Objective 1
Key terms and Characteristics
Key Terms:
-
Erythrocytes (RBCs): Red blood cells
- responsible for oxygen transport
-
Leukocytes (WBCs): white blood cells
-for immunity
-
Thrombocytes: Platelets
- assist in clotting
Characteristics
-
Sticky, opaque fluid with metallic taste
Colour depends on oxygen content:
-high O2 = scarlet red
-low O2 = dark red
- PH: 7.35-7.45
- Volume: 5-6L in males, 4-5L in females
Formation Elements
1. Red blood cells (RBCs)
2. White blood Cells (WBCs)
3. Platelets
Cellulare Terms
●
●
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The human body has over 250 different types of cells, each specialized for
specific functions.
Cyte: A suffix in anatomical language that means “cell.”
Thrombo: A prefix related to clotting or the formation of clots.
Recall
● In steady state (normal condition): Ions (charged particles)
move through the cell membrane to keep the right balance of
concentrations and pH.
● In altered states (when something goes wrong): The flow of
ions into or out of the cell is messed up, which can cause
problems in the body and lead to illness or disease.
Functions of Blood
1. Regulation
2. Transportation
3. Protections
Functions of Blood: Regulation
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Maintain body temperature by absorbing and disturbing heat
Maintain normal PH using buffer(alkaline reserve of bicarbonate
ions)
Maintain adequate fluid volume in circulatory system
Function of Blood: Transportation
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Delivery all O2 and nutrients to body cells
Transports waste to lungs & kidneys; elimination
Transports hormones from endocrine to target organ
Function of Blood: Protection
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Preventing blood loss
Prevents infection
Agents of immunity are carried in blood
Includes cells such as:
○ Antibodies
○ Complete proteins(create antibodies & hemoglobins)
○ WBCs
BLOOD CLOTTING
Blood Clotting to Prevent Blood Loss:
●
●
When you get a cut, blood clotting stops you from losing too much
blood.
Plasma proteins and platelets (a type of blood cell) work together to
form a clot.
BLOOD CLOTTING
Preventing Infection:
●
●
Blood cells help protect against infection.
In earlier lessons (N109), we talked about the glycocalyx (a layer on
the surface of cells). In N209, we will learn more about how blood
cells fight infection.
BLOOD CLOTTING
Blood Helps with Immunity:
● Blood carries agents that protect the body, including:
○ Antibodies (help fight infections)
○ Complement proteins (help destroy invaders)
○ White blood cells (fight off infections)
BlOOD & TISSUE
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Blood is the only liquid tissue in the body.
It’s a type of connective tissue.
The matrix (background substance) is a non-living fluid called
plasma.
The cells in blood are living and are called formed elements.
These cells float around in the plasma.
SPUN TUBE
●
When blood is spun in a tube, it separates into 3 layers:
1. Erythrocytes (Red Blood Cells): Bottom layer (~45% of total blood).
2. Plasma: Top layer (clear fluid).
3. Buffy Coat: Middle layer (white blood cells + platelets).
Hematocrit:
●
The hematocrit is the percentage of blood made up of red blood cells in the tube(RBCs).
Normal Hematocrit Values:
●
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Males: 47% ± 5% (Range: 42% - 52%)
Females: 42% ± 5% (Range: 37% - 47%)
WHAT IS A COMPLETE CELL
ONLY WHITE BLOOD CELLS ARE COMPLETE CELLS
What Makes a "Complete" Cell?
●
A complete cell has a nucleus and all the normal cell parts (like DNA, etc.).
Why Are RBCs and Platelets Incomplete?
●
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RBCs don’t have a nucleus (they lose it when they mature).
Platelets are actually tiny pieces of cells, not full cells, so they don’t have a nucleus
either.
ERYTHROCYTES
●
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Small and help carry gases (like oxygen) around the body.
Shape: Biconcave disc (like a doughnut with a thin middle, but no hole).
○ Anucleate (no nucleus) and no organelles (no other parts like mitochondria).
Why This Shape Helps Gas Transport:
1.
2.
3.
Biconcave shape: Gives a large surface area for better gas exchange (more oxygen can
be picked up or dropped off).
Hemoglobin: Makes up 97% of the cell (except water) and helps carry oxygen.
No mitochondria: RBCs don’t use the oxygen they carry. They make energy without
oxygen (anaerobic), so all the oxygen can be used by tissues.
HEMOGLOBIN
Hemoglobin and Oxygen:
●
Hemoglobin binds to oxygen but can also release it (this is what "reversibly" means—attach and
detach).
