Liver function test Flashcards by louisa wegbe

Function of the liver ?

0 Excretion - removal of toxic compounds from the blood - drugs , alcohol.

( pathology effects this - drug metabolism effected - careful of dosing )

0 Protein synthesis and cell membrane component synthesis

  - Albumin 
  - proteins associated with clotting.

( liver pathology can cause oedema and increased prothrombin time - blood takes longer to clot)

0 Maintenance of Serum Glucose
- storage of glucose as glycogen

postprandial (after food) - Perivenous cells at the edge of liver take up Glucose . Glucose —-> Glycogen. Glycogen stored )
Fasting state - Gluconeogenesis - liver converts other fuels / substances to glucose. Glc - 6 -P allows for glucose release.

(liver pathology which effects 8 -12 hour storage of glucose made worse if already have diabetes.
0 Acute liver failure - liver not able to maintain blood glucose concentration (Hypoglycaemia )
0 Chronic liver failure - failure of glucose storage - hyperglycaemia.

0 Barrier -

Controls solutes entering systemic circulation
Controls excretions in bile

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Protein metabolism - liver ?

In the liver the proteins are altered - need specific enzymes (deaminases, transaminases)

animo acid delivered to liver via portal vein
removal of animo group - NH
Transanimation - animo group transferred to keto acid acceptor - create new animo acid (this is how non essential animo acids made )
Deamination - removal of amino group as ammonia
* sometimes too much ammonia can be produced - toxic - hyperammonaemia.
Urea created in kidney by combining 2 NH3 (ammonia) groups and CO2. - secreted from liver and incorporated into kidney and urine.

IMPORTANT-
0 branched amino acid - broken down mainly by muscle
0 Aromatic - mainly broken down by liver.
Decreased branched AA/ Aromatic AA ratio in Acute liver disease (liver pathology—-> less aromatic AA broken down —-> less branched than aromatic

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Obesity and fatty liver disease

(non -alcoholic fatty liver disease?

Non - alcoholic fatty liver disease - build up of fat in the liver

4 stages

0 Steatosis - simple fatty liver in liver cells.

non alcoholic steatohepatitis - liver becomes inflamed.
Fibrosis - persistent inflammation causes scar tissue around liver and nearby BV. - liver cam still function normally
Cirrhosis - most severe - liver strinks , becomes lumpy and scarred.
damage is permanent and can lead to liver failure and cancer.

ca take years for fibrosis and cirrhosis to occur.

lifestyle changes can help prevent this .

Fat changes the structure of the liver - eventually cannot carry out function.

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Symptoms of Non alcoholic liver fatty disease -NAFLD ?

early stage - not usually symptoms

0 more sevre stages
- dull ,aching pain in right upper quadrant ( lower side of quadrant )

0 extreme tiredness

0 unexplained weight loss

0 weakness

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What proteins does the liver produced ?

0 Albumin - produced only in liver - control oncotic pressure.
2 weeks half-life - hypoalbuminemia thus not present in acute liver disease but in chronic .
Liver disease not only cause of low albumin - reduced dietary intake , alcohol consumption.

0 C -reactive protein - produced in response to inflammation

0 apolipoprotein - most of them.

0 hepcidin - regulate iron levels.

0 Insulin growth factor 1

0 proteins involved in coagulation

liver mostly syntheses glycoproteins - disturbances in glycosylation (- alter protein function and affect protein folding. protein cant carry out function and body has to find way to excrete it. )
except albumin , transcobalamin II and c -reactive protein.

*altered conc of proteins - useful indicator of liver function.

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LFT - significance of transanimases ?

AST - found in places in the body other than liver

ALT - more specific to liver.

Intracellular role - removal of amino group from animo acid.
increased levels indicate hepatocellular damage -HEPATITIS as transaminases released from cell.

0 Values >10x normal = primary hepatic damage

0 Values <10x normal = non-specific, no obvious aetiology

when AST and ALT are extremely suggest paracetamol toxity

comparison to ALP.

IF AST risen by ALT has not - suggest problen is elsewhere not liver.
( if you suspect muscle problem - measure CPK - creatine phosphate kinase) - high serum level suggest breakdown of muscle ( rhabdmyolysis - severe , myocardial infarction , muscular dystrophy etc )

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Comparison of AST to ALP.

0 Higher AST to ALP or ALT to ALP ratio and = more likely damage is due to hepatitis
Lower
- A greater than 10-fold increase in ALT and a less than 3-fold increase in ALP suggests a predominantly hepatocellular injury.

