You are on page 1of 10

Far Eastern University

Nicanor Reyes Medical Foundation

Institute of Medicine
1D Batch 2020

Physiology A - Blood Physiology (Part 1)
Dr. Joseph U. Olivar

Main Functions of the Blood 1. Capillary Hydrostatic Pressure

- Force generated by the
1. Maintains homeostasis blood pressure
2. Transports oxygen and a little bit - Force that tends to push
of carbon dioxide the plasma into the
3. Transport of absorbed nutrients interstitial space
4. Transport of waste products to
the kidneys for excretion 2. Oncotic Pressure
5. Transport of hormones - Maintains the plasma
6. Acid base balance (Plasma inside the capillary
proteins acts as buffer)
7. Water and electrolyte balance Note:
8. Immunity to diseases (White
Blood Cells or Leukocytes) Altering the forces means
9. Thermoregulation Filtration and absorption of the
plasma out of the capillaries
Normal Blood Volume Example:
Increase blood pressure =
Depends on the gender and body
Increase Capillary
weight of the person
Hydrostatic Pressure
70 kg adult male: approximately 5
Plasma will go to the
interstitial space: OUT OF
Composition: 60% Plasma; 40%
formed elements (WBC, RBC &
Decrease oncotic pressure
plasma will go OUT OF
Centrifuged Blood THE CAPILLARIES
o Upper/liquid portion:
Formed elements like the RBCs,
WBCs, and platelets are
o Middle portion: Buffy Coat
balanced by its production as well
(WBC and platelets)
as its wear and tear
o Bottom: RBC (dense part)
- Hematocrit is the Plasma
percentage of the
blood that is RBC Predominantly water (91-92%)
Major components of the plasma
Forces that Regulates the Plasma are proteins:
- Albumin
Plasma is within the capillaries because - Globulin (Antibodies)
of the two forces: - Fibrinogen (Coagulation

1 of 10

Functions of Plasma Proteins Myeloid cells Thrombocytes,

Red Blood cells, Granulocytes
1. Maintain water balance between and Monocytes
the intravascular and
extravascular space (pressure RED BLOOD CELLS
which holds on to the plasma)
Non-nucleated in the circulation
Plasma proteins are PRODUCED Biconcave shape
by the liver Very deformable due to excess
Kidneys made it possible that the cell membrane
plasma proteins are NOT Major Function: carries
EXCRETED in the urine (Plasma hemoglobin in the circulation and
proteins are too big to be HEMOGLOBIN inside the red
excreted in the urine) blood cell CARRIES THE
OXYGEN in return
Kidney Diseases: low levels of
Plasma Proteins (PP) Oncotic Anemia Decreased production
pressure decreases, Capillary Below the normal Increased destruction
Hydrostatic pressure value of RBCs
predominates Plasma goes Polycythemia Increased production
into the interstitial space resulting Above the normal Decreased
to EDEMA value of RBCs destruction

2. Contributes in the viscosity of the

blood. **but viscosity is primarily Red Blood Cell production begins in-utero
due to the red blood cells
3. Sources of antibodies
Organs Responsible for
4. Sources of coagulation factors Stage of Life Red Blood Cell
Hematopoiesis 8-10 weeks of Yolk Sac
embryonic life
Describes where blood cells Middle trimester of Liver (primary), spleen &
originate from in the bone marrow pregnancy lymph nodes
All cells in the circulating blood
Last month of
begin their lives inside the bone gestation and after Bone marrow
marrow from a single Pluripotent the baby is born (5
or Multipotent Hematopoietic years old)
Stem Cells Only the axial skeleton
20 years old and (RSVP: Ribs, Skull,
Hematopoietic stem cells gives rise to above Sternum, Vertebra, Pelvic
two progenitor cells (myeloid and Bone)
Lymphoid cells T and B
Lymphocytes Bones of the extremities cant
produce RBCs because they
become infiltrated with fats.