Comparison to Myoglobin:
●
Myoglobin (from muscles) is similar but it only holds onto oxygen and doesn’t release it as easily.
It’s more like a storage container for oxygen in muscles.
Why Reversible Binding is Important:
●
It allows hemoglobin to pick up oxygen in the lungs and release it where it's needed in the body
(like in muscles or tissues).
HEMOGLOBIN (COND’T)
Normal Hemoglobin Levels:
●
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Males: 13–18 g/100ml of blood
Females: 12–16 g/100ml of blood
Hemoglobin Structure:
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Hemoglobin has a red heme pigment that’s attached to a protein called globin.
The red color of blood comes from the heme.
Each heme has an iron atom that binds to one oxygen (O₂).
Each hemoglobin molecule can carry four oxygen molecules.
Hemoglobin O2
Each RBCs contains 250 million Hb molecules
● O2 loading in lungs -> produces oxyhemoglobin (ruby red)
● O2 unloading in tissue -> Produces deoxyhemoglobin, or reduces
hemoglobin (dark red)
● CO2 loading in tissue - 20% of CO2 in blood binds to Hb, producing
carbaminohemoglobin
Loading & lungs = ox
Unloading & tissue = de
Loading & tissue = carb
Hematopoiesis
Hematopoiesis (Blood Cell Formation):
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Hematopoiesis is the process of making all blood cells.
○ Recall: You might have seen this term in N109 (previous lessons on blood cell development).
Where Does Hematopoiesis Occur?
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Happens in the red bone marrow (found in bones).
In adults, it mainly takes place in:
○ Axial skeleton (spine, ribs, skull)
○ Girdles (shoulder and pelvic bones)
○ Proximal ends of the humerus (upper arm) and femur (thigh)
Hematopoiesis (cont’d)
Hematopoietic Stem Cells (Hemocytoblasts):
●
Hematopoietic stem cells (also called hemocytoblasts) are special cells that
can turn into any type of blood cell.
○ These stem cells are the starting point for creating red blood cells, white
blood cells, and platelets.
Story of How Hematopoietic Stem Cell Becomes an
Erythrocyte (Red Blood Cell):
Hematopoietic Stem Cell (Hemocytoblast): This is the "parent" cell that can become any kind of blood
cell.
Erythropoiesis: Process of formation of RBCs that takes about 15 days
Reticulocyte: Almost a full red blood cell, but still has some leftover material inside.
Erythrocyte (Red Blood Cell): The final stage—now it’s a fully mature, biconcave red blood cell, ready
to carry oxygen!
Erythropoiesis
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Erythropoiesis is the process where red blood cells (RBCs) are made. It takes
about 15 days.
Why RBCs Are Incomplete:
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RBCs are incomplete because they lose their nucleus and organelles as they
mature.
This process shows why RBCs are incomplete: early in development, they still have
some organelles (like ribosomes), but they lose them by the time they become
mature RBCs.
Stages of RBC Development:
1.
2.
Reticulocyte:
○ These are young RBCs that still have some ribosomes inside.
○ They're not fully mature yet.
Mature Erythrocyte:
○ After about 2 days, the ribosomes break down, and the cell becomes a fully mature RBC.
○ Now it has no nucleus or organelles, which is why it’s considered incomplete.
Reticulocyte Count:
●
The reticulocyte count tells us how fast RBCs are being made.
○ A higher count means more RBCs are being produced.
○ A lower count could mean a problem with RBC production.
Regulation & Requirements of Erythropoiesis
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To few RBCs leads to tissue hypoxia
Body tissue aren’t getting enough oxygen (tissue Hypoxia)
S/S
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Fatigue, SOB, pallor/blue skin (lips & fingers), dizzy, increase HR,
headache, confusion, chest Pain
Can cause organ damage
Regulation & Requirements of Erythropoiesis
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Too many RBCs increased blood viscosity
Cause problem with blood flow & increase risk for clot
S/S
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Headache, dizzy, blurred vision, fatigue, SOB, chest pain, increase
BP, red/flushed skin, increase risk for stroke, or heart attack
Can cause -> blood clots, stroke, heart attack
Regulation & Requirements of Erythropoiesis
Balance Between RBC Production and Destruction:
1.
2.
3.
4.
5.
Hormonal Controls
○ RBC production and destruction are controlled by hormones, mainly EPO (erythropoietin).
What system controls this?
○ Endocrine system (hormones released by glands like kidneys and liver) controls RBC balance.
