131 blood physio report

8/8/2019 131 Blood Physio Report

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Blood PhysiologyExercise 12Exercise 12



I. Intr oduction



Karl Landsteiner

noted for his development in

1901 of the modern system of classification of blood groups

from his identification of the

presence of agglutinins in the

blood

in 1930 he received the Nobel

Prize in Physiology or Medicine

with Alexander S. Wiener, he

identified the Rh factor in

1937.



Blood Typing

Agglutination

refers to the clumping of red cells together

the clumping of cells such as bacteria or red blood cells in the

presence of an antibody. The antibody or other molecule

binds multiple particles and joins them, creating a large

complex.

Why would agglutination be dangerous?



Antigen

macromolecules that elicit an immune response in the body

there are at least 30 commonly occurring antigens in surfaces

of cell membrane in human blood cells.



Two Particular types of Antigens:

ABO system of antigen

Rh systems of antigens



A BO System of A ntigen

A and B Antigens

Found on the surf aces of red blood cells

RH system

Spontaneous agglutinins

almost never occur

ABO system

Plasma agglutinins

responsible for causing

transfusion reactions

develop spontaneously

Rh System



Bleeding Time

a measure of how quickly blood clots, using platelets,

coagulation factors, and small vessel vasospasm.

Normal bleeding time is largely dependant upon both the

number and function of platelets.

Bleeding time is usually within a normal range when the

platelet count is greater than 100,000 per microliter.



Clotting Time

time interval in between onset of bleeding and appearance of

jelly like semisolid mass such as a blood clot.

The normal clotting time ranges from 4 to 9 minutes.

If the clotting time is shorter than the normal clotting time, itis classified as reduced , if longer than the normal clotting, it is

prolonged and if same as the normal clotting time, it is

normal .



Fibrin Formation

The formation of a fibrin clot at the site of an injury to the

wall of a normal blood vessel is an essential part of theprocess to stop blood loss after vascular injury.

The reactions that lead to fibrin clot formation are commonly

described as a cascade, in which the product of each step isan enzyme or cofactor needed for following reactions to

proceed efficiently.



II. Results



Blood TypingPositive (+) in Blood Type O.



Positive (+) in Blood Type B.

Positive (+) in Blood Type A.



Blood CoagulationA. Bleeding Time

On the first 15 second interval a distinct round blot due todrop of blood is observed. After 30 minutes or in the second

15-second interval, a distinct round drop of blood is also

observed however, its size is smaller than the first blot. The

blood stain stopped appearing on the filter paper after 45

seconds or in the 3rd 15-second interval.



Blood CoagulationB. Clotting Time

The on the first 30-second interval, when the capillary tubewas broken off, there was no threadlike formation visible.

After one minute, or in the 2nd 30-second interval, when the

capillary tube was broken off, a small, fragile, threadlike

formation was already observed. On the 3rd interval, after 1

minute and 30 seconds, a small part of the tube was again

broken off, but this time, the threadlike formation was

already firm and very visible. Therefore, the final clotting

time is 1 minute and 30 seconds.



Blood CoagulationC. Observation of Fibrin Strand Formation

The strand formation was observed in about 1 minutes and45 seconds.



III. Discussion



Principles be

hind Blood Typing



What are Antibodies?

Antibodies are

proteins made by a B-cell which can

recognize and attach

t o specif ic sites onantigens t o block their

eff ect.



Where are they produced in the body?

Antibodies are made

in plasma cells, whichare a type of white

blood cell, and are an

integral part t o thebodys nat ural def ense

system.



What is its mechanism of production?

Clonal Selection Theory

This theory states that there are a variety of B-

lymphocytes present in the immune system which produce

a small number of antibody molecules without any

antigenic stimulation, and these antibody molecules

integrate int

othe cyt

oplasmic memb

rane

of thei

rpro

du

cer

lymphocyte t o serve as recept or site for specif ic antigen.



