Hepatic Flashcards
why is liver disease relevant to dentistry
liver is main production site for clotting factors 2, 7, 9, 10 = reduced clotting = more bleeding
chronic liver disease often accompanies hep B and C blood borne disease
where does the main blood flow come from to the liver
hepatic portal venous system
all blood from gut goes to liver
where does the main blood flow come from to the liver
hepatic portal venous system
all blood from gut goes to liver
what organ will be enlarged in haemolytic anaemia and why and what is a possible side effect of this
the spleen
splenomegaly
The RBC’s are stored and broken down in the spleen so it gets enlarged
pre-hepatic jaundice, yellow eyes and skin
what is the main cause of ‘too little liver’
cirrhosis
end stage liver disease
how would cirrhosis present histologically
regenerating cells seperated by bands of fibrosis
what causes cirrhosis (3) and give the process (2)
constant liver abuse, viruses such as hepatitis, alcohol
usually after liver cells are damaged = inflammation = regeneration
under constant, prolonged abuse, the cells will heal by fibrosis (scarring)
name 6 viruses that cause cirrhosis
Hep B, C, D, E
Cytomegalovirus
Epstein Barr Virus
why does Hep A not cause cirrhosis
this is an acute attack on the liver, not chronic (unline B, C, D, E, EBV,)
may kill patient but if recover, the virus is cleared completely from the liver and doesn’t cause chronic damage and fibrosis
what are the consequences of cirrhosis (4)
liver failure = jaundice
Portal hypertension = raised BP in portal venous system
Ascites =
Hepatocellular cancer =
what are varices and what causes them
Varices are dilated veins in the distal oesophagus or proximal stomach caused by elevated pressure in the portal venous system, typically from cirrhosis.
what is a treatment for varices
Varices are dilated veins in the distal oesophagus or proximal stomach caused by elevated pressure in the portal venous system, typically from cirrhosis.
inject sclerosing agent or place rubber band over it
what is the only symptom of varices and how would we diagnose
massive bleeding and being sick with blood
endoscopy
explain the blood flow through the liver
from the gut, the portal vein takes blood to the liver and this goes to capillary level
blood then leaves via the hepatic vein
give 2 reasons why fibrosis from cirrhosis causes problems in the liver and what does this lead to
fibrosis may disrupt blood supply = death of tissue and difficulty pushing blood through liver
hepatocytes are aligned along blood vessels in health but under cirrhosis, the cells form in nodules leading to th cells being harder to get to for the blood
This leads to portal vein hypertension
what is ascites and what causes this (explain mechanism (2))
a build up of fluid in the abdomen causing bloating and swollen abdomen
cirrhosis
Reduced albumin production = reduced fluid absorption into blood = increased external fluid
portal hypertension = high pressures in the gut = swelling
how would ascites present and what is its cause
large swollen abdomen which is dull to tap and would show up as high volume liquid under a scan
what is albumin and where is it produced
most abundant serum protein helping regulate osmosis and blood content and also helps carry proteins and hromones
absorbs fluid back into the blood at venous end of capillaries
produced in the liver
how might we vaccinate against hepatocellular carcinomas
vaccine against hepatitis B
stops hep B infection
stops cirrhosis therefor no fibrosis
reduces turnover of hepatocytes
reduces risk of hepatocellular carcinomas
what is the major cause of bile flow blockage
gall stones
what are the main signs and symptoms of jaundice
yellow skin
yellow eyes
itchiness
pale stool
dark urine
high Bilirubin levels in blood
what affects does gall bladder blockage have on the skin
this can cause jaundice = yellow skin
if a patient never drinks alcohol or doesn’t have hepatitis but suddenly gets pain and jaundice, what is the likely cause?
