تجميع اسئله الاخصائين 1

shadoy@windowslive.
com

1

-It is Formation of different blood cells (RBCs-WBCs-PLATELATE).
- Site: Red Bone Marrow in all bone of children (Yolk sac), But in adult restricted to
Central Skeleton (skull, sternum. rib, hips, and vertebra).
* Factors Necessary For Erythropoiesis (Formation of RBCs):
1-Erythropoietin hormone. 2-Iron
3-Vit B12 4-Folic Acid
5-Ascorbic Acid (Vit C) 6-Vit B6 (Pyridoxine)
7-Amino Acid.
* RBCs: Red color, un nucleated, biconcave shape.
-About 1% of RBCs per day are Breakdown, Life span 120 days.
Function of RBCs:
Transport Oxygen + CO2 + Hormone + Enzyme +Vitamins + Nutrients
*Reticulocytes:
-It is immature RBCs.N.R 0.5-3% and stained by Brilliant Cresyl Blue.
Reticulocytosis:
1-hemorrhage. 2-megalobastic anemia 3-hemolytic anemia.
Reticulocytopenia:
1-B.M suppression (by drugs). 2- B.M failure (aplastic anemia).
*Erythrocytosis: (Increase in RBCs count with physiological causes):
1- High altitudes. 2- Physical training.
3- Drugs. 4- Smokers.
*Polycythemia:
-It is increased RBCs count, Hb, and PCV with Pathological causes.
-The Increase of RBCs is not by physiological causes.
Types of polycthemia:
1-Primary polycythemia. 2-Secondary polycythemia.
3-Relative polycythemia.
Relative polycythemia:
-It is due to decreased plasma volume with normal RBCs count.
-Relative increase PCV but normal WBCs and Platelets.
e.g: Burns, diuretic ttt
*Erythrocytopenia: -Decrease in Red Blood Cells count by:
1- Hemorrhage 2- Hemolysis
3- Lack substance needed for RBCs Production.
4- Chemotherapy or radiation 5- Leukemia.

shadoy@windowslive.com

2
*Parameters of CBC (Complete Blood Count):
- Hemoglobin: Hb(13-17 g\dl) = PCV/3
- Hematocrite: HCT (40-50% )
- Mean cell volume: MCV (80 100 FL) =PCV/RBCs
- Mean cell hemoglobin weight: MCH (27 33 pg) =Hb/RBCs
- Mean cell hemoglobin concentration: MCHC (32 36 %) =Hb/PCV
* Alteration in Size of RBCs:- anisocytosis.
* Alteration in Shape of RBCs: Poikilocytosis
*Hemoglobin(Hb):
-Consist of 4 Protein (94%) + 4 Heme groups (6%)
Hb F: Most found in children70% and 2% only found in adult.
2 chains and 2 chains.
-Cannot be estimated by alkaline hematine method. Dilution 1/200
Hb A: Most found adult 96 %.
Hb A2: found in adult 2 %.

Hb S: found in sickle cell anemia.
Hb H: found in alpha thalassemia with 3 deletions of alpha chain.
Hb C:
Hb E:
Hb D:
Hb Bar: found in alpha thalassemia with 4 deletions of alpha chain.

*ESR (Erythrocyte Sedimentation Rate):
-Pipette used for it called Westergen's pipette.
N.R: Male < 15 mm\hr Female < 20 mm\hr
*ESR Depends on:-
1- Plasma protein change. 2- Hb Concentration.
3- RBCs changes.
*ESR Very High (100 mm\hr) the pathognomonic of:
1-Malignancy 2-Autoimmune disease (SLE)
3-Active T.B 4-Myeloma 5-Rheumatic Fever
* Diseases associated with normal ESR:
1-Polycythemia 2-viral diseases
3-Sickle cell anemia 4-congestive heart failure


3
*Leucocytosis: increased in WBCs count.
*Neutrophilia: increased in neutrophil count
Causes:
-physiological:
1-Pregnancy 2-After exercise 3-Lactation. 4-Neonates (new borne).
-pathological:
1-Acute pyogenic infection (Bacterial) 2-Hemorrhage or hemolysis
4- CML 5-Polycythemia rubra vira
3-Trauma or surgery 6-Dohle bodies seen
*Eosinphilia: increased in eosinophil count.
Causes:
1-Allergy 2-Parasitic infestation
3-Steven'sjohnson syndrome. 4-Dermatitis
5-Loffler's syndrome 6-Hodgkin's disease
*Lymphocytosis: increased in lymphocytic count.
Causes:
-Physiologic: 1-infants 2-children
-Pathological:
1-Viral infection 2-T.B
3- CLL 4-Whooping cough (Bordetella pertussis)
5-Infection mononucleosis- CMV (detect by pual bunnel test)
*Monocytosis: increased in monocyte count.
Causes:
1-Infection (TB) 2-Typhoid fever. 3-Hodgkin's disease.
*Leucopenia: Decreased in WBCs number.
*Neutropenia: Decreased in neutrophil count.
Causes:
1-Drugs: cytotoxic drugs 2-Immune: SLE 3-X-Ray
4-Infections: a-Viral: hepatitis b-Bacterial: TB
*Lymphopenia: Decreased in lymphocytic count.
Causes:
1-Infections: HIV 2-Drugs: cytotoxic drugs
3- Radiotherapy 4- Immune: SLE
5-Cushing's syndrome 6- Hodgkin's disease


4
-It is reduction in the amount of circulating Hb, RBCs or both.
General Classification of Anemia:4
A-Microcytic anemia: (MCV less Than 80 FL)
1- Iron deficiency anemia. 2-Sideroblastic anemia.
3-Anemia of chronic disorder. 4-Lead poisoning. 5-Thalassemia.
B-Macrocytic: (MCV more than 100 FL)
1- Megaloblastic anemia (Pernicious anemia, Folic acid deficiency anemia).
2- Alcoholism.
C-Normocytic anemia: (MCV is Normal 80-100 FL)
-Aplastic anemia (AA).
D-Hemolytic anemia:
A-Congenital hemolytic:
1-Membrane defect: (Hereditary Spherocytosis, Hereditary eliptocytosis).
2-Enzyme defect: (G6PD deficiency).
3-Hb defect: (Sickle cell anemia, Hb pathies).
B-Acquired autoimmune hemolytic anemia
- AID, SLE, Blood group incompatibility.

