Transcript Nerve activates contraction

Chapter 10
Blood
Physical Characteristics of Blood
 Color range
- O2-rich blood is
scarlet red
- O2-poor blood is dull
red
 pH betw 7.35–7.45
 slightly higher than
body temp
Blood
 Only fluid classified as connective tissue
- Living cells = formed elements
- Non-living matrix = plasma
Hematocrit
Depends on age and, after
adolescence, the sex of the
individual.
•Newborns: 55-68%
•One (1) week of age: 47-65%
•One (1) month of age: 37-49%
•Three (3) months of age: 30-36%
•One (1) year of age: 29-41%
•Ten (10) years of age: 36-40%
•Adult males: 42-54%
•Adult women: 38-46%
Low hematocrit = anemic
High hematocrit = high altitudes, smokers,
dehydration, lung disease, tumors
Blood Plasma
 55% of blood sample
 ~ 90 % water
 Many dissolved substances
- Salts/electrolytes (metal
ions)
- Proteins
- Respiratory gases
- Hormones
- Nutrients
- Waste products
Plasma Proteins
 Albumin – regulates
osmotic pressure
 Clotting proteins – help
to stem blood loss
when a blood vessel is
injured
 Antibodies – help
protect the body from
antigens
Formed Elements
1. Erythrocytes =
red blood cells
2. Leukocytes =
white blood cells
3. Platelets =
cell fragments
1. Erythrocytes (Red Blood Cells)
 Carry O2 & little CO2
 Anatomy- Biconcave disks
- Essentially bags of hemoglobin
- Anucleate (no nucleus)
- Contain very few organelles
 Outnumber WBCs 1000:1
Hemoglobin
 Iron-containing protein
 Binds strongly, but
reversibly, to oxygen
 has four oxygen binding
sites
 Each RBC has 250
million hemoglobin
molecules
 Normal blood contains
12-18 g of hemoglobin
per 100 ml.
2. Leukocytes (White Blood Cells)
 Defense against
disease
 Have nucleus &
organelles
 move into and out of
vessels (diapedesis)
 ameboid motion
 Respond to chemicals
released by damaged
tissues
Leukocyte Levels in the Blood
 Normal 4,000 - 11,000 cells per ml
 Abnormal leukocyte levels
- Leukocytosis
+ 11,000 WBC/ml
Indicates an infection
- Leukopenia
- 4,000 WBC/ml
Commonly caused by drugs
Types of Leukocytes
Granulocytes
 Have granules
 neutrophils,
eosinophils, &
basophils
Agranulocytes
 No visible
granules
 lymphocytes &
monocytes
Figure 10.4
 Neutrophils
Granulocytes
- Multilobed nucleus w/granules
- phagocytes at infection
 Eosinophils
- Large brick-red granules
- Respond to allergies & parasitic worms
 Basophils
- histamine-containing granules
- Initiate inflammation
Agranulocytes
Lymphocytes
 Nucleus fills most of the cell
 important role in immune
response
Monocytes
 Largest of the WBC
 macrophages
 Fight chronic infection
L
3. Platelets
 Derived from
ruptured
multinucleate cells
(megakaryocytes)
 Needed for the
clotting process
 Normal platelet
count = 300,000/ml
Hematopoiesis - Blood cell formation
 Red bone marrow
 Adults – flat bones &
epiphyseal plates, not
shaft
 Hemocytoblast –
common stem cell
 Differentiation
- Lymphoid stem cell
make lymphocytes
- Myeloid stem cell
produces other
formed elements
Starts in the Red Bond Marrow
Leukemia
• Chronic Leukemia —Early in disease, abnormal blood
cells can still work; people may not have any
symptoms. Symptoms increase as leukemia cells
increase.
• Acute Leukemia —blood cells abnormal; cannot work.
Abnormal cells increases rapidly. Worsens quickly.
• Leukemia can arise in lymphoid cells or myeloid cells.
Fate of Erythrocytes
 Can’t divide, grow, or make proteins
 Wear out in 100 to 120 days
 Eliminated by phagocytes in spleen or
liver
 Replaced by division of hemocytoblasts
Control of Erythrocyte Production
 Rate is controlled by a hormone (erythropoietin)
 Kidneys produce most erythropoietin
 Negative feedback from blood O2 levels
Control of Leukocytes
• colony stimulating factors (CSFs) and interleukins
stimulate production of leukocytes.
