UERM

COLLEGE OF MEDICINE CLASS 2021B

2.01 Intro to Hematology/Plasma & RBC
Juliet Ver-Bareng, MD | August 25, 2017
PHYSIOLOGY
LE 2 TRANS 1

OUTLINE  Plasma= 5%
I. BLOOD • Specific Gravity
A. Major components of blood  Whole Blood = 1.050
B. Whole blood  Plasma = 1.025
C. Hematopoiesis • Viscosity
D. Functions of blood  3.5-5.5x more viscous than H O 2

II. PLASMA  due to hematocrit (RBC) and fibrinogen (plasma protein)

III. ERITHROCYTES
IV. HEMOGLOBIN B. WHOLE BLOOD
A. Structure • Plasma – 55%
B. Synthesis
 Water – 91.5%
C. Abnormalities
 Proteins – 7.5%
D. Oxygen dissociation curve
▪ Albumin (54%) – smallest, most abundant; transport fatty
Carbon dioxide dissociation curve
acids
V. LIFESPAN OF RBC
▪ Globulins (38%) – from plasma and liver cells e.g. gamma
VI. IRON
globulins and immunoglobulins
A. Iron transport
▪ Fibrinogen (7%)
B. Heme and Non-heme iron
 Solutes/Waste – 1%
VII. CLINICAL CORRELATES
A. Anemia and polycythemia • Formed elements – 45%
B. Hb1Ac and diabetes  RBC – 99%
C. Osmotic fragility test  WBC and platelets – 1%
D. Blood typing • Buffy coat – <1%
1. ABO Blood system
2. Rh Factor
3. Other minor blood types
E. Blood transfusion
1. Reasons for transfusion
2. Indications
3. Contradictions
4. Complications
F. RBC Disorders
1. Anemia
VIII. REFERENCES
IX. QUIZ

OBJECTIVES
1. Discuss the components of blood
1.1 Enumerate the substances dissolved in plasma
1.2 Identify the cellular elements
2. Describe the functions of blood
3. Determine the factors needed for hematopoiesis
4. Give the significance of the erythrocyte structure to its Figure 1. Whole Blood cell components
function
5. Discuss the factors needed in erythropoiesis C. HEMATOPOEISIS
6. Explain the oxygen dissociation curve (ODC) • Pluripotent Hematopoietic Stem Cell (PHSC) – Originated
6.1 Relate the shape of the curve to the molecular from bone marrow; where all cells of circulating blood are
characteristics of hemoglobin derived
6.2 Determine changes in the ODC in a given clinical  Differentiate to become:
condition ▪ Colony forming unit (CFU) – produce colonies or
7. Describe the recycling of blood components specific types of blood cells
8. Discuss causes of abnormal red blood cell indices  Aka committed stem cell
▪ Lymphoid stem cell (LDC)
LEGEND ▪ Another PHSC
Remember Lecturer Book Previous Presentation • Growth inducers – Controls the growth and development of
Trans the stem cells
 Factors that help in cell differentiation:
▪ Interleukin-3 (IL-3) – promotes growth and reproduction of
almost all different types of committed stem cells
I. BLOOD ▪ Interleukin-5 (IL-5)
A. MAJOR COMPONENTS OF BLOOD ▪ Thrombopoietin (TPO) – involved in platelet growth
● Volume ▪ Erythropoietin (EPO) – involved in RBC growth
▪ Granulocyte-Macrophage Colony Stimulating Factor (GM-
 Male - 4-6L
CSF) – involved in WBC growth
 Female - 4.5-5.5L
• Differentiation inducers – promotes differentiation of cells
• Body Weight Percentage
IL-3 – Promotes growth and reproduction of virtually all the
 Whole Blood = 6-8% different types of committed stem cells

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 2.01 Introduction to Hematology/Plasma & RBC LE 2

