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BDS2 BAMS > Jaundice and Liver Failure > Flashcards

Jaundice and Liver Failure Flashcards

1
Q

4 liver issues

A
  • viral liver diseases (hepatitis)
  • jaundice
  • cirrhosis
  • liver failure
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2
Q

when can the liver be palpable on the back

A

Liver pushed down the way when breathe in

Large liver (unhealthy) can palpate even when not breathing in

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3
Q

how many lobes does the liver have

A

3

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4
Q

location of the liver

A

under the ribs, adjacent to the lung but separated from the lung by the diaphragm

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5
Q

how does the liver cope with varying degrees of function

A

Lobes
- Can function individually – can transplant one lobe

Liver regenerates and expand to cope with function
- Can cope with some damage

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6
Q

function of gallbladder

A

bag which collects bile from the liver, at the back

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7
Q

what ducts join together to make ampulla of Vater entering the jejunum?

A

common bile duct joins the pancreatic duct

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8
Q

what is jaundice

A

accumulation of bilirubin in the skin

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9
Q

signs of jaundice

A

yellow-orange pigmentation

itch (bothers patient)

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10
Q

icteric

A

term used to describe jaundice patient

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11
Q

what is bilirubin

A

normal metabolic product of haem
- Recycle material inside the haem, exerted through kidneys

Bilirubin level in blood should be relatively low
- most recycled or lost

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12
Q

what can jaundice be a result of?

A

liver failure

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13
Q

scleral effects of jaundice

A

yellow-orange white of eye

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14
Q

what does the liver do to bilirubin

A

conjugates bilirubin so it can be excreted from the body

Not conjugated then not water soluble so cannot be excreted by urine
- Some reabsorbed into blood stream and kidney to be excreted

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15
Q

stool and urine colour if liver functioning well

A

normal/dark

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16
Q

stool and urine colour if liver not functioning well

A

pale/unpigmented as lack of bilirubin excretion

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17
Q

what is in excess when a patient has jaundice

A

bilirubin in the circulation

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18
Q

3 ways to define jaundice

A

pre-hepatic

hepatic

post-hepatic

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19
Q

pre-hepatic jaundice due to

A

increased haem load

  • autoimmune, spleen, abnormal RBCs
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20
Q

hepatic jaundice due to

A

liver cell failure

  • cirrhosis, hepatitis
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21
Q

post-hepatic jaundice due to

A

biliary, gall bladder and pancreatic disease

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22
Q

unconjugated bilirubin found

A

in blood

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23
Q

conjugated bilirubin found

A

in bile (liver passed to small intestine or kidney)

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24
Q

what is pre hepatic jaundice factors due to

A

due to factors before liver metabolism

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25
Q

what is the level of unconjugated bilirubin like in pre-hepatic jaundice?

A

higher than it should be

usually excessive quantities of RBC breakdown products

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26
Q

3 possible causes of pre-hepatic jaundice

A

Haemolytic anaemia

Post transfusion (bad match)

Neonatal (maternal RBC induced)

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27
Q

how can haemolytic anaemia cause pre-hepatic jaundice

A
  • RBC broken down faster
  • Turnover doubles
  • More bilirubin to deal with
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28
Q

how can a transfusion cause pre-hepatic jaundice

A
  • All new unmatched RBC broken down by immune system

- Straightforward as know if they have had a transfusion

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29
Q

what is a neonatal cause of pre-hepatic jaundice

A
  • Jaundice when born

- Maternal and baby blood mixed – don’t match so destroyed so excess of haemoglobin in liver and bilirubin in blood will

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30
Q

proportion comparisons of unconjugated and conjugated bilirubin

A

more unconjuageted than conjugated

greater unconjugated passed through blood circulation
- As not enough capacity in cells (liver cannot process it all)

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31
Q

hepatic jaundice due to impaired enzyme action

A

Reduced number of hepatocytes so reduced amount bilirubin that can be processed

Less liver hepatocytes and enzymes functioning

Less bilirubin that can be processed

  • Same amount made
  • more unconjugated in blood circulation
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32
Q

what are 2 causes hepatic jaundice

A

cirrhosis

drug induced liver dysfunction

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33
Q

what is a rare type of hepatic jaundice

A

secretion failure
- defective secretion of conjugated bilirubin from hepatocytes

liver cell membrane becomes impermeable to conjugate bilirubin - enters blood circulation instead

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34
Q

what causes post-hepatic jaundice

A

obstruction to bile outflow

  • cannot escape liver to small intestine
  • so conjugated and unconjugated bilirubin in blood
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35
Q

where are the 2 possible sites of problem for post-hepatic jaundice

A

intrahepatic biliary system

extrahepatic biliary system

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36
Q

what is an intrahepatic biliary system that can lead to post-hepatic jaundice

A

primary biliary scelrosis

  • No functioning bile ducts in liver
  • Immune disease
  • Scarring and blocking of ducts
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37
Q

