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48 Cards in this Set
- Front
- Back
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Innate Immunity can be described as...
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Defenses that are present at birth
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Which of the following is not a part of the bodies first line of defense?
A. Skin B. Mucous membranes C. Saliva D. Fever |
Fever
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The so called ciliary escalator functions by
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Moving microbes towards the throat
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The pH of skin is...
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3-5
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Which of the following bacteria neutralizes stomach acid, allowing the bacterium to grow in the stomach
A. Clostridium botulinum B. Streptococcus mutans C. Lactobacillus pyogenes D. Helicobacter pylori |
Helicobacter pylori
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What is the most abundant leukocyte?
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Neutrophil
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Which leukocytes function to produce toxins against certain parasites?
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Eosinophils
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Which of the following is classified as an agranulocyte
A. Monocyte B. Neutrophil C. Eosinophil D. Basophil |
A. Monocyte
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What substance released by damaged cells intensifies the effects of inflammation?
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Prostoglandins
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During inflammation their is activation and increased concentration of a group of proteins in the blood called?
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Acute-phase proteins
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Phagocytes may be activated by components of bacteria such as lipid A or...
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Lipopolysaccharides
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Which macrophages are located in certain tissues and organs of the body?
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Fixed macrophages
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Fixed macrophages that are found in the liver are called
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Kupffer's cells
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The indigestible material in the phagolysosome is called the...
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Residual body
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Which of the following organisms has the ability to escape from a phagosome before it fuses with a lysosome?
A. Shigella B. Chlamydia C. Plasmodium D. Leishmania |
A. Shigella
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Complement proteins are labeled...
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1-9
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Interferons are produced by certain animal cells after being stimulated by...
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Viruses
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How many principal types of interferons do humans have?
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3
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Antimicrobial peptides may be one of the most important components of...
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Innate Immunity
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Some bacteria evade the complement system by means of their...
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capsule
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Which of the following is NOT a physical form of defense for the respiratory & gastrointestinal tracts?
A. Mucus B. Cilia C. Hairs D. Epidermis |
D. Epidermis
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Which chemical factor digests peptidoglycan in perspiration, tears, and saliva?
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Lysozome
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What inhibits cell wall synthesis, forms pores in the plasma membrane, and destroys DNA & RNA in microbes?
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Antimicrobial peptides
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What process intensifies the effects of interferons?
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Fever
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What do activated fixed macrophages secrete to bring about vasodilation, increased permeability & clot formation?
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Cytokines
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The high temperature in a fever increases the production of
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Transferrins
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All of the following are effector mechanisms of antibody-mediated disease EXCEPT:
A. Opsonization and phagocytosis of cells B. Fas-dependent apoptosis of cells C. Complement- and Fc receptor–mediated inflammation and tissue injury D. Antibody stimulation of cell surface receptors in the absence of the physiologic ligands E. FcεR crosslinking |
B. Fas-dependent apoptosis is a regulatory mechanism in T cell–mediated responses and may be involved in T cell–mediated damage to other cells, but the Fas pathway is not stimulated by antibodies. Antibody-mediated (types I to III) hypersensitivity diseases involve four main effector mechanisms: (1) IgE coats mast cells and links the presence of allergens with mast cell activation and release of inflammatory mediators; (2) antibody-mediated opsonization of cells and activation of complement promotes phagocytosis of cells through phagocyte Fc or C3 receptors; (3) antibody binding to tissues can promote recruitment of leukocytes via binding to Fc receptors on leukocytes or by activation of complement with release of chemotactic byproducts; and (4) autoantibodies specific for cell surface receptors either stimulate receptor activity in the absence of the physiologic ligand or inhibit binding of physiologic ligands to their receptors.
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Which type of hypersensitivity disease is caused by deposition of antigen-antibody complexes in blood vessel walls?
A. Type I B. Type II C. Type III D. Type IV E. Type V |
C. Hypersensitivity diseases are often categorized by numerical designation. Type III is immune complex disease. Type I is immediate hypersensitivity (allergic) disease. Type II is disease caused by antibodies binding to antigens in tissues. Type IV is T cell–mediated disease. There is no type V hypersensitivity.
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Which of the following statements about immune complex–mediated diseases is NOT true?
