chapter 27 part 2 Flashcards

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??)
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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
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3
Q

ameboid moement

A

irregular movement and how wBCs move around

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4
Q

positive chemotaxis

A

when a WBC follows a trail to a trauma area

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5
Q

leukocytosis

A

WBC count over 11,000, this is a normal response to a bacterial or viral infection

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6
Q

granulocytes

A

Neutrophils, eosinophils, and basophils

  • cytoplasmic granules
  • larger and shorter lived than RBCs
  • lobed nuclei
  • phagocytic
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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
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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
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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
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10
Q

histamine

A

an inflammatory chemical that acts as a vasodilator and attracts other WBCs to inflamed sites

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11
Q

Agranulocytes

A

lymphocytes and monocytes

  • lack visible cytoplasmic granules
  • have spherical or kidney shaped nuclei
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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
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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

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14
Q

B cells

A

give rise to plasma cells, which produce antibodies

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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
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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
Q

platelet plug formation (simple)

A
  • injury to lining of vessel exposes collagen fibers; platelets adhere
  • platelets release chemicals that make the nearby platlets sticky; platelets plug formation
26
Q

coagulation (simple)

A

firbrin forms a mesh that traps RBCs and platelets, form the clot

27
Q

vascular spasm (detail)

A
  • vasoconstriction of damaged blood vessels
  • triggers
    • direct injury
    • chemicals released by endothelial cells and platelets
    • pain reflexes
28
Q

platelet plug formation (detail)

A
  • 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
Q

ADP during platelet plug form

A

causes more platelets to stick and release their contents

30
Q

serotonin and thromboxane A2

A

vasoconstrictor, granules found within platlets, enhance vascular spasms and more platlet plug formation

31
Q

Coagulation (detail)

A
  • turn blood from liquid to gel
  • reinforces the platelet plug w fibrin threads
    3 phases
32
Q

phase 1 of coagulation

A

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
Q

intrinsic pathway

A
  • triggered by tissue damaging events

- activated platelets, collagen

34
Q

extrinsic pathways

A

triggered by exposure to tissue factor (TF) of plasma factor lll (an extrinsic factor) outside the circulatory system ( due to damaged vessel)

35
Q

coagulation phase 2

A

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
Q

prothrombin

A

a glycoprotein found in plasma

37
Q

thrombin

A

changes fibrinogen to fibrin

38
Q

coagulation phase 3

A

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