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98 Cards in this Set

  • Front
  • Back
what's grading and staging of liver disease
grading: degree of inflammation
staging: degree of fibrosis
4 causes of ACUTE liver failure (ALF)
DRUGS
alcohol
bile obstruction
viruses (e.g hepA)
jaundice can be classified in 2 ways
SITE: pre, intra, post - hepatic

TYPE: conjugated/ unconjugated (by liver)
what's the cause of pre-hepatic jaundice
excess bilirubin (unconjugated) from too much haem broken down:
- haemolysis
- haemolytic anaemias

unconj = not water-soluble (not excreted in urine)
what causes intra-hepatic jaundice
liver cells INJURED/ DEAD + some cholestasis (intra-hepatic bile ducts):
- ALF
- hepatitis (alcoholic, autoimmune, viral, drug-induced)
- cirrhosis (acute-on chronic/ decompensated)
- bile duct loss (PBC, PSC)
- preg
- storage diseases (Wilson's, haemoachromatosis, a1-antitrypsin def)
what causes post-hepatic jaundice
bile OBSTRUCTION--> conjugated bilirubin (water-soluble= dark urine, pale stools):
- gallstones in CBD
- congenital biliary atresia
- CBD strictures
- tumours (head of pancreas, cholangiocarcinoma)
- PSC, PBC
what the pathology behind liver cirrhosis
final common END-PT ....IRREVERSIBLE liver damage
fibrosis & nodular regeneration 
loss function
final common END-PT ....IRREVERSIBLE liver damage
fibrosis & nodular regeneration
loss function
2 important complications of liver cirrhosis
- what does each complication lead to (effects)
2 important complications of liver cirrhosis
- what does each complication lead to (effects)
1) PORTAL HTN: ascites, splenomegaly, varices, caput medusae...

2) liver FAILURE: coagulopathy, encephalopathy (liver flap, confusion), hypoglycaemia, sepsis

(also: hepatocellular carcinoma & mallnutrition)
what's the progression of alcoholic liver disease with time & which is reversible:
- 2-3d
- 4-6wks
- months-yrs
- yrs
- 2-3d.................reversible FATTY liver
- 4-6wks............reversible HEPATITIS
- mnths-yrs.....irreversibleFIBROSIS
- yrs...................irreversible CIRRHOSIS
features of ALCOHOLIC hepatitis & NASH/NAFLD (4)
features of ALCOHOLIC hepatitis & NASH/NAFLD (4)
hepatocyte NECROSIS
NEUTROPHILS
MALLORY-BODIES
pericellular FIBROSIS
hepatocyte NECROSIS
NEUTROPHILS
MALLORY-BODIES
pericellular FIBROSIS
what's non-alcoholic steatohepatitis (NASH)
- who
- may lead to fibrosis & cirrhosis (& liver ca)
identical pathology to alcoholis liver disease
- non-drinkers
- DM, obese, hyperlipidaemia
common & rare causes of viral hepatitis
hep A,B,C,D,E
delta agent
EBV
CMV
HSV
yellow fever virus
compare outcomes of hep B and C viral hepatitis
B: acute fulimant (death), chronic, cirrhosis, ca, asymp

C: chronic, cirrhosis
6 causes of CHRONIC hepatitis
viral: hep B & C
PBC
PSC
autoimmune
drug-induced
PBC;
- pathology & effects
- serology/ test results
- age & sex presentation
PBC;
- pathology & effects
- serology/ test results
- age & sex presentation
rare AUTOIMMUNE chronic non-caseating GRANULOMATOUS inflammation = progressive CHOLESTASIS, CIRRHOSES & portal HTN
- obstructive jaundice, AMA (M2 antimicrobial ab's), IgM
- F~50yrs
rare AUTOIMMUNE chronic non-caseating GRANULOMATOUS inflammation = progressive CHOLESTASIS, CIRRHOSES & portal HTN
- obstructive jaundice, AMA (M2 antimicrobial ab's), IgM
- F~50yrs
autoimmune hepatitis:
- path
- specific features (test results)
- age & sex presentation
Chronic inflammatory.
Auto-ab's: ANA, SMA, LKM, ↑IgG, ↑γGT

young/middle-aged F
clinical presentation S&Ss of PBC
clinical presentation S&Ss of PBC

specifics in CAPS
F~50yrs
asymp
↑Alk phos & γGT
fatigue
PURITIS (itch)
XANTHELASMA
jaundice/ skin pigmentation
portal HTN
hepatomegaly
clinical presentation S&Ss of autoimmune hepatitis
young/ middle-aged F
ACUTE-on-chronic: jaundice, fatigue, abdo pain, nausea