2 sites of extrahepatic biliary system that can lead to post-hepatic jaundice

A

gall bladder

common bile duct

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38
Q

what can happen in the gall bladder that can lead to post-hepatic jaundice

A

gall stone formation

- block biliary tree so cannot get bilirubin passed

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39
Q

what 2 carcinomas can occue in the common bile duct region that can lead to post-hepatic jaundice

A

pancreatic carcinoma
- Pancreatic head by bile duct – expand and squash duct to prevent bile passing through

Cholangiocarcinoma

  • Tumour of bile duct itself
  • Usually when it enters the duodenum
  • 60s, Wake up and suddenly have jaundice
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40
Q

circulation components of post-hepatic jaundice

A

uncojugated and conjugated bilirubin

Unconjugated bilirubin in blood
Passing through cell – conjugated

And try to pass into bile 
- Cannot 
Back through liver cells and into blood 
- Mix in blood 
- Conjugated and unconjugated
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41
Q

circulation components of pre-hepatic jaundice

A

greater proportion of unconjugated bilirubin as excess RBC products and not enough hepatocyte capacity to process it all

42
Q

circulation components of hepatic jaundice (secretion failure)

A

unconjugated and conjugated bilirubin

liver cell membrane become impermeable to conjugated bilirubin

43
Q

circulation components of hepatic jaundice (impaired enzyme/hepatocyte function)

A

unconjugated bilirubin

Bilirubin cannot get processed due to disease in cells or not enough to do job
- Very little If any pass into bile

44
Q

pale stool and dark urine suggests

A

post hepatic cause of jaundice

obstructive jaundice (yellow skin, eyes and pale poo and dark urine as pass back up through the liver to kidneys)

45
Q

normal coloured stool and urine is indicative of which type of jaundice

A

pre-hepatic

  • excess bilirubin is unconjugated in blood
  • everything normal coloured
46
Q

pale stools and urine is indicative of which type of jaundice

A

hepatic

  • no conjugation of bilirubin occurring as liver not functioning
47
Q

where do gall stones form

A

in the gall bladder

collect like bag and pop out into biliary tree and get stuck
- multiple stones usually

48
Q

what does gall stones do

A

block biliary tree —> obstructive post-hepatic jaundice

cause inflammation

  • wall - seen on US
  • and adjacent tissues (phrenic nerve impact)
49
Q

acute cholecystitis

A

inflammation of the gall bladder

50
Q

role of the gall bladder

A

store bile made in the liver

bile moves in until gall bladder contracts
- squirts out and moves into small intestine by pressure when needed (fat digestion)

51
Q

3 gall bladder symptoms

A

Pain in SHOULDER tip

Abdominal Pain Right side (where liver is)
- Radiates to the back

Pain brought on by eating Fatty food
- Stimulates bile release by contraction of the gall bladder.

52
Q

what is the most common issue of gall bladder

A

Usually Gall stones

- Rarely Cholangiocarcinoma (bile duct cancer)

53
Q

3 ways of imaging the jaundiced patient

A

ultrasound

plain radiographs

ERCP
- Endoscopic Retrograde Cholangio Pancreatography

CT scans (computerised tomography)

54
Q

ultrasound of liver detects

A

Detects dilated bile channels WITHIN the liver
- Also dilated biliary tree

Show echoes of what’s happening in abdomen

Width of gallbladder, stones

55
Q

plain radiographs of the gall bladder show

A

radiopaque gall stones only (not all)

56
Q

main imaging techniques of liver and gall bladder are

A

ultrasound and CT scans (computerised tomography)

57
Q

ERCP

A

Endoscopic Retrograde Cholangio Pancreatography

Dye into bile tree and see if blockage into the bile tree
- Pass down from stomach into duodenum and small canula into the duct

Instrument down so can do work whilst there (instrument to make small incision to allow stones out)

Can only reach so far up the duct

58
Q

how can you receive a patient of a carcinoma of a bile duct and jaundice temporarily

A

by a stent - helps to widen the lumen in case of a carcinoma

until decide on best treatment

59
Q

when is pancreatitis and Cystic Fibrosis common

A

if drink a lot of alcohol

60
Q

why is the inflammation of the pancreas an issue

A

release digestive enzyme

- in gland can cause digestion from inside out

61
Q

what supplements may be needed in CF

A

oral pancreatic enzyme supplements

Viscous secretion of pancreases, mean cannot move out duct properly

Pancreatic enzyme in gland can cause pancreatitis

62
Q

pancreatitis

A

when pancreatic enzyme (digestive enzymes) are released inside the pancreas because of inflammation rather than in the small intestine

