Liver Disease Flashcards
Where is the liver located?
right upper quadrant
In the right 5th intercostal space to the costal margin
How much does a healthy liver weigh?
1.4-1.7 kg
You should be able to palpate the liver in a healthy patient. True or false
False
you should not be able to feel the liver in a healthy patient
What is an anatomical variation of the liver ?
Riedels lobe
it can simulate a mass
What is riedels lobe?
it is a tongue like inferior projection on the right love of the liver beyond the level of the most inferior costal cartilage on cross-sectional images
Riedels lobe is more palpable than the rest of the liver. True or false
True
The liver is responsible for the production of bile. What is the role of bile?
an emulsifying agent that makes fat more “absorbable”
What is the function of the gallbladder with high consumption of fatty meals?
gall bladder and cystic duct constrict to ensure that bile enters the duodenum to reach the small intestine
Where liver receives blood (carrying nutrients) from all of the GI tract via what blood vessel ?
The hepatic portal vein
What is an advantage of sublingual medication?
by passes first pass metabolism of the liver
does not go into systemic circulation as it has its own circulation
75% of the livers blood supply is from what blood vessel?
the hepatic portal vein
The common hepatic artery which carries what kind of blood?
oxygen rich blood
The common hepatic artery constitutes ____% of the livers blood supply
25
How is the liver drained?
the hepatic vein carries blood to the inferior vena cava
GTN (glyceryl trinitrate) is absorbed in the floor of the mouth. What are the characteristics of the FoM that allow absorption?
thin
non-keratinized
has its own blood supply
List some functions of the liver
Synthesis of plasma proteins (albumin and clotting factors: 2,7,9,10)- liver makes all of the clotting factors
Metabolism of drugs and toxins
Immunity via hepatic macrophages (kupffer cells)- liver filters the blood
Metabolism of fats, proteins and carbohydrates
Storage of glycogen, vitamins and minerals (vitamin A, D, E, K)
Bile production and excretion
Excretion of cholesterol and sex hormones
What is the function of the gallbladder?
stores and concentrates bile produced in the liver
What are the parenchymal (functional) tissue of the liver?
Hepatocytes
Hepatocytes constitute _____% of the liver volume
80
What are the non-parenchymal tissue of the liver?
sinusoidal endothelial cells
Phagocytic kupffer cells
Hepatic stellate cells
Parenchyma are to be distinguished from what other kinds of tissue ?
Supporting and connective tissue
What is a liver sinusoid?
the are a larger caliber of capillaries, they have a specialised endothelial lining known as the sinusoidal endothelial cells.
Be able to label a sinusoid
The central hepatic vein drains into the ______________.
Vena cava
At the sinusoid there is a mixing of …
portal (vein) and arterial blood
this usually drains into the central hepatic vein
Briefly describe the state of the blood that arrives at the hepatic central vein?
cleansed version of the blood which is sent back to the heart
Drugs and toxins are metabolised before they reach the hepatic central vein
Give examples of liver function tests
ALT / AST
ALP/ GGT
Bilirubin total
Albumin
Clotting studies (PT/INR/factors)
What is the normal range for serum levels of alanine aminotransferase (ALT)?
<40 IU/L
What is the normal range for serum levels of aspartate aminotransferase
6-40 IU/L
ALT and AST are enzymes found in hepatocytes. Raised serum levels of these enzymes are an indication of what ?
leakage from damaged hepatocytes
damage to liver cells
Alkaline phosphatase (ALP) enzymes are commonly found in the __________ and are an indication of _________.
bile duct cells (also found in sinusoid complex)
indication of damage to the bile duct (bile is produced by hepatocytes and secreted into the bile ducts.
What is the normal range for serum levels of ALP?
30-130 IU/L
What is the normal range for serum levels of GGT?
50-420 IU/L
Gamma glutamyl transferase (GGT) are enzymes commonly found in the _________ and are an indication of ____________.
bile duct cells (also found in sinusoid complex)
indication of damage to the bile duct (bile is produced by hepatocytes and secreted into the bile ducts.
Aside from bile ductal cell damage, what other situation can lead to an increase in ALP?
high bone turnover
bone growth resulting from bone healing / pathological bone resorption
What is the normal range of serum levels of bilirubin?
0.1-1.0 mg/dL
What is the normal range of serum levels of albumin?
3.5-5.3 g/dL
What is the norma range of serum levels of clotting factors?
