1
Q
Why is horseshoe crab blood blue?
A
Because it contains hemocyanin, a copper-based oxygen-carrying protein instead of hemoglobin.
2
Q
What is blood doping?
A
The removal of red blood cells to induce hypoxia and EPO release, followed by reinfusion to increase RBC count.
3
Q
What is the athletic advantage of blood doping?
A
Increased endurance and reduced fatigue due to increased oxygen-carrying capacity.
4
Q
What is a major danger of blood doping?
A
Increased blood viscosity, raising risk of stroke and heart attack.
5
Q
How does aspirin affect hemostasis?
A
It blocks thromboxane A2, inhibiting platelet plug formation.
6
Q
What is hemostasis?
A
A three-step process that stops excessive blood loss.
7
Q
What is a vaccine?
A
Introduction of a weakened or harmless antigen to stimulate antibody production.
8
Q
Why do vaccines provide faster future protection?
A
They create memory cells that respond quickly to later exposure.
9
Q
Why is HIV difficult to vaccinate against?
A
High mutation rate causes many viral strains.
10
Q
What percentage of HIV DNA transcripts contain errors?
A
More than 50%.
11
Q
Why was smallpox so deadly historically?
A
High mortality rates, especially in infants.
12
Q
Who developed the smallpox vaccine?
A
Dr. Edward Jenner.
13
Q
How did Jenner discover smallpox immunity?
A
Observation that cowpox exposure protected milkmaids.
14
Q
What disease was used to vaccinate against smallpox?
A
Cowpox.
15
Q
Where does the word vaccine come from?
A
Latin word ‘vacca’ meaning cow.
16
Q
What percentage of body weight is blood?
A
Approximately 8%.
17
Q
Average blood volume in adult men?
A
5–6 liters.
18
Q
Average blood volume in adult women?
A
4–5 liters.
19
Q
What is normal blood pH?
A
7.35–7.45.
20
Q
What color is oxygenated vs deoxygenated blood?
A
Bright red when oxygenated, darker red when deoxygenated.
21
Q
Primary functions of blood?
A
Transport, temperature regulation, disease protection.
22
Q
How does blood transport oxygen?
A
Hemoglobin in red blood cells binds oxygen.
23
Q
How does blood regulate body temperature?
A
Through vasodilation and vasoconstriction.
24
Q
What is vasodilation?
A
Widening of blood vessels to release heat.
25
What is vasoconstriction?
Narrowing of blood vessels to conserve heat.
26
How does blood protect against disease?
White blood cells fight pathogens.
27
What is plasma?
The non-living fluid matrix of blood.
28
What percentage of blood is plasma?
Approximately 55%.
29
Main component of plasma?
Water (over 90%).
30
How many solutes are in plasma?
Over 100.
31
Three most abundant plasma proteins?
Albumin, globulins, fibrinogen.
32
Function of albumin?
Maintains osmotic balance and buffers pH.
33
Function of globulins?
Immune response and lipid transport.
34
Function of fibrinogen?
Blood clotting.
35
What are formed elements?
Cells and cell fragments in blood.
36
Three formed element types?
Erythrocytes, leukocytes, platelets.
37
What are leukocytes?
White blood cells involved in immunity.
38
What percentage of blood do leukocytes make up?
Less than 1%.
39
Are leukocytes complete cells?
Yes, they have nuclei and organelles.
40
Two main leukocyte classifications?
Granulocytes and agranulocytes.
41
Granulocyte types?
Neutrophils, eosinophils, basophils.
42
Agranulocyte types?
Lymphocytes and monocytes.
43
What percent of blood do leukocytes make up?
Less than 1% of total blood volume.
44
Are leukocytes complete cells?
Yes, they contain nuclei and organelles.
45
Two main types of leukocytes?
Granulocytes and agranulocytes.
46
Which leukocytes are granulocytes?
Neutrophils, eosinophils, basophils.
47
Which leukocytes are agranulocytes?
Lymphocytes and monocytes.
48
Primary function of neutrophils?
Highly phagocytic; major role in innate immune defense.
49
Primary function of eosinophils?
Defense against parasites; involved in allergies and asthma.
50
Primary function of basophils?
Release histamine to promote inflammation.
51
Where are lymphocytes mostly found?
Lymphoid tissues.
52
Function of T lymphocytes?
Attack virus-infected cells and tumor cells.
