Hepatic Flashcards

1
Q

why is liver disease relevant to dentistry

A

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

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2
Q

where does the main blood flow come from to the liver

A

hepatic portal venous system
all blood from gut goes to liver

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3
Q

where does the main blood flow come from to the liver

A

hepatic portal venous system
all blood from gut goes to liver

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4
Q

what organ will be enlarged in haemolytic anaemia and why and what is a possible side effect of this

A

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

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5
Q

what is the main cause of ‘too little liver’

A

cirrhosis
end stage liver disease

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6
Q

how would cirrhosis present histologically

A

regenerating cells seperated by bands of fibrosis

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7
Q

what causes cirrhosis (3) and give the process (2)

A

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)

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8
Q

name 6 viruses that cause cirrhosis

A

Hep B, C, D, E
Cytomegalovirus
Epstein Barr Virus

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9
Q

why does Hep A not cause cirrhosis

A

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

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10
Q

what are the consequences of cirrhosis (4)

A

liver failure = jaundice
Portal hypertension = raised BP in portal venous system
Ascites =
Hepatocellular cancer =

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11
Q

what are varices and what causes them

A

Varices are dilated veins in the distal oesophagus or proximal stomach caused by elevated pressure in the portal venous system, typically from cirrhosis.

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12
Q

what is a treatment for varices

A

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

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13
Q

what is the only symptom of varices and how would we diagnose

A

massive bleeding and being sick with blood
endoscopy

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14
Q

explain the blood flow through the liver

A

from the gut, the portal vein takes blood to the liver and this goes to capillary level
blood then leaves via the hepatic vein

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15
Q

give 2 reasons why fibrosis from cirrhosis causes problems in the liver and what does this lead to

A

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

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16
Q

what is ascites and what causes this (explain mechanism (2))

A

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

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17
Q

how would ascites present and what is its cause

A

large swollen abdomen which is dull to tap and would show up as high volume liquid under a scan

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18
Q

what is albumin and where is it produced

A

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

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19
Q

how might we vaccinate against hepatocellular carcinomas

A

vaccine against hepatitis B
stops hep B infection
stops cirrhosis therefor no fibrosis
reduces turnover of hepatocytes
reduces risk of hepatocellular carcinomas

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20
Q

what is the major cause of bile flow blockage

A

gall stones

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21
Q

what are the main signs and symptoms of jaundice

A

yellow skin
yellow eyes
itchiness
pale stool
dark urine
high Bilirubin levels in blood

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22
Q

what affects does gall bladder blockage have on the skin

A

this can cause jaundice = yellow skin

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23
Q

if a patient never drinks alcohol or doesn’t have hepatitis but suddenly gets pain and jaundice, what is the likely cause?

A

gall stone in bile duct

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24
Q

if a patient rarely drinks alcohol, doesnt have hepatitis and has no pain but comes in with jaundice, what is the liekly cause

A

a cancer in the bile duct or pancreatic/duodenal cancer that is blocking the bile duct

