Blood Flashcards
(122 cards)
1
Q
Blood
A
Specialised connective tissue that contains cells suspended in a fluid matrix
2
Q
Functions of blood
A
- Transport (gases, nutrients, hormones, metabolic wastes)
- pH and ion concentration of interstitial fluid
- Restricting fluid loss at injury sites
- Defence
- Body temperature
3
Q
Characteristics of blood
A
- 38 degrees C
- 5 times as viscous as water
- Slightly alkaline
4
Q
Whole blood
A
Fluid plasma and formed elements
5
Q
Fractionated blood
A
Separated for clinical purposes
6
Q
Components of plasma
A
Plasma proteins, other solutes, water
7
Q
Plasma proteins
A
Albumins, globulins, fibrinogens
8
Q
Albumins
A
- Most abundant
Important for - Osmolarity
- Transport of fatty acids, thyroid hormones
9
Q
Globulins
A
- Body defence e.g. antibodies
- Transport globulins e.g. hormone-binding proteins
10
Q
Fibrinogens
A
Important for clotting
11
Q
Serum
A
The remaining fluid when clotting proteins are removed from a blood sample
12
Q
Which organ synthesises more than 90% of plasma proteins?
A
The liver
13
Q
Formed elements
A
Red blood cells, white blood cells and platelets
14
Q
Hemopoiesis
A
Process of formed elements formation
15
Q
Erythrocytes
A
RBCs
16
Q
Which pigment do RBCs contain?
A
Hemoglobin
17
Q
Hematocrit
A
Percentage of blood sample that consists of formed elements (mostly RBCs)
18
Q
Venipuncture
A
Blood sample from anterior elbow
19
Q
Arterial puncture
A
Blood sample from arteries at wrist or elbow used for blood gas analysis (lung function)
20
Q
Which stem cell populations are important for production of formed elements?
A
Myeloid stem cells and lymphoid stem cells
21
Q
Shape of RBC
A
Biocave disc with a thin central region and thicker outer margin
22
Q
Benefits of RBC shape and flexible membrane
A
- Surface area
- Ability to form stacks
- Ability to bend when moving through small capillaries
23
Q
Rouleaux
A
Stacks of RBCs
24
Q
Do mature RBCs have nucelei?
A
No
25
How do mature RBCs obtain energy?
Through anaerobic metabolism (no nuclei = no mitochondria = no aerobic metabolism)
26
Why do mature RBCs lack mitchondira?
So the absorbed oxygen will be carried to peripheral tissues and not stolen by mitochondria
27
Hemoglobin
Responsible for RBCs ability to transport oxygen and carbon dioxide
28
Hemoglobin structure
Complex quaternary: 2 alpha chains and 2 beta chains
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Heme
- Non protein pigment complex
- Holds an iron ion
- Contained in a single hemoglobin chain
30
Oxyhemoglobin
When oxygen binds to iron in heme unit
31
Why is the binding of an oxygen molecule to the iron in a heme unit reversible?
The iron-oxygen interaction is very weak
32
Deoxyhemoglobin
A hemoglobin molecule whose iron is not bound to oxygen
33
What kind of blood is dark red?
Blood containing RBCs filled with deoxyhemoglobin
34
Fetal hemoglobin
Binds oxygen more readilt than does adult hemoglobin
35
Carbaminohemoglobin
Alpha and beta chains of hemoglobin bind to carbon dioxide
36
Anemia
Interferes with oxygen delivery to peripheral tissues
37
When do embryonic blood cells appear in the bloodstream?
Third week of development
38
Myeloid tissue
Red bone marrow, where RBCs are formed
39
Hemocytoblasts or hematopoietic stem cells (HSCs)
- Found in red bone marrow
| - Divide to form myeloid stem cells and lymphoid stem cells
40
Myeloid stem cells
Divide to produce RBCs and several classes of WBCs
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Lymphoid stem cells
Divide to produce lymphocytes
42
Myeloid stem cells
Divide to produce RBCs and several classes of WBCs
43
Lymphoid stem cells
Divide to produce lymphocytes
44
What accounts for the differences in hematocrit values between males and females?