53
Function of B lymphocytes?
Produce antibodies.
54
What happens to monocytes after leaving circulation?
They differentiate into macrophages in tissues.
55
What cell gives rise to all leukocytes?
Hematopoietic stem cell.
56
Which stem cell produces granulocytes and monocytes?
Myeloid stem cell.
57
Which stem cell produces lymphocytes?
Lymphoid stem cell.
58
Main function of platelets?
Blood clotting.
59
Platelet lifespan?
About 10 days.
60
Platelets are fragments of which cell?
Megakaryocytes.
61
Normal platelet count?
150,000–400,000 platelets per µL.
62
What hormone regulates platelet production?
Thrombopoietin.
63
Primary function of erythrocytes?
Transport oxygen.
64
How does erythrocyte shape relate to function?
Biconcave shape increases surface area for gas exchange.
65
Normal erythrocyte count?
4.2–6.1 million cells per µL.
66
Erythrocyte lifespan?
100–120 days.
67
What is hemoglobin?
An iron-containing protein that binds oxygen.
68
Hemoglobin structure?
Globin protein with four heme groups containing iron.
69
What is oxyhemoglobin?
Hemoglobin bound to oxygen.
70
What is deoxyhemoglobin?
Hemoglobin after oxygen has been released to tissues.
71
What is carbaminohemoglobin?
Hemoglobin bound to carbon dioxide.
72
What is hematopoiesis?
Formation of blood cells.
73
Where does hematopoiesis occur?
Red bone marrow.
74
What cells initiate hematopoiesis?
Hematopoietic stem cells.
75
What is leukopoiesis?
Production of white blood cells.
76
What is hematocrit?
The percentage of whole blood volume composed of red blood cells (erythrocytes).
77
What is erythropoiesis?
The process of red blood cell (RBC) production in red bone marrow.
78
How many red blood cells are produced per second?
More than 2 million RBCs are produced per second.
79
What hormone primarily stimulates erythropoiesis?
Erythropoietin (EPO).
80
Where is erythropoietin (EPO) released from?
The kidneys.
81
What does erythropoietin act on?
Red bone marrow.
82
What effect does EPO have on its target tissue?
Stimulates increased red blood cell production.
83
How does testosterone affect erythropoiesis?
Testosterone increases EPO production.
84
Why do males generally have a higher RBC count than females?
Because testosterone increases EPO production.
85
What is hypoxia?
A condition of low oxygen availability in tissues.
86
What role does hypoxia play in erythropoiesis?
Hypoxia stimulates the release of EPO.
87
Why does hypoxia trigger EPO release?
To increase red blood cell production and improve oxygen delivery.
88
What happens if there are too many erythrocytes?
Blood becomes too thick (viscous), increasing risk of stroke.
89
Why can excess erythrocytes cause a stroke?
Thickened blood may not pass easily through blood vessels.
90
What happens if there are too few erythrocytes?
Reduced oxygen delivery to tissues, leading to anemia.
91
Why is balance between erythrocyte production and destruction important?
Imbalance can cause anemia or dangerous blood thickening.
92
Where does erythrocyte destruction primarily occur?
In the spleen.
93
What happens to hemoglobin during erythrocyte destruction?
Hemoglobin degenerates and is separated into heme and globin.
94
What happens to the globin portion of hemoglobin?
It is broken down into amino acids and released into circulation.
95
What happens to the heme portion of hemoglobin?
It is split into iron and a pigment.
96
What happens to iron from heme?
Iron is salvaged and reused.
97
What pigment is formed from degraded heme?
Bilirubin.
98
Where is bilirubin processed?
In the liver.
99
How does bilirubin leave the body?
It is secreted into bile and leaves in feces.
100
What is anemia?
A condition characterized by too few red blood cells or insufficient hemoglobin.
101
What is the treatment for anemia caused by blood loss?
Blood transfusion.
102
What is renal anemia?
Anemia caused by insufficient EPO production by the kidneys.
103
What is the treatment for renal anemia?
Synthetic erythropoietin (EPO).
104
What is aplastic anemia?
Anemia caused by destruction or inhibition of red bone marrow.
105
What is hemolytic anemia?
Anemia caused by excessive destruction of red blood cells.
106
What is thalassemia?
A genetic disorder where one globin chain is absent.
107
What is sickle cell anemia?
A genetic disorder caused by one incorrect amino acid in the beta globin chain.
