LFT / Jaundice / Gallstones Flashcards
ALT
AST
ALP
GGT
ALT: Alanine transaminase (3-40 iu/l) (skeletal muscle, cardiac, kidneys)
AST: asperate aminotransferase (3-30iu/l) also raises in liver damage but if ALT not raised, likely to be other cause. produced by liver, skeletal muscle, cardiac, brain, RBC. in alcoholic liver disease AST>ALT
ALP: alkaline phosphatase (30-100umol/l) (<120)
biliary epithelium, bone, 3rd-trimester placenta, intestine, kidney (raised in biliary obstruction)
GGT: gamma-glutamyl transferase (8-60u/l) (liver-specific not sensitive, lots of things make it raise even sneezing) *monitor in abstinence for alcohol
*can help distinguish between hepatocellular damage and cholestasis
Assessing liver funcion
Bilirubin (3-17 umol/l)
Albumin (35-50 g/l)
Prothrombin time (10-14 s/l)
Amylase- pancreas
Lipase- pancreas
ALT
A raised ALT indicated hepatocellular damage
>x10
ALT > AST chronic liver disease
AST > ALT cirrhosis and acute alcohol hepatitis
ALP
ALP is concentrated in the liver, bile duct and bone tissue
Raises if there is obstruction/cholestasis
>x3
enzyme that hydrolyses phosphotaseester
*isolated raised ALP boney metastases/sarcoma vitamin d deficiency recent bone fracture renal osteodysotrophy
GGT
Gamma Glutamyl Transferase
If there is a raise in the ALP, check the GGT
raised GGT:
bile flow obstruction
biliary epithelial damage
alcohol and drugs (phentoin)
if ALP is raised but GGT normal= bone
if ALP raised, GGT raised= cholestasis
jaundice in
- pre hepatic
- hepatic
- post hepatic
pre hepatic: normal urine and normal stools (unconjugated bilirubin
hepatic: dark urine, normal stools
post hepatic: dark urine and pale stools because the bile and pancreatic lipase cannot reach the bowel - poor absorption (pale bulky stools)
albumin
synthesised in the liver
helps bind to water
oncotic pressure
- cirrhosis= decrease in the production of albumin (ascites)
- inflammation: in high temperature, there is a decrease in the production of albumin
- loss of albumin in nephrotic syndrome
acute hepatocellular damage
- poisoning (paracetamol OD)
- infection (hepatits a/b)
- liver ischaemia
ALT very raised
ALP, GGT, bilirubin high
DILI: drug-induced liver injury
commonly- flucloxacillin, co amoxiclav
differentials if all LFT raised:
congestive heart failure obstructive jaundice pre hepatic obstruction cholangiocarcinoma head of pancreas tumor pancreatitis
interpreting LFT’s
- ALT and ALP
(ALT >AST chronic liver disease)
AST> ALT cirrhosis / acute alcohol hepatitis
AST > ALP hepatitis
ALP > AST cholestatic
high amylase- pancreas
AST normal ALT unlikely to be due to liver. - GGT
if there is a raise in ALP, chek GGT. bile flow obstruction
high ALP, high GGT= cholestasis
high ALP, normal GGT= boney metastases.
bilirubin
RBC live for 120 days
then phagocytosed by macrophages into heme and globin
globin= amino acids
heme- protophoryn
protophoryn ic converted to unconjugated bilrubin
taken to liver = conjugated by UDP. water soluable, stored in bile duct
formation: haem (RBC)
metabolism: unconjugated binds to albumin. hepatocytes conjugated bilirubin (UDP glucosyl transferase enzyme)
conjugated is transferred to bile canaliculi
in the colon - bacteria degrades conjugated bilirubin to urobilinogen and stercobilinogen
pre haptic jaundice
increased load of bilirubin
causes:
haemolysis, malaria, haemoltyic anaemia, septicaemia
Gilbert syndrome (low UGT)
Crigler Najjar (no UGT)
Dubin Johnson (deficiency in the protein which moves CB from liver to bile)
physiological jaundice of the newborn
signs:
normal urine and normal stools (unconjugated bilirubin)
if bilirubin >2.5mg/dl yellow sin
hepatic jaundice
hepatocellular jaundice (raised ALT, ALP, AST)
drugs, alcohol, viral hepatitis, autoimmune, metabolic, hereditary, viral hepatitis
high UCB and CB
signs: dark urine (CB) normal stools
viral hepatitis
autoimmune hepatitis
drugs/toxins (paracetemol OD)
alcohol
rarer- metabolic disorders hereditary haemochromatosis Wilson's disease alpha 1 antitrpsyin deficiency primary hepatoma
post hepatic jaundice
cannot excrete (conjugated) bilirubin due to an obstruction e..g gall stones, pancreatic carcinoma
bile (conjugated bilirubin) builds up, leaks between hepatocytes in the blood vessels.