The fact that estrogens don't stimulate erythropoiesis
45
What stimulates erythropoiesis?
```
The hormone erythropoietin (EPO) (directly)
Other hormones (indirectly)
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46
Which organs make EPO?
Kidneys and liver
47
When does EPO appear in the plasma?
When peripheral tissues, especially the kidneys, are exposed to a low concentration of oxygen
48
Effects of EPO
1. Stimulates erythroblast division and eryhroblast-producing stem cell division
2. Speeds up maturation of RBCs by accelerating Hb synthesis
49
Blood doping
When athletes elevate their hematocrits by re-infusing packed RBCs that were removed and stored at an earlier date
50
Why is blood doping dangerous?
It makes blood more viscous and increases the workload on the heart
51
Hemolyzed RBCs
Ruptured RBCs
52
Hemoglobin recycling
Alpha, beta chains of Hb - eliminated
Globular proteins - metabolised or release for other use
Iron - recycled
53
Hemoglobinuria
When abnormally large numbers of RBCs break down in the bloodstream and urine may turn red or brown
54
Hematuria
Presence of intact RBCs in urine
| Occurs after kidney damage or damage to vessels along urinary tract
55
Fate of heme
1. Heme unit stripped of its iron and converted to biliverdin
2. Converted to bilirubin which is released to bloodstream
3. Bilirubin binds to albumin and is transported to the liver for excretion in bile
56
What causes jaundice?
When bile ducts are blocked or the liver can't absorb or excrete bilirubin, bilirubin diffuses into peripheral tissues
57
Recycling of iron
Iron ions extracted from heme molecules bound and stored in phagocytic cells or released into bloodstream where they bind to transferrin
58
How is transferrin recycled?
RBCs developing in red bone marrow absorb amino acids and transferrins from the bloodstream and use them to synthesise new Hb molecules
59
Antigens
Substances that can trigger an immune response
60
Surface antigens
Substances that the immune system recognises as self
61
How is your blood type determined?
By the presence or absence of specific surface antigens in RBC plasma membranes
62
Type A blood
RBCs with surface antigen A only
Plasma contains anti-B antibodies
63
Type B blood
RBCs with surface antigen B only
Plasma contains anti-A antibodies
64
Type AB blood
RBCs with both surface antigens A and B
Plasma has neither anti-A nor anti-B antibodies
65
Type O blood
RBCs with neither surface antigens A or B
Plasma has both anti-A and anti-B antibodies
66
Rh blood group
Based on the presence or absence of the Rh surface antigen
67
Rh factor
Rh surface antigen
68
Agglutinogens
Surface antigens
69
Agglutinins
Antibodies
70
Agglutinate
Foreign cells
71
Agglutination
When agglutinates clump together
72
Cross-reaction
When an antibody meets its specific surface antigen, the RBCs agglutinate
73
Compatibility test
1. Determination of blood type
| 2. Cross-match test
74
Cross-match testing
Involves exposing the donors RBCs to a sample of the recipients plasma under controlled conditions
75
Do WBCs have nuclei?
Yes
76
Where do WBCs circulate?