Table 1. Plasma Proteins and Their Functions TRANS 1

Plasma Proteins Function
Transthyretin Binds T3, T4 and vitamin A
Albumin Oncotic pressure, binds steroids, T3
and bile
α 1-Antitrypsin Protease inhibitor, causes
emphysema
α 2-Macroglobulin Broad spectrum protease inhibitor
Haptoglobulin Binds hemoglobin
Β-Lipoprotein Binds lipid
Transferrin Binds iron
Complement C3 Third component of complement
system
Fibrinogen Clotting factor, precursor of fibrin
IgA Mucosal immunity
IgD
IgE Binds to mast cells or basophils
IgG Humoral immunity
Figure 2. Formation of multiple different blood cells from the original PHSC
IgM Humoral immunity
in bone marrow

D. FUNCTIONS OF BLOOD III. ERYTHROCYTES

• Transport (free form or bound) A. RBC PRODUCTIONS SITES
 Nutrients – plasma • Yolk Sac – early embryonic life
 Gases – plasma and RBC • Liver, spleen, lymph nodes – 2 nd trimester of gestation (4-6
 Hormones, enzymes, electrolytes – plasma months)
 Waste materials for excretion – plasma • Bone marrow – last month of gestation up to 5 years of age
• Defense – WBC • Proximal portion of long bones – 6-20 years of age
• Repair – hemostasis • Marrow of membranous bones - >20 years of age
• Acid base balance – plasma and RBC
• Maintenance of body temperature – plasma B. ERYTHROPOIESIS
• Maintenance of adequate body fluid – plasma Stages of RBC Maturation
• Myeloid stem cell
II. PLASMA • Proerythroblast (Day 1) – first cell that can be identified in the
Components of Plasma RBC series
• Straw colored watery solution • Erythroblast (Day 2-4) – hemoglobin accumulation, nuclear
• 55% of blood volume condensation, decreases in cell size, decreased mRNA,
• SERUM – plasma without coagulating factors morphologically identifiable
 Factors 1, 2, 5, 8  Stages:
• Plasma Proteins (synthesized in the liver, except for γ globulins) ▪ Basophil erythroblast - 1st generation cells, stain with
basic dyes
 Albumin - main plasma component
▪ Polychromatophil erythroblast
 Globulin (α, β, γ)
▪ Normoblast
 Fibrinogen
• Reticulocyte (Day 5-7) - after enucleation; at this stage, RBC is
in circulation
 Contains small amount of basophilic material,
 Remnants of Golgi apparatus, mitochondria, and few other
cytoplasmic organelles
▪ Diapedesis – stage in reticulocyte where cells pass from
bone marrow into blood capillaries
▪ Retic count – indicator of rate of RBC production
 Normal: 2%
• Mature RBC/Erythrocyte

Figure 3. Serum protein electrophoresis showing amount of protein

distribution

Additional Information
• Greenish/yellowish plasma
 May indicate jaundice due to break down of heme
• Paler than straw color
 High lipid content
Figure 4. Stages of RBC Maturation

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 2.01 Introduction to Hematology/Plasma & RBC LE 2

