Last edited: 8/21/2021

1. HEMATOCRIT
Hematology - Hematocrit Medical Editor: Dr. Sofia Suhada M. Uzir

OUTLINE Classification of anemia

I) INTRODUCTION Based on the mean corpuscular volume (MCV)

II) LAYERS IN BLOOD SAMPLE o Microcytic
III) SUMMARY o Normocytic
IV) REVIW QUESTIONS o Macrocytic
V) REFERENCES The normal MCV is 80–100 fL.
o If more than one disorder is present, the MCV may be
an average of the different populations of RBCs
producing a normal MCV
o However, in mixed disorders, the red cell distribution
I) INTRODUCTION width (RDW) will be increased
o Other classification schemes stratify anemias based on
Hematocrit = Packed Cell Volume (PCV) increased RBC loss (due to bleeding or hemolysis) or
o Volume percentage of red blood cells in blood, impaired production
measured as part of a blood test [Oxford Medicine]
o The value is expressed as a percentage or fraction
of cells in blood
o For example, a PCV of 40% means that there are 40 (B) BUFFY COAT
milliliters of cells in 100 milliliters of blood It constitute of platelets & WBCs

Did you know? (1) Platelets

Red blood cells account for nearly all the cells in the blood. 150,00- 450,000 / ml blood
o The PCV rises when the number of red blood cells Function
increases or when the total blood volume is reduced o Plug up any damaged blood vessels
Example: dehydration
<150,000 = thrombocytopenia
o The PCV falls to less than normal, indicating anemia o Increase chance of bleeding
when your body decreases its production of red blood
cells or increases its destruction of red blood cells. >450,000 = thrombocytosis
[The Association for Clinical Biochemistry & Laboratory Medicine] o More clots formation
(2) WBC/ leukocytes
II) LAYERS IN BLOOD SAMPLE 4800 - 11,000 / ml blood
Example: < 4800 = leukopenia
o 1 mm3/ ml from brachial vein taken out and >11,000 = leukocytosis
centrifuged o Leukemoid reaction
Coated with heparin to prevent blood clots o Leukemia
o This will be separated by densities into 3 different o Infections
layers: (C) PLASMA
Erythrocytes
Buffy coat 0.55 ml = 55 % of the total blood sample taken
Plasma 90-93% of plasma is water
8% is protein
Others:
o Oxygen, Co2, NO
o Electrolytes
Sodium
Potassium
Chlorine
o Nutrients
Glucose
Amino acids
Fatty acids
o Enzymes
o Hormones
o Metabolic waste products
The plasma transports the waste product to the
kidney/liver where it could be excreted in the
urine/feces
Figure 1. Layers of centrifuged blood sample [Wikipedia]
Lactic acid
(A) ERYTHROCYTES Uric acid
It is the most dense layer Creatinine
o It constitutes about 5-6 million/ ml of blood
About 0.45 ml / 45% of the total blood taken
< 45% = anemia
> 45% = polycythemia

Hematocrit HEMATOLOGY: Note #1. 1 of 3

(1) Water Regarding the water in plasma volume, which is
true?
90-93% of plasma
a. It doesn’t transport RBCs
o Universal solvent
b. It is 98% of the total plasma volume
Helps transport RBCs
c. It is 90% of the total plasma volume
Dissolve certain types of solutes, protein,
d. It is a type of buffy coat
molecules within the blood vessels
Controls blood volume and blood pressure
Regarding platelets which is false?
(2) Plasma Protein a. Platelets is a component of the buffy coat
b. Less than 150,000 is considered thrombocytopenia
8% of plasma
c. More than 450,000 is called thrombocytosis
(i) Albumin d. It always increases with RBCs
o 60% of the total plasma proteins
o Regulate water balance (osmotic pressure) Regarding the plasma, which is false?
a. Water is one of its components
(ii) Globulins b. It is free of nutrients
o Alpha + beta c. It helps in excreting metabolic waste products
Transport proteins d. Oxygen is one of its components
Transport substances that are not soluble within
the blood plasma
Examples: Which is true regarding the layers of a centrifuged
Transferrin blood sample?
o Iron a. There are 4 layers
If not bounded, can cause free radicals b. There are 5 layers
c. There are 2 layers
Thyroxine binding globulins (TBG)
d. There are 3 layers
o Hormones T3/T4
o Gamma
Antibody like Erythrocytes, which is true?
Produced by plasma cells (differentiated B cells) a. Less than 45% is called anemia
For fighting different types of pathogens by b. More than 45% is seen in high mean corpuscular
volume
Opsonization
c. It constitutes about 4-5 million/ml of blood
Activating certain pathways
d. It constitutes about 5-8 million/ml of blood
III) SUMMARY
Regarding albumin, which is true?
Hematocrit is also known as PCV a. Alpha and beta is a subtype of albumin
There are 3 layers in centrifuged blood sample which are b. Gamma is a subtype of albumin
o Erythrocytes – 45% c. It helps in regulating water balance
o Buffy coat d. It helps in fighting pathogens by opsonization
o Plasma – 55%
The buffy coat is made out of platelets and WBCs CHECK YOUR ANSWERS
The plasma contains mainly water, which is a universal
solvent V) REFERENCES
Lab Tests Online UK PCV. The Association for Clinical
IV) REVIW QUESTIONS Biochemistry & Laboratory Medicine (2020)
The following is true considering gamma globulins https://labtestsonline.org.uk/tests/pcv
Sumana Devata. Anemia, Oxford Medicine (2018)
except? https://oxfordmedicine.com/view/10.1093/med/9780190862800.001.
a. It is antibody like 0001/med-9780190862800-chapter-62
b. Is produced by plasma proteins Blood fractionation [digital image]
https://en.wikipedia.org/wiki/Blood_fractionation
c. It helps in regulating blood pressure through Le T, Bhushan V, Sochat M, Chavda Y, Zureick A. First Aid for
elimination of pathogens the USMLE Step 1 2018. New York, NY: McGraw-Hill Medical; 2017
d. It is involved in opsonizations of pathogens Marieb EN, Hoehn K. Anatomy & Physiology. Hoboken, NJ:
Pearson; 2020.
Boron WF, Boulpaep EL. Medical Physiology.; 2017.
The following is true regarding hematocrit except? Urry LA, Cain ML, Wasserman SA, Minorsky PV, Orr RB,
a. It is the total amount of WBC in blood sample Campbell NA. Campbell Biology. New York, NY: Pearson; 2020.
Jameson JL, Fauci AS, Kasper DL, Hauser SL, Longo DL,
b. It is also known as packed cell volume Loscalzo J. Harrison's Principles of Internal Medicine. New York
c. It is expressed as a percentage etc.: McGraw-Hill Education; 2018.
d. It rises when the number of red blood cells increases Sabatine MS. Pocket Medicine: the Massachusetts General
Hospital Handbook of Internal Medicine. Philadelphia: Wolters
Kluwer; 2020.
Which of the following is true regarding blood
plasma?
a. It constitutes 65% of the total blood sample
b. It helps in regulating blood pressure
c. Erythrocytes is one of the constituents
d. It helps in the classification of anemia

Why is water is known as universal solvent?

a. Helps transport RBCs
b. Dissolve certain types of solutes, protein, molecules
within the blood vessels
c. Controls blood volume and blood pressure
d. All of the above

2 of 3 HEMATOLOGY: Note #1. Hematocrit

Hematocrit HEMATOLOGY: Note #1. 3 of 3
 Last edited: 8/11/2021

1. ERYTHROPOIESIS: RED BLOOD CELL FORMATION

Erythropoiesis: Red Blood Cell Formation | Part 1 Medical Editor: Dr. Sofia Suhada M. Uzir

OUTLINE (C) CELLS PRODUCED

I) ERYTHROPOIESIS
II) REVIEW QUESTIONS
III) REFERENCES

I) ERYTHROPOIESIS
Formation of RBCs is called erythropoiesis

(A) LOCATION
(1) Sites – In order Figure 2. RBCs [European Pharmaceutical Review]
Yolk Sac
Liver
(D) GROWTH FACTORS/ MOLECULES REQUIRED
Spleen
Bone marrow (RED) (Spongy bone trabeculae) (1) Erythropoietin (EPO)
o Skull
Made by PCT cells in kidney due to hypoxia
o Sternum
Hypoxia stimulus:
o Pelvis
o Anemia
o Epiphyses of long bones
o Obstructive Lung disease
o Restrictive Lung Diseases
o Obstructive sleep apnea
o Heart Failure
o Circulatory Shock
o Atherosclerosis
o Thromboembolisms
o Cyanide or Carbon monoxide poisoning
(2) EPO production
Hypoxia
o Degradation of hypoxia inducible factor (HIF)
o HIF in kidney cells
HIF transcription factor
o Activates genes that become expressed and lead to
synthesis of a protein called EPO
o EPO then travels to red bone marrow where it acts on
Figure 1. Hematopoiesis - bone marrow [News Medical] myeloid stem cells
This converts myeloid stem cells into RBC
precursor cells
(2) Mnemonic
Young Liver Synthesizes Blood cells

(B) DRIVING FACTOR

Blood loss
o Ulceration
o Stab wound
Hypoxia
o Inadequate oxygen delivery to tissue
o Production of more RBC to supply more oxygen
Anemia

Figure 3. Erythropoiesis induced by hypoxia [Learnhaem]