A-Microcytic anemia:
-All are microcytic hypochromic in P.B.P except sidroplastic may be dimorphic
picture (normocytic normochromic or microcytic hypochromic).
-Hb, PCV, MCV, MCH are reduce in all and MCHC is normal (not affected) in all.
1-Iron deficiency anemia:
-It is the commonest anemia in the world.
-Iron deficiency develop slowly and symptoms only seen when Hb <8g/dl.
-The Iron store in liver in the form of Ferritin and Hemsiderin.
- Ferritin circulated in plasma but hemsiderin cannot enter the circulation only in liver.
-Cause plumer vinson syndrome and pencil cells shaped may target cells.
Diagnosis:
1- Microcytic Hypochromic (MCV< 80FL), (MCH<27pg).
2- S.Iron (N.R 60-190 ug) and S.Ferritin are decrease.
3-TIBC is increase. 4-Free erythrocyte protoporphyrin is increase.
5-Percentige saturation of transferrin is decrease. N.R 35-40%.
6- Erythropoiesis is normoblast. 7-Target cells.
8-Decreased or absent of hemosiderin stained by Prussian blue stain to give golden
brown and blue granules.


5
2-Sidroblastic anemia:
A-Hereditary Sidroblastic anemia: related with chromosomal abnormalities.
B-Acquired Sidroblastic anemia: due to chemical or drugs.
-The defect in protoporphyrin due to deficiency of delta amino lesulimik synthetase
enzyme which responsible for synthesis of protoporphyrin. Lead to decrease
protoporphyrin and increase S.iron.
*Sidrocyte: Mature RBCs containing non heam iron but cannot appear in PBP
because it removed by spleen.
*Sidroblast: Immature RBCs in B.M.
-Type I:
-Contain iron but cannot utilize for Hb synthesis. Hb is normally synthesis in this type.
-30-40% normally found in circulation.
- Type II:
- Contain iron but cannot utilize for Hb synthesis. Hb is normally synthesis and iron in
this type more than type I.
-Type III:
- Contain iron but cannot utilize for Hb synthesis.
-Hb is abnormal and iron form granules around the nucleus called ring sidroblast.
Diagnosis:
-The diagnosis is closely opposite to iron deficiency anemia except dimorphic picture
present only in sidroblstic anemia (normcytic normochromic or microcytic).

3-Anemia of chronic disorder:
-Characterized by decrease releasing of iron from macrophage to plasma and so to
erythroblast.
-Causes:
1-Chronic inflammatory disease such as T.B, rheumatic arthritis & SLE.
2-Malignant disease such as carcinoma, lymphoma & sarcoma.
- Diagnosis: -Elliptocyte short, sharp projection VI
1-S.iron decrease. 2-TIBC decrease.
3-S.firritin increase (Fe is present but cannot able to reach circulation).
4-Percentige saturation of transferring is Normal. (S.Transferrin)
5-Free protoporphyrin Increase.

4-Lead poisoning:( (
-Lead to hemolysis of RBCs due to poisoning and patients are usually death before
diagnosis in the lab.


6
5-Thalassemia:
-The defect of thalassemia occurs in globins gene.
1-Alpha thalassemia:
-The defect in alpha globins gene due to deletion of 1 or 2 or 3or 4 alpha globins gene.
-Deletion in one gene called Silent carrier.
-In 2 gene called alpha thalassemia trait: (RBCS Increase).
-In 3gene called Hb H disease or beta 4: (golve ball inclusion bodies).
-In 4 genes called hydrofetalis Hb or Hb Bar disease (4 gammas): the patient
is in compatible for live due of 4 gama are high affinity to oxygen.
-The symptoms of this are depend on the number of gene deleted.
2-Beta thalassemia:
-The defect in beta globins gene.
A-Beta thalassemia major (Coolys anemia):
-Homozygous.due to total absence of beta globins gene production or the beta globins
gene are present but not functional.
B-Beta thalassemia minor:
-Heterozygous carrier and usually no clinical symptoms.
Diagnosis of Thalasemia:
1-All are Microcytic Hypochromic.
2-Sever anemia Hb 2-3g/dl in Coolys anemia.
3- Defective in Hb F (more than 70% or 90% in Hb electrophoresis test).
4- Absence or decrease of HbA.
5-Basophilic stippling(RNA remnant). 6-nucleated red cells. 7-Target cells.
8- S.iron, S.ferritin, TIBC, Free protoporphyrin and percentage saturation of transferrin
are normal because the defect in globins gene not in heam.

B-Macrocytic: (MCV more than 100 FL)

1-Megaloblastic anemia
- Due to deficiency of Vitamin B12 or Folic Acid or both.
- Function of Vitamin B12 and Folic Acid:
-It is important in formation of DNA & RBCs.
A-Pernicious anemia:
-Causes due lack of Intrinsic factor or gastrictomy.
- I.F transport Vit B12 from stomach to the site of absorption (terminal Ilium).
-Transcoblamin 1(alpha globulin-not effect-granulocyte) or Transcoblamin 2(Beta
globulin-V.I) transport Vit B12 from terminal Ilium to B.M for uses or to the site of
storage in liver.
-Cause Neurological symptoms. Howell-jolly (DNA remnant) bodies and Cabot ring
in severe cases. -Diagnosis by Schilling test.


7
Vit B12:
-The daily requirement of vit B12 in the body is 2ug. N.R=3-5 mg.
-Any deficiency in vit B12 with normal I.F called megablastic anemia
- Vit B12 synthesis by M.O inside the body but cannot absorb by body.
-It is a disease of later life usually age of > 40 years.
- Vit B12 store mainly in liver called adenocylecobalomin.
- Vit B12 in plasma called methyl coblamin.
-Diphylobothrium latum parasite cause Vit B12 deficiency because it is taking up
from blood and cause megablastic anemia due to this.
B-Folic acid deficiency anemia:
-The daily requirement of folate in the body is 100-200 ug.
-Cause macrocytic anemia due to Folate deficiency.
-Absorption in duodenum and upper duodenum.
- Folate in plasma called methyl tetrahydroflate monoglutamate.in RBCs and liver
called methyl tetrahydroflate polyglutamate.
-Not cause Neurological symptoms and sore tongue.
Diagnosis of Megaloblastic anemia:
1- Macrocytic anemia (MCV more than 100FL)
2- Decreased Serum Level of Vit B12 or Folic Acid.
5-Pancytopenia + hyper segmented neutrophil. V.I
3- Horse shoe shaped cell. 4- Reduce red cell life span.
2- Alcoholism:
-Any liver disease cause round macrocytic anemia not megablastic.