Variable
Low levels of albumin and clotting factors are indicative of …
liver tissue loss
What is the purpose of osmotic pressure in the blood ?
maintains fluid in the blood and prevents swelling
What is bilirubin?
a breakdown produce of red blood cells
Briefly describe how bilirubin arrives at the gut?
absorbed through the blood (after break down of RBCs) into the liver
It is usually retained in the biliary system and ejected out of the common bile duct before arriving in the gut
it gives faecal matter its characteristic colour
Describe an instance that leads to the presence of bilirubin in the urine
Gall stones
bilirubin can be absorbed in the blood and therefore some of it is also excreted in the kidney
In the presence of a gall stone/obstruction, bilirubin ends up being present in the urine as opposed to the faeces.
This is because excretion via the gut is divested as it is unable to leave the gall bladder through the common bile duct
Where does the production of bilirubin occur?
Heme is broken down to bilirubin in the macrophages of the reticuloendothelial system (tissue macrophages, spleen and liver)
How does bilirubin reach the liver?
unconjugated bilirubin is transported through the blood complexed to albumin to the liver
How is bilirubin taken up in the liver cells?
bilirubin is then taken up by facilitated diffusion by the liver and then conjugated with glucoronic acid
Give a summary of bilirubin metabolism
- senescent red cells are a major source of haemproteins
-break down of heme to bilirubin occurs in macrophages of reticuloendothelial system
-unconjugated bilirubin is transported in the blood complexed to albumin to the liver
-bilirubin is taken up via facilitated diffusion in the liver and conjugated to glucoronic acid
-conjugated bilirubin is actively secreted into bile and then the intestine
-in the intestine glucoronic acid is removed by bacteria which results in bilirubin being converted to urobilinogen
- some of the urobilinogen is reabsorbed from the gut and enters portal blood
-a portion of urobilinogen participates in enterohepatic urobilinogen cycle
-the remainder of urobilinogen is transported by the blood to the kidney where it is converetd to urobilin and excreted, giving urine its characteristic colour
-urobilinogen is oxidises by intestinal bacteria to brown stercobilin
What derivative of bilirubin gives the brown colour that can be observed in faeces?
stercobilin
What derivative of bilirubin gives urine its characteristic yellow colour ?
urobilin
Liver disease is the ___ “big killer” in England and wales.
5TH
after heart, cancer, stroke and respiratory disease
What dental considerations should you make for patients with liver disease?
LA- metabolism of LA; to prevent systemic toxicity
Risk of bleeding due to reduced clotting factor synthesis
Rates of alcohol- related mortality were substantially greater for those in more disadvantaged socio-economic classes. True or false.
True
What are the general classifications of alcohol related disease?
Acute Intoxication
Chronic dependency
What are the risks associated with acute intoxication of alcohol ?
acute alcoholic hepatitis
acute pancreatitis
risk of coma
aspiration
trauma
hypothermia
death
What are the risks associated with chronic alcohol dependency?
chronic liver disease
chronic pancreatitis
cardiomyopathy
brain atropy
peripheral neuropathy
malnutrition
malignancy- x6 increased risk of cancer
stroke
CVD
psychosocial aspects cause significant morbidity
What are the risks associated with chronic alcohol dependency?
chronic liver disease
chronic pancreatitis
cardiomyopathy
brain atropy
peripheral neuropathy
malnutrition
malignancy- x6 increased risk of cancer
stroke
CVD
psychosocial aspects cause significant morbidity
In order to keep health risks from alcohol to a low level, what is the recommendation for alcohol consumption weekly?
no more than 14 units per week
What is the best way to consume the recommended 14 units per week and why ?
best to spread drinking evenly over 3 or more days
one or two heavy drinking episodes a week will increase risk of death from long term illness and from accidents and injuries
What is the best way to cut down the amount of drinking?
have several drink free days each week
How much pure alcohol does one unit of alcohol contain ?
8g or 10ml of pure alcohol
How do you calculate the number of units of alcohol ?