CLD: leuconychia, clubbing palmar erythema, spider naevi, DUPUYTREN's contrapture (cirrhosis), hepatomegaly, ascites, portal HTN
encephalopathy

PBC, PSC, UC, Graves, EXTRAHEPATIC (urticaria)
don't forget drug-induced hepatitis:
- which drugs
- presentation
MANY!
mimics any liver disease (acute/ chronic)
PSC: 
- patho
- age & sex
- stong assoc with which disease
- specific features
PSC:
- patho
- age & sex
- stong assoc with which disease
- specific features
CHRONIC inflammation/ fibrosis/ strictures intra- & extra- HEPATIC BILE ducts, F~40yrs
- 80% have UC
- post-hepatic jaundice: chronic biliary obstruction
- ↑Alk phos, may have ↑AMA & SMA
- secondary biliary cirrhosis
difference between PBC & PSC
PBC: commoner, granulomas, intra-heaptic +ve AMA & IgM

PSC: UC, intra & EXTRA hepatic, biliary obstruction- abnormal LFTs, jaundice, cholangitis
3 liver storage diseases
Haemochromatosis (iron)
Wilson's (copper)
a1-antitrypsin def
Haemochromatosis:
- how inherited
- how acquired

- what are the outcomes if untreated (2)
1) Autosomal RECESSIVE = ↑iron deposition in liver (& other sites)
2) ↑diet iron/ transfusion/ iron therapy

- cirrhosis, hepatocellular carcinoma
clinical presentation & features of haemochromatosis (incl age & gender)
middle-aged MEN
asyp...then...
fatigue
arthralgia (iron deposits in joints)
slat-grey skin
DM ('bronze DM')
CLD: hepatomegaly, cirrhosis
what's wilson's disease
- key features for Dx

- what 2 diseases does it cause
autosomal RECESSIVE ↑Cu in liver & CNS....treatable. 
- Kayser-Fleischer rings (deposits in iris)
- lo serum caeruloplasmin
- Cu in urine 

CHRONIC hepatitis & NEUROLOGICAL deterioration
autosomal RECESSIVE ↑Cu in liver & CNS....treatable.
- Kayser-Fleischer rings (deposits in iris)
- lo serum caeruloplasmin
- Cu in urine

CHRONIC hepatitis & NEUROLOGICAL deterioration
what's a1-antitryprin def
- inheritance
- what 2 diseases does it cause
autosomal RECESSIVE
↓synthesis in liver (enzyme inhibitor)....globules trapped in liver

CLD (cirrhosis) & EMPHYSEMA
2 primary tumours of the liver
hepatocellular ADENOMA.......................benign ♀

hepatocellular CARCINOMA (HCC)......malignant- 90% of 1° tumours
hepatocellular ADENOMA.......................benign ♀

hepatocellular CARCINOMA (HCC)......malignant- 90% of 1° tumours
secondary tumours (mets) in the liver are much more common than primary ones. 
- S&Ss
secondary tumours (mets) in the liver are much more common than primary ones.
- S&Ss
fever, malaise, anorexia, loss wt, RUQ pain (liver capsule stretch)
late- jaundice
hepatomegaly
what diseases is HCC (hepatocellular carcinoma) related with (3)

how does it normally present
HBV, HCV
cirrhosis

mas, pain, obstruction
cancer associated with the biliary tree
cholangiocarcinoma
cholangiocarcinoma
all hepatitis viruses can be ACUTE

which viruses can be CHRONIC?
all hepatitis viruses can be ACUTE

which viruses can be CHRONIC?
[A (only Acute)]
B C D E
whats the lab confirmation for hepatitis infection
CLOTTED blood for SEROLOGY

