Transcript Chapter 19: Blood

Chapter 19:
Blood
Primary sources for figures and content:
Marieb, E. N. Human Anatomy & Physiology. 6th ed. San Francisco: Pearson Benjamin Cummings, 2004.
Martini, F. H. Fundamentals of Anatomy & Physiology. 6 th ed. San Francisco: Pearson Benjamin Cummings, 2004.
The components
of the cardiovascular system,
and their major functions.
The Cardiovascular System
• Cardiovascular system = Anatomical division
– A circulating transport system:
• heart
• blood vessels
• blood
• Circulatory system = Clinical division
– Cardiovascular system
– Lymphatic system
Functions of the
Cardiovascular System
• To transport materials to and from
cells:
–
–
–
–
–
oxygen and carbon dioxide
nutrients
hormones
immune system components
waste products
The important components and
major functions of blood.
Blood
• Is specialized fluid of connective tissue
• CT = cells in matrix
• Functions:
– Distribution
– Regulation
– Protection
Functions of Blood
1. Distribution
-
Deliver oxygen and nutrients to cells
Remove metabolic waste
Transport hormones to targets
2. Regulation
-
Maintain body temp  distribute heat
Maintain pH & fluid volume
3. Protection
-
Restrict loss at injury (clotting)
Prevent infection (leukocytes)
Characteristics of Blood
1. pH 7.4
2. Temperature 38⁰C/100.4⁰F
3. Total volume 4-6 Liters (9-11 pints)
Estimate your own blood volume:
7% body weight in kg = blood in Liters
1kg = 2.2lb
(weight lb/2.2) x 0.07 = blood in Liters
Composition of Blood
• Fractionation = Process of separating whole
blood into plasma and formed elements
• Blood matrix = Plasma
– ~55% (water + soluble proteins)
• Blood cells: formed elements
• Erythrocytes: ~45%, transport oxygen
• Leukocytes: < 1%, defense
• Platelets: < 1%, cell fragments and for clotting
Plasma
• 90% water + dissolved solutes
– Nutrients, gasses, hormones, wastes, ions,
proteins
• Plasma Proteins (~8% of total plasma)
– 7.6g/100ml of plasma
– 5x more proteins than interstitial fluid
– Proteins remain in plasma, not absorbed by cells
for nutrients
3 Classes of Plasma Proteins
• Albumins (60%)
• Globulins (35%)
• Fibrinogen (4%)
Plasma Proteins
1. Albumins (60% of plasma proteins)
-
Produced by the liver
Functions:
1. Act as pH buffer for blood
2. Contribute to osmotic pressure of blood
- Keep water in blood
3. Transport fatty acids
4. Transport Thyroid hormones
5. Transport Steroid hormones
Plasma Proteins
2. Globulins (35% of plasma proteins)
1. Gamma globulins / Antibodies /
Immunoglobulins:
-
Produced by plasma cells in the lymphatic system
Function to attack foreign substances
2. Alpha and Beta globulins/Transport globulins:
-
Produced by the liver
Function to transport small or insoluble
compounds to prevent filtration loss by the kidney
Plasma Proteins
3. Clotting Factors (4% plasma proteins)
-
Produced by the liver
11 total, fibrinogen most abundant
All function to promote or form a clot
Fibrinogen produce long, insoluble
strands of fibrin
**Serum = plasma (-) minus fibrinogen
Plasma Proteins
4. Other (1% of plasma proteins)
-
From Liver:
-
-
Metabolic enzymes and antibacterial proteins
From endocrine organs:
-
Hormones
*Liver disease = leads to blood disorders b/c
plasma proteins are produced by the liver
Figure 19–1b
Hemopoiesis
• Process of producing formed elements
– Blood cell production
• All formed elements arise from the
same progenitor cell
– The hemocytoblast, located in the red
bone marrow
KEY CONCEPT
• Total blood volume (liters) = 7% of
body weight (kilograms)
• About 1/2 the volume of whole blood is
cells and cell products
• Plasma resembles interstitial fluid, but
contains a unique mixture of proteins
not found in other extracellular fluids
What would be the effects of a
decrease in the amount of plasma
proteins?