Erythropoietin (EPO)
○ EPO is a hormone that stimulates the production of red blood cells.
Basal (steady) level of EPO
○ There’s always a small amount of EPO in the blood to keep RBC production at a steady level.
EPO released by kidneys
○ Most EPO comes from the kidneys (a little from the liver too).
○ EPO is released when there’s low oxygen (hypoxia) in the body.
Regulation & Requirements of Erythropoiesis
Balance Between RBC Production and Destruction part 2:
1.
2.
3.
4.
5.
EPO released by kidneys
○
Most EPO comes from the kidneys (a little from the liver too).
○
EPO is released when there’s low oxygen (hypoxia) in the body.
Too many RBCs or high oxygen
○
When there are too many RBCs or oxygen levels are high, EPO production is reduced.
EPO speeds up RBC maturation
○
EPO helps immature RBCs mature faster, so they can carry oxygen.
Testosterone and RBC production
○
Testosterone boosts EPO production, leading to more RBCs, which is why males usually have higher RBC
counts than females.
Athletes abusing EPO
○
Some athletes use artificial EPO to increase RBC count and boost oxygen levels for better performance.
Regulation & Requirements of Erythropoiesis
Balance Between RBC Production and Destruction part 3
Key Points:
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EPO controls RBC production.
Low oxygen → more EPO → more RBCs.
Too many RBCs or high oxygen → less EPO.
Testosterone increases EPO, giving males higher RBC counts.
Artificial EPO abuse is used by some athletes to enhance performance.
Regulation & Requirements of Erythropoiesis
Dietary Requirements for RBC Production:
1.
2.
3.
4.
Amino Acids, Lipids, and Carbs
○
Needed for general cell function and energy production.
Iron
○
Iron is important for making hemoglobin, the protein in RBCs that carries oxygen.
Where Iron Is Found
○
65% of iron is in hemoglobin.
○
The rest is stored in the liver, spleen, and bone marrow.
Why Iron Needs to Be Bound to Proteins
○
Free iron is toxic to cells, so the body keeps it bound to proteins for safety.
Regulation & Requirements of Erythropoiesis
Dietary Requirements for RBC Production part 2:
1.
Iron Storage
○ Iron is stored as ferritin and hemosiderin in cells.
Iron Transport
○ Iron is carried through the blood by a protein called transferrin.
Vitamin B12 and Folic Acid
○ These are important for rapidly dividing cells, like the developing red blood cells (RBCs).
2.
3.
Key Points:
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Iron is needed for hemoglobin.
Stored safely in ferritin and hemosiderin, carried by transferrin.
Vitamin B12 and folic acid are key for making new RBCs.
FATE & DESTRUCTION OF ERYTHROCYTES
Life Span and Breakdown of RBCs:
1.
2.
3.
4.
RBC Life Span:
○
RBCs live for about 100–120 days.
Old RBCs Become Fragile:
○
Over time, RBCs get weaker, and their hemoglobin (Hb) starts to break down.
Macrophages in Spleen:
○
Macrophages (special cells) in the spleen eat and break down old RBCs.
RBC Breakdown Process:
○
Hemoglobin (Hb) is separated into:
■
Iron
■
Heme
■
Globin (protein part)
FATE & DESTRUCTION OF ERYTHROCYTES CONT’D
1.
2.
3.
4.
5.
Iron:
○ Iron is recycled and stored for future use.
Heme:
○ Heme gets broken down into bilirubin, which is yellow.
Bilirubin and Jaundice:
○ If the liver can’t process bilirubin properly, it builds up in the body and causes
jaundice (yellow skin and eyes).
Bilirubin Secretion:
○ The liver sends bilirubin into the bile, which goes into the intestines.
○ Bilirubin leaves the body in feces (poop).
Globin:
○ Globin is broken down into amino acids, which can be reused by the body.
FATE & DESTRUCTION OF ERYTHROCYTES (FLOW CHART)
Key Points:
How the Breakdown Happens (Flow Chart):
1.
2.
Old RBC → Fragile RBC
○
→ Macrophages in spleen break it down
Hemoglobin (Hb) → Iron, Heme, Globin
○
Iron → Stored for reuse
○
Heme → Bilirubin → Secretes in bile
■
Bilirubin → Causes jaundice if not processed
properly
■
Leaves body in feces
○
Globin → Broken into amino acids
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RBCs live about 120 days, then break down.
Iron is reused, heme becomes bilirubin, and
globin becomes amino acids.
Jaundice happens if bilirubin builds up in the
body.
