Download Veins returning blood

Veins returning blood
Veins have large radii
and low resistance.
Walls are thin, not
elastic
Most blood volume is in
veins
Veins
Valves prevent
engorgement and backflow
Sympathetic NS constricts
veins to increase venous
return
Skeletal muscles also help
return
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Baroreceptor reflex
Baroreceptors detect
fluctuations in blood
pressure and send info
to medulla
Signals go to ANS
Baroreceptors
Response to low pressure
Problems with vessels
Hemorrhage
Why do aneurysms form?
Hypertension, inflammation,
arteriosclerosis, genetics…
Aneurysm
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Blood pressure problems
Hypertension – Blood pressure over 140/90
Baroreceptors can adjust to higher BP
High BP puts stresses on vessels, elasticity
(atherosclerosis, strokes) and stresses on heart
(heart attacks), kidneys
Blood pressure problems
Treatments for hypertension:
Low salt diet, reduce stress, increase exercise
ACE inhibitors (reduce blood volume)
Alpha, beta blockers (reduce sympathetic effects)
Calcium blockers (reduce cardiac contractions)
Blood pressure problems
Circulatory shock – blood pressure drops
too low to serve tissues.
 From weak heart, blood loss, dilation from
allergic response
 Body compensates w/sympathetic signals,
fluid shifts
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Components of blood
Plasma
Blood cells: erythrocytes (RBC)
leukocytes (WBC), and
platelets
Hematocrit is the % of
blood occupied by RBC.
What is plasma?
Ions: mostly Na+ and Cl-.
Gasses, waste, nutrients, hormones
Plasma proteins:
 Albumins establish an osmotic gradient,
carry some hormones
 Globulins (alpha, beta, gamma) transport
molecules, serve as antibodies
 Fibrinogen - blood clotting
RBCs
RBCs have no nuclei, ribosomes, or
organelles
Packed with hemoglobin
“Doughnut-like” shape
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Hemoglobin
Heme - contains iron and
binds with one molecule of
O2
Globin - 4 protein chains
Turns bright red when
combined with oxygen
CO2, CO, H+ can also bind
RBCs replenished every second
 Spleen removes old RBCs, RBCs last
about 4 months
 RBCs are produced in bone marrow
from pluripotent stem cells (2 M/sec)
Kidney controls RBC production
 Kidney is sensitive to anemia and
releases erythropoietin
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Blood doping
Banned in competitive sports:
Erythropoietin (EPO) can be synthesized and
injected to enhance endurance
An athlete’s own blood can be stored and
reinjected to boost RBC’s
Hematocrit can detect
Causes of anemia?
Anemia – O2 to tissues is low
Due to RBC, erythropoiesis, or hemoglobin
“Pernicious anemia” – lack of B12 results in low
RBC production
Aplastic anemia – bone marrow production
How the body repairs itself
Initial response:
vascular spasm - reduces blood flow
through the vessel
platelet plug - Aggregation of platelets.
Platelets attach to areas with exposed
collagen
These processes are stimulated by ADP
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Platelets
 Platelets are cell fragments that are
functional for 10 days
 Reduce blood loss (maintain hemostasis)
Platelets and a RBC
Positive feedback at injury site
Initial stimulus is exposed collagen
Repair is contained to site of injury
Inhibits platelet
aggregation
Prostacyclin
and nitric oxide
Vessel
wall
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ADP
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Platelets
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Normal endothelium
Plug
Inhibits platelet
aggregation
Prostacyclin
and nitric oxide
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Normal endothelium
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Injury site
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How the body repairs itself
Stopping blood loss:
Fibrinogen (plasma protein) is converted into
fibrin (thread-like protein). This conversion is
catalyzed by thrombin
Fibrin threads trap RBCs, forming a clot
How the body repairs itself
Stopping blood loss:
Fibrinogen (plasma protein) is converted into
fibrin (thread-like protein). This conversion is
catalyzed by thrombin
Fibrin threads trap RBCs, forming a clot
Thrombin is formed from inactive prothrombin
in plasma
The clotting cascade...!
Clotting cascade is a series of reactions activating
enzymes in a series... final conversion is fibrinogen into
fibrin
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Vessel damage
Exposed collagen
Platelet
aggregation
Hageman
factor
PF3
Cascade is initiated
when a platelet plug is
present or from exposed
collagen.