A. Decrease in plasma osmotic pressure
B. Decrease in ability to fight infection
C. Decrease in transport and binding of
some ions, hormones, and other
molecules
D. All of the above
What would be the effects of a
decrease in the amount of plasma
proteins?
A. Decrease in plasma osmotic pressure
B. Decrease in ability to fight infection
C. Decrease in transport and binding of
some ions, hormones, and other
molecules
D. All of the above
Which plasma protein would you expect
to be elevated during a viral infection?
A.
B.
C.
D.
albumin
fibrinogen
immunoglobulins
regulatory proteins
Which plasma protein would you expect
to be elevated during a viral infection?
A.
B.
C.
D.
albumin
fibrinogen
immunoglobulins
regulatory proteins
What are the
characteristics and
functions of red blood cells?
Erythrocytes: Red Blood Cells
• 99.9% of blood’s formed elements
• 1/3 of total body cells
– Average human = ~75 trillion cells
• Average RBC count = 4.2-6.3 million/µl
Measuring RBCs
• Red blood cell count:
– reports the number of RBCs in 1 microliter
whole blood
• Hematocrit (packed cell volume, PCV):
– % of whole blood occupied by formed
elements
– Mostly erythrocytes: 99.9%
– Males have a greater percentage of RBC
then females
Blood Counts
• RBC: Normal Blood Counts
– male: 4.5–6.3 million
– female: 4–5.5 million
• Polycythemia = excess erythrocytes but
normal blood volume
– Usually due to bone marrow cancer
–
hematocrit = viscosity 
heart strain and stroke
Erythrocyte Structure
• Small and highly specialized biconcave disc
• Thin in middle and thicker at edge
Figure 19–2d
Importance of RBC
Shape and Size
1. Large surface area for gas exchange:
– quickly absorbs and releases oxygen
2. Folds and form stacks:
– passes through narrow blood vessels
3. Discs bend and flex entering small
capillaries:
– 7.8 µm diamater passes through capillary
Erythrocytes
• Mature erythrocytes lack all organelles
– Lack nuclei, mitochondria, and ribosomes
• No division, no repair
• Life span < 120 days
• Cell is 97% hemoglobin protein (red color)
• Hemoglobin transports oxygen and some
carbon dioxide
The structure and function of
hemoglobin.
Hemoglobin Structure
• Complex quaternary structure
• 2 α chains and 2 β chains
• Each chain has one heme group with iron in
center: iron binds oxygen
Figure 19–3
Hemoglobin (Hb)
• Oxyhemoglobin = oxygen bound, RED
• Deoxyhemoglobin = no oxygen, BURGUNDY
• Fetal Hb binds oxygen stronger than adults
– Insures transfer of oxygen from mom
• Most oxygen is carried in blood bound to
Hb, some in plasma
• Only 20% carbon dioxide carried by Hb:
– Carbaminohemoglobin – carbon dioxide bound
to amino acids on α / β chains, not on heme
Hemoglobin (Hb)
• 280 million Hb/RBC, 4 hemes/Hb, each
heme binds 1 oxygen = >1 billion
oxygen/RBC
• 25 trillion RBC per person
• Normal hemoglobin (adult male):
– 14–18 g/dl whole blood
• When plasma oxygen is low, Hb releases
oxygen and binds carbon dioxide
• At lungs carbon dioxide exchanged for
oxygen by diffusion
Anemia
• Hemoglobin levels are below normal
• Oxygen starvation, due to:
1. Insufficient # RBC’s
2. Low Hb
3. Abnormal Hb
1. Thalassemia
2. Sickle-cell anemia
Abnormal Hb
1. Thalassemia = inability to produce α or β
chains
-
slow RBC production
cells fragile and short lived
2. Sickle-cell anemia = single amino acid
mutation in β chain high oxygen
-
cells normal low oxygen
Hb misfolds
RBC’s deform into crescent shape
-
RBC’s are fragile, blocks capillaries
Components
of old or damaged
red blood cells are recycled.
