ANEMIA

ANEMIA
Anemia is present when the Hb concentration is below the reference range for
the age and sex of an individual.
Referenge range of Hb concentration (g/dl)
Cord blood 13.5 20.5
First day of life 15.0 23.5
Children 6 months 6 years 11.0 14.5
Children 6 years 14 years 12.0 15.5
Adult males 13.0 17.0
Adult females (non-pregnant) 12.0 15.5
Pregnant females 11.0 14.0
In healthly individuals, there are strong correlations between the Hb, red cell
count and PCV.
Referenne rang of erythrocytres in adult males is 4.4 5.8 millions / mm3 and
in adult females is 4.1 5.2 millions / mm3.
The PCV in adult males is 40 51 % and in adult females is 36-46 %.

ADAPTIVE RESPONSES TO ANEMIA
Compensatory mechanism in anemia:
* Increased production of 2,3-DPG by red cells.
This causes a reduction of O2 affinity of Hb and causes an increased release
of O2 at tissues.
* When the Hb falls below 7-8 g/dl, changes occur in the CV system: increased
cardiac output at rest, mainly by an increase in stroke volume and also by an
increase in the heart rate.

SYMPTOMS AND SIGNS IN ANEMIA
Underlying mechanism of symptoms and signs in anemia are:
1. Decreased tissue oxygenation, causing widespread organ dysfunction
2. Adaptive changes, particularly in the cardiovascular system
SYMPTOMS OF ANEMIA
Easy fatiguability, dyspnoe on exertion, palpitation, angina and
intermittent claudication (in older patients with degenerative arterial
disease), heartache, vertigo, light-headidness, visal disturbances,
drowsiness, menstrual disturbances and loss of libido.

SIGNS OF ANEMIA
Pallor, tachycardia, wide pulse pressure with capillary pulsation, hemic
murmurs, signs of congestive heart failure and hemorrhages and occasional
exudates in the retina.
Severe anemia ( Hb less than 6 g/dl) may also causes slight proteinuria,
mild impairment of renal function and low grade fever.
MECHANISMS OF ANEMIA
Blood loss
Hemolytic anemia
* Congenital defects
* Acquired defects
Impairment of red cell formation
* Insufficient erythropoiesis
* Ineffective erythropoiesis
Pooling and destruction of red cells in an enlarged spleen
Increased plasma volume
MORPHOLOGICAL CLASSIFICATION OF ANEMIA

1. Hypochromic and microcytic
Decreased values of MCHC, MCV and MCH

2. Normochromic and normocytic
Normal values of MCHC, MCV and MCH

3. Macrocytic
Increased MCV
NORMOCYTIC ERYTHROCYTE
Normal MCV 76 96 fl
Diameter of red cell = diameter of the nucleus of small lymphocyte

MICROCYTIC ERYTHROCYTE
Decreased MCV
Diameter of red cell < diameter of the nucleus of small lymphocyte

MACROCYTIC ERYTHROCYTE
Increased MCV
Diameter of erythrocyte > diameter of the nucleus of small lymphocyte

NORMOCHROMIC ERYTHROCYTE
Normal MCHC 32 36 % (g/dl)
Central area of pallor occupying about 1/3 of the cell diameter

HYPOCHROMIC ERYTHROCYTE
Decreased MCHC
Central area of pallor increased > of the cell diameter

HYPOCHROMIC AND MICROCYTIC ANEMIA
1. Iron deficiency anemia
2. Thalassemia
3. Anemia of chronic diseases
4. Sideroblastic anemia

NORMOCHROMIC AND NORMOCYTIC ANEMIA
1. Anemia in Acute blood loss
2. Hemolytic anemia, except due to pathologic hemoglobin
3. Aplastic anemia
MACROCYTIC ANEMIA
1. Megaloblastic anemia
* Folic acid deficiency
* Vitamin B12 deficiency
* Abnormalities of nucleic acid synthesis

2. Non-megaloblastic anemia
Post acute blood loss and hemolysis
Chronic liver disease
Chronic alcoholism

IRON DEFICIENCY ANEMIA
DISTRIBUTION OF IRON IN THE BODY
Total body iron of a healthy adult 2 5 g.
About 2/3 ( 66.4 %) of the iron is found in the Hb of red cells;
1 ml red cells contains about 1 mg of iron
Myoglobin of muscle cells ( 3.3 %) and respiratory enzymes of all cells
(cytochrome oxidase, catalase, peroxidase) contains 0.15 g iron
Storage iron: ferritin and hemosiderin about 1 g ( 30 %)
Transferrin (1-globulin) 0.1% of total iron.


IRON ABSORPTION
Daily intake of iron 0.5-2 mg
Adults with normal iron stores absorps about 5 10 % of total daily intake
Absorption takes place in the duodenum and proximal portion of jejunum


INCREASED ABSORPTION DECREASED ABSORPTION
Ferro - ion Ferri - ion
Anorganic iron Organic iron
Acid state, e.g. HCl, Vit C Base state: antacide
secrete of
pancreas
Increased solubility, e.g.
fructose,
amino acids
Decreased solubility,
e.g.phytate,
phosphate, oxalate.
Iron deficiency Iron excess
Increased erythropoiesis Decreased erythropoiesis
GE tract infection, e.g.
diarrhea
HEMATOLOGICAL CHANGES
Hb decreases before decrease of red cells
Decrease of MCHC, MCV and MCH resulting in a hypochromic and
microcytic anemia
Morphology of blood film
- hypochromic and microcytic red cell
- pencil cell
- target cell
Morphology of bone-marrow film (Giemsa staining)
- defective erythropoiesis
- normoblastic hyperplasia, decreased acidophilic normoblasts
- smaller normoblasts due to decrease of cytoplasm
- ragged cytoplasm of normoblasts with pycnotic nuclei
- naked nuclei (normoblast without cytoplasm)


Morphology of bone marrow film (Prussian blue staining)
- decreased sideroblast to 0 10 % (Normal 30 50 %)
BIOCHEMICAL CHANGES
Decreased serum iron concentration < 40 Ug/dl
Increased Iron Binding Capacity (IBC) > 370 Ug/dl
Decreased transferrin saturation < 15%
Decreased serum ferritin concentration < 12 ng/ml
Increased erythrocyte protoporphyrin.
Increased transferrin receptor concentration
RESPONSE OF IRON TREATMENT
1. Reticulocytosis
2. Increased Hb concentration of 2 g/dl in 3 weeks
HEMOGLOBIN S
Hb S: glutamic acid in position 6 of the normal -chain is
replaced (substituted) by valine molecule.
This results in deoxygenated HbS being 50 times less soluble
than deoxygenated HbA.
The deoxygenated HbS molecules initially polymerize without
forming fibres then polymerize into long fibres (tactoids) which
deform the red cell into the typical sickle-shape.
Red cells from heterozygotes HbS sickle at much lower PO2
values than those from homozygotes and do not usually sickle in
vivo.
SICKLE-CELL ANEMIA
Homozygote of HbS.
Red cells contain 80% or more HbS, the remainder being
mainly HbF.
The red cells sickle at the O2 tension normally found in venous
blood. The red cells (sickled or unsickled) containing
deoxygenated HbS are less deformable than normal red cells
and suffer mainly extravascular hemolysis. The increased
rigidity of the cells may cause them to be jammed in and
obstruct small vessels, thus causing tissue infarction.
Symptoms due to infarction occur in episodes, with painful
crises e.g. affecting the chest, limbs. Accompanied with low
grade fever.
Pigment gallstones formation are caused by frequent hemolysis
of the red cells.