[ABV% x volume of drink (ml)]/1000
What does the disability-adjusted life year (DALY) refer to ?
extends the concept of potential years of life lost due to premature death to include equivalent years of “healthy” life lost by virtue of being in states of poor health or disability
Causal relationships have been established between harmful drinking and incidence of infectious diseases such as… (name the infectious diseases)
tuberculosis
HIV/AIDs
What impacts can alcohol have in dentistry ?
dental erosion due to sugars/acid
dental erosion due to vomiting
halitosis
tooth staining
oral cancers (with and without smoking)
dental trauma
poor oral hygiene
reduced bone density
Briefly explain the impact of alcohol on bone density
alcohol affects vitamin D metabolism
this therefore reduces calcium absorption via the intestine and impacts bone density
Dental surgeries should not be taking part of alcohol screening. True or false
false
What are the CAGE alcohol screening questions?
C- do you think you should CUT down alcohol?
A- do you get angry when people say you drink too much ?
G- do you feel guilty?
E- do you have to have a drink in the morning to get your eye open?
What is regarded as the “best” screening tool for alcohol?
AUDIT
alcohol use disorders identification test
What format can the AUDIT screening tool be delivered in?
Interview
self reported questionnaire
What is a potential disadvantage of the AUDIT screening tool over the CAGE screening tool?
it takes longer
What is the intervention for a zone I AUDIT screening score of 0-7
alcohol education
What is the intervention for a zone II AUDIT screening score of 8-15?
Simple advice
What is the intervention for a zone III AUDIT screening score of 16-19?
simple advice plus brief counselling and continued monitoring
What is the intervention for a zone IV screening score of 20-40 ?
referral to specialist for diagnostic evaluation and treatment
What causes chronic liver disease?
continuous or repetitive injury to the liver which can cause inflammation
In some patients, inflammation of the liver can lead to ____________.
progressive scarring (fibrosis)
connective tissue
What are the stages of liver damage?
Healthy liver
Fatty liver
Liver fibrosis
Cirrhosis
What is the initial response of the liver to injury?
to lay down fat
this causes enlargement of the liver
On a cellular level, briefly state what occurs in cirrhosis
the growth of connective tissue causes the destruction of the liver cells
List some causes of chronic liver disease
alcohol
obesity/diabetes
viral hepatitis
Other autoimmune diseases (PBC - primary biliary cirrhosis, PSC- primary sclerosing cholangitis, AIH- autoimmune hepatitis, haemochromatosis, alpha-1 antitrypsin)
How can alcohol, obesity and diabetes lead to the development of CLD ?
leads to the accumulation of fatty deposits in the liver which can leads to inflammation
How can viral hepatitis lead to the development of CLD?
leads to host immunity activation which leads to inflammation
Inflammation can lead to fibrosis
growth of connective tissue can lead to death of liver cells
What is haemochromatosis ?
this is when there is an overload of iron being laid down in the liver
A deficiency in alpha-1 anti-trypsin can cause CLD, how?
a-1 anti-trypsin protects against natural damaging reactions in the liver
The removal of aetiology of CLD can halt or reverse damage to the liver, why is this ?
this is because the liver has immense capacity to regenerate and repair
What are the two main hepatic pathways for alcohol metabolism ?
alcohol dehydrogenase
cytochrome P450 2E1
How does alcoholism damage the liver via the ADH pathway?
[ethanol —> acetaldehyde—> acetic acid]
[CH3CH2OH—> CH3CHO—> CH3COOH]
The dehydration of ethanol to acetalcehyde requires ADH enzyme as well as cofactor NAD+
When ethanol is converted to acetaldehyde, NAD+ is reduced to NADH
NAD+ is also reduced to NADH when acetaldehyde is oxidised to acetic acid
In alcoholism there is excessive NADH in relation to NAD
NADH inhibits gluconeogenesis and increases fatty acid oxidation (use of fatty acids for energy)
fatty acid oxidation leads to fatty infiltration of the liver and thus leads to inflammation
Acetaldehyde is a carcinogen. True or false
True
What is the MOA of the disulfiram reaction observed in metronidazole ?
metronidazole inhibits conversion of acetaldehyde to acetic acid
this leads to the build up of acetaldehyde which can lead to sickness/hang over feeling
How does alcoholism lead to liver damage via the CYP2E1 pathway
CYP2E1 facilitates the dehydration of ethanol to acetaldehyde
[CH3CH2OH —-> CH3CHO]
NAPDH is used as a co-factor in this reaction and leads to the production of NADP and free radicals
The free radicals generated in this reaction cause direct cellular damage
chronic alcohol consumption causes up-regulation of CYP2E1
This means that more alcohol is metabolised via this hepatic pathway; more free radicals are produced and thus cause cellular damage
What are the 3 additional pathways of destruction for alcohol related liver disease?
