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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

Ch 16: Blood

Plasma and Cellular Elements of Blood

Hematopoiesis

RBC Physiology

Coagulation

slide2

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
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 acid valine (aa #6 of 146)

HbA HbS  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 flow platelet 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:

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