Nerve activates contraction
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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