Flocculation & Turbidity test

Principle :
Reagent + serum flocculation. The grade of the flocculation
is determined by colorimeter.
1. Cephalin Cholesterol Flocculation Test ( CCFT )
Reagent : cholesterol & cephalin emulsion
Result : neg until 4 pos.
Disadvantage : reagent is difficult to be made, expensive and
unstable.
Advantage : Very sensitive for early diagnosing virus hepatitis.
2. Thymol Turbidity Test ( TTT )
Reagent : Thymol solution in barbital buffer
Result : 0-4 unit
disadvantage : false positive in hyperglobulinaemi disease
( acute Malaria, typhoid, multiple myelomac,
infectious mononucleosus, collagen disease )
Advantage :cheap and stable reagents
3. Thymol Flocculation Test
Reagent + Serum incubation 24 h
Result : 0 - 4
Disadvantage : less sensitive
Advantage : rarely false positive

4. Kunkel (Zinc - Sulfate Turbidity Test)

Reagent : Zinc - sulfate solution
Result : 4 - 12 unit
Disadvantage : * less sensitive for diagnosing acute Hepatitis
* False Positive, (antibody formation)
Advantage : fast, cheap & stable
5. Moncke Sommer
Reagent : Na2 Co3 & HgCl3
Result : flocculation with clear supernatan at 70 mg % HgCl3
Disadvantage : * False Positive in collagen diseases
Advantage : cheap & most sensitive

6. Cobalt Reaction
Reagent : Co Cl26H2O 1 %
Result : + pos sedimen, clear supernatan
negative : neg sedimen -, turbid supernatan
trace : pos sedimen +, turbid supernatan

Interpretation : tube I pos 1/2

II neg

Normal = 3/4 - 4/5

Notes :
Shiff to the left : 1/2 or 2/3 alpha 2 globulin
choledocholithiasis
liver abses
liver carcimo
gastric cancer

* Shift to the right : 5 / 6 or 6 / 7 gamma globulin

Hepatic cirrhosis
Acute yellow atrophy
Chronic hepatitis
Multiple myeloma
Kallaazan disease
FIBRINOGEN

is sintezised in liver, may be in RES

Function : blood clotting process

Determination : quantitative
semi quantitative
qualitative

Normal : 250 - 400 mg/dL

Decrease in : severe liver disease ( acute hepatic necrosis )

Prothrombin

is synthesized in liver
Decrease :
1. Poor Vitamin K in diet
2. Vitamin K absorption is lack
3. Liver cannot synthesized proth.

Obstructive jaundice : prothrombin can be normalized by

parenteral vit. K.
Parenchymatous jaundice : prothr cannot be normalized by
parenteral vit. K

Prothrombin occurred in severe liver disease ( end stage )

very bad prognose

Prothrombin Time ( PTT ) : 10 - 14 sec.

SPECIFIC PROTEIN

A. Haptoglobin :

- glyco protein

- concentration is expressed as Hemoglobin or

methemoglobin binding capacity

Normal : 100 - 200 mg/dl Hb binding capacity

Increase : post hepatic jaundice

Decrease : hepato - cellular disease

B. Lipoprotein-X (Lp-X)

* in cholestatic jaundice & Lecithin Cholesterol acyl transferase

deficiency
* Sensitive determinant for cholestatic (if there is no LCAT
deficiency) but cannot differentiate intra / extra hepatal
cholestatic

C. Alpha fetoprotein (AFP)

- is the principal fetal protein
- in children > 1 year until adult normal : < 30 mg/ml
can be detection only by Radioimmuno assay (RIA)
- Gross elevations of AFP serum in Hepatocellular carcinoma
Teratoblastoma testis / ovarium
* Hepato-cellular carcinoma
* Teratoblastoma lestis / ovarium
Elevation < 500 mg / ml in

Pancreatic carcioma Pancreas cancer

Colon cancer
Lung cancer
On protein electrophoresis move as fast as alpha 1 globulin

Not for liver function test, but for tumor marker

( monitoring therapy of carcinoma )

On non-neoplastic liver disease :

* Chronic active hepatitis
* alcoholic cirrhosis
* regenerative activy of hepatocyte
D. Ceruloplasmin

