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Histology > [2] Lecture 14-blood And Hemostasis > Flashcards

[2] Lecture 14-blood And Hemostasis Flashcards

1
Q

Blood is ___ % of the body’s weight

A

8

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2
Q

Ph range of blood

A

7.35-7.45

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3
Q

Blood - formed elements [calls/PLTs] =

A

Plasma

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4
Q

Plasma w/o blood-clotting proteins:

A

Serum

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5
Q

3 layers in heparinized and centrifuges blood:

A

Supernatant
Buffy coat
Precipitate

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6
Q

Supernatant

A

Plasma

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7
Q

Buffy coat

A

Leukocytes

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8
Q

Precipitate

A

Sedimented red blood cells

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9
Q

Average male blood stats

A

5-6 L
44-54% formed elements
47% hematocrit

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10
Q

Average Female blood stats

A

4-5 L
38-48% formed elements
42% hematocrit

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11
Q

3 types of blood proteins:

A

Fibrinogens
albumins
Globulins

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12
Q

Made in liver

Function in blood clotting
Target for thrombin

A

Fibrinogen

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13
Q

Made in liver

Exert major osmotic pressure on blood vessel walls

A

Albumin

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14
Q

Immunoglobulins

A

Globulins

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15
Q

Hormone that increases # of RBC-erythrocytes

A

Erythropoietin

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16
Q

4-5 x10^3/µL in males

3.5-5x10^3/µL in females

A

Norm RBC count

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17
Q

What organ produces erythropoietin?

A

Kidney

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18
Q

RBC are devoid of:

A

Granules and organelles

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19
Q

Major contents of RBCs:

A

Lipids, ATP, Carbonic anhydrase, hemoglobin

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20
Q

Proteins in RBCs:

A

50% are integral membrane proteins

Spectrin and actin are peripheral proteins

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21
Q

RBC have been useful for studying what?

A

Cortical cytoskeleton

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22
Q

Why’re RBC membranes and proteins easily isolated?

A

No nucleus or organelles

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23
Q

Principal determinant of cell shape in RBC?

A

Cortical cytoskeleton

No cytoskeletal components

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24
Q

Major structural protein in RBCs and is a member of the calponin family of actin-binding proteins.

A

Spectrin

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25
Q

This is a tetramer of 2 polypeptide chains, alpha and beta.

Ends of the tetramers asso. W/ short actin filaments

A

Spectrin

The asso. Results in spectrin-actin network.

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26
Q

Links the spectrin-actin network and the plasma membrane by binding to spectrin and a transmembrane protein [band 3]

A

ankyrin

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27
Q

Another link that binds spectrin-actin junctions and the transmembrane protein glycophorin

A

Protein 4.1

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28
Q

Difference btw ankyrin and protein 4.1:

A

Protein 4.1 links glycophorin

Ankyrin links to band 3 [anion transport channel w/ HCO3-

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29
Q

Protein 4.1 can also be called:

A

Beta sheet domain

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30
Q

Polymorphonuclear leukocytes (PMNs)

A

Neutrophils

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31
Q 
7-9µm
3-5 nuclear lobes 
Active amoeboid 
phagocytes 
Granulocyte containing lysozyme and other proteases and elastase and myeloperoxidases
A

Neutrophils

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32
Q

How long do neutrophils stay in circulation? After circulation?

A

10-12 hours in circulation

1-2 days out of circulation in tissue [out circulation]

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33
Q

How is neutrophil capable of destroying bacteria?

A

Secretion of enzymes by forming free radicals [superoxides] and release of lysozyme and lactoferrin [which destroy bacterial walls

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34
Q

What is the point of the nucleus of the neutrophil?

A

Barb= tells that it is female neutrophil. It shows inactive X chromosome.

Named after patient “barb” it was first noticed.

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35
Q 
7-9 µm 
Bilobed 
Large, membrane-bound  granules 
Contains: serotonin, heparin, kallikrein 
Can produce leukotrienes
A

Basophils

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36
Q

Heparin

A

Anticoagulant

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37
Q

Kallikrein

A

Attracts eosinophils

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38
Q

What do leukotrienes do?

A

Increases vascular permeability

Slow contraction of smooth muscles

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39
Q 
9-10µm 
Bilobed nucleus 
Respond to allergic rxn and parasites 
Phagocytize antibody-antigen complexes and parasites 
3 specific granules:
A

Eosinophil

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40
Q

3 specific granules for eosinophils:

A

Major basic protein (MBP)-parasite disruption

Peroxidase

Cationic protein: neutralizes heparin and anti-parasitic effect

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41
Q

Eosinophil is stained: color?

