Transcript Circulatory System -Cardiovascular & Lymphatics

Circulatory
System
-Cardiovascular &
LymphaticsChapters 17 - 19
Chapter 17 - BLOOD

Components
 Only
fluid connective tissue
 Formed elements – living cells
 Fluid matrix – plasma
 Spun tube – 45% RBC’s, 1%
buffy coat (WBC’s, Platelets),
55% plasma
 Characteristics
 Salty
 Alkaline (7.35 – 7.45 pH)
 Varied in color due to O2
content
 5-6 L in males; 4-5 L in
females
 8% of body weight
 Functions (transportation &/or
protection)
Distribution
O2 and food nutrients
Wastes to lungs and kidneys
Hormones from endocrine
glands to target organs
Maintains body temperature
(absorbs and distributes
body heat)
Protection
Maintains pH (reservoir for
bicarbonate ions)
Maintains fluid volume
Prevents blood loss
(through platelet action and
blood proteins)
Prevents infection (through
WBC’s and antibodies)
 Formed Elements
Erythrocytes (RBC’s)
Characteristics
Lacks nucleus and
organelles – “bag
of hemoglobin molecules”;
33% of RBC is hemoglobin
~ 8 mm in diameter; look like
flat discs with depressed
centers
Shape provides large surface
area ideal O2 transport
Flexible due to spectrin
(fibrous protein) which allows
Rouleaux movement (stacking)
when traveling through
capillaries
800:1 RBC’s : WBC’s = blood
viscosity
4.3 – 5.2 million cells/cc RBC
count in women
5.1 – 5.8 million RBC count
in men
Number of cells correlates
with viscosity; more RBC’s =
more viscous blood = slower
moving
Function
Carry O2 through their
contained hemoglobin
Hemoglobin consists of
“globin” protein bound to
red “heme” iron pigment
Each hemoglobin contains
4 ringlike heme groups
Each globin protein
consists of 4 polypeptide
chains; each chain is
bound to a heme group
Each iron atom can
combine with one O2
Thus each hemoglobin
can carry 4 O2’s
Each RBC contains 250
million hemoglobin
molecules = transporting 1
billion O2’s.
Also carries CO2 on the
globin so there is no
competition for binding sites
~ 20% of CO2 is carried this
way
Production of RBC’s
In red bone marrow of long
and flat bones
Arise from stem cells
“Hemocytoblasts” which reside
in bone marrow
Hemocytoblast is transformed
into a proerythroblast
Proerythroblast give rise to
early erythroblast (produce
large amounts of ribosomes)
Early erythroblast
transforms into late
erythroblast as hemoglobin
production increases
Late erythroblast
transforms into normoblast
when hemoglobin content
reaches 34%
Nucleus ceases functions
and is ejected causing the
center of cell collapse (thus
the depressed center or disc
shape)
Normoblast transforms into
reticulocyte (named for
remaining rough ER)
Up to this point takes 3-5
days
Reticulocytes enter
circulation and become
mature erythrocytes in ~ 2
days.
Process is balanced
between production and
destruction (about 2
million/sec) under hormonal
control and with adequate
amounts of iron and B
vitamins.
Hormonal Control
RBC production is directly
linked to erythrocyte hormone
(which is in system at low
levels all the time to maintain
production as basal levels)
Erythropoietin hormone is
produced when kidney cells
release REF (renal
erythropoietin factor) in
response to cell hypoxia.
Hypoxia is due to
Declining # of RBC’s due
to hemorrhaging or
excessive RBC destruction
Reduced availability of O2
due to altitude or pneumonia
Increased O2 demands by
tissues during exercise
It’s not the number of cells
that controls erythropoietin,
but the cell’s ability to
transport O2
Erythropoietin stimulate red
marrow to MATURE already
committed cells at a faster rate
than otherwise (1-2 days faster)
Testosterone can stimulate
kidneys to release REF
(accounting for high RBC levels
in men than women; conversely
those with kidney failure have
RBC counts less than half of
normal individuals
Dietary needs for
erythropoietin production
Need carbs, proteins, lipids,
iron B-complex vitamins
65% of body’s iron supply is in
hemoglobin, the rest is stored in
liver, spleen and marrow
(because free iron is toxic to
tissues) as ferritin, hemosiderin,
or transferrin
Iron loss is 1.7 mg and 0.9
mg per day in women and
men respectively
B-12 and folic acid are
needed for DNA synthesis
in immature RBC’s
Destruction of RBC’s
Because they are anucleate,
they cannot synthesize
proteins, reproduce, grow,
etc.