ERYTHROPOIESIS: RED BLOOD CELL FORMATION HEMATOLOGY: Note #1. 1 of 3

(3) Requirements (iii) In the ileum
B12 o Intrinsic factors bind with the transport protein
Folate Receptor mediated endocytosis
Iron Vitamin B12 is released into the circulation
Carbohydrates through the basolateral membrane
Fats Binds with transcobalamin I & II
Amino acids
(4) Iron metabolism
(E) SEQUENCE OF DEVELOPMENT
Iron ingested from food/supplements in Fe3+ state
(1) RBC pathway
(i) In duodenum – enterocytes
o A ferro-reductase enzyme known as duodenal
cytochrome B converts Fe 3+ into Fe 2+
o Then Fe 2+ is brought into duodenal cell with H+ by (RBC) Figure 5
DMT-1
o Once in duodenal cell: (i) Basophilic erythroblasts
Fe 2+ binds with apoferritin converting into ferritin o Stain blue
Ferritin can bind with multiple ferritins forming RNA stains blue
hemosiderin
Ferritin can release Fe 2+ on basal surface of cell (ii) Polychromatic Erythroblasts
where a feroportin channel transports Fe2+ from o Stain blue & red
duodenal cell into blood RNA is being translated into proteins which stain
Before the Fe 2+ binds to transferrin red
It is oxidized to Fe 3+ by hephaestin
Transferrin carries the Fe 3+ in the blood to (iii) Orthochromatic Erythroblasts
various organs o Stain red
o Must bound to transferrin because it can RNA has been translated to proteins which stains
undergo Fenton reaction producing free red
radicals
(iv) Reticulocytes
(ii) In the liver
o Have no nucleus or organelles after the
o There are hepatocytes that can detect the changes in orthochromatic erythroblast spit them out
iron levels o The reticulocytes mature into erythrocytes in 2-3 days
It produces hepcidin
B12 and folate are needed for DNA synthesis and
Hepcidin controls the activity of feroportin by
maturation in developing RBC’s
blocking it
This is to control the amount of iron
Too much iron is toxic
o HFE protein
Controls hepcidin
In hemochromatosis, there is no production of
functional HFE protein
Hence, iron overload occurs

(iii) In red bone marrow

o The red bone marrow is the organ we need it in for
erythropoiesis
Once Fe 3+ is taken to red bone marrow
It is taken up into developing RBCs
Binds with heme pigment called protoporphyrin
with the help of ferro-chelatase
Eventually the heme will bind with the globin
chains and make hemoglobin
(5) Vitamin B12 and folic acid metabolism
Vitamin B12 and folic acid are ingested from food such as
leafy vegetables and red meat

(i) In duodenum
o Folic acid is absorbed across the gut, into the blood
stream

(ii) In stomach
o Parietal cells make proteins called intrinsic factors
Intrinsic factors bind to vitamin B12

Figure 4. Causes of ineffective erythropoiesis

[Keep Maturation on Track]

2 of 3 HEMATOLOGY: Note #1. ERYTHROPOIESIS: RED BLOOD CELL FORMATION

 The precursor of all lines of blood cells is the
a. Myeloblast
b. Hemocytoblast
c. Proerythroblast
d. Progranulocyte

Megakaryocyte give rise to

a. Erythrocyte
b. Agranulocyte
c. Granulocytes
d. Thrombocytes

The production of red blood cells in the bone

marrow is regulated by
a. Renin
b. Angiotensin
c. Erythropoietin
d. Calcium

Which of the following is true regarding

thrombopoiesis?
a. In the red bone marrow
b. Produce RBCs
c. Uses EPO
d. Doesn’t give rise to platelet

Process of formation of blood corpuscles is called

a. Hemolysis
b. Hemozoin
c. Hemopoiesis
d. Haemoter

The blood corpuscles are of _________ kinds.

a. 5
b. 4
c. 2
d. 3

CHECK YOUR ANSWERS

III) REFERENCES
Alila Medical Media. Shutterstock Hematopoiesis Bone Marrow
[digital image] https://www.news-medical.net/life-
Figure 5. Stages of erythropoiesis [Keep Maturation on Track] sciences/Hematopoiesis-Process.aspx
European Pharmaceutical Review. Red blood cells with ability to
deliver drugs. 2020. [digital image]
https://www.europeanpharmaceuticalreview.com/news/121018/rese
II) REVIEW QUESTIONS
archers-synthesise-red-blood-cells-with-ability-to-deliver-drugs/
The hormone erythropoietin stimulates red blood Erythropoietin and the control of erythropoiesis. Learn Haem.
2019. [digital image]
cell production in the red bone marrow. Where in https://www.learnhaem.com/courses/anaemia/lessons/normal-
the body is erythropoietin produced? haematopoiesis/topic/normal-erythropoiesis/
a. Spleen Keep Maturation on Track. [digital image]
https://keepmaturationtrack.eu/ineffective-erythropoiesis/
b. Kidney Oxford University Press. Gaskell & Rostron: Therapeutics and
c. Liver Human Physiology. [Quiz]
d. Thyroid https://global.oup.com/uk/orc/pharmacy/ifp_therapeutics/student/mc
qs/ch09/
Blood circulation. MCQ Biology. [Quiz]
Which of the following statements about https://www.mcqbiology.com/2014/02/mcq-on-haematopoietic-
erythrocytes is correct? system.html
a. They fight infection Le T, Bhushan V, Sochat M, Chavda Y, Zureick A. First Aid for
the USMLE Step 1 2018. New York, NY: McGraw-Hill Medical; 2017
b. They clot blood Marieb EN, Hoehn K. Anatomy & Physiology. Hoboken, NJ:
c. They lack a nucleus Pearson; 2020.
d. They are produced in the spleen Boron WF, Boulpaep EL. Medical Physiology.; 2017.
Urry LA, Cain ML, Wasserman SA, Minorsky PV, Orr RB,
Campbell NA. Campbell Biology. New York, NY: Pearson; 2020.
Where does hematopoiesis take place? Jameson JL, Fauci AS, Kasper DL, Hauser SL, Longo DL,
a. Lungs Loscalzo J. Harrison's Principles of Internal Medicine. New York
etc.: McGraw-Hill Education; 2018.
b. Pancreas Sabatine MS. Pocket Medicine: the Massachusetts General
c. Liver Hospital Handbook of Internal Medicine. Philadelphia: Wolters
d. Bone marrow Kluwer; 2020.

Platelets are formed from what type of cell?

a. Melanocytes
b. Macrophages
c. Astrocytes
d. Megakaryocytes

ERYTHROPOIESIS: RED BLOOD CELL FORMATION HEMATOLOGY: Note #1. 3 of 3

 Last edited: 8/11/2021

1. LIFESPAN AND DESTRUCTION

Erythropoiesis: Lifespan & Destruction | Part 2 Medical Editor: Dr. Sofia Suhada M. Uzir

OUTLINE II) SITES OF DESTRUCTION

I) THE BASICS (1) Sinusoidal capillaries

II) SITES OF DESTRUCTION
Found in:
III) SEQUENCES OF EVENTS
IV) REVIEW QUESTIONS Spleen
V) REFERENCES Liver
Red Bone marrow

I) THE BASICS
Lifespan of RBCs 100-120 days
o As RBCs reach this time the cytoskeleton and
hemoglobin function start declining
So, it’s out with the old and in with the new
Cytoskeleton
Proteins in the cytoskeleton help with flexibility and
pliability to squeeze through small capillaries
o Spectrin protein Figure 1. Cut section of sinusoidal capillary
Webbed-like protein [Pearson Education]
o Ankyrin
Bind spectrin to cell membrane
o Glycophorin
o Band 3 protein 4.1 & 4.2
As RBCs getting older, it becomes less flexible and more
rigid.

III) SEQUENCES OF EVENTS

(1) Old RBCs (B) GLOBIN CHAINS

Move through the sinusoids in these organs Is one of the products of hemoglobin break down by
o RBCs gets stucked in the intercellular clefts macrophages
o They get phagocytosed by macrophages The other is heme
o The hemoglobin in the RBC is broken down in the It will further break down into amino acids
macrophage into: o The amino acids can be recycled to help in the
Globin chains erythropoietic cycle again
Heme
Globin chains include
o Alpha
o Beta
o Delta
o Gamma

(i) Hemoglobin types

o Adults
2 alpha + 2 beta
o Fetal hemoglobin
2 alpha + 2 gamma
o Hemoglobin A2
Very rare type
2 alpha + 2 delta

Figure 2. Recycling of RBCs [Bio Ninja]

LIFESPAN AND DESTRUCTION HEMATOLOGY: Note #1. 1 of 3

 (C) HEME
Is one of the products of hemoglobin broken down by
macrophages
The other is globin chains
It will further break down into iron and biliverdin which
gets broken down into bilirubin Figure 3.
(1) Iron
The iron that is released from heme can bind with
apoferritin
o Forming ferritin
Ferritin molecules polymerize
o Form hemosiderin that is stored in tissues like the
liver and macrophages
(2) Bilirubin
Biliverdin get broken down into bilirubin
Bilirubin is very toxic if it gets into the blood stream
causing neurotoxicity
Spit out of macrophage in the unconjugated form and
binds to albumin where it is transported to the liver

(i) In the liver

o Unconjugated bilirubin binds with glucuronic acid Figure 3. Bilirubin metabolism simplified
Forms conjugated bilirubin [Lab Technologist Farukh]
Soluble
Will be secreted into bile
Bile helps with fat digestion
Will be released in the duodenum through the
hepatopancreatic ampulla

(ii) In the duodenum

o The bile is released into the duodenum
Helps to emulsify fat
o Bilirubin in the bile gets broken down to
urobilinogen by the bacteria enzymes (such as
proteases)
Small amounts of urobilinogen is absorbed across
GIT and into blood where it is taken to kidneys
and added into urine
This is called urobilin
Causes yellow coloration of the urine
Some of it can be recycled and reconjugated with
glucuronic acid through the enterohepatic
circulation Figure 4.
The remaining urobilinogen in the GIT gets
stercobilin by bacteria in colon
This pigment gives feces its brown hue