Hemostasis
 Stoppage of blood flow
 Result of a break in a blood vessel
 Hemostasis involves three phases
1. Platelet plug formation
2. Vascular spasms
3. Coagulation
1. Platelet Plug Formation
 Collagen fibers are exposed by
a break in a blood vessel
 Platelets become “sticky” and
cling to fibers
 Anchored platelets release
chemicals to attract more
platelets
 Platelets pile up to form a
platelet plug
2. Vascular Spasms
 Anchored platelets
release serotonin
 Serotonin causes
blood vessel
muscles to spasm
 Spasms narrow the
blood vessel,
decreasing blood
loss
3. Coagulation
 Injured tissues release thromboplastin
 PF3 (a phospholipid) interacts with
thromboplastin, blood protein clotting factors,
and calcium ions to trigger a clotting cascade
 Prothrombin activator converts prothrombin
to thrombin (an enzyme)
 Thrombin joins fibrinogen proteins into hairlike fibrin
 Fibrin forms a meshwork
(the basis for a clot)
Blood Clotting
 Blood usually clots
within 3 to 6 minutes
 The clot remains as
endothelium
regenerates
 The clot is broken
down after tissue repair
 Vitamin "K" is derived from the German
"koagulation" -essential for the functioning of
several proteins involved in blood clotting
Undesirable Clotting
Thrombus
 Clot in unbroken vessel
 Deadly in heart
Embolus
 Thrombus that breaks
away and floats in
bloodstream
 Can later clog vessels in
critical areas such as the
brain
Bleeding Disorders
1.Thrombocytopenia
 Platelet (thrombocyte)
deficiency
 normal movements can cause
bleeding
 Petechiae – purple blotches
2. Hemophilia
 Hereditary bleeding disorder
 Normal clotting factors are
missing
 Sex-linked genetic disorder
Bleeding Disorders
3. Anemia
a. Hemorrhagic – massive bleeding
b. Hemolytic – bacterial infection
c. Pernicious – lack of B12 absorption
d. Aplastic – damage of bone marrow
e. Iron-deficiency – diet, menstral
flow, bleeding ulcer
f. Sickle-cell – recessive genetic
disorder; sickling due to increase
O2 levels
Bleeding Disorders
4. Polycythemia – abnormal increase of RBCs; from
bone cancer or response to high altitude; causes
high viscosity.
5. pH disorders – regulated by kidneys & resp. sys.
a. alkalosis – too basic
b. acidosis – too acidic
Blood Groups and Transfusions
 Large losses of blood have serious
consequences
15 to 30 % = weakness
+ 30 % = shock; can be fatal
 Transfusions = only way to replace
blood quickly
 Transfused blood must be of the same
blood group
Human Blood Groups
 over 30 common RBC antigens (proteins)
 Worst transfusion reactions caused by
ABO and Rh antigens
 Unmatched blood types:
Lysed RBCs release hemoglobin which
blocks kidneys, causes fevers, vomit,
etc.
Human Blood Groups
 Blood contains genetically determined
proteins
 A foreign protein (antigen) may be
attacked by the immune system
 Blood is “typed” by using antibodies that
will cause blood with certain proteins to
clump (agglutination)
ABO Blood Groups
 Based on the presence or absence of two
antigens (A & B)
 Blood Types
 Type A – has A antigen, anti-B antibody
 Type B – has B antigen, anti-A antibody
 Type AB – has both A & B antigens, Universal Recipient
 Type O – lacks A & B antigens, has both anti-A anti-B
antibodies; Universal Donor
Rh Blood Groups
 Named because one of eight Rh
antigens (agglutinogen D) found first in
Rhesus monkey
 Most Americans are Rh+
 Anti-Rh antibodies not automatically
formed; formed after exposed to Rh+
 Problems can occur in mixing Rh+ blood
into a body with Rh– blood
Rh Dangers During Pregnancy
 Rh– mom with Rh+ baby- problems for
the unborn child
 1st pregnancy usually no problems
 2nd pregnancy, the mom’s antibodies
attack the Rh+ blood
- hemolytic disease of the newborn
- Destruction of RBCs, anemia, brain
damage, death
- Fetal transfusions
• Give RhoGAM serum to prevent sensitivity
to Rh antigen
Blood Typing
 Blood mixed with anti-A and anti-B serum
 Coagulation or no coagulation leads to
determining blood type
 Cross matching – testing for
agglutination of donor RBCs by the
recipient’s serum, and vice versa
Developmental Aspects of Blood
 Sites of blood cell
formation
- fetal liver and spleen
- bone marrow takes over
by 7th month
 Fetal hemoglobin can
pick up more O2
 Physiological Jaundice – liver can’t keep up
with rapid fetal RBC destruction