2 of 10

Hepatosplenomegaly 3. Reticulocyte
- First cell to be released
Enlargement of the liver and - Still color blue due to
spleen when the bone marrow is several cytoplasmic
unable to produce RBCs. remnants remaining
The SPLEEN and LIVER are - After 2 days, the
supposedly, only functional cytoplasmic remnants
during the middle trimester of become pinkish non-
pregnancy but they are called to nucleated RBCs
function again when the bone - The cell passes from the
marrow has failed. THEY bone marrow into the
ENLARGE DUE TO EXCESS blood capillaries by
WORK. diapedesis
Extramedullary Hematopoiesis Hemoglobin
Seen in aplastic anemia and
bone marrow dysplasia when the - carries oxygen
liver and spleen produces RBCs 4 Pyrole molecules have to
again combine to form the
Protoporphyrin IX
Erythropoiesis Protoporphyrin IX + Fe++ will
produce HEME
RBC production 1 Heme + polypeptide globin to
1. Hemocytoblast form 1 chain of Hemoglobin
- Other name for pluripotent 4 Chains of Hemoglobin (2
hematopoietic stem cell and 2 chains) are needed to
- Produces 2 genitor cells: produce an adult hemoglobin.
myeloid and lymphoid In an adult hemoglobin,1 heme contains
- Myeloid: source of RBCs 1 iron (1 Hemoglobin = 4 Iron)
- Myeloid transforms to
become proerythroblast It is the IRON CONTENT of the
2. Proerythroblast Hemoglobin which actually binds the
- Committed to form RBC Oxygen so each iron in the Hemoglobin
- Once formed, can combine with one molecule of
the development and the The transport of oxygen (97% are
nucleus condenses and transported) in the blood is primarily in
is completely extruded combination with hemoglobin
out of the cell.
23% carbon dioxide is transported by
** Intermediate Cells big and deeply Hgb and 77% are dissolved in the
staining due to presence of nucleus Plasma
(Basophil Erythroblast,
Polychromatophil erythroblast, The combination of hemoglobin and
Orthochromatic erythroblast) oxygen is reversible - it attaches or

3 of 10

detaches whether the concentration of Transferrin - transport form of

oxygen is increased or decreased iron.
The deoxygenated blood It does not always donate iron for
reaching the lungs is devoid of RBC production because most of
oxygen (lungs is rich in oxygen the time, the iron absorbed from
due to inspiration of air), since the diet is stored as ferritin but
there is a gradient between the when the RBCs needing iron
lungs and the deoxygenated for synthesis, transferrin will
blood, Oxygen attaches to the transfer iron for hemoglobin
Hemoglobin through the process synthesis
of Diffusion Red blood cells produced in the
bone marrow will go in the
When the blood is on the level of circulation for 120 DAYS ONLY
the tissues (devoid of oxygen due then it will rupture or be
to usage of oxygen for destroyed primarily in the spleen.
metabolism), the Hemoglobin RBCs will be dissociated from
releases the oxygen so they can hemoglobin that will release iron
go to the tissues. and will be brought back and
stored in the bone marrow to
Iron be used in the next
erythropoietic series.
Approximately we have 4-6 The iron used in erythropoiesis is
grams of Iron in the body recycled from senescent RBCs
In the blood: most of the time
iron exists as Hemoglobin (2/3 of
Iron is in this form) Iron Elimination
In the muscle: Myoglobin Eliminated thru:
In the Storage tissue primarily
in the duodenum intestinal Stool (bile)
mucosa: Ferritin Urine
Some Iron perform in cytochromic Sweat
and enzymatic reactions. Menstruation heavy
PRIMARY SOURCE: RED MEAT menstruation indicates that you
there is a little absorption in the need to take Iron supplements to
diet prevent iron deficiency
In order for iron to be absorbed in
the duodenum (part of the small Vitamin B12 and Folic Acid
intestine), it has to COMBINE
with APOTRANSFERRIN Important for the final
(protein produced in the liver) maturation of the RBCs
which together with the bile goes Important for the synthesis of
to the duodenum. Once the iron DNA
combines with the apotransferrin Vitamin B12 needs an intrinsic
from the liver it is now absorbed factor produced by the stomach
in the blood as transferrin. to be absorbed.