NOTE: Figure 4. Detailed destruction of erythrocyte [Oncohema Key]

o Another name for urobilinogen in the GIT is fecal
stercobilinogen
o The colour of stool and urine is a good clinical indicator
if there is an obstruction in the biliary pathway where
bilirubin cannot be secreted
o Gallstone obstructed in the common bile duct can push
bilirubin into the blood stream
tissues
Yellowish coloration = jaundice

2 of 3 HEMATOLOGY: Note #1. LIFESPAN AND DESTRUCTION

 IV) REVIEW QUESTIONS
All of the following are the site of RBCs
What is the approximate formation of bilirubin in destruction, except
adults? a. Liver
a. 150-220 mg b. Lung
b. 50-70mg c. Spleen
c. 250-350 mg d. Bone Marrow
d. 500-700 mg
CHECK YOUR ANSWERS
Which of the following statement is NOT true?
a. Bilirubin is lipophilic in nature V) REFERENCES
b. Biliverdin reductase is an ATP dependent soluble Cut section of sinusoidal capillary. Pearson Education [digital
enzyme image] https://slideplayer.com/slide/17455779/
Bio Ninja. Human Physiology. Recycling of erythrocyte [digital
c. Albumin has 2 binding sites for bilirubin image] https://ib.bioninja.com.au/options/option-d-human-
d. Heme oxygenase enzyme produces biliverdin, physiology/d3-functions-of-the-liver/erythrocyte-recycling.html
ferrous ion and CO Lab Technologist Farukh. Bilirubin Metabolism in The Body
Simplified [digital image]
https://m.facebook.com/1681813371896372/posts/bilirubin-
Which form of energy is required for the working of metabolismin-in-bodythe-heme-present-in-the-hemoglobin-and-
complex enzyme system? other-prote/3133705743373787/
a. ATP Oncohema Key. Introduction to Increased Destruction of
Erythrocytes [digital image] https://oncohemakey.com/introduction-
b. ADP to-increased-destruction-of-erythrocytes/
c. NAD Oxford University Press. Gaskell & Rostron: Therapeutics and
d. None of the above Human Physiology. [Quiz]
https://global.oup.com/uk/orc/pharmacy/ifp_therapeutics/student/mc
qs/ch09/
What happens to the globin part of hemoglobin after GPATINDIA. Pharamcophore Edulabs India. Catabolism of
its dissociation? Hemoglobin and MCQs For Pharmacist, GPAT, NEET, GATE and
CSIR NET Exams. 2021. [Quiz] https://gpatindia.com/catabolism-of-
a. Excreted through urine hemoglobin-and-mcqs-for-pharmacist-gpat-neet-gate-and-csir-net-
b. Stored in liver exams/APA citation guide. (2016). http://www.bibme.org/citation-
c. Degraded to its amino acid guide/apa/
Le T, Bhushan V, Sochat M, Chavda Y, Zureick A. First Aid for
d. None of the above the USMLE Step 1 2018. New York, NY: McGraw-Hill Medical; 2017
Marieb EN, Hoehn K. Anatomy & Physiology. Hoboken, NJ:
What would happen to red blood cells if the heme Pearson; 2020.
group were removed from hemoglobin? Boron WF, Boulpaep EL. Medical Physiology.; 2017.
Urry LA, Cain ML, Wasserman SA, Minorsky PV, Orr RB,
a. Red blood cells would not be able to bind oxygen Campbell NA. Campbell Biology. New York, NY: Pearson; 2020.
b. Red blood cells would not be able to reproduce Jameson JL, Fauci AS, Kasper DL, Hauser SL, Longo DL,
c. White blood cells would not be able to reproduce Loscalzo J. Harrison's Principles of Internal Medicine. New York
etc.: McGraw-Hill Education; 2018.
d. Blood clot formation would be inhibited Sabatine MS. Pocket Medicine: the Massachusetts General
Hospital Handbook of Internal Medicine. Philadelphia: Wolters
The secretion of bilirubin from hepatocytes to Kluwer; 2020.
canaliculi are an energy-dependent process. The
transporter protein involved in this protein is
a. MRP2 protein
b. Active transport coupled with Na K ATPase
c. Bilirubin transporting protein
d. Chylomicron

In the intestine, bacterial degradation of bilirubin

forms urobilinogen. Urobilinogen is a colorless
bilirubin derived product that is further oxidized to
form the following pigments except
a. Urobilin
b. Mesobilin
c. Stercobilin
d. Exobilin

When red blood cells are worn out, part of their

components are recycled while others are
disposed. Select the incorrect statement about
destruction of red blood cells.
a. The greenish pigment, biliverdin, is recycled to the
bone marrow
b. Iron is carried to the bone marrow by a protein called
transferrin
c. Biliverdin and bilirubin impart color to bile
d. Macrophages in the liver and spleen destroy worn
out red blood cells

Life span of RBC is

a. Around 90 days
b. Around 50 days
c. Around 125 days
d. Around 115 days

LIFESPAN AND DESTRUCTION HEMATOLOGY: Note #1. 3 of 3

 Last edited: 9/11/2021

1. TYPES OF ANEMIAS
Hematology | Types of Anemias Medical Editor: Dr. Ana Guerra

OUTLINE Table 1-2. Types of anemia according to their morphology

[LabPedia.net].
I) OVERVIEW Microcytic Normocytic Macrocytic
II) IRON DEFICIENCY ANEMIA hypochromic normochromic
III) PERNICIOUS ANEMIA MCV <80 fl 80-95 fl >95 fl
IV) HEREDITARY SPHEROCYTOSIS
V) G6PDH MCH <27 pg >27 pg
VI) SICKLE CELL ANEMIA MCHC <32% N N
VII) HEMORRAGIC ANEMIA Hemolytic Vit B12
VIII) APLASTIC Iron
anemias deficiency
IX) THALASSEMIA deficiency
Thalassemia Acute blood Folic acid
X) APPENDIX loss deficiency
Sideroblastic
XI) REVIEW QUESTIONS E.g. Bone marrow Aplastic
anemia
XII) REFERENCES failure anemia
Chronic
diseases Renal
diseases
I) OVERVIEW Lead
poisoning
(A) DEFINITION
Anemia is defined as a low carrying capacity condition due (C) COMMON CLINICAL PRESENTATION
to decrease in hemoglobin concentration.

Table 1. Diagnostic criteria for anemia in males and females

[LabPedia.net].
RBCs values Male Female
Hemoglobin 13.5-17.5 g/dL 11.5-15.5 g/dL
Hct % 36-48%
Hematocrit (D) DIFFERENTIAL DIAGNOSIS STUDIES
40-52%
PCV
(i) Red cell distribution width (RDW)
Packed cell volume
MCV 80-95 fL Helps in the differential diagnosis of iron deficiency
80-95 fL anemia and thalassemia.
Mean cell volume
MCH 27-34 pg (ii) Serum iron
27-34 pg
Mean cell hemoglobin
Helps differentiating between hemochromatosis and
MCHC % 30-37%
hemosiderosis.
Mean cell hemoglobin 30-37%
concentration (iii) Transferrin
Reticulocytes count 0.5-1.5% 0.5-1.5%
Cand help in diagnosis of anemia of chronic disease and
differential diagnose with iron deficiency anemia.
(B) CLASSIFICATION
(iv) Transferrin saturation
There are several types of classifications for anemia, but
two of the widely accepted are based on: Cand help in diagnosis of anemia of chronic disease and
differential diagnose with iron deficiency anemia.

(v) Ferritin
It correlates with total body iron stores.
(i) Classification based on etiology
Increased RBC’s destruction (hemolysis).
(vi) Total Iron binding capacity (TIBC)
Increased blood loss, which may be acute or chronic. Always done along serum iron levels.
Defective maturation of erythropoiesis.
(vii) Peripheral blood smear
Informs abnormalities of the RBC shape, size and
(ii) Morphological classification
inclusions.
Normochromic and normocytic anemia (normal MCV
and MCHC). (viii) Bone marrow examination
Hypochromic and microcytic anemia (low MCV, MHC Helpful study when there are signs and symptoms of
and MCHC). aplastic anemia.
Normochromic and macrocytic (high MCV, normal or
increase MHC and normal MCHC). (ix) Coombs test
Very useful to differentiate between hereditary
spherocytosis and autoimmune hemolytic anemia.

TYPES OF ANEMIAS HEMATOLOGY: Note #1. 1 of 7

 II) IRON DEFICIENCY ANEMA III) PERNICIOUS ANEMIA

(1) Etiology (1) Etiology

Excessive bleeding. Autoimmune.
Menorrhagia. Deficiency in diet.
Iron deficiency in diet (common in vegetarians).
(2) Pathogenesis
Increased demand by the body
o Infancy, pregnancy, lactation. (i) B12 deficiency
Autoimmune condition where the body creates antibodies
against Intrinsic Factor.
(2) Pathogenesis
Absence of iron: In order to be absorbed, B12 binds to intrinsic factor
o Protoporphyrin can’t form heme inside the GI tract.
Dysfunctional hemoglobin.
Erythrocyte volume decrease:

Figure 1. Pathogenesis of iron deficiency anemia.

(3) Specific symptoms
Koilonychia: Spoon-shaped nails.
Hair loss.
Pica: Some patients may like to eat clay, ice and starch.
Glossitis (smooth, red tongue).
Stomatitis.
Angular cheilitis.

Figure 1-2. Pathogenesis of pernicious anemia.

