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Physl 210 > Blood > Flashcards

Blood Flashcards

1
Q

What are the general functions of blood?

A

transport of oxygen, carbon dioxide, nutrients, waste products, ions, hormones etc., regulation of ion and pH balance, defense (immune protection) and hemostasis

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2
Q

What is the hematocrit?

A

% of total blood volume occupied by packed red blood cells

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3
Q

What is the white blood cell layer called?

A

buffy coat

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4
Q

What is polycythemia?

A

high amount of red blood cells

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5
Q

What is the liquid fraction of the blood?

A

plasma

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6
Q

What is the interstitial fluid?

A
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7
Q

How is most of the carbon dioxide transported through the body?

A

through plasma

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8
Q

Where are plasma proteins made?

A

liver

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9
Q

When clotting factors have been removed from plasma what does it become?

A

serum

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10
Q

What is hematopoiesis?

A

process of formation of blood cells

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11
Q

Where does hematopoiesis happen prenatally?

A

yolk sac, liver, spleen

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12
Q

Where does hematopoiesis happen postnatally?

A

bone marrow

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13
Q

What does multipotent mean?

A

can specialize into many cells

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14
Q

How is hematopoiesis regulated?

A

Cytokines

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15
Q

What are cytokines?

A

small proteins that are hormone-like in their mechanism of action

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16
Q

What are hematopoietins

A

another word for cytokines. They act as growth factors

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17
Q

What are erythropoietins?

A

cytokines that develop red blood cells

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18
Q

What are thrombopoietins?

A

cytokines, that develop platelets

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19
Q

What shape are blood cells?

A

biconcave

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20
Q

What gives red blood cells their color?

A

hemoglobin

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21
Q

What is hemoglobin?

A

responsible for 98-99% of total oxygen transport, binds to the oxygen in loose and reversible manner

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22
Q

What is oxygenation?

A

loose physical binding of oxygen

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23
Q

What makes CO inhalation fatal?

A

Hemoglobin (Hb) can bind to other gases and it has 200x more affinity for CO than O2. It is hard to identify CO because it is colorless and odorless.

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24
Q

What is the most important dietary factor for RBC production?

A

iron

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25
Q

How is iron lost?

A

through sweat, urine, menstrual flow

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26
Q

How does body iron reserve distribute % wise?

A

50% Hb
25% other iron containing proteins
25% bound with Ferritin

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27
Q

What happens when there is a lack of Vitamin B12 ?

A

it causes pernicious anemia

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28
Q

What is anemia?

A

decreased oxygen-carrying capacity of the blood due to a deficiency of RBCs and/or hemoglobin contained in the RBCs

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29
Q

What causes anemia?

A

1) decreased production of RBC in the bone marrow
2) Increased destruction of the RBCs in the body (hemolytic anemia)
3) Increased blood loss leading to loss of RBCs (hemorrhagic anemia)
4) Abnormal hemoglobin production

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30
Q

What is the abnormal structure of hemoglobin called?

A

sickle cell disease

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31
Q

What are leukocytes?

A

white blood cells

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32
Q

What are erythrocytes?

A

red blood cells

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33
Q

Why is the erythrocyte shaped the way it is?

A

to increase surface-area-to-volume ratio, allowing oxygen and carbon dioxide to diffuse more efficiently

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34
Q

What is a consequence for erythrocytes lacking nuclei and a lot of organelles?

A

that they can not reproduce themselves and they will not last long

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35
Q

What is the breakdown product of hemoglobin?

A

bilirubin which is returned to the circulation and gives plasma its yellow color

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36
Q

Why is iron important?

A

it is what oxygen binds to on the hemoglobin

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37
Q

What is the opposite of iron deficiency?

A

hemochromatosis

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38
Q

What is transferrin?

A

an iron-transport plasma protein that delivers almost all iron to the bone marrow which will then be incorporated onto new blood cells

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39
Q

What is folic acid?

A

vitamin found in large amounts of leafy plants, yeast, liver. When in low amounts it will effect erythrocyte production (decreasing it)

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40
Q

the vitamin that is required for the action of folic acid?

A

vitamin B12

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41
Q

Diet to get vitamin B12 in system?

A

only found in an animal diet and not on a vegetarian one

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42
Q

How is vitamin B12 absorbed from the gastrointestinal tract?

