Hepatobiliary lab diagnostics Flashcards
A 61 year-old man lost 8 kg during the last 4 months. He complains of pruritus and frequently occurring dull epigastric pain. He has noted dark-colored urine, but lightcolored stools lately. He has jaundice. The gall bladder is palpable, but non-tender.
Laboratory results:
serum bilirubin: 310 μmol/l, mostly direct
urine Ubg: negative
ASAT: 82 U/l
ALAT: 91 U/l
alkaline phosphatase: 540 U/l
prothrombin time: INR = 2.6
What is the cause of his jaundice? What further tests do you consider?
Serum bilirubin: < 17 μM
Alkaline phosphate: < 150 U/L
ASAT: < 45 U/L
ALAT: < 45 U/L
INR: 0,9-1,2 (generally 1)
Serum bilirubin is drastically elevated, by a Direct hyperbilirubinemia, which is increased Conjugated Bilirubin cB.
Urine UBG is absent, which is not normal and serum UBG is absent as well, which is not normal. It is therefore obstructive jaundice, because no bile is getting into the gut for reabsorption as UBG.
INR prothrombin time is elevated, so there is decreased liver coagulant secretion, probably due to the absent bile secretion and lipid soluble vitamin malabsorption.
The ASAT and ALATs are also both elevated, meaning there is some liver damage.
Alkaline phosphatase (ALP) is elevated which is a specific indicator of obstructive jaundice or bone disease. Gamma Glutamyl Transferase (GGT) is the other one that is more specific for obstruction.
Itchiness is commonly occuring during jaundice due to the depositions in the skin.
The palpable and enlarged but non-painful upper right quadrant, is called Curvoisier’s sign with all of these other symptoms and weight loss indicate an obstructive jaundice from a tumor. The most frequent site for this kind of obstructive jaundice is a tumor in the head of the Pancreas.
Tests to perform:
Ultrasound
ERCP: Endoscopic Retrograde Cholangio-Pancreatogram
PTC: Percutaneous Transhepatic Cholangiography
MRI of pancreas.
An icteric woman has the following laboratory parameters:
serum indirect bilirubin: 54 μmol/l
serum direct bilirubin: 5,1 μmol/l
urine bilirubin: negative
ASAT: 19 U/l
ALAT: 22 U/l
LDH: 720 U/l
Ht: 0.33 l/l
Plasma haptoglobin and hemopexin concentrations are significantly decreased
What is the cause of her jaundice?
Total bilirubin < 17 uM
Direct bilirubin < 5 uM
Ratio 5/54 = 0.1, an indirect hyperbilirubinemia, non-conjugated hyperbilirubinemia.
Urine bilirubin should not be present so this is normal. Normally all the bilirubin is conjugated in liver and then converted to UBG in the gut. It is UBG that is normally present in urine.
ASAT and ALAT are both normal, <45 Units / L
LDH: is high, > 160 Units/ L.
Hematocrit is low: normal is 40-54 L/L in males, 38-48 L/L in females.
Haptoglobin and Hemopexin are both Hemeoglobin binding proteins. They are decreased, indicating that they are being used/consumed at a higher than normal rate
Diagnosis: A hemolytic jaundice, some kind of Intravascular originating jaundice for sure.
A 38 year-old man, who regularly drinks alcohol. He has never been ill before, but he has grown icteric in the last couple of days. He has a temperature, and is a little anemic.
His liver is palpable an inch below the ribs, it is slightly tender. Laboratory results:
urine color: dark brown
serum total bilirubin: 150 μmol/l
ASAT: 160 U/l
ALAT: 60 U/l
GGT: 490 U/l
MCV: 103 fl
What is the cause of his jaundice?
Dark brown urine -> indicates cB in the urine.
Serum total bilirubin is very elevated
ASAT and ALAT are both elevated beyond 45 uM, indicating liver damage.
GGT is very elevated beyond 60uM, indicating obstructive jaundice
MCV: Mean Corpuscular Volume, the size of the red blood cells. Normal is 80-95 femtoliters. Increased MCV indicates bone marrow problem, which is this case is caused by alcoholism.
The cause is acute alcoholic hepatitis and macrocytic anemia. indicated by the ASAT and ALAT liver damage, along with the GGT and MCV, and fever.
The palpable and enlarged liver also indicates that there is chronic alcohol induced liver fibrosis or fatty liver in the backround.
4
A 47 year-old man, who has been on hemodialysis for 5 years before he got his kidney transplantation. He has little body hair, a large, protruding belly, slim extremities and gynecomastia. Laboratory results:
ASAT: 85 U/l
ALAT: 76 U/l
prothrombin time: INR = 2.7; it does not change after vitamin K administration
albumin: 28 g/l
K+: 3.3 mmol/l
Ht: 0.36
What is the most likely diagnosis?
ASAT and ALAT are elevated, but not as darastically as in an accute liver damage, indicates chronic damage.
Prothrombin INR is increased, indicating coagulant defeciency. It doesn’t elevate after vit K administration indicating it is a liver problem and not malnutrition or absorption.
Albumin is low. Normal albumin range is 35-50 g/L and normal total protein is 60-80 g/l.
Potassium is low, due to the ascites, causing hypovolemia and RAS activation, and impaired hormone breakdown by the liver, causing aldosterone retention.
Hematocrit is low
Physical findings: Protruding belly is ascites, Gynecomastia from impaired estrogen clearance.
The diagnosis is Liver Cirhossis.
The dialysis is a risk factor for viral Hepatitis B and C.