ANEMIA
What is Anemia?
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Anemia means the blood can't carry enough oxygen
because there aren’t enough healthy RBCs or
hemoglobin.
This makes it hard for the body to function properly.
Symptoms of Anemia:
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Fatigue (feeling tired all the time)
Pallor (pale skin)
Dyspnea (shortness of breath)
Chills (feeling cold)
Types of Anemia:
1.
2.
Hemorrhagic Anemia (Blood Loss Anemia):
○
Rapid blood loss (e.g., from a severe
wound).
○
Treatment: Blood replacement (getting a
transfusion of blood).
Chronic Hemorrhagic Anemia:
○
Slow, steady blood loss (e.g., from
hemorrhoids or a bleeding ulcer).
○
Treatment: Fix the cause of the blood loss
(like treating the ulcer or hemorrhoids).
ANEMIA PT. 2
Iron-Deficiency Anemia:
Key Points:
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Cause: Lack of enough iron, which could be due to:
○ Blood loss (hemorrhagic anemia).
○ Low iron intake from food.
○ Poor absorption of iron.
Symptoms:
○ RBCs are small and look pale.
○ They can’t make enough hemoglobin because there
isn’t enough iron.
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Anemia is when the blood can't
carry enough oxygen.
Causes of anemia include blood
loss or lack of iron.
Iron-deficiency anemia makes
RBCs smaller and paler because
they can’t make enough
hemoglobin.
ANEMIA PT. 3
Aplastic Anemia:
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Cause: The red bone marrow is damaged or doesn't work properly, so not enough RBCs
are made.
Sickle-Cell Anemia:
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Cause: Abnormal hemoglobin (the protein in RBCs that carries oxygen).
Genetic: You inherit it from your parents.
More common in: People of African descent.
Effect: RBCs become sickle-shaped, which makes them get stuck and not carry oxygen well.
ANIMA PT. 4
Polycythemia:
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1.
Cause: Too many RBCs in the blood.
Effect: Makes the blood thicker (more viscous), which makes it flow slower and more sluggish.
Polycythemia Vera: A type of bone marrow cancer that makes the body produce too many RBCs.
Blood Doping:
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What it is: Athletes take out some of their own RBCs, store them, and then put them back in before a
competition.
Purpose: Increases oxygen levels in the blood, which helps improve stamina during the event.
ANIMA PT.5
Key Points:
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Aplastic anemia: Red bone marrow stops making enough RBCs.
Sickle-cell anemia: Abnormal RBCs that can't carry oxygen properly
(genetic).
Polycythemia: Too many RBCs, making blood thick and sluggish.
Blood doping: Athletes boost RBC count for better performance.
White Blood Cells
What Are Leukocytes (WBCs)?
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Leukocytes are white blood cells (WBCs).
They are the only blood cells that are complete cells (they have a nucleus and organelles).
Make up less than 1% of the total blood volume.
Function: They help fight disease and infections
How Leukocytes Work:
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Diapedesis: WBCs can leave blood vessels (capillaries) and move into tissues to fight infections.
Leukocytosis:
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Leukocytosis means an increase in WBC count.
This is a normal response when the body is fighting an infection.
Types of WBC
Two Major Types of Leukocytes:
1.
2.
Granulocytes (cells with visible granules in the cytoplasm):
○ Neutrophils
○ Eosinophils
○ Basophils
Agranulocytes (cells without visible granules in the cytoplasm):
○ Lymphocytes
○ Monocytes
Memory Tip for Leukocytes:
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"Never let monkeys eat bananas" =
Neutrophils, Lymphocytes, Monocytes, Eosinophils, Basophils.
Key Points:
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WBCs are complete cells that fight
infections.
They can leave the blood and go
into tissues.
There are two main types:
granulocytes (with granules) and
agranulocytes (without granules).
GRANULOCYTES
Granulocytes:
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Neutrophils, Eosinophils, Basophils
Larger and shorter-lived than RBCs.
All are phagocytic (they eat and digest things like bacteria or debris).
Key Points:
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Neutrophils fight bacterial infections.
Eosinophils attack large parasites and help with allergies.
Basophils release histamine to cause inflammation and attract other WBCs.
NEUTROPHILS
Neutrophils:
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Most common WBCs (50–70% of all WBCs).
Act as the body’s first defenders against bacterial infections (e.g.,
appendicitis, meningitis).
Attracted to areas of infection or inflammation and are active eaters
(phagocytes).
EOSINOPHILS
Eosinophils:
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2–4% of WBCs.