LABORATORY FINDINGS in SICKLE CELL ANEMIA
Positive result of HbS in routine Hb electrophoresis.
Hb varying between 6 9 g/dl
Morphology of blood film:
Hypochromic microcytic red cells
Sickle cell positive.
Howell-Jolly bodies positive post spleen atrophy
Decreased Erythrocyte Sedimentation Rate


SICKLE-CELL TRAIT
Heterozygote (one gene for HbA and one for HbS)
HbS between 20-45%, the rest mainly HbA. Mixing of HbA
and HbS in routine Hb-electrophoresis.
Usually asymptomatic. Hemolytic crisis can occur after severe
stress or severe infection.
The red cells do not sickle until the O2 saturation falls below
40%.
Detection of sickle cell in blood film after mixing with reducing
agents in the SICKLING TEST.

HEMOGLOBIN E
HbE : substitution of glutamic acid with lysine at the 26
th

position of the -chain.
HbE is very common in South-East Asia.
Homozygotes with mild anemia and low MCV (microcytic)
and many circulating target cells up to 60% in the blood film.
Heterozygotes have about 20-30% HbE, are asymptomatic
and usually not anemic.
HEMOGLOBIN C
HbC : substitution of glutamic acid with lysine at the 6
th

position of the -chain.
Prevalence in Nigeria and northern part of Ghana 7-22%
Homozygotes have mild anemia, MCV normal or low and
many target cells 25-90% in the circulation.
HbC crystals are formed in the red cells if HbC > 44%
Heterozygotes are asymptomatic and non-anemic.
Target cells 6-40% in the blood.
DEFICIENCY OF RED CELL ENZYMES
Hemolytic anemias may also result from congenital
abnormalities of the enzyme system concerned with energy
transfer in glucose metabolism. The red cell requires a
continuous supply of energy for the maintenance of membrane
flexibility and cell shapes, the regulation of Na and K pumps and
the maintenance of Hb in the reduced ferrous form.
Energy is transferred through the energy-rich compounds ATP,
reduced NADH (nicotinamide-adenine dinucleotide), the related
phosphorylated compound NADPH, and reduced glutathione
(GSH).
The most common enzyme deficiency is G6PD, an enzyme
within the aerobic pentose-phosphate shunt.
Deficiency of pyruvate kinase, an enzyme within the anaerobic
glycolytic (Embden-Meyerhof) pathway


G6PD DEFICIENCY
The defective gene is present on the X-chromosome, thus the
clinical features of G6PD deficiency are mainly seen in males.
Homozygous women are uncommon.
Low activities of G6PD result in low concentrations of the
reducing compounds NADPH and GSH. The purpose of these
compounds is to maintain Hb and other erythrocytic proteins in
a reduced and active form. People with G6PD deficiency are
poorly protected against drugs which are oxidants. When
oxidants enter the cell they first convert Hb to methemoglobin
and finally denature it so that it precipitate in the red cell in the
form of rounded masses called Heinz bodies. Components of the
red cell membrane may undergo marked oxidation leading to
intravascular hemolysis.
Oxidant drugs or chemicals that can cause hemolytic anemia in
G6PD deficiency are:
anti-malarial drugs, e.g. primaquine, chloroquine
sulphonamides
analgetics, e.g. aspirin (high doses), phenacetin, para-
cetamol, and salicylic acid
vitamin K and fava beans.
Other condition causing hemolytic episodes are infection and
acidosis.
Laboratory findings:
Heinz bodies and schistocytes in the blood film
Evidence of extra- and intra-vascular hemolysis
Decreased G6PD, normally 6.3-11.5 IU/g Hb
PYRUVATE KINASE DEFICIENCY
Only homozygotes have symptoms.
Anemia varies from mild to severe
Not sensitive to drugs
Occurs in infants and young adults.
DEFECTS OF RED CELL MEMBRANE
HEREDITARY SPHEROCYTOSIS
Defect of spectrine, band 3 or protein 4.2
Family history of pallor, mild jaundice and splenomegaly.
Presence of spherocytes in stained blood film
Increased plasma bilirubin
Reticulocytosis 5-20%
Increased osmotic fragility of the red cells, lysis starts at
0.6-0.8 g/dl saline concentration.
MCV decreased, MCHC normal.
HEREDITARY ELLIPTOCYTOSIS
The defect lies in abnormality of the red cell membrane,
mutations affecting the spectrine genes or the protein 4.1 or
glycophorin C genes.
Elliptocytes 25-90% , in normal persons only 0-5%.
Homozygotes have a severe anemia from infancy
HEREDITARY STOMATOCYTOSIS
Mild to moderate anemia and reticulocytosis
Stomatocytes 20-40%
DD/ stomatocytes found in Acute alcoholism, Alcoholic
cirrhosis, Pb intoxication, Thalassemia minor, Infectious mono-
nucleosis and malignancy.
HEREDITARY ACANTHOCYTOSIS
Acanthocytes > 40% in peripheral blood smear
Abnormalities found in serum:
a- lipoproteinemia
decreased lecithin, lipid and cholesterol
DD/ Acanthocytes can be found in blood film of:
Hepatic cirrhosis with hemolytic anmeia
Hemangioma in the hepar
Neonatal hepatitis
HEMOSTASIS
+ A PROCESS TO STOP BLEEDING FROM SPONTANEOUS
VASCULAR DAMAGE

HEMOSTASIS DEPENDS ON :
1. VASCULAR FACTOR
2. THROMBOCYTE FACTOR
3. COAGULATION FACTOR
VASCULAR PHASE
ARTERIAL CAPILLARY VENOUS
ARTERY
MICRO
CIRCULATION
VEIN
-THICK MUSCLED
-ELASTIC
-HARD TRAUMATIC DAMAGE
-SOFT
-EASILY DAMAGE
-THIN
-LIGHT TRAUMATIC DAMAGE
THE WHOLENESSOF VASCULAR SYSTEM DEPENDS ON NUMBER AND FUNCTION OF
THROMBOCYTE

