chronic liver disease Flashcards
presentation of liver infection (5)
enlarged liver lymphadenopathy fever riggors general malaise
enlarged smooth edged liver suggestive of
hepatitis
infective causes of hepatomegaly (6)
- infectious mononucleosis
- viral hepatitis
- malaria
- amoebic
- hydatid cysts
- leishmaniasis
cancers causing heptomegaly (4)
leukemia
lymphoma
hepatocellular carcinoma
signs of liver cirrhosis (3)
jaundice
spider naevi
palmar erythema
metabolic causes of liver disease (3)
Wilson’s syndrome
Haemochromatosis
acute porphyria
3 drugs causing hepatitis
statins
amiodarone
macrolides
2 main liver enzymes -released after hepatocellular injury
AST
ALT
which liver enzyme is more specific for hepatic injury
ALT
where can AST be found (3)
Skeletal and cardiac muscle
hepatocytes
RBCs
ratio of AST and ALT increase in liver injury
1:1
alcoholic liver disease ratio of AST to ALT
AST>ALT above 2:1
ALP increased in
biliary tree obstruction -but not specific to liver
where can ALP be found
liver
bone
placenta
if ALP is raised from bone what will be normal
GGT
3 tests for hepatic function (not liver enzyme tests)
serum albumin
serum bilirubin
PT/INR
cholestatic pattern of liver enzymes
- marked increase ALP and GGT
- mild increase ALT and AST
hepatic pattern of liver enzymes
- marked ALT and AST increase
- minimal to no ALP increase
increase AST + ALT by several 100 = (3)
- chronic hepatitis
- alcohol induced hepatitis
- NAFLD
increase AST and ALT by several 1000
acute viral heptitis
increase AST and ALT by >10,000 (2)
- toxin related paracetamol (paracetamol)
- liver ischaemia
5 manifestations of liver disease
- coagulopathy
- ascites
- hepatorenal syndrome
- variceal bleeding
- hepatic encephalopathy
what substances accumulation causes hepatic encephalopathy
ammonia
what happens to ammonia in the brain
absorbed and removed by astrocyte brain cells
how do the astrocyte cells metabolise ammonia
via converting glutamate to glutamine to metabolise the ammonia
what does increasing glutamine stores do to brain cells
causes osmotic pressure changes and causing water movement into the brain causing cerebral oedema
mental state changes in hepatic encephalopathy (5)
- forgetfulness
- confusion
- irritability
- inverted sleep pattern
- personality change
LFTs hepatic encephalopathy
increased AST, ALT, albumin, bilirubin, PT,
management of hepatic encephalopathy (5)
- lactulose
- antibiotics
- increased protein and kcal diet
- BCAA and protein supplements
- transplant
pathology of variceal bleeding
fibrosis compresses veins and arteries–> portal hypertension –> high pressure in collateral circulation –> veins in lower oesophagus dilated and prominent –> more prone to damage from coughing/ eating etc –> hematemesis
hepatorenal synrome=
rapid deterioration in renal function with cirrhosis or fluminant liver failure
when does hepatorenal syndrome often occur
sudden insult to the liver -infection of GI bleed
what happens causing renal hypotension
cirrhosis causes release of NO, prostaglandins and other vasoactive substances causing splanchnic vasodilation
what does hypotension in the kidneys trigger
RAS - further hypoperfusion of the kidneys -kidney failure
hepatorenal syndrome 1=
- rapid deterioration circulation and renal function -
- terlipressin resists hypovolemia
- may need haemodialysis
- median survival <2 weeks
hepatorenal syndrome 2 =
- steady deterioration
- may need TIPS
- 6 months median survival
medical management of hepatorenal syndrome
terlipressin
octreotide
midodrine
surgical management of hepatorenal syndrome
liver transplant +/- kidney transplant
ascites pathology
portal hypertension causing splanchnic vasodilation –> hypoperfusion of kidneys +RAS –> Na+ reabsorption + aldosterone –> fluid retention
aldosterone released from
zona glomerulosa of adrenal gland
what in liver failure contributes to ascites formation
less albumin formation decreasing osmotic pressure
causes of ascites
portal hypertension
hypoalbuminemia
malignancies
infections
complications of ascites (3)
bacterial peritonitis
hepatorenal syndrome
thrombosis
3 clinical features of ascites
abdominal swelling
SOB
weight gain
what does serum ascites albumin gradient (SAAG) determine
if ascitic fluid is due to portal hypertension
SAAG >1.1=
ascites due to portal hypertension
SAAG <1.1 =
etiology other than portal hypertension -nephrotic syndrome, cancer
investigations of an ascitic tap
albumin measurement neutrophil count amylase culture cytology
