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U N I T VI

Textbook of Medical Physiology, 11th Edition

Chapter 35:
Blood Types; Transfusion;
Tissue and Organ Transplantation
Slides by Robert L. Hester, Ph.D.

GUYTON & HALL


Copyright 2006 by Elsevier, Inc.

Overview of Blood Types


Blood Video\What are Blood Types-.mp4

Copyright 2006 by Elsevier, Inc.

Blood Groups
Red blood cell surface antigens: glycolipids or glycoproteins

A-B-O System
agglutinogens: 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

Copyright 2006 by Elsevier, Inc.

Blood Groups
GENOTYPE

BLOOD TYPE

AGGLUTINOGENS AGGLUTININS

OO

------

ANTI-A and
ANTI-B

OA or AA

ANTI-B

OB or BB

ANTI-A

AB

AB

AB

------

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Titer of Agglutinins

After birth almost


zero
2-8 months after birth
begin production
8-10 years old
maximum titer
Gradually declines
remaining years of life

Copyright 2006 by Elsevier, Inc.

Blood Typing
BLOOD TYPE

ANTI-A

ANTI-B

------

------

------

------

B
AB

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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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Hemolytic Disease of the Newborn or


Erythroblastosis fetalis
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

Copyright 2006 by Elsevier, Inc.

Hemolytic Disease of the Newborn or


Erythroblastosis fetalis
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 fetus
and cause agglutination
Maternal blood with anti-D usually circulate in infants
blood for another 1-2 months after birth destroys more
RBC
More critical with 2nd and succeeding Rh positive child

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Hemolytic Disease of the Newborn or


Erythroblastosis fetalis

Signs and Symptoms


1. Jaundice
2. Pallor or anemia at birth
3. Hepatosplenomegaly forming nucleated blastic
RBCs
4. kernicterus

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Hemolytic Disease of the Newborn or


Erythroblastosis fetalis

Treatment
1. Exchange Transfusion
Replace neonates blood with Rh (-) blood
> 6 weeks - transfused Rh (-) blood is replaced by
infants own Rh (+) blood and mothers anti-D is
destroyed
2. Injection of IgG anti-D or Rh Ig or Rhogam
to expectant mother starting at 28-30 weeks AOG

Copyright 2006 by Elsevier, Inc.

Hemolytic Disease of the Newborn or


Erythroblastosis fetalis

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 large
amounts 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

Copyright 2006 by Elsevier, Inc.

Transfusion Reaction
Hemolysins
IgG agglutinins contain 2 binding sites
IgM agglutinins contain 10 binding sites

Agglutination = clumping of cells by activation of


complement system (Ag-Ab reaction) release
proteolytic enzymes destroys membrane of
agglutinated cells (either by physical distortion of
cells or phagocytosis by WBC) release of Hb
hemolysis

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Transfusion Reaction

Transfusion reaction due to agglutination of


donor blood and rarely recipients blood
due to plasma portion of donor blood
immediately becomes diluted by plasma of
recipient decreasing titer of transfused
agglutinins
DONORS BLOOD undergoes hemolysis
Copyright 2006 by Elsevier, Inc.

Transfusion Reaction

Signs and Symptoms


1.
2.
3.
4.
5.

Fever and chills


Shortness of breath
Jaundice
Shock
Renal shutdown

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Transfusion Reaction

Renal Shotdown or Renal Failure


1. Renal Vasoconstrictor toxic substance
released by hemolyzed blood
2. Circulatory Shock due to loss of circulating
RBC, the produced toxic substances and from
immune 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 > Hb
bound to haptoglobin excess leaks thru the
glomerular membrane into kidney tubules, which
precipitates 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 and
tissue cells)

HLA Typing test for rate of transmembrane uptake by WBC of a special dye
OBTAIN THE BEST POSSIBLE MATCH

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Transplantation

Rejection ---- mainly due to activation of


T-cells
Suppressive therapy---- inhibit immune
response not protected from infectious
diseases and sometimes even cancer
1. glucocorticoids limits growth of all lymphoid
tissues decrease formation of Ab and T cells
2. azathioprine - inhibits formation of Ab and T cells
3. cyclosporine --- specific inhibitor of helper T-cell
formation; most valuable because it does not
suppress other portions of the immune system

Copyright 2006 by Elsevier, Inc.

RECAP
Blood Video\Blood Types.mp4

Copyright 2006 by Elsevier, Inc.

U N I T VI
Textbook of Medical Physiology, 11th Edition

Thank you

GUYTON & HALL


Copyright 2006 by Elsevier, Inc.

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