(B: surface antigens & ab's also)
which hepatitis virus can only co-exist with hepB and exacerbates the infection
hepD
hep E:
- similar to which hep virus (clinically and transmission)
- where is it common
- associated with severe disease when
similar to hep A (think vowels!)- young adults, ingestion
common in tropics/ INDIA

severe in PREG!
similar to hep A (think vowels!)- young adults, ingestion
common in tropics/ INDIA

severe in PREG!
how is hep A transmitted?
peak incidence what age?
incidence in UK?
can only cause ACUTE infection (not chronic)
can cause OUTBREAKS!
INGESTED!
faecal-oral
poor hygiene/ overcrowding
food & water
- travellers
- young adults
reducing in UK
what ab assoc with hep A

control/ prevention?
Treatment
clotted blood for serology- IgM

VACCINE & hygiene
monitor for encephalopathy & resolution
NO ANTIVIRALS
clotted blood for serology- IgM

VACCINE & hygiene
monitor for encephalopathy & resolution
NO ANTIVIRALS
how is hep B & C transmitted (4)
BLOOD (IVDUs)
SEX
DIRECT
VERTICAL transmission (chronic infection more likely)
lab confirmation of Hep B
- how long classifies chronic infection 
- which component indicates INFECTIVITY
- which component in ACUTE / recent infection 
- which component = IMMUNITY
lab confirmation of Hep B
- how long classifies chronic infection
- which component indicates INFECTIVITY
- which component in ACUTE / recent infection
- which component = IMMUNITY
>6months = chronic
HBsAg/HBeAg & DNA = INFECTIVE
ant-HBc IgM = current/ recent ACUTE infection
Anti-HBs = IMMUNITY
>6months = chronic
HBsAg/HBeAg & DNA = INFECTIVE
ant-HBc IgM = current/ recent ACUTE infection
Anti-HBs = IMMUNITY
which components in the blood indicates chronic hep B carrier
HBsAg >6mnth
Anti-HBc IgG
(+/- eAg/anti-eAg, c IgM)
HBsAg >6mnth
Anti-HBc IgG
(+/- eAg/anti-eAg, c IgM)
what does anti-HBsAg alone indicate
vaccination w/o disease
(or transfusion with blood possessing immunity)

no anti-HBc IgG
what does presence of HBsAg & HBeAg indicate
incubating infection
incubating infection
what does ↑↑↑LFTs, HBsAg/HBeAg, Anti-HBc IgM & anti-HBc IgG indicate
ACUTE infection
ACUTE infection
what does anti-HBs & anti-HBc IgG indicate
recovery from INFECTION
recovery from INFECTION
which antibody after HBV infection indicates immunity from NATURAL infection that vaccination doesn't give in addition to anti-HBsAg
anti-HBcAg IgG
anti-HBcAg IgG
clinical features of viral hepatitis
fever, malaise, anorexia, nausea, arthralgia, jaundice, hepatomegaly, splenomegaly, lymphadenopathy

(extra-hepati common in HBV)
clinical features of HBV
viral hep: fever, malaise, anorexia, nausea, arthralgia, jaundice, hepatomegaly, splenomegaly, lymphadenopathy

+ EXTRA-hepatic: arthralgia, urticaria (itchy rash- pic)
viral hep: fever, malaise, anorexia, nausea, arthralgia, jaundice, hepatomegaly, splenomegaly, lymphadenopathy

+ EXTRA-hepatic: arthralgia, urticaria (itchy rash- pic)
control and treatment of HBV
minimise blood exposure & safe sex

VACCINATION prophylaxis (e.g travel) & after
ANTIVIRALs:
- peginterferon
- suppresive antivirals (entecavir, Tenofovir)
which viral hepatitis (B,C,D,E) is more commonly chronic
~85% HCV chronic
if an individual tests +ve for anti-HBV, what test is done to assess if they have an active/ past infection
VIRAL RNA PCR
which 2 viral hepatitis's can be prevented with VACCINE
which 2 viral hepatitis's can be prevented with VACCINE
A (acute) & B (prophylaxis & after)
A (acute) & B (prophylaxis & after)
3 outcomes for hep A
asymp & resolution
acute infection ---> resolution
acute liver failure (rare) ---> death/ resolution