Additional Information C. RBC SHAPE AND SIZE TRANS 1

• RBCs are enucleated, thus they are unable to: Functions of RBCs
 Synthesize protein ● Transport of gases - bound to hemoglobin
 Engage in oxidative metabolism  O2 - oxyhemoglobin
▪ They get their energy from  CO2 - carbaminohemoglobin
• Glycolysis ● Acid Base Buffer
• Pentose shunt pathway ● Contain carbonic anhydrase
▪ catalyzes the reaction: CO2 + H2O ⇆ H2CO3 which is
Factors Affecting RBC Production important in respiration
• Erythropoietin – a hormone secreted by the kidneys that
increases the rate of production of red blood cells in response to Normal RBC Shape and Size
failing levels of oxygen in the tissues • Top view – biconcave disks in shape
 Produced in response to decreased O2 in blood (Hypoxia) • Side view – discoid dumbbell shape
 Effects: • Mean diameter – 7.8 μm
▪ Stimulate the proliferation and differentiation of committed • Thickness
erythroid cells  2.5 μm at thickest point
▪ Prevents the apoptosis of erythrocytic progenitors
 1 μm or less in center
▪ Increases the viability of erythrocytes
• Average volume of RBC – 90-95 cubic μm
 From interstitial cells in the peritubular capillaries (kidney)
• RBCs are “bags” that deform into almost any shape and can
and perivenous hepatocytes
squeeze through capillaries
▪ Kidney: 90% (from the Juxtaglomerular apparatus/JGA )
▪ Liver: 10%
 Increased number of RBCs will activate a negative feedback Advantages of RBC Shape
mechanism to stop RBC production • Large surface area:volume ratio increases diffusional exchange
across the RBC membrane
• Facilitates flow through narrow vessels
 Rouleaux formation – RBCs stack in single-file like dinner
plates
▪ Occurs in increased fibrinogen and globulin
▪ Erythrocyte sedimentation rate – rate of how fast RBCs
settle
 0-15 mm/hr in males
 0-20 mm/hr in females
 Elevated in infection but non-specific
• Allows bending and flexing of the RBC
 Can flow through 4 μm vessels (sinusoids of spleen and
liver)

Abnormal RBC Shapes and Size

Figure 5. Function of the erythropoietin mechanism to increase • Anisocytosis – unusual size
production of RBCs when tissue oxygenation decreases  Microcytic - <7 μm due to iron deficiency (sideropenic
anemia) or hemoglobinopathia
Additional Information  Macrocytic - >7.8 μm due to deficiency in maturation factors
• Hypoxia-inducible factor-1 (HIF-1) – Renal tissue hypoxia  Megaloblastic - RBCs too large with odd shapes for
 Helps in EPO synthesis Hemoglobin A (most common): 2α (red) and 2β (green)
 Stimulus: Hypoxia, Androgens and Cobalt salts chains
 Others: Norepinephrine, Epinephrine and Prostaglandin ▪ Folic acid or vitamin B12 deficiency (macrocytic
megaloblastic anemia)
• Iron  Gigantocytes - 4x the normal size; young RBC
• Vitamin B12 – maturation factor; absorption in the body needs • Poikilocytosis - unusual shape
intrinsic factor produced by the stomach  Acanthocytes – spur/spike cells
 Low intrinsic factor, low B12 absorption, decrease in RBC  Codocytes – target cells
maturation, pernicious anemia  Stomatocytes – mouth
 Mechanism  Drepanocytes – sickle
▪ Intrinsic Factor binds tightly with vitamin B 12 making it in  Echinocytes
bound state during bound state, B12 is protected from  Burr cells
digestion by the gastrointestinal secretions.  Elliptocytes
▪ (Still during bound state) Intrinsic factor binds to specific  Ovalocytes
receptor sites on the brush border membranes of the  Spherocytes
mucosal cells in the ileum.  Tear drop
▪ Vitamin B12 is transported into the blood; during the next
few hours by pinocytosis, carrying both intrinsic factor and
the vitamin through the membrane
• Folic acid – maturation factor

Additional Information
• Folic acid and Vitamin B12 are essential for DNA synthesis
and formation of thymidine triphosphate

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 2.01 Introduction to Hematology/Plasma & RBC LE 2
TRANS 1
A. STRUCTURE OF HEMOGLOBIN