Figure 19–4
Recycling RBCs
• Macrophages (phagocytes) of liver, spleen,
and bone marrow:
– monitor RBCs
– engulf old/damaged RBCs
• Replaced by new
– 1% of circulating RBCs replaced per day:
•about 3 million RBCs per second
Hemoglobin Recycling
• Phagocytes break cells down:
1. Protein  globulin amino acids, released for use
2. Heme  hemoglobin into components:
1. Iron is removed:
- It is bound to transferrin in blood for recycling back to
bone marrow (new RBCs)
2. Pigment  heme to biliverdin (green), Biliverdin 
bilirubin (yellow-green)
- Bilirubin is released into blood
- Filtered by liver
- Excreted in bile
3. In gut, bilirubin  urobilins (yellow),stercobilins (brown)
- urobilins is excreted in urine
- stercobilins remain in feces
Blood Disorders
• Jaundice
– Failure of bilirubin to be excreted in bile,
collects in peripheral tissues
– Causes yellow skin and eyes
• Hemoglobinuria:
– Cause  Hemolysis, RBC rupture in blood
– Red/brown urine due to kidney filtering
intact α and β chains of hemoglobin
How would the hematocrit change
after an individual suffered a
hemorrhage?
A. The hematocrit would be higher.
B. The hematocrit would be lower.
C. The hematocrit would show a
larger percent WBC.
D. No change would be seen.
How would the hematocrit change
after an individual suffered a
hemorrhage?
A. The hematocrit would be higher.
B. The hematocrit would be lower.
C. The hematocrit would show a
larger percent WBC.
D. No change would be seen.
How would the level of bilirubin in
the blood be affected by a disease
that causes damage to the liver?
A.
B.
C.
D.
The level would decrease.
The level would increase.
The level would fluctuate wildly.
The level would not change.
How would the level of bilirubin in
the blood be affected by a disease
that causes damage to the liver?
A.
B.
C.
D.
The level would decrease.
The level would increase.
The level would fluctuate wildly.
The level would not change.
Erythropoiesis:
The stages of
red blood cell maturation,
and red blood cell production.
Erythropoiesis
• Red blood cell formation
• Occurs in reticular CT in red bone
marrow, in spongy bone
• Stem cells mature to become RBCs
• 2 million/sec (1 oz new blood per day)
RBC Maturation
Figure 19–5
Hemocytoblasts
• Stem cells in bone marrow divide to
produce:
– myeloid stem cells:
• become RBCs, some WBCs
– lymphoid stem cells:
• become lymphocytes
Erythropoiesis
1. Hemocytoblast differentiates into myeloid stem cells
2. Followed by many stages of differentiation, all
involve an increase in protein synthesis
3. Cell fills with Hb
- loses organelles including the nucleus
4. 3-5 days reticulocytes are formed (Hb + some
ribosomes), released into blood.
- 1-2% of total blood RBCs
5. 2 days in circulation lose ribosomes = mature
erythrocytes
- No more protein synthesis
Components
• Building red blood cells requires:
– amino acids
– iron
– vitamins B12, B6, and folic acid
• Lack B12 = pernicious anemia
– Low RBC production
Stimulating Hormones
• Erythropoietin (EPO)
– Also called erythropoiesis-stimulating
hormone:
– secreted by the kidney
– Secreted when oxygen in tissues is low
(hypoxia = low oxygen level)
– due to disease or high altitude
– No EPO = Kidney failure b/c low RBCs
Erythropoietin (EPO)
• Stimulate RBC production:
– Increase cell division rates (up to 30
million/sec)
– Increase Hb synthesis = decrease maturation
time
• “blood doping” = injection EPO or RBC to
enhance athletic performance:
– Increase oxygen to tissue
– Increase hematocrit/viscosity = clots, stroke,
and heart strain
RBC Tests
Table 19–1
KEY CONCEPT
• Red blood cells (RBCs) are the most
numerous cells in the body
• RBCs circulate for approximately 4
months before recycling
• Several million are produced each
second
• Hemoglobin in RBCs transports:
– oxygen from lungs to peripheral tissues
– carbon dioxide from tissues to lungs
Blood typing.
The basis for ABO
and Rh incompatibilities.
