Jaundice and Liver Failure Flashcards
4 liver issues
- viral liver diseases (hepatitis)
- jaundice
- cirrhosis
- liver failure
when can the liver be palpable on the back
Liver pushed down the way when breathe in
Large liver (unhealthy) can palpate even when not breathing in
how many lobes does the liver have
3
location of the liver
under the ribs, adjacent to the lung but separated from the lung by the diaphragm
how does the liver cope with varying degrees of function
Lobes
- Can function individually – can transplant one lobe
Liver regenerates and expand to cope with function
- Can cope with some damage
function of gallbladder
bag which collects bile from the liver, at the back
what ducts join together to make ampulla of Vater entering the jejunum?
common bile duct joins the pancreatic duct
what is jaundice
accumulation of bilirubin in the skin
signs of jaundice
yellow-orange pigmentation
itch (bothers patient)
icteric
term used to describe jaundice patient
what is bilirubin
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
what can jaundice be a result of?
liver failure
scleral effects of jaundice
yellow-orange white of eye
what does the liver do to bilirubin
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
stool and urine colour if liver functioning well
normal/dark
stool and urine colour if liver not functioning well
pale/unpigmented as lack of bilirubin excretion
what is in excess when a patient has jaundice
bilirubin in the circulation
3 ways to define jaundice
pre-hepatic
hepatic
post-hepatic
pre-hepatic jaundice due to
increased haem load
- autoimmune, spleen, abnormal RBCs
hepatic jaundice due to
liver cell failure
- cirrhosis, hepatitis
post-hepatic jaundice due to
biliary, gall bladder and pancreatic disease
unconjugated bilirubin found
in blood
conjugated bilirubin found
in bile (liver passed to small intestine or kidney)
what is pre hepatic jaundice factors due to
due to factors before liver metabolism
what is the level of unconjugated bilirubin like in pre-hepatic jaundice?
higher than it should be
usually excessive quantities of RBC breakdown products
3 possible causes of pre-hepatic jaundice
Haemolytic anaemia
Post transfusion (bad match)
Neonatal (maternal RBC induced)
how can haemolytic anaemia cause pre-hepatic jaundice
- RBC broken down faster
- Turnover doubles
- More bilirubin to deal with
how can a transfusion cause pre-hepatic jaundice
- All new unmatched RBC broken down by immune system
- Straightforward as know if they have had a transfusion
what is a neonatal cause of pre-hepatic jaundice
- Jaundice when born
- Maternal and baby blood mixed – don’t match so destroyed so excess of haemoglobin in liver and bilirubin in blood will
proportion comparisons of unconjugated and conjugated bilirubin
more unconjuageted than conjugated
greater unconjugated passed through blood circulation
- As not enough capacity in cells (liver cannot process it all)
hepatic jaundice due to impaired enzyme action
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
what are 2 causes hepatic jaundice
cirrhosis
drug induced liver dysfunction
what is a rare type of hepatic jaundice
secretion failure
- defective secretion of conjugated bilirubin from hepatocytes
liver cell membrane becomes impermeable to conjugate bilirubin - enters blood circulation instead
what causes post-hepatic jaundice
obstruction to bile outflow
- cannot escape liver to small intestine
- so conjugated and unconjugated bilirubin in blood
where are the 2 possible sites of problem for post-hepatic jaundice
intrahepatic biliary system
extrahepatic biliary system
what is an intrahepatic biliary system that can lead to post-hepatic jaundice
primary biliary scelrosis
- No functioning bile ducts in liver
- Immune disease
- Scarring and blocking of ducts
2 sites of extrahepatic biliary system that can lead to post-hepatic jaundice
gall bladder
common bile duct
what can happen in the gall bladder that can lead to post-hepatic jaundice
gall stone formation
- block biliary tree so cannot get bilirubin passed
what 2 carcinomas can occue in the common bile duct region that can lead to post-hepatic jaundice
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
circulation components of post-hepatic jaundice
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
circulation components of pre-hepatic jaundice
greater proportion of unconjugated bilirubin as excess RBC products and not enough hepatocyte capacity to process it all
circulation components of hepatic jaundice (secretion failure)
unconjugated and conjugated bilirubin
liver cell membrane become impermeable to conjugated bilirubin
circulation components of hepatic jaundice (impaired enzyme/hepatocyte function)
unconjugated bilirubin
Bilirubin cannot get processed due to disease in cells or not enough to do job
- Very little If any pass into bile
pale stool and dark urine suggests
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)
normal coloured stool and urine is indicative of which type of jaundice
pre-hepatic
- excess bilirubin is unconjugated in blood
- everything normal coloured
pale stools and urine is indicative of which type of jaundice
hepatic
- no conjugation of bilirubin occurring as liver not functioning
where do gall stones form
in the gall bladder
collect like bag and pop out into biliary tree and get stuck
- multiple stones usually
what does gall stones do
block biliary tree —> obstructive post-hepatic jaundice
cause inflammation
- wall - seen on US
- and adjacent tissues (phrenic nerve impact)
acute cholecystitis
inflammation of the gall bladder
role of the gall bladder
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)
3 gall bladder symptoms
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.