obstructive- high ALP, high GGT
- extra hepatic
mechanical obstrction (gallstones)
malignancy
pancreatitis (acute/chronic)
2. intrahepatic primary biliary cirrhosis primary sclerosing cholangitis sarcoidosis pregnancy drugs/alcohol dubin johnson syndrome rotor syndrome
signs:
pale stools, dark urine (bile flow is obstructed)
pruritis (bile salts)
haemolytic jaundice
jaundice, anaemia
raised UCB
low hb, low haptoglobin, raised reticulocyte in haemolytic jaundice
ALT, ALP, GGT normal
*a type of prehepatic jaundice
pancreatitis
epigastric pain which radiates to the back
raised lipase and amylase (pancreatic enzymes)
causes: I GET SMASHED
hepatitis
fever, RUQ pain, jaundice, dark urine
raised ALT, raised AST, high ALP (ALT>AST)
hep A: faecal oral. incubatino is 2-4 weeks. flu, jaundice, hepatosplenomegaly
hep B: blood/bodily fluids. mom-child viral transmission. incubation 6-20 weeks
hep C: blood/bodily fluids/IV drug use. incubation 6-9 weeks
hep D: bodily fluids. can only co-infect if hep b+ve
liver disease clinical signs
ascites hepatic encephalopathy (ammonia) portal hypertension palmar erythema gynaecomastia in men menstural irregularities GI varices spider naevi brusing hepatorenal syndrome
UGT activity
hepatic impaired conjugation of bilirubin
inherited: Gilbert syndrome, Crigler Najjar type I and II
glucuronidation can be inherited/acquired by certain drugs.
autoimmune hepatitis
primarily affects females
(commonly have other immune diseases like thyroid disease)
LFT hepatic: raised AST
hyperglobulinaemia (elevated IgG)
non-specific autoantibodies0 antinuclear antibodies
diagnose on liver biopsy
tx; immunosuppressive therapy (prednisolone)
(azathioprine therapy)
Gilbert syndrome
bengin condition
isolated, mild unconjugated hyperbilirubinaemia (<80)
autosomal dominant inhertiance
most common of the hereditary hyperbilirubinaemias of the population
more common in males
jaundice if illl/fasting
reduction in UGT
- Cholelithiasis
- cholecystitis
- choledocolithiasis
- cholangitis
- presence of gallstones in the gallbladder
- inflammation of the gallbladder after a cystic duct obstruction
- gall stones in the common bile duct
- inflammation/infection of biliary tract
cholelithiasis
gallstones in the gallbladder (oversaturation and precipitation)
RUQ pain <6 hours
diagnose with US (posterior acoustic shadow)
treatement: elective cholecystectomy
types and content of bile
- cholestrol (yellow) cholestrol and bile salts
- bilirubin/pigmented: unconjugated bbilirubin binds wiht calcium (black stones on xray)
- brown stones (infected) infection of the gallbladder/bile duct. bacteria brings hydrolyti enzymes that hydrolyste the bilirubin and phosphates.
bile salts acids cholestrol phospholipids protein bilirubin water electrolyte bicarbonate
cholecystitis
inflammation of the gallbladder as a stone has been lodged in the cystic duct
RUQ pain- shifts to shoulder dull and achey mid epigastric pain nausea and vomiting Murphey's sign (rebound tenderness) raised CRP raised WBC bile stasis irritates the mucosa
investigate: US, ERCP
treat: IV abx, IV fluids, analgesia, cholecystecomty
Murphey’s sign
ask the patient to take deep breathe in
diaphragm goes down
put hand underneath
pain- makes the patient stop breathing
choledocolithiasis
gallstone migrates into the common bile duct
RUQ >6 hours
ALP, AST, ALT and total bilirubin is raised
investigation: US dilated, ERCP, MRCP
* obstructive jaundice
cholangitis
infection of the biliary tract due to bile stasis (from an gallstone)
e.coli, klibsella, entercoccus
Charcot’s triad: fever, RUQ pain, jaundice,
Reynolds pentad +confusion +hypotension
bloods: WBC, CRP, ALP, AST, AST
US
IV abx
urgent biliary decompression