0 lower AST/ALP ration = more likely damage is cholestatic 
         - A less 
           than 10- 
           fold 
           increase 
           in ALT 
           and a 
           more 
           than 3- 
           fold 
           increase 
           in ALP 
          suggests
      cholestasis.
     -  
can have a mixed picture.

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Comparison of AST to ALT

both transanimases

Ratio of AST/ALT useful in alcohol diagnostic

AST raised to higher level than ALT in alcohol related damage (acute alcoholic hepatitis )
      - AST/ALT >2 
(AST higher than ALT )
        with 
        presumed 
        hepatic 
        disease = 
        most likely 
        alcohol 
        involvement

*ALT > AST - suggest chronic liver disease.

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significance of ALP and GGT?

ALP - hydrolyses phosphate esters.
Found in liver, bone ,intestine and placenta.

Raised ALP indicates obstuction in billary tract e.g CHOLESTATIC.

raised ALP usually presents before onset of clinical jaundice.

ALP expected to be higher in pregnant women.

raised ALP with raised gamma- Glutamyltransferase (GGT) suggest cholestatic cause

Isolated ALP rise -GGT not raised suggest another cause.

0 Bony metastases or primary bone tumours (e.g. sarcoma)
0 Vitamin D deficiency
0 Recent bone fractures
0 Renal osteodystrophy

Chronic alcohol problems – goes up and stays up even when they stop drinking . Help to see if liver damage due to alcohol

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what test can help determine

0 hepatocellular damage

0 cholestasis

0 liver excretory function

0 biosynthetic function

(basically what test can help differientiate btw pre - hepatic , hepatic , post - hepatic or conjugated or unconjugated jaundice )

Hepatocellular disease - AST , ALT

0 Cholestasis - ALP/GGT

0 Liver excretory function - serum , urine bilirubin, blood ammonia

( Bilirubin unconjugated (water insoluble - does not pass into urine) or conjugated (pass into urine as urobilogen -makes it darker)
bowel blockage - digestive pancreatic enzymes cant reach bowel so fat not absorbed , stools pale, bulky and more difficult to flush.

normal urine +
normal stools =
pre-hepatic
cause

 - Dark urine + 
   normal stools = 
   hepatic cause

     - Dark urine + 
       pale stools = 
       post-hepatic 
      cause 
     (obstructive)

0 Biosynthetic function - Albumin , coagulation factors , prothrombin
( biosynthetic - liver ability to generate specific proteins )

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Patient jaundice but normal ALT and AST - causes ?

0 Gilbert’s syndrome - most common cause. - genetic condition (- higher than normal level of bilirubin build up in blood. )

Haemolysis: - 
       check a 
       blood film, 
       full blood 
       count, 
      reticulocyte 
      count, 
      haptoglobin 
      and LDH 
      levels to 
      confirm.

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Causes of unconjugated hyperbilirubinemia ?

Haemolysis (e.g. haemolytic anaemia)

0 Impaired hepatic uptake (e.g. drugs, congestive cardiac failure)

0 Impaired conjugation (e.g. Gilbert’s syndrome)

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Causes of conjugated hyperbilirubinemia ?

Hepatocellular injury

Cholestasis

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Causes of acute hepatocellular injury ?

0 Poisoning (paracetamol overdose)

0 Infection (Hepatitis A and B)

0 Liver ischaemia

If onset within days - indicates an acute reason

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Causes of Chronic hepatocellular injury ?

0 Alcoholic fatty liver disease

0 Non-alcoholic fatty liver disease

0 Chronic infection (Hepatitis B or C)

0 Primary biliary cirrhosis

less common

0 Alpha-1 antitrypsin deficiency

0 Wilson’s disease

0 Haemochromatosis

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What are the different types of hepatitis ?

Where are the found ?

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HEPT A - faecal - oral route

HEPT B - Bodily fluids - blood, milk, amniotic fluid , vaginal secretions, semen.

MODE OF TRANSMISSION:

       1. sexual 
       contact with 
       infected 
       2. 
    contaminated 
    blood :
       - blood 
       transfusions   
       - sharing 
        needles - intravenous drug use. 
        3. Childbirth - pass from mother to a baby.

HEPT C
HEPT D - same hept B - but only present in those with an active hept b infection.
HEPT E

HEPT D AND HEPT B ?

What are they ?

What do they cause ?

How does it damage the body ?

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HEPT B and HEPT D - cause hepatitis (inflammation the liver )

HEPT D - can cause infection without HEPT B as it it lives within its structure - needs B to replicated.

