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BDS2 - GIT system > liver disease > Flashcards

liver disease Flashcards

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1
Q

what are some liver issues

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

where does the liver sit

A
  • under the ribs adjacent to the lungs

- it is separated from the lungs by the diaphragm

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3
Q

how can you feel your liver

A
  • if you take a deep breath in

- if it is not healthy, and is inflamed the you can feel your liver without taking a deep breath

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4
Q

how many lobes does the liver have

A

3

- each lobe can function separately so you can transplant just one lobe to someone

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5
Q

how does the liver cope with its function

A
  • it can regenerate and expand
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6
Q

what is the gall bladder

A
  • collects bile from the liver
  • sits up against the diaphragm
  • the duct that takes bile from the gall bladder is the common bile duct which goes down to the pancreas
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7
Q

what is jaundice

A
  • an accumulation of bilirubin in the skin
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8
Q

what is bilirubin

A

it the normal metabolic product of haem = breakdown haem and it is absorbed and excreted
- bilirubin in the blood should be low and undetectable

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9
Q

what can jaundice cause

A
  • if it is high then it will spread from the blood stream and into the skin to cause pigmentation
  • can cause an itch = bilirubin in the skin can upset the nerve endings and cause an itch
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10
Q

what is the other term for jaundice

A
  • icteric
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11
Q

what colour is bilirubin

A
  • yellowy/orange which then makes the skin that colour
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12
Q

what are the scleral effects of jaundice

A
  • easier to see jaundice around the eyes

- it is the first place you will begin to see it

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13
Q

what is the pathway for bilirubin

A
  • haem –> biliverdin –> bilirubin
  • get bilirubin from haem metabolism = most haem is recycled but small amount is lost in each cycle
  • liver takes bilirubin and conjugates it to be removed from the body = not conjugated means it is not water soluble so can’t be removed from the body in the urine
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14
Q

what does the colour of stool depend on

A
  • depends on the conjugation of bilirubin
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15
Q

how much bilirubin is there in jaundice

A
  • excess in circulation
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16
Q

what are the 3 ways to describe jaundice

A
  • pre-hepatic
  • hepatic
  • post-hepatic
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17
Q

what is pre-hepatic

A
  • increased haem load
  • autoimmune, spleen, abnormal RBC’s
  • increased bilirubin production beyond the liver’s capacity to conjugate it
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18
Q

what is hepatic

A
  • liver cell failure

- cirrhosis, hepatitis

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19
Q

what is post-hepatic

A
  • biliary, gall bladder and pancreatic disease
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20
Q

what is the normal bilirubin metabolism

A
  • blood has a small amount of unconjugated bilirubin
  • some passes through the cells through the endoplasmic reticulum and others remain in the blood
  • the bilirubin that goes through the cells then enters the canaliculus in the liver and becomes conjugated and it then excreted out of the body
  • most of the bilirubin goes through the cells - only a very small amount is left in the blood
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21
Q

what causes pre-hepatic jaundice

A
  • jaundice due to factors before the liver metabolism

- usually excessive quantities of red blood cells breakdown products

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22
Q

what happens in pre-heptic jaundice

A
  • too much bilirubin so stops the liver ability to conjugates so the amount of non-conjugated bilirubin in the blood is higher than it should be
  • could be due to
    = haemolytic anemia - bed blood cells broken down faster than they should be (60 days instead of 120)
    = post tranfusion - from a bad match so there is more red blood cells for liver to deal with
    = neonatal - at birth when maternal red blood cells mix with baby blood during delivery so overload baby’s liver function
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23
Q

how much bilirubin is there in pre hepatic

A
  • there is more than normal amounts of both conjugated and non-conjugated bilirubin
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24
Q

what is a disease from pre-hepatic

A

Gilbert’s disease

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25
Q

what is Gilbert’s disease

A
  • decreased bilirubin uptake by liver cells
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26
Q

what causes hepatic jaundice

A
  • due to liver failure = cirrhosis of drug induced liver dysfunction
  • number of hepatocytes are reduced so reduced ability of the liver to process the bilirubin, so the amount of unconjugated bilirubin accumulates
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27
Q

what happens in hepatic jaundice

A
  • prevents metabolism of red blood cells breakdown products
  • imparted bilirubin conjugation
  • too few cells to do the job = so bilirubin passes through the liver but then goes straight back out into the blood instead of passing right through, returns to the blood unchanged
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28
Q