Attack large parasites (like worms) by releasing enzymes that break
them down.
Also involved in allergies and asthma and help modulate the immune
system.
BASOPHILS
Basophils:
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Rarest WBCs (only 0.5–1% of WBCs).
Contain histamine in their granules:
○ Histamine makes blood vessels widen (vasodilator) and helps bring more
WBCs to the site of infection or inflammation.
AGRANULOCYTES
Agranulocytes (cells without visible granules in the cytoplasm):
○
○
Lymphocytes
Monocytes
Key Points:
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Lymphocytes: T cells fight virus-infected and tumor cells; B cells make antibodies.
Monocytes: Turn into macrophages that eat and destroy harmful invaders and
help activate the immune system.
AGRANULOCYTES
Lymphocytes:
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1.
2.
Second most common WBC (about 25% of all WBCs).
Crucial for immunity – they help protect the body from infections.
T Lymphocytes (T cells):
○ Attack virus-infected cells and tumor cells.
B Lymphocytes (B cells):
○ Make plasma cells that produce antibodies to fight infections.
AGRANULOCYTES
Monocytes:
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Largest WBCs (about 3–8% of all WBCs).
Leave the blood and move into tissues, where they turn into macrophages.
Macrophages are big eating cells that fight:
○ Viruses
○ Bacteria inside cells
○ Chronic infections
They also help activate lymphocytes to boost the immune response.
LEUKOPOIESIS
Leukopoiesis (WBC Production):
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Leukopoiesis is the process of making white blood cells (WBCs).
Stimulated by chemical messengers from the red bone marrow and mature WBCs.
Stem Cells and Their Pathways:
1.
2.
3.
Hemocytoblast Stem Cell:
○ The starting cell that can turn into different types of blood cells.
○ It splits into two pathways:
Lymphoid Stem Cells:
○ These produce lymphocytes (a type of WBC).
Myeloid Stem Cells:
○ These produce all other blood cells, including most types of WBCs.
LEUKOPOIESIS PT.2
Disorders from Abnormal WBC Production:
1.
2.
Leukemia:
○ Overproduction of abnormal WBCs (cancer of the blood cells).
Infectious Mononucleosis:
○ A viral infection that causes an increase in certain WBCs.
Key Points:
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●
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WBCs are made from stem cells in the bone marrow.
Lymphoid stem cells make lymphocytes; myeloid stem cells make other blood cells.
Too many or abnormal WBCs can lead to diseases like leukemia or mononucleosis.
PLATELETS
Platelets are tiny fragments that come from larger cells called megakaryocytes.
Function of Platelets:
●
Platelets form a temporary plug to help seal breaks in blood vessels when they get injured.
How Platelets Are Kept Inactive:
●
Nitric oxide (NO) and prostacyclin (both released by the blood vessel lining) keep platelets inactive and
mobile in the blood, so they don’t stick to the walls of blood vessels unless there’s a problem (like a cut).
Platelet Formation:
●
Platelet production is controlled by a hormone called thrombopoietin.
PLATELETS PT.2
Comparison to Erythropoietin:
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Thrombopoietin (for platelets) and erythropoietin (for red blood cells) are both
hormones that help stimulate the production of blood cells.
Both are important for maintaining healthy blood cell numbers, but one regulates
platelet production, and the other regulates red blood cell production.
Key Points:
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●
Platelets help seal wounds by forming a plug.
Thrombopoietin controls platelet formation, just like erythropoietin controls red blood
cell formation.
PLASMA
Plasma is a straw-colored, sticky fluid that makes up the liquid part of your blood.
What Plasma Is Made Of:
●
●
About 90% water.
Contains over 100 different dissolved substances, like:
○ Nutrients (like glucose)
○ Gases (like oxygen and carbon dioxide)
○ Hormones
○ Waste products
○ Proteins
○ Inorganic ions (like sodium and potassium)
PLASMA PT.2
Plasma Proteins:
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Plasma proteins are the most
abundant solutes in plasma.
These proteins stay in the blood and
are not taken up by cells.
Main Plasma Protein – Albumin:
●
Albumin is the most abundant protein in
plasma.
Functions of Albumin:
1.
2.
3.
Carries other molecules (like hormones and drugs).
Helps maintain blood pH as a blood buffer.
Regulates plasma osmotic pressure, which helps
keep the right amount of fluid in the blood vessels.
Key Points:
●
●
Plasma is mostly water and has lots of dissolved
substances.
Albumin is the most important protein in plasma,
helping carry things, balance pH, and keep fluid in the
blood.