HEPT B virus - virus is released from hepatocytes without causing damage (does not cause inflammation)
0 Damage is due to immune system - the T cells find infected hepatocyte and eliminate them - causing liver damage.
( b cells also release antibodies HB antigens in blood )

0 HEPT D - when newly replicated hept D virus leaves cell - the HDAg - delta antigens damage the liver as they leave - liver damage.

Structure of HEPT B AND D ?

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HEPT B AND D have an envelope surrounded by a membrane - contains Hepatitis B viral proteins e.g Hbs surface antigen.

Membrane
Capsid - beneath the membrane -

0 HEPT B has HBc (HB core) & , HBe - variant of HBc but not part of virus - (secreted - found in blood / serum of infected people)

0 HEPT D - has HDAg - delta antigen in the caspid.

DNA - genetic material - contained within the caspid.

0 HEPT B - partial double stranded circular DNA. - long & short strand.

0 HEPT D - single stranded circular DNA.

Hoe does HEPT B infect cells ?

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Hepatitis B binds to hepatocyte and fuses with its membrane. ——> releases capsid into cell ——-> partial double stranded circular DNA is completed and passes to the nucleus ————-> mRNA created and virus uses cells ribosomes to synthesise viral proteins ( e.g hbs, hbc ,
hbe antigen etc )

hbe leaves cells and is found in serum

hbc and hbs incorpated into viral structure.

Symptoms of hepatitis ?

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Jaundice - Yellowing of skin = sclera of eyes - destruction of liver cells release bilirubin.

0 Itchiness - caused by bile salts getting into skin.

0 increased bilirubin in urine

0 Pale , hard to flush stools.

Chronic hepatitis caused if prolonged - 5 - 10 % of cases.

 - insufficient T Cell response     - Increasing HBs bind t neutralising antibodies

2/3rds develop mild asymptomatic acute hepatitis.

Symmptomatic

0 preicteric phase ( before jaundice ) 
      - body aches 
     - headcahes 
- nausea 
- fatigue 
( few days - a week )

0 icteric phase - Jaundice + dark urine
(1 -2 weeks )

Recovery phase( if better)

Fulminant hepatitis - (if worsen - 
      - sudden 
       fever
     - abdominal 
       pain
     - jaundice 
     - confusion 
     - coma

Chronic - similar but often milder.

Consequences of hepatitis ?

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Chronic hepatitis

- liver scarring
- Cirrhosis     - Liver failure.

increasing risk of hepatocellular carcinoma.

How does HEPT D infect cells /

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HEPT D binds to cells and fuses with membrane
host cell RNA plymerase used to copy the viral RNA.

cell’s ribosomes used to produce HDg ( delta antigen )

viral rna packaged into caspid and HBs anitgens used to get caspid eneveloped
leaves cell - delta antigen harmful to cell and cause liver damage (unlike hept B -

Diagnosis of HEPT B or HEPT B & D co infection ?

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HBs antigen detected in blood - present 1-2 weeks after exposure

HBc antigens- present after 1-2 week but cleared quickly

after HBc antigens cleared HBc antibodies appear

 - HBc core IgM apppear before shortly symptoms
 - HBg core IgG antibodies apear 1 - 2 weeks after symptoms.

anti HBs antibodies appear during recovery.

ACUTE HEPATITIS - what is dectected ?

O Anti HB core IgM antibodies
O Hbs antigens
O HBc antigens
O Viral DNA

O HB core IgG is present depending ot time of testing

O In recovery phase - only :
- anti HB core IgM & anti HB antibodies detected.

Diagnosis of HEPT B or HEPT B & D co infection ?

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ACUTE HEPATITIS - what is dectected ?

O Anti HB core IgM antibodies
O Hbs antigens
O HBc antigens
O Viral DNA

O HB core IgG is present depending ot time of testing

O In recovery phase - only :
- anti HB core IgM & anti HB antibodies detected.

What periods of time are the are the hept antigens and antibodies dectected after exposure to hept b or hept b and d co infection ?

HBs antigen detected in blood - present 1-2 weeks after exposure HBc antigens- present after 1-2 week but cleared quickly after HBc antigens cleared HBc antibodies appear - HBc core IgM apppear before shortly symptoms - HBg core IgG antibodies apear 1 - 2 weeks after symptoms. anti HBs antibodies appear during recovery.

Diagnosis of chronic Hepatitis B ?

NEGATIVE 0 Anti HB cre IgM antibodies POSITIVE 0 Anti HB core IgG antibody 0 HBs antigen These are present for more than 6 months . 0 Viral DNA 0 HBc antigen 0 HBc antibodies can be detected as well.

Diagnosis of resolved hepatitis ?