108
What is hemostasis?
The process that stops bleeding.
109
What are the three broad steps of hemostasis?
Vascular spasm, platelet plug formation, and coagulation.
110
What is hemostasis?
A series of reactions that stop bleeding.
111
What are the three main steps of hemostasis?
Vasoconstriction, platelet plug formation, and coagulation.
112
What happens during vasoconstriction?
The blood vessel near the injury constricts to slow blood flow.
113
Why does vasoconstriction occur after vessel injury?
To reduce blood loss at the site of injury.
114
What is platelet plug formation?
Activated platelets form a temporary plug at the injury site.
115
What do platelets stick to during plug formation?
Collagen fibers exposed by vessel damage.
116
What happens to platelets when they are activated?
They swell and release chemical messengers.
117
What chemicals are released by activated platelets?
ADP, thromboxane A2, and serotonin.
118
What is platelet aggregation?
Platelets sticking to one another to build the plug.
119
What type of feedback loop occurs in platelet activation?
Positive feedback loop.
120
How do platelets reinforce vasoconstriction?
Serotonin enhances vessel constriction.
121
Why does platelet plug formation usually only occur during vessel rupture?
Because collagen fibers are only exposed when vessels are damaged.
122
What is coagulation?
The process that reinforces the platelet plug with fibrin threads.
123
What is the end result of coagulation?
Blood becomes gel-like and forms a clot.
124
What are the two pathways of coagulation phase 1?
Intrinsic and extrinsic pathways.
125
What triggers the intrinsic pathway?
Factors within the blood.
126
What triggers the extrinsic pathway?
Factors outside the blood.
127
What is formed at the end of phase 1 of coagulation?
Prothrombin activator.
128
What happens during phase 2 of coagulation?
Prothrombin is converted into thrombin.
129
What happens during phase 3 of coagulation?
Thrombin converts fibrinogen into fibrin.
130
What is the role of fibrin?
Forms a mesh that stabilizes the clot.
131
What is clot retraction?
Platelets contract and pull fibrin strands together.
132
What proteins allow platelets to contract?
Actin and myosin.
133
What happens to serum during clot retraction?
It is squeezed out of the clot.
134
How does clot retraction aid vessel repair?
It pulls ruptured vessel edges together.
135
What growth factor promotes muscle cell and fibroblast division?
Platelet-derived growth factor (PDGF).
136
What growth factor restores endothelial lining?
Vascular endothelial growth factor (VEGF).
137
What is fibrinolysis?
The process of breaking down fibrin strands.
138
When does fibrinolysis begin?
Within about two days.
139
What enzyme digests fibrin?
Plasmin.
140
What is a thromboembolic condition?
A condition involving abnormal clot formation that can block vessels.
141
What is thrombocytopenia?
A condition with abnormally low platelet count.
142
How is thrombocytopenia treated?
Platelet transfusion.
143
What causes bleeding disorders?
Deficiency or inability to synthesize procoagulants.
144
What is hemophilia A?
Deficiency of clotting factor VIII.
145
What percentage of hemophilia cases are type A?
About 77%.
146
What is hemophilia B?
Deficiency of clotting factor IX.
147
What is hemophilia C?
Mild hemophilia caused by factor XI deficiency.
148
What is disseminated intravascular coagulation (DIC)?
Widespread clotting in intact vessels with severe bleeding.
149
What commonly causes DIC?
Pregnancy complications or incompatible blood transfusions.
150
What are the main types of blood transfusions?
Red blood cells, plasma, white blood cells, and platelets.
151
Why are platelets often removed from stored blood?
To reduce clotting and immune reactions.
152
When is a blood transfusion compatible?
When donor antigens do not trigger recipient antibodies.
153
What happens during an incompatible transfusion?
Agglutination and hemolysis of red blood cells.
154
What are the consequences of incompatible transfusion?
Kidney failure, shock, and potentially death.
155
What is immunity?
Resistance to disease.
156
What are the two main types of immunity?
Innate (non-specific) and adaptive (specific).
157
What is innate immunity?
Non-specific defenses present at birth.
158
What is adaptive immunity?
Specific defenses that develop after exposure to antigens.
159
What are the three lines of defense?
First: surface barriers; Second: internal innate defenses; Third: adaptive immunity.
160
What is the first line of defense?
External body membranes such as skin and mucous membranes.