Figure 7. Structure of hemoglobin

● Heme - contains the iron part, where the oxygen binds

● Globin - synthesized by ribosomes; combines with heme,
forming a subunit of hemoglobin called hemoglobin chain
Figure 6. RBC morphology
B. SYNTHESIS OF HEMOGLOBIN
1. 2-succinyl-CoA is produced in the Krebs cycle binds to 2
RBC Indices glycine molecules to form a pyrrole molecule
• Mean cell volume (MCV) 2. 4 pyrrole molecules bind together to form Protoporphyrin IX
 It is the measure of average volume of RBC 3. Protoporphyrin IX binds Fe2+ (ferrous iron) to form heme
• Mean cell Hemoglobin (MCH) 4. Heme combines with globin, a long polypeptide chain
 It is a measurement of the average weight of hemoglobin in synthesized in the ribosome to form a hemoglobin chain
individual erythrocytes
• Mean Cell Hemoglobin Concentration (MCHC)
 It is the average concentration of hemoglobin in erythrocytes
• Red cell distribution width(RDW)
 It is a measure of variability of erythrocyte size
Table 2. RBC Indices
INDICES MALE FEMALE
Hematocrit (%) 42±5 37±
RBC count (106
4.5-5 4-4.5
/μL)
MCV (fL)
87 87
(Hctx10)/RBC
MCH (pg) Figure 8. Hemoglobin Synthesis
29 29
(HbX10)/RBC
MCHC ● There are variations in hemoglobin chains based on the amino
(HbX100)/Hct
34 34 acid of the polypeptide chain (⍺, β, ε or γ chains)
MCD (mean  Hemoglobin A - 2 ⍺ chains + 2 β chains; most common in
diameter of 500 7.5 7.5 adult body
cells in smear)  Fetal Hb - 2 γ chains + 2 ⍺ chains
 Embryonic Hb - 2 ⍺ chains + 2 ε chains
Additional Information ● Red blood cells contain several hundred thousand hemoglobin
• Hematocrit = percent of volume of blood occupied by molecules which transport oxygen
RBC  Male - 14-16 g/dL
• Concentration of RBCs in the blood  Female - 12-14 g/dL
 Male – 5,200,000 ( 300,00) ● 1 gm of Hb capable of combining 1.34 ml O2
 Female – 4,700,000 ( 300,00)  Male
▪ At average 15 gm% Hb
• Quantity of Hemoglobin in RBCs
▪ Carries maximum amount of 20 ml O2
 RBCs can concentrate hemoglobin about 34g per 100
 Female
mL ▪ At average 14 gm% Hb
 Normal hematocrit: 40-45% ▪ Carries maximum amount of 19 ml O2

Constituents of RBC
C. HEMOGLOBIN ABNORMALITIES
 Hemoglobin (Hb) - provides the red pigment
● Structural or qualitative – the amino acid sequence is altered
 2,3-diphosphoglycerate (2,3 DPG) - reduces Hb affinity to O 2
because of incorrect DNA code
 Glutathione - protects RBC from oxidant damage
 Hemoglobinopathy
 Carbonic Anhydrase
● Quantitative - Production of one or more globin chains is
reduced or absent
IV. HEMOGLOBIN
 Thalassemia
• Where oxygen binds to be transported in the body

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● Hereditary persistence of fetal hemoglobin (HPFH) - TRANS 1

complete or partial failure of γ globin to switch to β globin
C. OXYGEN DISSOCIATION CURVE
● Sigmoid shape
● 50% saturation - 28 mmHg of oxygen; rapid increase until 50%
● Further increase in oxyhemoglobin lead to slowing down of
saturation until 90%, until it’s 100% (Plateau stage, Boron)
● At the level of tissue, ~40% saturation; at the level of alveoli -
~100% saturation
● Shift to the Right (less affinity of Hb for O2 → O2 is released)
 Decrease in pH (Acidic)
 Increase in 2,3-Bisphosphoglycerate
 Increase in Temperature
 Increase in Carbon Dioxide
● Shift to the Left (greater affinity of Hb for O2 → O2 remains
bound to Hb)
 Increase in pH (Basic) Figure 10. Carbon Dioxide Dissociation Curve
 Decrease in 2,3-Bisphosphoglycerate
 Decrease in Temperature V. LIFESPAN OF RBCS
 Decrease in Carbon Dioxide ▪ Life span of RBC: 120 days in circulation
 Erythrocytes form in the bone marrow
 RBCs stay in circulation for 120 days
 Senescent RBCs are phagocytosed in the liver and
spleen
 Hemoglobin dissociates to become heme and globin
 Heme components are recycled in the body - ferrous
irons are transported in the body while remaining heme is
converted to biliverdin and then to bilirubin, then secreted
in form of bile by the liver
 Membrane proteins and globin proteins are broken down
to amino acids by the body