Table 1. Blood Types with Their Genotypes andTheir Constituent Agglutinogens and Agglutinins

Genotypes Blood Types Agglutinogens Agglutinins

OO O -- Anti-A & Anti-B

OA or AA A A Anti-B

OB or BB B B Anti-A

AB AB A and B --



Table . Blood Typing, Showing Agglutination of Cellsof the Different Blood Types with Anti-A or Anti-B

Agglutinins in the Sera

Red Blood CellTypes

SeraAnti-A Anti-B

O - -

A + -

B - +

AB + +



Hemostasis a complex process which changes blood from a fluid to a solid

state the arrest of bleeding from an injured blood vessel, requires

the combined activity of vascular, platelet, and plasma factors

proceeds in two phases: primary and secondary hemostasis.



Primary Hemostasis

formation of the primary platelet plug and involves platelets,

the blood vessel wall and von Willebrand factor.

characterized by:

[1] vascular contraction

[2] platelet adhesion[3] formation of a soft aggregate plug



When these vessels are damaged, there are three basicmechanisms that promote hemostasis or the stoppage of

bleeding.



Following damage, there is an immediate reflex that promotesvasoconstriction, thus diminishing blood loss.



Exposed collagen from the damaged site will promote

the platelets to adhere.



When platelets adhere

to the damaged vessel,

they undergo

degranulation and

release cytoplasmic

granules, which

contain serotonin, a

vasoconstrictor, andADP and Thromboxane

A2.



The ADP attracts more platelets to the area, and thethromboxane A2 promotes platelet aggregation,

degranulation, and vasoconstriction.



Secondary Hemost asis

defined as the formation of fibrin through the coagulation

cascade.

The coagulation cascade is traditionally separated into 3

pathways: intrinsic, extrinsic and common pathways.



The extrinsic pathway involves the tissue factor and

factor VII complex, which activates factor X.



The intrinsic pathway involves high-molecular

weight kininogen, prekallikrein, and factors XII, XI, IXand VIII. Factor VIII acts as a cofactor for the factor

IX-mediated activation of factor X.

The extrinsic and intrinsic pathways converge at theactivation of factor X.



The common pathway involves the factor X-mediated generation of thrombin from prothrombin,

with the ultimate production of fibrin from

fibrinogen.



The final hemostatic

mechanism is coagulation.Damaged tissue releases

factor III, which with the aid

of Ca++ will activate factor

VII, thus initiating the

extrinsic mechanism.



Prothrombin activator converts prothrombin to thrombin.

Thrombin converts fibrinogen to fibrin.



Both active factor

VII and active

factor XI will

promote cascade

reactions,

eventuallyactivating factor

X.



Active factor X,

along with factor III,factor V, Ca++, and

platelet

thromboplastic

factor (PF3), will

activateprothrombin

activator.



Fibrin initially forms a

loose mesh, but then

factor XIII causes theformation of covalent

cross links, which

convert fibrin to a

dense aggregation of

fibers.



Blood Coagulation TestsBleeding Time

Bleeding ordinarily lasts for 1 to 6 minutes

Lack of any one of several of the clotting factors can prolong the bleeding

time

Especially prolonged by lack of platelets

Clotting Time Normal clotting time is 6 to 10 minutes

Clotting time varies depending on the method used for measuring it



Observation of Fibrin Formation

Fibrinogen high-molecular weight protein that occurs in plasma

formed in the liver and liver disease can decrease the

concentration of circulating fibrinogen



IV.Cli

nical Applications



Blood Typing Blood Transfusion

Hemolytic Disease of the Newborn

Blood Products

Red Blood Cell Compatibility



Blood CoagulationBleeding Disorders:

von Willebrand Disease (VWD)most common inherited bleeding disorder. It is caused by

deficiencies or defects in a certain substance in the blood that

helps clots to form. VWD occurs about as often in men as it

does in women

131 blood physio report

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