ABO ppt

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U N I T VI

Textbook of Medical Physiology, 11th Edition

GUYTON & HALL

Copyright © 2006 by Elsevier, Inc.

Chapter 35:Blood Types; Transfusion;

Tissue and Organ Transplantation

Slides by Robert L. Hester, Ph.D.

8/20/2019 ABO ppt



Overview of Blood Types

• Blood Video\What are Blood Types-.mp4

http://localhost/var/www/apps/conversion/tmp/scratch_5/Blood%20Video/What%20are%20Blood%20Types-.mp4






8/20/2019 ABO ppt



Blood Groups

Red blood cell surface antigens: glycolipids or glycoproteins

A-B-O Systemagglutinogens: surface antigens (A,B)

genes (A, B, O)

inherited (two surface chromosomes)

OO OA OB AA BB AB

also present on all cells in the body

agglutinins: gamma globulins, anti-A, anti-B, IgM, IgG

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Blood Groups

GENOTYPE BLOOD TYPE AGGLUTINOGENS AGGLUTININS

OO

OA or AA

OB or BB

AB

O

A

B

AB

------

A

B

AB

ANTI-A

ANTI-B

ANTI-A and

ANTI-B

------

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Titer of Agglutinins

• After birth – almostzero

• 2-8 months after birth – begin production

• 8-10 years old – maximum titer

• Gradually declinesremaining years of life

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Blood Typing

BLOOD TYPE ANTI-A ANTI-B

O

A

B

AB

------

++

------

------

+

+

------

8/20/2019 ABO ppt

http://slidepdf.com/reader/full/abo-ppt 7/21Copyright © 2006 by Elsevier, Inc.

Blood Groups

Rhesus System

agglutinogens: 6 rhesus factors (C, D, E, c, d, e)

inherited as triplets

CDE, CDe, Cde, CdE, cDE, cDe, cde

antigen D =Rhesus positive (widely

prevalent & more antigenic)

agglutinins: do not occur spontaneously, only after

exposure to Rh antigens

Rh+ blood into Rh negative person:

sensitization to further Rh+ transfusion

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•Disease of the fetus and newborn child

•Fetal blood enters maternal circulation

•Agglutination & phagocytosis of fetus’ RBCs

• ABO incompatibility

•O mother and A or B fetus

•IgG anti-A and anti-B cross placenta

•very mild effects

Hemolytic Disease of the Newborn or

Erythroblastosis fetalis

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•Rh incompatibility

•Rh positive fetus and a Rh negative mother

•Anti-D agglutinins form in mother from exposure to

fetus’ Rh Ag

diffusion thru the placenta into the fetusand cause agglutination

•Maternal blood with anti-D usually circulate in infant’s

blood for another 1-2 months after birth destroys more

RBC

•More critical with 2nd and succeeding Rh positive child



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• Signs and Symptoms

1. Jaundice

2. Pallor or anemia at birth3. Hepatosplenomegaly – forming nucleated blastic

RBCs

4. kernicterus

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• Treatment

1. Exchange Transfusion

• Replace neonate’s blood with Rh (-) blood

• > 6 weeks - transfused Rh (-) blood is replaced byinfant’s own Rh (+) blood and mother’s anti-D is

destroyed

2. Injection of IgG anti-D or Rh Ig or Rhogam

• to expectant mother starting at 28-30 weeks AOG



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• Prevention

• Administer Rhogam to Rh (-) mother who delivered

Rh (+) babies to prevent sensitization of mother to

the D Ag, thus, reducing the risk of developing largeamounts of anti-D during 2nd pregnancy

Mechanism of Rhogam

• inhibits Ag-induced B lymphocytic Ab production in

expectant mothers• Attaches to D-Ag sites on Rh (+) fetal RBC that

may cross the placenta



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Transfusion Reaction

Hemolysins – IgG agglutinins contain 2 binding sites

– IgM agglutinins contain 10 binding sites

Agglutination = “clumping” of cells by activation ofcomplement system (Ag-Ab reaction) release

proteolytic enzymes destroys membrane of

agglutinated cells (either by physical distortion ofcells or phagocytosis by WBC) release of Hb hemolysis

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• Transfusion reaction due to agglutination of

donor blood and rarely recipient’s blooddue to – plasma portion of donor blood

immediately becomes diluted by plasma of

recipient decreasing titer of transfused

agglutinins

• DONOR’S BLOOD undergoes hemolysis

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• Signs and Symptoms

1. Fever and chills2. Shortness of breath

3. Jaundice

4. Shock

5. Renal shutdown

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• Renal Shotdown or Renal Failure1. Renal Vasoconstrictor – toxic substance

released by hemolyzed blood

2. Circulatory Shock –

due to loss of circulatingRBC, the produced toxic substances and fromimmune reaction (Ag-Ab reaction) – hypotension,decrease renal blood flow, decrease urine output

3. Renal Tubular Blockage – total amount of free

Hb released into the circulating blood > Hbbound to haptoglobin excess leaks thru theglomerular membrane into kidney tubules, whichprecipitates and blocks renal tubules

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Transplantation

• Autograft – same animal

• Isograft – identical twin• Allograft – same species

• Xenograft – different species

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Transplantation

• HLA Ab

– Most important Ab causing graft rejection

–150 Ab 6 on tissue cell membrane (WBC andtissue cells)

• HLA Typing – test for rate of trans-

membrane uptake by WBC of a special dye

• OBTAIN THE BEST POSSIBLE MATCH

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Transplantation

• Rejection ---- mainly due to activation ofT-cells

• Suppressive therapy---- inhibit immune

response not protected from infectiousdiseases and sometimes even cancer

1. glucocorticoids – limits growth of all lymphoidtissuesdecrease formation of Ab and T cells

2. azathioprine - inhibits formation of Ab and T cells3. cyclosporine --- specific inhibitor of helper T-cell

formation; most valuable because it does notsuppress other portions of the immune system

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RECAP

• Blood Video\Blood Types.mp4

http://localhost/var/www/apps/conversion/tmp/scratch_5/Blood%20Video/Blood%20Types.mp4




8/20/2019 ABO ppt


U N I T VI

Textbook of Medical Physiology, 11th Edition

GUYTON & HALL

Thank you

ABO ppt

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