Chapter 17 - blood

ursinus college A&P study

What is RBC formation, where, and how?

Erythropoiesis in red bone marrow

hemopoietic stem cell→proerytheroblast (committed cell)→ (beginning of developmental pathway) phase 1 is ribosome synthesis, Basophilic erthyroblast→phase 2 hemoglobin accumulation polychromatic erythroblast→ orthochromatic erythroblast→ejection of the nuculeus→reticulocyte this will enter blood stream and become a mature erythrocyte after a few days. (15 day process)

What regulates RBC formation/production

Depending on hormones, iron levels, AA and B vitamins, the hormone in charge is erythropoietin, erythropoietin is stimulated by the accumulation of HIF.

the kidney’s cells are hypoxic (oxygen-deficient), HIF is degraded by oxygen-sensitive enzymes, but it cannot be degraded in poor oxygen, the accumulation of HIF from oxygen deficiency will casue EPO to be synthesizes and stimulated from the kidneys,

→ so hypoxia is what determines erythropoiesis.

blood typing

Antigens are what blood type is named after, they are like a marker to show if they belong.

Agglutinins or antibodies are what will cause clumping of blood cells if there is that type of blood, opposite of Antigen

type AB has antigens A and B, they have no agglutinins can receive any blood

type A has antigen A, the agglutinin is B

type B has antigen B, the agglutinin is A

type O has no antigen’s, but has B and A agglutinins

leukocytes

white blood cells

Granulocytes→

neutrophil=phagocytize bacteria

eosinophil= kills parasitic worms (complex in allergies/asthma)

basophil=release histamine/other mediators of inflammation

Agranulocytes→

lymphocyte= mount immune response by direct cell attack or w/ antibodies

Monocyte=phagocytosis develop into macrophages in tissues

platelets

seal small tears in BV, important to blood clotting

platelet formation

stem cell→megakaryocyte stage I→stage II/III→stage IV→ platelets

what is the first step of hemostasis to prevent blood loss?

1. vasual spasm- vasocontriction caused by injury to vascualr smooth muscle, chems released by endothelial cells/platelets, or pain relfexes initated by local pain receptors

what is the second step of hemostasis to prevent blood loss

platelet plug formation- platelets do not normally stick-

endothelial cells release nitric oxide and prostacyclin that prevent aggregation after injury. Plates aggregate, forming a temp plug and signal for clot formation →when endothelial cells are damaged and underlying collagen fibers are exposed platelets adhere strongly to collagen →von Willebrand (plasma protein) forms bridge between platelet and collagen→platelts activate forming spikes and become stickier → the platelets release ADP which is an aggregating agent to enhance platelets sticking and serotonin/thromboxane A2 which enhance vascular spams and platelet aggregation→ positive feed back as more platelets aggerate and release chemicals after one minute platelet plug built and blood loss further reduced.

Granules released during blood clotting

serotonin, Ca+(cofactor), ADP, enzymes, platlet derived growth factor

functions of blood

transport of nutrients, waste, hormones

regulation of body temp, body ph, fluid volume of the circulatory system

protection from blood loss by clotting and preventing infections w antibodies

Components of blood

CT w/ cells(formed elements), matrix(plasma), fibers (soluble fibrinogen that can become insoluble when clotting)

thrombopoiesis

formation of thrombocytes which is needed for forming platelets

hemapoetic stem cell>myloeid stem cell (mitosis wihtout seperation)>megakaroctye>fragments into platelet

Serotonin and Thromboxane

Serotonin is released from platelets and causes vasoconstriction to limit blood flow from the area

thromboxane is produced and released from platelets and causes platelet aggregation to form the platelet plug as well as asocontriction

platelet plug

step in hemostasis where the exposed damaged endothelial cells and underlying collagen fibers are exposed and the von Willebrand factor is a plasma protein that forms bridges between platelets and collagen, EC factor.

→ platelets become activated and become spikey sticky and release chemicals. The chemicals are

ADP, which is an aggregating agent that enhances platelets to stick and release contents

serotonin and thromboxane A2 enhance the vascular spasm and platelet aggregation.

coagulation / blood clotting step of hemostasis

last step, turns blood from a liquid to a gel by reinforcement from fibrin which is like a protein glue, all things except the tissue factor that circulate in blood are inactive, vitamin k is required for synthesizing four of the clotting factors, activation turns most factors into enzymes, this signals a cascade.