2 effects of decreased thrombopoietin synthesis
thrombocytopenia
portal hypertension
hepatitis acute symptomatic disease (4)
Hep A
Hep B
Hep B+D
Hep E
possible hepatitis chronic disease
Hep B
Hep B+D
Hep C
transmission route of Hep A
fecal oral route
recovery from Hep A
99%
diagnosis of Hep A
high ALT + bilirubin
symptoms of Hep A
jaundice
epigastric pain
nausea
dark urine/ pale stools
Hep B transmission route
blood-blood sexual unsterile needle vertical tattooing and body piercing
Hep B more prevalent in
health care workers
if Hep B not treated can lead to
HCC
HBsAg=
antigen present of outside of virus
HBsAg antibodies without antigens=
non-infected immunity
HBcAg=
core antigen
HBcAg indicates
active viral replication and infection
Hep C infection presentation
remains asymptomatic and develops into chronic disease
Hep C spread=
blood-blood contact
test for Hep C
Anti-HCV antibody test
if anti-HCV positive next step =
HCV polymerase chain reaction -positive in chronic infection
most common cause of viral hepatitis worldwide=
Hep E
host of Hep E=
pig
most cases of Hep E=
asymptomatic
range of disease in NAFLD
steatosis
steatohepatitis
fibrosis
cirrhosis
what causes NAFLD
fatty deposits in the liver unrelated to alcohol or viral cause
metabolic syndrome = 3 of the following (5)
obesity hypertension diabetes hypertriglyceridemia hyperlididemia
what factor is a major contributor to NAFLD
insulin resistance
macroscopic view of liver in NAFLD
large
soft
yellow
greasy
clinical features of NAFLD -My hepatocytes no more fast food
- micro/ macrovesicular steatosis
- hepatocyte balloon degeneration with necrosis and apoptosis
- neutrophil rich inflammation
- mallory denk bodies
- fibrosis
complications of NAFLD
cirrhosis
HCC
LFTs of NAFLD
ALT> AST
liver cirrhosis =
end stage liver damage by disruption of normal hepatic parenchyma by bands of fibrosis and nodules
inflammatory changes in cirrhosis=
TGF-beta sub-endothelial fibrosis from stellate cells
where are stellate cells
beneath endothelial cells lining sinusoids
causes of cirrhosis (7)
-alcoholic liver disease
-NAFLD
-Chronic hep A and C
-PBC and PSC
-haemochromatosis and wilsons disease
alpha-1 antitrypsin
-cystic fibrosis
why do you get palmar erythema
hyperestrinism since liver removes estrogen from blood
compensated cirrhosis classical presentation (3)
fatigue
weight loss
weakness
decompensated cirrhosis presentation (6)
confusion ascites edema pruritis hematemesis melena
what score can predict mortality and survival in liver disease
Child-pugh score -A BEAP
Child-pugh score=
Albumin Bilirubin Encephalopathy Ascites PT (INR)
liver failure=
development of coagulopathy and encephalopathy
hemochromatosis=
excess iron in body which deposits in tissues
primary hemochromatosis =
autosomall recessive defect -HFE gene
secondary hemochromatosis (3)
chronic transfusions
CLD
ineffective erythropoiesis
when does hemochromatosis present
late adulthood 30-50 years old
classical triad of disease from hemochromatosis
- micronodular cirrhosis
- diabetes mellitus
- bronze skin
complications of hemochromatosis
HCC cirrhosis CHF cardiac arrhythmia's thyroid dysfunction sepsis
treatment of hemochromatosis
venesect
avoid iron rich food
Wilsons disease=
increased copper from
- lack of copper transport into bile
- lack of copper incorporation into ceruloplasmin
- decreased ceruloplasmin secertion into blood
when does wilsons disease usually present
<30 years old
neurological changes of wilsons (4)
- change in behaviour
- dementia
- chorea
- parkinsonian symptoms
eye change in wilsons
kayser-fleischer rings in descemet membrane of cornea
skin changes in wilsons (3)
- blue lunulae in nails
- grey skin
- hypermobile joints
complications of wilsons (7)
HCC Coombs arthritis neurological deficits psychiatric problems amino aciduria nephrocalcinosis
management of wilsons (6)
- avoid copper
- lifelong D-penicillamine
- anticholinergics, GABA antagonist
- antiepileptics
- lactulose
- liver transplant
A1 anti-trypsin deficiency =
defect in protease inhibitor
consequence of a1 anti-trypsin deficiency
emphysema and liver
when does a1 anti-trypsin present
30-40
symptoms of panacinar emphysema
SOB
wheezing
cough
three systems affected with PiZZ genotype of a1 anti-trypsin deficiency
lungs
liver disease
skin disease
what is affected by the PiSZ genotype of a1 anti-trypsin deficiency
predisposed to lung disease
management of a1 anti-trypsin (3)
- quit smoking
- IV augmentation via infusion of pooled human a1 antiprotease
- transplant