what is the most common issue of gall bladder
Usually Gall stones
- Rarely Cholangiocarcinoma (bile duct cancer)
3 ways of imaging the jaundiced patient
ultrasound
plain radiographs
ERCP
- Endoscopic Retrograde Cholangio Pancreatography
CT scans (computerised tomography)
ultrasound of liver detects
Detects dilated bile channels WITHIN the liver
- Also dilated biliary tree
Show echoes of what’s happening in abdomen
Width of gallbladder, stones
plain radiographs of the gall bladder show
radiopaque gall stones only (not all)
main imaging techniques of liver and gall bladder are
ultrasound and CT scans (computerised tomography)
ERCP
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
how can you receive a patient of a carcinoma of a bile duct and jaundice temporarily
by a stent - helps to widen the lumen in case of a carcinoma
until decide on best treatment
when is pancreatitis and Cystic Fibrosis common
if drink a lot of alcohol
why is the inflammation of the pancreas an issue
release digestive enzyme
- in gland can cause digestion from inside out
what supplements may be needed in CF
oral pancreatic enzyme supplements
Viscous secretion of pancreases, mean cannot move out duct properly
Pancreatic enzyme in gland can cause pancreatitis
pancreatitis
when pancreatic enzyme (digestive enzymes) are released inside the pancreas because of inflammation rather than in the small intestine
what disease is a consequence fo chronic pancreatic disease
type 2 diabetes
what is the prognosis like for a pancreatic malignancy (adenocarcinoma)
poor
- developed
- tumour present for many years
how to manage pre-hepatic jaundice
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
how to manage post-hepatic jaundice
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
methods of prevention of gall stone recurrence
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
what type of births are at higher risk of neonatal jaundice
Natural births over C sections
risk in neonate of neonatal jaundice
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
kernicterus
- 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
how to treat neonatal jaundice
phototherapy
- blue wave light (energy sufficient to cause break down of bilirubin)
what is the ultimate consequence of liver failure
death
- cannot detoxify many toxins
- cannot maintain carbohydrates in blood properly
what is a cause of acute liver failure
paracetamol poisoning
other drug reaction
what is acute liver failure
Sudden loss of liver function
- recovery or Rapid death
2 ways liver failure can cause death
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
how many days does it take to use up premade clotting factors by the liver
4 days
clotting factors will not last the weeks needed to repair hepatocytes to normal
what is the time window to reduce damage to liver after insult
36-48 hours
- after this need a liver transplant
clotting factors will not last the weeks needed to repair hepatocytes to normal
3 types of chronic liver failure
cirrhosis
primary liver cancer
- often after hepatitis
secondary liver cancer
- metastases
cirrhosis
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
aetiology of cirrhosis
Alcohol
Primary Biliary Cirrhosis
viral disease - chronic active hepatitis
autoimmune chronic hepatitis
Haemachromatosis
Cystic fibrosis
signs and symptoms of cirrhosis
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
how can spider naevi and palmer erythema occur due to cirrhosis
- 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
how can an acute bleed/portal hypertension occur due to cirrhosis
- 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
ascites and cirrhosis
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
2 functions of liver
synthetic
metabolic
synthetic function of liver
plasma proteins
- Transporting proteins
- Gamma globulin - ascites
clotting factors
- bleeding
metabolic function of liver
drug metabolism (esp. 1st pass)
detoxification of unpleasant things
conjugation of RBC breakdown products
–> jaundice
liver function tests
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
what 2 functions of the liver are impaired in liver disease
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
what is INR specific to
normal liver function
- Should be 1
If on medicine that effects INR have different function (e.g. warfarin)
If not then not working properly
what does INR measure
prothrombin time against control
warfarin INR therapeutic range
2-4
INR normal therapeutic range
1
if not 1 than significant liver dysfunction
effects of liver failure
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
liver failure treatment
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
only cure for liver failure
transplantation
liver transplantation
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
alcohol cessation and liver failure
cirrhosis and stop drinking
- will get better
acute or chronic liver failure and stay off alcohol can improve
3 general end stage liver disease effects on dentistry
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
3 metabolic consequences of liver disease on dentistry
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
4 synthetic consequences of liver failure on dentistry
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