what happens in secretion failure of hepatic jaundice

A
  • defective secretion of conjugation bilirubin from liver cells
  • liver cell membrane is impermeable so bilirubin can’t get through to be excreted
  • means that non-conjugated bilirubin that passed through the cells and became conjugated returns to the blood conjugated as it can get through to be excreted
  • means there is a mixture of both conjugated and unconjugated bilirubin in the blood
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29
Q

what happens in post-hepatic jaundice

A
  • bile tree is blocked so bile can’t escape into the intestine so backs up and goes into the blood
  • there is an obstruction to bile outflow
  • intra-hepatic biliary system = primary biliary sclerosis, the bile system doesn’t work
  • extra-hepatic biliary system = gall bladder or common bile duct
  • there is an obstruction somewhere in the biliary network
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30
Q

what bilirubin is in the blood due to post-hepatic jaundice

A
  • both unconjugated and conjugated
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31
Q

how can the gall bladder be blocked in post-hepatic jaundice

A
  • gall stones
  • these are the most common forms of bile duct blockage
  • if you have a bile duct blockage you want it to be gall stones as these are easiest treated
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32
Q

how can the common bile duct be blocked in post hepatic jaundice

A
  • pancreatic carcinoma = tumour of the head of the pancreas, as it extends it will squash the bile duct and block it
  • cholangiocarcinoma = tumour of the bile duct itself
  • poor outcome for patients with either of these = 1-2 years at most
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33
Q

what are the clinical features of jaundice

A
  • conjugated bilirubin is excreted in the urine and faeces = colour changes with cause of jaundice
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34
Q

what is the colour of stool in post hepatic jaundice

A
  • pale stool and dark urine
  • conjugated bilirubin causes jaundice
  • if block the bowel tree then conjugated bilirubin can’t get to the small intestine so stool will be pale
  • obstructive jaundice = yellow eyes, dark urine and pale stool
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35
Q

what makes stool dark

A
  • if get bilirubin through, excess bilirubin
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36
Q

what colour of stool is in pre hepatic

A
  • everything is normal as normal function of bilirubin still happening
  • will get dark urine and stool
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37
Q

what happens if there is a problem with the liver itself (hepatic jaundice)

A
  • will get pale stool and pale urine
38
Q

how can you tell between pre-, post- and hepatic jaundice

A
  • by the colour of the stool
39
Q

what are gall stones

A
  • form within the gallbladder
  • they collect in the gall bladder then one is released, and it can block the biliary tree
  • can cause obstructive jaundice
40
Q

what can happen when you get inflammation of the tissues and gallbladder

A
  • means you can get an inflamed diaphragm as it is next to the gall bladder
  • can irritate the phrenic nerve and the sensory skin it supplies is on the shoulder, so the Brian thinks that is where the pain is coming from
41
Q

where is gall bladder pain often felt

A
  • in the shoulder
42
Q

what is acute cholecystitis

A
  • inflammation of the gall bladder
43
Q

what are gall bladder symptoms

A
  • pain in the shoulder is a tip off that there could be a problem in gall bladder
  • abdominal pain on the right side = radiates to the back
  • pain is brought on by eating fatty food = stimulates bile release by contraction of the gall bladder
44
Q

how is gall bladder pain brought on by eating fatty food

A
  • bile constrictions emulsify fat and so when eating fatty food there is a lot of fat to emulsify so it can be sore eating fatty foods
45
Q

what is the function of the gall bladder

A
  • storage bag
  • if there is enough of a contraction, then stones can go out and block the pathway
  • a tumour in the head of the pancreas can squash the bile ducts to prevent getting through
46
Q

who was it originally believed to be more likely to get gall stones

A
  • fair, female, fertile, fat, forty
47
Q

who can get gall stones

A
  • anyone can get gall stones - these people may be at more risk, but they are not the only ones who can get gall stones
48
Q

what size are gall stones

A
  • 1cm in size roughly

- if you have one stone you are likely to have more than ons tone, probably lots of stones

49
Q

how can you image jaundice patient

A
  • ultrasound
  • plain radiographs
  • ERCP
50
Q

how is the ultrasound used to image jaundice

A
  • detects dilated bile channels within the liver
  • also dilated biliary tree is detected = shows the width of the duct
  • shows echoes of what’s going on
51
Q

how are plain radiographs used to image jaundice

A
  • show radiopaque gall stones

- only useful if gall stones have something in them to make them radiopaque, or else won’t see them