63
Q

what disease is a consequence fo chronic pancreatic disease

A

type 2 diabetes

64
Q

what is the prognosis like for a pancreatic malignancy (adenocarcinoma)

A

poor

  • developed
  • tumour present for many years
65
Q

how to manage pre-hepatic jaundice

A

Identify and treat the cause

Blood transfusion – settle as cells remove

Anaemia – found out why

Congenital reason – deal with different

Mostly due to medicine given which effects breakdown of RBC

66
Q

how to manage post-hepatic jaundice

A

Remove obstruction
- Gall stones via ERCP

  • Gall Stones via lithotripsy (ultrasound)
    Focus energy and pressure waves on gall stones and US will fracture
  • Maybe 5-6cm under skin can absorb energy. Do from 3 angles and focus on 1 particular place to minimise absorption
  • Force open channel with a stent
67
Q

methods of prevention of gall stone recurrence

A

Remove gall bladder (Cholecystectomy) – easiest option

Prevent build up of bile acid by medicine

  • Ursodeoxycholic Acid
  • Low calorie & low cholesterol diet - Prevent issues of gall stones forming

Prevent Bile Acid reabsorption from the GIT

  • Small drip of bile passing into – not large enough to deal with single large fatty meals
  • cholesytramine – lower high cholesterol levels and treat itching by liver disease
68
Q

what type of births are at higher risk of neonatal jaundice

A

Natural births over C sections

69
Q

risk in neonate of neonatal jaundice

A

Increased Haem breakdown

  • Birth trauma
  • ABO & Rhesus incompatibility

Poor liver function in neonate
- Worse if <37 weeks gestation

Risk of KERNICTERUS
- Brain damage from bilirubin
- Permanent loss of function
High bilirubin in brain can cause permanent brain damage

Not in adults as brain more segregated from blood than in neonate

70
Q

kernicterus

A
  • Brain damage from bilirubin due to neonatal jaundice
  • Permanent loss of function
    High bilirubin in brain can cause permanent brain damage

Not in adults as brain more segregated from blood than in neonate

71
Q

how to treat neonatal jaundice

A

phototherapy

- blue wave light (energy sufficient to cause break down of bilirubin)

72
Q

what is the ultimate consequence of liver failure

A

death

  • cannot detoxify many toxins
  • cannot maintain carbohydrates in blood properly
73
Q

what is a cause of acute liver failure

A

paracetamol poisoning

other drug reaction

74
Q

what is acute liver failure

A

Sudden loss of liver function

- recovery or Rapid death

75
Q

2 ways liver failure can cause death

A

Bleeding
- Not able to make clotting factors

Encephalopathy

  • Damage to brain due to toxic materials
  • Build-up in blood due to liver not detecting and removing them
76
Q

how many days does it take to use up premade clotting factors by the liver

A

4 days

clotting factors will not last the weeks needed to repair hepatocytes to normal

77
Q

what is the time window to reduce damage to liver after insult

A

36-48 hours
- after this need a liver transplant

clotting factors will not last the weeks needed to repair hepatocytes to normal

78
Q

3 types of chronic liver failure

A

cirrhosis

primary liver cancer
- often after hepatitis

secondary liver cancer
- metastases

79
Q

cirrhosis

A

Mixed picture of damage, fibrosis & regeneration of liver structure

Combination of healing and scarring

  • Permanent damage after each time
  • More damage than recovery able (regenerate cells but not in correct architecture)

so fewer hepatocytes able to process and eliminate material

80
Q

aetiology of cirrhosis

A

Alcohol

Primary Biliary Cirrhosis

viral disease - chronic active hepatitis

autoimmune chronic hepatitis

Haemachromatosis

Cystic fibrosis

81
Q

signs and symptoms of cirrhosis

A

NONE! - large or small liver

  • Inflamed liver (bigger) can detect at start
  • More fibrotic and less functioning liver – shrink in size

Acute bleed - portal hypertension

Jaundice

Oedema & ascites (abdominal fluid in excess)