A

through protein called intrinsic factor which is secreted by the stomach

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43
Q

What are some functions of the immune system?

A

to protect against infection of pathogens, isolate or remove foreign substances, destroy cancer cells (immune surveillance)

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44
Q

What does the immune system have to identify first?

A

the self vs the non-self

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45
Q

What are the non-specific defenses/ innate immunity?

A

they defend against foreign substances/cells without having to specifically identify them. They use general protection mechanisms not one for a specific cell and one for another.

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46
Q

Where are non-specific defenses (innate immunity) found?

A

skin, enzymes in saliva, tears and mucus

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47
Q

What are specific defenses (acquired immunity)?

A

defense depends on the specific identification by the lymphocytes on intruders

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48
Q

What are some inappropriate (bad) roles that the immune systems can take?

A

can respond in an exaggerated way to harmless substances (allergies) and autoimmune reactions (attacking its own immune system)

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49
Q

What are the 2 groups that leukocytes can be classified into?

A

it is based on the stem cell that they derived from, but the 2 groups are myeloid cells and lymphoid cells

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50
Q

What are included as myeloid cells?

A

neutrophils, basophils, eosinophils and monocytes

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51
Q

What are the myeloid-derived cells that are distinct from macrophages but have characteristics like macrophages (e.g. phagocytosis)?

A

dendritic cells (do not confuse with dendrites)

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52
Q

What are mast cells?

A

cells found throughout connective tissue, when they are mature they are not found in the blood. They secrete histamine

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53
Q

What initiates inflammation?

A

non-specific innate response to tissue injury

54
Q

What are the key mediators in inflammation?

A

cells that function like phagocytes e.g. neutrophils, macrophages and dendritic cells

55
Q

What are examples of possible inducers of inflammation?

A

cuts, bullet wound, injuries to sun burn, infected sutures, infection of tonsil by cold virus

56
Q

What are the main goals of inflammation?

A

healing and resolution

57
Q

What are the 4 main physical characteristics of inflammation?

A

redness (rubor), swelling (tumor), heat (calor) and pain (dolor)

58
Q

What are the causes of rubor, tumor and calor? and agent?

A

increased blood flow and histamine

59
Q

What does increased blood flow do for inflammation?

A

increases delivery of proteins and leukocytes

60
Q

What is the vasculature (blood vessel wall) responsible for?

A

release of inflammatory mediators, increased blood flow, increased permeability of small blood vessels

61
Q

What is emigration?

A

when cells move out from within the blood vessel into the interstitial space

62
Q

What does taxis mean?

A

movement

63
Q

What is chemotaxis?

A

ability of WBCs to move against a concentration gradient (L to H) in response to chemical factors (chemotactic)

64
Q

How do phagocytes recognize bacteria?

A

they use PRR (pattern recognition receptor) which help them recognize common patterns or patterns that are not expressed by body cells and only the non-self agent

65
Q

How do you increase the efficiency of phagocytosis of the bacteria by receptors?

A

by adding opsonin (the butter that white blood cells like on the bacteria)

66
Q

What are the host factors that bacteria are coated with?

A

factors made by “self” or own body called opsonins

67
Q

What are the 2 types of opsonins?

A

antibodies and complement proteins

68
Q

What is oxygen dependent killing by neutrophils?

A

when they act like bleach (able to kill almost any virus or bacteria) by producing corrosive free radicals like O2- and H2O2

69
Q

What is oxygen-independent killing by neutrophils?

A

using enzymes found in the neutrophils like lysozyme (which acts inside the cell), lactoferrin (ferrin means iron and they act in the extracellular space) and defensins (which act outside cell) to kill bacteria

70
Q

Why is neutrophilic killing in the long term bad?

A

because when they kill they produce a lot of chemical factors which do not discriminate between our body’s healthy cells and the non self agent (intruder to destroy) this causes inevitable collateral damage

71
Q

What is a result of long term inflammation?

A

pus (a yellow fluid in open wound area that has become too infected)

72
Q

What are complement proteins?

A

inactive proteins that are involved in innate defense (first line of defense)

73
Q

When the complement proteins are activated what are some of their functions?

A

OIL
Opsonization: they can act as opsins and be used as a tag on bacteria

Immunol and inflammatory competent cells: they will attract these cells (e.g. neutrophils and macrophages) to help with inflammation

Lysis: they can lyse (breakdown) bacteria in immediate surrounding

74
Q

What is clonal selection?

