Human phys chapter 7

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134 Terms

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What are the two learning objectives of the infection lecture?

Explain resistance to infection and distinguish innate from acquired immunity.

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What types of threats does the immune system defend against?

External microorganisms and internal abnormal cells including potential tumor cells.

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What are the three defense categories named in the lecture?

Anatomical barriers, inflammatory responses, and immune responses.

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What is innate immunity?

A rapid general nonspecific defense against threats recognized as nonself.

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What is adaptive immunity?

An antigen-specific defense involving B and T lymphocytes and immunological memory.

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Which response typically begins sooner: innate or adaptive immunity?

Innate immunity responds within minutes to hours; adaptive immunity generally develops over days.

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Which cells are highlighted as innate defenses?

Epithelial barrier cells, neutrophils, macrophages, dendritic cells, and natural killer cells.

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Which soluble mediators are highlighted in innate immunity?

Complement and interferons.

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How does active immunity differ from passive immunity?

Active immunity produces the person's own immune response; passive immunity provides ready-made antibodies.

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Give a natural example of active immunity.

Developing immunity after exposure to an infectious agent.

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Give an artificial example of active immunity.

Vaccination or immunization.

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Give a natural example of passive immunity.

Maternal antibodies transferred to the infant.

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Give an artificial example of passive immunity.

Administration of antibodies from an external source.

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What is inflammation?

A coordinated response to injury or pathogens that recruits defense cells and mediators to affected tissue.

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What are the five local signs of inflammation?

Redness (rubor), heat (calor), swelling (tumor), pain (dolor), and loss of function (functio laesa).

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What causes redness and warmth during inflammation?

Capillary or arteriolar dilation increases local blood flow.

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What causes swelling during inflammation?

Increased vascular permeability permits fluid to leave vessels and enter tissue.

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What recruits leukocytes to an injured area?

Chemotactic signals and inflammatory mediators.

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What is chemotaxis?

Directed movement of leukocytes toward chemical signals at an injury or infection site.

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What is diapedesis?

Migration of white blood cells out of the bloodstream through vessel walls into tissues.

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Which cytokine is linked to fever in the lecture?

IL-1 beta acts on the brain to promote fever and other sickness responses.

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What does IL-6 stimulate in the lecture?

The liver's production and release of acute-phase proteins.

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What is the major role of IL-8?

Recruitment and activation of neutrophils.

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Which interleukins are listed as activating NK cells?

IL-2 and IL-12.

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What is the general effect of TNF-alpha in inflammation?

It promotes inflammatory responses and reinforces several cytokine effects.

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What are PAMPs?

Pathogen-associated molecular patterns: features of microbes recognized by innate immune receptors.

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Which receptor family recognizes PAMPs according to the lecture?

Toll-like receptors are one example.

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What is phagocytosis?

Engulfment and ingestion of particles or pathogens by cells such as macrophages and neutrophils.

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What do macrophages release to recruit more immune defenses?

Cytokines that stimulate inflammation and recruit immune cells.

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What is complement?

A cascade of circulating proteins that supports immune defense through opsonization, inflammation, and cell lysis.

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What is opsonization?

Marking a target to enhance its recognition and engulfment by phagocytes.

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Which complement component is highlighted for opsonization?

C3b.

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Which complement components are associated with inflammatory activation and mast-cell effects?

C3a and C5a.

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Which complement component is a major recruiter and activator of neutrophils?

C5a.

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What does MAC do?

The membrane attack complex forms pores that can lyse target cells.

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Which phagocyte is most numerous and often first to reach an injury?

Neutrophils.

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What are antigen-presenting cells (APCs)?

Cells that process antigens and display peptide fragments for recognition by adaptive immune cells.

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How do NK cells recognize some abnormal cells?

Reduced or abnormal inhibitory recognition of MHC on target cells can permit killing.

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Which cells mediate humoral immunity?

B lymphocytes and their antibody-secreting plasma-cell descendants.

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Which cells mediate cell-mediated immunity?

T lymphocytes.

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What do CD markers designate?

Cluster-of-differentiation surface markers on immune cells.

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Which two CD markers are specifically highlighted in the lecture?

CD4 and CD8.

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What two signals does the lecture say lymphocyte activation requires?

Recognition of a specific antigen and activating chemical signals.

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What is the function of IgG highlighted in the lecture?

An antibody in blood that can cross the placenta to the fetus.

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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.

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What is the sequence of adaptive immune response stages?

Antigen recognition, lymphocyte activation, effector attack, decline or contraction, and memory-cell persistence.

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Why does the adaptive response contract after an antigen declines?

Many activated lymphocytes die, helping restore homeostatic balance.

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Why are memory cells important?

They remain after an immune response and support faster responses to later exposures.

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What can happen if inflammation fails to resolve?

Persistent inflammation can contribute to chronic inflammatory disease.