THE ROLE OF VASCULAR PHASES :
REFLECTION : DECREASE OF BLOOD FLOW
A. VASOCONSTRICTION
LOCAL :
1. SEROTINE = 5 HT = 5 HIDROXYTRIPTAMINE
2. EPINEPHRINE
3. THROMBOXAN A
2
B. BEGINS THE OTHER HEMOSTSIS PROCESS
THROMBOCYTE : COLLAGEN PROTUBERANCE ADHESION AGGREGATION
COAGULATION : INTRINSIC : F XII F XII a
EXTRINSIC : RELEASE F III = THROMBOPLASTIN TISSUE
VASOCONSTRICSION
MICROCIRCULATION BLEEDING :
PLATELET PLUG
BLEEDING > MORE : HEMOSTATIC PLUG
THROMBOCYTE PHASE
TOTAL : 150.000. - 400.000/mm
AGE : + 10 DAYS
: 2 - 3 O
1 MEGACARYOSITE : 3.000 - 4.000 THROMBOCYTE
INFLUENCED BY : THROMBOPOEITIN (RENAL) 7 - 8 x
NO NUCLEUS








MAKE THROMBOCYTES FORM
FILAMENT SUB MEMBRANE CYTOSCELET
MICROTUBULES
MICRO FILAMENT
FUNCTION : 1. PSEUDOPODI
2. CONTRACTION WHEN AGGREGATION

PROTEIN CONTRACTILE RESOURCE :
2. SOL GEL ZONE
THROMBOSTENIN
THROMBOSTENIN A
(ACTIN)
THROMBOSTENIN M
(MYOSIN)
1. PERIPHERAL ZONE
a. EXTERIOR COAT
P
3
b. UNIT MEMBRANE
c. SUB MEMBRANE
IS A PLACE FOR : ADHESION - AGGREGATION
HAS RECEIVER FOR :
THROMBIN, COLLAGEN, ADP, ADRENALIN
3. ORGANEL ZONE
SPREAD FREELY IN CYTOPLASM
FUNCTION : - RESPIRATION
- EXCRETION
- PRODUCTION
- STORAGE
- RELEASE ENERGY
-ORGANIZE THE THROMBOCYTES CHEMIST AND
PHYSIOLOGY RESPONSE TO STIMULATION

3 GRANULES TYPE
1. LISOSOM HYDROLYTIC ENZIM
2. SOLID GRANULE a. ATP
b. ADP
c. Ca
++

d. SEROTONIN
e. EPINEPHRINE
f. NOR-EPINEPHRINE
3. ALPHA GRANULE a. -THROMBOGLOBULIN
b. PLATELET FACTOR 4 P4
c. PLATELET DERIVED GROWTH FACTOR PDGF
d. GLYCO PEPTIDE STIMULATING SOFT MUSCLE AND
FIBROBLAST REPLICATION
e. PROTEIN ~ PLASM - F.V
- F. VIII
- FIBRINOGEN
- FIBRONECTIN
f. THROMBOSPONDIN TSP
THROMBOCYTE FUNCTION :
1. ADHESION
2. AGGREGATION
3. RELEASE REACTION
ADHESION
THROMBOCYTE ADHESION AT FOREIGN SURFACE ESPECIALLY
COLLAGEN FIBRE
1. COLLAGEN
2. MICROFIBRILE
3. SUBENDOTHELIAL TISSUE
VIII : v WF (FACTOR VIII VON WILLEBRANDS
1. THROMBIN
2. ADP
3. COLLAGEN
4. ADRENALIN
5. ADHESION - AGGREGATION
FACTOR VIII : VW : SYNTEZISED BY ENDOTHELIAL CELLS AND MEGACARYOCYT

COAGULATION FACTORS
I FIBRINOGEN
II PROTHROMBIN
III THROMBOPLASTIN = TISSUE FACTOR
IV CALSIUM
V PROACCELERIN, LABILE FACTOR
VI -
VII SERUM PROTHOMBIN CONVERSION ACCELERATOR
(SPCA), STABLE FACTOR
VIII ANTIHEMOPHILIC FACTOR
IX CHRISTMAS FACTOR, PLASMA THROMBOPLASTIN
COMPONENT (PTC)
X STUART FACTOR, STUART POWER FACTOR
XI PLASMA THROMBOPLASTIN ANTECEDENT (PTA)
XII FIBRIN STABILIZING FACTOR
COAGULATION PHASE
CLASIC THEORY OF BLOOD COAGULATION
MORAWITZ 1904
PROTHROMBIN

THROMBIN

TROMBOPLASTIN

FIBRINOGEN

FIBRIN

THROMBIN

Ca ++

SURFACE CONTACT

XII

XIIa

XI

XIa

IX

IXa

VIII

VIIIa

X

Xa

V

Va

II

IIa

I

Ia

CASCADE THEORY
MACFARLANE 1964

XII

XIIa

XI

XIa

IX

IXa

Ca ++

X

Ca ++ PHOSPHOLIPID

VIII

Xa

II

IIa

Ca ++

V

PHOSPHOLIPID

I

Ia

WATERFALL THEORY
DAVIE & RATNOFF
1964 1969

INTRINSIC EXTRINSIC
ACTIVE SURFACE PREKALLIKREIN
XII
XII
a XII
f

PLASMA
HMWK
KALLIKREIN
HMWK
HMWK
XI XI
a

IX
Ca
++
VII
VII
a

IX
a

P
+
f3

Ca
++
(II
a
Pf
3
Ca
++
VIII)
Ca
++
TISSUE FACTOR
Ca
+++


(VII/VII
a
Ca
++
TISSUE FACTOR)

COMMON
X
Ca
++
X
a

V
+
P
+
f
3
Ca
++
(X
a
V-Pf
3
Ca
++
)
(PROTHROMBINASE)
PROTHROMBIN THROMBIN
FIBRINOGEN
FIBRIMONOMER + PEPTIDES
SOLUBLEFIBRIN
STABILIZED FIBRIN
XIII
a
XIII

Ca
++
Ca
++
Ca
++
COAGULATION INHIBITOR
- ANTI THROMBIN III
- PROTEIN C
AT III BLOCK AT III : XIIa, XI a, IX a, Xa, IIa

PROTEIN C BLOCK : VIII : C, Va

FIBRINOLYSIS SYSTEM
ENDOTHELIUM
ACTIVATOR
ACTIVATOR PLASMA
- F XIIa
- KALLIKREIN
FIBRIN
FORMATION
BOUND
PLASMINOGEN
(FIBRIN)
PLASMINOGEN
BOUND
PLASMIN
(FIBRIN)
PHYSIOLOGIC
PROTEOLYSIS
(FIBRINOLYSIS)
FREE
PLASMIN
(PLASMA)
PATHOLOGIC
PROTEOLYSIS
(FIBRINOLYSIS)
INHIBITOR
ANTIPLASMIN
(PLASMA)
FREE
PLASMINOGEN
(PLASMA)
SYSTEM
FIBRINOLYSIS
SYSTEM
COAGULATION
- C
2 ANTI PLASMIN
- C
2 MACROGLOBULIN
- C
1 ANTI PLASMIN