C-Normocytic anemia: (MCV is Normal 80-100 FL)

Aplastic anemia(AA):
-It is pancytopenia due to Bone Marrow failure or decrease B.M production.
Causes:-
A- Congenital: fanconi's anemia defect in DNA.
B- Acquired: Idiopathic
1- Drugs (chloroamphinicol). 2- Chemical: Benzene 3- Radiation
4- Viruses: (hepatitis C, Epstein-Barr virus)
Diagnosis of aplastic anemia:
1-Normocytic normochromic or macrocytic 2-Pancytopenia.
4- marked increased of erythropoietin hormone level in serum and urine.
6-Neutrophil alkaline phosphates Increase. 5- Enlargement of spleen.

*Pure red cell aplasia: -Affect only the erythropoietin cells.
-patient with aplasia have anemia + reticuloculocytopenia with normal WBC and
platelet count.


8
D-Hemolytic anemia:
Clinical feature of hemolytic anemia:
1- Normocytic normochromic except MCHC is normal or increase in
Spherocytosis.
2- Reticulocytosis (Erythroid hyperplasia).
3-Splenomegally except in Sickle cell anemia is Atrophy. V.I
4- Haptoglobin decrease. (Alphaglycoprotin) react with free Hb.
5-Pollar and mild jaundice.
7- Fragmented cells + Schistocyte. V.I
8-Ostomatocyte and acanthocyte.
9-Hemoglobinemia: free Hb in circulation.
-Plasma hemopoxin react with free Hb converted to mess Hb then dissociated.
-Any inclusion body not appear in circulaton because it removed by spleen.

1-Hereditary Spherocytosis:
-The defect in cell membrane proteins (Spectrin) either:
Quantitative: due to decrease amount of cell membrane proteins (Spectrin).
Qualitative: the proteins (Spectrin) is present but not functional.
Any defect in cell membrane proteins cause release of membrane lipid and lead to
decrease surface area. (Spherocyte).
Diagnosis of Spherocytosis anemia:
1-Spherocyte lacks the central parel.
2-Osmatic fragility test increase. V.I
3-Acidified glycerol lysis time.

2-Hereditary Eliptocytosis:
-Same of spherocytosis but deferent in PBP appear as eliptocytosis.

3-G6PD deficiency anemia (Favism):
-It is sex linked disorders due to defect in enzyme of G6PD.
-Any sex linked disorders carrier in female and diseases in male.
-Type B is common type.
-The defective gene is present on the chromosome X, mainly seen in males.
-Female heterozygous G6PD deficiency can resistant the malaria falciprum.
-G6PD deficiency leads to NAPPH deficiency lead to precipitation of Heinz body.
-Heinz body stained by supravital stain.
-Pyruvate Kinase deficiency: lead to G6PD deficiency must be homozygous.
-Special test is enzyme level for G6PD and collected in EDTA anticoagulant only. V.I.
FAVISM:
-It is acute hemolytic anemia result from G6PD deficiency, usually effect children and
combined with Hb urea.
-Causes see Heinz bodies in the peripheral red cells.


9
4-Sickle cell anemia (Drepanocytes):
-Caused by substitution of one aa (valine) instead of glutamic acid at position No 6 in
the Beta chain of Hb resulting in abnormal HbS.
-Sickle cell causes atrophy of the spleen, not cause spleenomegaly.
-Sickle cell trait in heterozygous.
-ESR reduced only in hemolytic anemia.
Tests For diagnosis of Sickle cell anemia:
1- Sickiling test.
2-Hb solubility test +ve.
3- Hb electrophoresis (Hb A, Hb S, Hb F).
-Hb S and Hb- ---are migrated as the same strand in electrophoresis.

5-Hb pathies:
-It is condition due to qualitative defect in globins polypeptide chain.
Classified into 3groups:
A-Due to structure variant of Hb:
1-Single aa substitution: eg: Hb S, Hb C, Hb E, Hb D.
Hb C:
-Caused by substitution of one aa (Lysine) instead of glutamic acid at position No 6 in
the Beta chain of Hb resulting in abnormal Hb C.
V.I . Target cells are Prominent in Hb C -
-In soluble and less soluble than Hb A.
-Blood incubation with 3%Nacl in W.P at 37 C.
-Wet preparation
-Hb C, Hb E, Hb A2 at the same position in electrophoresis technique.
-Hb C trait no anemic, Target cell.
Hb E:
-Caused by substitution of one aa (Lysine) instead of glutamic acid at position No 26
in the Alpha chain of Hb resulting in abnormal Hb E.
Hb D:
-Caused by substitution of one aa (Protamine) instead of glutamic acid at position No
121 in the Alpha chain of Hb resulting in abnormal Hb D.
2-Multi aa substitutions:
Eg: Hb bar
B-Due to failure synthesis of Hb normally:
Eg: Beta talassemia
C- Due to failure to complete new switch from Hb F to Hb A.

*Hb pathies abnormality due to change in behavior of Hb may be due to aggregation,
insolubility, high O2 affinity and instability (release of aa lead to precipitation and
denaturation of globins in side RBCs and RBCs become abnormal).


10
6-Autoimmune Hemolytic anemia:
-It is group of hemolytic anemia result from Ab direct against self antigens.
-eg: IgG, IgM less common, IgA and some bind complement.
-It classified according to Temp and according to etiology.
A-according to Temp in to worm Ab and cold Ab:
1-Worm Ab:
-IgG react at 37C. Most are anti Rh antigen.
2-Cold Ab:
a-Cold hemoaglutination disease:
-It is IgM react in 4 C. Most are anti i and anti I.
b-Paroxysmal cold Hb urea (PCH):
-IgG react in 4 C. Anti D
B-According to etiology:
-Idiopathic or secondary.
Lab diagnosis of worm Ab AIH:
-Hb, PCV decrease. WBCs, Plt normal. MCV mild increase, MCH, MCHC normal.
-In PBP spherocytosis and reticulocytosis. -polychromasia.
-To differentiate between spherocytosis in AIH and in hereditary make DAT is +ve in
worm AIH anemia.
-Direct comb test is +ve in all hemolytic anemia. V.I
-S.folate and cell folate are decrease.
Lab diagnosis of cold PCH:
-Donald Landsteiner Ab test:
-It is special test for Hb urea.
*Relation between erythroid hyperplasia and reduced M/E ratio:-
-M/E ratio is: ratio between number of cell of neutrophile series and the number of
erythroblast in the bone marrow. Normal range: 2:8
- Reduction of M/E ratio is taken as evidence of erythroid hyperplasia.


11
-It is the substance remains inside the RBCs.
-All inclusion bodies are stained by supravital stain.
-All inclusion bodies are stained by Wright Giemsa stain except reticulocyte and
Heinz bodies.
-All inclusion bodies are not stained by iron stain except pappenheimer bodies.