5
A 38 year-old woman complains of recurrent, sharp pain in the right upper quadrant of her abdomen. She has been vomiting, has fever and jaundice.
Laboratory results:
serum bilirubin: 50 μmol/l, mostly direct
Ubg: negative
ASAT: 180 U/l
alkaline phosphatase: 640 U/l
What is the cause of her symptoms, and how can you prove the diagnosis?
Serum bilirubin: Elevated, direct hyperbilirubinemia conjugated
Serum UBG is negative, indicating obstructive jaundice.
ASAT is elevated, indicating liver damage/inflammation.
ALP is elevated, indicating obstruction.
So: Obstruction, pain, and inflammation. It is either a gall stone or gall bladder infection, Cholelithiasis or Cholangitis.
Ultrasound,
test for other acute phase reaction proteins to see if it is an acute inflammation.
6
A 25 year-old man has been icteric for a few days. His laboratory values:
serum indirect bilirubin: 47 μmol/l
serum direct bilirubin: 4 μmol/l
ASAT: 18 U/l
ALAT: 23 U/l
alkaline phosphatase: 66 U/l
Ht: 0.48
Hb: 162 g/l
What is the cause of his jaundice? What further tests are necessary?
Indirect bilirubin is very high,
Direct bilirubin is actually normal
Indirect, non-conjugated hyperbilirubinemia.
ASAT and ALAT are both normal
ALP: is normal
Hematocrit is normal
Hemoglobin is normal
This weird one is Gilbert’s Disease (french guy, “Zhilbear’s” disease)
aka
Familial Nonhemolytic Jaundice caused by a mild defecit in liver’s ability to process bilirubin, and its resulting mild accumulation in a mild indirect hyperbilirubinemia that is usually not associated with any other symptoms or problems.
does not require any treatment.
7
A 32 year-old man has been complaining of fatigue, malaise and a temperature for a week. His liver is palpable ¾ of an inch below the ribs, it is a bit tender. His laboratory results:
serum indirect bilirubin: 28 μmol/l
serum direct bilirubin: 24 μmol/l
Ubg: increased
ASAT: 870 U/l
ALAT: 1180 U/l
alkaline phosphatase: 310 U/l
What is the most likely diagnosis, and how can you prove it? What further tests are necessary?
Serum direct bilirubin is elevated
Direct bilirubin is elevated
The ratio indicates a direct hyperbilirubinemia
Serum UBG is increased
ASAT and ALAT are both massively increased
ALP is increased
This looks like a severe acute hepatitis. You need to test urine UBGand cB values as well. Blood values for hematocrit and hemoglobin.
Conclusion: Acute panreatitis due to due to toxins (e.g. mushrooms) or acute viral hepatitis
Further tests: Test for Amanitin or other toxins, Specific antibodies against heptatitis A / B and PCR against hepatitis C
8
A 28 year-old woman. She is complaining of fatigue, malaise and nausia. Her laboratory results:
serum total bilirubin: 45 μmol/l
ALAT: 220 U/l
alkaline phosphatase: 200 U/l
γ-globulins: 33 g/l (↑)
RF and ANA: positive
What is the most likely diagnosis, and what tests should be done?
Serum bilirubin elevated, but less than 50, and this is subicterus.
ALAT increased
ALP increased
gamma globulins are increased
RF: Rehumatoid factor It is defined as an antibody against the Fc portion of IgG
ANA: Anti-nuclear antibody
Probably Autoimmune hepatitis, although Hep B and C can also produce autoantibodies.
Tests:
Must exclude Hep B and Hep C, serology tests, and PCR.
Must also take a liver biopsy to verify the autoimmune hepatitis.
9
A 30 year-old woman, who is 164 cm tall, her body weight is 81 kg. She saw her doctor, because she had noted a yellow discoloration of her skin accompanied by itching. She mentions she has had unpleasant gastrointestinal symptoms after meals for a long time: feeling full, having nausea. Physical examination reveals: yellow skin and sclera, spleen is not palpable, liver enlarged by an inch. The right upper quadrant of her abdomen is clearly sensitive on palpation. Laboratory findings:
serum bilirubin: 150 μmol/l
urine bilirubin: positive
Ubg: decreased
ASAT: 53 U/
alkaline phosphatase: 710 U/l
GGT: 390 U/l
What is the most likely diagnosis?
164 cm is 5.4 feet. and she is 81kg. Obese.
jaundice
hepatomegaly with pain
symptoms after meals indicate malabsorption or GI obstruction
Serum bilirubin is elevated
Urine bilirubin is positive indicating obstructive jaundice/cholestasis.
ASAT is very mildly elvated
ALP and GGT strong elevation, obstruction
Cholelithiasis causing obstructive jaundice
Check via ultrasound and possibly ERCP
10
A newborn baby is admitted to the hospital with a complaint of increasing jaundice. The serum bilirubin is 160 μmol/l.
What can be the cause of the jaundice if this bilirubin is mainly:
A. direct, or
B. indirect reacting?
A) If it is Direct hyperbilirubinemia:
Congenital stenosis aka atresia of the bile duct.
B) Indirect hyperbilirubinemia
If it is severe, it may be hydrops fetalis, caused by Rh incompatibility or ABO incompatibility.
mild it is most likely the frequent hemolytic jaundice of the newborn.
or a genetic defect of bilirubin conjugation: Imparied conjugation: Crigler-Najjar syndrome: type I (no expression of conjugating enzyme) or type II (reduced expression of conjugating enzyme).