A

when only one B cell out of the many in the lymph node recognize the antigen

75
Q

What are the roles of B and T cells (lymphocytes)?

A

3 R
R: recognize antigens (foreign agents) in a specific manner
R: respond to antigens (destruction of them)
R: remembers the first encounter with an antigen so that they can respond better next time if exposed

76
Q

What are secondary lymphoid tissues?

A

where T and B lymphocytes first encounter foreign antigen to become fully activated (if they do not encounter any foreign antigen they will not be fully activated)

77
Q

What are the primary lymphoid tissues?

A

organs or sites where B and T lymphocytes develop/ originate like thymus and bone marrow

78
Q

How do complement proteins kill by MAC formation?

A

when they are activated they can be deposited on the surface of the bacteria and organize themselves in the form of a pore. Fluid from outside can rush into the bacteria through the pore and this will kill it

79
Q

B vs T lymphocytes in recognizing an antigen

A

T cells are picky so they can not just recognize any foreign antigen like B cells but have to undergo processing and presentation of the foreign antigen

80
Q

How does the interaction between antigen-presenting cells (APC) and T cells work?

A

1) APC presents antigen on MHC
2) the macrophage or dendritic cell (APC) expresses a molecule on its surface that the T cell will them match to bind to it (co-stimulatory)
3) the APC secrete cytokines that will influence the helper T cell to finally become activated

81
Q

Where is MHC II present on?

A

specialized antigen-presenting cells like macrophages or dendritic cells

82
Q

How is active immunity acquired?

A

by exposure to a disease or through vaccines

83
Q

What is the purpose of active immunity?

A

to combat FUTURE infection

84
Q

How is passive immunity acquired?

A

through ingestion of antibodies in placenta or in mother’s milk

85
Q

What is the purpose of passive immunity?

A

to combat EXISTING infection

86
Q

What is the difference between primary and secondary response? similarity?

A

primary is slower to develop and the secondary is quick to develop. But they are both part of acquired or adaptive immunity

87
Q

What is hemostasis?

A

not to be confused with hOMEOstasis it is the mechanisms by which our bodies prevent blood loss

88
Q

What are pro-hemostatic or pro-coagulant factors?

A

pro (means work towards gaining something)

therefore, they work to prevent blood loss

89
Q

What are anti-hemostatic or anti-coagulant factors?

A

anti (against)

therefore, they keep blood fluid to circulate normally and do not favor hemostasis

90
Q

What are the steps to hemostasis?

A

1) Vasoconstriction as soon as there is a rupture
2) Primary hemostasis (platelet plug formation/ white thrombus because platelets look white)
3) Secondary hemostasis (blood clotting/ red thrombus)

91
Q

How is the structure of platelets like?

A

do not have a nucleus, are small cells that do not live very long

92
Q

What are alpha granules?

A

contain relatively large molecules, adhesion molecules like von Willebrand factor and growth factors

93
Q

What are dense granules?

A

contain relatively small molecules like ADP and ATP (that are meant for platelets), Ca++ and serotonin

94
Q

What are the steps for platelet plug formation (primary hemostasis)?

A

3As

1) adhesion of platelets- stick to damaged vessel wall
2) activation (change of shape) of platelets- they change shape, express various receptors and secrete various substances
3) aggregation of platelets- they stick and form a plug

95
Q

What are the proteins that make the platelet plug?

A

fibrinogen

96
Q

Why does platelet plug not continuously expand from cut side?

A

adjacent endothelial cells to the cut site containing NO and PGI2 do not favor platelets to form there so the platelets stay in their platelet plug area not expanding

97
Q

What is the effect of secondary hemostasis?

A

formation of gel-like fibrin clot where RBC are trapped inside of

98
Q

What are the 4 important factors involved with blood clotting?

A

I: fibrinogen
II: Prothrombin
III: tissue factor
IV: calcium

99
Q

How is thrombin activated?

A

it is activated through the merge of the intrinsic (inside blood vessels) and extrinsic (outside blood vessles) pathways to create the common activated factor that will change prothrombin (inactive enzyme) to thrombin (active enzyme)

100
Q

Genotype making a person O blood type

A

OO (homozygous)

101
Q

Genotypes that will make someone have B blood type

A

BB or BO

102
Q

Genotypes that will produce an A blood type

A

AA or AO (A dominant over O)

103
Q

What are ABO class of antigens made of?