1-Heinz bodies:
-Nature of globins chain precipitate in side RBCs and stained by supravital stain.
-Found in hemolytic anemia in G6PD and megaloblastic anemia.
2-Howell jolly bodies:
-It is DNA or nucleus remnant and stained by supravital stain.
-Found in megaloblastic anemia and sickle cell anemia.
3-Pappenheimer bodies:
-Abnormal accumulation of iron granules and stained by perls Prussian and
Rowmansky stain.
-Found in sideroblastic anemia.
4-Hb H inclusion:
-Precipitate of Hb in side RBCs and stained by supravital stain.
- Found in thalassemia.
5-Basophilic stippling:
-It is RNA remnant and stained by any stain.
-Found in megaloblastic anemia and thalassemia.
6-Cabot ring:
-Through to be remnants of mitotic spindle.
-Found in megaloblastic anemia and myelodysblastic syndrome.
7-Reticulocyte:
-Immature RBCs contain precipitated RNA and stained by supravital stain (new
methylene blue).
-Found in hemolytic anemia.


12
-It is malignant proliferation of hematopoietic cells characterized by abnormal
accumulation of WBCs in B.M and peripheral blood.
Causes of leukemia:
1-unknown causes. 2- Ionizing radiation.
3- Drugs and chemical. 4- Genetics. 5- Retrovirus.
6- Immune states.
Classification of leukemia:
A- Acute leukemia: (high malignancy).
- It is malignant proliferation of Immature hematopoietic cells (blast cells).
1-AML:
- Most common in adult. With Auer rods.
-have 8 subtypes from m0 to m7.FAB
2-ALL:
-Most common in children.
-have 3 sub types L1, L2, L3. FAB (French American British) V.I
B-Chronic leukemia: (Low malignancy).
-It is malignant proliferation of mature and immature hematopoietic cells.
1-CML: (40 -60)
-Most common in adult and diagnostic by Philadelphia (Ph)-chromosome.
- Philadelphia chromosome due to cross link between long arms of chromosome 9
with long arm of chromosome 22.
-Neutrophil alkaline phosphates (NAP) are decrease.
2-CLL: in >50year (50-60)
-It is accumulation of abnormal lymphocyte in B.M and peripheral blood.
-Smudge cell character in peripheral blood.
Leukomoid reaction:
-Leucocytosis characterized by presence of Immature cells and high neutrophil
alkaline phosphates (NAP).
Causes: 1-Malignant tumor 2-Acue infection
2-Acute hemolysis. 3-Burns PP.
-It is classified into granulocytic LR and lymphocytic LR.
Different between LLR and CLL:
LLR CLL
1-occur in >40 year and in children also in >50year
2-No hepatospleenomegaly hepatospleenomegaly
3-by infection virus, T.B. No infection
4-Typical lymhopathy No


13


14


15
-It is the mechanism by which the blood is kept in fluid state inside the blood vessels.
Function of homeostasis:
A-To stop blood bleeding by:
1-Blood vessels. 2-Platelets. 3-Coagulation factors.
B-To prevent thrombosis by:
1-Blood flow. 2-Inhibitors 3-Fibrinolytic system. 4-Platelets (some time).
1-Blood vessels (B.V):
-Intima of B.V consists from endothelial (non thrombogenic layer) and sub endothelial.
-The sub endothelial layer contain:
1- -ve charge collagen which responsible for activation of Plt and C.F.
2-Elastic fiber 3-Protoglycan or glycoprotein.
Functions of endothelial layer:
1-Produce angiotensin II (vasoconstriction).
2-Produce Vonwillebrand factor (VWF) (50% carry factor VIII in the circulation and
50% enter the sub endothelial layer to adhesion of plt with endothelial cells).
3-glycocaylx contain heparin sulphate which activating antithrombin III (strong
inhibiter) to inhibit IIa, IXa, Xa, XIa
4-Produce prostacyclin to prevent Plt aggregation in normal condition.
5-Contain receptor thrombomodulin which bind with thrombin to activate protein C
to inhibit factor Va, VIIIa.
6-Thrombin activate endothelial to produce plasminogene.
7-Synthesis protein S which is cofactor for protein C.
2-Platelete (Plt):
-Discoid, non nucleated and formed in the B.M by megakaryocytic.
-Life span is 10 days and N.R 150000-450000/L.(contain actins, mycin)
The cytoplasm of Plt contains 3 types of granules:
1-Dense granules: contain ADP, ATP, and Serotonin, calcium when release in
circulation act as agonist.
2-Alpha granules: produce PDGF to act on B.M to increase production of Plts.plt
factor 4 anti heparin. -VWF present also in plts.
3-Lysosomal granules: produce lysosomal enzyme which help in destruction of
any invading M.O and hence the Immune response.
Functions of Plt: formation of haemostatic plug at the site of damage by:
1-Adhesion 2-Release reaction 3-aggregation by glycoprotein 2B,3A.
4-procoagulant activity: -contain activation for factor XI.
-Source of tissue thromboplastin and phospholipids.


16
-Plt contains TXA2 vasoconstriction, agonist (short life span 1min) not present
normally.
3-Coagulation factors (C.F):
-It is plasma protein circulate in active form called pro-enzyme.
-All C.F produce by liver except VIII are produce by endothelial cells.
Classification of C.F based on functional and biochemical properties into 4 groups:
1-Vit K dependant C.F :(gama carboxylic acid in terminal by vit K).
-Factor II, VII, IX, X, Protein C and S.
-Warfarin is oral anticoagulant which stop the activity of Vit K (PIVKA state) Vit K
is present but not functional.
2-Contact factors:
- Factor I, XI, XII, Prekallekerin. HMWK.
3-Thrombin sensitive factors:
-Factor I, V, VIII, XIII.
4-Labile factor:
-Factor V, VIII
- Factor VIII circulates in combination with VWF (8-12Hrs).if not 1-2min.
Activation of C.F by 3 pathways:
1-Internsic pathway:
-Contain ve charge collagens fiber, XII, XI, IX (VIIIa+Ca+phospholipid) called
teanase enzyme, X.
2-Externsic pathway:
-from out circulation Contain Tissue thromboplastin (damage tissue+plat), VII, X.
3-Common pathway:
-Contain X, Prothrombinase enzyme(Va +Ca+ phospholipids), prothrombin II,
thrombin IIa, fibrinogen I, Fibrin Ia(monomer).
-Thrombin IIa activate V to Va and VIII to VIIIa and XIII to XIIIa. And also
activate protein C, S. system inhibitor.
- Ia(monomers) polymerization by the action of XIIIa to Ia(polymers).
-Plts has receptor called fibrinogen receptor attach to Ia polymers to form secondary
haemostatic plug.
Type of Inhibiters:*******************************************
1-Blood flow. 2-Serine protease 3-fibrinolytic system.
Test used to asses haemostatic mechanism:
A-Bleeding time (BT):
-This test depends on platelets and B.V (capillary fragility).
1- IV method: normal 1- 4 min with IVY method.
2-Dukes method: normal 2-6 min.
3-Standraized template method: normal 2-6 min.