Figure 9. Oxygen Dissociation Curve

Additional Information
• 2,3-Biophosphoglycerate
 Produced during glycolysis

D. CARBON DIOXIDE DISSOCIATION CURVE

• Carbon dioxide dissociation curve Figure 11. Lifespan of RBC
 Tissues: 46 mmHg V. LIFESPAN OF RBCS
 Alveoli: 40 mmHg VI. IRON
 Lower curve dependent on ▪ Transport and Storage of Iron:
 Haldane Effect  When Iron is absorbed by the small intestine, it combines
▪ when oxygen is bound to hemoglobin, carbon dioxide is in the blood plasma with a beta globulin, apotransferrin to
released form transferrin, which is transported in the plasma
▪ contributes more to carbon dioxide transport than Bohr  The Iron is loosely bound in the transferrin and can be
effect released to any tissue cell at any point in the body
▪ due to increase acidity in Hemoglobin as oxygen binds;  Excess Iron in the blood is deposited in the liver
more acidic Hb = lower tendency for Hb to bind with CO2, hepatocytes and less in the reticuloendothelial cells of
and release of H+ which binds to bicarbonate and dissociate the bone marrow
to water and carbon dioxide, to be released from the body
 In cytoplasm, Iron combines with apoferritin to form
 Bohr Effect ferritin
▪ increased in carbon dioxide causes oxygen to be  Storage Iron - Iron stored as ferritin
displaced in Hb  Hemosiderin - smaller quantities of iron in the storage pool
are in an extremely insoluble form
 Daily loss of Iron
▪ 0.6 mg of iron each day, into the feces

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Table 3. Two types of heme like, it 1

Heme Iron
found in meat, poultry, and
fish
readily absorbed by the body
(23% absorbed)
absorption not changed by
other food
transported by heme
transporter on apical portion
● In hereditary spherocytosis where RBC is sphere or ball TRANS
Non Heme Iron will easily burst as it cannot accommodate more water due to its
found in vegetables, fruit, and shape; hemolyzed at higher NaCl concentration
eggs ● In sickle cell and thalassemia, it will burst at lesser tonicity
not absorbed as well (3-8%
absorbed); vegans are
advised to take in more iron to
compensate
absorption can be increased
or decreased by other food
transported by DMT-1
transporter on apical portion

Figure 13. Effects on RBCs in different solutions

Figure 12. Iron Transport & Metabolism

Table 4. Recommended Dietary Allowance of Iron (in mg); varies among Figure 14. Osmotic Fragility Test
sex during reproductive years; more iron needed for women in reproductive
years
AGE MALE FEMALE
C. BLOOD TYPING
0-6 mos. 0.27 0.27
7-12 mos. 11 11 The ABO Blood System
1-3 yrs 7 7
4-8 yrs 10 10
9-13 yrs 8 8
14-18 yrs 11 15
19-30 yrs 8 18
31-50 yrs 8 18
51-70 yrs 8 8
>70 yrs 8 8
Pregnant women 27

VII. CLINICAL CORRELATES

A. Hb1Ac AND DIABETES
• Hemoglobin and Glucose
 Glucose rapidly diffuses into RBC by facilitated diffusion
 N terminal valine of hemoglobin alpha chain is available for
Figure 15. Major Blood Types
irreversible glycation:
 Hemoglobin Hb -> Hba1c Table 5. Blood types and their agglutinins and the plasma they agglutinate
 Hb glycation level (+HbA1c level) is proportional to glucose
concentration in plasma; high levels = possibility of diabetes FREQUENCY
PLASMA
 Normal hemoglobin A1c level = 4% to 5.9% BLOOD AGGLUTININS (%)
AGGLUTINATES
● Transporters in the RBC membrane TYPE IN PLASMA
RBC OF TYPE
 CL- - HCO3- exchanger = AE1 or Band 3 USA PH
 Glycophorin – contribute the major portion of glycosylation O. Anti A, Anti B 46 45 A, B, AB
 Water channel (Aquaporin) = AQP1
A Anti B 40 25.8 B, AB
B. OSMOTIC FRAGILITY TEST
● Measures the ability of red blood cells to retain their integrity in
hypotonic solutions B Anti A 10 22.8 A, AB
● Depending primarily on: AB None 4 6 None
 Volume of the cell
 Surface area
 Cell’s membrane function