VASCULAR DISORDERS
- LIGHT BLEEDING DISORDERS
- PETECHIAE, ECCHYMOSES OR BOTH
- MUCOUS MEMBRANE BLEEDING : <
- ORGAN / MUSCLES BLEEDING : <<
- SPECIAL TEST : ( - )
A. HEREDITERY HEMORRHAGIC TELEANGIECTASIRE
(OSLER - RENDU - WEBER DISEASE)
B. HEREDITERY CAPILLARY FRAGILITY
( VASCULAR PSEUDOHAEMOPHILIA)
C. EHLERS - DANLOS DISEASE
I. CONGENITAL
D. OTHERS
- ORTHOSTATIC PURPURA
- MECHANICAL PURPURA
- FAT EMBOLISM
- AUTO ERYTHROCYTE SENSITIZATION
- SYSTEMIC DISORDERS COLLAGEN DISEASE,
POLYARTERITIS NODOSA, AMYLOID DISEASE, ALLERGY.
A. PURPURA SIMPLEX
B. SENILE PURPURA
C. NON THROMBOCYTOPENIC PURPURA
1. INFECTION
2. DRUGS
3. UREMIC
4. CUSHING DISEASE (CORTICOSTEROID ABUSE)
5. SCURVY
6. DYSPROTEINAEMIA
7. HENOCH - SCHONLEIN PURPURA
II. ACQUIRED
CONGENITAL
A. HEREDITARY HAEMORRHAGIE TELEANCIECTASIE
- VERY RARELY
- =
- SKIN BLEEDING & MUCOUS BLEEDING
- CAPILLARY MULTIPLE DILATATION AND ARTERIOL SENSITIVE
WALL BAD VASOCONSTRICTION
INCREASE BLEEDING

B. HEREDITARY CAPILLARY FRAGILITY
- IS A VARIANT OF VON WILLEBRAND DISEASE
- INCREASE BLEEDING TIME

C. EHLERS - DANLOS SYNDROME
- COLLAGEN DISORDERS
- CAPILLAARY FRAGILITY >> BLEEDING HEMATOM
- INCREASE BLEEDING TIME
ACQUIRED:
A. PURPURA SIMPLEX :
- REPRODUCTION PERIOD
- TORNIQUET TEST : weak (+)
- NORMAL BLEEDING TIME

B. SENILE PURPURA
- = ; > 60 THN
- LIGHT TRAUMA PURPURA
- COLLAGEN ATROPHY EASILY MOVEMENT SKIN
- TORNIQUET TEST : ( -)

C. NON THROMBOCYTOPENIC PURPURA
- CAPILLARY FRAGILITY & PERMEABILITY >>
- TOTAL THROMBOCYTE : N
- TORNIQUET TEST : ( + )
- BLEEDING TIME : N SOMETIMES >
-MOST OFTENLY FINDING IN CLINIC
1. INFECTION
- TYPHOID
- SUB ACUTE BACTERIAL ENDOCARDITIS
- SEPTICEMIC
- SMALL POX
- TOXIN DAMAGE THE ENDOTHELIAL
2. DRUGS
- PENICILLIN, STREPTOMYCIN
PHENACETIN ASPIRIN, SULPHONAMIDE, ANTIHISTAMIN
BARBITURAT, ETC..
- STOP DRUGS SYMPTOM ( - )
3. UREMIC
- OFTEN EPISTAXIS
- TROMBOCYTE FUNCTION DISORDERS SOMETIMES
THROMBOCYTOPENIC
- UREA VALUE DISORDER
4. CUSHING DISEASE / CORTICOSTEROID ABUSE
- MENOPAUSE
- PREDNISON - PREDISOLON >> CORTISON
- DISRUBTION: FRAGILE VASCULAR
- TORNIQUET TEST : SOMETIMES (+ )
5. SCURVY : VIT. C DEFICIENCY
- INTERCELLULER MATERIAL
- VIT. C DEF. CAPILLARY FRAGILITY >> EASILY DAMAGE PETECHIAE
- CHILDREN : GUMS OEDEM BLEEDING
- HYPERKERATOSE
- ADULTS : GERIATRIC
- LEAVING ALONE INADEQUATE FOOD ALCOHOL

6. DYSPROTEINEMIC
PROTEIN PLASMA DISORDER
- CRYOGLOBULINEMIC
- HYPERGLOBULINEMIC
- MACROGLOBULINEMIC
- MULTIPLE MYELOMA
THROMBOCYTE FUNCTION DISTURBANCY BECAUSE OF THE THROMBOCYTE IS
COVERED BY THE PROTEIN

7. HENOCH SCHONLEIN SYNDROME
(ANAPHYLACTOID PURPURA)

-MOSTLY FINDING
- HYPERSENSITIVE TO BACTERIAL
- 1 3 WEEKSBEFORE:UPPER RESPIRATORY TRACT INFECTION BY :

p - STREPTOCOCCUS HEMOLYTICUS

DISORDERS : - PURPURA
- JOINT
- RENAL
- CHILDREN YOUTH : >
- IT COULD BE BECAUSE OF FOOD,INSECT BITE, VACCINATION
- INFLAMATION REACTION FROM ARTERIOL AND CAPILLARY PERMEABILITAS >>
EXUDATION AND BLEEDING
THROMBOCYTE DISORDERS
I. NUMBER DISORDER
A. THROMBOCYTOSE
B. THROMBOCYTEMIA
C. THROMBOCYTOPENIC
II. FUNCTION DISORDER
A. ADHESION DISORDER
B. THROMBOCYTEMIA
C. THROMBOCYTOPENIC
A. THROMBOCYTOSE :
- NUMBER OF THROMBOCYTE :
INCREASE FOR A WHILE
- PHYSIOLOGIE : PHYSICAL EXERCISE
- PATHOLOGIE : - TRAUMA
- CARCINOMA
- INFLAMATION
- NO STIMULUS N

B. THROMBOCYTEMIA :
- PERMANENT THROMBOCYTOSE
- FUNCTION : ABNORMAL
C. THROMBOCYTOPENIC
STEM CELL POOL
HYPOPLASIA
IMMATURE
MEGAKARYOEXTE
POOL
MATURE
DISORDERED
REGULATION
THROMBOPOITIC
STIMULI
INEFFECTIVE
THROMBOPOISIS
PLATELET
PRODUCTION
CIRCULATING
PLATELET POOL
SPLENIC PLATELET
POOL
NORMAL :
70%
30%
10 - 40%
60 - 90%
ABNORMAL POOLING
OR DISTRIBUTION
PLATELET
UTILIZATION
ACCELERATED
DESTRUCTION
ABNORMAL
ACCELERATED DESTRUCTION
DESTRUCTION MOSTLY THROMBOCYTOPENIC