Encephalopathy – not detoxifying so brain poisoned

Spider naevi, palmar erythema

  • High oestrogen levels from reduced metabolism (liver metabolism oestrogen)
  • Causes vascular changes – red palms with pale centres (many fascia not musculature), blood vessels on skin
82
Q

how can spider naevi and palmer erythema occur due to cirrhosis

A
  • High oestrogen levels from reduced metabolism due to reduced functioning hepatocytes (liver metabolism oestrogen)
  • Causes vascular changes – red palms with pale centres (many fascia not musculature), blood vessels on skin
83
Q

how can an acute bleed/portal hypertension occur due to cirrhosis

A
  • portal hypertension leads to oesophageal varices
  • change liver architecture cannot connect systemic to portal vein
  • becomes oedematous
  • causes fluid transudation out of vessels into tissues
  • oesophagus and rectal area stretch – direct connection from gut to systemic veins
  • bulging into oesophageal lumen
  • no longer able to pass into liver

fragile veins, catch = tear, bleed

84
Q

ascites and cirrhosis

A

Fluid accumulate in peritoneum
- Abdomen is a bag which contains intestines and sealed at top and bottom
- Cannot escape into pelvis
(Unlike heart failure – drain to ankles)

cirrhosis causes…
High portal venous pressure
Low plasma protein synthesis (made by liver but cannot pass out)
- Low oncotic pressure

85
Q

2 functions of liver

A

synthetic

metabolic

86
Q

synthetic function of liver

A

plasma proteins

  • Transporting proteins
  • Gamma globulin - ascites

clotting factors
- bleeding

87
Q

metabolic function of liver

A

drug metabolism (esp. 1st pass)

detoxification of unpleasant things

conjugation of RBC breakdown products
–> jaundice

88
Q

liver function tests

A

Traditionally use hepatic cell enzyme levels
- ALT, GGT
Raised in liver inflammation
- Don’t test function – test liver inflammation (not that useful)

Proportional to the number of hepatic cells
- Falls in end stage liver disease

International Normalised Ratio (INR) most useful
- clotting factors

89
Q

what 2 functions of the liver are impaired in liver disease

A 
synthetic 
> plasma proteins 
-Transporting proteins
-Gamma globulin - ascites
>clotting factors 
-bleeding
metabolic
>drug metabolism (esp. 1st pass)
>detoxification of unpleasant things 
>conjugation of RBC breakdown products 
--> jaundice
90
Q

what is INR specific to

A

normal liver function
- Should be 1

If on medicine that effects INR have different function (e.g. warfarin)

If not then not working properly

91
Q

what does INR measure

A

prothrombin time against control

92
Q

warfarin INR therapeutic range

A

2-4

93
Q

INR normal therapeutic range

A

1

if not 1 than significant liver dysfunction

94
Q

effects of liver failure

A

fluid retention – ascites

raised INR and prolonged bleeding
- 1.3 is HIGH for non warfarin patient

Portal Hypertension

  • Inability of GI blood to re-enter the vena cava
  • Leads to Oesophageal vein dilatation (Varices)

inability to remove ‘waste’ - urea
- Encephalopathy

build up of haem breakdown products
- JAUNDICE

95
Q

liver failure treatment

A

Sometimes you cannot – will usually die from it unless get a transplant which are rare to get

Supportive

  • end stage disease
  • acute failure - recovery likely

“Artificial Liver”
- Experimental stage

Transplantation
- only ‘cure’ possible
- don’t need whole liver – can be lobe
cadaveric donor – can do 3 separates lobes
- one lobe can increase in size and carry out full job, regenerate

liver vascular anatomy is unpredictable, so risk of death is live donor

96
Q

only cure for liver failure

A

transplantation

97
Q

liver transplantation

A

only cure for liver failure

  • don’t need whole liver – can be lobe
    cadaveric donor – can do 3 separates lobes
  • one lobe can increase in size and carry out full job, regenerate

liver vascular anatomy is unpredictable, so risk of death is live donor

98
Q

alcohol cessation and liver failure

A

cirrhosis and stop drinking
- will get better

acute or chronic liver failure and stay off alcohol can improve

99
Q

3 general end stage liver disease effects on dentistry

A

clotting disorders

abnormal drug metabolism

Liase with the physician – if they have specialist, have significant degree of liver problems
- INR very useful - DIFFERENT RANGE
- 1.1-1.3 abnormal in liver disease patients
PLATELETS - make sure they are normal

100
Q

3 metabolic consequences of liver disease on dentistry

A

Prolonged effect of sedatives
- Avoid intravenous sedation!! – can take longer to wear off
Different effect – cannot know as not sure what their function is, need to ask is ok

Reduce drug doses?

  • Discuss with the patient’s physician
  • Care with antifungals – avoid miconazole, erythromycin and tetracycline

Suitable analgesics?
- Paracetamol probably the safest – ASK!
- In normal doses – good analgesic
NSAIDS increase bleeding risk

101
Q

4 synthetic consequences of liver failure on dentistry

A

Reduced clotting factor synthesis

  • Bleeding tendency
  • Work with Haematologist - fresh frozen plasma?

Reduced plasma transport protein synthesis
- Drug binding reduced - dose may need reduced

Reduced ‘gamma globulin’ synthesis
- More prone to infections?

No problem with Local Anaesthesia
- Metabolised in the plasma, not the liver

BDS2 BAMS (54 decks)

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