4 of 10

Lack of Vitamin B12 and folic acid will It is NOT the number of RBCs that
result to: stimulates its production of RBCs.
Erythropoiesis proceeds very
slowly Erythropoietin
Intermediate cells (big and deeply main hormone that stimulates the
staining because they contain production of RBCs
nucleus) go out to the circulation - 90% produced by kidney
because of a very slow DNA - 10% produced by liver
synthesis. Once the EPO is produced, it will
Presence of macrocytes STIMULATE the bone marrow to
Megaloblastic Anemia produce RBCs BUT if the
Pernicious Anemia - type of HEMOGLOBIN IS ENOUGH, IT
megaloblastic anemia secondary WILL SEND A NEGATIVE
to the absence of intrinsic factors FEEDBACK on the kidneys and
(produced by the stomach) that liver to stop its production of
disables the person to absorb erythropoietin.
vitamin B12
Sprue malabsorption of vitamin The number of RBCs in the
B12 and folic acid in the GIT circulation is determined by the
balance between production and
Control of RBC Production destruction.
Level of Tissue Oxygenation is the Going back to Osmosis, it is
most important regulator of RBC defined base on the
production concentration of solute.
Osmosis is the movement of
- Low level of tissue
the solvent from an area of low
solute to an area of high solute
- Due to Anemia (RBC and concentration.
In the clinic, only Isotonic
Even with a normal number of solution (example: 0.9% NaCl,
RBCs, people going to high Normal Saline, 5% Dextrose) is
altitude places will produce being used because Hypertonic
increased number of RBCs due solution shrinks or crenates the
to decreased level of tissue RBCs while Hypotonic solution
oxygenation lyses the RBCs
People with pulmonary Clinical Correlation
tuberculosis, even though they
have normal number of RBCs, 1. Anemia
the oxygen cant traverse the a. Deficiency due to rapid
lungs so the oxygenation is loss or slow production
decreased resulting to an b. Maybe due to blood loss
increase production of RBCs.

5 of 10

c. Maybe due to Iron blood decreased

deficiency oxygenation blood
- Small RBC size vessels are dilated
(microcytic) blood goes back
- pale looking immediately in the right
(hypochromic) side of the heart
- hemoglobin INCREASED workload in
- Give iron the heart.
supplementation - Tolerated by young
d. Megaloblastic Anemia individuals because
- Macrocytic of strong heart
- Hyperchromic muscles.
- hemoglobin
- Give Vit. B12 and 2. Polycythemia
Folic Acid a. Secondary if living in
e. Hemolytic Anemia places with high altitude
abnormality of the shape
f. Hereditary b. Primary due to genetic
Spherocytosis aberration. Polycythemia
- RBCs are spherical Vera (no negative
in shape (should be feedback/inhibition, RBC is
biconcave) continually produced)
- Can be caused by a
defective c. Effect on the circulatory
membrane due to system: the viscosity is
abnormal increased, sluggish flow of
membrane proteins. blood balanced by
- Dysfunctional Na-K increase volume of blood
pump (Na is resulting to a normal
maintained inside) workload. Although there
- Spherical shaped is normal workload, the
RBCs when passing blood flow is sluggish, it
thru the smallest will increase the formation
capillaries, they of spontaneous blood
rupture because of clotting resulting to a high
the shape. probability of stroke.
Resulting to
anemia. d. Very high amount of
g. Effect on the circulatory hemoglobin can be
system: the viscosity corrected by removal of
(embarked by RBCs) is some blood to lessen the
decreased less viscosity.
resistance to flow many
blood goes back to the
right side of the heart
decreased RBCs in the

6 of 10

ABO Blood Grouping Types of Transfusion Reaction

Immediate (ABO) Delayed (Rh)

IgM (Antibody) is IgG (Antibody) is

involved. M: mabilis involved
Very fast, involves Delayed
the complement because
system and will agglutination will
immediately result occur and it will
to hemolysis. call the WBCs
hemolysis can
Forward Reverse
Antigens in
Reagent Antibodies in
Known A and Cross Matching for the Compatibility
Contains: the anti-sera
Known B cells
To detect 1. Major Reaction
Antigens Antibodies P.S.D.R - Patient Serum
presence of:
ANTIGEN ANTIBODIES (antibody) vs. Donor Red
present in present in Cell (antigen)
RED CELL PLASMA Transfusion is NOT
Type A A Anti B possible if the major
Type B B Anti A reaction is reactive
Type A,B AB None 2. Minor Reaction
Anti A or Anti Transfusion is possible
Type O None even if there is a reaction
between a patient cell and
Reagents for direct or forward donor serum
blood typing from commercially It is possible to transfuse type O blood in
prepared anti-sera. the form of packed red blood cells
Reagents for indirect or reverse because the amount of antibody is very
blood typing from prepared little and it will be easily diluted by the
known A and known B cells patients blood.
Agglutination interaction of
antibody with its corresponding Major Reaction:
antigen. Universal Donor: Type O no antigen
Universal Recipient: Type A,B no
ADVERTISMENT: Monster Energy antibodies
Drink. Unleash the Beast!
Positive reaction: Agglutination
(destruction of RBCs) that will
cause renal shutdown and
patients death

7 of 10

Rhesus (Rh) Blood Grouping attack the fetal RBCs. Endpoint:

