Ch 16 blood
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Ch 16: Blood. Plasma and Cellular Elements of Blood Hematopoiesis RBC Physiology Coagulation. Blood = connective tissue. Extracellular matrix:. Specialized cells:. Fig 16-1. Plasma. Blood Components Overview. Blood. 20-40%. Total WBC: 4,000 - 11,000. 2-8%. Cellular Elements.

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Ch 16: Blood

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Ch 16 blood

Ch 16: Blood

Plasma and Cellular Elements of Blood

Hematopoiesis

RBC Physiology

Coagulation


Ch 16 blood

Blood = connective tissue

Extracellular matrix:

Specialized cells:

Fig 16-1


Blood components overview

Plasma

Blood Components Overview

Blood

20-40%

Total WBC: 4,000 - 11,000

2-8%

Cellular

Elements

50-70%

1- 4%

Fig 16-1/3


Red blood cells

Red Blood Cells

O2

Fig 16-5


Hem at opoiesis blood cell formation

Hem(at)opoiesis = Blood Cell Formation

  • Few uncommitted stem cells in red bone marrow throughout life time (Fig 16-2)

  • Controlled by cytokines. Examples:

    • Erythropoietin

    • CSFs and ILs: e.g. M-CSF, IL-3 (= multi CSF)

    • Thrombopoietin

  • Leukemia vs. leukocytosis vs. leukopenia


Ch 16 blood

Controlled by ____________,specifically CSFs and ILs

Compare to Fig 16-2


Epo regulates rbc production

EPO Regulates RBC Production

  • “Hormone” synthesized by kidneys in response to hypoxemia

  • EPO gene cloned in 1985  Recombinant EPO now available (Epogen, Procrit)

  • Use in therapy, abuse in sport


Erythropoiesis

Erythropoiesis

EPO release

Mitotic rate 

Tissue O2

RBC bag of Hbfor carrying O2

lifespan ~ 120 days

source of ATP for RBC?

Maturation speed 

Tissue O2

Reticulocytes

enter

circulation


Hemoglobin hb

Hemoglobin (Hb)

  • Requires iron (Fe) + Vit. B12 (cobalamin) p.698/Ch21

  • Quaternary protein structure ?

  • Reversible binding between Fe & O2

  • CO: a toxic gas (not in book)

  • Bilirubin to bile. Hyperbilirubinemia

  • HbA vs. HbF


Hb structure

Hb Structure

Porphyrin ring with Fe in center

How many O2 can 1Hb carry?


Rbc disorders

RBC Disorders

  • Polycythemia vera (PCV ~ 60-70%)

  • Anemias(O2 carrying capacity too low)

    • Hemorrhagic anemia Fe deficiency anemia

    • Hemolytic anemia, due to genetic diseases (e.g. Hereditary spherocytosis) or infections

    • Pernicious anemia

    • Renal anemia


Sickle cell anemia

Sickle Cell Anemia

1st genetic illness traced to a specific mutation:

DNA:CAC CTC

aa: glutamic acidvaline (aa #6 of 146)

HbAHbS  crystallizes under low oxygen conditions


Platelets thrombocytes

Platelets = Thrombocytes

  • Megakaryocytes (MKs) are polyploid. Mechanism?

  • MK produces ~ 4,000 platelets which live an average of 10 days.

  • Platelets contain gra-nules filled with clotting proteins & cytokines

  • Activated when blood vessel wall damaged


Hemostasis

Hemostasis

= Opposite of hemorrhage  stops bleeding

Too little hemostasis  too much bleeding

Too much hemostasis  thrombi / emboli

Three major steps:

  • Vasoconstriction

  • Platelet plug(temporary blockage of hole)

  • Coagulation (clot formation seals hole until tissues repaired)


Steps of hemostasis

Steps of Hemostasis

Vessel damage exposes collagen fibers

Platelets adhere to collagen & release factors

local vasoconstriction& platelet aggregation

decreased blood flowplatelet plug formation

+ feedback loop

Fig 16-11


Platelet plug formation

Platelet Plug Formation

Platelet activating factor (PAF)


Steps of hemostasis cont

Steps of Hemostasis cont.

Two coagulation pathways converge onto common pathway

  • Intrinsic Pathway. Collagen exposure. All necessary factors present in blood. Slower.

  • Extrinsic Pathway. Uses TF released by injured cells and a shortcut.

  • Usually both pathways are triggered by same tissue damaging events.

Fig 16-12


The coagulation cascade

The Coagulation Cascade

“Cascade” is complicated network!

Numbering of coagulation factors according to time of discovery

Fig 16-12


Common coagulation pathway

Common Coagulation Pathway

Intrinsic pathway

Extrinsic pathway

Active factor X

Prothrombin  thrombin

fibrinogen  fibrin

reinforces platelet plug

clot


Structure of blood clot

Structure of Blood Clot

Plasmin, trapped in clot,

will dissolve clot by fibrinolysis

Clot formation limited to area of injury: Intact endothelial cells release anticoagulants (heparin, antithrombin III, protein C).

SEM x 4625


Clot busters anticoagulants

Clot Busters & Anticoagulants

Dissolve inappropriate clots

Enhance fibrinolysis

Examples:Urokinase, Streptokinase & t-PA

Prevent coagulation by blocking one or more steps in fibrin forming cascade

Inhibit platelet adhesion  plug prevention

Examples:


Hemophilia

Hemophilia


Ch 16 blood

Hemophilia A (Factor VIII Deficiency)


Ch 16 blood

Blood Doping

the end


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