BLOOD HOPSY
BLOOD HOPSY
T1
Blood, whole blood (Blood cells & plasma)
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Blood, function and Characteristics
Functions 2. Defense
1. Transport Presence of WBC that
defend the body from
Gases; O2 from lung to infectious attacks
tissues and CO2 from 3. Regulation
tissues to the lung.
a. Temperature reg.
Nutrients: organic
water has high specific
(glucose, aa, lipids)
heat (great heat storage
and inorganic
than other liquids and
substances like Na+,
solids, so prevents
Ca2+ are carried by
sudden changes in T0 .
blood
b. Acid-base balance:
Waste products: urea, uric
acid, creatinine etc to The Hb in RBC is an
the kidney etc. important chemical
buffer 3
(Cont…) Properties of blood
a. Color:
c. pH : 7.4 (blood is
a.1. bright red
slightly alkaline)
(oxygenated blood)
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(Cont…) Types of plasma proteins
Plasma proteins
A. Albumin (~ 60% or
4.5 gm/dl)
B. Globulins (~ 40%, or
2.5 g/dl)
• (alpha, beta, gamma)
Determined by means of
Electrophoresis
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(Cont…) Functions of plasma proteins
A. Albumin:
- is produced in the liver
- It is responsible for Colloid osmotic pressure (COP)
or oncotic pressure.
- Oncotic pressure helps to keep plasma fluid back in
circulation by causing reabsorption pressure.
- Albumin also transports nutrients (e.g., lipids,
hormones, bilirubin etc.
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B. Globulin are of 3-types: alpha1&2, beta, and
gamma globulins.
-Alpha & gamma are made in the liver and
transport lipoproteins, iron hormones etc.
-Gamma globulins act as antibodies
C. Fibrinogen
Synthesized in the liver and are involved in
the process of blood clotting
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(Cont…) Blood. RBC (erythrocytes)
Shape: Flexible
biconcave shaped cells,
thinner at the center
and thicker at the ages.
Diameter: ~ 7.5 um
Mature RBC’s have no
nucleus and the shape
gives them greater
surface area-to-volume
ratio.
Thus, RBC’s can bend
and twist very easily to
pass through the
narrow capillary bed. 10
(Cont…) Blood, Normal RBC No.
Carries hemoglobin (Hb)
1. carries O2 and CO2 gas
2. Hb also helps as a
buffer in the cell
(good for pH-regulation
(Cont…) 3-different stages of RBC production
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(Cont…) Blood, RBC, factors that stimulate
erythropoietin and its inverse relation with Hct
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(Cont…) Hemoglobin (Hb), structure and function
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(Cont…) Blood, Hb-function and structure
Each polypeptide has one
Heme group and each
Heme contains one
Fe2+ that carries 1-O2
molecule.
• Phagocytosis by
macrophage, spleen,
liver and bone marrow
takes place cells.
• The macrophages
release the Hb-molecule
that is broken down into:
a. Globin (protein) and,
b. Heme part
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(Cont…) Blood physiology, RBC-indices
Knowing the RBC-indices will help one to realize the
size, Hb-level in the blood, and type of RBC
abnormalities or pathologies.
Thus the 3-important facts that need to be assessed in
RBC-indices include measuring:
• a. The Hb-concentration
• b. The RBC-count (No of RBCs)
• c. The Ht (hematocrit) values
• From the above indices, other important blood
parameters can be calculated. These include:
1. MCV : Mean Cell Volume
2. MCH : Mean Cell Hemoglobin
3. MCHC: Mean Cell Hemoglobin Concentration
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(Cont…) Anemia
Anemia in general can be defined as a decrease in the O2-transport capacity of the blood.
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(Cont…) Blood physiology, diseases
a. Blood loss anemia:
During hemorrhage persons loose too much
blood. The Fe2+ absorbed from the intestine
is not enough to produce adequate Hemoglobin to
replace the lost Hemoglobin that took place
during bleeding.
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(Cont…) Blood physiology, diseases
b. Aplastic anemia: Aplasia means lack of functioning bone
marrow. It is caused by exposure to excess chemicals,
drugs and gamma or X-ray that destroy the bone marrow.
Effect is lower RBC production
c. Megaloblastic anemia (nutritional deficiency) :
Maturation failure anemia (pernicious anemia) is
caused by inability to absorb Vitamin-B12 and folic
acid from the intestine. Absence of intrinsic factor
(gastrechtomy) is another cause. Effect
is that RBC can not proliferate properly, b/s
DNA synthesis does not occur. As the result the
RBC’s become big, oversized (megaloblastic )
and have fragile membranes that easily rupture
and decrease the No.
• -
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(Cont…) Blood physiology, diseases
c. Hemolytic anemia: hereditarily acquired and makes
the RBC’s to easily rupture as they cross through narrow
blood vessels like capillaries, spleen etc. Examples are:
a. Hereditary spherocytosis: spherical shaped
RBC (not biconcave) that rupture easily
b. Sickle cell anemia: is caused by abnormal beta
chain in Hb-structure. When exposed to
low O2 (hypoxia), the Hb precipitates
forming long crystals and damaging and
rupturing the cell-membrane, their by
causing anemia.
c. Erythroblastosis fetalis: Destruction and
decrease of RBC’s number of the fetus by
antibodies from Rh-negative mother.
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(Cont…) Blood physiology, polycethemia
Polycethemia: is production of too much RBC in the
circulation. Polycethemia has a physiological or a
pathological cause:
A. Physiological cause is known as Secondary
Polycethemia :
When ever the tissues become hypoxic
b/s of low O2-tension) like in high altitude,
the marrow produces excessive RBC (6-7
mill/mm3).