Through the loose and dense connective tissues of the body
77
Characteristics of WBCs
1. All can migrate out of the bloodstream
2. All are capable of amoeboid movement
3. All are attracted to specific chemical stimuli
78
Amoeboid movement
A gliding motion made possible by the flow of cytoplasm into slender cellular processes extended in the direction of movement
79
Positive chemotaxis
Characteristic of WBCs that guide them to invading pathogens, damaged tissues and other active WBCs
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Margination
When WBCs in the bloodstream are activated, they contact and adhere to the vessel walls
81
Granular leukocytes
Neutrophils, eosinophils, and basophils
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Agranular leukocytes
Monocytes and lymphocytes
83
Nonspecific defenses
Neutrophils, eosinophils, basophils, monocytes
84
Microphages
Neutrophils and eosinophils
85
Specific defences
Lymphocytes
86
Hemolytic disease of the newborn (HDN)
When mother's antibodies cross placenta and attack fetus' RBCs
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Hemolytic disease of the newborn (HDN)
When mother's antibodies developed during first pregnancy cross placenta and attack fetus' RBCs
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Neutrophils
Highly mobile, specialised cells for attacking and digesting bacteria that have been marked with antibodies or complement proteins
89
Eosinophils
Attack objects that are coated with antibodies mostly through exocytosis
90
Basophils
Migrate to injury sites and cross the capillary endothelium to accumulate in damaged tissue and discharge granules containing histamine and heparin into interstitial fluid
91
Neutrophils
Highly mobile, specialised cells for attacking and digesting bacteria that have been marked with antibodies or complement proteins
92
Eosinophils
Attack objects that are coated with antibodies mostly through exocytosis
93
Basophils
Migrate to injury sites and cross the capillary endothelium to accumulate in damaged tissue and discharge granules containing histamine and heparin into interstitial fluid
94
Histamine
Dilates blood vessels
95
Heparins
Prevents blood clotting
96
Monocytes
Becomes a tissue macrophage
97
Lymphocytes
T cells
B cells
NK cells
98
T cells
- Responsible for cell-mediated immunity
| - Defence against invading foreign cells and coordinating immune response
99
B cells
- Responsible for humoral immunity
| - Production of antibodies
100
What do activated B cells differentiate into?
Plasma cells
101
NK cells
- Responsible for immune surveillance
| - Detection and subsequent destruction of abnormal cells
102
Which lymphocyte is important in preventing cancer?
NK cells
103
Leukopenia
Inadequate numbers of WBCs
104
Leukopoiesis
Hemocytoblast divisions produce myeloid stem cells and lymphoid stem cells
Myeloid stem cells divide to create progenitor cells which give rise to all formed elements except lymphocytes
105
What does extreme leukocytosis usually indicate?
The presence of some form of leukemia
106
Lymphocytopoiesis
Some lymphocytes are derived from lymphoid stem cells that remain in red bone marrow - differentiate into B cells or NK cells
Some lymphocytes are produced in lymphatic tissues
107
Lymphatic tissues
Thymus, spleen, and lymph nodes
108
Colony-stimulating factors (CSFs)
Regulate WBC populations
109
Platelets
Disc-shaped cell fragments
110
Thrombocytopoiesis
- Occurs in red bone marrow
| - Megakaryocytes shed cytoplasm in packets = platelets
111
Hemostasis
Stopping of the bleeding
1. Vascular phase
2. Platelet phase
3. Coagulation phase
112
Vascular phase
Period of local blood vessel constriction (vascular spasm)
113
Platelet phase
Platelets are activated, aggregate at the site and adhere to damaged surfaces
114
Coagulation phase
Occurs as factors released by platelets and endothelial cells interact with clotting factors to form a blood clot
115
Clot retraction
Platelets contract and pull the torn edges of the damaged vessel closer together
116
Fibrinolysis
When the clot gradually dissolves through the action of plasmin, the activate form of circulating plasminogen
117
Hemostasis
Stopping of the bleeding
1. Vascular phase
2. Platelet phase
3. Coagulation phase
118
Vascular phase
Period of local blood vessel constriction (vascular spasm)
119
Platelet phase
Platelets are activated, aggregate at the site and adhere to damaged surfaces
120
Coagulation phase
Occurs as factors released by platelets and endothelial cells interact with clotting factors to form a blood clot
121
Clot retraction
Platelets contract and pull the torn edges of the damaged vessel closer together
122
Fibrinolysis
When the clot gradually dissolves through the action of plasmin, the activate form of circulating plasminogen
