1
Q
Leukopoiesis
A
- production of WBCs
- stimulated by chemical messengers from bone marrow and mature WBCs
- all leukocytes originate from hemocytoblasts
- stimulated by a hormone ( what hormone??)
2
Q
leukocytes
A
- make up <1% of blood vol
- can leave the capillaries via diapedesis
- move thru tissue spaces via ameboid and positive chemotaxis
3
Q
ameboid moement
A
irregular movement and how wBCs move around
4
Q
positive chemotaxis
A
when a WBC follows a trail to a trauma area
5
Q
leukocytosis
A
WBC count over 11,000, this is a normal response to a bacterial or viral infection
6
Q
granulocytes
A
Neutrophils, eosinophils, and basophils
- cytoplasmic granules
- larger and shorter lived than RBCs
- lobed nuclei
- phagocytic
7
Q
neutrophils
A
- granulocyte
- most numerous
- last 6hrs to a few days
- fine granules
- when stained, cytoplasm has lilac color
- granules contain hydrolyticenzymes/ defensins
- 1st to arrive at site of infection
- carries out phagocytosis
8
Q
Eosinophils
granulocyte
A
- digest parasitic worms that are too large to be phagocytized
- roll in allergic reactions and inflammation
- 8 to 12 days, circulate for 4-5 days
9
Q
Basophils
granulocyte
A
- Rarest WBCs
- large, ourpleish blackish granues contain histamines
- functionally similar to mast cells
- a few hours to a few days
- release hystomine
- release heparine
10
Q
histamine
A
an inflammatory chemical that acts as a vasodilator and attracts other WBCs to inflamed sites
11
Q
Agranulocytes
A
lymphocytes and monocytes
- lack visible cytoplasmic granules
- have spherical or kidney shaped nuclei
12
Q
Lymphocytes
A
- large, dark purp. circular nuclei with a thin rim of blue cytoplasm
- crucial to immunity
two types - T cells and b cells
13
Q
T cells (lymphocytes)
A
act against virus- infected cells and tumor cells- memory, cytotoxic, regulatory (suppressor), helper, natural killer
-memory cells can last years, weeks for all else
14
Q
B cells
A
give rise to plasma cells, which produce antibodies
15
Q
monocytes
A
- largest leukocytes
- abundant pale blue cytoplasm
- u or kidney shaped
- leave circulation, enter tissues, and differentiate into macrophages
- actively phagocytic cells; crucial against viruses, intracellular bacterial parasites, and chronic infections
- activate lymphocytes to mount an immune response
16
Q
Leukocyte disorders
A
- leukopenia
- leukemias
- acute leukemia
- chronic leukemia
17
Q
Leukopenia
A
abnormally low WBC count- drug induced
18
Q
Leukemias
A
- cancer conditions involving WBCs
- named according to the abnormal WBC clone involved
- Myelocytic leukemia involves myeloblasts
- lymphocytic leukemia involves lymphocytes
19
Q
acute leukemia
A
involves blast type cells and primarily affects children
20
Q
chronic leukemia
A
more prevalent in older people
21
Q
leukemia
A
- bone marrow totally occupied w cancerous leukocytes
- immature nonfunctional WBCs in the blood stream
- death caused by internal hemorrhage and overwhelming infections
- treatments include irradiation, antileukemic drugs, and stem cells transplants
22
Q
platelets
A
- small frags of megakaryocytes
- formation regulated by thrombopoietin
- granulescontain serotonin, Ca2+, enzymes, ADP, and platelet derived growth factor
- form a temp seal on breaks in blood vessels
- circulating platlets are kept inactive and mobile by NO (nitrous oxide) and prostacyclin from INTACT ENDOTHEIAL CELLS OF BV
23
Q
hemostasis
A
- fast series of reactions for stoppage of bleeding
1. vascular spasm
2. platelet plug formation
3. Coagulation
24
Q
Vascular spasm (simple)
A
smooth muscle contracts, causing vasoconstriction
25
platelet plug formation (simple)
- injury to lining of vessel exposes collagen fibers; platelets adhere
- platelets release chemicals that make the nearby platlets sticky; platelets plug formation
26
coagulation (simple)
firbrin forms a mesh that traps RBCs and platelets, form the clot
27
vascular spasm (detail)
- vasoconstriction of damaged blood vessels
- triggers
- direct injury
- chemicals released by endothelial cells and platelets
- pain reflexes
28
platelet plug formation (detail)
- positive feedback cycle
- at site of injury, platelets ;
- stick to exposed collagen fibers w the help of von willebrand factor, a plasma protein
- swell, become spiked and sticky, and release chemical messengers (their granules)
- ADP
- serotonin and thromboxane A2
29
ADP during platelet plug form
causes more platelets to stick and release their contents
30
serotonin and thromboxane A2
vasoconstrictor, granules found within platlets, enhance vascular spasms and more platlet plug formation
31
Coagulation (detail)
- turn blood from liquid to gel
- reinforces the platelet plug w fibrin threads
3 phases
32
phase 1 of coagulation
prothrombin activator
2 ways
intrinsic pathway
- triggered by tissue damaging events - activated platelets, collagen
extrinsic pathway
- triggered by exposure to tissue factor (TF) of plasma factor 111 ( an extrinsic factor) outside the circulatory system (due to damaged vessels)
33
intrinsic pathway
- triggered by tissue damaging events
| - activated platelets, collagen
34
extrinsic pathways
triggered by exposure to tissue factor (TF) of plasma factor lll (an extrinsic factor) outside the circulatory system ( due to damaged vessel)
35
coagulation phase 2
pathway to thrombin
- prothrombin activator ( 12 coagulation factors) catalyzes the transformation of prothrombin ( a glycoprotein found in plasma) to the active enzyme thrombin ( which changes fibrinogen into fibrin)
36
prothrombin
a glycoprotein found in plasma
37
thrombin
changes fibrinogen to fibrin
38
coagulation phase 3
common pathway to the fibrin mesh
- thrombin convert soluble fibrinogen to fibrin
- fibrin strands form the bases of a clot
- fibrin causes plasma to become a gel like trap for formed elements
- thrombin (with CA2+) actvates clotting factor Xlll which;
cross links fibrin
strengthens and stabilizes the clot
A&P 2 Chapter 16
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