COMPENSATED MEGACARYOCYTE THROMBOCYTOPENIC (-)
1. ITP POST SPLEENECTOMY
2. ARTIFICIAL HEART VALVES USING

DECOMPENSATED THROMBOCYTOPENIC (+)

INTRACORPUSCULAR
DISORDER SOMETIMES
EXTRA CORPUSCULAR
IMMUNOLOGY DISORDER >>

SMASHED CELL COUGHT BY : - SPLEEN
- LIVER
- RES
USES
1. THROMBUSE FORM
2. DIC = DISSEMINATED INTRA VASCULAR COAGULATION
3. TTP = THROMBOTIC THROMBOCYTOPENIC PURPURA
PRODUCTION : AMEGACARYOCYTIC THROMBO CYTOPENIC
1. MYELOPHTHISIS
- Ca PROSTATE
- Ca MAMMAE METASTASE WILL HAPPEN IF SPREAD WIDELY
2. PRIMARY BONE MARROW DISOEDERS
- ACUTE LEUKEMIA
- CLL
- MM
- APLASTIC ANEMIA
3. INFECTION :
MOST OFTEN VIRAL INFECTION
- MEGACARYOCYTE INVATION
- THROMBOCYTE SMASHED
- VIRAL ANTIGEN ANTIBODY - COMPLEX
4. DRUGS
- THIAZIDE
- ALCOHOL
- ANTI CANCER DRUGS
- IMMUNOSUPRESSIVE
- CHLORAMPHENICOL
1. MEGALOBLASTIC ANEMI : - MOST OFTENLY
- PANCYTOPENIC
2. SIDEROBLASTIC ANEMIA
3. PRELEUKEMIA
4. PAROXYSMAL NOCTURAL HEMOGLOBINURIA
ABNORMAL POOLING
THROMBOCYTE PRODUCTION : N or 7
AT SPLEENOMEGALI : 60-90% THROMBOCYTE ARE IN THE SPLEEN (N : 30%)
THROMBOCYTE DILUTION
STORAGE BLOOD FAST TRANSFUSION
1. THROMBOCYTOPENIC
2. RECEIVERS BLOOD DILUTION
3. LABILE BLOOD COAGULATION <<
PLASMA EXPANDER USING AS :
DEXTRAN THROMBOCYTOPENIC
1. DILUTION
2. THROMBOCYTE DAMAGE

INEFFECTIVE THROMBOPOISIS
IDIOPHATIC THROMBOCYTOPENIC PURPURA
ACUTE
- CHILDREN : 2 - 6 y.o.
- =
- DURATION: 2 - 6 weeks
- REMISSION : 80 %
- THROMBOCYTE : <20.000/mm
3

CHRONIC
PUBERTY - 50 y.o.
>
FEW MONTHS FEW YEARS
(-) FLUCTUATION
30.000 - 80.000/mm
3
( I T P )
- THROMBOCYTE AGE :
- 50.000/ mm
3 :

- < 10.000/ mm
3 :

- AUTOANTIBODY :
INTO PLACENTA

2 - 3 DAYS (C
r
51)
1 - 2 DAYS
< 2 HOURS
Ig G
CONGENITAL ITP
ACUTE ITP : IN WINTER RESPIRATORY TRACT INFECTION ITP
LABORATORY : THROMBOCYTE v
- < 50.000/ mm
3
-

FINDING : MEGATHROMBOCYTE (GIANT THROMBOCYTE)
- BLEEDING TIME >> BAD COAGULATION RETRACTION
- RUMPELEED TEST : (+)
- BONE MARROW : MEGACARYOCYTE 77 ; GRANULE <<
ACQUIRED COAGULATION FACTOR DISORDERS :
3 INHERITANCE PATTERNS
1. F.VIII and F.IX DEFICIENCY : X-LINK RECESSIVE
2. VON WILLE BRAND DISEASE
- DISFIBRINOGENIA DISEASE : AUTOSOMALDOMINANT.
- F. XI DEFICIENCY
3. F. I, II, V, VII, X, XII, XIII DEFICIENCY : AUTOSOMAL RECESSIVE.
- 85 % F. VIII DEF.
- 12 % F. IX DEF.
- 1 % F. XI DEF.
HEMOPHILIA A = F. VIII DEF. = CLASSIC HEMOPHILIA
- THE DISORDER ONLY AT : , = CARRIER
- CHINA : RARE
- NEGRO UNUSUAL
- DISEASE LEVEL F. VIII VALUE
- SEVERE 0 - 2 %
- MODERATE 2 - 5 %
- LIGHT 5 - 25 %
- SUBHEMOPHILIA 25 - 50 %
THROMBOCYTE FUNCTION DISORDERS
1. ADHESION TOWARDS COLLAGEN DISORDER
- EHLERS-DANLOS SYNDROME (VASCULAR DISORDER)
2. ADHESION TOWARDS SUBENDOTHELIAL
- BERNARD SOULIER SYNDROME (THROMBOCYTE DISORDER)
- VON WILLERBRAND SYNDROME (PLASMA DISORDER)
3. RELEASING DISORDERS
- HERMANSKY - PUDIAIL SYNDROME
- WISKOTT - ALDRICH SYNDROME STORAGE POOL DEFICIENCY
- CHEDIAK - HIGASHI SYNDROME
CYCLO - OXYGENASE DEFICIENCY (RELEASING MECHANISM DISTURBANCE)
GLYCOGEN STORAGE DISEASE TIPE I (NUCLEOTIDE METABOLISME DISTURBANCE)
4. ADP AGGREGATION (THROMBOCYTE DISORDER)
- THROMBASTHENIA GLANZMANN
- AFIBRINOGEMIA
(PLASMA DISORDERS)


FIBRINOGEN RECEPTOR DEFICIENCY
(GLICO PROTEIN II b/ III a = GP II b / GP III a)
CLINICAL SYMPTOMS :
1. SPONTANEOUS BLEEDING