(4) Diagnosis
History of patient. (ii) Folic acid deficiency
Physical examination. Usually due to folic acid deficiency in diet.
Blood test with complete blood count (CBC).
Levels of serum ferritin, iron, TIBC and/or transferrin.
Folic acid is also needed for RBC to condense and
mature
Table 1-3. Useful tests in the diagnosis of iron deficiency
anemia [Hematología. La sangre y sus enfermedades]. (3) Diagnosis
RBC
Hg
Table 1-4. Useful tests in the diagnosis of pernicious anemia
Hct [Hematología. La sangre y sus enfermedades].
MCV RBC
MCH Hg
MCHC N Hct

Reticulocytes N/ MCV

Leukocytes N/ MCH N

Hypochromic and MCHC N

Blood smear microcytic RBC, Reticulocytes N/
elliptocytes. Leukocytes
Platelets N Macrocyte RBC,
Blood smear
Serum iron teardrop cells
Ferritin Platelets
TIBC
RDW
(4) Treatment

2 of 7 HEMATOLOGY: Note #1. TYPES OF ANEMIAS

 IV) HEREDITARY SPHEROCYTOSIS VI) SICKLE CELL ANEMIA

(1) Etiology (1) Etiology

Hereditary condition with mutations in membrane proteins Hereditary condition: Missense mutation
and erythrocyte cytoskeleton.
(2) Pathogenesis
Sickle cell anemia occurs due to a substitution on the
position 6 of the chain of Hb A1
o Glutamine is substituted by valine
(2) Pathogenesis
Abnormal erythrocyte membrane due to proteins
mutations.
o They only take a sickle form when they’re not bound
to O2 every time they get oxygenated, RBCs go
back to their normal structure.

o On their sickle form they can undergo hemolysis or

(3) Diagnosis
occlude blood vessels causing a vaso-occlusive
Table 1-5. Useful tests in the diagnosis of hereditary crisis
spherocytosis [Hematología. La sangre y sus enfermedades]. Priapism: Vessels of the penis get clogged with
RBC sickle cells, causing a painful erection.
Hg Splenomegaly due to the hemolysis
Hct
In some cases splenectomy will be needed.
MCV
MCH N/
MCHC N
Reticulocytes
Blood smear Microspherocytes
Platelets N/
Coombs Test Negative

V) G6PDH Figure 1-3. Red blood cells: Normal form and sickle form
[MedlinePlus].
Glucose 6-phosphate Dehydrogenase deficiency
(1) Etiology Nice to know
Hereditary condition People with sickle cell anemia have been found to be resistant
to malaria.
(2) Pathogenesis
In order to obtain energy, RBC can only do glycolysis:
(3) Treatment
Glucose Transfusions.
Oxygen.
Glucose-6-phosphate
dehydrogenase 6-Phosoho- Opioids depending on the severity of the pain.
Glucose Fluids
6-phosphate glucanolactone
Hydroxy urea – helps producing fetal hemoglobin
GSSG
NADP NADPH (oxidized
glutathione) VII) HEMORRAGIC ANEMIA

(1) Etiology
GSH Peptic ulcers due to H. pylori or aspirin
(reduced Aneurisms
glutathione) Traumas
Erythrocytes generate energy. Cancer
The NADPH obtained thanks to the action of the G6PD Hemorrhoids
enzyme, reduce glutathione allowing it to catch free (2) Pathogenesis
radicals that are harmful for the RBC.
Excessive bleeding RBC’s

(3) Treatment

Transfusions
Fluids
(3) Diagnosis
Surgery to stop bleeding

TYPES OF ANEMIAS HEMATOLOGY: Note #1. 3 of 7

 VIII) APLASTIC ANEMIA IX) THALASSEMIA

(1) Etiology (1) Etiology

Idiopathic in 65% Hereditary condition where there is an absence of a
Drugs (e.g. chloramphenicol, benzenes, streptomycin, globin chain
etc.). o If there is an -chain missing -thalassemia.
Viruses (CMV, EBV).
Radiation. o If there is a -chain missing -thalassemia.

(2) Pathogenesis
Destruction of the myeloid stem cells
Nice to know
Hemoglobin is formed with two -chains and two -chains.

(2) Pathogenesis
Low functional hemoglobin due to its structure mutation
o MCV >90 ft
Microcytic anemia.

(3) Diagnosis
Figure 1-4. Aplastic anemia.
Table 1-7 Differential diagnosis of thalassemia and iron
deficiency anemia [Hematologïa. La sangre y sus
(3) Specific symptoms enfermedades].
Current infections due to leucopenia. Thalassemia Iron deficiency
Petechiae ( bruising). RDW N
Bleeding.
Serum ferritin N/
(4) Diagnosis Serum iron N
Transferrin
N
Table 1-6. Useful tests in the diagnosis of aplastic anemia saturation
[Hematología. La sangre y sus enfermedades].
RBC
Hg
Hct (4) Treatment
MCV N Transfusions.
MCH N Iron supplements.
Oxygen.
MCHC N
Bone stem cell transplant.
Reticulocytes N/
L:
Leukocytes
N:
Platelets
Bone marrow
Hypocellularity
examination

(5) Treatment
Bone marrow transplant.
Transfusions.

4 of 7 HEMATOLOGY: Note #1. TYPES OF ANEMIAS

 X) APPENDIX

Figure 5. Summary of types of anemias.

TYPES OF ANEMIAS HEMATOLOGY: Note #1. 5 of 7

 XII) REFRENCES
XI) REVIEW QUESTIONS
Le T, Bhushan V, Sochat M, Chavda Y, Zureick A. First Aid for
1) A 31 year old woman is presented with history of the USMLE Step 1 2018. New York, NY: McGraw-Hill Medical; 2017
Marieb EN, Hoehn K. Anatomy & Physiology. Hoboken, NJ:
fatigue, dizziness and headaches since three months Pearson; 2020.
ago. Boron WF, Boulpaep EL. Medical Physiology.; 2017.
Urry LA, Cain ML, Wasserman SA, Minorsky PV, Orr RB,
A blood test was performed and results showed Hb Campbell NA. Campbell Biology. New York, NY: Pearson; 2020.
10 g/dL; Hct 40%; MCV 78 fl; MHC 25 pg and MCHC Jameson JL, Fauci AS, Kasper DL, Hauser SL, Longo DL,
30%. Loscalzo J. Harrison's Principles of Internal Medicine. New York
etc.: McGraw-Hill Education; 2018.
According to laboratory findings, how would you Sabatine MS. Pocket Medicine: the Massachusetts General
morphologically classify this type of anemia? Hospital Handbook of Internal Medicine. Philadelphia: Wolters
Kluwer; 2020.
a) Microcytic normochromic. Pérez, J.C. Hematología. La sangre y sus
b) Macrocytic hypochromic. enfermedades (4.a ed.). Editorial McGraw-Hill; 2015.
c) Microcytic hypochromic. Anemia: Part 1 - Anemia Classification, Diagnosis, and Routine
Work up. (2021, 1 junio). Labpedia.Net. https://labpedia.net/anemia-
d) Normochromic normocytic. part-1-anemia-classification-diagnosis-and-routine-workup/

2) The following test comes to be very useful in the

differential diagnosis of hereditary spherocytosis and
autoimmune hemolytic anemia:
a) RDW
b) Peripheral blood smear
c) TIBC
d) Coombs test

3) G6PDH deficiency is a condition where glucose can’t

turn into 6-phospho-glucanolactone due to lacking of
G6PDH, which leads damage to RBC’s membranes.
What is exactly the mechanism of this damage?
a) NADP can’t turn into NADPH so glutathione can’t be
oxidized, leading to increased free radicals.
b) NADP can’t turn into NADPH so glutathione can’t be
reduced, leading to increased free radicals.
c) NADPH can’t turn into NADP so glutathione can’t be
reduced, leading to increased free radicals.
d) NADPH can’t turn into NADP so glutathione can’t be
oxidized, leading to increased free radicals.

4) If you’re suspecting of pernicious anemia on your

patient, which finding on a blood smear test would
support your diagnosis?
a) Teardrop cells.
b) Elliptocytes.
c) Heinz bodies.
d) Microspherocytes.

5) The followings are specific symptoms of iron

deficiency anemia EXCEPT for:
a) Pica.
b) Tachycardia.
c) Koilonychia.
d) Angular cheilitis.

CHECK YOUR ANSWERS

6 of 7 HEMATOLOGY: Note #1. TYPES OF ANEMIAS

TYPES OF ANEMIAS HEMATOLOGY: Note #1. 7 of 7
 Last edited: 8/21/2021

1. POLYCYTHEMIA
Hematology: Polycythemia Medical Editor: Dr. Sofia Suhada M.Uzir

OUTLINE

I) INTRODUCTION
II) ERYTHROPOIETIN (EPO)
III) POLYCYTHEMIA VERA
IV) BLOOD DOPING
V) SECONDARY POLYCYTHEMIA
VI) SUMMARY
VII) REVIEW QUESTIONS
VIII) REFERENCES

I) INTRODUCTION
Polycythemia is an abnormally increased concentration of
RBCs in the blood, either through reduction of plasma Figure 2. JAK STAT pathway [ResearchGate]
volume or increase in red cell numbers. [Oxford Languages]
There are two types:
o Polycythemia vera (primary) (A) EFFECTS OF POLYCYTHEMIA
o Secondary polycythemia Polycythemia causes:
o Increase RBC to water ratio
II) ERYTHROPOIETIN (EPO) Viscosity of blood will increase thicker blood
EPO is made by the kidneys at the distal convoluted Increase incidence of clot formations
tubules (thrombi/emboli)
o It stimulates myeloid stem cells and proerythroblasts In veins deep vein thrombosis (DVT) may
into erythropoietic process Figure 1 develop
o EPO increases RBCs through JAK STAT pathway In coronary artery myocardial infarction
In pulmonary arteries pulmonary embolism
In the proximal convoluted tubules, there are also cells
In cerebrum stroke
that are constantly secreting EPO
o Increase bleeding longer prothrombin time
Note:
JAK STAT IV) BLOOD DOPING
o Janus Kinase and Signal Transducer and Activator of
Transcription Causes transient polycythemia
For example, in the Olympics (non-ethical!)
o Athletes take their blood out and store it to be
reinserted into the circulatory system a day before
their event

