Faculty: Faculty of Health and Applied Sciences
Department: Department of Health Sciences
Program: Biomedical Sciences Program
Liver Function
Surname Thomas
Name Jackson
Email address thomashamalwa@gmail.com
Name of course Work Integrated Learning
Course code WILB821S
Couse coordinator Ms. Eva Uumati
Name of training institution Oshakati NIP
Discipline in which training is Chemistry
received
Name of training officer Mrs. Rosalia Shaumbwa
Period of training
23/09/24 14/11/24
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Contents
Introduction...................................................................................................................... 3
Methods........................................................................................................................... 4
Results............................................................................................................................. 5
Discusion..........................................................................................................................6
Conclusion....................................................................................................................... 8
References.......................................................................................................................9
Appendix........................................................................................................................ 10
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INTRODUCTION
The liver is an organ that is functionally complex organ that has an important role in
biochemical processes including; anabolism, catabolism, detoxification, and removal of
waste substances from the body. The liver processes and excretes the major red blood
cell waste product, bilirubin. It also responsible for maintenance of cholesterol
homeostasis and clotting as it produces bile salts and clotting factors respectively
(Bishop et al., 2009).
Damage to the tissue of the liver may result in the blockage of the blood flow the the
organ and prevents it from working optimally as its functioning deteriorates over time
(Minter., 2023).
Liver function tests are measured via the photometric technology, which measures the
end-point reaction of LFTs. Photometry is the measurement of the amount of light a
sample absorbs and involves passing a beam of light through a sample and measuring
the intensity of light that reaches a detector (Abbott Laboratories, 2013).
The photometry method works as follows; light from a tungsten halogen lamp is
converged with a convex lens and passed into a reaction cuvette where changes in
absorbance are detected as the reaction proceeds. Another convex lens concentrates
the onto a reflector or mirror, the mirror then reflects the light onto a diffraction grating
through a slit. This is followed by the light spectrum being reflected to the photodiode
array by the grater, which results in the division of the concentrated light beam into 16
independent wavelengths from 340 to 804 nanometers. The light intensity at various
wavelengths is then measured by a photodiode array. A preamplifier board converts
and amplifies the signal coming from the photodiode array through the DAQ board and
CPU board allowing the signal to be sent to the system control center where the data
reduced and the calculation of the results is performed (Abbott Laboratories, 2013).
Liver function tests (LFTs) are used to assess the functionality of the liver and to
determine the site of hepatic injury thereby helping to orchestrate a differential
diagnosis. LFTs include total bilirubin, direct bilirubin (conjugated), indirect bilirubin
(unconjugated), total protein, globulins and enzymes (Bishop et al., 2009). The enzymes
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that are most clinically significant include, aminotransferases (alanine aminotransferase
[ALT] and aspartate aminotransferase [AST]), alkaline phosphatase [ALP], gamma-
glutamyl-transferase (GGT), and lactate dehydrogenase (LD) (Minter., 2023).
Elevations in AST and ALT with normal ALP and bilirubin is indicative of hepatic disease
or injury. Elevations in levels of the concentration of ALP and bilirubin with normal levels
of ALT and AST may be suggestive of cholestatic complications. When we have an
increase of bilirubin alone it is termed isolated hyperbilirubinaemia were ALP, AST and
ALT are normal. An increase in levels of ALP and AST/ALT is identified as a mixed
injury pattern (Minter., 2023).
The proficiency of the liver can be assessed utilizing its propensity to synthesize
albumin and vitamin K-dependent clotting factors (Lisman & Porte, 2017) .
METHODS
A yellow top tube containing a clot activator and serum separating gel is used for the
patient blood sample. The tube is centrifuged at a centrifugal speed of 1800 XG for ten
minutes. This separates serum from the red cells, white cells and serum since they all
have different densities.
After the tube is centrifugation the sample are taken to the sorting bench to separate
chemistry, immunochemistry and serology samples. After sorting the chemistry samples
are scanned to see whether they are registered onto the laboratory information system
(LIS). The samples are then checked for lipaemia and hemolysis followed by the action
stipulated by the standard operating procedure. After the integrity of the samples is
observed the volumes are then checked and if the volumes are not sufficient the plasma
is poured into sample cups that are place into the test tube. All the caps on the tubes
are then removed followed by placing the test tubes in the Architect machine rack,
which is loaded onto the Architect machine, which then starts to run the tests.
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RESULTS
TEST REFERENCE RESULT FLAG
Urea and Electrolytes
Potassium 3.6 – 5.1 mmol/mol 3.8
Sodium 136 – 144 mmol/l 129 Low
Urea 2.1 – 7.1 mmol/l < 1.1 Low
Creatinine 35 – 88 mmol/l 77.4
Estimated GFR >90 ml per minute 102.9 Low
Liver function tests
Total Bilirubin 0 – 20.5 umol/l 21 High
Alkaline Phosphatase 32 – 91 U/l 139 High
Gamma Glutamyl Transferase 7 – 50 IU/l 230 High
Aspartate Amino Transferase 15 – 41 IU/l 159 High
Alanine Transaminase 7 – 35 IU/l 96 High
Lactate Dehydrogenase 98 – 192 IU/l 250 High
Total Protein 61 – 79 g/l 88
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DISCUSION
Liver function tests
Patient identified as ChemP03 has markedly elevated bilirubin and liver enzymes (AST,
ALT, ALP, LD and GGT) which are indicative of liver associated complications and hints
to a differential diagnosis of a mixed liver injury. These tests measure the
concentrations of proteins (globulins), enzymes and other substances synthesized or
processed by the liver. The enzymes measured include, aspartate amino transferase
(AST), alanine transferase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase
(LD) and gamma-glutamyl-transferase (GGT).