A. Immune complexes may contain antibodies bound to either self or foreign antigens. B. Immune complex–mediated diseases generally show systemic manifestations. C. Pathologic features of immune complex diseases are determined by the cellular source of the antigen. D. Small complexes are deposited in vessels more than large complexes, which are usually efficiently phagocytosed. E. Complexes containing cationic antigens are more likely to produce severe, long-lasting injury by depositing in blood vessels and renal glomeruli. |
ANS: C. A hallmark of immune complex–mediated disease is that pathologic features reflect the site of immune complex deposition and are not determined by the cellular source of the antigen. As such, immune complex–mediated diseases tend to be systemic, with little or no specificity for particular tissues. Immune complexes that cause disease may be composed of either self antigens or foreign antigens with bound antibodies. These complexes are produced during normal immune responses, but they cause disease only when they are produced in excessive amounts or are not efficiently cleared so that they become deposited in tissues. Small complexes are often not phagocytosed and tend to be deposited in vessels more readily than large complexes, which are usually cleared by phagocytes. Complexes containing cationic antigens bind tightly to negatively charged components of basement membranes of blood vessels and kidney glomeruli, typically producing long-lasting injury.
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In which of the following disorders is the underlying pathogenic mechanism NOT due to antibody-mediated damage to cells or tissues?
A. Pernicious anemia B. Autoimmune hemolytic anemia C. Pemphigus vulgaris D. Acute rheumatic fever E. Hyperacute allograft rejection |
ANS: A. Pernicious anemia is caused by neutralizing autoantibodies specific for intrinsic factor, which is a secreted protein required for absorption of vitamin B12 in the gastrointestinal tract. The lack of vitamin B12 absorption leads to decreased erythropoiesis, with subsequent anemia. Autoimmune hemolytic anemia is caused by opsonizing antibodies specific for erythrocyte membrane antigens, leading to their destruction by phagocytes. Pemphigus vulgaris occurs when autoantibodies specific for epidermal cell intracellular junctions cause inflammatory disruption of the skin, leading to formation of skin vesicles. Acute rheumatic fever is caused by antistreptococcal cell wall antibodies that cross-react with myocardial antigens, leading to inflammation and damage to myocardium. Hyperacute allograft rejection is caused by antibodies specific for alloantigens on graft endothelial cells, leading to blood vessel wall damage and thrombosis.
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Which of the following is NOT associated with increased relative risk of developing systemic lupus erythematosus?
A. Female gender B. Deficiency in complement protein C2 C. African-American ethnicity D. Presence of HLA-DR3 E. Defect in B cell maturation |
E. Systemic lupus erythematosus (SLE) is a chronic, remitting and relapsing, multisystem disease that affects predominantly women, with an incidence of 1 in 700 in women between the ages of 20 and 60 years. Incidence increases to about 1 in 250 in African-American women. The female-to-male ratio is 10:1. Deficiencies of classical complement proteins, especially C2 or C4, are seen in about 10% of patients with SLE; abnormal complement levels may result in defective clearance of immune complexes.
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A 5-year-old girl is taken to the emergency department with lethargy, confusion, vomiting, abdominal pain, and flushed skin that is warm to the touch. Respirations are fast and shallow (Kussmaul) and emanate a strong, fruity odor. The mother notes that the child has been excessively thirsty over the past week and that she began wetting her bed during naps. Urine dipstick testing reveals markedly elevated levels of glucose and ketones.
A. Type I hypersensitivity B. Type II hypersensitivity C. Type III hypersensitivity D. Type IV hypersensitivity |
ANS: D. This patient is in diabetic ketoacidosis, a serious complication of her previously undiagnosed insulin-dependent diabetes mellitus (type 1). Her insulin deficiency results from destruction of the insulin-producing beta cells of the islets of Langerhans in the pancreas. Several mechanisms may contribute to beta cell destruction. Prominent among these mechanisms are type IV (delayed-type) hypersensitivity reactions mediated by CD4+ TH1 cells reactive with islet antigens, and cytotoxic T-lymphocyte (CTL)-mediated lysis of islet cells.
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A 29-year-old woman gives birth to an infant who is lethargic, jaundiced, and severely anemic and has an enlarged liver and spleen. The mother is RhD negative and the father is homozygous RhD positive. This is their second child.