52
Q

how is ERCP used to image jaundice

A
  • endoscopic retrograde cholangiopancreatography
  • shows contrast radiograph of biliary tree
  • use a dye into the bile tree to see any blockages in it
  • can put a stent in the bile duct to open it up
  • is good but can only reach so far up the duct with it
53
Q

how is cystic fibrosis linked with pancreatitis

A
  • need oral pancreatic enzyme supplements in cystic fibrosis
  • aetiological role in alcohol in chronic pancreatitis
  • pancreatitis is common with alcohol
  • possible role in mumps virus - usually temporary
54
Q

what type of diabetes is a consequence of chronic pancreatic disease

A
  • will be type 2 diabetes
55
Q

what is the prognosis of pancreatic malignancy

A
  • poor prognosis as it is often not found till it is too late
  • not found until patient presents with jaundice
56
Q

how can the pancreas digest itself

A
  • can be inflamed and produced digestive enzymes and can produce these into the gland which can cause the gland to digest itself inside out
57
Q

how do you manage pre hepatic jaundice

A
  • identify and treat he cause
58
Q

how do you manage post hepatic jaundice

A
  • remove obstruction
59
Q

how can you remove the obstruction in post hepatic jaundice

A
  • gall stones removed vie ERCP
  • gall stone vie ultrasound
    = use sonic waves to breakdown stones
    = 3 different direction of waves and pressure blows up the stones
    = if you hit a hard structure with an ultrasound it will fracture
    = means you can focus on one area and not damage the surrounding tissue
  • can force one the channel with a stent
    = opens up bile duct, little mesh metal opening up to allow bile to flow through
60
Q

how can you prevent the recurrence of gall stones

A
  • remove the gall bladder (cholecystectomy) = if removed, then can’t make stones, simplest and most effective treatment
  • prevent build up of bile acid = low calorie and low cholesterol diet
  • prevent bile acid reabsorption from the GIT = cholestyramine
61
Q

what can be an issue if you remove your gallbladder

A
  • means you only have a small drip of bile coming from the liver instead of the big amount from the gall bladder
  • means you would have to change diet to decrease amount of fatty foods consumed
  • would have to eat in small doses
62
Q

what is neonatal jaundice

A
  • doesn’t happen if you have a C-section
  • increased haem breakdown = birth trauma, ABO and Rhesus incompatibility
  • poor liver function in neonate = worse if <37 weeks gestation
  • risk of Kernicterus
63
Q

what is kernicterus

A
  • high levels of bilirubin in the brain can cause damage to the developing brain
  • can get permanent brain damage
  • don’t get in adults as the brain is much more separated from blood
64
Q

how do you treat neonatal jaundice

A
  • phototherapy
  • in old time used to put the baby’s cot next to the window to allow sunlight in to make the jaundice go away
  • nowadays, have phototherapy which is blue light phototherapy = the blue light break down the bilirubin in the skin and causes it to then be removed
65
Q

what can cause acute liver failure

A
  • paracetamol poisoning

- another drug reaction

66
Q

how does paracetamol poisoning occur

A
  • can take 4 days to use all clotting factors
  • only takes 20 tablets
  • is a painful death
  • can’t detoxify all the tables so will die
  • will bleed to death as can’t produce clotting factors in time
  • encephalopathy = damage to the brain due to the presence of toxic materials
67
Q

what happens if you can survive the acute period of liver failure

A
  • then you will survive
  • the liver will switch itself off for a while the restart - but the problem is you can’t survive without a liver and we have no machine to work as liver for that period
68
Q

what is chronic liver failure

A
  • Cirrhosis
  • primary liver cancer
  • secondary liver cancer = metastases
69
Q

what is cirrhosis

A
  • circle of scarring and healing of the liver = mixed picture of image, fibrosis and regeneration of liver structure
  • eventually there is more damage than functioning liver = architecture of the liver is very specific so if the damage is too much then the liver cells may not regenerate in correct way
  • eventually get fewer and fewer hepatocytes than can do their function
70
Q

what can cause cirrhosis

A
  • lots of things
  • alcohol
  • primary biliary cirrhosis
  • viral disease = chronic active hepatitis
  • autoimmune chronic hepatitis
  • haemochromatosis
  • cystic fibrosis
71
Q

how can you get primaru biliary cirrhosis

A
  • from an autoimmune disease
72
Q

what are the signs and symptoms of cirrhosis

A
  • can get a larger or smaller liver = as it becomes more fibrotic then the liver becomes smaller and smaller
  • acute bleed = portal hypertension
  • jaundice
  • oedema and ascites (abdominal fluid)
  • encephalopathy
  • spider naevi, palmer erythema
73
Q

