Liver Flashcards
Functions of liver
detoxification carb and glucose regulation bile drainage blood circulation and filtration synthesis and storage of amino acids and proteins fats and viatmins
Ligamentum teres, falciform ligament, caudate lob, quadrate lobe - where
in middle of lobes is falciform
What are the ligaments of the liver
right traingluar ligament, coronary lig, left triangular ligamnet, venosum
Porta hepatitis, which way do the structures go
free edge of lesser omentum attaches here (carrying structures with it)
-Contains the Heaptic artery, portal vien and bile duct
BVA - anterior
Contributions from hepatic artery and portal vien
1/4 heptic artery , 3/4 portal vien
where does falciform ligament go to?
to umbilicus
Lymphatic drainage of liver
nodes at porta hepatits (coeliac nodes) (on hepatic artery)
ANS - visceral supply and pain to liver
coeliac plexus, parasympathtic - vagus
sympathetic - greater splanchnic nerves
Pain in epigastric region
cyctic duct
from neck of gall bladder joins with pancreas
how is bile released into duodenum
smooth muslce at distal end of bile duct and ampulla relax
is the gall bladder covered in visceral peritonium?
yes
Arterial supply to gall blader
cystic artery (from right hepatic artery) - passes through the triangle of calot
Venous supply gall bladder
Cystic vien (into portal vien)
nerve, pain of gall bladder
ans - via coeliac plexus (same as liver), epigastric region
lymph of gall bladder
cystic nodes - hepatic - coeliac
Cholelithiasis
Presence of gall stones
-cholesterol (green or yellow/whtite), and pigment stones (bilirubin, calcium salts usualy small and dark)
3 main places of porto-systemic shunting
-causes
-alternative vessels enlarge to try and divert blood back from portal circulation back to heart
Oesopahgeal varacies
Caput medusae (around umbilicus)
-Anus - anorectial varices
Due to portal hypertension - causes included cirrhosis
-in submucosa
-can rupture and bleed if pressure to high
Patterns of hepatic injury
5 general responses degeneration and intracellular accumulation Necrosis and apoptosis inflammation regeneration firbosis
What happens in hepatic failure and what are the clinical features
sudden and massive destruction/endpoint
loss of 80-90% capacity
increased demand - infection, gastrointestinal bleeding
High mortality
Clinical features - jaundice, hypoalbuminaemia, elevated ammonia (neurological function)
Cirrhosis process and what happens
- fibrous septae
- damage to hepatocytes
- micro and macronodules - parancheal nodules (hepatocyes encircled by fibrosis)
- change in structure - shunts, blood bypasses the liver
- progressive fibrosis
Process - kupffer cells released cytokines, causes inflammatory response
- results in change to hepatocytes
- undergo apoptosis
- inflammatory repsonse increase
Portal Hypertension
Pre, post and intra hepatic
increased resistance to portal flow
- due to cirrosis blocking pathways of blood
- prehepatic - obstructive thromobsis
- posthepatic - server right sided heart failure
- intrahepatic - cirrosis
Consequences of portal hypertension
Ascities, portal systemic shunts
Hep A
Self limiting
Does not cause chronic hepatitis
hygiene and sanitiation
asymptomatic , mild ilness, jaundice
Hep B
acute hepatitis with resolution
chronic hepatitis may lead to cirrhosis or massive necrosis
blood and body fluid borne
immune repsone to viral antigens expressed on infected hepatocytes leads to liver damage
Hep C
major cause of liver disease
Risk - injections and blood transfusions, medical treatments poor sanitation
acute infection usually undetected
chronic disease occurs in majority
20% develop cirrosis after 5-20 years
-most people who get acute will develop chronic hepatitis
Autoimmune hepatitis
chronic progressive hepatits
genetic predisposition, presence of autoantibodies
-immunosuppression
-association with other autoimmune disease
Drug and toxic induced liver injury
predictable Hepatotoxins - dose-dependent matter
-and unpredicatable
-may directly cell toxic, or act through ehpatic conversion to an active toxin activated
-cholestasis, hepatocellular necrosis, fatty liver disease, fibrosis, granulomas, vascular lesions, neoplams
-most common acute liver failure = paracetamol
most common chronic - alcohok
Alcoholic liver disease
change in lipid metabolism
decreasesd export of lipoprotien and cell injury caused by reactive oxygen species and cytokines
-hepatic steatosis, alcoholic heptitis, cirrhoisos
Non-alcoholic fatty liver disease
-what it is associated with
- metabolic syndrome, obesity, type 2 diabetes, dyslipidemia, hypertension