Figure 1. EPO stimulating proerythroblast in erythropoiesis

[Science Direct]

Figure 3. Summary blood doping [Sports247]

III) POLYCYTHEMIA VERA (1) Why blood doping?
Increase in RBC production primarily due to hyper Blood doping helps to increase in the number of RBCs in
functional JAK STAT pathway in the bone marrow the body
There is a problem in the receptor in which EPO binds to o Increases oxygen carrying capacity
o Causes increased in functions of JAK STAT pathway More blood oxygen supply to the muscle
Signal nucleus for proliferations More endurance
Activating genes to undergo transcription and
translations (2) Drawbacks
o Hyperfunctioning amplified effects increase in Increase in viscosity
erythropoiesis = increase in the RBCs o Thicker blood increase incidence clot formation,
Remember: thrombi/emboli especially if not properly hydrated
Polycythemia = abnormal increase in production of o Increase peripheral resistance increase in the
RBCs blood pressure (may cause hypertension)
Dizziness
Headaches

Polycythemia HEMATOLOGY: Note #1. 1 of 3

 V) SECONDARY POLYCYTHEMIA The following may be caused by polycythemia
except
Due to the enhance of EPO production a. Thrombi formation
Causes: b. Decrease in functioning RBCs
o Hypoxia/low amount of oxygen c. Stroke
High altitudes d. DVT
Cardiovascular diseases
Decrease oxygen carrying capacity What causes secondary polycythemia?
Renal cancer a. Low oxygen levels
Enhance production of EPO b. Renal cancer
Increase EPO increase JAK STAT pathway c. Heart diseases
increase erythropoiesis increase in RBCs d. All of the above

The following typically distinguishes polycythemia

vera from other causes of erythrocytosis
a. Massive splenomegaly
b. Aquagenic pruritis
c. High hematocrit
d. High hemoglobin

The following cause microcytic erythrocytosis

Figure 4. Number of cells producing erythropoietin a. Beta thalassemia trait
[Vivo Pathophysiology] b. Hypoxic erythrocytosis
c. Polycythemia vera
d. All of the above
VI) SUMMARY
Polycythemia is primarily due to hyper functional JAK Regarding polycythemia vera all are true except
STAT pathway in the bone marrow. a. Erythroid progenitor cells are resistant to apoptosis
o This triggers more erythropoiesis hence, more RBCs b. Autonomous clonal form of erythrocytosis
formation. c. Elevated plasma erythropoietin level excludes
polycythemia vera as the cause for erythrocytosis
Secondary polycythemia is caused by the increase in d. Abundant bone marrow iron
production of EPO Increases the JAK STAT pathway
and RBCs
CHECK YOUR ANSWERS

VII) REVIEW QUESTIONS VIII) REFERENCES

Regarding polycythemia, which is correct? Oxford Languages (2021) https://languages.oup.com/google-
dictionary-en/
a. There are 2 types NatBoardMCQ (2015) [Quiz]
b. There are 3 types http://www.natboardmcqs.com/hematology-mcq-exercise-19/
c. There are 4 types Hong-MouShih Journal of the Formosan Medical Association.
Physiology and pathophysiology of renal erythropoietin-producing
d. There are 5 types cells (2018)
https://www.sciencedirect.com/science/article/pii/S09296646183006
In polycythemia vera, which is true? 39
VIVO Pathophysiology (2018) [digital image]
a. There is hyper functionality of erythropoiesis in the http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/otherend
liver o/epo.html
b. There is hyper functionality of JAK STAT pathway in Blood doping (2017) [digital image]
the liver https://www.sports247.my/blood-doping-doesnt-work-least-not-
amateurs-study/
c. There is hyper functionality of erythroblasts in the JAK STAT pathway [digital image]
bone marrow https://www.researchgate.net/figure/JAK2-receptor-signaling-and-
d. There is hyper functionality of JAK STAT pathway in activation-of-STAT-pathway-The-binding-of-
erythropoietin_fig1_261957679
the bone marrow Le T, Bhushan V, Sochat M, Chavda Y, Zureick A. First Aid for
the USMLE Step 1 2018. New York, NY: McGraw-Hill Medical; 2017
In secondary polycythemia, which is false? Marieb EN, Hoehn K. Anatomy & Physiology. Hoboken, NJ:
Pearson; 2020.
a. It is due to enhance of EPO production Boron WF, Boulpaep EL. Medical Physiology.; 2017.
b. It can be seen in certain renal cancers Urry LA, Cain ML, Wasserman SA, Minorsky PV, Orr RB,
c. It decreases the oxygen carrying capacity Campbell NA. Campbell Biology. New York, NY: Pearson; 2020.
Jameson JL, Fauci AS, Kasper DL, Hauser SL, Longo DL,
d. Hypoxia is one of the main causes Loscalzo J. Harrison's Principles of Internal Medicine. New York
etc.: McGraw-Hill Education; 2018.
Thrombosis in polycythemia vera is due to Sabatine MS. Pocket Medicine: the Massachusetts General
Hospital Handbook of Internal Medicine. Philadelphia: Wolters
a. Erythrocytosis
Kluwer; 2020.
b. Leukocytosis
c. Thrombocytosis
d. all of the above

True regarding pathogenesis of polycythemia vera

a. erythropoietin independent erythroid colony
formation
b. hypersensitivity of polycythemia vera erythroid
progenitor cells to EPO
c. resistance of polycythemia vera progenitor cells to
apoptosis
d. all of the above

2 of 3 HEMATOLOGY: Note #1. Polycythemia

Polycythemia HEMATOLOGY: Note #1. 3 of 3
 Last edited: 8/22/2021

1. LEUKOPOIESIS (WHITE BLOOD CELL FORMATION)

Leukopoiesis: White blood cell formation Medical Editor: Dr. Sofia Suhada M. Uzir

OUTLINE (C) NEUTROPHILS

Relative abundance (%)
I) LEUKOCYTES o 50-70% relative abundance in differential
II) LEUKOPOIESIS
III) SEQUENCE OF DEVELOPMENT (1) Structure
IV) THROMBOPOIESIS
V) SUMMARY OF CELL FUNCTIONS Multi-lobulated nucleus also referred to as
VI) REVIEW QUESTIONS polymorphonuclear leukocytes (PMNs)
VII) REFERENCES Granules stains pink
o Absorbs red (eosin) acid
o Absorbs blue (methylene) base
I) LEUKOCYTES
(2) Function
Normal range
Phagocytosis of pathogens
o 4,000-11,000 WBCs/mm3
Contain granules with leukocyte alkaline phosphatase
(LAP)
Performs respiratory burst
o Uses hydrogen peroxide to kill bacteria
o This process causes neutrophil to die as well and
release its DNA which creates a net on pathogen
tagging them to be destroyed
(3) Clinical significance

o Bacterial infections
Most common: Strep Pneumoniae, S. Aureus
o Inflammation
o Drugs
Corticosteroids

Figure 1. Different types of WBCs [Medical News Today] o Bone marrow failure
Aplastic anemia
(A) GRANULOCYTES Chemotherapy
Radiation therapy
Visibly stained granules after wright's stain o Drugs
Figure 2 Clozapine
o Neutrophils
o Eosinophils (D) EOSINOPHILS
o Basophils Relative abundance (%)
(B) AGRANULOCYTES o 2-4% relative abundance in differential

No visibly stained granules after wright's stain (1) Structure

o Monocytes Granules stain red
o B-lymphocytes o Absorbs red (eosin) acid
o T-lymphocytes
Contains Bilobed (Telephone shaped) Nucleus
(2) Function
Kills parasitic worms with major basic proteins and
cationic peptides
Involved in allergic reactions
Involved in asthma
(3) Clinical significance
Eosinophils eosinophilia
o Atopic dermatitis
o Asthma
o Parasitic Infections
o Acute Interstitial Nephritis
Figure 2. Agranular vs granular lymphocytes [Shutterstock]
Caused by drugs like macrolides and allopurinol
o Churg Strauss Syndrome
o Adrenal Insufficiency
Eosinophils eosinopenia
o Cushing’s Syndrome
o Drugs:
Corticosteroids

Leukopoiesis (White blood cell formation) HEMATOLOGY: Note #1. 1 of 6

 (E) BASOPHILS (3) Clinical significance
Relative abundance (%) Lymphocytes lymphocytosis
o 0.5-1% relative abundance in differential o Viral Infections
EBV
(1) Structure
Mumps
Contain S-shaped nucleus o Lymphoma
Granules stains blue o Tuberculosis
o Absorbs blue (methylene) base Lymphocytes lymphopenia
(2) Function o Immunosuppression
HIV/AIDS
Release histamines, leukotrienes and serotonin during DiGeorge Syndrome
inflammation and allergic reactions to cause vasodilation Drugs: Chemo-radiation
of capillaries and cause chemotaxis of WBC’s o Lymphoma
Contain heparin granules which are important for
preventing blood clots II) LEUKOPOIESIS
(3) Clinical significance Leukopoiesis is the formation of white blood cells
Basophils basophilia The stem cell associated with the process is
o Allergic reactions hemocytoblast
o Chronic myelocytic leukemia (CML)
Basophils basopenia
o Rare