17
B-Clotting Time (CT):
-Screening test for all C.F I XIII except VII. (glass test tube)****************
-Used whole blood clotting time with water path at 37. Normal time = 3 9 min.
C-Plasma clotting time:
-Include: PT, PTT, and TT.
1-Prothrombin time (PT):
- Screening test for Extrinsic and Common pathway.
-Consist of 2 factors: a-Tissue thrombo blast with acetone to remove portion of
phosholipid and Cal2 b- VII
- It is prolonged when deficiency of ( I , II , V , VII , X ).
- Sensitive special to deficiency of (V, VII, X).
- We measure PT by adding thromboplastin, Calcium to activate extrinsic path way.
Prothrombin ratio % = PT of test
PT of control
-International Normalized Ratio (INR) = PT of test
Or Sensitivity of reagent (IST) PT of control
-Prolong: defect in liver or Vit K deficiency or oral anticoagulant.
- This test used for control or anticoagulant treatment (warfarin).
-Normal time = 10 15 sec
2-Partial thromboplastin time (PTT,APTT,KCCT):
- Screening test for Intrinsic and Common pathway.
-Consist of 6 factor (XII (Prekallerin, HmwK), XI, IX, X, II, I)V.
-It is prolonged when there is deficiency of factor (VIII-IX).
-When VIII deficiency it causes: hemophilia A (Von willebrand disease)
-when IX deficiency it causes: hemophilia B (Christmas disease)
We measure PTT by adding:
1- kaolin (KCCT) 2-Phospholipids 3-Calcium.
- Normal time = 30 40sec.
-This test used for control or anticoagulant treatment (heparin).
3-Thrombin time (TT):
-Screening test for fibrinogen (detect defect or deficiency of fibrinogen).
-It is prolonged when there is deficiency of fibrinogen I and presence of heparin.
- Conversion prothrombin to fibrinogen by adds thrombin. From outside the body.
-Normal time = 10 20 sec.heparin, SDP,-------,#########################
D- Clot solubility test:
-Specific test for XIII.
-Use 1% of monochloroactic acid.
-Fibrin polymers: clot remains for 2hrs without dissolving.
-Fibrin monomers: clot dissolved < 2hrs (XIII deficiency).


18
*Antithrombin III: VI
-It is strong inhibitor mainly inhibit IIa, IXa, Xa, XIa.
-It is potentiated by heparin.
*There is 6 factors should be known:
1-VIII anti-hemophilic. 2- IX Christmas.
3- II prothrombin. 4- IIa thrombin.
5- I fibrinogen. 6- Ia fibrin.
*Protein C and protein S:
-Protein C is protease and degrades Va, VIIIa.
-Protein S is potentiated and effect of activated protein C.
*Some convert of factor: V.I
-Plasminogen converts to plasmin by:
1-kallikarin (most strong). 2-Urokinase 3-Streptokinase.
-Fibrin converts to fibrin degradation product by plasmin.
-Fibrinogen to fibrin by thrombin.
*Anticoagulant drugs: VI
-Most common 2 drug heparin and warfarin.
1-Heparin:
-It is acidic mucopolysaccaride and does not cross placenta.
-It is potentiates action of anti thrombin III to inhibit IIa, IXa, Xa, XIa.
-Overdose of heparin cause hemorrhage managed by stopping heparin and giving
protamine sulphate.
-Controlled and monitoring of heparin treatment by PTT test.
2-Warfarin:
-It is Vit K antagonist and cross placenta.
-Cause hemorrhage managed by stopping warfarin and infusing fresh frozen plasma
and give Vit K.
-Controlled and monitoring of warfarin treatment by PT test.

Disorder of haemostatic mechanism:
-Due to bleeding tendency or thrombosis.
-In bleeding tendency the defect in primary H-disorder (B.V, Plts) or secondary
H-disorder (C.F).
-In thrombosis the defect in Inhibitor or fibrinolytic system.
1-Primary H-disorder: divided in to:
A-Disorder of vascular H:
-Mainly congenital due to elastic fiber deficiency, collagen deficiency or acquired
due to damage of B.V resulting of increase vascular permeability.
-It is diagnosis by clinical no specific test.


19
B-Platelets Disorder: either:
1-Numerical disorder:
-If the Plts < 50.000 cell/cum the bleeding occur.
-If the Plts < 10.000 cell/cum the bleeding occur spontaneously.
2-Funtional disorder: either:
1-Congenital: due to chromosomal abnormalities and divided into:
Receptor defect, enzyme defect, granules defect.
2-Acquired: such as: Aspirin, heparin, multiple myeloma, myelofibrosis.
-Aspirin Inhibit Cyclo oxygenase enzyme lead to decrease TXA2 (agonist).
-Test used for primary H-disorder called Hiss test or tourniquet test: N.R < 20 dotes
2-Secondary H-disorder (C.F): either:
A-Congenital disorder:
-Always deficiency in simple C.F such as:
1-Haemophilia. 2-VWF disease. 3-Fibrinogen disorder.
B-Acquired disorder:
-Deficiency in multiple C.F such as:
1-DIC 2-Liver disease 3-Vit K deficiency.

1-Hemophilia A:
-Congenital deficiency in VIII called Classical hemophilia most sever in Royal
disease.
2-Hemophilia B:
-Congenital deficiency in IX called Christmas disease.
3-Hemophilia C:
-Congenital deficiency in factor XI.
4-Para hemophilia:
-Congenital deficiency in factor V.
-Hemophilia A and B are inherited as sex linked recessive.
-Male ---------hemophilia 50%normal 50%heamophilic
-Female-------carrier 50%normal 50%carrier (daughter)
-N.R: OF factor:
************** *** VWF, VIII, IX, XI, XIII. ontain C : Cryoprecipitate *

*FFP contain:*************************************


20

: (direct) orward grouping *F
-Detecting ABO grouping by using the cells (RBCs) of the patient.
: (indirect) everse grouping *R
-Detecting ABO grouping by using the serum of the patient.
- = blue = A sera - The color of anti -
- == yellow B sera - the color of anti
- == gray D sera - the color of anti
V.I differentiated by Lectin react only with A1. anti A1 ) A2 20% A1 80%, (
immune response. specific substance capable of inducing : *Antigen
-Blood group Ag is attached to cell membrane.
Antibody Ab (Immunoglobulin (IG):
-are the proteins that synthesized by B-lymphocyte.
: Class of antibody -
1-IgG.(lowest M.W) 2- IgM(highest M.W) 3- IgA. 4- IgD. 5- IgE.
ABO blood group system: *
-The most blood group system.
- Essential for prevent of hemolytic transfusion reaction.