A

W/ eosin- stained

Pink.
Lighter than basophils

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42
Q

Large round sometimes slightly indented nucleus, fills most of cell
Variation in size from 6-18µm-small, medium, large
B and T

A

Lymphocytes

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43
Q

Precursor of plasma cell

A

B lymphocyte

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44
Q

Precursor of T lymphocyte.

A

T lymphocyte

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45
Q

How do T and B lymphocyte differ on microscope slide?

A

Cant distinguish difference

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46
Q 
Largest leukocyte
9-12µM
Eccentrically located: one side of the cell
Kidney shaped nucleus 
Granular cytoplasm d.t small lysosomes 
Precursor of macrophages and osteoclasts
A

Monocytes

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47
Q

2µM
200,000-400,000 /mL of blood
Enhance aggregation by release of factors, and they promote clot formation, retraction,and dissolution

A

Platelets

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48
Q

Dervied from megakaryocytes

A

PLT’s

49
Q

How do platelets repair damage to endothelium?

A

By forming platelet plug

50
Q

Adhesion of PLT involves:

A

Integrins

51
Q

PLT release _____to increase PLT aggregation:

A

Thromboxane

52
Q

Endothelial cells secrete ______ which decreases PLT aggregation

A

Prostacyclin

53
Q

The elimination of bleeding

A

Hemostasis

54
Q

Where does most effective mechanisms for hemostasis occur in vasculature?

A

Small vessels: capillaries, arterioles, and venules

55
Q

Accumulation of blood in tissues

A

Hematoma

56
Q

Hemostasis sequence of events:

A
  1. constriction of vessel smooth muscle
  2. constriction of vessels
  3. slowing of blood
  4. formation of PLT plug
  5. blood clotting (coagulation)
57
Q

Notable characteristic that intimates formation of PLT plug:

A

Injury to endothelial lining exposing the underlying collagen fibers

58
Q

What do PLT’s adhere to?

A

Exposed collagen fibers.

59
Q

What is the chemical rxn that occurs in the PLT plasma membrane?

A

PLT release contents of their secretory vesicles, including ADP and cause conversion of arachidonic acid to thrombaxane A2

60
Q

Sure her stimulates PLT aggregation

A

Thromboxane A2

61
Q

ADP and other factors cause the PLT’s to:

A

to aggreagate to form plug

62
Q

A plasma protein, released from weibel-palate bodies in endothelial cells that facilitate the adherence of PLT’s to the walls of the damaged blood vessel.

A

Von willebrand factor

63
Q

Releases von willebrand factor

A

Weibel-palade bodies

64
Q

Where is prothrombin and fibrinogen found?

A

In the blood of all norm individuals. It is in inactive form.

65
Q

What activates prothrombin

A

Factor XII

66
Q

What activates factor XII is activated ?

A

Contact w/ collagen in the damaged vessel.

67
Q

Active form of prothrmbin

A

Thrombin

68
Q

What catalyzes the conversion of fibrinogen to fibrin?

A

Thrombin

69
Q

A mesh-work in which PLT’s, blood cells, and plasma become entrapped to form the actual clot

A

Fibrin

70
Q

Where is fibrinogen formed?

A

Liver

71
Q

Fibrin mesh work forms in the presence of _______

A

Factor XIII

72
Q

What activates factor XIII

A

Thrombin

73
Q

Are Factor number sequential?

A

No they were numbered as they were discovered

74
Q

Fibrinogen is split into a number of polypeptides by

A

Thrombin

75
Q

Fibrinogen polypeptides are then chemically linked y the enzymatic action of:

A

Factor XIII

76
Q

Dissolution of fibrin clots through activation of ___________________ and ___________

And what is this process called?

A

Plasminogen activator system ; Action of plasmin

This is called fibrinolysis

77
Q

Produced by injured endothelial cells:

A

Tissue plasminogen activator

T-Pa

78
Q

t-Pa plays role in plasminogen activator system

A

Converts inactive plasmimnogen into enzymatic form plasminogen.

79
Q

T-pa is activated by endothelial cell and by

A

Fibrin- so fibrin actually initiates its own destruction

80
Q

What 2 substances dissolve clot?

A

Plasmin and t-PA

81
Q

What event initiates the clotting process?

A

The activation of prothrombin to thrombin

82
Q

Why is it called cascade?

A

Sequential activation of inactive proteins into active enzymes

83
Q

Typically initiated by endothelium of the blood vessel exposing collagen fibers
Everything necessary for it to occur is already within the blood, including Ca+, req’d as a cofactor for many of the sequential steps in the clotting cascades.
LOCAL DAMAGES to endothelial surface

A

Intrinsic pathway- in the blood.