B. Pathological cause is called Polycethemia Vera
(erythremia) or primary polycythemia. It is about
7-8 million / mm3.
Is mainly due to genetic causes as in
Tumerous or cancerous production of
RBC. Moreover, increases are also seen in WBC
and platelet numbers. 25
(cont…) polycythemia
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Summary about blood picture
• To summarize , CBC (complete blood count) should be a
routine medical examination.
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(Cont…) Blood Physiology, types of blood groups
There are several different types of antigens on RBC surfaces, but the
most known and clinically important antigens for blood grouping are:
a. The ABO-blood groups, and
b. The Rh-factors
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(Cont…) Blood Physiology, ABO-blood
groups
• Whenever there is an antigen on RBC surfaces, the
plasma will not contain its specific antibody
(agglutinine).
• A person whose red cells possess the antigen-A
(agglutinogen-A) has anti-B antibody (agglutinin) in
his serum and is classified as blood group A
• If B-antigen is present in the Red cell membranes,
Anti-A antibody is present in his serum and the
person is designated as blood group B.
• If Both AB-antigens are present on Red cells, then he
has no antibody, so is AB-blood group.
• If No antigens are present on red cells, he is O Type
and has both anti A and B antibody in his serum.
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(Cont…) Blood Physiology, relative frequencies of
blood groups
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(Cont…) Blood Physiology, Universal donor
Blood group “O” is called universal donor,
because people with this blood types have no
antigens on their cell-membrane surfaces and
therefore can not agglutinate if transfused to
any blood types.
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(Cont…) Blood Physiology, Universal recipient
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(Cont…), Blood physiology, Rh-blood typing
In comparison to ABO blood group, the Rh-factor is slow acting
and is not found in other secretion like saliva etc.
Rh- incompatibility: Usually causes serious problems
The Incompatibility:
Father Rh + = Rh + means he has D-antigen on his RBC
membrane
Mother Rh- = No Rh factor, so it is depicted as Rh-
Marriage:
1. Rh+ father X Rh- mother = Rh + fetus
2. During birth through placenta , Rh+ blood (antigens) of the
fetus leak (enter) to mothers blood and sensitizes her.
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(Cont…) Blood physiology, Rh- incompatibility
3. Mother ‘s blood produces anti-Rh antibodies (anti-D antibodies )
against the Rh+ blood.
4. During the 2nd pregnancy and there after, the Anti-Rh+ antibodies
(agglutinins) enter into the fetus and agglutinate or hemolyze the
RBC’s the fetus.
The passage of the bile pigment to the brain causes Kernicterus (damage
of the basal ganglia with subsequent motor disturbances)
Typing of blood for Rh-system is the same as for ABO system. That is,
Rh+ RBC’s are agglutinated when exposed to serum containing anti-
D antibodies, but Rh- RBC’s are not agglutinated.
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(Cont…) Blood physiology, Blood transfusion
• Importance of blood transfusion:
• Transfusion of whole blood or its parts (plasma, or red
blood cell concentrates or other specific clotting factors
is supplied in order to:
A. Restore blood volume
B. Improve O2 transport to tissues
C. Correct bleeding abnormalities etc.
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Blood Physiology
Hemostasis
(blood clotting mechanisms)
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Hemostasis
• Definition:
• Hemostasis (blood clotting) refers to stopping or arrest of bleeding.
Blood cells involved in blood clotting processes are platelets
(Thrombocytes).
What are platelets?
• Platelets are type of blood cells which are small, colorless, and non-
nucleated and have a life span of about 10 days.
• Platelets develop from fragments of big cytoplasmic structures in the
bone marrow called megakaryocytes.
• The cytoplasm of platelets produce many chemicals like:
a. Thromboxane A2,
b. Serotonin,
c. Histamine,
d. von Willbrand’s factor
e. Ca2+, Cu, Fe2+ etc
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Blood clotting
Some properties of platelets
include Adhesiveness,
Aggregation
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Steps in the formation of blood clotting
There are 4-to- 5 stages of
hemostasis:
1. Vasoconstriction
(vascular
spasm)
2. Platelet plug (platelet
aggregation)
3. Clotting processes
4. Clot retraction
5. Clot dissolution
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Clotting factors
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Intrinsic and extrinsic clotting
mechanisms
There are more than 50 different types of anticoagulants and pro-coagulants
circulating in the blood.
-Anti-coagulants dominate a little over procagulants when blood circulates in the
circulatory system.
-During tear or injury, procagulants dominate near the site of injury, otherwise they
remain more or less in balance.
Be it through intrinsic (damage to the blood itself) or extrinsic (rupture of the vessel)
blood clotting mechanism, both of them have a common ending.
That is, they end in producing a substance called Prothrombin activator
Be it through intrinsic (damage to the blood itself) or extrinsic (rupture of the vessel)
blood clotting mechanism, both of them have a common ending.
That is, they end in producing a substance called Prothrombin activator
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Coagulation, Prothrombin activator
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Extrinsic pathway
Extrinsic pathways
It begins with traumatized (injured)
tissues that release a substance
called tissue thromboplastin and
together with factor VII*(SPCA)
activates factor X*(Stuart factor) to its
active form X.
thrombin converts
Fibrinogen ------------- to Fibrin
(loose solid
clot)
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Intrinsic mechanism
Intrinsic mechanism begins with trauma
to the blood itself or exposure of the
blood to collagen at injured blood
vessel wall. The blood then activates
Factor XII to its active form XIIa
Then cascade of reactions continue until
the formation of activated Factor Xa
Factor VIII + IX + platelet
phospholipids.
The absence of Factor VIII causes classic
hemophilia and deficiency in platelet
number causes the bleeding disease
thrombocytopenia.
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