- initially hepatic steatosis which can progress to inflammation and then can turn to cirrosis
Haemochromatosis
- excessive accumulation of body iron
- deposited in liver and pancreas
- genetic defect - excesive iron abosption
- autoskomal resessive
- can get cirrosis, diabetes, skin pigmentation
Cholestasis of sepsis
decreased bile flow, obstruction of intra or extrahepatic bile ducts
- sepsis - infection from bacteria and toxins
- can result as a direct effect of intrahepatic infection (bacteria cholangitis)
- can get ischaemia related to hypotension
- circulation microbial products (particular in context of gram negative infection)
Autoimmune cholangiopathies
- primary biliary cirrhosis (autoimmune disorder leading to destruction of bile canaliculi)
- primarey sclerosing cholangitis (autoimmune disoer leadign to scaring of bile ducts)
Passive congestion and centriolobular necrosis
Right sided cardiac decompesnation, commonly seen at autopsy, element fo preterminal circulatory failure with most deaths
Liver tumours
benign neoplams - cavernous haemangiomas, hepatocellular adenoms, malignant neoplasms - hepatoceellulra carcinoma, hepatoblastoma
Causes of jaundice - unconjugated, conjugated
unconjugated (indirect) - haemolysis, gilberrst syndrome
Inside liver - cholestasis - drugs, pregnancy, thyroid diesease
Obstruction inside liver - hepatitis, cirrhosis, bilary cirrhosis, large liver masses
Outside liver - obstrucion outside - galstones, bilayr pancreatic cancer, pancreatitis
ALP
obstruction outside liver
increase with cancer, gall stones (anything blocking bile)
GGT
obstruction outside liver
Alcohol, drugs, phenytoin, ritampicin, also fatty liver - mainly alcohol (can have fat obstructing)
ALT and AST
liver specific
hepatitis , inflammation and hepatocellular injury
-ALT more liver specific
-if these are really really high than could be acute drug poisoning
Albumin
liver is only source
decrease with cirrosis, illness (non-specific)
-long term ilness
Globulins
Inflamation -decreases with hepatitis, cirrhosis
-decreases if synthetic function is impaired
Prothrombin raito
increases with liver failyre - if syntheitic funciton is imparied
Glucose
liver maintains fasting glucose, inability to maintain glucose
- decreases
- liver failure
Ammonium
increases
CEA
cancer marker-can be fore bening cirossis and hepatitis
Gilberts syndrome
variant in billirubin conjugaction - so billirubin is unconjugated
other liver tests normal
jaudice
-can test - if fasting for 48 hrs and bilirubin rises 2 times
Main causes of Liver function test abnormalities
Fatty liver - obesity, diabetes ect
-Viral hepatitis, alcohol
Old treatment for Hep C
regiems were interferon based (made cytokines), however not very good and could get flu like symptoms
(injection)
Current treatment
Antiviral agents - tablets , better cure rates
How to treat varicies that have ruptured
can tie around them however need to also sort hypertension
Causes of portal hypertension
Pre-hepatic - portal vien thrombosis
Intrahepatic - cirrhosis
Post hepatic - heaptic vien thrombosis, right heart failrure
Hepatic encephalopathy
result of chronic liver failure
Early symptoms - mood and personality change, inverted sleep
Late - confusion, bizarre behaviour, drowsiness and coma
-advanced cirrhosis with liver failure
Mechanisms of Hepatic encephalopathy
Chronic liver failure i.e functioning poorly
Liver unable to detoxify substances produce by bacteiral metbaolsim
-portosystemic collaters shunt blood back to portal ciruclaiton- does not go back to liver, so is not detoxified
-Ammonia build up in blood brain barrier
disturbs normal brain funciton
Treatment of hepatic encephalopathy
lactulose - just to manage symptoms (normally a laxative)
-however will convert ammonia to a non-absobable molecule
What is ascites
Fluid in peritoneum causing abdominal distention
- can be caused by portal hypertension
- increased pressure in protal vien, fluid shifts out inot circulation into perritoneum
- less able to hold on to fluid in circulation
What can be seen with portal hypertension
Varacies, acsites, hepatic encepahlopathy
Budd chari syndrome
- what it is
- and sypmtoms
- cause
- management
acute thrombosis of hepatic vien
outflow of blood from liver obstructed
liver becomes acutely congested, hepatocellular damage
Porral hypertension occurs - ascities develop
Symptoms - acute rapdily progressive servere upper abdominal pain
jaudice, hepatomgaly, ascities, hepatic enchaplopathy
Cause - mainly no obvious cause
management - protocaval shunting often performed to divert blood flow , anticoagulants, diruertics