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25
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
26
what is hepatitis
inflammation of the liver
27
what can cause hepatitis
infections e.g. viral, bacterial, fungal non infectious = alcohol, drugs, autoimmunity, metabolic problems
28
what is the general pathway of drestuction of the liver (3)
hepatitis (inflammation Cirrhosis = permanent damage hepatocellular carcinoma - HCC - with cirrhoisis
29
what is HCC
hepatocellular carcinoma
30
symptoms of hepatitis
jaundice pale fatty stools dark urine malaise serum biochemical tests/ serological tetss
31
how do we diagnose hepatitis
symptoms serum biochemistry and serological tests
32
what is a virion
complete virus
33
what are the major types of hepatitis virus
A-E
34
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
35
which types of hepatitis virus are oral facieses route
A and E spread through food contamination
36
whcih hepatitis virus is DNA and RNA
B = DNA ACDE = RNA
37
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
38
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
39
what type of vaccine do we have for hep A
whole formalin killed virus
40
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
41
what age group is often asymptomatic for Hep A
3-5 year olds risk as they are not very hygienic and add to spread
42
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
43
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
44
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)
45
how does Hep B become chronic in some patients
HBV integrates into hepatocyte DNA so constantly produces antigens
46
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
47
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)
48
what 3 forms does Hep B come in
Dane particle = whole = infectious Filamentous = non infectious sphere = non infectious
49
what is the hep B core made up of (3)
dsDNA DNA polymerase HBcAg core antigen
50
what would we see in a serology of acute hep B (2)
HBsAg and IgM of HBcAg
51
what 4 genes are in HBV
S protein = surface antigen C protein = core antigen P = polymerase antigen X = unknown, reguatory
52
which antigen is causing illness in Hep B
E antigen HBeAg - breakdown of HBcAg core protein
53
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
54
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.
55
how much chronic hep B leads to chronic liver disease
10%
56
what increases chances of getting chronic hep B
getting it earlier in life
57
what antigen is genetically engineered for vaccine for Hepatitis B
HbsAg surface antigen
58
what do we need before we can get Hepatitis D
Hepatitis B
59
which hepatitis viruses are related
hepatitis D needs hepatitis B
60
what percent of Hep B carriers also carry HepD
5%
61
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.
62
what is the structure of hep D
RNA surrounded by Delta antigen Surface formed from HBsAg
63
what do we use to detect HDV
hep D virus Delta antigen found at the core of Hep D
64
what is the effect if having Hep D
rarely progressive 'supervirus' makes Hep B more likely to be chronic and destructive
65
what percent of IV drug users are infected by Hepatitis C
80%
66
what hepatitis virus is very common in IV drug users
hep C
67
how is Hepatitis C transferred
IV drug abuse needle sticks, tattoos, ear piercing 80% iv drug users infected Previously blood products, haemodialysis, transplantation minor routes - saliva; sexual; vertical
68
when does the Hep C antigen show up
6 weeks to 6 months (97% by 6 month)
69
is acute Hep C serious
very mild acute infection 1% get jaundice
70
describe Hepatitis C chronicity
50 - 85% become chronic 50% fatigue (10y); 25% cirrhosis (20y); 5% HCC(30y) 350 000 to 500 000 people die each year from hepatitis C-related liver diseases.
71
what percent of HCV get cirrhosis after chronicity
25% after 10 years
72
what percent of HCV get HCC after chronicity
5%
73
if a patient is on interferon alpha and Ribavirin
hep C (outdated)
74
what drugs have historically been used for Hep C
Ribavirin and Alpha Interferon
75
which hep virus has there been recent cures and targets for elimination by
hep C
76
how can we reduce Hep C (4)
safe IV drug use with good hygeien control cures more screening and protection find a vaccine
77
which hep virus has a large 10 gene genome
Hep C
78
which antigen is responsible for Hep C attachment to host cells
E2
79
which hepatitis virus causes epidemics in middle aged patients
Hep E
80
whats the incubation period for Hep E
6 weeks
81
which group has particularly high mortality/chronicity with hep E
pregnancy and immunocomprimsied
82
which hepatitis virus has high mortality with pregnancy
hep E
83
how is Hep E mainly spread
food contamination epidemics
84
how do we diagnose Hep E
PCR or IgM or IgG serology
85
how do we reduce Hep E
good hygiene, cooking food thouroughly, no vaccine, observe for liver problems
86
where is the liver positioned
mid right abdomen to upper left abdomen Infront of stomach and bile duct
87
what vessels provide oxygenated and non-oxygenated blood to the liver
proper hepatic artery = oxygenated hepatic portal vein = deoxygenated
88
what does the portal vein carry and from where
