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
2
Q
What is the hematocrit?
A
% of total blood volume occupied by packed red blood cells
3
Q
What is the white blood cell layer called?
A
buffy coat
4
Q
What is polycythemia?
A
high amount of red blood cells
5
Q
What is the liquid fraction of the blood?
A
plasma
6
Q
What is the interstitial fluid?
A
7
Q
How is most of the carbon dioxide transported through the body?
A
through plasma
8
Q
Where are plasma proteins made?
A
liver
9
Q
When clotting factors have been removed from plasma what does it become?
A
serum
10
Q
What is hematopoiesis?
A
process of formation of blood cells
11
Q
Where does hematopoiesis happen prenatally?
A
yolk sac, liver, spleen
12
Q
Where does hematopoiesis happen postnatally?
A
bone marrow
13
Q
What does multipotent mean?
A
can specialize into many cells
14
Q
How is hematopoiesis regulated?
A
Cytokines
15
Q
What are cytokines?
A
small proteins that are hormone-like in their mechanism of action
16
Q
What are hematopoietins
A
another word for cytokines. They act as growth factors
17
Q
What are erythropoietins?
A
cytokines that develop red blood cells
18
Q
What are thrombopoietins?
A
cytokines, that develop platelets
19
Q
What shape are blood cells?
A
biconcave
20
Q
What gives red blood cells their color?
A
hemoglobin
21
Q
What is hemoglobin?
A
responsible for 98-99% of total oxygen transport, binds to the oxygen in loose and reversible manner
22
Q
What is oxygenation?
A
loose physical binding of oxygen
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.
24
Q
What is the most important dietary factor for RBC production?
A
iron
25
How is iron lost?
through sweat, urine, menstrual flow
26
How does body iron reserve distribute % wise?
50% Hb
25% other iron containing proteins
25% bound with Ferritin
27
What happens when there is a lack of Vitamin B12 ?
it causes pernicious anemia
28
What is anemia?
decreased oxygen-carrying capacity of the blood due to a deficiency of RBCs and/or hemoglobin contained in the RBCs
29
What causes anemia?
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
30
What is the abnormal structure of hemoglobin called?
sickle cell disease
31
What are leukocytes?
white blood cells
32
What are erythrocytes?
red blood cells
33
Why is the erythrocyte shaped the way it is?
to increase surface-area-to-volume ratio, allowing oxygen and carbon dioxide to diffuse more efficiently
34
What is a consequence for erythrocytes lacking nuclei and a lot of organelles?
that they can not reproduce themselves and they will not last long
35
What is the breakdown product of hemoglobin?
bilirubin which is returned to the circulation and gives plasma its yellow color
36
Why is iron important?
it is what oxygen binds to on the hemoglobin
37
What is the opposite of iron deficiency?
hemochromatosis
38
What is transferrin?
an iron-transport plasma protein that delivers almost all iron to the bone marrow which will then be incorporated onto new blood cells
39
What is folic acid?
vitamin found in large amounts of leafy plants, yeast, liver. When in low amounts it will effect erythrocyte production (decreasing it)
40
the vitamin that is required for the action of folic acid?
vitamin B12
41
Diet to get vitamin B12 in system?
only found in an animal diet and not on a vegetarian one
42
How is vitamin B12 absorbed from the gastrointestinal tract?
through protein called intrinsic factor which is secreted by the stomach
43
What are some functions of the immune system?
to protect against infection of pathogens, isolate or remove foreign substances, destroy cancer cells (immune surveillance)
44
What does the immune system have to identify first?
the self vs the non-self
45
What are the non-specific defenses/ innate immunity?
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.
46
Where are non-specific defenses (innate immunity) found?
skin, enzymes in saliva, tears and mucus
47
What are specific defenses (acquired immunity)?
defense depends on the specific identification by the lymphocytes on intruders
48
What are some inappropriate (bad) roles that the immune systems can take?
can respond in an exaggerated way to harmless substances (allergies) and autoimmune reactions (attacking its own immune system)
49
What are the 2 groups that leukocytes can be classified into?
it is based on the stem cell that they derived from, but the 2 groups are myeloid cells and lymphoid cells
50
What are included as myeloid cells?
neutrophils, basophils, eosinophils and monocytes
51
What are the myeloid-derived cells that are distinct from macrophages but have characteristics like macrophages (e.g. phagocytosis)?
dendritic cells (do not confuse with dendrites)
52
What are mast cells?
cells found throughout connective tissue, when they are mature they are not found in the blood. They secrete histamine
53
What initiates inflammation?
non-specific innate response to tissue injury
54
What are the key mediators in inflammation?
cells that function like phagocytes e.g. neutrophils, macrophages and dendritic cells
55
What are examples of possible inducers of inflammation?
cuts, bullet wound, injuries to sun burn, infected sutures, infection of tonsil by cold virus
56
What are the main goals of inflammation?
healing and resolution
57
What are the 4 main physical characteristics of inflammation?
redness (rubor), swelling (tumor), heat (calor) and pain (dolor)
58
What are the causes of rubor, tumor and calor? and agent?
increased blood flow and histamine
59
What does increased blood flow do for inflammation?
increases delivery of proteins and leukocytes
60
What is the vasculature (blood vessel wall) responsible for?
release of inflammatory mediators, increased blood flow, increased permeability of small blood vessels
61
What is emigration?
when cells move out from within the blood vessel into the interstitial space
62
What does taxis mean?
movement
63
What is chemotaxis?
ability of WBCs to move against a concentration gradient (L to H) in response to chemical factors (chemotactic)
64
How do phagocytes recognize bacteria?
