Blood Group & Coagulation

8/12/2019 Blood Group & Coagulation

1/24

ANEMIA

o Iron-Deficiency Anemia (most common)

o Aplastic Anemia - bone marrow does not

produce enough RBC

o Hemorrhagic anemia - due to extreme blood

loss

o Pernicious anemia - B12 deficiencyo Sickle Cell Anemia (genetic)


2/24

Sickle Cell Anemia

Genetic disease

Red blood cells become

sickle shape

Cant carry as muchoxygen


3/24

RED BLOOD CELL MORPHOLOGY

Sickle cell anemia. Note the sickle shaped

red blood cell.


4/24

Thalasemia

Normal hemoglobin is composed of two

chains each of and globin. Thalassemia

patients produce a deficiencyof either or

globin, unlike sickle-cell diseasewhich

produces a specific mutant form of globin.
http://en.wikipedia.org/wiki/Sickle-cell_diseasehttp://en.wikipedia.org/wiki/Sickle-cell_diseasehttp://en.wikipedia.org/wiki/Sickle-cell_diseasehttp://en.wikipedia.org/wiki/Sickle-cell_disease


5/24

LEUKEMIA

o Type of cancer

o Overproduction of immature white blood

cells

o They take the place of RBCs

o Treatable with bone marrow transplants,

chemothemotherapy, radiation


6/24

BLOOD POISONING

SEPTICEMIA

An infection enters theblood stream, can be

deadly

Treated with antibiotics

THROMBOCYTOPENIA

Low production ofPlatelets, Causing

bleeding or bruising


7/24

Haemophilia

In general symptoms are internal or externalbleeding episodes, which are called "bleeds

Deficiency in coagulation factor VIII is the

most common cause of haemophilia.Haemophilia A

Haemophilia B: Deficiency in coagulation

factor IX Haemophilia C : Deficiency in coagulation

factor XI
http://en.wikipedia.org/wiki/Haemophilia_Bhttp://en.wikipedia.org/wiki/Haemophilia_Bhttp://en.wikipedia.org/wiki/File:XlinkRecessive.jpg


8/24
http://en.wikipedia.org/wiki/File:XlinkRecessive.jpg


9/24

Transfusion Reactions

People with Type A blood makeantibodies to Type B RBCs, butnot to Type A

Type B blood has antibodies to

Type A RBCs but not to Type B Type AB blood doesnt have

antibodies to A or B

Type O has antibodies to bothType A & B

If different blood types aremixed, antibodies will causemixture to agglutinate

Fig 13.513-16


10/24

When RBCs carrying one or both antigens are exposed to thecorresponding antibodies, they agglutinate; that is, clump together.People usually have antibodies against those red cell antigens thatthey lack.

Human RBC before (left) and after (right) adding serum

containing anti-A antibodies. The agglutination reaction

reveals the presence of the A antigen on the surface of the

cells.

http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/B/BloodGroups.html


11/24

Illustration of the forward and reversegrouping reaction patterns of the ABOgroups using a blood group tile

http://www.bh.rmit.edu.au/mls/subjects/abo/resources/genetics1.htm


12/24

Transfusion Reactions continued

If blood types don't match,recipients antibodiesagglutinate donors RBCs

Type O is universal donor

because lacks A & B antigens Recipients antibodies

wont agglutinate donorsType O RBCs

Type AB is universalrecipient because doesntmake anti-A or anti-Bantibodies Wont agglutinate donors

RBCs

Insert fig. 13.6

13-17


13/24

3. Platelets (Thrombocytes)

* Cell fragments bound to megakaryocytes

* Bud Off and are released into the blood


14/24

Platelets (thrombocytes)

Are smallest of formedelements, lack nucleus

Are fragments of

megakaryocytes; amoeboid Constitute most of mass of

blood clots

Release serotonin tovasoconstrict & reduce bloodflow to clot area

Secrete growth factors tomaintain integrity of bloodvessel wall

Survive 5-9 days


15/24

Function of Platelets

Stop bleeding from a damaged vessel

* Hemostasis

Three Stepsinvolved in Hemostasis

1. Vascular Spasm

2. Formation of a platelet plug

3. Blood coagulation (clotting)


16/24

Steps in Hemostasis

Immediate constrictionof blood vessel

Vessel walls pressed togetherbecome

sticky/adherent to each other

Minimize blood loss

*DAMAGE TO BLOOD VESSELLEADS TO:

1. Vascular Spasm:


17/24

Steps in Hemostasis

a. PLATELETSattach to exposed collagen

b. Aggregation of platelets causes release ofchemical mediators (ADP, Thromboxane A2)

c. ADPattracts more platelets

d. Thromboxane A2(powerful vasoconstrictor)

* promotes aggregation & more ADP

2. Platelet Plug formation: (figure 11-10)

Leads to formation of platelet plug !


18/24

Figure 11-10

(+)Feedback promotes formation of platelet Plug !


19/24


20/24

Final Step in Hemostasis

a. Transformation of blood from liquid to solid

b. Clot reinforces the plug

c. Multiple cascade steps in clot formation

d. Fibrinogen (plasma protein) FibrinThrombin

3. Blood Coagulation (clot formation):

Clotting Cascade


21/24


22/24

Clotting Cascade

Participation of 12 different clotting factors

(plasma glycoproteins)

Factors are designated by a roman numeral

Cascade of proteolytic reactions

Intrinsic pathway/ Extrinsic pathway

Common Pathwayleading to the formationof a fibrin clot !


23/24

inactive

active

Hageman factor (XII)

CLOT !

X


24/24

Clotting Cascade

Intrinsic Pathway:

Stops bleeding within (internal)a cut vessel

Foreign Substance (ie: in contact with test

tube) Factor XII (Hageman Factor)

Extrinsic pathway:

Clots blood that has escaped into tissues

Requires tissue factors externalto blood

Factor III (Tissue Thromboplastin)

Documents

Blood Group & Coagulation