Blood Types
• All cell membranes have surface
antigens
– Antigens indicate “self”
– Antigen = substance that triggers immune
response
• Normal cells are ignored and foreign
cells attacked
Blood Types
• Are genetically determined
• Classified by the presence or absence
of RBC surface antigens A, B, or D (Rh)
• RBCs have 3 important antigens for
transfusion, agglutingens A, B, D (Rh)
4 Basic Blood Types
Figure 19–6a
4 Basic Blood Types
•
•
•
•
A (surface antigen A) = 40%
B (surface antigen B) = 10%
AB (antigens A and B) = 4%
O (neither A nor B) = 46%
Agglutinogens
• Antigens on surface of RBCs
• Screened by immune system
• Plasma antibodies attack (agglutinate)
foreign antigens
Blood Plasma Antibodies
• Type A:
– type B antibodies
• Type B:
– type A antibodies
• Type O:
– both A and B antibodies
• Type AB:
– neither A nor B
The Rh Factor
• Also called D antigen
+
• Either Rh positive (Rh ) or Rh negative
(Rh—)
• Only sensitized Rh— blood has anti-Rh
antibodies
Cross-Reaction
Figure 19–6b
Cross-Reaction
• Also called transfusion reaction
• At birth, blood contains antibodies
against A or B antigens that are not
present
• Plasma antibody meets its specific
surface antigen
• Antibodies will cause blood
agglutination (clumping) of antigen
(agglutinogen) and hemolyze
• If donor and recipient blood types not
compatible
Blood Type Test
• Determines blood type and compatibility
Figure 19–7
Cross-Match Test
• Performed on donor and recipient
blood for compatibility
• Without cross-match, type O— is
universal donor
– It lacks all agglutinogens (A, B, and D)
• No risk of agglutination by antibodies in
anyone
Erythroblastosis fetalis
• Aka Hemolytis disease of the newborn
• Antibodies against D antigen only form upon exposure
and can cross the placenta
• Rh- mom pregnant with Rh+ baby
– Gets exposed to D antigen during birth
– Makes anti-D antibodies
– Pregnant with second Rh+ baby
– Antibodies cross placenta
– Causes agglutination and lysis of fetal RBCs 
anemia and death
• Prevention = treat mom with RhoCAM during first
birth to prevent antibody formation
What are surface antigens on RBCs?
A. glycoproteins in the cytosol
B. receptor proteins in the cell
membrane
C. peripheral proteins of the cell
membrane
D. glycolipids in the cell membrane
What are surface antigens on RBCs?
A. glycoproteins in the cytosol
B. receptor proteins in the cell
membrane
C. peripheral proteins of the cell
membrane
D. glycolipids in the cell membrane
Which blood type(s) can be transfused
into a person with Type O blood?
A.
B.
C.
D.
Type A
Type B
Types A and B
Type O
Which blood type(s) can be transfused
into a person with Type O blood?
A.
B.
C.
D.
Type A
Type B
Types A and B
Type O
Why can’t a person with Type A blood
safely receive blood from a person with
Type B blood?
A. Type B blood will break down in the
person’s veins.
B. Type B blood will destroy Type A cells.
C. Type A blood contains agglutinating
agents for Type B.
D. Type B blood contains agglutinating
agents for Type A.
Why can’t a person with Type A blood
safely receive blood from a person with
Type B blood?
A. Type B blood will break down in the
person’s veins.
B. Type B blood will destroy Type A cells.
C. Type A blood contains agglutinating
agents for Type B.
D. Type B blood contains agglutinating
agents for Type A.
The types of white blood cells,
and
the factors that regulate the
production of each type.