deoxygenated blood from SI, LI, pancreas and spleen oxygen been used in these organs and blood travels through liver
89
how does fat stimulate biliary secretion
fat detected in liver = release of CCK CCK causes gall bladder constriction presses out bile into the small intestine
90
what shape are hepatocytes
hexagonal
91
what is the structure of liver tissue
haxagonal hepatocytes surrounded by portal triads in the corner with branch of bile duct, portal vein and portal artery
92
what are portal triads
triad of hepatic portal vein, hepatic artery and bile duct found in corners of hepatocytes
93
the liver have ~500 functions, give the main ones
Detoxification: Filters & cleans blood of waste products (drugs, hormones) - ammonia (excess = swelling brain = confusion, first function that goes with liver disease) Immune functions: Fights infections and diseases (RE system) Involved in Synthesis of clotting factors, proteins, enzymes, glycogen and fats Production of bile & breakdown of bilirubin Energy storage (glycogen and fats) Regulation of fat metabolism Ability to regenerate
94
how might liver failure result in confusion
liver is responsible for detoxification of ammonia if not occurring, ammonia builds up causes swelling of the brain presses on parts of the brain = confusion
95
what is one of the first signs of liver failure
build-up of ammonia = confusion
96
give 2 ways that liver failure means a pt is more prone to bleeding
1: cirrhosis = portal hypertension = splenomegaly = increased platelet destruction = less platelets = reduced primary haemoastasis 2: liver is site of vitamin K dependant clotting factor production = reduced this = reduced clotting factors = reduced Extrinisc and intrinsic pathways of secondary haemostasia
97
give 4 ways liver disease is classified
By time line: Acute vs chronic By pattern: Hepatic vs cholestatic (more to do with bile ducts) vs mixed By presentation: asymptomatic vs symptoms By severity: cirrhotic vs non-cirrhotic
98
compare hepatic and cholestatic liver disease
h = liver tissue c = more to do with bile ducts most are mixed
99
give 4 ways we might get acute liver injury
Hepatitis A, B or E Epstein Barr Virus drug overdose = paracetamol vascular problems e.g., hepatic thrombosis
100
compare acute liver damage and acute liver failure
damage = recovery is likely failure = complete lack of function = need transplant
101
give some causes of chronic liver damage, and what might this lead to
alcohol viral (hep B,C) autoimmune Vascular metabolic = NAFLD, iron, copper leads to cirrhosis and chronic liver failure
102
give some examples of presenting factors of acute liver injury
Asymptomatic (mainly) abnormal LFTs &coagulopathy Malaise, nausea, anorexia Jaundice Confusion – think ALF ! Bleeding - rare Upper right Liver pain - rare
103
give some signs and symptoms of chronic liver damage
abnormal LFTs hepatomegaly, malaise, abdo discomfort itching Ascites, oedema Haematemesis (varices) Easy bruising (coagulopathy) Jaundice Confusion Anorexia, wasting
104
give some important markers tested in LFTs (5)
LFT = liver function tests Albumin ALT – Alanine Aminotransferase AST – Aspartate Aminotransferase Bilirubin Globulin
105
what is indicative of ALT and AST increase to 1000’s from blood tests
liver failure
106
what two proteins found in the blood would be in the thousands with liver failure
ALT and AST
107
what two liver enzymes are increased when drinking alcohol
ALT and AST
108
what 2 blood tests can be done, other than enzyme/protein markers, to test for ALF
platelet count INR
109
what is jaundice (2)
yellow pigmented sclera and skin due to build of unconjugated bilirubin in the blood
110
what 2 things can be the cause of jaundice
increased breakdown on RBC = increased bilirubin liver failure = reduced conjugation of bilirubin
111
what does pale faces and dark urine mean
reduced steroicobilogen reduced bilirubin conjugation = liver failure
112
briefly explain the breakdown of haemoglobin and metabolism of bilirubin
haemoglobin = haem and globin (in spleen) haem = iron and bilirubin (liver or spleen) unconjugated biliburin attached to albumin is conjugated in liver travels down intestine, 10% reabsorbed, most is converted to sterocobiligen = brown pigment in feces of the re-absorbed 10%, half is metabolised in kidney as urobiligen (yellow pigment in urine)
113
why does dark urine and pale feces indicate liver disease
post-hepatic jaundice reduced conjugated bilirubin = reduced sterocobiligen= brown pigment in faeces reduced liver metabolism of bilirubin = increased renal metabolism = increased urobiligen = darker urine
114
what is and what causes pre-hepatic jaundice
jaundice caused by things other than liver increased substrate = more RBC breakdown splenomegaly, thallasaemia, sickle cell Haemolytic anaemia Gilbert’s syndrome Criggler-Najjar syndrome
115
what causes hepatic jaundice
Cirrhosis Infiltration of the liver by tumours Acute hepatitis (viral, alcoholic, autoimmune, drug-induced)
116
what causes post-hepatic jaundice
Post-hepatic, or obstructive jaundice, happens when bilirubin can’t be drained properly into the bile ducts or digestive tract because of a blockage therefor overflows into blood (and gets metabolised in kidneys more = dark urine)
117
give some causes of post-hepatic jaundice