Lifespan of 100-120 days
Dying cells become trapped
in capillaries of spleen and
are engulfed by roaming
phagocytes
Hemoglobin is degraded into
billirubin and secreted in the
bile by the liver
Released iron is salvaged
and recycled
 Disorders
(anemias or
polycythemia)
Anemias – reduced O2
carrying ability of blood
(really a symptom rather than
a disease)
Hemorrhagic anemia –
results from blood loss;
corrected by blood
replacement
Hemolytic anemia –
erythrocytes are ruptured
prematurely (hemoglobin
abnormalities, blood
mismatch, bacterial or
parasitic infection,
congenital defects in plasma
membrane)
Aplastic anemia – destruction
or inhibition of red marrow
(cancer and the drugs used to
treat cancer can cause
marrow to be replaced by
connective tissue); blood
transfusions are used until a
bone marrow transplant can be
performed
Iron deficiency anemia –
inadequate intake of ironcontaining foods, impaired
iron absorption
Pernicious anemia –
deficiency in vitamin B-12,
usually due to lack or
intrinsic factor necessary to
absorb B-12 from the diet
Thalassemia – genetic in
origin, RBC count is less
than 2 million cells/cc,
RBC’s are small and delicate
due to hemoglobin molecule
abnormality
Sickle-cell anemia –
abnormal hemoglobin is
spiky and sharp causing
cells to become crescent
shaped; cells rupture
prematurely causing vessels
to dam up and cause clots.
Polycythemia – excessive or
abnormal increase in the
number of erythrocytes.
Viscosity is increased causing
sluggish blood flow. Usual
cause is bone cancer.
Secondary polycythemia
– normal in those living at
high altitudes due to
secretion of
erythropoietin in
response to reduced O2
levels.
Leucocytes
(WBC’s)
800: 1 RBC’s:WBC’s
4,000-11,000 WBC/cc (anymore
= leukocytosis)
1% of total blood volume
Contain nuclei and organelles
Protect from damage caused by
viruses, bacteria, toxins,
parasites, cancer
 Display
diapedesis (slip in and
out of blood vessels) by amoeboid
movement
Can respond to chemical
distress signals given out by
damaged and dying tissues
(positive chemotaxis)
2 major categories based on
structural and chemical
characteristics:
Granulocytes
– lobed nuclei and stained
granules – appears “grainy”
Neutrophils
most numerous
2x RBC size
½ of WBC population
3-5 lobes, hard to see granules
digest bacteria
#’s elevate with staph, salmonella,
systemic yeast, and appendicitis
infections
Basophils
Least
numerous
Slightly larger than RBC’s,
U or S shaped nucleus
Few purple granules
When found in tissues are called
“mast cells”
When bound to antibodies
release heparin (anticoagulant)
and histamine (vasodilator) to
help WBC migration
Eosinophils
2x
RBC size
1-4% of WBC population
Nucleus is bi-lobed
Large, coarse red granules
Eat antigen-antibody complexes
Elevation can indicate allergic
reactions, parasitic worm or
protozoan infections
Reside in intestines, lungs and
skin
 Agranulocytes
– lack granules
 Lymphocytes
 2nd most numerous
 Found in lymph tissue
 Small portion in bloodstream
 Immune cell (T and B cells) production
 Large, dark, purple nucleus which
occupies most of the cell
 May have a thin rim of pale blue
cytoplasm
 Act against virus infected cells and
tumors
Monocyte
Largest
WBC
Also called “macrophages”
Gray-blue cytoplasm,
dark blue-purple U or kidney
shaped nucleus
Elevation may indicate a chronic
viral or bacterial infection such
as leprosy or tuberculosis
3
Monocyte
1 Basophil
4
2
Lymphocyte
5
Neutrophil
Eosinophil
Production
of WBC’s
Leukopoiesis – hormonally
triggered
All arise from
hemocytoblasts
Some mature in the thymus
gland; others in the bone
marrow
Disorders
Leukemia
– “white
blood”
Abnormal WBC’s which
fail to respond to
regulatory mechanisms