Leukocytes (WBCs)
• < 1% of total blood volume
– 6000-9000 leukocytes/µl blood
– Use blood to travel to tissues
• Not permanent residents of blood
• Most in connective tissue proper and lymphatic
system organs
• Function:
– Defend against pathogens
– Remove toxins and wastes
– Attack abnormal/damaged cells
• All have nuclei & organelles, no hemoglobin
Circulating WBCs
1. Migrate out of bloodstream (diapedesis)
-
Margination = adhere to vessel
Emigration = pass between endothelial cells in
vessel walls
2. Have amoeboid movement in bloodstream
3. Attracted to chemical stimuli (positive
chemotaxis)
4. Some are phagocytic:
–
Engulf pathogens and debris
neutrophils, eosinophils, and monocytes
5 Types of WBCs
Figure 19–9
5 Types of Leukocytes
Granulocytes vs. Agranulocytes (on handout)
1. Neutrophils
2. Eosinophils
3. Basophils (in tissues = mast cells)
4. Monocytes (in tissues = macrophages)
5. Lymphocytes
Neutrophils
•
•
•
•
•
•
Also called polymorphonuclear leukocytes (PMNs)
Non-specific defense
Phagocytic
50–70% of circulating WBCs
3-5 lobed nucleus
Pale cytoplasm granules with:
– lysosomal enzymes and defensins
– bactericides
• hydrogen peroxide and superoxide
• Very mobile: first at injury
• Life span less than 10 hours
Neutrophil Function
1. Respiratory burst
-
H2O2 and O2- , kills and phagocytize
2. Degranulation:
-
Release defensins (against some bacteria,
fungi, and viruses), lyse bacteria
3. Release prostaglandins
-
Induce inflammation to stop the spread of
injury
4. Release leukotrienes
-
Attract phagocytes
Degranulation
• Defensins (host defense proteins):
– peptides from lysosomes
– attack pathogen membranes
Eosinophils
•
•
•
•
•
•
•
•
Also called acidophils
Phagocytic
2–4% of circulating WBCs
Bilobed nucleus
12µm diameter
Granules contain toxins
Life span 9 days
Attack large parasites
Eosinophil Functions
1. Phagocytosis of antibody covered
objects
2. Defense against parasties:
-
Exocytose toxins on large pathogens
3. Reduce inflammations
-
anti-inflammatory chemicals/enzymes
that counteract inflammatory effects of
neutorphils and mast cell
Basophils
In Tissues = Mast cells
•
•
•
•
•
Non-specific defense
Not phagocytic
Are less than 1% of circulating WBCs
Are small, 8-10µm diameter
Granules contain
– Histamine: dilate blood vessels
– Heparin: prevents clotting
• Accumulate in damaged tissue
• Life span 9 days
Basophil Functions
1. Inflammation (Histamine)
2. Allergic response, also via histamine
Monocytes
In Tissues = Macrophages
•
•
•
•
Non-specific defense
Phagocytic
2–8% of circulating WBCs
Are large and spherical, kidney shaped
nucleus
• Circulate 24 hours, exit to tissues =
macrophage
• Life span several months
Macrophage Functions
1.
2.
3.
4.
Phagocytosis: virus & bacteria
Attract phagocytes
Attract fibroblasts for scar formation
Activate lymphocytes:
– Mount immune response
Lymphocytes
•
•
•
•
•
•
Immune response
20–30% of circulating WBCs
Large round nucleus
5-17µm diameter, larger than RBCs
Migrate between blood and tissues
Mostly in connective tissues and
lymphatic organs
• Life span days to lifetime
3 Classes of Lymphocytes
1. T cells
2. B cells
3. Natural killer (NK) cells
Lymphocyte Functions
1. B cells:
-
Humoral immunity
Differentiate into plasma cells
Synthesize and secrete antibodies
2. T cells
-
cell-mediated immunity
attack foreign cells
3. NK cells:
-
Immune surveillance
Destroy abnormal tissues
KEY CONCEPT
• RBCs outnumber WBCs 1000:1
• WBCs defend against infection, foreign
cells, or toxins
• WBCs clean up and repair damaged
tissues
KEY CONCEPT
• The most numerous WBCs:
– neutrophils
• engulf bacteria
– lymphocytes
• are responsible for specific defenses of
immune response
Which type of white blood cell
would you find in the greatest
numbers in an infected cut?
A.
B.
C.
D.
eosinophils
neutrophils
lymphocytes
monocytes
Which type of white blood cell
would you find in the greatest
numbers in an infected cut?
A.
B.
C.
D.
eosinophils
neutrophils
lymphocytes
monocytes
Which type of cell would you find in
elevated numbers in a person who is
producing large amounts of circulating
antibodies to combat a virus?
A.
B.
C.
