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What are the two learning objectives of the infection lecture?
Explain resistance to infection and distinguish innate from acquired immunity.
What types of threats does the immune system defend against?
External microorganisms and internal abnormal cells including potential tumor cells.
What are the three defense categories named in the lecture?
Anatomical barriers, inflammatory responses, and immune responses.
What is innate immunity?
A rapid general nonspecific defense against threats recognized as nonself.
What is adaptive immunity?
An antigen-specific defense involving B and T lymphocytes and immunological memory.
Which response typically begins sooner: innate or adaptive immunity?
Innate immunity responds within minutes to hours; adaptive immunity generally develops over days.
Which cells are highlighted as innate defenses?
Epithelial barrier cells, neutrophils, macrophages, dendritic cells, and natural killer cells.
Which soluble mediators are highlighted in innate immunity?
Complement and interferons.
How does active immunity differ from passive immunity?
Active immunity produces the person's own immune response; passive immunity provides ready-made antibodies.
Give a natural example of active immunity.
Developing immunity after exposure to an infectious agent.
Give an artificial example of active immunity.
Vaccination or immunization.
Give a natural example of passive immunity.
Maternal antibodies transferred to the infant.
Give an artificial example of passive immunity.
Administration of antibodies from an external source.
What is inflammation?
A coordinated response to injury or pathogens that recruits defense cells and mediators to affected tissue.
What are the five local signs of inflammation?
Redness (rubor), heat (calor), swelling (tumor), pain (dolor), and loss of function (functio laesa).
What causes redness and warmth during inflammation?
Capillary or arteriolar dilation increases local blood flow.
What causes swelling during inflammation?
Increased vascular permeability permits fluid to leave vessels and enter tissue.
What recruits leukocytes to an injured area?
Chemotactic signals and inflammatory mediators.
What is chemotaxis?
Directed movement of leukocytes toward chemical signals at an injury or infection site.
What is diapedesis?
Migration of white blood cells out of the bloodstream through vessel walls into tissues.
Which cytokine is linked to fever in the lecture?
IL-1 beta acts on the brain to promote fever and other sickness responses.
What does IL-6 stimulate in the lecture?
The liver's production and release of acute-phase proteins.
What is the major role of IL-8?
Recruitment and activation of neutrophils.
Which interleukins are listed as activating NK cells?
IL-2 and IL-12.
What is the general effect of TNF-alpha in inflammation?
It promotes inflammatory responses and reinforces several cytokine effects.
What are PAMPs?
Pathogen-associated molecular patterns: features of microbes recognized by innate immune receptors.
Which receptor family recognizes PAMPs according to the lecture?
Toll-like receptors are one example.
What is phagocytosis?
Engulfment and ingestion of particles or pathogens by cells such as macrophages and neutrophils.
What do macrophages release to recruit more immune defenses?
Cytokines that stimulate inflammation and recruit immune cells.
What is complement?
A cascade of circulating proteins that supports immune defense through opsonization, inflammation, and cell lysis.
What is opsonization?
Marking a target to enhance its recognition and engulfment by phagocytes.
Which complement component is highlighted for opsonization?
C3b.
Which complement components are associated with inflammatory activation and mast-cell effects?
C3a and C5a.
Which complement component is a major recruiter and activator of neutrophils?
C5a.
What does MAC do?
The membrane attack complex forms pores that can lyse target cells.
Which phagocyte is most numerous and often first to reach an injury?
Neutrophils.
What are antigen-presenting cells (APCs)?
Cells that process antigens and display peptide fragments for recognition by adaptive immune cells.
How do NK cells recognize some abnormal cells?
Reduced or abnormal inhibitory recognition of MHC on target cells can permit killing.
Which cells mediate humoral immunity?
B lymphocytes and their antibody-secreting plasma-cell descendants.
Which cells mediate cell-mediated immunity?
T lymphocytes.
What do CD markers designate?
Cluster-of-differentiation surface markers on immune cells.
Which two CD markers are specifically highlighted in the lecture?
CD4 and CD8.
What two signals does the lecture say lymphocyte activation requires?
Recognition of a specific antigen and activating chemical signals.
What is the function of IgG highlighted in the lecture?
An antibody in blood that can cross the placenta to the fetus.
What is the function of IgM highlighted in the lecture?
An antibody found on B-cell surfaces or secreted in blood and associated with early immune responses.
What is the sequence of adaptive immune response stages?
Antigen recognition, lymphocyte activation, effector attack, decline or contraction, and memory-cell persistence.
Why does the adaptive response contract after an antigen declines?
Many activated lymphocytes die, helping restore homeostatic balance.
Why are memory cells important?
They remain after an immune response and support faster responses to later exposures.
What can happen if inflammation fails to resolve?
Persistent inflammation can contribute to chronic inflammatory disease.
How is immunity linked to the rest of the body?
Nervous and endocrine systems help regulate immunity; many tissue and blood cells participate.