Antibody
(AB)
Antigen (AG) GROUP
B A A
A B B
------ AB AB
AB ------- O

. ve - O : Universal donor *
. +ve AB : Recipient donor *
Compatible donor blood Recipient ABO
group
A O A
B O B
AB A B O AB
O O


21
. e c E D - C are: Ags 5 contain *Rhesus group:
in this group. antigens most is ntigen D: A -
-The presence or absence of D-antigen determine if Rh +ve or Rh ve.
- Fisher race terminology is used to describe Rh antigen.
- If D antigen found Rh is positive (85%).
- If D antigen not found Rh is negative (15%).
- Du antigen is weak type of D antigen.

*Other blood group system:

system: kell blood group - 1
-kell Abs are IgG, they can cause hemolytic disease of newborn.
Duffy blood group system: - 2
-Duffy Abs are IgG, they can cause HDNand detect malaria parasites.
Kidd blood group system: - 3
-Kidd Abs are IgG, they can cause hemolytic disease of newborn.
6. Chromosome are controlled by the : HC M or HLA antigen *

. cord cells except all red cell with reacting it is : I Anti *
. cord cell with reacting it is : i Anti *
- That means we can differentiate between anti I & anti i by cord cells.

- ): Antiglobulin test (AHG *
- Antibody is gamma globulin.
- Most incomplete antibodies are IgG (worm Ab).
-AHG serum contains Anti-IGg and Anti C3.*****************************
- AHG serum used by most labs for pre-transfusion IAT Anti-IgG.
-when doing DAT to detect in vivo sensitization with IgG or C3.

*Anti-human Immunoglobulin:
1-Coombs test. 2-Anti-Ab = anti-antibody. 3-Anti-IgG.
: * Direct and indirect antiglobulin test (coomb's test)
-Binding of IgM to red cell is usually cause agglutination and IgG bind to red cell is
not cause agglutination.
-IgG can be detect by antiglobulin test (coomb's test).
irect antiglobulin test (DAT): D - A
-Used to detect sensitized RBCs in patient blood.
pplication of DAT: A
1- Hemolytic disease of newborn.
2- Autoimmunohemolytic anemia
3- Drug induced hemolytic anemia
4- Transfusion reaction.


22
): Indirect antiglobulin test (IAT - B
-Used to detect sensitized antibody in patient serum.
-The RBCs are washing several times to remove unbounded proteins (IGg).
- Application of IAT:
1- Cross matching.
2- Antibody Screening.
3- Phenotyping.
- : Cross matching *
- Types of cross matching:
Donor red cells o determine compatibility between T : Major cross matching - 1
and patient serum (plasma).
and Donor serum determine compatibility between To Minor cross matching: - 2
patient red cells.

Common causes of false positive in both IAT and DAT: *
1-Cold agglutination.
2-Rouleaux.
3-Reagent contamination.
4-Antibody low incidence antigen.
5-Human errors.
Common causes of false negative in both IAT and DAT: *
1-Failure to add antiglobulin reagent. (Anti Sera).
2-Add wrong antiglobulin reagent (Anti Sera).

(hydroxyl fetalis): Hemolytic disease of newborn (HDN) *
-Can develop when mother Rh negative and Fetus Rh positive during pregnancy.
must be the same group to occur HDN.********************************** -
- Mother Rh -ve administrate Rh immunoglobulin (RhIG) to prevent hemolytic
disease in newborn.

: donor in KSA *Selection of blood
-blood donor must meet the following criteria:
1-age: at least 17 years old.
2- weight: at least 50 kg.
3- Hb: 13-18g /dl.
4- three month from last donation.
5- Blood pressure: 120/70.
6- Body temperature: 37 C
7- Pulse rate: 70/min
e donor reaction: Advers *
1-Syncope (fainting): the most common donor adverse reaction.
2- Nausea and vomiting.
3-Hematoma.


23
Serological test for blood donor: *
1-HIV 1&2 2- HBV
3-HCV 4-HTLV
5-Syphilis. 6- Malaria.
HIV (human immunodeficiency viruses): - A
-the etiologic agent of AIDS
Serological test of AIDS:
1-ELISA
2- Western blot (WB) is confirmatory test.
: HBV (hepatitis B) - B
-Serological test for HBV by ELIZA.
HCV (hepatitis C): - C
Serological test
1- ELIZA. 2-RIBA (confirmatory test).
SYPHILIS: - D
-is complex sexually transmitted disease.
-Serological test:
1-RPR (rapid plasma region).
2- VDRL. 3-TRUST
cell lymphotropic virus): - HTLV (human T - E
Serological test:
1-ELISA 2- Western blot (WB) is confirmatory test
MALARIA: - F
-Diagnosis by THICK FILM.

*Transfusion reaction screening of blood:
Transfusion screening test: -
1- Patient blood group & antibody detection.
2- Donor blood group.
3- Screening of donor blood for infectious disease.
4- Cross matching.
*Anticoagulant and Preservative:
-Anticoagulant used for blood donor bags are:

Expiration Temp Preservative
21 1-6 C 1-citrate phosphate dextrose (CPD)
21 1-6 C 2- citrate phosphatedextrose- dextrose
(CP2D)
35 1-6 C 3- citrate phosphate dextrose-adenine
(CPDA-1)


24
blood bank. in used anticoagulant is most common 1 - CPDA -
The storage time of saline adenine glucose mannitol (SAGM) is 42 days. -
-Citrate: prevent coagulation.
-Phosphate: act as buffer to decrease PH.
- Dextrose: used for ATP generation.
- Adenine: substrate for the red cell to synthesize of ATP.