A. Type I hypersensitivity B. Type II hypersensitivity C. Type III hypersensitivity D. Type IV hypersensitivity |
ANS: B. This condition, called erythroblastosis fetalis, is a severe form of hemolytic disease of the newborn that occurs when an Rh-negative mother gives birth to an infant who is Rh positive (since the father is homozygous Rh positive). In this disease, the mother produces IgG antibodies against Rh-positive cells to which she has been previously exposed (i.e., during the delivery of her first Rh-positive child). Because the mother’s immune system recognizes Rh antigen as “foreign,” she produced large amounts of anti-Rh antibody when she encountered the antigen during the second pregnancy. This antibody crossed the placenta and mediated cellular injury in the second infant. Therefore, this is an example of type II hypersensitivity. Note that the most commonly involved antigen in erythroblastosis fetalis is RhD.
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A 23-year-old medical student is taken to the emergency department because of diffuse facial erythema (redness), tightness of the chest, and difficulty breathing. He reports that the symptoms began shortly after he ate a shellfish dinner at a nearby Thai restaurant. On physical examination, he appears to be in acute distress with elevated heart rate and respiratory rate and a dangerously low blood pressure. He is treated with epinephrine.
A. Type I hypersensitivity B. Type II hypersensitivity C. Type III hypersensitivity D. Type IV hypersensitivity |
ANS: A. This young man is in anaphylactic shock, secondary to systemic exposure to shellfish antigens, to which he produced IgE antibodies when he was previously exposed. This is a classic example of type I (immediate) hypersensitivity.
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Innate immunity mechanism for preventing viral infection
A. Type I interferons (IFN-α, IFN-β) B. CD8+ cytolytic T lymphocyte C. Antibody D. Natural killer cell |
ANS: A. One of the key innate immunity responses that can prevent viral infection is the production of type I interferons (IFNs), which are secreted by various cell types in response to double-stranded RNA interacting with Toll-like receptors. Type I IFNs induce an antiviral state in cells, which makes them resistant to host viral replication.
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Adaptive immunity mechanism for eradicating established viral infection
A. Type I interferons (IFN-α, IFN-β) B. CD8+ cytolytic T lymphocyte C. Antibody D. Natural killer cell |
ANS: B. Once viruses have infected cells, they produce cytoplasmic proteins that are processed and presented by the class I MHC pathway. CD8+ cytotoxic T lymphocytes recognize viral peptide-class I MHC complexes on the surface of infected cells and kill these cells. The killing mechanism leads to apoptosis, which ensures degradation of viral DNA as well as host cell DNA.
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Innate immunity mechanism for eradicating established viral infection
A. Type I interferons (IFN-α, IFN-β) B. CD8+ cytolytic T lymphocyte C. Antibody D. Natural killer cell |
ANS: D. Natural killer (NK) cells are innate immunity effector cells that can kill infected cells by mechanisms similar to cytotoxic T lymphocytes (CTLs). However, they are activated by different receptors than are CTLs, and they are inhibited by receptors that bind class I MHC on other cells. Viruses have the ability to evade detection by CTLs by inhibiting class I MHC expression on their host cell surfaces. When this occurs, NK cells may provide a backup defense mechanism, since they are activated by host cells that lack normal class I MHC expression.
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Adaptive immunity mechanism for preventing a viral infection
A. Type I interferons (IFN-α, IFN-β) B. CD8+ cytolytic T lymphocyte C. Antibody D. Natural killer cell |
ANS: C. Antibodies can neutralize viruses before they infect cells. Immunity imparted by many antiviral vaccines is due to antibodies.
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Good induction of mucosal immunity but risk of developing a viral disease, especially in immunocompromised hosts
A. Live attenuated or killed bacteria B. Live attenuated oral virus C. Synthetic viral subunit vaccines D. Conjugate vaccines E. Recombinant viral vectors F. DNA vaccines G. Purified subunit vaccines |
ANS: B. Live attenuated viral vaccines infect recipient cells, and viral proteins are processed and presented to T cells. This method of vaccination induces good T cell–dependent antibody responses. Attenuation makes risk of serious disease from the vaccine very low. Live attenuated oral poliovirus vaccines, which induced good IgA responses in the gastrointestinal tract, are no longer used routinely in the United States because of low but definable risk of vaccine-associated cases of paralytic polio.
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Induction of a T cell–dependent antibody response to polysaccharides, such as Haemophilus influenzae B and pneumococcal capsular polysaccharides
A. Live attenuated or killed bacteria B. Live attenuated oral virus C. Synthetic viral subunit vaccines D. Conjugate vaccines E. Recombinant viral vectors F. DNA vaccines G. Purified subunit vaccines |
ANS: D. Conjugate vaccines are composed of bacterial capsular polysaccharides covalently coupled to proteins. This hapten-carrier arrangement promotes T cell–dependent responses to the polysaccharides, which is required for protective IgG memory responses. Polysaccharides alone do not activate T cells and therefore do not induce isotype switching or memory cell generation.