[NB: no chronic infection]
outcomes for hep B & C viruses
.
in chronic viral hepatitis, how many yrs is taken to cirrhosis and hepatocellular carcinoma
>20rs Cirrhosis
>30yrs carcinoma
what's significant about vertical transmission of hep B to a baby- what pattern of infection do they show
more likely to show CHRONIC infection & complications
when are antivirals used in viral hepatitis
CHRONIC infection only (not acute!)
infalmmation
before complications
adults
what test results would confirm you could treat chronic infection with
- HBV
- HCV

how long is considered chronic infection
HBV: HBsAg & DNA
HCV RNA present (active)

>6 months
what's peginterferon-α
what is it used to treat
✔advantages
✕. disadvantages
immune response to viral infection- given via injection as adjuvant for HBV & HCV:
✔sustained
✔predict who will benefit
✕.side effects!
✕. suppression rather than cure
✕. minority benefit
2 drugs used in HBV & HCV
peginterferon-a & ribavirin

(HBV- also other antivirals)
(HBC- antiviral PROTEASE inhibitors: triple therapy)
antivirals for HBV
✔advantages
✕. disadvantages
eg Entecavir, Tenofvir
✔safer
✕. supression
✕.resistance
✕.life-long Rx
adverse effect of ribavirin (1)
anaemia
what's triple therapy for HBC
- name 2 antivirals used in triple therapy
newer antivirals give in combination with PEGINTERFERON & RIBAVIRIN

PROTEASE inhibitors: TELAPREVIR & BOCEPREVIR
side effects of protease inhibitors used in HCV triple therapy:
- Telaprivir
- Boceprevir
TELAPRIVIR: puritis, nause, rash, anaemia, rectal pain, diarrhoea

BOCEPREVIR: anaemia, distorted sense & smell
define ACUTE liver disease
rapid development of liver dysfunction w/o prior liver problems
<6mths
ENCEPHALOPATHY
difference between LFTs & TRUE LFTs
LFTs: ALT/AST, Alk phos, GGT

TRUE: BR, Alb, PTT
important Q's to ask when suspecting ACUTE liver failure (ALF) (6)
symps
duration
DH (OTC, herbal, supplements)
TOXINS
INFECTIONs
ALCOHOL
TRAVEL
Ix's for acute liver disease (ALD)
LFT's (incl alb, BR, PTT)
glucose
Virology & micro (bloods, urine) & AUTOab's (e.g IgM, AMA)
ferratin, caeruloplasmin, a1-antitrypsin
USS
rare- biopsy
treatment of ALD
3mnth REST
FLUIDS, no alcohol
↑CALORIES- metabolic considerations
treat ITCH (eg. UDCA)
treat hypoglycaemia!!!
treatment of PBC & PSC
PBC: uresodeoxycholic acid (UDCA)

PSC: corticosteroids & uresodeoxycholic acid (UDCA)
what's Budd-chiari syndrome
- what disease / presentations S&Ss can it cause
what's Budd-chiari syndrome
- what disease / presentations S&Ss can it cause
hepatic vein obstruction (eg thrombosis, hypercoaguable, tumour)
acute epigastric pain, N&V, shock, insidious portal HTN, ascites, jaundice & cirrhosis, tender hepatomegaly.