gall stone in bile duct
if a patient rarely drinks alcohol, doesnt have hepatitis and has no pain but comes in with jaundice, what is the liekly cause
a cancer in the bile duct or pancreatic/duodenal cancer that is blocking the bile duct
why does bile blockage cause jaundice
if the bile cannot exit the gall bladder/liver, this causes a build up of bile in the liver
causes overflow into the blood
what is hepatitis
inflammation of the liver
what can cause hepatitis
infections e.g. viral, bacterial, fungal
non infectious = alcohol, drugs, autoimmunity, metabolic problems
what is the general pathway of drestuction of the liver (3)
hepatitis (inflammation
Cirrhosis = permanent damage
hepatocellular carcinoma - HCC - with cirrhoisis
what is HCC
hepatocellular carcinoma
symptoms of hepatitis
jaundice
pale fatty stools
dark urine
malaise
serum biochemical tests/ serological tetss
how do we diagnose hepatitis
symptoms
serum biochemistry and serological tests
what is a virion
complete virus
what are the major types of hepatitis virus
A-E
what are the two main ways of classifying hepatitis viruses
Genome = All RNA apart from Hep B - DNA (vaccine)
Route of transmission = A and E oro-faecal route
BCD are all parental route e.g. saliva, blood, needles
which types of hepatitis virus are oral facieses route
A and E
spread through food contamination
whcih hepatitis virus is DNA and RNA
B = DNA
ACDE = RNA
how many types of Hep A are there, which ones are relevent (3)
I-VII
I-III and VII are human viruses
I is 80% relevant and III is very common too
how does Hep A and E get into the faeces (3)
enters through stomach and intestine
absorbed in the blood and makes way to liver causes hepatitis
secreted from liver in bile into the intestine = faeces
what type of vaccine do we have for hep A
whole formalin killed virus
what is the infection and serum levels rates for Hep A (3)
2 week incubation (no serum antibodies)
4-10 day prodrome period (symptoms but general also Ig start showing)
resolves in a few weeks
what age group is often asymptomatic for Hep A
3-5 year olds
risk as they are not very hygienic and add to spread
would we see antibodies in the blood, or pathogen in the faeces first and why is this relevent for Hep A
pathogen in faeces first
this is a problem as the patient is shedding and contagious before we can detect disease and prevent
why is Hep B more dangerous than Hep A
most Hep A patients recover in 2 weeks
2.5% of Hep B patients go into chronic hepatitis
either persistant (‘health’) hepatitis or active hepatitis which is very damaging
what happens to 2.5 percent of hepatitis B surfferers
they develop chronic carrier state, being either
Chronic persistent hepatitis (‘healthy carrier’) - just spread
Chronic active hepatitis (damaging and spread)
how does Hep B become chronic in some patients
HBV integrates into hepatocyte DNA so constantly produces antigens
compare chronic persistant hepatitis and chronic active hepatitis
both 2.5% of Hep B patients, both very infective, both HBV integrated DNA
CPH - non symptomatic and no damage
CAH - symptomatic, cirrhosis, very damaging, very infecitious
describe the structure of Hepatitis B virus dane particle (4)
full particle = ‘dane particle’
DNA with DNA polymerase
plasmid with HBcAg (core antigen)
Capsule with HBsAg (surface antigen)
what 3 forms does Hep B come in
Dane particle = whole = infectious
Filamentous = non infectious
sphere = non infectious
what is the hep B core made up of (3)
dsDNA
DNA polymerase
HBcAg core antigen
what would we see in a serology of acute hep B (2)
HBsAg
and IgM of HBcAg
what 4 genes are in HBV
S protein = surface antigen
C protein = core antigen
P = polymerase antigen
X = unknown, reguatory
which antigen is causing illness in Hep B
E antigen
HBeAg - breakdown of HBcAg core protein
what is HBeAg and when is it seen in serology
a breakdown molecule of HBcAg - hepatitis B core antigen
seen when there are high levels of antigen and very infectious
what would be a serological diagnosis of Chronic Hep B infection
characterized by the persistence of HBsAg for at least 6 months (with or without concurrent HBeAg). Persistence of HBsAg is the principal marker of risk for developing chronic liver disease and liver cancer (hepatocellular carcinoma) later in life.
how much chronic hep B leads to chronic liver disease
10%
what increases chances of getting chronic hep B
getting it earlier in life
what antigen is genetically engineered for vaccine for Hepatitis B
HbsAg surface antigen
what do we need before we can get Hepatitis D
Hepatitis B
which hepatitis viruses are related
hepatitis D needs hepatitis B
what percent of Hep B carriers also carry HepD
5%
why can a pt not be ONLY infected by Hepatitis D (3)
Hep D is caused by a ‘defective’ RNA virus which coexists with HBV
Outer coat derived from HBsAg – cannot survive without HBV.
~5% HBV carriers are HDV positive.