Remain unspecialized
Enhanced
lymphoblastic
ability to
divide
Impair or suppress
normal bone marrow
function
Named according to
cell type: “myelocytic”
or “lymphocytic”
leukemias
promyelocytic
Infectious
mononucleosis
Viral (Epstein-Barr
virus)
Elevated monocytes
and lymphocytes
Leukopenia – decreased
number of WBC’s; usually
due to chemotherapy
Platelets
(Thrombocytes)
Not true cells; are fragments
Anucleated
Arise from stem cells,
become megakaryocyte then
fragment
250,000
– 500,000 /cc
Essential for clotting
Degenerate in 10 days
 Hemostasis
– (stopping blood
flow)
Vasconstriction –
Constriction of blood vessels
triggered by injury to smooth
muscle wall of vessel,
compression of vessel by
escaping blood, chemicals
released by platelets, pain
receptors being stimulated
20-30
minutes of reduced
blood flow
More efficient when
vessel is crushed rather
than blunt cut . Blunt cuts
have less tissue damage
and more profuse blood
flow
Platelet
Plug
(+) charged platelet clings
to the (-) charged collagen
tissue under the
endothelium
Platelets develop swollen,
spiky processes
Platelet granules degenerate
and release chemicals
This
sets up a series of
clotting events which calls
more platelets to the
injury site
Aspirin inhibits plug
formation
Takes about 1 minute
Plug Formation
Coagulation
(blood clotting)
Prothrombin ------>
thrombin
Thrombin + fibrinogen =
fibrin mesh
30 different factors involved;
+
each require Ca
Most
are plasma proteins
made in the liver
Absence of any one of
these factors results in the
inability to coagulate
blood (hemophilia is an
example)
Takes about 3-6 minutes
COAGULATION
Clot
Retraction
Within 30 – 60 minutes,
platelets shrink and pull
fibrin fibers closer
together, further sealing
edges of wound
Fibrinolysis
– Clot disposal
Within 2 days, plasmin
enzyme (activated by
healing endothelium and
factors in the clot itself)
will begin to eat away at
the clot
Fibrinolysis
Pathology
Thrombus
– undesirable clot
in an unbroken vessel
Embolus – thrombus that
has broken free and is
traveling in the circulatory
system
Any
roughening of vessel
walls can exacerbate this
(atherosclerosis, burns,
inflammation,
immobilization, etc)
Ruptured cholesterol plaque with thrombus
Thrombocytopenia
– decrease in the
number of platelets, causes numerous,
small, hemorrhages body wide
(petechiae). Caused by anything that
would destroy bone marrow (drugs,
radiation). Diagnosed with a platelet
count under 50,000/cc. Often need
blood transfusions
Impaired
Liver Function –
can’t manufacture
coagulants due to vitamin
K deficiency, hepatitis,
cirrhosis, etc
 Hemophilia
 Type
A – lack
Factor VIII – 83%
 Type
B – lack
Factor IX
 Type
C – lack
Factor X
 Plasma
90%
water
10% “other stuff” – gases,
hormones, nutrients,
wastes, ions, proteins
(albumin, clotting proteins,
globulins), etc.
 Transfusions
 Losses
of 15 – 30 % causes
paleness and weakness; more
than 30% = severe shock
 RBC’s have specific antigens
(flags) on their surface
Plasma
has agglutinogens
(soldiers) floating in it
which attach to and clump
foreign antigens
Foreign blood will be
agglutinated (clumped) and
destroyed
Type
A – A antigens, Anti-B
agglutinogens – can receive A
and O blood
Type B – B antigens, Anti-A
agglutinogens – can receive B
and O blood
Type
AB – A & B antigens, no
agglutinogens – can receive all
blood types (universal recipient)
Type O – no antigens, Anti-A &
Anti-B agglutinogens – can
receive only O (universal donor)
 Rh
factor is another type of antigen
 Transfusion reactions can involve
lowered oxygen carrying ability,
blocked blood vessels, renal shut down
from liberated hemoglobin in the
system, fever, chills, nausea, vomiting
Any Questions?