A

carbohydrate molecules

104
Q

What is the role of the helper T cells?

A

like their name they do not do the attacks themselves but instead help the B cells, macrophages and cytotoxic T cells

105
Q

What are cytotoxic T cells?

A

they are attack cells, they bind to the target via the antigen on the target and kill them directly through chemicals

106
Q

What are some symptoms of hemolytic disease in newborns?

A

fever, chills, nausea, clotting in blood vessels and Hb in urine. They can have an extended abdomen too

107
Q

Rhesus mismatch between mother and child

A

women Rh- has a baby that is Rh+, some of its Rh+ blood will mix with the mother’s and she will develop anti-D. In a second pregnancy, now with the anti-D in her blood stream the anti-D will cross the barrier and get to the fetal tissue. This result in complications

108
Q

Mismatch blood transfusion in the Rh system

A

transfusion of Rh+ blood in a Rh- person will create the anti-D antibodies so when you try to get another transfusion these anti-D will bind to the Rh+ transfusion and cause clumping/hemolysis

109
Q

What class do the antibodies of the rhesus system belong to?

A

IgG

110
Q

Antibodies of the ABO system are part of which class?

A

IgM

111
Q

What is the universal recipient?

A

blood type AB

112
Q

What is the universal donor?

A

blood type O

113
Q

What is a sign that there is a mismatch of blood in a transfusion?

A

clumping or hemolysis

114
Q

Rhesus system

A

Rh D+ and Rh D- (do not express D antigen)

115
Q

What is agglutination?

A

red blood cell clump

116
Q

How is ABO blood type determined?

A

1) separating a unknown sample of a person’s blood into RBC and plasma
2) putting a drop or two of the RBC into a known solution of antibodies A or B
3) checking mixture to see if it agglutinated or not
- e.g. Blood type A has agglutination with anti-A but not with anti-B

117
Q

What are the roles of an antigen?

A

depends on the antigen present on its red blood cell surface (A antigen= blood type A etc. except AB has both A and B antigens and O has none)

118
Q

What is anti D?

A

an antibody that binds to the D antigen

119
Q

What is anti B?

A

an antibody that binds to the B antigen

120
Q

What is the anti A?

A

an antibody that binds (is complementary to) to A antigen

121
Q

What does plasmin do?

A

makes fibrin (insoluble) into FDPs ( soluble fibrin fragments)

122
Q

What are clinical clot busters or thrombolytic drugs?

A

used to treat patients with heart attacks, they are made in the lab

123
Q

What is the plasminogen activator?

A

what is released with increased exercise from the endothelial cells that turns plasminogen into plasmin

124
Q

How does the breakdown of a fibrin clot work (fibrinolysis)?

A

Converts naturally occurring protein (plasminogen) into plasmin. Plasmin in close contact to fibrin clot will make it into soluble fibrin fragments that will dissolve clot and let it float away in blood circulation

125
Q

What does thrombin do ?

A

it converts fibrinogen into fibrin, activates platelets, activates clotting factors V, VIII, XI and XIII and activates protein C(anticoagulant activity)

126
Q

Effects of deficiency of factor VII and VIII?

A

severe bleeding

127
Q

Effects of deficiency of factor XI?

A

moderate bleeding

128
Q

Effect of deficiency of factor XII on clotting?

A

no bleeding problem in vivo/ not a requirement to start blood clotting (in body) but failure to clot in vitro (out of body)

129
Q

What is Hemophilia B?

A

it is a problem expressed in males due to a deficiency of factor IX, there is not treatment available

130
Q

How does thrombin convert from having pro-coagulant properties by itself to anti-coagulant activity?

A

It binds to thrombomodulin which is found on the surface of an endothelial cell. This will then make it convert inactive protein C to active protein C which is responsible for breaking down factor V and VIII both important factors in blood clotting compromising their abilities and thereby acting as an anticoagulant

131
Q

How does the clinical anticoagulant calcium chelators work?

A

it works in vitro removing ionized Ca++

132
Q

How does the clinical anticoagulant heparin work?

A

it works in vitro and in vivo by increasing effect of antithrombin 3 (natural anticoagulant)

Physl 210 (2 decks)

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