*Storage of blood component:

Expiration Component Blood

1-6 C Whole blood

1 years (-80C) RBC

5 days(22-25 C) Platelet
1 years (-18 C) Fresh Frozen Plasma FFP

1 years (-18 C) Cryoprecipitate

*Red Cell Component:
RBC (packed red cell): - A
removed. plasma are unit of whole blood with most of the RBCs -
used for hemolytic also symptomatic anemia is the component of choice RBC: -
newborn exchange transfusion.
- RBC can be store by frozen for years by adding Glycerol.
WBCs: - B
-Can be reduced in the whole blood bag by several methods:
1- Centrifugation. 2- Saline washing. 3- Freezing. 4- Filtration.
-Filtration is the best method choice today in blood bank.
Plasma Components: - C
: Fresh Frozen Plasma FFP - 1
Used to treatment for patient associated with: -
1-Clotting factor deficiency.
2-Disseminated intravascular coagulation (DIC).
3-Vit K deficiency.


25
: Cryoprecipitate - 2
-It is cold- Insoluble portion of plasma that precipitates when FFP is thawed between
1-6 C.
-Used to control bleeding associated with fibrinogen deficiency or factor XIII
deficiency.
- Cryoprecipitate also used for treatmentment: -
1-hemophilia A. 2- Von willebrand disease.
: Platelets - D
-Used for treatment of bleeding in patient with thrombocytopenia or platelet
dysfunction.
-Platelets are extremely sensitive to temperature and PH changes.

: Store Temperature for blood components *

Temperature Components
1-6 C 45 days Whole blood
1-6 C Red blood cell (RBC)
1 years (-18 C) Fresh frozen plasma (FFP)
5 days(22-25 C) Platelets
20-24 C Granulocytes
1 years (-18 C) Cryoprecipitate


26
*Thrombocytosis:
-It is increased platelets count.
Types: 1-Primary (essential). 2-Secondary
-------------------------------------------------------------------------------------------------

*Thrombocytopenia:
-Decreased in platelets count
Causes:
1-Aplastic Anemia. 2-Megaloblstic anemia. 3-Malignancy or leukemia
4-Idiopathic thrombocytopenic purpura (ITP).
5-Viral: CMV 6-Drugs

*multiple myeloma:
-Disease arising from malignant transformation of B cell.
-Most common symptoms present are bone pain.
Diagnosis of multiple myeloma:
-Normocytic+ Normochromic: (common)
1-Bence jounce protein present. V.I
2-Thrombocytopenia + neutropenia. 3-increased basophile.
4-Increased red cell 5-ESR high 6-plasma cell high
7-Monoclonal Ig in serum, monoclonal light chain in urine.


27
*Malignant lymphoma:
-Tumor of lymphoid tissue.
*Hodgkin's disease:
-This diseases affect the lymph tissues.
-Large binucleate or multinucleate cell called ReedSternberg cells.
-Affected lymph node contains Epstein Barr virus genome (EBV).
Diagnosis:
1-normocytic + normochromic anemia.
2-high ESR 3- neutrophilia 4-eosinphillia
5-lymphopenia
*NON Hodgkin's disease:
-The etiology is unknown
-This disease associated with patient they have acquired immune deficiency (AIDS).

*Systemic Lupus Erythematosis
(SLE):
-It is Autoimmune Disease affecting many organs.
*Tests of SLE:
- By Detection of anti-body (Abs):
1-Antinuclear Ab (ANA): But not specific test for SLE.
2-Anti-Double Stranded- DNA Ab (Ads DNA): it is specific test for SLE.
* Diagnosis of SLE:
- Blood Analysis: 1-pancytopenia 2-high ESR
-Urine analysis: 1-proteinuria. 2-hematuria. 3-RBCs &WBCs Casts.


28


29
*Anticoagulant:
-The sample of hematological lab must be < 3 hrs in room temp and < 6 hrs in blood
film.
1-EDTA (Sequesterin):
-Used 0.2 mg + 1 ml blood.
-If used >2mg: PCV decrease, MCH increase, Plts increase.
2-Trisodium citrate:
-Used 1ml + 9 ml blood 1:9
-Not used in RBCs count.
3-Heparin:
-Used only in osmotic fragility test and acidified glycerol lysis time in hereditary
spherocytosis and eliptocytosis because is not affect on the shape of RBCs.
-Not used in blood film count because it clumping of leukocyte.
*Blood count:
1-WBCs count:
-Used 2% GAA which lysis RBCs, Plts and stained nuclei of WBCs.
-Dilution 1/20
-Used hemocytometer (chamber) in most blood count.
2-RBCs count:
-Used 1% formal citrate which preserves RBCs and destruction WBCs only.
-Dilution 1/200.
3-PLTs count:
-Used formal citrate.
4-Reticulocyte count:
-By thin blood film stained by methylene blue (supravital stain).
5-Hb:
- by alkaline hematin method except Hb F.
-Dilution by 0.02 ml + 4 ml drabkins solution.
Hb F:
-Cannot be estimated by alkaline hematin method.
-Dilution 1/200.


30


31

- General information about blood bank :

cells ( RBCs ) of the patient. detecting ABO grouping by using the - : forward grouping
serum of the patient. detecting ABO grouping using the - : reverse grouping

- sera A == blue - the color of anti
- sera B == yellow - the color of anti
- sera D == gray - the color of anti

*antigen : substance capable of inducing specific immune response .
* blood group antigen are attached to cell membrane .
* antibody AB (immunoglobulin ) :are the protein that synthesized by B-lymphocyte .
* class of antibody :
1-IgG.
2- IgM.
3- IgA.
4- IgD.
5- IgE.

*ABO BLOOD GROUP SYSTEM :
system . most blood group the -
- essential for the prevent of hemolytic transfusion reaction .

Antibody (AB) Antigen (AG) GROUP
B A A
A B B
------ AB AB
AB ------- O

* universal donor : O .
* recipient donor : AB .

*Rhesus group : contain six antigen are : C- D E c d e .
in this group . most antigen : is antigen D -
-the presence or absence of D-antigen determine if Rh positive or Rh negative
- fisher race terminology is used to describe Rh antigen .
- if D antigen found Rh is positive ( 85%).
- if D antigen not found Rh is negative (15%).
- Du antigen is weak type of D antigen .

COMPATIIBLE DONOR BLOOD RECIPTION ABO
GROUP
A O A
B O B
AB A B O AB
O O


32

*other blood group system :
1- kell blood group system : kell antibody are IgG , they can cause hemolytic disease for newborn .
2-duffy blood group system :duffy antibody are IgG , they can cause hemolytic disease for newborn .
and detect malaria parasites .
3- kidd blood group system :kidd antibody are IgG , they can cause hemolytic disease for newborn .