ACUTE LIVER DISEASE (ALD)
how long do hepatic reactions to drugs take
- 3 commonly used medication that can cause ALD
6 wks
- NSAIDs, amox, co-amoxiclav
(also: euphomisms & imported illegal drugs)
define FULMINANT hepatic failre
JAUNDICE & ENCEPHALOPATHY in a pt with prev normal liver!!!!!!!!!!!
S&Ss of fulminant liver failure
JAUNDICE & ENCEPHALOPATHY
hypoglycaemia
coagulopathy
circulatory failure]renal fulure]infection
treatment for fulminant hepatic failure:
- SUPPORTIVE
- DEFINITIVE
SUPPORTIVE: inotropes & FLUIDS
- renal replacement
- manage complications

TRANSPLANT (life-long immunosupression)
some criteria for liver transplants in acute liver FAILURE
<pH
↑PTT (clotting) / INR (bleeding)
↑creatinine (renal failure)
jaundice/ encephalopathy
↑lactate
↑bilirubin
>40yrs
which cells initiate fibrosis (which eventually leads to cirrhosis)? (2types)
activated quiescent hepatic STELLATE cells (HSC)
by-prods of activated KUPFFER cells
activated quiescent hepatic STELLATE cells (HSC)
by-prods of activated KUPFFER cells
what type of liver disease does metabolic syndrome predispose to?
(type 2 DM, obese, low HDL, HTN, hyperlipidaemia)
NAFL (non-alcoholic fatty liver disease)
what type of gramulomas are seen in PBC
non-caseating
non-caseating
what test results are characteristic for PBC

key
↑↑↑alk phos (obstructive LTF's)
AMA ab's type M2 (anti-mitochondrial)

fatigue, itch (PRURITIS), XANTHELASMA, hepatomegaly
treatment of PBC

what symptom is a poor indicator
uresodeoxycholic acid (helps itch)

jaundice poor indicator
distinguish between the 2 types of autoimmune hepatitis
- age
- serum ab's
type 1: ADULT, ANA +/- SMA

type 2: CHILDREN, LKM-1
histopathology of autoimmune hepatitis- BIOPSY to rule out:
- Wilson's disease, a1-antitrypsin def, viral hep, drug-induced, ...
INTERFACE hepatitis
necrosis
eosinophils, lymphocytes & inflam cells
fibrosis / cirrhosis
INTERFACE hepatitis
necrosis
eosinophils, lymphocytes & inflam cells
fibrosis / cirrhosis
treatment of autoimmune hepatitis
corticosteroids (prednisolone)
azathioprine
treatment of haemochromatosis
venesection
venesection
hwo to Dx & treat Budd-Chiari syndrome (obstruction of hepatic veins)
USS

Recanalisation/ TIPS (transjugular intrahepatic portosystemic shunt)
which drug used to treat RA & psoriasis shows does-dependent liver toxicity
what does it cause (in the liver)
METHOTREXATE
fibrosis
what causes cardiac cirrhosis
secondary to RHF:
- tricuspid valve incompetence
- congenital
-rheumatic fever
- constrictive pericarditis/ cardiac tamponade/ effusion)
presentation of cardiac cirrhosis
CCF/ RHF
hepatomegaly
portal HTN: ascites, varices, caput medusa, liver impairment....
which viral hepatitis is most common worldwide
HCV
treatment for compensated liver cirrhosis
reduce salt intake
avoid aspirin & NSAIDs
good nutrition (support)
no alcohol
score used to cirrhosis to predict prognosis & variceal bleeding risk
CHILD-PUGH
how does portal HTN cause renal failure
hepatic vessels release vasodilators = ↓systemic MAP = baroreceptor reflex = renal artery myogenic response 'autoregulation' = renal hypoperfusion = failure = accumulate creatinine & urea = toxicity
Ix's for ascites
spontaneous bacterial infection?- tap & neutrophil count
USS
treatment for ascites spontaneous bacterial peritonitis (3)
ABX's
TERLIPRESSIN for vascular instability
maintain renal PERFUSION

NUTRITION & NO Na+
which drugs to avoid in ascites
NSAIDs & aspirin
treatment for ascites
SPIRONOLACTONE (monitor U&Es)
PARACENTESIS- rapid relief
TIPS
transplant
how to quickly relieve ascites
paracentesis
x. risk infection
x. encephalopathy
x. hypovolaemia
what causes asterixis (liver flap)
ammonia not metabolised by liver--> circulates to CNS, affects signalling
what can asterixis indicate
liver disease
salbutamol use (tremor)
CO2 retention
alcohol-withdrawal
anything neurological