Hepatic macrophage activation
Antioxidant deficiency
Endotoxaemia
How can hepatic macrophage activation lead to alcohol related liver disease?
chronic exposure to alcohol activated macrophages that produce TNF-a and induce reactive oxygen species (ROS) in mitochondria
ROS- hunt for other atoms electrons which can lead to unstable reactions
How can antioxidant deficiency in alcoholics lead to liver disease
poor diet and general poor health can lead to a reduction in antioxidant deficiency in alcoholics
this leads to higher levels of oxidative stress and apoptosis
How can alcohol encourage endotoxemia ?
alcohol directly affects the barrier function of the GI mucosa
> > when gram -ve bacteria dies, their endotoxins such as LPS can be released«
these endotoxins can cause an acute inflammatory reaction«
The endotoxins can now travel via compromised GI mucosa and end up in the blood stream. This is known as endotoxaemia.
The endotoxins can cause hepatic inflammation
What is the presentation for alcohol related liver disease ?
Abdominal pain
hepatomegaly
presence of risk factors
Ascites
Weight loss- loss of muscle mass
Weight gain- water retention
malnutrition/wasting- loss of appetite
anorexia
fatigue
What are the risk factors for alcohol related liver disease?
Prolonged and heavy alcohol comsumption
Hep C
Female sex
cigarette smoking
obesity
>65 years old
hispanic ethnicity
family history
What is Ascites?
this is the collection of fluid in the peritoneal cavity
(>25ml)
It is use to low blood levels of albumin which causes a loss of osmotic pressure. Fluid is lost from the vessels which leads to abdominal swelling
What are the signs of liver disease?
Leukonychia- white nails
Palmar erythema- red palms
Spider naevi- dilated superficial capillaries
Dyputrens contracture
Gynaecomastia- unable to convert hormones
Finger clubbing (linked to many disorders)
Where are spider naevi commonly found and why?
Head
Neck
Upper limbs
This is because they are only found in the region of the superior vena cava
What is Dyputrens contracture?
this is the presence of a fibrous band which prevents straightening of the pinky and ring finger
Ascites is caused by __________ and ___________
portal hypertension
low blood levels of albumin (portal hypertension means that nothing is being metabolised including albumin)
What is portal hypertension and what are the consequences?
portal hypertension is when there is elevated blood pressure in the portal venous system
nothing is being metabolised, nothing is being detoxified
toxins will continue to be present in the blood
A dilated vein is known as a…
variceal
Portal hypertension can cause…
Ascites
Variceal bleeding
Encephalopathy
Explain how portal hypertension can cause encephalopathies
portal hypertension prevents the blood from being detoxified
this means that the toxins are able to reach the brain and act as false neurotransmitters- disturbance of circulating toxins
Explain how portal hypertension leads to variceal bleeds?
portal hypertension leads to increase in blood pressure in veins in the lower oesophagus and stomach
The veins begin to expand as they are not designed for high pressure; lead to formation of varices.
There is very little structure/mucosa over them which means they can burst- hence variceal bleeds
What is Jaundice?
this is the accumulation of bilirubin in the bloodstream and deposition in the skin, sclera and mucous membranes
What happens to bilirubin in the liver?
Conjugation with glucorinic acid
Bacterial deconjugation of bilirubin leads to…
formation of urobilinogen
Urobilinogen can be used to form stercobilin
What are some pre-hepatic causes of jaundice?
pre-hepatic causes often have to do with too much bilirubin in the blood as a result of haemolysis of RBCs
Malaria
Sickle cell Anaemia
Spherocytosis
Autoimmune
These conditions all cause damage to RBCs thus reducing their lifespan and increasing bilirubin blood levels
So much RBC destruction which causes uncharacteristic rise in blood bilirubin levels
Name some hepatic causes of jaundice?
Hepatic causes of jaundice indicate that bilirubin is not being metabolised.
The following conditions can lead to reduced bilirubin metabolism (conjugation- first step of metabolism of bilirubin)
-viral hepatitis
-alcohol liver disease
-NAFLD- non alcoholic fatty liver disease
-drug induced
-autoimmune hepatitis
What are some post hepatic causes of jaundice?
also known as obstructive jaundice
conjugated bilirubin often passes through the cystic and biliary duct (common hepatic and common bole ducts)
A blockage in these ducts prevents further metabolism of bilirubin and this can lead to increase in blood levels of bilirubin
Obstructive jaundice can be caused by:
Gallstones
Pancreatic cancer (tumour blockage)
Pancreatitis
How is alcohol related liver disease diagnosed?