(F) MONOCYTES
Relative abundance (%)
o 3-8% relative abundance in differential
(1) Structure
Kidney bean shaped nucleus
Largest WBC
(2) Function
Become macrophages when they leave blood and enter
tissues
Types of macrophages:
o Kupffer cells in liver
Figure 3. Summary of WBCs formations [Teresa Winslow]
o Microglia in brain
o Alveolar macrophages in lungs
o Osteoclasts in bone
(A) LOCATION
o Langerhans cells in skin
Site of leukopoiesis:
Phagocytosis of pathogens
o Red bone marrow
Antigen presenting cell
Has sinusoidal capillaries
o Presents antigens to T-cells on its MHC-II complex
o Skull
(3) Clinical significance o Sternum
o Pelvis
Monocytes monocytosis o Epiphyses of long bones (trabeculae/spongy bone)
o Tuberculosis
o Hodgkin’s lymphoma (B) CELLS PRODUCED
o Chronic Myelocytic leukemia
White blood cells
Monocytes monocytopenia
o HIV (C) GROWTH FACTORS / MOLECULES REQUIRED
o EBV Granulocyte growth factors
o Acute Myelocytic Leukemia o Neutrophils
o Chemo-Radiation IL-3, IL-6 and G-CSF
o Eosinophils
(G) LYMPHOCYTES
IL-4 and IL-5
Relative abundance (%) o Basophils
o 20-30% relative abundance in differential IL-3 and IL-4
(1) Structure Agranulocytes
o B-Lymphocytes
Spherical nucleus takes up most of cell volume Made in red bone marrow
Small amount of cytoplasm IL-6
(2) Function o T-Lymphocytes
Made in red bone marrow
T-lymphocytes Go to thymus to mature into:
o T-helper (CD4+ cells)
T helper
Activate B cells and turn them into plasma cells to
T regulatory
make antibodies
Cytotoxic
o Cytotoxic T cells (CD8+ cells)
IL-2, IL-4, IL-6, IL-7
Kills viral infected cells and cancer cells
Monocytes
B-lymphocytes
o M-CSF
o Become plasma cells and release antibodies
2 of 6 HEMATOLOGY: Note #1. Leukopoiesis (White blood cell formation)
 III) SEQUENCE OF DEVELOPMENT (i) B-lymphocyte
Pathways: o Functional
o Granulocyte pathways o Settles in lymphatic tissue
o Agranulocyte pathway Spleen
o Monocyte pathway Lymph nodes
MALT
(A) GRANULOCYTE PATHWAY
(ii) T-lymphocyte
Hemocytoblast myeloid stem cell myeloblast
Myeloblast will divide into 3 different promyelocyte o Non-functional
Figure 3 o Goes to thymus gland (primary lymphoid organ) and
Neutrophilic matures into
Eosinophilic Cytotoxic, T-helper or T-regulatory cells then
Basophilic settles in lymphatic tissue
Spleen
These will continue to their corresponding myelocyte
Lymph nodes
o beginning to form U-shaped nucleus constriction with
MALT
granules
metamyelocyte (C) MONOCYTE PATHWAY
band cell Hemocytoblast myeloid stem cell monoblast
o perfectly constricted U-shaped nucleus promonocyte monocyte leaves blood enters
granulocyte tissues becomes macrophage
o Nuclei segmented GM-CSF is needed for monoblast pathway
Basophil IL-3, IL-5, AG-CSF are needed for monoblast formation
U-shaped / S-shaped
Stain blue with methylene blue based
Eosinophil
Bilobed nucleus
Granules stain red with red (eosin) acid
Neutrophilic
Polymorphonuclear leukocytes
Granules stains pink
o Absorbs red (eosin) acid
o Absorbs blue (methylene) base
GM-CSF is needed for myeloid cell formation
IL-3, IL-5, G-CSF is needed for myeloblast formation

Remember:
Myeloid stem cell can divide into 3 cell lineages forming:
o Red blood cells – EPO dependent
o Platelets – TPO dependent
o Granulocytic white blood cells and monocytes

Figure 4. Granulocyte pathway [SpringerLink]

(B) AGRANULOCYTE PATHWAY

Hemocytoblast lymphoid stem cell lymphoblast Figure 5. Monocyte pathway [ResearchGate]
prolymphocyte
Lymphocyte
o B-lymphocyte (mature)
o T-lymphocyte
IL-3, IL-5, AG-CSF are needed for lymphoblast formation

Leukopoiesis (White blood cell formation) HEMATOLOGY: Note #1. 3 of 6

 IV) THROMBOPOIESIS

Formation of platelets is called thrombopoiesis Figure 6

(A) LOCATION
(1) Sites
Bone marrow (RED)
o Skull
o Sternum
o Pelvis
o Epiphyses of long bones

(B) CELLS PRODUCED

Platelets

(C) GROWTH FACTORS/MOLECULES REQUIRED

(1) Thrombopoietin (TPO)
Made by PCT cells of kidney and liver
Goes to red bone marrow and stimulates platelet pathway
Figure 7

(D) SEQUENCE OF DEVELOPMENT

Platelet pathway
Hemocytoblast myeloid stem cell megakaryoblast
promegakaryocyte megakaryocyte platelets

Figure 7. The actions of TPO [Wiley Online Library]

V) SUMMARY OF CELL FUNCTIONS

(1) Monocyte

(i) Functions in the tissue

o Phagocytosis
o Antigen presenting cells (APCs)

(ii) Types of macrophages

o Can be free in the lymphatic system or reside at
several places Figure 6
Central nervous system
Microglia
Liver
Kupffer cells
Alveoli
Alveolar macrophages
Bones
Osteoclasts

Figure 6. Stages of thrombopoiesis [Wikivet]

Figure 8. Macrophages in different organs [OncohemaKey]

4 of 6 HEMATOLOGY: Note #1. Leukopoiesis (White blood cell formation)

 (2) Basophil
Granules can secrete
o Heparin
natural anticoagulant
o Histamines
regulate inflammation by vasodilation

(3) Eosinophil
Secrete very toxic proteins killing parasites/worms
o Cationic peptide
o Major basic protein
Plays a role in type 1 hypersensitivity reaction
(4) Neutrophil
Phagocytosis
Oxidative/respiratory burst
o Release free radicals
o Take oxygen
Hydroxide radical
Hypochlorous acid
o Damage DNA, proteins and cell membrane
(5) Platelets
Play a role in blood clots
o Plug the blood vessel to prevent blood loss
(6) B-lymphocyte
Plays a role in humoral immunity
o Turns into plasma cells secreting antibodies
(7) T-lymphocyte
Divide into lineages
o T-helper cells
Help B-lymphocytes turn into plasma cells
React with APCs
o Cytotoxic T-cells
Induce apoptosis of infected cells
Viral
Cancer cells

(B) MNEMONIC
Differentiated white cell count (DWC)
o Percentage of each when taking 1 blood sample
Never Let Monkeys Eat Bananas
o Neutrophils – 50%-70%
o Leukocytes – 20%-30%
o Monocytes – 3%-8%
o Eosinophils – 2%-4%
o Basophils – 0.5%-1%

Leukopoiesis (White blood cell formation) HEMATOLOGY: Note #1. 5 of 6

 VI) REVIEW QUESTIONS VII) REFERENCES
The common progenitor cell for granulocytes and Deborah Weatherperson. (2020) Medical News Today
[digital image] https://www.medicalnewstoday.com/articles/327446
monocytes which gives rise to the myeloblast Teresa Winslow. (2007) WBCs formation [digital image]
a. GM-CSF https://slidetodoc.com/body-defense-blood-lymph-membranes-
b. Eo-CSF immunity-blood-cells/
c. GM-CFC Granulocyte development [digital image]
https://link.springer.com/chapter/10.1007/978-3-319-41873-5_10
d. A and C Agranulocyte vs granulocyte [digital image]
e. None of the above https://www.shutterstock.com/image-vector/leukocytes-types-
scheme-editable-vector-illustration-1226857036
Monocyte pathway. ReasearchGate [digital image]
They proliferate in response to immunologic https://www.researchgate.net/figure/Schematic-representation-of-
stimulation (e.g. allergic reactions) developmental-stages-of-macrophages-HSCs-in-the-presence-
a. Neutrophils of_fig1_334715225
OncohemaKey. Macrophages in different organs [digital image]
b. Eosinophils// https://oncohemakey.com/8-the-white-cells-1-granulocytes-
c. Basophils monocytes-and-their/
d. Monocytes Proprofs Hematology (2013) [Quiz]
https://www.proprofs.com/quiz-school/story.php?title=hematology-
e. Lymphocytes leukopoiesis-blood-smear-cytochemistry
Stage when cell may be recognized specifically as a Wikivet. Thrombopoiesis Pathway. 2008 [digital image]
neutrophil, eosinophil, or basophil. https://en.wikivet.net/File:Thrombopoiesis_pathway.jpg
Markus Peck. The action of TPO. Wiley Online Library. 2016.
a. Myeloblast
[digital image] https://onlinelibrary.wiley.com/doi/10.1111/liv.13317
b. Promyelocyte Le T, Bhushan V, Sochat M, Chavda Y, Zureick A. First Aid for
c. Myelocyte// the USMLE Step 1 2018. New York, NY: McGraw-Hill Medical; 2017
d. Metamyelocyte Marieb EN, Hoehn K. Anatomy & Physiology. Hoboken, NJ:
Pearson; 2020.
e. Stab Form Boron WF, Boulpaep EL. Medical Physiology.; 2017.
Urry LA, Cain ML, Wasserman SA, Minorsky PV, Orr RB,
Has a ground-glass appearance Campbell NA. Campbell Biology. New York, NY: Pearson; 2020.
Jameson JL, Fauci AS, Kasper DL, Hauser SL, Longo DL,
a. Metamyelocyte Loscalzo J. Harrison's Principles of Internal Medicine. New York
b. Megakaryocyte etc.: McGraw-Hill Education; 2018.
c. Promyelocyte Sabatine MS. Pocket Medicine: the Massachusetts General
Hospital Handbook of Internal Medicine. Philadelphia: Wolters
d. Myeloblast Kluwer; 2020.
e. Promonocyte//