Erythroblastosis fetalis
Rh Positive: D antigen is present
in the cell membrane In Ultrasound, there is a fluid collection
Rh negative: D antigen is not surrounding the heart, surrounding the
present in the cell membrane abdomen and underneath the skin, this
is called FETAL HYDROPS.
In contrast to ABO blood grouping 9-10% Rh negative pregnant women,
wherein you already have the preformed the newborn can suffer from Hemolytic
antibodies in the plasma, the Rh blood disease with varying manifestations of
grouping, you will not produce the Rh hemolytic anemia as well as hydrops
antibodies unless you are exposed to fetalis.
the D antigen.
Correlation of the Effect of Anemia to
Example: Rh negative doesnt the Circulatory System
have Anti-D, but will have an Anti-
D when exposed to the D Decrease resistance vasodilation
antigen. increase workload of the heart
Fetal heart will also fail
CASE ANALYSIS No longer pumps the blood forward
Rh positive blood given to an Rh negative
patient The blood goes back to the right side
NOTHING will happen to the patient of the heart
He will develop antibodies after 4 Increase capillary hydrostatic
months. pressure
After 4 months, Rh positive blood given Plasma goes out/into the interstitial
AGAIN to an Rh negative patient space resulting to edema formation
The patient will die because the patient called fetal hydrops.
already has been exposed/positive to
Rh antibodies. Liver and spleen enlarged because it will
try to compensate to produce more
Hemolytic Disease of the Newborn RBCs
Hemoglobin from the destruction of the
Will only occur if the mother is RBCs, will be converted to bilirubin and
Rh negative and the father is if it is going to be deposited in the brain
Rh positive - there is a 50% will result to KERNICTERUS.
chance that baby will become Rh
positive Treatment
Rh Negative mother plus Rh 1. RhoGAM
Positive baby: the blood of the a. Anti D Immunoglobulin
fetus can mix with the blood of b. Source: Extracted from the
the mother (Rh negative) so after antibodies developed by
several months, the mother Rh Negative Males
produces a VERY SMALL Anti-D transfused with Rh
immunoglobulin IgG that CAN Positive Blood

8 of 10

c. MECHANISM OF given and fetus suffers

ACTION: The fetal blood is from hydrops fetalis.
exposed to the maternal b. The Rh positive blood of
blood who is Rh negative. the baby is withdrawn and
The maternal blood replaced with Rh negative
generates antibodies. blood just to temporarily
Injected RhoGAM coats stop the maternal antibody
the fetal RBCs so that from destroying the RBCs.
when the fetal and
maternal blood meets, *Prevention through the giving of
there will be no recognition RhoGAM
and the mother will not
*Treatment by means of exchange
produce an antibody
d. Single dose of RhoGAM
given at 28 weeks of Hemolytic Disease of the Newborn
pregnancy (given
intravascularly, effective Rh negative blood given to an Rh
for only for 12 weeks) positive patient
Nothing will happen, sensitization
If pregnancy is not will happen if negative is exposed
yet delivered 12 to the positive.
weeks after after
the the first dose is First thing to do when a pregnant
given, a second woman is Rh Negative:
dose is given to Check Rh type of the partner.
prevent Do NOT give RhoGAM
alloimmunization. immediately.
The 2nd dose is
given after 40 Will you give RhoGAM during the first
weeks. pregnancy?
The first pregnancy is not
If the fetus is Rh positive, affected because the
post-partum dose is given development of antibody is
within 72 hours after the delayed. RhoGAM is given to
delivery. prevent the mother from being
sensitized and produce the
Post partum dose will NOT antibodies.
be given if the baby is Rh Once the antibodies are
negative because there produced, it will be lifetime. So
will be no sensitization with the second and the subsequent
an Rh negative mother. pregnancies will be affected.
First pregnancy should always be
administered with RhoGAM;
a. This is the only treatment
given that the mother is Rh
given if RhoGAM is not
negative and the father is Rh

9 of 10

Will you still give RhoGAM to a

patient undergoing tubal ligation after
5th pregnancy? (History includes: All
4 children did not suffer from HDN
since the obstetrician gave RhoGAM
during the first pregnancy)
RhoGAM will still be given even if
there is no 6th pregnancy
because if the baby is Rh
positive, the mother will be
sensitized and lose the chance of
receiving an Rh positive blood in
cases of emergency.

Why so much concern with Rh and

not with ABO?
ABO involves the IgM antibodies
and they cannot cross the
placenta and will not harm the
fetal RBCs unlike in Rh whose
antibodies are IgG, they cross the

Ad Astra
Per Aspera

10 of 10