Raised AST/ALT
Normal or elevated ALP
Elevated GGT
Macrocytic anaemia (bone marrow produces abnormally large cells)
deranged clotting and protein
Ultrasound: hepatomegaly, fatty liver, cirrhosis, ascites, portal hypertension
CT/MRI
Liver biopsy
What is the first line management of ALD?
alcohol abstinence with or without alcohol withdrawal management
weight reduction
nutritional supplementation
immunisation ?
What is the second line treatment of ALD?
liver transplant
What are some dental considerations of patients with ALD?
resistant to sedation with benzodiazepines (GABAa enhancement)
NSAIDs should be avoided due to GI bleed and renal impairment risk
Half the dose of paracetamol
Routine procedures should not be performed in the context of jaundice without work up to assess thrombocytopenia/coagulopathy. Urgent medical advice is required if jaundiced
Why are NSAIDs contraindicated for liver disease ?
this is because NSAIDs are highly bound to serum albumin (which is synthesised by the liver)
With low serum albumin, bioavailability of NSAIDs as they are free in serum
This increases the risk of toxicity
Briefly describe the pathophysiology of non-alcoholic fatty liver disease (NAFLD)
-Steatosis- insulin resistance leads to accumulation of excessive triglyceride in the liver (is this due to gluconeogenesis?); fatty overload in liver
-Non-alcoholic steatohepatitis- second hit, additional oxidative injury which manifests as necro-inflammation.
-Cirrhosis- Scar tissue then replaces normal hepatic parenchyma (functional hepatocytes/tissue)
What is associated with steatosis ?
obesity
____% of obese people have non-alcoholic steatohepatitis (NASH)
5-10%
___% of morbidly obese people have NASH
19%
What is the presentation of NAFLD?
most patients have no symptoms or non-specific symptoms such as fatigue
no clinical features until the development of cirrhosis
Hepatomegaly and features of CLD may be present
blood tests usually show ALT (alanine aminotransferase)
ultrasound will show fatty liver
Biopsy
What is the gold standard for diagnosis of NAFLD?
biopsy
What is the first line treatment of NAFLD without end-stage LD?
diet and exercise
adjunct weight loss pharmacotherapy
adjunct gastric bypass
with diabetes- add insulin sensitiser
with dyslipdaemia- lipid lowering therapy
What is the management of NAFLD with end-stage LD?
Liver transplantation
Trans-jugular intra-hepatic portosystemic shunt (TIPS)
What is the route of transmission for Hepatitis A ?
Faeco-oral
What is the route of transmission for Hepatitis B ?
sexual contact
blood borne
vertical transmission (mother to child)
What is the route of transmission for Hepatitis C ?
Blood borne
small risk with vertical transmission and sexual contact
What is the route of transmission for Hepatitis E ?
UK genotypes are probably transmitted via porl
Reports of blood borne transmission
Indian subcontinent genotypes are likely faeco-oral
What is the route of transmission for EBV (epstein barr virus)?
saliva and genital fluid
EBV is a herpes virus
Vaccinations are available for which hepatitis viruses?
Hepatitis A and B
C, E and EBV have no vaccinations
Hepatitis A causes _________ infection
acute
Hepatitis B causes _______ and _______ infection
acute and chronic
Hepatitis C is _________ in 80% of cases
chronic
Acute forms of Hepatitis C are rarely ___________.
symptomatic
Hepatitis E causes ________ infection.
Acute
When is hepatitis E able to cause chronic infection ?
when immunosuppression is reported
EBV causes ________ infection
acute
Why is hepatitis B endemic in parts of Asia and Africa?
this is due to mother-to-child transmission
more prevalent in migrant populations
What demographic is more likely to develop chronic infections from hepatitis B ?
Children
How is hepatitis B often contracted in adulthood?
sexual contact
IVDU (intravenous drug use)
Infection of hepatitis B in adulthood is usually cleared spontaneously with non-specific flu like symptoms of seroconversion. True or false
True
What can occur in the acute phase of hepatitis B infection ?
fulminant liver failure
What causes damage to the liver in hepatitis B infection ?