D.
B lymphocytes
T lymphocytes
neutrophils
basophils
Which type of cell would you find in
elevated numbers in a person who is
producing large amounts of circulating
antibodies to combat a virus?
A.
B.
C.
D.
B lymphocytes
T lymphocytes
neutrophils
basophils
How do basophils respond
during inflammation?
A.
B.
C.
D.
secrete antibodies
phagocytize foreign particles
release histamine
reduce inflammation
How do basophils respond
during inflammation?
A.
B.
C.
D.
secrete antibodies
phagocytize foreign particles
release histamine
reduce inflammation
Leukopoiesis:
WBC Production
Figure 19–10
Leukopoiesis
• All blood cells originate from hemocytoblasts which
produce:
– myeloid stem cells and
– lymphoid stem cells
• Lymphoid stem cells  Lymphocytes
– Production involves the immune response
• Myeloid stem cells  Basophils, Eosinophiles,
Neutrophils, Macrophages as directed by specific
colony stimulating factors (CSF)
– CSF is produced by Macrophages and T cells
• Different CSF results in different cell
Myeloid Stem Cells
• Differentiate into progenitor cells:
– which produce all WBCs except
lymphocytes
Lymphocytes
• Are produced by lymphoid stem cells
• Lymphopoiesis:
– the production of lymphocytes
WBC Development
• WBCs, except monocytes:
– develop fully in bone marrow
• Monocytes:
– develop into macrophages in peripheral
tissues
Other Lymphopoiesis
• Some lymphoid stem cells migrate to
peripheral lymphoid tissues (thymus,
spleen, lymph nodes)
• Also produce lymphocytes
WBC Disorders
• Leukopenia:
– abnormally low WBC count
• Leukocytosis:
– abnormally high WBC count in normal blood
volume
– Normal infection increases WBCs from 7,500
to 11,000/µl
• >100,000/µl  leukemia, cancerous stem cells
• Leukemia: WBC > 100,000/µl
– extremely high WBC count
– WBC produced  immature and abnormal
Infectious Mononucleosis:
• Epstein Bar virus infection causes:
– Production of excess agranulocytes that
are abnormal, self limiting
Table 19–3
The structure
and function of platelets
and how are they produced.
Platelets (Thrombocytes)
•
•
•
•
Cell fragments involved in clotting
Flattened discs, no nucleus
2-4µm diameter, 1µm thick
Constantly replace
– 9-12 days in circulation
– Phagocytosed by cells in spleen
• 350,000/µl blood
• 1/3 of total platelets held in reserve in
spleen, mobilized for crisis
Platelet Counts
• 150,000 to 500,000 per microliter
• Thrombocytopenia: < 80,000/µl
– abnormally low platelet count
– Results in bleeding
• Thrombocytosis: > 1 million/µl
– abnormally high platelet count
– Due to cancer or infection
– Results in a clotting risk
3 Functions of Platelets
1. Transport clotting chemicals, and
release important clotting chemicals
when activated
2. Temporarily form patch (platelet
plug) over damaged vessel walls
3. Actively contract wound after clot
formation
-
Contain actin and myosin
Platelet Production
• Also called thrombocytopoiesis:
– occurs in bone marrow
1. Induced by thrombopoietin from kidney
and CSF of leukocytes
2. Megakaryocyte in bone marrow breaks off
membrane enclosed cytoplasm to blood
3. Each megakaryocyte can produce ~4,000
platelets
Mechanism that controls blood
loss after injury,
and the reaction
sequence in blood clotting.