Has a pale clear blue cytoplasm

a. Metamyelocyte
b. Megakaryocyte
c. Promyelocyte
d. Myeloblast //
e. Promonocyte

Has an indented kidney shaped nucleus

a. Myeloblast
b. Promyelocyte
c. Myelocyte
d. Metamyelocyte//
e. Stab form

Also called a "juvenile cell"

a. Myeloblast
b. Promyelocyte
c. Myelocyte
d. Metamyelocyte//
e. Megakaryoblast

Has a partially constricted nucleus

a. Segmented form
b. Band form//
c. Metamyelocyte
d. Myelocyte
e. Promyelocyte

Has a streaked chromatin pattern

a. Monocyte//
b. Megakaryocyte
c. Neutrophilic Myelocyte
d. Mast cells
e. Plasma cells

Contain heparin, peroxidase, and histamine

a. Neutrophil
b. Basophil
c. Eosinophil
d. Mast cells
e. B and D//

CHECK YOUR ANSWERS

6 of 6 HEMATOLOGY: Note #1. Leukopoiesis (White blood cell formation)
 Last edited: 10/24/2021

1. HEMOSTASIS: COAGULATION CASCADE

Hemostasis: Coagulation Cascade Medical Editor: Mariel Antoinette L. Perez

OUTLINE

I) INTRODUCTION
II) FIVE STEPS OF HEMOSTASIS
III) APPENDIX
IV) REVIEW QUESTIONS
V) REFRENCES

I) INTRODUCTION

(1) HEMOSTASIS
Word Etiology
o “hemo” – blood; “stasis” – stop
Localized blood stopper
Usually occurs when there’s damage to blood vessels
o E.g., ruptured, lacerated, leaking out
A sequence of five steps

(2) NATURAL ANTI-COAGULATION OF BLOOD

Before studying the process of hemostasis, it’s important
to understand what keeps the blood naturally thin
o Prevents blood from becoming thrombotic,
coagulating on its own, and forming a clot
There are three general layers to take note of:
o Endothelial cells
secrete chemicals
Nitric Oxide (NO)
Prostacyclin (PGI2)
o Subendothelial cells
underneath the endothelial layer
made up of connective tissue, specifically collagen
collagen-rich layer
o Smooth muscle cells with specific types of receptors
nociceptors = pain receptors Figure 1 Natural Nanti coagualtion mechanisms

(1) Platelet Inactivation

II) FIVE STEPS OF HEMOSTASIS
There are two things in the blood: plasma and cells
o Cells (or formed elements) such as White Blood Cells
(WBCs), Red Blood Cells (RBCs), and platelets
o Platelets
Microscopic (tiny), cytoplasmic fragments
Derived from megakaryocytes
Naturally inhibited by NO and PGI2
keeps platelet inactive to prevent it from
binding onto the surface of the endothelial cell
(2) Heparin Sulfate
Glycosaminoglycan present on the membrane
Natural anti-coagulant
Binds and activates protein Anti-Thrombin III (ATIII)
o Degrades and inactivates clotting factors II, IX, X
Clotting factors are naturally just circulating in the
bloodstream
(3) Thrombomodulin
Binds with protein called Thrombin (Factor II/ FII)
o Activates Protein C
Degrades and inactivates factors V and VIII

HEMOSTASIS: COAGULATION CASCADE HEMATOLOGY: Note #7. 1 of 6

 (1) VASCULAR SPASM (2) PLATELET PLUG FORMATION
(1) Trigger With the endothelial cells damaged,
o There will be a decreased release of NO and PGI2
injured blood vessel endothelial damage Platelets will not be inactivated
o May also cause damage to the underlying tissue Allow platelets to attach to endothelium
o Blood may leak out and decrease blood volume o Damaged heparin sulfate will not be able to keep
(2) Purpose clotting factors inactivated
o Damaged thrombomodulin will not be able to activate
Prevent blood loss from occurring by contracting or protein C cannot keep FV and FVIII inactivated
constricting blood vessels
(1) Platelet Activation
(3) Mechanism
Platelets are activated when GP1b binds with vWF
(i) Endothelin o GP1b (glycoprotein-1b)
Secreted by injured endothelial cells Platelet receptor that specifically binds to vWF
binds on to receptor on smooth muscle o von Willebrand Factor (vWF)
activates intracellular PIP2-Calcium mechanism secreted by injured endothelial cells
smooth muscle contracts triggers vessel (2) Platelet chemical release
vasoconstriction decreases blood vessel
diameter prevents blood loss Once activated, will release the following
o Adenosine Diphosphate (ADP)
(ii) Myogenic Mechanism o Thromboxane A2 (TXA2)
o Serotonin (5-hydroxytryptamine or 5-HT)
Direct contact or injury to smooth muscle causes
smooth muscle contraction (3) Platelet Aggregation

(iii) Nociceptor Activation Platelets have receptors on their membrane that

specifically bind with ADP and TXA2
Inflammatory chemicals are released when there’s
ADP & TXA2 stimulates platelets to come and aggregate
inflammation
at area of injured vessel
E.g., histamine, leukotrienes, prostaglandins, Platelets bind with other platelets via their GP2b/3a, with
These chemicals stimulate the nociceptors fibrinogen bridging them together
Nociceptors (pain receptors) will initiate pain
Pain reflex induces vasoconstriction (4) Vascular Spasm Effect Enhancement
TXA2 and serotonin bind to the smooth muscle
o Cause contraction
oT
o Enhances the vascular spasm effect
(5) Clinical Significance
Aspirin: TXA2 release
Clopidogrel, Prasugrel, Ticagrelor: ADP release
Abciximab: inhibits GP2b/3a inhibitors
Von Willebrand Disease: VWF production

Figure 2 Vascular Spasm

Figure 3 Platelet plug formation

2 of 6 HEMATOLOGY: Note #7 HEMOSTASIS: COAGULATION CASCADE

 (3) COAGULATION CASCADE o Activates XIII XIIIa
Requires Ca2+
Intrinsic pathway
o Independent of the extrinsic pathway Factor XIIIa
For example, someone’s blood in a test tube is not o Also known as Fibrin Stabilizing Factor
heparinized (no heparin coating) o Crosslinks fibrin stands together
Glass has rough, charged surface hence, Crosslinked fibrin
XIIa from the intrinsic pathway gets activated o Creates a fibrin mesh
This shows that the intrinsic pathway can occur in Mesh will hold down the platelet plug in place
a test tube independent of the extrinsic pathway. Mesh prevents platelets from dislodging and going
o Takes 4-6 minutes to different areas to cause an embolism
Extrinsic pathway o Thickens the blood passing through the area to slow
o Dependent on some of the factors and proteins within down the blood flow and prevent blood loss
the intrinsic pathway
(3) Extrinsic Pathway
o Takes 30 seconds
Note: An “a” after the roman numeral indicates an Blood vessel injury triggers release of Tissue factor
activated factor. (Factor III)
Factor III activates Factor VII VIIa
(1) Intrinsic Pathway o requires Ca2+ and PF4
Liver constantly creates clotting proteins that are normally VIIa can activate IX IXa
inactivated while circulating in the blood VIIa can converge into or stimulate the common pathway
Activated platelets express phosphatidyl serine groups on o Requires Ca2+ and PF4
their membrane, causing a negative charge
Negative charge will interact with and activate Factor XII Note: Tip for Remembering the Coagulation Cascade
(Hageman Factor)
o XII XIIa X marks the spot in the middle = Factor X
Left (intrinsic pathway) count downwards
XIIa activates XI FXIa o 12 8 (skip 10)
XIa activates IX IXa
Right (extrinsic pathway)
IXa forms a complex with VIIIa o 3 + 7 = 10
o Complexation requires PF3 and Ca2+
Common Pathway
VIIIa-IXa activates X Xa o 5 x 2 x 1 = 10
(2) Common Pathway (4) Clinical Significance
X Xa is the start of the common pathway Hemophilia A in factor VIII
Xa, Va, and Ca2+ will activate prothrombin activator
Hemophilia B in factor IX
o converts prothrombin (II) to thrombin (IIa)
Hemophilia C in factor XI
Thrombin reacts in two ways:
Heparin, Factor X inhibitors (Rivaroxaban) factor X
o Links together Fibrinogen (I) into Fibrin (Ia)
Fibrinogen is soluble Heparin, Factor II Inhibitors (Dabigatran) thrombin or
Fibrin is insoluble in the plasma also known as Factor II
Helps turn liquid blood into a jelly-like Warfarin formation of Thrombin, Factor VII, Factor IX,
substance to slows down blood flow in the Factor X
area and prevent loss of RBCs