* Copper oxidase

* Normal : 34 mg/dl

* Decrease : - Wilson's disease

- Protein Energy Malnutrition
- Nephrosis

* Increase : Chronic infection ( tbc, pneu )

Lupus erythematous
Rheumatic arthritis / fever
Myocardial infarction
Physiological stress
ACUTE HEPATITIS

I. Preicterus stadium
Symptom : fever, anorexia, malaise, abdominal discomfort

Laboratories : Abnormal BSP

Positive CCFT
AST & ALT
Urine urobilinogen : positive
others : normal

II. Icterus Stadium :

Symptom : Icteric, liver tender, afebril

Laboratories : Abnormal liver function tests

III. Post - Icterus Stadium :
The symptoms disappear
Lab. : liver function tests decrease to normal level
serum bilirubin still , negative urine urobilinogen

Hematological lab.
* Leucopeni, lymphopeni & neutropeni in preicteric stage
* Aplastic anemi, rare
* PTT protonged
* ESR on preicteric stage
N on icteric stage
if icteric begin to disappear
N on convalescence stage
CHRONIC HEPATITIS
Chronic inflamation > 6 month
Classification :
1. Chronic persistent hepatitis
2. Chronic lobular hepatitis
3. Chronic active hepatitis
1. Chronic persistent hepatitis
Etiology : Hepatitis B virus
Hepatitis Non A Non B virus
Alcoholism
Unknown
Lab. : Normal serum bilirubin or mildly elevated serum
IgG
2. Chronic lobular hepatitis

Etiology : acute viral Hepatitis like illness

Hepatitis Non A Non B virus
Lab. : increase of transaminases
3. Chronic active hepatitis

Etiology : Hepatitis B virus

Hepatitis Non A Non B virus

Unknown

Lab. : serum bilirubin

transaminases

gamma globulin
HEPATIC CIRRHOSIS
Is a diffuse process with fibrosis and nodule formation. It has
followed hepato-cellular necrosis. Although the causes are
many, the end result is the same
Etiology :
- Hepatitis B, non A - non B virus
- Alcoholism
- Metabolic : hemochromatosis
diabetes mellitus
Wilson's disease
- Prolonged intra & extrahepatal cholestatis
- Abnormal immunity
- Toxin & therapeutic agent
Laboratory : Compensated transminases
GGT
urine urobilinogen
Decompensated :

Urine : urobilinogen
(+) bilirubin
sodium in ascites

Blood : bilirubin
albumin
gamma globulin
transaminases
alkaline phosphatase
cholesterol ester

Normochrom normocyter anaemi, PTT prolonged

HAEMOCHROMATOSIS
A. PRIMARY HAEMOCHROMATOSIS
Normal Iron Metabolism :

The normal daily diet contains about 10 - 20 mg of iron of

this 1 - 1,5 mg is absorbed depends on body stores more
being absorbed the greater the need

Fasting iron serum is 250  / dl.

The normal total body content of iron is about 4 g., of wich

3 g are present in hemoglobin, myoglobulin , catalase, etc

Storage iron comprises 0,5 g ; of this 0.3 is in the liver.

When its capacity is ezcceded, iron is deposited in other

parenchymol tissues.
Definition :
Primary Haemochromatosin is a metabolism disturbance of
elevated iron absorpstion for years.
Etiology : Genetic
Patologi : * A. fibrous tissue reaction is found where even the iron
is deposited
liver intestine
pancreas heart
spleen, gaster brain, nerve
endocrine skin
lab. : - abnormal liver function tests
- serum iron
- transferrin 90 % saturated
- hyperglycemia
HEPATOCELLULAR FAILURE
Disfunction of liver cells can cause several manifestations :
1. Jaundice
2. Hepatic coma
3. Endocrine imbalance
- testicular atrophy
Oesterogen
- gynecomastia
in
- lost of body hair
- arterial spider Oesterogen inactivation
- palmar erythem
4. Fetor hepaticum
5. Ascites :
* serum osmotic coloid ( albumin )
* electrolyte retention ( hormonal imbalance )
* portal vein pressure