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Composed of viral proteins synthesized from recombinant viral genes
A. Live attenuated or killed bacteria B. Live attenuated oral virus C. Synthetic viral subunit vaccines D. Conjugate vaccines E. Recombinant viral vectors F. DNA vaccines G. Purified subunit vaccines |
ANS: C. Synthetic subunit viral vaccines are composed of viral proteins synthesized from recombinant genes. The hepatitis B virus vaccine, now in widespread use, was the first synthetic viral subunit vaccine to be developed and contains the recombinant hepatitis B surface antigen (HBsAg).
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Composed of antigens purified from microbes or inactivated toxins, such as the tetanus toxoid vaccine
A. Live attenuated or killed bacteria B. Live attenuated oral virus C. Synthetic viral subunit vaccines D. Conjugate vaccines E. Recombinant viral vectors F. DNA vaccines G. Purified subunit vaccines |
ANS: G. The most commonly used purified subunit vaccines are the diphtheria and tetanus toxoid vaccines, which induce protective antibody responses against toxins produced by the bacteria.
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Composed of a recombinant nonpathogenic virus carrying genes of a pathogenic virus, such as HIV
A. Live attenuated or killed bacteria B. Live attenuated oral virus C. Synthetic viral subunit vaccines D. Conjugate vaccines E. Recombinant viral vectors F. DNA vaccines G. Purified subunit vaccines |
ANS: E. Genes encoding immunodominant epitopes of a pathogenic virus can be cloned into the genome of nonpathogenic viruses, and the resulting recombinant virus can be used as a vaccine against the pathogenic virus. This is one of the approaches under development for HIV (human immunodeficiency virus) vectors, and trials of canarypox virus containing SIV (simian immunodeficiency virus) genes have been used in primates with some success.
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A common strategy by which microbes survive their host’s immune responses involves changing the structures of the molecules they produce so that they are no longer recognized by the host’s immune system. This strategy, called antigenic variation, is most likely to allow evasion of which type of immune recognition?
A. Toll-like receptor–dependent recognition of microbes by cells of the innate immune system B. Mannose receptor–dependent recognition of microbes by cells of the innate immune system C. Antibody recognition of microbial cell surface molecules D. Natural killer cell inhibitory receptor recognition of class I major histocompatibility complex (MHC) molecules on infected cells E. T cell receptor recognition of microbial cell wall lipid antigens |
ANS: C. Antigenic variation allows microbes to evade adaptive immune recognition, usually by antibodies, but also by T cells. Antigenic variation usually involves mutations or recombination events in microbial genes encoding cell surface proteins or encoding enzymes involved in synthesis of cell surface sugars. The result changes microbial surface antigens. This is an effective strategy, because many of the microbial antigenic structures that the adaptive immune system recognizes, are not essential for survival or virulence of the microbe. In contrast, most structures recognized by receptors of the innate immune system (e.g., Toll-like receptor and scavenger receptor ligands) are essential for microbial survival and, as such, cannot undergo antigenic variation. Although some viruses may block class I major histocompatibility complex (MHC) expression by infected cells, this renders the cells more susceptible to natural killer cell–mediated killing and is not antigenic variation by the virus. Only a small subset of T cells recognizes lipid antigens, usually in association with CD1 molecules. There is no evidence for antigenic variation of the lipid antigens recognized by these T cells.
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1) A commensal bacterium
A) Does not receive any benefit from its host. B) Is beneficial to its host. C) May be an opportunistic pathogen. D) Does not infect its host. E) B and D only. |
Answer C
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2) Which of the following statements is true?
A) Symbiosis refers to different organisms living together. B) Members of a symbiotic relationship cannot live without each other. C) A parasite is not in symbiosis with its host. D) Symbiosis refers to different organisms living together and benefiting from each other. E) At least one member must benefit in a symbiotic relationship. |
A
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3) A nosocomial infection is
A) Always present but is inapparent at the time of hospitalization. B) Acquired during the course of hospitalization. C) Always caused by medical personnel. D) Only a result of surgery. E) Always caused by pathogenic bacteria. |
B
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4) The major significance of Koch's work was that
A) Microorganisms are present in a diseased animal. B) Diseases can be transmitted from one animal to another. C) Microorganisms can be cultured. D) Microorganisms cause disease. E) Microorganisms are the result of disease. |
D
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