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 deficiency
o Sickle Cell Anemia (genetic)
Sickle Cell Anemia
Genetic disease
Red blood cells become
sickle shape
Cant carry as much
oxygen


RED BLOOD CELL MORPHOLOGY
Sickle cell anemia. Note the sickle shaped
red blood cell.
Thalasemia
Normal hemoglobin is composed of two
chains each of and globin. Thalassemia
patients produce a deficiency of either or
globin, unlike sickle-cell disease which
produces a specific mutant form of globin.

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

BLOOD POISONING
SEPTICEMIA

An infection enters the
blood stream, can be
deadly
Treated with antibiotics


THROMBOCYTOPENIA


Low production of
Platelets, Causing
bleeding or bruising
Haemophilia
In general symptoms are internal or external
bleeding 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

Transfusion Reactions
People with Type A blood make
antibodies to Type B RBCs, but
not 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 both
Type A & B
If different blood types are
mixed, antibodies will cause
mixture to agglutinate

Fig 13.5
13-16
When RBCs carrying one or both antigens are exposed to the
corresponding antibodies, they agglutinate; that is, clump together.
People usually have antibodies against those red cell antigens that
they 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.ultran
et/BiologyPages/B/BloodGroups.html


Illustration of the forward and reverse
grouping reaction patterns of the ABO
groups using a blood group tile

http://www.bh.rmit.edu.au/mls/subjects/abo/resources/genetics1.htm
Transfusion Reactions continued
If blood types don't match,
recipients antibodies
agglutinate donors RBCs
Type O is universal donor
because lacks A & B antigens
Recipients antibodies
wont agglutinate donors
Type O RBCs
Type AB is universal
recipient because doesnt
make anti-A or anti-B
antibodies
Wont agglutinate donors
RBCs
Insert fig. 13.6
13-17
3. Platelets (Thrombocytes)
* Cell fragments bound to megakaryocytes
* Bud Off and are released into the blood
Platelets (thrombocytes)
Are smallest of formed
elements, lack nucleus
Are fragments of
megakaryocytes; amoeboid
Constitute most of mass of
blood clots
Release serotonin to
vasoconstrict & reduce blood
flow to clot area
Secrete growth factors to
maintain integrity of blood
vessel wall
Survive 5-9 days

Function of Platelets
Stop bleeding from a damaged vessel
* Hemostasis

Three Steps involved in Hemostasis
1. Vascular Spasm
2. Formation of a platelet plug
3. Blood coagulation (clotting)


Steps in Hemostasis

Immediate constriction of blood vessel

Vessel walls pressed together become
sticky/adherent to each other

Minimize blood loss

*DAMAGE TO BLOOD VESSEL LEADS TO:

1. Vascular Spasm:
Steps in Hemostasis
a. PLATELETS attach to exposed collagen
b. Aggregation of platelets causes release of
chemical mediators (ADP, Thromboxane A
2
)
c. ADP attracts more platelets
d. Thromboxane A
2
(powerful vasoconstrictor)
* promotes aggregation & more ADP
2. Platelet Plug formation: (figure 11-10)
Leads to formation of platelet plug !
Figure 11-10
(+) Feedback promotes formation of platelet Plug !
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) Fibrin
Thrombin
3. Blood Coagulation (clot formation):
Clotting Cascade
Figure 11-11
Thrombin in Hemostasis
Factor X
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 Pathway leading to the formation
of a fibrin clot !


inactive

active
Hageman factor (XII)
CLOT !
X
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 external to blood
Factor III (Tissue Thromboplastin)