones via ERCP - gall stones via lithotripsy (ultrasound) - force open channel with a stent prevent gall stone recurrent
40
How can you prevent gall stone recurrence?
- 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
How can neonatal jaundice occur
increased haem breakdown - birth trauma - ABO and Rh incompatibility poor liver function in neonate (especially if premature)
42
what does neonatal jaundice give a risk of
kernicterus | - brain damage from bilirubin
43
what is brain damage from bilirubin in a neonate called
kernicterus
44
How do you treat kernicterus
phototherapy (put baby in blue light)
45
How can acute liver failure occur
- paracetamol poisoning (very slow death as need to use up clotting factors first) - other drug reaction
46
What happens during acute liver failure
- sudden loss of liver function | - rapid death (bleeding as can't produce clotting factors, encephalopathy- damage to brain because of toxic materials)
47
How can chronic liver failure occur
- cirrhosis - primary liver cancer - secondary liver cancer (metastases)
48
what is cirrhosis
combination of healing and scarring, eventually more damaged than functioning liver
49
what causes cirrhosis
- 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
What is a common way to get liver cancer
following on from hep infection
51
Signs and symptoms of cirrhosis
- None! - acute bleed (portal hypertension) - jaundice - oedema and ascites (abdominal fluid) - encephalopathy - spider naevi, palmar erythema (high oestrogen levels from reduced metabolism)
52
How does ascites occur
major sign of liver failure - high portal venous pressure - low plasma protein synthesis (low oncotic pressure)
53
How does oesophageal varices occur? what is it a sign of
liver failure | - acute bleed (portal hypertension)
54
What are the functions of the liver? i.e. what do you loose when it fails
SYNTHETIC function - plasma proteins - clotting factors METABOLIC function - drug metabolism - detoxification - conjugation of RBC breakdown products
55
How can you test the function of the liver
- traditionally use hepatic cell enzyme levels (raised in inflammation, proportional to the number of hepatic cells - International normalised ratio (INR) useful
56
What does INR test do
measures PROTHROMBIN time against a control | prothrombin --> thrombin
57
what is a normal INR value
1.0
58
if on warfarin what is the therapeutic INR range
2.0-4.0
59
If not on warfarin and INR is not 1.0, what might that indicate
significant liver synthetic dysfunction (i.e. not enough clotting factors)
60
What effects on the body does liver failure have
- fluid retention (ascites) - raised INR and prolonged bleeding - portal hypertension - inability to remove 'waste' - build up of haem breakdown products (jaundice)
61
What is the treatment for liver failiure
Supportive - end stage disease - acute failure - recovery lively "artificial liver" - experimental Transplantation - only 'cure' possible
62
what effect does alcohol cessation have on liver failure
greatly improved 5 year survival expectation
63
What is relevant to dentists for hepatic disease
- what do 'liver function tests' mean - end stage liver disease - liase with the physician - metabolic consequences - synthetic consequences - no problem with LA
64
what do dentists need to know about end stage liver disease
- clotting disorders | - abnormal drug metabolism
65
what do dentsits need to liase with physicians about with hepatic disease
- INR test | - platelets (make sure they are normal)
66
What metabolic consequences in hepatic disease do dentists need to know about
- Prolonged effect of senatives - Reduce drug doses? Care with antifugals - suitable analgesics? (paracetamol probably safest but ask)
67
What synthetic consequences in hepatic disease do dentists need to know about?
- 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
Why is giving LA not a problem for people with hepatic disease
it's metabolised in the plasma, not the liver

BDS2 BAMS Gastroenterology (5 decks)

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