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Rh- 1
▪ Rh-positive erythrocytes from fetus enter blood ofTRANS
negative woman during the birth process
▪ Anti-RH antibodies are produced by woman’s immune
system that remain in the women’s bloodstream
▪ During succeeding pregnancy, antibodies pass
placental barrier and enter fetal blood causing
destruction of erythrocytes
● Prevention
 Mother receives anti Rh D immunoglobulins on the 28 th week
of gestation and right after delivery
● Management
 Baby receive exchange transfusion of Rh- blood

D. BLOOD TRANSFUSION
● Process of transferring whole blood or blood components from
donor to recipient
● Indications
 Active blood loss
▪ To replace circulating volume & O2 delivery
 Perioperative anemia
▪ To ensure adequate O2 delivery during preoperative
phase
 Symptomatic chronic anemia without hemorrhage or
impending surgery
Figure 16. Blood typing with addition of antisera causing agglutination due ▪ Hb < 6 g/dl
to antibody-antigen reactions ● Indications of blood transfusion
 Whole Blood
▪ Acute blood loss
▪ Shock
▪ Exchange transfusion in neonate
 Packed red blood cells
▪ Chronic severe anemia
▪ Leukemia
▪ Thalassemia
 Platelets concentrate
▪ Thrombocytopenia
▪ Bleeding due to platelet dysfunction
▪ Malignancy
▪ Major surgery
● The Contraindications of Blood Transfusion
 Acute pulmonary edema
 Congestive heart failure
 Pulmonary embolism
 Malignant hypertension
 Hypercythemia
 Serious renal failure
 Serious allergy to blood transfusion
● Complication of Blood Transfusion
 Acute – during transfusion/within 24 hours
 Delayed – after 24 hours
 Transfusion reactions occurs within first 10-15 mins or 50 cc
Figure 17. Cross matching - done before exchange transfusion; donor RBC of blood
cross matched with recipient’s plasma; agglutination = do not give blood; ▪ Allergic - facial flushing, rash to low BP
not compatible ▪ Febrile - tachycardia, fever, chills, headache
▪ Hemolysis - chest pain, low back pain, low BP
Other minor blood types
● Rhesus factor: C, D, E Table 6. Complication of Blood Transfusion
● Duffy IMMUNE MEDIATED NON-IMMUNE MEDIATED
● Kidd Acute Delayed Acute Delayed
● MNS -Septic
● P -Circulatory
-Hemolytic overload
Hemolytic
reaction -Metabolic
Rh Blood Type reaction
- Post -Hyper- -Infection
• Rh(+) = presence of Rh antigen -Febrile non-
transfusion kalemia -Iron
● Rh(-) = absence of Rh antigen hemolytic
purpura -Hypo- overload
● Development of anti Rh of mother during subsequent pregnancy -Urticaria
-Graft vs. calcaemia
-Anaphylactic
 Erythroblastosis fetalis or Hemolytic Disease of the host disease -Metabolic
Newborn alkalosis