What are the five learning-objective themes in the blood lecture?
Blood composition and functions; roles of RBCs, WBCs, and platelets; primary versus secondary hemostasis; coagulation models and regulation; bleeding/thrombotic disorders and lab tests.
What are the three overarching functions of blood?
Transport, regulation, and protection.
What are the two main components of whole blood?
Plasma and formed elements.
About what fraction of blood is plasma in the lecture diagram?
Approximately 55%.
About what fraction of blood is formed elements in the lecture diagram?
Approximately 45%.
What is the most abundant component of plasma?
Water, about 91% by weight in the lecture diagram.
Which plasma proteins are shown in the lecture diagram?
Albumins, globulins, fibrinogen, and prothrombin.
What do erythrocytes primarily do?
Transport oxygen and help transport carbon dioxide and buffer blood pH.
What do leukocytes primarily do?
Defend against infection and other threats.
What do platelets primarily do?
Support hemostasis and formation of a temporary platelet plug.
What is the typical shape of a red blood cell?
Biconcave disc.
Why is the biconcave shape of RBCs useful?
It provides surface area and flexibility for gas exchange and passage through capillaries.
Do mature human RBCs have nuclei?
No; mature circulating erythrocytes lack nuclei.
What is the approximate lifespan of an RBC?
About 120 days.
What enzyme in RBCs speeds CO2 conversion to carbonic acid?
Carbonic anhydrase.
What reaction does carbonic anhydrase catalyze?
CO2 plus H2O reversibly forms H2CO3, supporting bicarbonate-based CO2 transport.
What is erythropoiesis?
The process of producing red blood cells.
Where does RBC formation begin?
Red bone marrow from hematopoietic stem cells.
What stimulates erythropoietin-mediated RBC production?
Reduced tissue oxygenation.
What is the homeostatic goal of erythropoietin?
Increase RBC production when oxygen delivery is inadequate.
What is hemoglobin made of?
Four globin chains, each associated with a heme group.
How many oxygen molecules can one hemoglobin bind?
Up to four O2 molecules.
What is anemia in the lecture?
A reduction in the number or volume of functional RBCs per unit of whole blood.
What is hematocrit?
The fraction of whole blood volume occupied by red blood cells after centrifugation.
What is the buffy coat?
The thin layer containing leukocytes and platelets between plasma and RBCs after centrifugation.
What is leukopenia?
An abnormally low white blood cell count.
What is leukocytosis?
An increased white blood cell count that may occur with infection, stress, or other conditions.
Name the three granulocyte categories in the lecture.
Neutrophils, eosinophils, and basophils.
Name the two agranulocyte categories in the lecture.
Lymphocytes and monocytes.
What are platelets derived from?
Fragments of megakaryocytes.
What is thrombocytopenia?
An abnormally low platelet count associated with increased bleeding risk.
What happens when incompatible blood is transfused?
Antibodies can bind RBC antigens, causing agglutination and hemolysis.
What is hemostasis?
The physiological process that limits blood loss after vessel injury while keeping blood fluid elsewhere.
What is the overall sequence of hemostasis shown in the lecture?
Vessel injury, primary hemostasis, secondary hemostasis, stable clot, then fibrinolysis.
What is the initial vascular response to vessel injury?
Transient vasoconstriction or vascular spasm to reduce blood loss.
What causes vascular spasm according to the lecture?
Nervous reflexes, local humoral factors, and local myogenic responses.
What is primary hemostasis?
Formation of a temporary platelet plug by platelet adhesion, activation, and aggregation.
What is secondary hemostasis?
Coagulation-factor reactions that generate thrombin and fibrin to reinforce the platelet plug.
What is exposed after endothelial injury that promotes platelet adhesion?
Subendothelial collagen and related structures.
What is von Willebrand factor's role in platelet adhesion?
vWF bridges exposed collagen and platelet GPIb receptors.
Which platelet receptor binds vWF during adhesion?
GPIb.
What happens during platelet activation?
Adherent platelets change shape and release mediators such as ADP and thromboxane A2 to recruit more platelets.
What do ADP and thromboxane A2 promote?
Additional platelet activation and aggregation.
Which platelet receptor binds fibrinogen for aggregation?
GPIIb/IIIa.
How does fibrinogen help platelet aggregation?
Fibrinogen bridges GPIIb/IIIa receptors on neighboring activated platelets.
What is the sequence of primary platelet events?
Adhesion, activation, and aggregation.
How do primary and secondary hemostasis cooperate?
Platelets form the initial plug, while thrombin-generated fibrin stabilizes it.
What is the role of vWF beyond platelet adhesion?
It helps protect and carry coagulation factor VIII.
Which pathway begins with tissue factor exposure after injury?
Extrinsic pathway.
Which coagulation factor is associated with tissue factor in the extrinsic pathway?
Factor VII, which becomes VIIa.