2. LATE BLEEDING STOP
CRANIAL BLEEDING
3. BLEEDING LEVEL >< F. VIII VALUE
4. BLEEDING TIME: NORMAL

HEMOPHILIA
Y

X
X
+ NORMAL
NORMAL
X

Y
X
X


Y
X
Y
X
Y Y


X




Y Y X




X




HEMOPHILIA
HEMARTROSE
HEMATOMA
HEMATURI
TRAUMA
OPERATION
25 % 25 % 25 % 25 %
25 % 25 % 25 %
X
Y
X
25 %
X
carier
HEMOPHILIA B = CHRISTMAS DISEASE
- F. IX DEFICIENCY
- SYMPTOM : GENETIC AND DISTRIBUTION
SEX = HEMOPHILIA A.
HEMOPHILIA C
- F. XI DEFICIENCY
- AUTOSOMAL DOMINANT
- ESPECIALLY JEWISH
- BLEEDING >LIGHT
- HEMARTHROSE RARELY HAPPENED
- BLEEDING MANIFESTED IF THERE IS WOUND OR OPERATION
-COULD BE MANIFESTED TO
VON WILLEBRAND DISEASE
- AUTOSOM DOMINANT >
- v F. VIII - vW
- BLEEDING TIME >
- TORNIQUET TEST (+)
- ADHESION <
- OFTEN EPISTAXIS anD MENORHAGIA
- HEMARTHROSIS : RARE
ACQUIRED
LIVER DISEASE = PRODUCE IN LIVER : FACTOR I, II, V, VII, IX, X
1. LIVER FUNCTION v COAGULATION FACTOR PRODUCTION v
HEMOSTATIC FAILURE
2. FIBRINOLYSIS SYSTEM 7
3. THROMBOCYTOPENIC
VITAMIN K DEFICIENCY = VITAMIN K DISTURBANCE : FAKTOR II, VII, IX, X
1. VITAMIN K NEEDED =FEW
2. FOOD SOURCE, INTESTINE FLORA BACTERIAL
3. DEF. BECAUSE OF : - GALL BILE OBSTRUCTION
- SPRUE
- STEATORRHEA
UREMIC
1. THROMBOCYTE FUNCTION v BECAUSE OF:
- GUANIDINOSUXINATE ACID
- HYDROXYPHENOL ACETATE
2. COAGULATION FACTORS VALUE : II, VII, IX, X DECREASE
FIBRINOLYTIC SYSTEM DISORDERS
NORMAL FUNCTION :

1. RESTRICTION OF FIBRIN PRODUCTION
2. FIBRIN COAGULANT LIQUEFACTION
NORMAL REACTION :
COAGULATION FIBRINOLYSIS
Fast
FIBRIN DEVELOPMENT tissue repairs FIBRIN tissue liquefaction
slow
PRECURSOR
ACTIVATOR
INHIBITOR
FIBRINOGEN BM 340.000
FIBRINOLYSIS
FIBRIN FRAGMEN X 280.000
FIBRINOGENOLYSIS
FRAGMEN Y 155.000
FRAGMEN E 50.000 FRAGMEN D 83.000
FIBRIN(OGEN) DEGRADATION PRODUCT = FDP
FRAGMEN Y, D, E = COAGULATION INHIBITOR
DISSEMINATED INTRAVASCULAR COAGULATION (DIC)
TISUUE DAMAGE TISSUE FACTOR VASCULARITY
STIMULATE :
FIBRIN FORMATION
1. THROMBOCYTE USAGE THROMBOCYTOPENIC
2. COAGULATION FACTOR I, II, V, VIII, XIII USAGE
DEFICIENCY HEMOSTATIC FAILURE
FIBRINOLYTIC SYSTEM ACTIVATION
FPD PRODUCTION RES
FDP7 BLOOD CIRCULATION 7 URINE
severe light DIC depends on NUMBER and SPEED of
TISSUE THROMBOPLASTIN COME INTO BLOOD CIRCULATION
- FIBRINOLYSIS SECUNDER
3 (three) PROBLEMS APPEAR:
1. COAGULATION FACTOR and THROMBOCYTE v
- BLEEDING
- FIBRINOLYSIS 7
2. ORGAN ISCHEMIC ESPECIALLY RENAL
3. ERYTHROCYTE FRAGMENTATION ANEMIA MICROANGIOPATHIC
HEMOLYTIC ANEMIA
FRAGMENTATION
SCHISTOCYTE
MICROSPHEROCYTE
LABORATORY :
1. PROTHROMBIN TIME (PT) : INCREASE
2. ACTIVATED PARTIAL THROMBOPLASTIN TIME (aPPT) :INCREASE
3. THROMBIN TIME (TT) :INCREASE
4. JUMLAH THROMBOSIT :INCREASE
5. PERIPHERAL BLOOD SMEAR :
ERYTHROCYTE
CLINICAL
ACUTE: - ABRUPTIO PLACENTAE
- AMNION EMBOLISM
- INTRA UTERINE FETAL DEATH
- ABORTUS SEPSIS
- CARDIAC and PULMONARY OPERATIONS
- HEMOLYTIC REACTION in TRANSFUSION
- SEPTIKEMIC ESPECIALLY HUMAN and MENINGOCOCCUS
- PULMONARY EMBOLISM
- POISONOUS SNAKE BITE
SUBACUTE/CHRONIC :
- LOCAL CARSINOMA DIFFUSE
- ACUTE LEUKEMIA and PROMIELOCYTIC
- INTRA UTERINE FETAL DEATH
- THROMBOTIC THROMBOCYTOPENIC PURPURA
- FULMINANS PURPURA
- GIANT HEMANGIOMA
PLASMA
ENDOTHELIAL
OTHER TISSUE
PRIMARY FIBRINOLYSIS
ACTIVATOR
PLASMINOGEN PLASMIN
DAMAGE
HEMOSTATIC
FAILURE
FDP
INHIBISION
- FIBRINOGEN
- F. V
- F. VIII
PHYSIOLOGIE: - HARD WORK
- EMOSIONAL DISORDER
- ANXIETY
- ANOXIA
PATHOLOGIE: C CHIRROSIS HEPATIC
C PROSTATE CARCINOMA
- URIKINASE 7 RENAL ACTIVATOR and
URINARY TRACT
NORMAL : LIVER COULD CLEAN THE ACTIVATOR
TEST
SECOND
FIBRINOLYSIS (DIC)
a
PRIMARY
FIBRINOLYSIS
b
MECHANISM
TT
X PT
a PTT
X THROMBOCYTE
FDP
X FIBRINOGEN
FIBRIN MONOMER
EUGLOBIN CLOT
LYSIS TIME
PLASMINOGEN
F. V
F.VIII
>
>>
>
v
few 7
v v
(+)
(-)
v/N
v
v
>
>
>
N
Real 7
N/v
usually (-)
(+)
v
v
v/N
FDP, F. I v
FDP, F. I v, F.V v
FDP, F. I v, F.V v,
F. VIII v.
PLASMIN
- THROMBIN
- PLASMIN
THROMBIN
PLASMIN
a. Used
b. Damaged
a. Used
b. Damage
TORNIQUET TEST
5 cm
5 cm
TENSION
SYSTOLIC
DIASTOLIC
5 minutes
100 mmHg
Wait 5 Minutes
PETECHIAE
: > 10 ABNORMAL
CAPILLARY FRAGILITY COARSE EXAMINATION
ABNORMAL :
- THROMBOCYTOPENIC
- PURPURA
- VON WILLEBRAND DISEASE
= RUMPEL LEEDE TEST
= HEST TEST
BLEEDING TIME
- ANTISEPTIC with ALCOHOL 70 %
- PRICK WITH A BLOOD LANCET
ROUNDED
FILTER
PAPER
5 mm
EVERY 30 SECONDS TOUCH
THE COMING BLOOD with ROUND FILTER PAPER.
BLEEDING TIME: 5 x 30 = 2 Minutes
If BLEEDING TIME > 10 STOP THE EXAMINATION
1. DUKE METHOD : EAR LOBE
VASCULAR FACTOR
THROMBOCYTE FACTOR
N : 1 - 3 MINUTES
- 3 fingers
- 3 mm
THE COMING BLOOD TOUCH BY ROUNDED FILTER PAPER
EVERY 30 SECONDS
CALCULATION METHOD is the same as DUKE, NORMAL: 1 - 7 Minutes
The PUNCTURE HAVE TO BE DEEP ENOUGH that the DIAMETER of
BLOOD SPOTS on the skin > 5mm.
T : 40 mmHg
BLOOD LANCET
2. METODA IVY :
CLOT RETRACTION
-NUMBER OF THROMBOCYTE SHOULD BE NORMAL
-TAKE + 5 CC OF BLOOD PLACE IN A SCALE
CENTRIFUGE TUBE AS 5 CC
-PLACE A WOODEN RIB INTO THAT
-LET IT BE IN ROOM TEMPERATURE 2 3 JAM
-RELEASE THE BLOOD CLOT CAREFULLY FROM
TUBE WALL LIFT THE DLOT BY CATCHING THE WOODEN RIB
- WRITE THE SERUM VOLUME