Gallstones External compression: -pancreatitis -pancreatic tumour -ampullary tumour
118
what are the most common causes of chronic liver disease
NAFLD & NASH Alcohol Viral hepatitis (B, C - cause chronic)
119
what are NAFLD and NASH
NAFLD = non-alcoholic fatty liver disease NASH = nonalcoholic steatohepatitis
120
compare NAFLD and NASH
both caused by fatty diets and have fatty liver NAFLD = little, no inflammation NASH = inflamationa and pre-cirrhotic hepatitis
121
what is wilsons disease involved with
copper deposits on the liver = chronic liver damage
122
give some risk factors of NAFLD
Hypertension, diabetes, high alcohol, obesity
123
what autoimmune disease can affect the liver and who is more likely to get this
autoimmune hepatitis - affect more women ~ middle-aged 10:1
124
what can an ultrasound of the liver look at
bile duct blockage cirrhosis big spleen portal hypertension Metastasis
125
how many units of alcohol class as binge drinking, safe limit, hazerdous drinking
>10 in one sitting = binge <14 over three days = safe >28 = hazardous
126
how many units of alcohol class as binge drinking, safe limit, hazerdous drinking
>10 in one sitting = binge <14 over three days = safe >28 = hazardous
127
what is the commonest, and rising commonest cause of liver disease
alcoholic liver disease NAFLD is on the rise and is often un-recognised
128
why does fat cause liver damage
fat deposits on the liver = more likely to get blood clots enlarged liver = need more blood supply hypertension cirrhosis
129
what hepatitis viruses cause chronic liver damage and how many people worldwide have this
Only hepatitis B and C generally can cause chronic hepatitis = 500 million people worldwide are infected with Hepatitis B or C
130
how can we reduce HCV
PREVENTION = screening blood donations, no IV drug use, wear gloves and cross contamination control treat = 90% of pts within 8-12 weeks no vaccine
131
how can we reduce HCV
PREVENTION = screening blood donations, no IV drug use, wear gloves and cross contamination control treat = 90% of pts within 8-12 weeks no vaccine
132
what year did blood donations start getting screened for e.g. hep C
1991
133
what are the three stages of scarring of the liver
NCPH = non-cirrhotic portal hypertension Often due to vascular problems in the liver Tolerating bleeding well and clotting generally intact; Relatively rare (patients generally aware) Pre-cirrhotic No effect on dental work May be asymptomatic Liver cirrhosis Compensated & decompensated
134
compare compensated and uncompensated cirrhosis
compensated= Invisible Blood can be normal Risk low uncompensated= Visible Big belly, thin limbs Jaundice high alcohol take Abnormal blood tests Risks high
135
what is ascites
bloating and swollen tummy (liver cirrhosis)
136
as time goes on, what changes with liver disease and how do we use these to score liver disease
bilirubin increases albumin decreases risk of ascites and encephalopathy increase INR increases used in child pugh scoring
137
what is the child pugh score
bilirubin albumin INR Ascites Encephalopathy use of all these factors to classify grade of cirrhosis
138
what is the implication of a child-pugh score of C
mortality increases to 50% in two years if child-pugh C
139
what is the major cancer found in liver
hepatocellular carcinoma
140
what is palmer erythema and what is it related to
red palms of hands many diseases - liver disease
141
what are and what causes spider navaei
red marks on skin = small clumps of blood vessels which appear on the surface of the skin found in many diseases, late cirrhosis
142
what are and what causes spider navaei
red marks on skin = small clumps of blood vessels which appear on the surface of the skin found in many diseases, late cirrhosis
143
what does >10 spider naevi above the chest =?
high risk of hypertension
144
why might liver damage cause Gynaecomastia
liver is involved in testosterone production testosterone inhibits oestrogen if testorone reduces and oestrogen increases, breatss may form Gynecomastia is men growing breasts
145
what is gynaecomastia
men growing breasts due to low testosterone and high oestrogen
146
what does hypoalbuminemia cause
white nail beds sign of liver disease
147
what is a cause of white nail beds
hypoalbuminaemia could be due to liver disease
148
how might we tests for decompensation liver failure encephalopathy
pt will be confused Pt may struggle with sleep cycle, change in personality, not able to concentrate, worse with infection = confusion ask to count back from 100 in 7sor draw 5 sided star OR test for albumin levels
149
how do we treat the symptoms of liver disease (3)
Diuretics = removes ascites Nutrition support Supplements Propranolol = reduced portal hypertension
150
how does liver disease effect us as dentists
possible contamination of hep B prescribing drugs metabolised in the liver increased toxicity of drugs metabolised in the liver
151
what drugs must we avoid with liver failure patients
NSAIDs, anticoagulants or antiplatelets - any drug that cause coagulopathies increased DILI with Flucloxacillin and Co-Amoxyclav
152
what two antibiotics ahve increased DILI
drug induced liver injury Flucloxacillin and Co-Amoxyclav
153
how much paracetamol is safe for patient siwht liver disease
3g a day, not 4