84
Q

Involves the formation of tissue factor (thromboplastin or Factor III)

Activated by physical trauma

A

Extrinsic pathway

85
Q

A membrane bound lipoprotein exporessed at sites of cell injury;
Derived from the plasma or organelle membranes of damaged cells in the disrupted tissue and enters into circulating blood.

A

Thromboplastin

86
Q

Beginning of intrinsic pathway:

A

Exposed collagen fibers leads to activation of Factor XII (hageman factor)

87
Q

Steps in intrinsic pathway:

A
  1. Exp. collagen
  2. Factor XII activation
  3. Factor XI and kallikrein activation by XII
88
Q

Involved in the formation of bradykinin and in the kinin cascade and in the conversion of plasminogen to plasmin

A

Kallikrein

89
Q

Increases vascular permeability

A

Bradykinin

90
Q

Can activate and feedback more hageman factor [factor XII]

A

Kallikrein

91
Q

Thrombin involved in activating:

A

Factor XI and factor VIII

92
Q

Factor XI activates

A

Factor IX

93
Q

Factor IX combines w/ activated factor VIII and Ca+ to activate:

A

Factor X

94
Q

Factor VIII is activated by:

A

Thrombin

95
Q

What ion is needed in intrinsic pathway ?

A

Ca++

96
Q

Steps of extrinsic pathway:

A
  1. Damaged cell membrane release thromboplastin in blood
  2. Thromboplastin activates factor VII
  3. Factor VII and Ca+ activate factor X
97
Q

Extrinsic and intrinsic lead to activation of what factor?

A

Factor X

98
Q

Factor X + Factor ___ + ___+ = activated prothrombin

A

V; Ca++

99
Q

Factor V is activated by

A

Thrombin

100
Q

What factor is thrombin?

A

Factor II

101
Q

Thrombin and Ca++ activates:

A

Fibrin and Factor XIII

102
Q

Which factor is necessary in the cross-linking of fibrin polymers to stabilize the fibrin gel?

A

Factor XIII

103
Q

Where are most clotting factors synthesized?

A

Liver

104
Q

Vitamin k is necessary for which clotting factors (3):

A

VII, IX, X,

105
Q

_____________ is activated by various cytokines released by mast cells, PLT’s, and damaged tissue cells.

A

Homing mechanism

106
Q

___ is released by endothelial cells and increases vascular permeability

A

NO

107
Q

Leukocytes must do what to be involved in homing mechanism?

A

Leave laminar flow and move toward the endothelium of the vessel wall

108
Q

What’re the 2 phases involving cellular adhesion molecules:

A

Selectin and integrin phase

109
Q

What is on exterior of leukocyte for binding during homing mechanism?

A

Sialyl lewis-x antigens [oligosaccharide ligands]

They bind to p-selectin binding on endothelial cell surface

110
Q

Steps of selectin phase in leukocyte extravasation

A
  1. Sialyl lewis-x antigen binds to selectin on cell surface.
  2. These oligosaccharides bind to CRD on p-selectins
  3. Binding of ligands to p-selectins causes leukocytes to roll along endothelium
111
Q

P-selectins on endothelial cell surface and bind to oligosaccharides of leukocyte (sialyl lewis-x antigens) are activated by:

A

Inflammatory signaling

112
Q

Leukocyte extravasation integrin phase:

A
  1. Integrins are activated on leukocyte membrane
    - -bind to ICAM-1and2 on endothelial cells
  2. Integrins ß1 and ß2 are activated on leukocyte membrane
    - -bind to VCAM and ICAM on endothelial cell membranes
  3. Integrins interacting w/ endothelial ligands promote the transendothelial migration of leukocytes.
113
Q

Antibody induced hemolytic disease in the newborn that is caused by blood group incompatibility btw mom and fetus

A

Erythroblastosis fetalis

114
Q

Incompatibility occurs when fetus inherits RBC antigenic determinants that’re foreign to the mother ___ and ___ blood group antigens are of particular interest.

A

ABO and Rh

115
Q

The major cause of Rh incompatibility

A

D antigen

116
Q

Why does erythroblastosis fetalis no occur during 1st pregnancy?

A

IgM is produced- too large to cross the placenta [to harm fetus].

During 2nd preg, B cells have formed IgG response to D antigen which can cross the placenta.

117
Q

Rh _______ mothers are given anti-D globulin soon after delivery of an Rh ______ baby.

A

Neg; pos

118
Q

_____________________ mask the antigenic sites on the fetal RBCs that may have leaked into the maternal circulation during childbirth.

A

Anti-D antibodies

119
Q

Hemolysis in erythroblastosis fetalis results in:

A
  • Hemolytic anemia which causes hypoxic injury to the heart and liver
  • jaundice which causes damage to the CNS
  • hyperbilirubinemia

Histology (13 decks)

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