161
What is the second line of defense?
Antimicrobial proteins, phagocytes, inflammation, and fever.
162
What is the third line of defense?
Adaptive immune responses targeting specific antigens.
163
What are surface barriers?
Skin and mucous membranes that block pathogen entry.
164
What are phagocytes?
White blood cells that engulf and destroy pathogens.
165
Which cells are major phagocytes?
Neutrophils and monocytes/macrophages.
166
What are natural killer (NK) cells?
Lymphocytes that kill virus-infected and tumor cells without antigen activation.
167
How do NK cells contribute to immunity?
They destroy abnormal cells and enhance inflammation.
168
What are antimicrobial proteins?
Proteins that attack microorganisms or hinder reproduction.
169
Name key antimicrobial proteins.
Interferons, complement proteins, and defensins.
170
What is fever?
A systemic increase in body temperature.
171
What causes fever?
Pyrogens released by leukocytes and macrophages.
172
What is inflammation?
A response to infection or injury.
173
What triggers inflammation?
Infection, extreme heat, and tissue injury.
174
What are the goals of inflammation?
Prevent spread, remove debris/pathogens, alert adaptive immunity, and enable repair.
175
What are the signs of inflammation?
Redness, heat, swelling, pain, and loss of function.
176
What is immunological memory?
The ability to respond faster and stronger to a known antigen.
177
What is the difference between primary and secondary exposure?
Secondary responses are faster and stronger.
178
What is humoral immunity?
Antibody-mediated immunity targeting extracellular antigens.
179
What cells are responsible for humoral immunity?
B lymphocytes.
180
What is cell-mediated immunity?
Immunity where lymphocytes directly act on infected cells.
181
What cells are responsible for cellular immunity?
T lymphocytes.
182
What are antibodies?
Proteins that bind antigens and mark them for destruction.
183
What are the classes of antibodies called?
Immunoglobulins.
184
Which antibody is produced first?
IgM.
185
Which antibody is most abundant?
IgG.
186
What percentage of antibodies is IgG?
Approximately 75–85%.
187
What are antigen-presenting cells (APCs)?
Cells that present antigens to T cells.
188
Which cells act as APCs?
Dendritic cells, macrophages, and B cells.
189
What is the role of APCs?
Engulf antigens and present them to T cells.
190
Where do B cells mature?
Bone marrow.
191
Where do T cells mature?
Thymus.
192
What is immunocompetence?
Ability to recognize one specific antigen.
193
What is self-tolerance?
Ability to avoid attacking self antigens.
194
What happens during primary antibody response?
Lag of 3–6 days, peak around 10 days, low antibody levels.
195
What happens during secondary antibody response?
Response within hours, higher and longer-lasting antibody levels.
196
What is active immunity?
Immunity produced by one's own immune system.
197
What is passive immunity?
Immunity acquired by receiving antibodies.
198
What is naturally acquired active immunity?
Immunity from infection.
199
What is artificially acquired active immunity?
Immunity from vaccination.
200
What is naturally acquired passive immunity?
Antibodies from mother to infant.
201
What is artificially acquired passive immunity?
Injection of antibodies.
202
What is the Rh (D) antigen?
An antigen found on red blood cells.
203
What is the Rhesus factor?
Presence or absence of the Rh antigen.
204
How is blood type determined?
Using antigen-antibody interactions.
205
What is erythroblastosis fetalis?
A condition where maternal antibodies destroy fetal RBCs.
206
When does erythroblastosis fetalis occur?
Rh-negative mother with Rh-positive baby.
207
What is the lymphatic system?
A system that returns leaked fluid to the bloodstream.
208
What are the main components of the lymphatic system?
Lymph, lymphatic vessels, lymph nodes, spleen, thymus, tonsils.
209
What is lymph?
Fluid inside lymphatic vessels.
210
What is the function of lymph nodes?
Clean lymph and house immune cells.
211
What cells are found in lymphatic tissue?
Lymphocytes, macrophages, dendritic cells, reticular cells.
212
Where do lymphocytes arise?
Red bone marrow.
213
What are macrophages?
Large phagocytic cells.
214
What do dendritic cells do?
Present antigens to T cells.
215
What do reticular cells do?
Produce reticular fibers.
216
How are plasma transfusions used?
To provide circulating antibodies to patients.
*BSCI 202 FINAL EXAM*
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