HEMOSTASIS: COAGULATION CASCADE HEMATOLOGY: Note #7. 3 of 6

 (5) FIBRINOLYSIS
(4) CLOT RETRACTION & REPAIR
(1) Breaking Down Fibrin Mesh
(1) Platelet Contraction
There’s a need to get rid of the clot
Platelet contraction is stimulated once the platelet plug is
o The clot may be big enough that it could occlude
anchored to injured vessel wall by fibrin mesh
blood flow and possibly cause ischemia
Platelets contains contractile proteins
o Actin and myosin7 Endothelium expresses protein Tissue Plasminogen
Activator (TPA)
When platelets contract, they pull the damaged edges of
TPA converts Plasminogen into Plasmin
the injured blood vessel close to each other
o Plasminogen is naturally occurring in the bloodstream
This squeezes some serum out of the injured vessel
(2) Platelet-Derived Growth Factor (PDGF) Secretion Plasmin breaks down Fibrin mesh into Fibrinogen and
If smooth muscle cells are damaged, PDGF triggers Fibrin degradation products like D-Dimer
mitosis or proliferation of smooth muscle cells o This process recanalizes the clotted vessel
Damage to connective tissue, PDGF forms connective (2) Clinical Significance
tissue patches to regenerate collagen fibers
TPA Drugs
(3) Vascular Endothelial Growth Factor (VEGF) o
Secretion Increased rate of blood clot breakdown
Regenerates the new endothelial lining o Given to patient who have stroke or some type of
The blood vessel then starts to go through healing & ischemic attack within hours
remodeling Elevated D-Dimers can be indicative of blood clots and
inflammation
o Specific blood tests can be done to determine if
patient has had some type of clot formation

od clot and stabilizes clot

Figure 4 Clot Retraction

Figure 5 Fibrinolysis

4 of 6 HEMATOLOGY: Note #7 HEMOSTASIS: COAGULATION CASCADE

 III) APPENDIX

Figure 6. Summary of Hemostasis

Figure 7. Coagulation Cascade

HEMOSTASIS: COAGULATION CASCADE HEMATOLOGY: Note #7. 5 of 6

 IV) REVIEW QUESTIONS
1) Which is not a natural way of the body to prevent
blood from becoming thrombotic?
a) Heparin Sulfate
b) Nitric Oxide
c) Thromboxane
d) Prostacyclin

2) Which of the following is more stable?

a) Fibrinogen
b) Fibrin
c) They are equally stable

3) What is the third step of hemostasis?

a) Platelet Plug Formation
b) Coagulation Cascade
c) Vascular Spasm
d) Fibrinolysis

CHECK YOUR ANSWERS

V) REFRENCES
Le T, Bhushan V, Sochat M, Chavda Y, Zureick A. First Aid for
the USMLE Step 1 2018. New York, NY: McGraw-Hill Medical; 2017
Marieb EN, Hoehn K. Anatomy & Physiology. Hoboken, NJ:
Pearson; 2020.
Boron WF, Boulpaep EL. Medical Physiology.; 2017.
Urry LA, Cain ML, Wasserman SA, Minorsky PV, Orr RB,
Campbell NA. Campbell Biology. New York, NY: Pearson; 2020.
Jameson JL, Fauci AS, Kasper DL, Hauser SL, Longo DL,
Loscalzo J. Harrison's Principles of Internal Medicine. New York
etc.: McGraw-Hill Education; 2018.
Sabatine MS. Pocket Medicine: the Massachusetts General
Hospital Handbook of Internal Medicine. Philadelphia: Wolters
Kluwer; 2020

6 of 6 HEMATOLOGY: Note #7 HEMOSTASIS: COAGULATION CASCADE

 Last edited: 12/9/2021

1. BLOOD TYPING
Blood Typing Medical Editor: Mariel Antoinette L. Perez

OUTLINE (B) ANTIBODIES

Found in the plasma or circulation
I) BLOOD TYPE DONATION Made by our immune system
II) ANTIGENS AND ANTIBODIES
Protects blood from incompatible blood
III) BLOOD TYPING COMPATIBILITY
As seen in Figure 2
IV) CLINICAL SIGNIFICANCE
V) APPENDIX o Type A blood has Anti-B antibodies
VI) REVIEW QUESTIONS o Type B blood has Anti-A antibodies
VII) REFRENCES o Type AB blood has neither antibodies
o Type O blood has both Anti-A and Anti-B antibodies
I) BLOOD TYPE DONATION (C) ANTIGEN-ANTIBODY REACTION
Three different dishes per plate or scenario
Each dish is coated with antibodies
o 1st dish is coated with Anti-A antibodies
o 2nd dish is coated with Anti-B antibodies
o 3rd dish is coated with Anti-Rh antibodies
Agglutination
o Clumping of red blood cells
o Produced when blood with a specific antigen interacts
Figure 1. Blood Type Compatible Donation with its respective anti-antibody
A-antigen reacts with Anti-A antibodies
In Figure 1, the arrow denotes “can donate to”
B-antigen reacts with Anti-B antibodies
ABO Typing
Rh-antigen reacts with Anti-Rh antibodies
o Type A can donate to A and AB
o Type B can donate to B and AB
o Type AB can only donate to AB Note: Anti-Rh is the same as Anti-D.
o Type O can donate to all blood types A, B, AB, and O
III) BLOOD TYPING COMPATIBILITY
Rh Typing
o Rh negative
can donate to both positive and negative
o Rh positive
can only donate to Rh positive
can’t donate to Rh negative

II) ANTIGENS AND ANTIBODIES

Figure 3. How to Read Blood Typing Results

Figure 3 shows a summary of agglutination reactions for
the different blood types
Blood Type O can be donated to all ABO blood types.
o Type O– is the universal donor.
Figure 2. ABO Blood Types and Their Corresponding Antigens They have all the antibodies in their plasma
and Antibodies Other blood types can benefit/receive.
All the antibodies in their plasma will attack
(A) ANTIGENS other blood types
Surface markers on red blood cells that let the immune Great donor, terrible recipient.
system know what your blood type is o Type O+ can donate to all positive blood types
All other blood types that’s not yours is considered foreign Remember: Rh+ can’t donate to Rh–
As seen in Figure 2 Blood Type AB can receive all ABO blood types.
o Type A blood has A antigen o Type AB– can receive from all negative blood types
o Type B blood has B antigen Remember: Rh+ can’t donate to Rh–
o Type AB blood has both A and B antigens o Type AB+ is the universal recipient.
o Type O blood has neither A nor B antigens can receive from ALL blood types
Blood Type or Rh typing does not matter
Note: To make it easier to remember, the “O” in Type O
is empty because there neither antigen is present!

Blood Typing HEMATOLOGY: Note #8. 1 of 3

 IV) CLINICAL SIGNIFICANCE

(A) HEMOLYTIC DISEASE OF THE NEWBORN

(1) Definition
Also called Erythroblastosis fetalis
One of the dangerous mismatched transfusions
Endogenous: happens within the person’s body
Usually not a problem for the first birth
o But first birth triggers it
o Sometimes not a problem for the second birth; but
generally, the risk increases with every birth.
(2) First Fetus/Birth
Mother: Rh–
o Has no Rh antibodies
Unless she has had some type of mismatched
transfusion in the past
Figure 4. Blood Typing 1
Fetus: Rh+
In Figure 4, o It has an Rh antigen on its membrane
o Top-Left
Blood Type A– In the first birth, when the placenta breaks away from the
Can donate to A (+/-), AB (+/-) uterus, some of the blood of the fetus leaks away and
mixes with the mother’s blood
Can receive A–, O–
o Fetal RBCs in mother’s circulation triggers
o Top-Right
immune system to make Anti-Rh antibodies
Blood Type A+
Can donate to A+, AB+ (3) Following Birth/s
Can receive A (+/-), O (+/-)
Rh– mother has another fetus with Rh+ RBCs
o Bottom-Left
The Anti-Rh antibodies that the mother’s immune system
Blood Type B–
produced during the 1st birth can cross placenta and
Can donate to B (+/-), AB (+/-)
attack fetus RBCs
Can receive B–, O– Fetal RBCs undergo agglutination and hemolysis
o Bottom-Right
Blood Type A+ (4) Effect on Affected Baby
Can donate to A+, AB+ Baby will have hemolytic anemia
Can receive B (+/-), O (+/-) Decreases baby’s RBCs
Increases bilirubin levels to the maximum
May cause kernicterus and mental retardation
(5) Treatment
This can be recognized during pregnancy
Diseases can be prevented by giving Rhogam
o Anti-Rh antibody drug
o Binds to the Anti-RH antibodies and renders them
ineffective

Figure 5. Blood Typing 2

In Figure 5. Blood Typing 2,
o Top-Left
Blood Type AB–
Can donate to AB (+/-)
Can receive A–, B–, AB–, O–
o Top-Right
Blood Type AB+
Can donate to AB+
Can receive A (+/-), B (+/-), AB (+/-), O (+/-)
o Bottom-Left
Blood Type O–
Can donate to A (+/-), B (+/-), AB (+/-), O (+/-)
Can receive O– only
o Bottom-Right
Blood Type O+
Can donate to A+, B+, AB+, O+
Can receive O (+/-)

2 of 3 HEMATOLOGY: Note #8 Blood Typing

 V) APPENDIX

Figure 6. Summary of Blood Typing Lecture

VI) REVIEW QUESTIONS VII) REFRENCES

Le T, Bhushan V, Sochat M, Chavda Y, Zureick A. First Aid for
1) Which of the following is considered a universal
the USMLE Step 1 2018. New York, NY: McGraw-Hill Medical; 2017
donor? Marieb EN, Hoehn K. Anatomy & Physiology. Hoboken, NJ:
a) Type AB+ Pearson; 2020.
b) Type AB– Boron WF, Boulpaep EL. Medical Physiology.; 2017.
Urry LA, Cain ML, Wasserman SA, Minorsky PV, Orr RB,
c) Type O+ Campbell NA. Campbell Biology. New York, NY: Pearson; 2020.
d) Type O– Jameson JL, Fauci AS, Kasper DL, Hauser SL, Longo DL,
Loscalzo J. Harrison's Principles of Internal Medicine. New York
etc.: McGraw-Hill Education; 2018.
2) Which of the following is considered a universal Sabatine MS. Pocket Medicine: the Massachusetts General
receiver? Hospital Handbook of Internal Medicine. Philadelphia: Wolters
Kluwer; 2020
a) Type AB+
b) Type AB–
c) Type O+
d) Type O–

3) Assuming that the following are valid results,

identify the blood type:

a)

b)

c)

d)
CHECK YOUR ANSWERS

Blood Typing HEMATOLOGY: Note #8. 3 of 3