-TO EXAMINE THROMBOCYTE FUNCTION
-INFLUENCED BY FIBRINOGEN VALUE

WAY :

-
-
-
-
-
-
-
WOODEN
RIB
5 CC
DARAH
-NORMAL : 40 60 % < 40 % BAD
-CONSISTENCY : SHOULD BE TOUGH
-BAD : SLACK & WEAK

-CLOT LIQUEFACTION VOLUME :
-SERUM VOLUME 40 %
-CLOT VOLUME 100 40% = 60 %
-HEMATOCRITE 22 %
-CLOT LIQUEFACTION VOLUME 60 % - 22 % = 38 VOL %

-NORMAL : 0 20 VOL % ABNORMAL : > 20 VOL %

PLATELET ADHESIVENESS TEST
(ADHESI FUNCTION )
10 CC
PRECENT A B 300.000 150.000
PLATELET = ---------- X 100 % = ------------------------------- X 100 %
ADHESIVENES A 300.000

150.000
= ------------ X 100 % = 50%
300.000
NORMAL : 26 60 %
PATOLOGIS : < 26 %
A : CALCULATE
NUMBER OF
THROMBOCYTE
300.000/mm
3
6 10 CC
/MINUTE

B : CALCULATE
NUMBER OF
THROMBOCYTE
150.000/ mm
3
GLASS BEAD SALZMANN
THROMBOCYTE AGGREGATION
PPP = PLATELET POOR PLASMA (3000 RPM)
PRP = PLATELET RICH PLASMA (1500 RPM)
0

2

4

6

8
ADP 10 M
SPD
CONTROL
TA
O
P
T
I
C
A
L

D
E
N
S
I
T
Y

P
L
A
T
E
L
E
T

R
I
C
H

P
L
A
S
M
A

0

2

4

6

8
ADP 1 M
SPD
CONTROL
TA
0

2

4

6

8
EPINEPHRINE 5 M
SPD
CONTROL
TA
0

2

4

6

8
COLLAGEN 1/100
SPD
CONTROL
TA
0 2 4 6 8 10 0 2 4 6 8 10
PRP : 0.1 CC TIME (MINUTE)
AT VON WILLE BRAND DISEASE AGGREGATION TO RISTOCETINE NEGATIVE
WHILE TO ADP, COLLAGEN, EPINEPHRIN ARE POSITIVE
SPD = STORAGE POOL DISEASE
TA = THROMBASTHENIA
CLOTING TIME
= COAGULUM TIME
= WHOLE BLOOD CLOTING TIME

METHOD : LEE & WHITE
BLOOD 3 CC
37
o
C
1 cc 1 cc 1cc
- AS THE BLOOD COME INTO SYRINGE, START STOPWATCH
- LOOK AT THE 1
ST
TUBE EVERY 30 UP TO THE CLOT APPEARS THAN
THE 2
ND
TUBE UP TO THE CLOT APPEARS FINALLY THE 3
RD
TUBE.
- STOP THE STOPWATCH IF THE 3
RD
TUBE. HAS THE BLOOD CLOT
WRITE THE TIME
* N : 5 11 MINUTES
CLOT MECHANISM MEASUREMENT BY INTRINSIC LANE
PROTHROMBIN TIME (PT)
TO MEASURE EXTRINSIC LANE ACTIVITIES F I, II, V, VII, X
CONTROL
PLASMA
PATIENTS
PLASMA
ORTHOBRAIN
THROMBO
PLASTIN
(OBT)
37
o
C
5 1 2
0,1 CC
0,2 cc
1
2
- ADD 0,2 CC OBT, START STOPWATCH
- EXPERIMENT ALWAYS DONE 2X
- STOP THE STOPWATCH IF THE FIBRIN HAS BEEN FORMED
* N : 11 14 SECONDS
ABNORNAL : THE DIFFERENCE BETWEEN PATIENTS PLASMA AND CONTROL
PLASMA IS MORE THAN 2 SECONDS
PATIENTS PLASMA
CONTROL PLASMA
I II
PARTIAL THROMBOPLASTIN TIME (PTT)
TO MEASURE PROCOAGULANT PLASMA ACTIVITIES, EXCEPT F. VII & XIII
(+) CAOLIN MAXIMUM CONTACT ACTIVITY ACTIVATED PARTIAL
THROMBOPLASTIN TIME = aPTT
CONTROL
PLASMA
PATIENTS
PLASMA
ACTIVATED
THROMBOFAX
(ORTHO)
37
o
C
5 5 3 5
0,1 CC
0,1 CC
0,2 cc
CaCl
2

0,02M
1
2
3
1. EXPERIMENT ALWAYS DONE 2X
2. NORMAL VALUE DEPENDS ON THE METHOD
* N : 25 40 SECONDS MANUAL OR AUTOMATIC
3. PATHOLOGIC IF THE DIFFERENCE BETWEEN PATIENTS PLASMA
AND CONTROL PLASMA IS MORE THAN 10 SECONDS
EXAMPLE : aPTT PATIENTS PLASMA : 60
aPTT CONTROL PLASMA : 44
PATIENTS PLASMA
CONTROL PLASMA
PTT SUBSTITUTIOIN TEST
ADSORBED PLASMA (AP) :
CONTENTS OF F. I,V,VIII,XI, XII

PRODUCTION : 3
I. 1 cc CITRATE PLASMA + 0.1 cc AlOH
3
CENTRIFUGE 3000 rpm, 10
37 C
take the SUPERNATANT
15
II. 1 cc OXALATE PLASMA + 100 mg BaSO
4
CENTRIFUGE 3000 rpm,10
37 C
take the SUPERNATANT