The immune response to the virus (antigen) damages the liver
What is the cellular immune response to hepatitis B?
induction of antigen specific T lymphocytes in lymphoid organs
Cytotoxic T cells (CD8+ cells)
T cells then mature and migrate to the liver
IFy (gamma) and TNFa cause down regulation of viral replication and trigger direct lysis of infected hepatocytes by HBV-specific CD8+ cytotoxic T cells
In hepatitis B, co-infection with ________ can increase the rate of fibrosis, cirrhosis and hepatocellular cancer
HCV
Hepatitis C virus
How is hepatitis B managed?
monitoring when in low risk phases of disease
Vaccination for health care professionals
Treatment with either a defined course of interferon to try to regain immune control and long-term nucleoside analogues (tenofovir/entacavir) to suppress viral load
What is ALT rise an indication of in hepatitis B infection ?
indication of active inflammation and transition to another phase of the disease
Patients with cirrhosis with hepatitis B are usually asymptomatic. True or false
true .
What is the main risk factor for hepatitis C infection?
IVDU
intravenous drug use
risk of getting HCV is mainly blood borne
Acute infection with HCV always results in presentation with jaundice and liver failure. True or false
false
it rarely results in presentation with jaundice and liver failure
Patients with HCV infection will usually report fatigue and “brain fog”, this is often a result of …
elevated ALT
There is a new direct antiviral therapy which is providing a “cure” for HCV infections. True or false
true
What are the dental considerations for viral hepatitis?
vaccination of health care professionals
appropriate PPE and needle stick injury protocols should be followed
direct antiviral agents have significant drug-drug interactions. Must check these before prescribing anyone with HCV treatment
What is cirrhosis?
this is abnormal scarring of the liver in response to inflammation
cirrhosis is irreversible
fibrosis and conversion of normal liver architecture to abnormal nodules “regenerative nodules”
In cirrhosis, stellate cells are activated, what is the result of this?
collagen deposits
Cirrhosis leads to _________.
end stage liver failure
decompensation is reached
Cirrhosis leads to _________.
end stage liver failure
decompensation is reached
Cirrhosis leads to…
portal hypertension
liver insufficiency
hepatic failure
What are the stages of cirrhosis?
Compensated
Decompensated
What is the compensated stage of cirrhosis
biochemical, radiological or histological findings consistent with a diagnosis of cirrhosis with preservation of synthetic function of liver (still synthesising proteins/enzymes)
No evidence of complications related to portal hypertension (where there is no metabolism and detoxification)
What is the decompensated stage of cirrhosis ?
reduced hepatic synthetic function
portal HTN (ascites, gastro-oesophageal varices, variceal bleeding, hepatic encephalopathy, jaundice) - these are consequences of portal HTN
What are the complications of cirrhosis ?
Jaundice
Coagulopathy
Portal hypertension
Malnutrition (protein deficiency)
hepatocellular carcinoma
Susceptibility to infection
What is portal hypertension ?
this is when there is an increase in pressure within portal vein which carries blood from the small intestine to the liver
Dental considerations for compensated cirrhosis
-Check FBC and INR prior to procedures
-dose reduction of paracetamol to max 500mg QDS
-avoid NSAIDs- leads to kidney injury
-may be sensitive to opiates and BZDs
-alcohol dependence (withdrawal syndrome)
-antibiotic prophylaxis for invasive procedures
-patients may complain of altered taste perception
Dental considerations for decompensated cirrhosis
thrombocytopenia and coagulopathy likely to cause an issue
give vitamin K prior to procedures if INR raised
recheck and consider FFP (Fresh frozen plasma)/platelet transfusion
consider capacity to consent
is procedure urgent?
patients on transplant list? wait until post transplant for procedures
Antibiotic cover as appropriate for invasive procedures
Dental considerations post-transplant
poor dentition post transplant is common
Immunosupression
Increased risk of opportunistic infection e.g. oral thrush, herpes simplex
Long term steroids can reduce bone density and impair wound healing- glucocorticoids increase bone resoprtion
Ciclosporin may cause gingiva hypertrophy
increased risk of malignancy- low threshold for referral/investigation of lymphadenopathy/oral lesions
Be aware of drug-drug interactions (e.g. fluconazole and tacrolimus)
What are the most common causes of CLD?
alcohol
obesity
chronic viral hepatitis