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How is immunity linked to the rest of the body?

Nervous and endocrine systems help regulate immunity; many tissue and blood cells participate.

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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.

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What are the three overarching functions of blood?

Transport, regulation, and protection.

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What are the two main components of whole blood?

Plasma and formed elements.

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About what fraction of blood is plasma in the lecture diagram?

Approximately 55%.

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About what fraction of blood is formed elements in the lecture diagram?

Approximately 45%.

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What is the most abundant component of plasma?

Water, about 91% by weight in the lecture diagram.

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Which plasma proteins are shown in the lecture diagram?

Albumins, globulins, fibrinogen, and prothrombin.

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What do erythrocytes primarily do?

Transport oxygen and help transport carbon dioxide and buffer blood pH.

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What do leukocytes primarily do?

Defend against infection and other threats.

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What do platelets primarily do?

Support hemostasis and formation of a temporary platelet plug.

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What is the typical shape of a red blood cell?

Biconcave disc.

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Why is the biconcave shape of RBCs useful?

It provides surface area and flexibility for gas exchange and passage through capillaries.

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Do mature human RBCs have nuclei?

No; mature circulating erythrocytes lack nuclei.

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What is the approximate lifespan of an RBC?

About 120 days.

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What enzyme in RBCs speeds CO2 conversion to carbonic acid?

Carbonic anhydrase.

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What reaction does carbonic anhydrase catalyze?

CO2 plus H2O reversibly forms H2CO3, supporting bicarbonate-based CO2 transport.

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What is erythropoiesis?

The process of producing red blood cells.

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Where does RBC formation begin?

Red bone marrow from hematopoietic stem cells.

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What stimulates erythropoietin-mediated RBC production?

Reduced tissue oxygenation.

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What is the homeostatic goal of erythropoietin?

Increase RBC production when oxygen delivery is inadequate.

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What is hemoglobin made of?

Four globin chains, each associated with a heme group.

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How many oxygen molecules can one hemoglobin bind?

Up to four O2 molecules.

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What is anemia in the lecture?

A reduction in the number or volume of functional RBCs per unit of whole blood.

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What is hematocrit?

The fraction of whole blood volume occupied by red blood cells after centrifugation.

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What is the buffy coat?

The thin layer containing leukocytes and platelets between plasma and RBCs after centrifugation.

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What is leukopenia?

An abnormally low white blood cell count.

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What is leukocytosis?

An increased white blood cell count that may occur with infection, stress, or other conditions.

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Name the three granulocyte categories in the lecture.

Neutrophils, eosinophils, and basophils.

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Name the two agranulocyte categories in the lecture.

Lymphocytes and monocytes.

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What are platelets derived from?

Fragments of megakaryocytes.

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What is thrombocytopenia?

An abnormally low platelet count associated with increased bleeding risk.

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What happens when incompatible blood is transfused?

Antibodies can bind RBC antigens, causing agglutination and hemolysis.

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What is hemostasis?

The physiological process that limits blood loss after vessel injury while keeping blood fluid elsewhere.

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What is the overall sequence of hemostasis shown in the lecture?

Vessel injury, primary hemostasis, secondary hemostasis, stable clot, then fibrinolysis.

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What is the initial vascular response to vessel injury?

Transient vasoconstriction or vascular spasm to reduce blood loss.

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What causes vascular spasm according to the lecture?

Nervous reflexes, local humoral factors, and local myogenic responses.

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What is primary hemostasis?

Formation of a temporary platelet plug by platelet adhesion, activation, and aggregation.

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What is secondary hemostasis?

Coagulation-factor reactions that generate thrombin and fibrin to reinforce the platelet plug.

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What is exposed after endothelial injury that promotes platelet adhesion?

Subendothelial collagen and related structures.

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What is von Willebrand factor's role in platelet adhesion?

vWF bridges exposed collagen and platelet GPIb receptors.

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Which platelet receptor binds vWF during adhesion?

GPIb.

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What happens during platelet activation?

Adherent platelets change shape and release mediators such as ADP and thromboxane A2 to recruit more platelets.

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What do ADP and thromboxane A2 promote?

Additional platelet activation and aggregation.

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Which platelet receptor binds fibrinogen for aggregation?

GPIIb/IIIa.

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How does fibrinogen help platelet aggregation?

Fibrinogen bridges GPIIb/IIIa receptors on neighboring activated platelets.

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What is the sequence of primary platelet events?

Adhesion, activation, and aggregation.

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How do primary and secondary hemostasis cooperate?

Platelets form the initial plug, while thrombin-generated fibrin stabilizes it.

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What is the role of vWF beyond platelet adhesion?

It helps protect and carry coagulation factor VIII.

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Which pathway begins with tissue factor exposure after injury?

Extrinsic pathway.

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Which coagulation factor is associated with tissue factor in the extrinsic pathway?

Factor VII, which becomes VIIa.