HEMOSTASIS
Hemostasis is the process that stops bleeding quickly.
It needs clotting factors and chemicals from platelets and damaged tissues.
Three steps to homeostasis: Vascular spasm, what triggers the vascular spasm,
effectiveness
Key Points:
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Vascular spasm is the first step in stopping bleeding: the blood vessel tightens to slow
blood loss.
It’s triggered by injury, chemicals, and pain signals, and works best in smaller vessels.
●
●
Platelet plug forms first, then coagulation makes it stronger with fibrin.
Coagulation turns blood from liquid to gel and needs Vitamin K to work.
Hemostasis PT.2
Step 1: Vascular Spasm
●
●
When a blood vessel is injured, it tightens up (called vasoconstriction) to reduce blood flow.
This helps slow down the bleeding until the next steps happen.
What Triggers Vascular Spasm?
1.
2.
3.
Direct injury to the smooth muscle of the blood vessel.
Chemicals released by endothelial cells (cells lining the blood vessels) and platelets.
Pain reflexes from the injury site.
Effectiveness:
●
●
This is especially useful in smaller blood vessels.
It can greatly reduce blood flow while other steps to stop bleeding take over.
Hemostasis PT.3
Step 2: Platelet Plug Formation
●
●
●
When a blood vessel is damaged, the collagen fibers inside the vessel are exposed.
Platelets stick to these exposed collagen fibers, forming a temporary plug to block the hole.
Platelets don’t stick to the walls of healthy blood vessels because collagen isn’t exposed there
Step 3: Coagulation (Blood Clotting)
●
●
Coagulation is the process that reinforces the platelet plug with fibrin threads (a protein).
This turns the blood from a liquid into a gel, creating a stronger seal over the damaged area.
Hemostasis PT.4: How Coagulation Works
How Coagulation Works:
●
●
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Blood clots are very effective at sealing larger breaks in blood vessels.
A series of reactions happen with clotting factors (also called procoagulants), which are
mostly plasma proteins.
Vitamin K is needed to make 4 clotting factors.
Coagulation Phases:
●
Coagulation happens in three phases, which work together to form a strong blood clot.
Might delete
Coagulation
Intrinsic Pathway:
Coagulation:
●
●
●
Coagulation is the process of forming a
blood clot to stop bleeding.
There are two pathways that help form a
clot:
Intrinsic pathway & Extrinsic Pathway
Key Points:
●
●
Intrinsic pathway uses factors already in the blood
and is slower.
Extrinsic pathway uses external factors, is faster,
and gets activated by tissue damage.
●
●
"Intrinsic" means that all the clotting factors needed
are already in the blood.
It’s the slower pathway because it takes more steps
to form the clot.
Extrinsic Pathway:
●
●
●
"Extrinsic" means that the clotting factors needed
come from outside the blood.
Triggered by tissue factor (TF), also called Factor III,
which is exposed when tissues are damaged.
This pathway is faster because it skips some steps in
the intrinsic pathway.
Coagulation PT.2
Phase 1: Two Pathways to Prothrombin Activator
●
●
●
●
This phase starts with either the intrinsic or extrinsic pathway (usually both are involved).
Triggered by tissue damage (like when you cut yourself).
Both pathways cascade (chain reaction) and eventually lead to the activation of Factor X.
Factor X activation leads to the formation of prothrombin activator, which is key for the next
phase.
Phase 2: Pathway to Thrombin
●
●
Prothrombin activator changes prothrombin (a protein in blood) into thrombin (an active
enzyme).
Thrombin is crucial because it starts the next steps in forming the blood clot.
Coagulation PT.3
Phase 3: Common Pathway to the Fibrin Mesh
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●
●
Thrombin (the active enzyme from Phase 2) turns fibrinogen (a protein in the blood) into fibrin.
Fibrin forms long strands that act as the foundation of the clot.
These fibrin strands make the blood turn into a gel-like substance, trapping blood cells and platelets to form a
solid clot.
Thrombin's Role (with Calcium):
●
Thrombin also activates Factor XIII (called fibrin stabilizing factor), which:
○
Cross-links the fibrin strands to make them stronger.
○
Stabilizes the clot, ensuring it stays in place.
Anticoagulants:
●
●
These are natural factors in the blood that prevent clotting from happening too much.
They help stop the blood from forming clots when it’s not needed.
CLOTTING STABILIZATION & REMOVAL
Once the blood vessel is repaired, the clot needs to be stabilized and then removed.