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TRANS 1
VIII. RBC DISORDERS Table 8. Primary vs. Secondary Absolute Polycythemia
PRIMARY SECONDARY
Anemia Physiologic adaptation to
• Deficiency in hemoglobin in the blood caused by either too few Polycythemia vera
hypoxia (high altitude and
(Eryhtremia)
RBCs or too little hemoglobin in the cells cardiac failure)
• Insufficient number of RBCs All cell lineage increases
Elevated EPO
 Blood loss anemia – occurs when chronic blood loss (RBC, WBC, platelets)
happens and cannot absorb enough iron from the intestines Genetic aberration – does not
to form hemoglobin as rapidly as it is lost stop producing cells
▪ Microcytic, hypochromic anemia Tumor/cancer or genetic
 Aplastic anemia - occurs when the immune system begins mutation
attacking healthy cells (bone marrow stem cells)
 Hemolytic anemia VIII. REFERENCES
▪ hereditary spherocytosis - RBCs are very small and
spherical rather than being biconcave disks
• Bareng, J.V. (2017). Lecture on Introduction to Hematology
PowerPoint Presentation.
▪ sickle cell anemia - contains abnormal type of
hemoglobin called Hemoglobin S (contains faulty beta • Boron and Boulpaep Medical Physiology, 2 nd Ed.
chains in the hemoglobin molecule) • Guyton and Hall Textbook of Medical Physiology, 13th Ed.
▪ Erythroblastosis fetalis - RH - positive RBCs in the fetus • Ganong’s Review of Medical Physiology, 23 rd Ed.
are attacked by antibodies from an Rh - negative mother • 2020 Transes
• Decrease/Abnormal Hemoglobin content
 Fe deficiency X. QUIZ QUESTIONS
 Vitamin b12 (Pernicious anemia)
 Folic Acid 1. What is the stimulus for the production of EPO?
 Abnormal amino acid chain (Thalassemia/sickle cell anemia) Hypoxia or decrease in oxygen in the body
• Parameters of Anemia 2. Give the content of RBC - Hemoglobin, carbonic
● RBC site (MCV) anhydrase, 2,3-bisphosphoglycerate, glutathione
● Hb content (MCHC) 3. Give one difference between plasma and serum? Plasma
● Normocytic - with coagulation factors; serum: without coagulation
factors
Table 7. Comparison between anemia and polycythemia 4. What do you call the immature RBC? Reticulocyte
ANEMIA POLYCYTHEMIA 5. Explain what will happen to the RBC if subjected to a
Deficiency of hemoglobin, Excess hemoglobin, hypertonic environment. Crenation/ Cell will shrink
hematocrit, or RBC in blood hematocrit, or RBC in blood 6. Give the cause of Jaundice. Breakdown of Heme to
Easy fatigability (lack of Billirubin
Headaches and dizziness
oxygen transport) 7. What happens to old senescent RBCs? Hemolysis in
Dizziness Pruritus spleen
Chest pain (may with a clog or 8. Differentiate serum from plasma. Plasma contains
Shortness of breath
slow blood flow in the heart) coagulation factors, while serum does not
Pallor (lacks redness) Painful swelling of the joints 9. What do you call the unusual size of RBC? Anisocytosis
Plethora or erythromelalgia
Tachycardia (fast heart beat) 10. Explain what will happen to the RBC if subjected to a
(tender palms and soles)
hypotonic environment. Swell/Hemolysis
Syncope (lack of oxygen in
Hypertensive 11. What is the main protein component of Plasma? Albumin
the brain)

Polycythemia
• Overproduction of RBCs (as well as WBCs and platelets)
• Absolute polycythemia
 Polycythemia vera
▪ RBC count may be 7 to eight million / mm3 and the
hematocrit may be 60 to 70% instead of the normal 40 -
45%
▪ Cause: genetic aberration in the hemocytoblast cells
that produce the blood cells (GOK!!!)
▪ Both hematocrit and total blood volume increases

 Effects of Polycythemia on circulatory system

▪ Due to increased viscosity of blood = sluggish blood
flow
 Secondary to hypoxia (physiologic, cardiopulmonary renal
disease)
▪ Physiological polycythemia – occurs in natives who
live in altitudes 14,000 to 17,000 ft., where the
atmospheric oxygen is low
• Relative Polycythemia
 Low plasma volume (diarrhea, vomiting, excessive
sweating)
 Prevention of thrombosis (ambulation when
possible/compression devices on lower extremities)

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