The aminotransferases AST (SGOT) and ALT (SGPT) convert aspartate and alanine
into oxaloacetate and pyruvate, respectively. In the absence of acute apoptosis or other
organ infarction, these enzymes are especially essential in diagnosing hepatocellular
(functional) liver damage. ALT is predominantly present in the liver (with minor amounts
in skeletal muscle and kidney), whereas AST is broadly spread in comparable amounts
in the heart, skeletal muscle, and liver, making ALT an even more "liver-specific"
biomarker of the liver compared to AST (Minter., 2023) & (Bishop et al., 2009).
ALP is mostly found in the liver, bones, intestines, kidneys, and placenta. The clinical
relevance of ALP arises from its ability to discriminate between hepatobiliary sickness
and bone-forming bone disease. The enzyme in the liver is restricted to the microvilli of
the bile canaliculi, therefore it functions as a superb biomarker of extrahepatic biliary
obstructions, such as a stone in the common bile duct, or in intrahepatic cholestasis,
such as medication cholestasis or primary biliary cirrhosis (Minter., 2023).
Lactate dehydrogenase (LDH) is a widely distributed enzyme throughout the body.
When cells in the body are injured or undergo necrosis it releases a non-specific marker
into the bloodstream (Bishop et al., 2009).
GGT is a cell-surface protein derived mostly from the liver that attributes to the
extracellular catabolism of glutathione. Glutathione (GHS) is a protein that acts as an
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anti-oxidant that is essential in guarding cells from oxidative stress and it is maintained
by GGT which transports the GHS into most types of cells to carry out its function.
Oxidative stress is linked to a various number of pathological conditions including
inflammation, carcinogenesis and reperfusion injury, these will in turn all increase the
level GGT in serum making it an essential marker of oxidative stress (Gohel & Chacko,
2013) & (Bishop et al., 2009).
Bilirubin is the breakdown product of red blood cells. When bilirubin is in its
unconjugated form which is insoluble in water it is transported to the liver while loosely
bound to albumin. In the liver unconjugated bilirubin is converted to the water soluble
conjugated bilirubin for excretion from the body. Jaundice is a condition characterized
by retention of bilirubin classified based on the site of the disorder: pre-hepatic, hepatic,
and post-hepatic. Pre-hepatic and post-hepatic jaundice, are caused by abnormalities
outside of the liver and is suggestive of a liver optimally functioning liver. Pre-hepatic
jaundice is characterized by unconjugated hyper-bilirubinemia since unconjugated
bilirubin is the increased fraction in pre-hepatic jaundice. On the other side hepatic
jaundice is an indication of primary liver damage or disease. This intrinsic liver defect or
disease can be due to disorders of bilirubin metabolism and transport defects or due to
diseases resulting in hepatocellular injury or destruction (Bishop et al., 2009) & (Minter.,
2023).
Urea and Electrolytes
Urea and electrolyte are important in understanding kidney function but to some degree,
they aid in identifying the health of the liver. The liver is responsible for the synthesis of
urea executed via the urea cycle; for this reason, elevated or lowered BUN levels are
often a sign of liver complications when used in conjunction with the above discussed
LFTs. Additionally, electrolyte abnormalities such as sodium and potassium deficiencies
can be present in cirrhosis and hepatic encephalopathy which is secondary to fluid
build-up and diuretic treatment (Simonetto et al., 2020).
Bleeding Disorders
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The association between liver disease and bleeding disorders is rooted from the liver’s
function in the production of vitamin k dependent clotting factors that are required for
hemostasis. Damage to the liver can lead to decreased production of these clotting
factors that will eventually result in coagulation disorders characterized by prolonged
prothrombin time (PT) and activated partial thromboplastin time (aPTT) (Lisman &
Porte, 2017) & (Minter., 2023).
CONCLUSION
Understanding the interactions between liver function tests, urea/electrolytes, lipograms,
inflammatory indicators such as CRP, and bleeding disorders is vital for correctly
identifying and treating liver-related conditions. The merging of these test results offer a
bird’s eye view of the condition being dealt with. However, flaws in experimental designs
include potential confounding factors such as concurrent diseases influencing laboratory
results or changes in sample handling practices that might bias data interpretation.
dependability.
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REFERENCES
Abbott Laboratories. (2013). ARCHITECT System Operations Manual 201837-111.
Bishop, M. L., Fody, E. P., & Schoeff, L. E. (2009). Clinical chemistry : techniques,
principles, correlations.
Gohel, M. G., & Chacko, A. N. (2013). Serum GGT activity and hsCRP level in patients
with type 2 diabetes mellitus with good and poor glycemic control: An evidence
linking oxidative stress, inflammation and glycemic control. Journal of Diabetes and
Metabolic Disorders, 12(1), 1–8. https://doi.org/10.1186/2251-6581-12-56
Lisman, T., & Porte, R. J. (2017). Pathogenesis, prevention, and management of
bleeding and thrombosis in patients with liver diseases. Research and Practice in
Thrombosis and Haemostasis, 1(2), 150–161.
https://doi.org/https://doi.org/10.1002/rth2.12028
Minter., V. L. M. Z. D. A. (2023). Liver Function Tests. StatPearls [Internet].
https://www.ncbi.nlm.nih.gov/books/NBK482489/%0A
Simonetto, D. A., Gines, P., & Kamath, P. S. (2020). Hepatorenal syndrome:
pathophysiology, diagnosis, and management. Bmj, 370.
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Appendix
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