. Chromosome 6 are controlled by the HLA antigen *

except cord cells it is react with all red cell - : Anti I *
with cord cell . it is react - : Anti i *
cord cells - by : i etween anti I & anti hat mean we can differentiate b T -

*Antiglobulin test ( AHG ) :-
. gamma globulin antibody are -
- most incomplete antibodies are IGg .
-AHG serum contain Anti-IGg and Anti C3 .
- AHG serum used by most lab for pre-transfusion IAT Anti-IGg .
-when doing DAT to detect in vivo sensitization with IGg or C3 .
-Anti-human Immunoglubin :-
1. coombs test .
2. anti-Ab = anti-antibody .
3. anti-IgG .

* direct and indirect antiglobulin test (coomb's test )
Binding of IgM to red cell is usually cause agglutination and IgG bind to red cell is not cause
agglutination .
-IgG can be detect by antiglobulin test (coomb's test )

*the direct antiglobulin test (DAT): test is positive when the patient red cell have sensitized in body .
-application of DAT:
1- hemolytic disease of newborn .
2- autoimmunohemolytic anemia
3- drug induced hemolytic anemia
4- transfusion reaction .

*Indirect antiglobulin test ( IAT) :- sensitized the antibody in the patient serum .
( IGg ) . unbonded proteins to remove several times RBCs are wash the -
-Application of IAT :-
1- Cross matching .
2- Antibody Screening .
3- Phenotyping .


33

* cross matching :-
Types of cross matching :-
Donor red cells and patient serum ( to determine compatibility between - Major cross matching : - 1
plasma )

Donor serum and patient red cells . to determine compatibility between - Minor cross matching : - 2

* common causes of false positive in both IAT and DAT :-
Cold agglutination - 1
2- Rouleaux .
3- Reagent contamination .
4- Antibody low incidence antigen .
5- human errors .
* common causes of false negative in both IAT and DAT :-
1- failure to add antiglobulin reagent . (( Anti Sera ))
2- Add wrong antiglobulin reagent (( Anti Sera )) .

* Hemolytic disease of newborn ( HDN ) :-
during pregnancy . Rh negative mother and Rh positive Fetus can develop when -
- mother Rh negative administrate Rh immunoglobulin ( RhIG ) to prevent Hemolytic disease in
newborn .

*selection of blood donor in KSA :
-blood donor must meet the following criteria :
1-age :at least 17 years old .
2- weight : at least 50 kg .
3- HB :14-18g /dl.
4- three mounth from last donation .
5- blood pressure :120/70 .
6- body temperature : 37 C
7- pulse rate : 70/min

* adverse donor reaction :
1-syncope (fainting ) :the most common donor adverse reaction .
2- nausea and vomiting .
3-hematoma .

*serological test for blood donor :
1-HIV 1&2
2- HBV


34
3-HCV
4-HTLV .
5-SYPHILLIS .
6- MALARIA .

*HIV (human immunodeficiency viruses ):
-the etiologic agent of AIDS
- serological test of AIDS :
1-ELISA
2- western blot (WB) is confirmatory test .

*HBV (hebatitis B)
-serological test for HBV :
1-ELIZA .
* HCV (hebatitis C) :
Serological test
1- ELIZA .
2-RIBA (confirmatory test ).

*SYPHILIS :
-is complex sexually transmitted disease
-serological test :
1-RPR (rapid plasma region ) .
2- VDRL.
*HTLV (human T-cell lymphotropic virus )
Serological test :
1-ELISA
2- western blot (WB) is confirmatory test .

* MALARIA :
-Diagnosis by THICK FILM .

*TRANSFUSION REACTION SCREENING OF BLOOD :
- transfusion screening test:
1- patient blood group & antibody detection .
2- donor blood group .
3- screening of donor blood for infectious disease .
4- crossmatch .

*ANTICOAGULANT AND PRESERVATIVE :
-anticoagulant used for blood donor bags are :
expiration temp Preservative


35
21 1-6 C 1-citrate phosphate dextrose (CPD)
21 1-6 C 2- citrate phosphate dextrose- dextrose (CP2D)
35 1-6 C 3- citrate phosphate dextrose-adenine (CPDA-1)

anticoagulant used in blood bank . 1 is most common - CPDA -
the storage time of saline adenine glucose mannitol (SAGM) is: 42 days -
-CITRATE :prevent coagulation .
-PHOSPHATE : act as buffer to decrease PH .
- DEXTROSE : used for ATP generation .
- ADENINE :substrate for the red cell to synthesize of ATP .

*STORAGE OF BLOOD COMPENENT :
EXPIRATION Compenent blood
Whole blood
1 years (-80C) RBC
5 DAYS PLATELETS
1 years (-18 C) Fresh frozen plasma FFP
1 years (-18 C) CRYOPRECIPTATE

*RED CELL COMPENENT :
1- whole blood
2- RBC ( packed red cell ) :
-RBC are unit of whole blood with most of the plasma removed
exchange used for hemolytic newborn also symptomatic anemia RBC: is the compenent of choice -
transfusion .

. Glycerol - for years by adding : n froze store by RBC can be -

- WBCs can be reduced in the whole blood bag by several methods :-
1- centrifugation . 2- saline washing . 3- freezing . 4- filtration.
choice today in blood bank. best method Filtration is the -

*plasma components :
1- fresh frozen plasma FFP : used to treat associated with:-
a- clotting factor deficiency .
b- Disseminated intravascular coagulation (DIC) .
c- vit K deficiency.

2- cryoprecipitate : is the cold insoluble portion of plasma that precipitate when FFP is thawed
between 1-6C .
Cryoprecipitate transfusion used to control bleeding associated with fibrinogen deficiency or factor
XIII deficiency .
Cryoprecipitate also used for treat:-
a- hemophilia A .
b- von willebrand disease

thrombocytopenia or platelet in patient with treat bleeding : platelets transfusion used to * platelets
dysfunction
- platelets are extremely sensitive to temperature and pH changes .


36

- for blood components : Store Temprature *

Temperature Compnents
1-6 C Whole blood
1-6 C Red blood cell ( RBC )
- 18 C Fresh frozen plasma (( FFP)
20-24 C Platelets
20-24 C Granulocytes

تجميع اسئله الاخصائين 1

Încărcat de

Informații document

Drepturi de autor

Formate disponibile

Partajați acest document

Partajați sau inserați document

Opțiuni de partajare

Vi se pare util acest document?

Este necorespunzător acest conținut?

Drepturi de autor:

Formate disponibile

تجميع اسئله الاخصائين 1

Încărcat de

Drepturi de autor:

Formate disponibile

shadoy@windowslive.

S-ar putea să vă placă și