Activation of
next thrombin
Activation
of thrombin
Clotting
cascade
Formation of
fibrin meshwork
Damaged vessel
is sealed
Clots are temporary
Fibroblasts form scar tissue for vessel repair.
The clot is dissolved slowly by the enzyme
plasmin (breaks down fibrin). Plasmin is
activated by the clotting cascade
Phagocytic WBC remove the products of clot
breakdown
Ok, but what is pus?
Well, pus comes from infected wounds
and consists of phagocytes, dead tissue
and bacteria.
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
End of exam 3 material (estimated)
White blood cells
There are five kinds of WBCs
WBCs defend against pathogens, cancer and
clean up debris
Introduction to the WBCs
Granulocytes
 Eosinophils - attack parasitic worms
 Basophils - make and store histamine and heparin
 Neutrophils - phagocytes, 1st to respond to infection
Monocytes - settle in tissue and become
macrophages
Lymphocytes Neutrophil
B and T cells of specific
immune response
Eosinophil
Monocyte
Lymphocyte
Basophil
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Production of WBCs
Produced from pluripotent stem cells in bone
marrow
Lymphocytes made in lymph tissue during
adulthood
Two-thirds of the leukocytes in the blood are
granulocytes, mainly neutrophils
Immune system
Body must resist disease in order to function
Defends against pathogens, identifies and destroys
abnormal cells.
The primary pathogens are bacteria and viruses.
Nonspecific immunity vs. Adaptive immunity
 Nonspecific responses work immediately - 1st line of
defense.
 Neutrophils, macrophages, inflammation, MAC
attack
 Adaptive immunity specifically targets certain
pathogens to which the body has been exposed
 B and T lymphocytes, antibodies
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Nonspecific response: inflammation
Redness and warmth
 Blood flow due to vasodilation
Swelling
 Increased capillary permeability
Pain
inflamed knee
 Nociceptors stimulated by fluid pressure
Inflammation : the beginning
First response involves cells
already in nearby tissue:
macrophages and mast cells
 Macrophages ‘eat’ bacteria
 Triggered by infection, mast
cells secrete histamine, causing
vasodilation
Mast cells in tissue
Fibrin walls off infection
Guided by chemotaxins,
neutrophils and monocytes go
to the area
How do phagocytes know what to eat?
Bacteria get labeled for destruction by opsonins
Opsonins are made from complement cascade,
helper T cells, antibodies
Bacteria acquire
opsonins, getting
labeled for macrophage
to engulf it
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Phagocytes also send signals
 They present antigens to helper T-cells
to induce a specific response
 They ‘wear what they eat’
plasma proteins
histamine
(including opsonins
and chemotaxins)
Phagocytes: stimulate histamine release, trigger clotting
cascade, release pyrogen which causes fever, induce
more WBC
Review
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What do those plasma proteins
do?
Some are clotting proteins..clotting cascade!
Some are antibodies! (discussed later)
Some are part of the complement system!
(discussed now…)
Nonspecific response : Complement system
Complement = cascade of
plasma proteins
Cascade activated by
molecules on surface of
bacteria or antibodies
MAC
Complement proteins are
opsonins, chemotaxins or
form MAC attack
Bacterial wall has
holes from membrane
attack complex
Complement has the
potential to be very
damaging to host tissues
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Nonspecific response:
What about viral infections?
Infected cells release interferon
Cause neighboring cells to produce virusfighting enzymes
Attracts natural killer cells
Host
Nasty
virus
Interferon
Adaptive immune response
Also fights viral and bacterial infections but uses
B and T lymphocytes found in lymph
 Pathogens have particular antigens, which
induce a specific response from B and T cells.
 Only cells with the antigen are attacked.
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B cell response
B lymphocytes respond to bacteria and toxins
An antigen stimulates some specific B cells to
become plasma cells and produce antibodies
 Contact with antigen can occur via macrophages
B cell response
How antibodies work
antigen
bacteria
binding site for this
specific antigen
Once labeled,
bacteria killed by:
MAC attack
Phagocytosis
Killer cells
Labels cell to be killed
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Result
of
labeling
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