AGED SERUM :
CONTENTS OF F. VII, IX, X, XI, XII
4 hours
WHOLE BLOOD CENTRIFUGE take the SUPERNATANT
37 C
24 hours divided 1 20cc FREEZER ( - 20C )
37 C





WAY :

1. INCUBATE : a. ACTIVATED THROMBOFAX 5
b. CaC
2
5 PLASMA : ( - )

2. MIX : PATIENT S PLASMA : ADSORBED PLASMA = 1 : 1
DONE PTT WITH THIS MIXED PLASMA

3. MIX : PATIENTS PLASMA : AGED SERUM = 1 : 1
DONE PTT WITH THIS MIXED PLASMA

4. MIX : PATIENTS PLASMA : NORMAL PLASMA = 1 : 1
DONE PTT WITH THIS MIXED PLASMA
SUBSTITUTION TEST
COAGULATION
FACTORS DEFICIENCY
XII
PTT
A
P T
N
TT
N
NP
C
AP
C
AS
C
XI A N N C C C
IX A N N C NC C
VIII A N N C C NC
X A A N C C
V A A N C C NC
VII N A - - - -
II A A N C NC NC
I A A A C C NC
NC
HEPARIN OR
INHIBITOR LIKE
HEPARIN
A A A NC - -
PTT - PARTIAL THROMBOPLASTIN TIME NP - NORMAL PLASMA
PT - PROTHROMBIN TIME AP - ADSORBED PLASMA
TT - THROMBIN TIME AS - AGED SERUM (SERUM TUA)


A = ABNORMAL
N = NORMAL
C = CONTROL
NC= NON
CONTROL
GENETIC COAGULATION DISORDERS
VII
EXTRINSIC
PTT A PT N
PTT N PT N
PTT N PT A
TOGETHER LANE
X, V, II, I
-VIII, IX, XI
BLEEDING
XII, HMWK,
PREKALLIKREIN
PTT A PT A
INTRINSIC
BLEEDING
UREACLOT
SOLUBILITY
TEST
XIII
HMWK = HIGH MOLECULE WEIGHT KININOGEN
ACQUIRED COAGULATION DISORDERS
- F. VIII INHIBITOR
- HEPARIN
INTRINSIC
SPECIAL TEST
PTT A PT N
PTT A PT A
PTT N PT A
EXTRINSIC
- LIVER DISEASE
- COUMARIN
(DRUG)
TOGETHER
LANE
- D I C
- HEPARIN
- LIVER DISEASE
ABNORMAL
TT
FIBRINOGEN VALUE
NORMAL
- LIVER DISEASE
- VIT. K DEFICIENCY
- COUMARIN
SPECIAL TEST
SCREENING TEST
1. NUMBER OF THROMBOCYTE
2. BLEEDING TIME
3. PTT
4. PT
A
B
C
D
E
F
G
NUMBER OF
THROMBOCYTE

N
N /
N
N
N
N
BLEEDING
TIME
>
>
>
N
N
N
N
P T T
N
>
N
>
>
N
N
P T
N
N
N
N
>
>
N

POSIBILITY
DIAGNOSIS

THROMBOCYTO
PENIC
VON WILLE
BRAND
FUNCTION
DISTURBANCES
INTRINSIC
DISTURBANCES
COMMON
DISTURBANCES
EXTRINSIC
DISTURBANCES
-
GENETIC
ALDRICH
SYND.
-
THROMBO
ASTENIA
HEMOFILIA
A & B
DEF F. I, II,
V, X
DEF F.VII
DEF F. .XIII
ACQUIRED
ITP, DRUGS
LE, INHIBI
TOR VIII ag
DRUGS, UREMIC
DYSPROTEIN
INHIBITOR
F. VIII c
DIC, LIVER DIS.
VIT K DEF.
-
ALERGY,
SCURVY,DRUGS
THROMBELASTOGRAPHY (TEG)
1. SCREENING TEST
2. THERAPEUTIC CONTROL
* PROFITS : 1. EASY
2. NO REAGENT / CHEAP
3. QUICK
WAY : BLOOD WHICH IS EXAMINATED COULD BE WHOLE BLOOD
(NATIVE BLOOD) OR CYTRATE BLOOD
1. TAKE BLOOD 2 CC TEG STARTED
2. PLACE BLOOD INTO CUVETE TO THE LIMIT SIGN
3. DROP PISTON COVER UPPER THE BLOOD WITH
PARAFIN
4. WAIT THE RESULT 2 HOURS WILL BE FORMED A
GRAPHIC
5. DEFINITE T, k AND Ma USING TEG METRE
PISTON
TEST RESULT PATERN T E G
Thrombelastography pattern in hemostasis defect (Franz & Coetzee, 1981)
Normal
Hemophilia
Thrombocytopenic
Hyperfibrinolysis
Hypercoagulation
r = normal
k = normal
m.a. = normal
r = longer
k = longer
m.a. =smaller / normal
r = normal
k = normal/longer
m.a. =smaller
r = normal
k = normal/longer
m.a. = normal/smaller
Regularly become small fastly
r = shorten
k = shorten
m.a. = bigger
1. TEG NORMAL PATTERN
TIME - r = REACTION TIME (W T)
FROM THE FIRST POINT AMPLITUDE 1MM
IDENTIC TO COAGULATION TIME
TIME k = ( W k )
TIME FROM FINAL W r - AMPLITUDE 20 MM
m .a = MAXIMUM AMPLITUDE
THE BIGGEST DEVIATION MEASURED IN mm
m . e = MAXIMUM CLOT ELASTISITY MEASURED
BY FORMULA :
m . e = ___________

r k
2
0

m
m

m
.

a

100 X a
100 - a
NORMAL : NATIVE BLOOD CYTRATE
r = 12 MINUTES r = 4 MINUTE
k = 6 MINUTE k = 2 MINUTE
m.e = 90 150 m.e = 100 - 160

R LONGER = - COAGULATION FACTOR DEFICIENCY
K LONGER = - THROMBOCYTOPENIC
- THROMBASTHENIA
- HYPOFIBRINOGENEMIC
- FIBRINOLYSIS activity increase
M. A SMALLER = - THROMBOCYTOPENIC
- THROMBASTHENIA
- HYPOFIBRINOGENEMIC
( < 100 mgr%)
N . fibrinogen : 200 400 mgr%
- F xiii decrease
r k
m
.

a

2. THROMBOCYTOPENIC PATTERN
r = normal
k = normal /longer
m.a. = smaller
3. HYPERFIBRINOLYSIS PATTERN
r k
r = normal
k = normal
m.a. = at first normal
suddenly become small
r k
4. HEMOPHILIA PATTERN
r = longer
k =longer
m.a. = normal/smaller
m
.

a

5. HYPERCOAGULATION PATTERN
r k
r = shorten
k = shorten
m.a = bigger