Hemostasis
• The cessation of bleeding:
– vascular phase
– platelet phase
– coagulation phase
The Vascular Phase
• A cut triggers vascular spasm
• 30-minute contraction
Figure 19–11a
3 Steps of the Vascular Phase
1. Endothelial cells contract:
–
expose basal lamina to bloodstream
2. Endothelial cells release:
–
chemical factors:
• ADP, tissue factor, and prostacyclin
–
–
local hormones
stimulate smooth muscle contraction
and cell division
3 Steps of the Vascular Phase
3. Endothelial cell membranes become
“sticky”:
–
seal off blood flow
The Platelet Phase
• Begins within 15 seconds after injury
Figure 19–11b
The Platelet Phase
• Platelet adhesion (attachment):
– to sticky endothelial surfaces
– to basal laminae
– to exposed collagen fibers
• Platelet aggregation (stick together):
– forms platelet plug
– closes small breaks
Activated Platelets
Release Clotting Compounds
•
•
•
•
•
Adenosine diphosphate (ADP)
Thromboxane A2 and serotonin
Clotting factors
Platelet-derived growth factor (PDGF)
Calcium ions
The Coagulation Phase
• Begins 30 seconds or more after the injury
Figure 19–12a
The Coagulation Phase
• Blood clotting (coagulation):
– Involves a series of steps
– converts circulating fibrinogen into
insoluble fibrin
Blood Clot
•
•
•
•
Fibrin network
Covers platelet plug
Traps blood cells
Seals off area
The Common Pathway
•
•
•
•
Enzymes activate Factor X
Forms enzyme prothrombinase
Converts prothrombin to thrombin
Thrombin converts fibrinogen to fibrin
Functions of Thrombin
• Stimulates formation of tissue factor
– forms positive feedback loop 
accelerates clotting
KEY CONCEPT
• Platelets are involved in coordination
of hemostasis (blood clotting)
• Platelets, activated by abnormal
changes in local environment, release
clotting factors and other chemicals
• Hemostasis is a complex cascade that
builds a fibrous patch that can be
remodeled and removed as the
damaged area is repaired
A sample of bone marrow has
unusually few megakaryocytes.
What body process would you expect
to be impaired as a result?
A.
B.
C.
D.
hematopoiesis
immune response
clotting
oxygen carrying capacity
A sample of bone marrow has
unusually few megakaryocytes.
What body process would you expect
to be impaired as a result?
A.
B.
C.
D.
hematopoiesis
immune response
clotting
oxygen carrying capacity
Vitamin K is fat-soluble, and some dietary
fat is required for its absorption. How could
a diet of fruit juice and water have an effect
on blood clotting?
A. Clotting time would increase.
B. Clotting time would decrease.
C. Clotting protein synthesis would
increase.
D. Vitamin K has no effect on
clotting.
Vitamin K is fat-soluble, and some dietary
fat is required for its absorption. How could
a diet of fruit juice and water have an effect
on blood clotting?
A. Clotting time would increase.
B. Clotting time would decrease.
C. Clotting protein synthesis would
increase.
D. Vitamin K has no effect on
clotting.
Bleeding Disorders
1. Thrombosis
- Clotting in undamaged vessels
- Slow or prevent flow
2. Embolus
- Free floating thrombosis
- Blocks small vessels  tissue damage, heart
attack, stroke
3. Disseminated intravascular coagulation
- Widespread clotting followed by systemic
bleeding
- Rare: complication of pregnancy or mismatched
transfusion
Bleeding Disorders
4. Hemophilia:
-
Inadequate production of clotting factors
Type A  Factor VIII (X linked)
Type B  Factor IX
Type C  Factor XI
Plasma Clotting Factors
Table 19–4
Blood Disorders
5. Dietary:
- Calcium required for clotting cascade
- Vitamin K required for liver to synthesize clotting
factors
- Iron required for hemoglobin production
- Vitamin B12 required for RBC stem cell division
6. Organ Health:
- Impaired liver =
- reduced clotting b/c of reduced clotting factors
- Impaired kidney =
- reduced RBC b/c of reduced EPO
- Reduced platelets b/c reduced thrombopoietin
SUMMARY
• Functions of cardiovascular system
• 5 functions of blood
• Structure of whole blood:
– plasma and formed elements
• Process of blood cell formation
(hemopoiesis)
• 3 classes of plasma proteins:
– Albumins, globulins, and fibrinogen
• RBC structure and function
• Hemoglobin structure and function
SUMMARY
• RBC production and recycling
• Blood types:
– ABO and Rh
• WBC structure and function
• 5 types of WBCs:
– Neutrophils, eosinophils, basophils,
monocytes, lymphocytes
• Differential WBC counts and disease
• WBC production
• Platelet structure and function
• Platelet production