Anti HB core IgG - marker of resolved hepatitis anti HBs & HBc antibodies can also be detcted. NEGATIVE 0 Viral DNA 0 Antigens 0 Anti HB core IgM antibodies ( signiffies acute infection - present before symptoms of hepatitis show )

Diagnosis of HEPT D ( with hept b ) ?

Presence of : 0 HEPT D RNA 0 HDAg - delta antigen 0 Anti HEP D anitbodies

diagnosis of cirrhosis / fibrosis ?

Cirhorrosis Transient elastography - uses soundwaves to measure the stiffness of liver tissue using ultrasound probe. if not suitable - liver biopsy Ultrasound - advanced fibrosis or cirrhosis for hepatocellular cancer.

What is HEPT A ?

Transmitted by faecal oral route self limiting - usually resolves within 2 months - Does not cause chronic liver disease Common to get it from shellfish SYMPTOMS - 0 Prodromal phase ( early symptoms - more advanced symptoms typical of the disease) - flu-like symptoms, - gastrointestinal symptoms - anorexia, - nausea, - vomiting, - abdominal right upper quadrant discomfort), - occasional headache, - cough, - pharyngitis, - constipation, - diarrhoea, - itch, - and urticaria. Usually, there are no specific signs on examination. ``` Icteric phase : - jaundice, - pale stools and dark urine (if there is cholestasis), - pruritus - Itch in the skin - sensation to stratch. - fatigue, - anorexia, - nausea, and vomiting ``` — symptoms often improve once jaundice occurs. *Hepatomegaly, splenomegaly, lymphadenopathy, and hepatic tenderness are often present on examination.

Treatment of HEPT A

Vaccine (don not give if current severe febrile illness or anaphylactic reaction ) Avoid public areas - prevent transmission.

HEPT E

Faecal -oral route can be caused by onions / spring onions. Usually acute but in in those with supressed immune systems can can cause chronic inflammation of the liver. Pregnant women - can be particularly fatal. common symptoms of heptatitis

Liver functional segments ?

Liver divided into segments - division based on plane of veins - important for surgery - can remove a particular segment - each of them have a branch of portal vein , hepatic proper and bile duct - can remove one without affecting other. segments are decided by location of veins not falciform ligament which separates right from left. ``` 1 - caudate lobe 2 3 4a 4b 5 6 7 8 ```

If onset of Jaundice is within weeks , what does it suggest may be the cause ?

Within weeks - subacute hepatits , bile duct obstruction vs *( if it was within days suggest acute hepatitis caused by infection , alchohol , drugs ) & Flucuating - suggest drug induced carcinoma, gallastones.

How can cirrhosis cause complications in the lungs?

Hepatic hydrothorax - presence of pleural effusion by cirrhosis. Cirrhosis - prevents liver functioning properly ------> portal hypertension ----------------------> build-up of fluid (ascites ) --------------------> if there are diaghragmatic defects - allows fluid (ascities ) to transfer to the plural space if Jaundiced & SOB check lung CXR. * note if jaundiced & cardiovascular exam is abnormal may be a sign of congestive right heart failure ( back of fluid because of reduced liver function)

What are the different types of liver derangement ? - Three then 2 non - offical ones (my own understanding) Typical alcohol liver disease pattern on LFTs? (and the reverse of this indicates what ?)

Cholestatic - elevation ALP (more than 3X) plus ( less than 10 x increase in AST ) + GGT increase Hepatocellular - more than 10 x increase in AST ( less than 3 x increase in ALP ) (FIGURES DO HAVE TO EXACT - BUT ROUGHLY THAT PROPORTION) Mixed - if indicates both hepatocyte damage & cholestasis. Alcohol liver disease : AST / ALT > 2 (if the ALT is more elevated than AST indicates concomitant viral hepatitis or non- fatty liver disease (in patients who misuse alcohol). Isolated rise in Bilirubin - Gilberts disease Low serum albumin - indicates chronic liver disease.

What may the AST , ALT levels be normal in a patient with cirrhosis?

they may be insufficient healthy liver tissue to produced elevated levels of these enzymes.

Compensated cirrhosis vs decompensated?

Compensate - when you don't have symptoms of the disease. Decompensated - cirrhosis has progressed to a point where the liver is having difficulty functioning and show symptoms of the disease. - DO ASCITIC TAP FOR ALL THESE PATIENTS - fluid examined for the neutrophil count, gram stain, microbiological culture & fluid albumin. absolute neutrophil count >250 cells / mm diagnostic of spontaneous bacterial peritonitis.

Liver function test Flashcards

(38 cards)