Clot Retraction:
●
●
●
Actin and myosin (proteins inside platelets) contract (tighten) within 30–60 minutes.
This contraction pulls on the fibrin strands in the clot, making it shrink and squeeze out the serum (the liquid
part of the blood, without the clotting proteins).
The retraction of the clot helps pull the edges of the blood vessel back together, promoting healing.
Where Have We Seen Actin and Myosin Before?
●
●
Actin and myosin are also found in muscle cells.
They work together to cause muscle contractions, and here they help platelets contract to shrink the clot.
CLOTTING STABILIZATION & REMOVAL: KEY POINTS
●
●
●
The clot shrinks to help close the wound.
Actin and myosin inside platelets contract to pull the clot together
and squeeze serum out.
This process closes the blood vessel to help it heal.
CLOTTING STABILIZATION & REMOVAL PT.2
Vessel Healing While Clot Shrinks:
●
While the clot is shrinking, the blood vessel is also healing.
Platelet-Derived Growth Factor (PDGF):
●
●
Platelets release PDGF.
PDGF helps smooth muscle cells and fibroblasts (cells that make connective tissue) multiply to
rebuild the blood vessel wall.
Vascular Endothelial Growth Factor (VEGF):
●
VEGF stimulates endothelial cells (cells lining the blood vessels) to multiply and repair the inside lining
of the vessel.
CLOTTING STABILIZATION & REMOVAL: KEY POINTS PT.2
● PDGF helps rebuild the blood vessel wall.
● VEGF helps repair the inner lining of the blood vessel.
FIBRINOLYSIS
Fibrinolysis is the process of removing clots after the vessel has healed.
This process starts within 2 days after the clot forms and continues until the clot is completely dissolved.
How It Works:
●
●
Plasminogen, a protein in the blood, is trapped inside the clot.
Over time, plasminogen is turned into plasmin, an enzyme that breaks down fibrin (the protein holding the clot
together).
Key Players in Fibrinolysis:
●
Tissue plasminogen activator (tPA), Factor XII, and thrombin all help convert plasminogen into plasmin.
Why Administer tPA During a Stroke?
●
tPA helps break down clots in blood vessels, so during a stroke, giving tPA can dissolve the clot blocking
blood flow to the brain and reduce damage.
FIBRINOLYSIS: KEY POINTS
●
●
Fibrinolysis breaks down clots after healing.
tPA helps speed up clot breakdown, especially during emergencies
like stroke.
Factors Limiting Clot Size:
There are two ways the body limits how big a clot can get:
1.
2.
Swift removal and dilution of clotting factors:
○
The body quickly removes or dilutes the substances that help form the clot.
Inhibition of activated clotting factors (Anticoagulants):
○
The body also has anticoagulants that stop clotting factors from becoming too active and making the
clot grow too large.
Types of Disorders:
1.
2.
Thromboembolic Disorders:
○
These are conditions that cause undesirable clot formation, leading to problems like blood clots in the
wrong places (e.g., deep vein thrombosis or stroke).
Bleeding Disorders:
○
These happen when the body can't form normal clots, leading to excessive bleeding (e.g., hemophilia).
Factors Limiting Clot Size: PT.2
Disseminated Intravascular Coagulation (DIC):
●
DIC is a serious condition where both types of problems happen at the same time:
○ Clots form in the wrong places.
○ Bleeding also occurs because the clotting factors are used up.
Key Points:
●
●
●
The body limits clot growth by removing clotting factors and using anticoagulants.
There are two main problems: too many clots or not enough clots.
DIC involves both problems at once, causing clots and bleeding.
THROMBOEMBOLIC DISORDERS
These are problems that involve blood clots forming in the blood vessels.
Thrombus:
●
●
A thrombus is a blood clot that forms and stays in a blood vessel that isn’t broken.
If the thrombus blocks blood flow, it can lead to tissue death because the tissue isn't getting
enough oxygen.
Examples of Thrombus Problems:
●
●
A clot in the leg veins (deep vein thrombosis - DVT) can block blood flow and cause swelling.
A clot in the heart can lead to a heart attack
THROMBOEMBOLIC DISORDER: PT.2
Embolus:
●
An embolus is a thrombus (clot) that breaks loose and floats through the bloodstream.
Embolism:
●
●
An embolism happens when the embolus (floating clot) blocks a blood vessel somewhere.
Example: A pulmonary embolism (clot in the lungs) or cerebral embolism (clot in the brain).