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
How do you increase the efficiency of phagocytosis of the bacteria by receptors?
by adding opsonin (the butter that white blood cells like on the bacteria)
66
What are the host factors that bacteria are coated with?
factors made by "self" or own body called opsonins
67
What are the 2 types of opsonins?
antibodies and complement proteins
68
What is oxygen dependent killing by neutrophils?
when they act like bleach (able to kill almost any virus or bacteria) by producing corrosive free radicals like O2- and H2O2
69
What is oxygen-independent killing by neutrophils?
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
Why is neutrophilic killing in the long term bad?
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
What is a result of long term inflammation?
pus (a yellow fluid in open wound area that has become too infected)
72
What are complement proteins?
inactive proteins that are involved in innate defense (first line of defense)
73
When the complement proteins are activated what are some of their functions?
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
What is clonal selection?
when only one B cell out of the many in the lymph node recognize the antigen
75
What are the roles of B and T cells (lymphocytes)?
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
What are secondary lymphoid tissues?
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
What are the primary lymphoid tissues?
organs or sites where B and T lymphocytes develop/ originate like thymus and bone marrow
78
How do complement proteins kill by MAC formation?
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
B vs T lymphocytes in recognizing an antigen
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
How does the interaction between antigen-presenting cells (APC) and T cells work?
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
Where is MHC II present on?
specialized antigen-presenting cells like macrophages or dendritic cells
82
How is active immunity acquired?
by exposure to a disease or through vaccines
83
What is the purpose of active immunity?
to combat FUTURE infection
84
How is passive immunity acquired?
through ingestion of antibodies in placenta or in mother's milk
85
What is the purpose of passive immunity?
to combat EXISTING infection
86
What is the difference between primary and secondary response? similarity?
primary is slower to develop and the secondary is quick to develop. But they are both part of acquired or adaptive immunity
87
What is hemostasis?
not to be confused with hOMEOstasis it is the mechanisms by which our bodies prevent blood loss
88
What are pro-hemostatic or pro-coagulant factors?
pro (means work towards gaining something)
| therefore, they work to prevent blood loss
89
What are anti-hemostatic or anti-coagulant factors?
anti (against)
| therefore, they keep blood fluid to circulate normally and do not favor hemostasis
90
What are the steps to hemostasis?
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
How is the structure of platelets like?
do not have a nucleus, are small cells that do not live very long
92
What are alpha granules?
contain relatively large molecules, adhesion molecules like von Willebrand factor and growth factors
93
What are dense granules?
contain relatively small molecules like ADP and ATP (that are meant for platelets), Ca++ and serotonin
94
What are the steps for platelet plug formation (primary hemostasis)?
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
What are the proteins that make the platelet plug?
fibrinogen
96
Why does platelet plug not continuously expand from cut side?
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
What is the effect of secondary hemostasis?
formation of gel-like fibrin clot where RBC are trapped inside of
98
What are the 4 important factors involved with blood clotting?
I: fibrinogen
II: Prothrombin
III: tissue factor
IV: calcium
99
How is thrombin activated?
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
Genotype making a person O blood type
OO (homozygous)
101
Genotypes that will make someone have B blood type
BB or BO
102
Genotypes that will produce an A blood type
AA or AO (A dominant over O)
103
What are ABO class of antigens made of?
carbohydrate molecules
104
What is the role of the helper T cells?
like their name they do not do the attacks themselves but instead help the B cells, macrophages and cytotoxic T cells
105
What are cytotoxic T cells?
they are attack cells, they bind to the target via the antigen on the target and kill them directly through chemicals
106
What are some symptoms of hemolytic disease in newborns?
fever, chills, nausea, clotting in blood vessels and Hb in urine. They can have an extended abdomen too
107
Rhesus mismatch between mother and child
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
Mismatch blood transfusion in the Rh system
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
What class do the antibodies of the rhesus system belong to?
IgG
110
Antibodies of the ABO system are part of which class?
IgM
111
What is the universal recipient?
blood type AB
112
What is the universal donor?
blood type O
113
What is a sign that there is a mismatch of blood in a transfusion?
clumping or hemolysis
114
Rhesus system
Rh D+ and Rh D- (do not express D antigen)
115
What is agglutination?
red blood cell clump
116
How is ABO blood type determined?
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
What are the roles of an antigen?
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
What is anti D?
an antibody that binds to the D antigen
119
What is anti B?
an antibody that binds to the B antigen
120
What is the anti A?
an antibody that binds (is complementary to) to A antigen
121
What does plasmin do?
makes fibrin (insoluble) into FDPs ( soluble fibrin fragments)
122
What are clinical clot busters or thrombolytic drugs?
used to treat patients with heart attacks, they are made in the lab
123
What is the plasminogen activator?
what is released with increased exercise from the endothelial cells that turns plasminogen into plasmin
124
How does the breakdown of a fibrin clot work (fibrinolysis)?
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
What does thrombin do ?
it converts fibrinogen into fibrin, activates platelets, activates clotting factors V, VIII, XI and XIII and activates protein C(anticoagulant activity)
126
Effects of deficiency of factor VII and VIII?
severe bleeding
127
Effects of deficiency of factor XI?
moderate bleeding
128
Effect of deficiency of factor XII on clotting?
no bleeding problem in vivo/ not a requirement to start blood clotting (in body) but failure to clot in vitro (out of body)
129
What is Hemophilia B?
it is a problem expressed in males due to a deficiency of factor IX, there is not treatment available
130
How does thrombin convert from having pro-coagulant properties by itself to anti-coagulant activity?
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
How does the clinical anticoagulant calcium chelators work?
it works in vitro removing ionized Ca++
132
How does the clinical anticoagulant heparin work?
it works in vitro and in vivo by increasing effect of antithrombin 3 (natural anticoagulant)