what can cause an acute bleed in cirrhosis

A
  • if you have changed architecture then may not be able to pass blood correctly from GIT so use smaller times connecting CIT so increased pressure and these will stretch (veins inside oesophagus) as trying to take more and more blood so become stretched and more fragile so can tear easier
  • can cause oesophageal varies
74
Q

what causes oesophageal varies

A
  • normally blood from the portal system passes into the liver then into the blood circulation, now as it can’t get into the liver it goes through the joining veins which increase in size and become fragile so if they tear can cause a big bleed
  • big cause of death
75
Q

what is oedema and ascites

A
  • high portal venous pressure
  • low plasma protein synthesis as liver makes these = lower oncotic pressure
  • get oedema in the abdomen
76
Q

what are spider naevi

A
  • high oestrogen levels from reduced metabolism
  • enlarged blood vessels from increased oestrogen
  • a red spot in skin and red lines radiating out of it
77
Q

what is palmer erythema

A
  • red fingers with white palm
78
Q

what is the function of the liver

A
  • synthetic = make plasma proteins and clotting factors

- metabolic = metabolism of RBC’s, detoxify

79
Q

what can happen when you get loss of synthetic functions

A
  • loss of plasma proteins = transporting proteins and gamma globulin
  • loss of clotting factors = should always test coagulation of someone with liver disease before extracting a tooth as they may not have a lot of clotting factors
80
Q

what happens when you get loss of metabolic function

A
  • loss of drug metabolism = especially 1st pass metabolism
  • loss of drug detoxification
  • loss of conjugation of RBC breakdown products
81
Q

what are liver function tests

A
  • traditionally use hepatic cell enzyme levels = ALT and GGT
  • raised in liver inflammation
  • proportional to the number of hepatic cells = falls in end stage liver disease
  • international normalised ratio (INR) most useful
82
Q

what does the INR look for

A
  • test to look at what it can do - is it making clotting factors for example
  • measure prothrombin time against control = prothrombin -> thrombin
  • specific to a normal liver function
  • normal value is 1.0
    = if on warfarin the therapeutic range is 2-4 (warfarin takes away ability to use INR to determine function)
  • if not on warfarin then INR should be 1
  • if INR is not on 1 then there is significant liver synthetic dysfunction (not enough clotting factors)
  • if INR is 1.1 then liver dysfunction
83
Q

what is the effect of liver failure

A
  • fluir 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 dilation
  • inability to remove waste - urea, get encephalopathy
  • build up of haem breakdown products = jaundice
84
Q

what is the treatment for liver failure

A
  • sometimes can’t treat
  • supportive treatment = end stage disease (can’t treat really), acute failure (recovery is likely)
  • ‘artificial liver’= experimental stage, need to culture hepatocytes as they can’t function normally
  • transplantation
85
Q

how is liver transplantation carried out

A
  • it is the only real option
  • only ‘cure’
  • relatively uncommon unless there is a good reason
  • can give one liver to 3 people as it has 3 lobes
  • also means there is the potential to take part of a living persons liver and give it to another person = vey risky, the liver has a lot of big vessel and it cut through one of these then you will bleed to death
86
Q

how does alcohol cessation affect liver disease

A
  • will get better if you stop drinking = even with cirrhosis, if you stop drinking then you will get better
  • people often fo well if they can just stop drinking
87
Q

how can end stage liver disease effect dentistry treatment

A
  • clotting disorders - need to consider for extractions
  • abnormal drug metabolism = may need to adjust the dose
  • need to liaise with the physician = need to make sure platelets are normal, INR is very useful, if a patient has a physician then you can assume that their liver disease id quite bad
  • patient can behave unpredictably
  • metabolic consequences
88
Q

what are metabolic consequences of liver disease to consider for dentistry

A
  • prolonged effects of sedatives = avoid intravenous sedation
  • reduce drug doses = discuss with the patient physician, care with antifungals (need to avoid miconazolem erythromycin and tetracycline)
  • suitable analgesics = paracetamol is probably the safest if kept to a safe dose, NSAID’s increase bleeding risk
89
Q

what are synthetic consequences of liver disease to consider for dentistry

A
  • reduced clotting factors= bleeding tendency, work with haematologist
  • reduced plasma transport protein synthesis = drug binding reduced, dosemay need reduced
  • reduced ‘gamma globulin’ synthesis = more prone to infection
90
Q

do those with liver disease have an issue with local anaesthetic

A
  • no

- metabolised in the plasma, not in the liver so it is safe to use

BDS2 - GIT system (5 decks)

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