Risk Factors for Clots:
●
●
●
Atherosclerosis (fatty buildup in blood vessels)
Inflammation in blood vessels
Slow blood flow or blood stasis (when blood doesn’t flow properly, like from being immobile for a long
time)
THROMBOEMBOLIC DISORDER: PT.3
Why Use Anticoagulants (Blood Thinners)?
●
Anticoagulants (blood thinners) help prevent clots from forming or growing bigger, reducing
the risk of blockages and serious complications like heart attacks, strokes, or pulmonary
embolism.
Key Points:
●
●
●
●
Thrombus = clot stuck in a blood vessel; Embolus = clot that moves.
Embolism happens when a moving clot blocks a vessel.
Risk factors include atherosclerosis, inflammation, and not moving enough.
Anticoagulants prevent clots from causing harm.
HUMAN BLOOD GROUPS:ANTIGENS
Red blood cells (RBCs) have different antigens on their surfaces.
What is an Antigen?
●
An antigen is something that the body sees as foreign and can trigger an immune response.
HUMAN BLOOD GROUPS:AGGLUTINOGENS
Agglutinogens:
●
The antigens on RBCs are also called agglutinogens because they can cause agglutination.
What is Agglutination?
●
●
Agglutination means the clumping of blood cells.
This happens when the immune system attacks foreign blood by clumping it together.
Why is Agglutination Dangerous?
●
●
●
If you get the wrong type of blood (like mismatched blood during a transfusion), the body sees it as foreign.
The body will attack the foreign blood, causing agglutination (clumping) and destroying the red blood cells.
This can cause a serious and potentially fatal reaction.
HUMAN BLOOD GROUPS
ABO and Rh Blood Groups:
●
●
The ABO and Rh blood groups are the most important because they cause the strongest
transfusion reactions when mismatched blood is given.
These groups are carefully typed to make sure blood transfusions are safe.
Key Points:
●
●
●
Antigens on RBCs can cause agglutination (clumping).
Agglutination happens when blood is mismatched and can be dangerous or deadly.
The ABO and Rh blood types are the most important to check before a transfusion.
ABO BLOOD GROUPS
Blood types are based on two antigens (ABO) found on the surface of red blood cells (Rh Factor).
Types of Blood:
●
●
●
●
Type A: Has only the A antigen on the RBCs.
Type B: Has only the B antigen on the RBCs.
Type AB: Has both A and B antigens on the RBCs.
Type O: Has no A or B antigens on the RBCs.
Key Points:
●
●
The blood type depends on which antigens are present on the RBCs.
A has A, B has B, AB has both, and O has neither.
Rh BLOOD TYPES
●
●
Rh+ means the D antigen is present on the RBCs.
About 85% of Americans are Rh+.
What Happens with Rh- People?
●
●
Rh- people don’t naturally have Anti-Rh antibodies in their blood.
Anti-Rh antibodies will form if an Rh- person gets Rh+ blood or if an Rh- mom carries an Rh+ baby.
What Happens with a Second Exposure?
●
If an Rh- person is exposed to Rh+ blood again, their body will have a bad reaction (a transfusion reaction)
because of the Anti-Rh antibodies they developed the first time.
Rh BLOOD TYPES: KEY POINTS
●
●
●
Rh+ has the D antigen; Rh- doesn’t.
Rh- people can develop antibodies if exposed to Rh+ blood or a Rh+
fetus.
Second exposure to Rh+ blood can cause a dangerous reaction.
Hemolytic Disease of the Newborn
(Erythroblastosis Fetalis):
This happens when an Rh- mom has a Rh+ baby.
First Pregnancy:
●
●
During the first pregnancy, the Rh- mom gets exposed to the Rh+ blood of her baby during
delivery.
The baby is born healthy, but the mom’s body starts to make anti-Rh antibodies.
Second Pregnancy:
●
●
In the second pregnancy, if the mom is carrying another Rh+ baby, her anti-Rh antibodies
can cross the placenta and attack the baby’s red blood cells.
This can cause serious problems for the baby, like anemia and jaundice.
Hemolytic Disease of the Newborn
(Erythroblastosis Fetalis):
How to Prevent It:
●
●
RhoGAM is a special shot that contains anti-Rh antibodies.
It helps prevent the mom from making her own anti-Rh antibodies, so her body won’t attack
future Rh+ babies.
Key Points:
●
●
●
Hemolytic disease happens when an Rh- mom carries an Rh+ baby.
The first baby is usually okay, but the second baby can be harmed if the mom’s body attacks it.
RhoGAM prevents the mom from developing harmful antibodies.
THE END.